WEEK 1 - GAS EXCHANGE/ PERFUSION

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Define the concept of gas exchange and the scope of the concept.
Definition: The process by which oxygen is transported to cells and carbon dioxide is transported from cells

- “Gas exchange” is a spectrum between optimal gas exchange to impaired gas exchange
Scope: - The more gas exchange is impaired, the more compromised the body becomes d/t hypoxia
- Cessation of gas exchange → anoxia

Define the concept of perfusion and the scope of the concept.

Definition: The flow of blood through arteries and capillaries, to deliver nutrients and oxygen to cells.
- It requires enough cardiac output to pump blood through blood vessels.

- Ranges from optimal perfusion to no perfusion

Scope: - Disorders that lead to changes in perfusion:
- Acute conditions (MI, stroke, shock)
- Chronic conditions (HTN, heart failure, sickle cell, hemophilia)

Compare the pathophysiological mechanisms that result in hypoxemic and hypercapnic respiratory failure.
Hypoxemic Respiratory Failure [oxygenation failure]

Definition: PaO2 ≤ 60mmHg when the pt is receiving inspired oxygen at a fractional concentration (FiO2) of ≥ 60%
- In other words, the pt's O2 level in their blood is 60mmHg or lower, even though they are breathing air with at least 60% O2

Primary Problem:
- Inadequate O2 transfer between alveoli and capillaries

Why is this considered hypoxemic respiratory failure?

- The PaO2 level indicates inadequate O2 sat of Hgb
- This PaO2 level exists despite the administration of supplemental O2 at 60% (which is 3x more than that of room air (21%))

Disorders that can cause hypoxemic respiratory failure:

- Pneumonia, pulmonary edema, pulmonary emboli
- Alveolar injury r/t inhalation of toxic gases
- Ventilator-induced lung injury, low cardiac output
 4 physiological mechanisms that cause hypoxemic respiratory failure:

- Normally, the amount of ventilation (V: air) should be equal to the amount of perfusion (Q: blood) in all parts of the lung
[VQ ratio is 1:1]
- So “VQ ratio” = the amount of air reaching the alveoli, compared to the amount of blood reaching the alveoli
A mismatch between - In a “VQ mismatch,” there may be more ventilation than perfusion or the other way around.
ventilation and perfusion (VQ - High VQ ratio: more ventilation compared to perfusion
mismatch) - Low VQ ratio: less ventilation compared to perfusion
- VQ mismatch is common in conditions where:
- There are ↑ secretions in the airways (e.g. COPD) or in the alveoli (e.g. pneumonia)
- Less air would reach the alveoli d/t all the secretions
- When bronchospasm is present (e.g. asthma)
- When there is alveolar collapse (e.g. atelectasis)
- Pain
- Each of these results in: ↑ metabolic demands, ↑ ventilatory demands, limited alveolar

- Definition: a situation where blood exits the heart without gas exchange occurring
- This would be caused by extreme VQ mismatch (low VQ since the blood is still passing through the heart, to
the lungs. But since there’s less air reaching the alveoli, there’s barely any gas exchange occurring.
Shunting - Two types of shunts:
- Anatomical shunt - where blood passes through an anatomical channel in the heart, bypassing the lungs
(e.g. ventricular septal defect)
- Intrapulmonary shunts - where blood flows through the pulmonary capillaries without participating in gas
exchange (occurs when alveoli fill with fluid)
- For this, O2 therapy is not enough because:
- The blood will pass from the right side to the left side of the heart without passing the lungs (anatomical shunt)
- Or, the alveoli will be filled with fluid, which will prevent gas exchange anyways (intrapulmonary shunt)

- Definition: ↓ in gas exchange across the alveolar-capillary membrane d/t processes that thicken or destroy the
Diffusion Limitation membrane
- Severe emphysema or recurrent pulmonary emboli can worsen diffusion limitation
- Pulmonary fibrosis, interstitial lung disease, ARDS thicken the alveolar-capillary membrane → slow gas transport
- Diffusion limitation causes more hypoxemia during exercise because during that time, blood travels through the lungs
much faster, but gas transport is still very slow → ↓ gas exchange

Hypoventilation - Definition: ↓ in ventilation → ↑ PaCO2 and ↓ PaO2

- Can be caused by restrictive lung disease, CNS disease, chest wall dysfunction, or neuromuscular disease
- Can cause both, hypoxemia AND hypercapnic respiratory failure
 Hypercapnic Respiratory Failure [ventilatory failure]

Definition: PaCO2 ≥ normal (45mmHg) + acidemia (arterial pH < 7.35).

Primary Problem: Insufficient CO2 removal

- There is an imbalance between ventilatory supply and ventilatory demand
- Ventilatory supply: maximum ventilation (gas flowing into and out of the lungs) that a person can handle without experiencing respiratory muscle
fatigue
- Ventilatory demand: the amount of ventilation needed to keep the PaCO2 levels normal
- NORMALLY: ventilatory supply > ventilatory demand
- But with lung diseases: ventilatory demand > ventilatory supply

Why is this considered hypercapnic respiratory failure?

- The PaCO2 is higher than normal
- There is evidence of the body’s inability to compensate for this increase (a.k.a. acidemia)
- The pH is at a level where a further ↓ can lead to severe acid-base imbalance

Disorders that can cause hypercapnic respiratory failure:

- Drug overdose with CNS depressants
- Neuromuscular diseases
- Trauma or diseases involving the spinal cord and its role in lung ventilation

4 categories of disorders that cause hypercapnic respiratory failure:

Abnormalities of the airways and - Patients with asthma, emphysema, chronic bronchitis, and cystic fibrosis are at high risk for hypercapnic
alveoli respiratory failure d/t airflow obstructions and air-trapping

Abnormalities of the CNS - Overdosing on opioids/CNS depressants → ↓ CO2 reactivity in brainstem → ↑ arterial CO2 levels
- Brainstem infarction or severe head injury → abnormal function of the respiratory centre in the medulla
- This will ↑ risk of hypercapnic resp failure because the medulla does NOT change RR to accommodate for
changes in the PaCO2
- Significant CNS depression → pt will not be able to protect their own airway

Abnormalities of the chest wall - Flail chest → rib cage cannot expand
- Kyphoscoliosis → changes in spinal configuration → lung compression → abnormal change expansion
- Massive obesity → weight of chest and abdominal contents limit lung expansion

Neuromuscular conditions - Guillain-Barré, muscular dystrophy, myasthenia gravis, MS → weakened or paralyzed respiratory muscles →
unable to maintain normal PaCO2 levels → risk of respiratory failure
Differentiate between early and late clinical manifestations of acute respiratory failure.
Early Clinical Manifestations Late Clinical Manifestations

- Change in mental status - Cyanosis - doesn’t occur until hypoxemia is severe

- Restlessness, confusion, agitation, combative behaviour - Angina, dysrhythmias
- Tachycardia and mild HTN - Permanent brain damage
- d/t the heart trying to compensate for low O2 delivery - Edema
- Severe morning headache - hypercapnia occurred at night - Uremia
- Rapid shallow breaths - Impaired renal function
Describe the nursing and interprofessional management of a patient with hypoxemic or hypercapnic respiratory failure.
Respiratory Failure: Nursing & Interprofessional Management

Nursing Assessment:
Subjective Data Objective Data Lab Findings/ Diagnostic Tests

PMHx: General - ↑/↓ pH

- Chronic lung disease - Restlessness, agitation - ↑/↓ PaCO2
- Potential occupational exposures to lung Skin - ↓ PaO2
toxins - Pale, cool, clammy skin - ↑/↓ bicarbonate
- Smoking (pack - years) - Or warm, flushed skin - ↓ SaO2
Meds: - Peripheral and central cyanosis - ↓ tidal volume
- Use of O2 Respiratory - ↓ forced vital capacity
- Inhalers (bronchodilators) - Shallow, ↑ RR, progressing to ↓ RR - ↓ minute ventilation
- Home nebulization - Use of accessory muscles with evidence of - ↓ negative inspiratory force
- OTC medications retractions - Needs to be documented q1h
Surgeries or other treatments: Cardio when a pt in the ICU is on a
- Previous intubation & mechanical - Tachycardia ventilator
ventilation - Dysrhythmias - Altered serum electrolytes, Hgb, WBC, and
- Recent thoracic or abdominal surgery - Extra heart sounds (S3, S4) HCT
Symptoms: Neuro - Abnormal findings on chest radiograph
- Anorexia, bloatedness, heartburn; weight - Somnolence - Abnormal pulmonary artery and pulmonary
gain/loss - Confusion artery wedge pressures (PAWP)
- Anxiety, depression - Slurred speech
- Changes in sleep pattern - Restlessness
- Dyspnea at rest, or with activity - Seizures
- Wheezing or coughing (productive or - Soma
non-productive) - Asterixis (flapping tremor)
- Sputum (volume, colour, viscosity) - ↓ deep tendon reflexes
- Fatigue, dizziness; diaphoresis
- Headache, chest pain, tightness
- Palpitations, swollen feet

Diagnoses, Goals of Care, Prevention:

Nursing Diagnoses Planning (Goals of Care) Prevention

- Inadequate gas exchange - Restore baseline ABG values - Thorough physical assessment and Hx
- Inadequate airway clearance - Restore baseline breath sounds - Appropriate nursing interventions
- Inadequate breathing pattern - Restore baseline breathing patterns (coughing, deep breathing, incentive
- Restore ability to clear secretions spirometry, ambulation, etc.)
 Respiratory Failure - Interventions

Oxygen therapy
- Type of O2 therapy for a pt with acute respiratory failure should: (a) be tolerated by the pt, (b) maintain PaO2 at
55-60mmHg and SaO2 ≥ 90% at the loewst O2 concentration possible
- O2 therapy is risky for patients with chronic hypercapnia (e.g. people with COPD) because their medulla may not
respond to CO2 levels (since it seems normal to them). Instead, their bodies will respond to hypoxia
- So, when they get supplemental O2, their body will no longer be hypoxemic, and they won't have any stimulus
Respiratory Therapy to force them to breathe → respiratory arrest

Mobilization of Secretions
- Effective coughing, adequate hydration and humidification
- Chest physiotherapy, tracheal suctioning

Positive-Pressure Ventilation
- Can be provided invasively through ET or nasotracheal intubation
- Can also be provided non-invasively through nasal or face mask
- Best for pts with hypoxemic respiratory failure

Relief of bronchospasm:
- Bronchodilators (e.g. salbutamol)
- IV aminophylline for severe bronchospasms
- Give bronchodilator with O2-enriched gas mixture to alleviate arterial hypoxemia
- IV magnesium for severe asthma or asthma refractory to conventional treatment

Reduction of airway inflammation:

- Corticosteroids (e.g. solumedrol)
- Inhaled flovent is preferred because it comes with less systemic adverse effects

Medication Therapy Reduction of pulmonary congestion:

- Can be caused by ARDS or right- or left-sided HF → ↓ alveolar ventilation, hypoxemia
- IV diuretics (e.g. Lasix) and nitroglycerine - will ↓ pulmonary congestion r/t HF
- Calcium-channel blockers and ϐ-blockers​​if Afib is present → will ↓ HR and improve CO

Treatment of pulmonary infections:

- IV antibiotics (e.g. Vancomycin, ceftriaxone)
- Make sure to do CXR and sputum culture beforehand

Reduction of severe anxiety, pain, and agitation:

- Sedation and analgesia with benzodiazepines (e.g. lorazepam, midazolam) and opioids (e.g. morphine, fentanyl) → ↓
anxiety, agitation, pain → will provide adequate oxygenation/ventilation
- Monitor pt for cardiovascular and respiratory depression
 Treating the underlying cause
- Reverse the disease process that caused acute respiratory failure (this is common sense buddy)

Supportive Therapy Maintaining adequate cardiac output

- IV fluids and meds will help ↑ CO
- Monitor for clinical indicators of adequate CO and tissue perfusion

Maintaining adequate hemoglobin concentration

- Hgb concentration ≥ 6mmol/L = adequate O2 saturation of Hgb
- Monitor pt for blood loss, and receive transfusions of PRBCs is enough Hgb cannot be maintained

- Maintain protein and energy stores

- This is important because nutrition depletion causes loss of muscle mass, including respiratory muscles →
Nutritional Therapy prolonged recovery time
- Enteral or parenteral nutrition preferred for pt at risk for aspiration d/t respiratory failure
- High-carb diet is avoided in people who retain CO2 because carbs metabolize into CO2 → ↑ CO2 load

Explain how the pathophysiological mechanisms that result in acute respiratory distress syndrome are related to the clinical
manifestations of this syndrome.
Pathophysiology of ARDS

Neutrophils damage alveolar wall → ↑ capillary permeability → fluid/protein/cells enter interstitium & alveoli → ↓ gas exchange → alveolar cells degenerate,
surfactant inactivation → hyaline membrane formation → ↓ compliance, fibrosis

- Type II pneumocytes will proliferate during the first week so that they can repair any damages
- Unusual organization of interstitial cells and collagen deposition
- Rapid progression, with respiratory distress occurring 12–18 hours after the initiating event

Early events → interstitial edema

- Lungs become stiff and less compliant
- Not easily resolved
- Might be missed on chest x-rays, but eventually shows up
- Waxy film (hyaline membrane + necrotic debris) form within 2 days → ↓ compliance, lack of gas exchange
- Results in ground-glass opacification in x-rays

Late stage:
- No more hyaline formation
- Macrophages digest hyaline
- Can heal (reversible), or progress into fibrosis
- Fibrosis destroys alveoli, respiratory bronchioles, and interstitium → acute respiratory failure (death)
Describe the nursing and interprofessional management of a patient with acute respiratory distress syndrome. Identify complications that
may result from acute respiratory failure or acute respiratory distress syndrome and measures to prevent or reverse these complications.
Acute Respiratory Distress Syndrome (ARDS) - What is it?

- Sudden and progressive form of acute respiratory failure, where the alveolar-capillary membrane becomes damaged and more permeable by
intravascular fluid
- ↑ capillary permeability → alveoli become filled with fluid → severe dyspnea and hypoxemia refractory to supplemental O2

ARDS - Causes

Direct lung injury

- Common causes:
- Aspiration
- Viral or bacterial pneumonia

- Less common causes:

- Chest trauma (e.g. airbags blowing during an accident) - Near-drowning
- Embolism: fat, air, amniotic fluid - O2 toxicity
- Inhalation of toxins - Radiation pneumonitis

Indirect lung injury

- Common causes:
- Sepsis (especially gram-negative infection)
- Severe massive trauma

- Less common causes:

- Acute pancreatitis - Opioid overdose (e.g. heroin)
- Anaphylaxis - Non-pulmonary systemic disease
- Blood transfusions - Severe head injury
- Cardiopulmonary bypass - Shock
- DIC
 ARDS - Pathophysiology

Phase 1 - injury or exudative phase - occurs 1–7 days after lung injury
- Neutrophils attach to capillaries in the lungs → damage to vascular endothelium → ↑ capillary permeability → protein-rich fluid builds up in the
peribronchial and perivascular interstitial spaces (interstitial edema) → fluid will shift from the interstitial space, into the alveoli → since alveoli are filled
with fluid, gas exchange cannot occur → intrapulmonary shunts are developed so that blood can still pass through
- Damage to type I and II alveolar cells → surfactant dysfunction → alveolar collapse (atelectasis) → ↓ compliance, ↓ gas exchange, hypoxemia
- Hyaline membranes line alveolar walls → fibrosis, ↑ atelectasis, VQ mismatch, shunting, diffuse limitation
- Hypoxemia → ↑ RR, ↓ tidal volume → ↑ CO2, respiratory alkalosis, ↑ CO
- Late: ↑ atelectasis, pulmonary edema, ↑ pulmonary shunting → failed compensatory mechanisms → hypoventilation, ↓ CO, ↓ tissue perfusion
- Primary changes: alveolar edema, atelectasis

Phase 2 - reparative or proliferative phase - starts 1–2 weeks after lung injury
- ↑ Neutrophils, ↑ monocytes, ↑ lymphocytes, fibroblast proliferation
- Lungs become dense with lots of fibrous tissue
- Fibroblasts and inflammatory cells destroy pulmonary vasculature → ↑ pulmonary vascular resistance, ↑ pulmonary HTN
- Interstitial fibrosis → ↓ lung compliance
- Hypoxemia → thickened alveolar membrane → diffusion limitation, shunting

Phase 3 - fibrotic phase - occurs 2–3 weeks after lung injury

- Lungs are filled with sparsely collagenous and fibrous tissues
- Diffuse scarring and fibrosis → ↓ lung compliance, hypoxemia
- Pulmonary vascular destruction and fibrosis → pulmonary HTN

ARDS - Manifestations

- From time of injury to 48hrs post-injury:

- Dyspnea, tachypnea, cough, restlessness
- Scattered, fine crackles
- ABGs: mild hypoxemia and respiratory alkalosis r/t hyperventilation
- CXR: minimal, scattered infiltrates
- As ARDS progresses:
- ↑ work of breathing (WOB)
- Tachypnea, tachycardia
- Intercostal and suprasternal retractions
- Diaphoresis, pallor, cyanosis
- Changes in sensorium and mentation
- Chest auscultation: diffuse crackles and wheezing
- CXR: extensive, bilateral interstitial and alveolar infiltrates
- Hallmark features:
- Severe hypoxemia
- PaO2/FiO2 ratio < 200, even when FiO2 is ↑ by a mask, cannula, or ET tube
 ARDS - Diagnostics

CXR
- New bilateral interstitial and alveolar infiltrates

Predisposing Condition
- Identification of a predisposing condition for ARDS within 48hrs of manifestations

Pulmonary Artery Wedge Pressure (PAWP)

- ≤ 18mmHg, and no evidence of heart failure
- PAWP will NOT increase in ARDS
- It only increases when a condition is related to the heart. So measuring PAWP will rule out cardiac conditions

Refractory Hypoxemia
- PaO2 < 50mmHg, with an FiO2 > 40%, and PEEP > 5cm H2O
- PaO2/FiO2 ratio < 200

How to remember:
A - acute hypoxemia
R - ratio (PaO2/FiO2) < 200
D - diffuse bilateral infiltrates
S - swan ganz (pulmonary artery catheter) shows PAWP ≤ 18mmHg)

ARDS - Complications

Hospital-acquired pneumonia
- Risk factors: impaired host defences, contaminated medical equipment, invasive monitoring devices, aspiration of GI contents, prolonged mechanical
ventilation
- Prevention: infection control, elevate HOB 45° or more to prevent aspiration

Barotrauma
- Rupture of distended alveoli during mechanical ventilation → air will be found in places where it’s not usually found → pulmonary interstitial emphysema,
pneumothorax, subcutaneous emphysema, pneumoperitoneum, etc.
- Prevention: ventilate pt with smaller tidal volumes

Volutrauma
- Large tidal volumes are used to ventilate non-compliant lungs → alveolar fractures, movement of fluids and proteins into alveolar spaces
- Prevention: ventilate pt with smaller tidal volumes

Stress Ulcers
 - Prevention: correct predisposing condition (i.e. hypotension, shock, acidosis), give anti-ulcer agents (i.e. famotidine, omeprazole, etc.), enteral feeds

Renal failure
- Caused by ↓ renal perfusion d/t hypotension, hypoxemia, hypercapnia, or administration of nephrotoxic meds (e.g. antibiotics: aminoglycosides)

ARDS - Nursing & Interprofessional Management

Nursing Assessment & Diagnoses:

Subjective Data Objective Data Lab Findings/ Diagnostic Tests

PMHx: General - ↑/↓ pH

- Chronic lung disease - Restlessness, agitation - ↑/↓ PaCO2
- Potential occupational exposures to lung Skin - ↓ PaO2
toxins - Pale, cool, clammy skin - ↑/↓ bicarbonate
- Smoking (pack - years) - Or warm, flushed skin - ↓ SaO2
Meds: - Peripheral and central cyanosis - ↓ tidal volume
- Use of O2 Respiratory - ↓ forced vital capacity
- Inhalers (bronchodilators) - Shallow, ↑ RR, progressing to ↓ RR - ↓ minute ventilation
- Home nebulization - Use of accessory muscles with evidence of - ↓ negative inspiratory force
- OTC medications retractions - Needs to be documented q1h
Surgeries or other treatments: Cardio when a pt in the ICU is on a
- Previous intubation & mechanical - Tachycardia ventilator
ventilation - Dysrhythmias - Altered serum electrolytes, Hgb, WBC, and
- Recent thoracic or abdominal surgery - Extra heart sounds (S3, S4) HCT
Symptoms: Neuro - Abnormal findings on chest radiograph
- Anorexia, bloatedness, heartburn; weight - Somnolence - Abnormal pulmonary artery and pulmonary
gain/loss, ↓ appetite - Confusion artery wedge pressures (PAWP)
- Anxiety, depression - Slurred speech
- Changes in sleep pattern - Restlessness
- Dyspnea at rest, or with activity - Seizures
- Wheezing or coughing (productive or - Soma
non-productive) - Asterixis
- Sputum (volume, colour, viscosity) - ↓ deep tendon reflexes
- Fatigue, dizziness; diaphoresis
- Headache, chest pain, tightness
- Palpitations, swollen feet

Planning & Goals of Care:

- Pt’s PaO2 should be within normal limits for age & baseline values on room air
- The SaO2 should be > 90%
- The pt’s airway should be patent
 - On auscultation, lungs should sound clear

Respiratory therapy: in
- O2 administration - nasal cannula/nasal prongs (max 6L), face mask (max 50%), NRB (max 100%)
- Invasive ventilation - mechanical ventilation with PEEP
- Prone positioning - laying on your stomach → allows for better lung expansion
- High-frequency oscillation - rapid RR small TV
- Lateral rotation therapy - improve ventilation oxygenation and prevent pressure ulcers

Medical & supportive therapy:

- Diuretics (e.g. lasix, furosemide), short-acting bronchodilators, corticosteroids (for inflammation)
- Inotropic or vasopressor medications (dobutamine, dopamine) to bring up the BP
- Hemodynamic monitoring - arterial catheter (to monitor BP), pulmonary artery catheter (to monitor PAWP)
- Identification & treatment of the underlying cause
- IV fluid administration (fluid resuscitation is done early, and less fluids are given later on)
- Airway suctioning, chest physiotherapy, effective coughing

Describe the characteristics of the respiratory system of the newborn (Table 25-1)
Outline the signs of respiratory distress in the newborn.
Sign of respiratory Distress Why it Occurs / What is Indicates

Nasal flaring

Intercostal or subcostal retractions (indrawing)

Grunting with respirations

Seesaw of paradoxical breathing (exaggerated rise in abdomen during

respiration, while the chest falls)

RR < 30 or RR > 60 breaths/min

Suprasternal or subclavicular retractions with stridor or gasping Indicates upper airway obstruction

Apneic episodes Can be d/t rapid ↑ in body temperature, hypothermia, hypoglycemia, or sepsis

Tachypnea Can be d/t inadequate clearance of lung fluid

Can also indicate newborn respiratory distress syndrome (RDS)

Change in skin colour Acrocyanosis: bluish discoloration of hands & feet → NORMAL in newborn
7-10 days after birth
Central cyanosis: bluish discoloration of the lips and mucous membranes →
ABNORMAL (late sign of hypoxemia)
Discuss respiratory distress syndrome and approaches to treatment in the newborn.
- A lung disorder that usually affects preterm infants
What is it? - Primary RDS:
- Caused by surfactant deficiency (since preterm infant doesn’t have full lung maturity to make surfactant)

- Diagnosis made based on manifestations & radiographic findings

- Characteristics of RDS found on a radiograph:
- Diffuse granular pattern over both lung fields that closely resembles ground glass (represents alveolar
Diagnosis atelectasis)
- Dark streak, or bronchograms, within the ground-glass areas → represents dilated, air-filled bronchioles
- Low lung volumes

- Immediate establishment of adequate oxygenation and ventilation

- Supportive care and measures for any preterm infant:
- Maintain adequate ventilation & oxygenation
Treatments - Maintain acid-base balance
- Maintain an NTE (neutral thermal environment)
- Maintain adequate tissue perfusion and oxygenation
- Prevent hypotension
- Maintain adequate hydration and electrolyte status
- Surfactant replacement therapy
- Inhaled nitric oxide (iNO) - pulmonary vasodilation- prevents stunting
- Extracorporeal membrane oxygenation (ECMO) - add O2 remove CO2 from blood
Compare methods of oxygen therapy for the high-risk infant.
Nasal Cannula Continuous Distending Pressure
- Administers low-flow oxygenation - CPAP provides positive pressure during inspiration & expiration
- Infant can still be breastfed or bottle-fed - Given via nasal prongs, nasopharyngeal tube, or face mask
- Should regularly check the nasal prongs to make sure they’re still in - Monitor infant for nasal damage or skin breakdown
place, are patent, and don’t cause any skin irritation - Orogastric tube may be used to decompress stomach while using
CPAP

Mechanical Ventilation Intermittent Mandatory Ventilation

- Used if other methods of therapy don’t correct gas exchange - Allows the infant to breathe spontaneously at their own rate
- Used for severe hypoxemia or severe hypercapnia - Provides mechanical cycled respirations and pressure at regular preset
- Indications: apnea, meconium aspiration syndrome (MAS), RDS, intervals
congenital malformations - Given via ET tube or ventilator

Synchronized Intermittent Mandatory Ventilation (SIMV) Volume Guarantee Ventilation

- Mechanically delivered breaths are synchronized to the onset of - Delivers predetermined volume of gas using inspiratory pressure that
spontaneous patient’s breaths varies according to infant’s lung compliance
- Involves signal detection of onset of spontaneous respiration from - Usually given with SIMV
abdominal movement, thoracic impedance, and airway pressure or flow
changes

High Frequency Jet Ventilation High Frequency Oscillation

- Uses a separate, parallel, low-compliant circuit and injector port to - Applies high frequency, low-volume, sine-wave flow oscillations to the
deliver small pulses/jets of fresh gas, deep into the airway airway
 WEEK 2 - GAS EXCHANGE/ PERFUSION
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Circulatory changes at birth.

- Oxygenated blood (which also carries nutrition) from the placenta, enters the fetal system via the umbilical vein.
- Blood travels to the liver and splits into:
- Portal and hepatic circulation.
- Inferior vena cava (IVC) via the ductus venosus
- Oxygenated blood enters the right atrium (RA) of the heart through the IVC
- High pressure directs blood from the RA through the foramen ovale to the left atrium (LA)
- Oxygenated blood is then pumped to the head and upper extremities from the left atrium and ventricle.
- Blood from the head and upper extremities enters the RA from the superior vena cava (SVC).
- This blood goes to the right ventricle (RV) and is pumped through the pulmonary artery.
- Most blood is shunted to the descending aorta via the ductus arteriosus.
- Minimal blood flows to the nonfunctioning fetal lungs.
- Before birth: High pulmonary vascular resistance and low systemic resistance exist
- At birth, clamping the umbilical cord and lung expansion cause abrupt hemodynamic changes.
- First breath → lungs expand → pulmonary vasodilation
- Pulmonary pressures fall and systemic pressures rise as the placenta is removed.
- Foramen ovale closes as LA pressure exceeds RA pressure
- Ductus arteriosus starts closing d/t ↑ oxygen concentration

Describe the pathophysiology and clinical manifestations of the different types of cardiomyopathies. Discuss nursing care and
interprofessional management of patients with different types of cardiomyopathies.
Dilated CM : Causes

- Cardiotoxic agents - alcohol, cocaine, doxorubicin - Muscular dystrophy

- Genetics (autosomal dominant) or familiar - Myocarditis
- Hypertension - Pregnancy
- Ischemia (CAD) - Valve disease
- Metabolic disorders
 Dilated CM: Pathophysiology

- Diffuse inflammation + degeneration of myocardial fibres → (1)left ventricular dilation → cardiomegaly → contractile dysfunction
- Diffuse inflammation + degeneration of myocardial fibres → (2) impairment of systolic function, atrial enlargement, stasis of blood in the LV

Dilated CM: Manifestations

Manifestation Why it Occurs

Fatigue Caused by ↓ CO → ↓ O2 supplying tissues → ↓ energy and fatigue

Dyspnea at rest Impaired LV function → ↑ pressure in pulmonary circulation → fluid

accumulation in the lungs & difficulty breathing even without exertion

Paroxysmal nocturnal dyspnea Lying down redistributes fluid from the lower extremities to the lungs →
pulmonary congestion is exacerbated → sudden, severe SOB

Orthopnea Same as paroxysmal nocturnal dyspnea

Abdominal bloating Caused by fluid buildup

Irregular HR, heart murmurs, palpitations Enlarged & weakened heart can cause arrhythmias

Dry cough Pulmonary congestion will irritate the airways

N/V, anorexia Caused by congestion of GI tract

Pulmonary crackles Caused by fluid buildup in the lungs

Edema Caused by fluid leaking into tissues

Weak peripheral pulses Caused by ↓ CO → ↓ blood flow

Systemic Embolism Poor blood flow → stasis of blood → blood clots

Cardiomegaly (moderate to marked)

 Dilated CM: Diagnostics

Diagnostic Study What do you see on there?

Doppler echocardiography Distinguishes DCM from other structural abnormalities

Chest XR Shows cardiomegaly with signs of pulmonary venous HTN & pleural effusion

ECG Tachycardia, bradycardia, and dysrhythmias

Lab studies ↑ B-type Natriuretic Peptide (BNP) if HF is present

Cardiac Catheterization Confirms or rules out CAD

Multiple gated acquisition (MUGA) Determines ejection fraction

Dilated CM: Nursing and Interprofessional Management

- ↑ myocardial contractility & ↓ afterload to control HF

- For secondary diluted CM, treat the underlying cause
- Medications
- Nitrates (e.g. nitroglycerin) - to ↓ preload → ↓ blood returning to the heart → ↓ workload on the heart
- Loop diuretics (e.g. furosemide [Lasix]) - ↓ preload → ↓ blood returning to the heart → ↓ workload on the heart
- ACE inhibitors (e.g. captopril, enalapril, lisinopril) → ↓ afterload → ↓ resistance to eject blood out of the heart during systole
- ARBS (e.g. Candesartan) → ↓ afterload → ↓ resistance to eject blood out of the heart during systole
- Angiotensin-neprolysin inhibitor (ARNI) → ↓ afterload → ↓ resistance to eject blood out of the heart during systole
- β blockers (e.g. bisoprolol) → controls neurohormonal stimulation that occurs during HF
- Aldosterone antagonists (e.g. spironolactone) → control neurohormonal stimulation that occurs during HF
- Digoxin → treats atrial fibrillation
- Antidysrhythmia meds (e.g. Amiodarone) → treats other dysthymias
- Nutrition therapy & cardiac rehabilitation will also help alleviate symptoms of HF, and will help improve CO and QoL
- Non-pharmacological therapies:
- Cardiac Resynchronization Therapy sync heart contractions btw ventricles
- Ventricular Assist Device
- Heart transplant or destination therapy with permanent/implantable VAD
- Patient Education:
- Teach pt to avoid situations that impair ventricular filling (e.g. strenuous activity, dehydration, anything that will ↑ SVR)
- Family should know how to access emergency care, and should know how to do CPR
 Hypertrophic CM: Causes

- Aortic stenosis - Hypertension

- Genetics (autosomal dominant)

Hypertrophic CM: Pathophysiology

Asymmetrical left ventricular hypertrophy without ventricular dilation

Interventricular septum becomes enlarged → obstructs blood flow LV → 4 main characteristics:
1. Massive left ventricular hypertrophy
2. Rapid, forceful contraction of the LV
3. Impaired relaxation (diastolic dysfunction)
4. Obstruction of left ventricular outflow tract [LVOT]
Leads to the ventricle becoming non-compliant & unable to relax → impaired ventricular filling → ↓ CO (especially during exertion)

Hypertrophic CM: Manifestations

Manifestation Why it Occurs

May be asymptomatic

Exertional dyspnea Caused by ↑ left ventricular diastolic pressure

Fatigue Caused by ↓ CO and exercise-induced flow obstruction

Angina Caused by ↑ left ventricular muscle mass, or compression of coronary arteries

Syncope (often during exertion) Caused by ↑ obstruction to aortic outflow during ↑ activity → ↓ CO &
cerebrovascular circulation. Also caused dysrhythmias

Palpitations Enlarged & weakened heart can cause arrhythmias

Cardiomegaly (mild to moderate)

 Hypertrophic CM: Diagnostics

Diagnostic Study What do you see on there?

Physical exam - palpation Forced apical impulse that may be displaced laterally

Physical exam - auscultation S4 and a systolic ejection murmur between the apex and sternal border

ECG ST-T-wave abnormalities, prominent Q waves, left-axis deviation, ventricular

and atrial dysrhythmias

Echocardiogram Left ventricular hypertrophy, wall motion abnormalities & diastolic dysfunction

Cardiac catheterization Confirms hypertrophic CM

Hypertrophic CM: Nursing and Interprofessional Management

Goals of interventions:
- Improve ventricular filling by ↓ ventricular contractility
- Relieving LVOT obstruction
Meds:
- β blockers (e.g. metoprolol) → ↓ ventricular contractility
- Calcium-channel blockers (e.g. amlodipine, verapamil) → ↓ ventricular contractility
- Antidysrhythmics (e.g. amiodarone) → treats dysrhythmias
- **Vasodilators (e.g. nitroglycerin) might worsen chest pain d/t ↓ venous return → obstructed blood flow from the heart
Non-pharm therapies:
- AV pacing if pt also has LVOT obstruction
- Surgery (ventriculomyotomy, myectomy) - recommended for those with severe symptoms with marked obstruction to aortic flow
- Alcohol-induced percutaneous transluminal septal myocardial ablasion (PTMSA)
- Avoid competitive sports, since it’ll ↑ SVR

Restrictive CM: Causes

- Amyloidosis - Post-radiation therapy

- Endomyocardial fibrosis - Sarcoidosis
- Neoplastic tumour
 Restrictive CM: Pathophysiology

Myocardial fibrosis, hypertrophy, infiltration → stiffening of ventricular wall + loss of ventricular compliance → too much rigidity of ventricular walls → ventricles
become resistant to filling → high diastolic filling pressure is needed in order to maintain CO

Restrictive CM: Manifestations

Manifestation Why it Occurs

Dyspnea The heart cannot ↑ CO by ↑ing HR, since this will compromise ventricular filling

Exercise intolerance The heart cannot ↑ CO by ↑ing HR, since this will compromise ventricular filling

Fatigue The heart cannot ↑ CO by ↑ing HR, since this will compromise ventricular filling

Angina ↓ CO → ↓ blood flow to the coronary arteries → ↓ O2 to the myocardium

Orthopnea

Syncope ↓ blood flow out of the heart → ↓ blood to the brain

Palpitations

Signs of HF: dyspnea, peripheral edema, ascites, hepatomegaly, JVD

Cardiomegaly (mild)
 Restrictive CM: Diagnostics

Diagnostic Study What do you see on there?

CXR May look normal, or show cardiomegaly from R & L atrial enlargement. May
also show pleural effusion in those progressing into HF.

ECG Mild tachycardia at rest, Atrial fibrillation, AV block

Echocardiogram Normal-sized LV with thickened wall, slightly dilated RV, dilated atria

Endmyocardial biopsy (EMB), CT scan, nuclear imaging

Restrictive CM: Nursing and Interprofessional Management

No specific treatment for restrictive CM exists

Goals of care:
- Improve diastolic filling
- Improve underlying disease process
Conventional therapy:
- Same treatment for HF and dysrhythmias
Patient Education:
- Teach pt to avoid situations that impair ventricular filling (e.g. strenuous activity, dehydration, anything that will ↑ SVR)

Demonstrate an understanding of hemodynamics, distinctive manifestations, and therapeutic management of congenital heart disease.
Describe the care for an infant or a child with a congenital heart defect and its surgical repair.
Congenital Heart Disease: Hemodynamics

- Normally, as blood is pumped through the heart, it does 2 things:

1. It flows from an area of high pressure to an area of low pressure
2. It takes the path of least resistance

- The pressure on the R side of the heart is lower than on the L side
- Pulmonary circulation has lesser resistance compared to systemic circulation

- If there is an abnormal connection between the heart chambers (e.g. septal defect), blood will go from an area of high pressure (L side) to an area of low
pressure (R side)
- This is called a “left-to-right shunt”
 Congenital Heart Disease: Manifestations

Classification system based on hemodynamic characteristics, to categorize CHD:

1. ↑ pulmonary blood flow
2. ↓ pulmonary blood flow
3. Obstruction to blood flow out of the heart
4. Mixed blood flow (saturated & desaturated blood mix in the heart or large arteries)

↑ Pulmonary blood flow - Manifestations ↓ Pulmonary blood flow - Manifestations

- Signs of HF - Hypoxemia
- E.g. Atrial septal defect (ASD) - Cyanosis
- E.g. Ventricular Septal Defect (VSD) - E.g. Tetralogy of Fallot (common defect)
- E.g. Patent ductus arteriosus (PDA) - should normally close after birth - E.g. Tricuspid atresia (common defect)
- E.g. Atrioventricular canal defect

Obstruction to blood flow out of the heart - Manifestations Mixed blood flow - Manifestations
- E.g. Coarctation of the aorta (narrowing of the aortic arch) - Cyanosis (severity depends on type and size of defect)
- E.g. Aortic stenosis - Cardiomegaly, heart failure (HF)
- E.g. Pulmonic stenosis (leads to hypoxemia if severe) - E.g. Transposition of the great arteries (TGA) → severe cyanosis
- Pressure load on the ventricle (↑ afterload), ↓ CO - E.g. Truncus arteriosus → severe HF
- Mild obstruction → asymptomatic - E.g. Hypoplastic left heart syndrome
- E.g. Total Anomalous Pulmonary Venous Connection

Tetralogy of Fallot Tricuspid Atresia Transposition of the Great Arteries

VSD, pulmonic stenosis, overriding aorta, and No tricuspid valve, so blood from RA → LA (via Aorta sends deoxygenated blood, pulmonary
hypertrophy of RV ASD) → LV → RV (via VSD) → pulmonary artery sends oxygenated blood
artery
 Truncus Arteriosus Total Anomalous Pulmonary Venous Hypoplastic Left Heart Syndrome
Connection (TAPVC)

One major arterial trunk, instead of a separate Blood from pulmonary vein → RA → LA (via LA → RA (via ASD) → RV → pulmonary artery
trunk for aorta and pulmonary artery ASD) → LV → aorta → ductus arteriosus → aorta

Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD) Patent Ductus Arteriosus (PDA)

Hole between both atria → blood moves from Hole between both ventricles → blood moves Ductus arteriosus stays open → blood moves
LA to RA from LV to RV from aorta to pulmonary artery
 Atrioventricular Canal Defect Coarctation of the Aorta Aortic Stenosis

Low ASD + high VSD → blood can mix Narrowing of the aorta → ↑ pressure towards Narrowing of aortic valve → hypertrophy of LV
between all 4 chambers the defect, low pressure past the defect

Pulmonic Stenosis

Narrowing of pulmonic valve → hypertrophy of

RV
** Decreased pulmonary blood flow, mixed blood flow, increased pulmonary blood flow, obstruction to blood flow**
Discuss the nurse’s role in helping the child and family cope with congenital heart disease.
Congenital Heart Disease: Nursing Care

Initial Reaction & Impact on Family:

- Shock, anxiety, and fear of child’s death.
- Need for time to grieve before understanding the defect.
- Immediate medical treatment and informed consent required
- Parents should be supported emotionally.
- Facilitate parent-newborn attachment through physical contact (holding, touching, looking)
Helping the Family Adjust Caring for the Child:
to the Disorder - Gradual teaching of care to a reliable person can ease parents' fears.
- Educate parents on the importance of discipline to prevent later issues
- Use behaviour modification techniques (e.g. concrete awards, social reinforcement)
Potential issues:
- Risk of over-dependency d/t parents’ fear that the child will die
- Nurses should teach parents about fostering independence and optimal development.
- Encourage social interaction with peers and self-paced activities.
Long-Term Family Crisis:
- Ongoing stress from physical care, financial costs, emotional strain, fear of death, and concern for the future
- Family will need to adjust their lifestyle even after the child’s condition is stabilized
- Support from other families with similar experiences can be beneficial.

Initial Explanation:
- Clear explanation based on the parents' level of understanding.
- Review basic heart structure and function.
- Use diagrams, pictures, or models to visualize the defect.
- Written information and glossary of terms are helpful
- Provide information on prognosis and treatment options.
Educating the Family - Assess and clarify understanding in subsequent encounters.
about the Disorder Internet and Support:
- Parents use the Internet and support groups for information.
- Caution parents about the accuracy of online information.
- Parents should discuss information they found online, with HCPs, especially the cardiologist.
Patient education - child”
- Tailor information to child’s developmental age.
- Preschoolers: Focus on experiences rather than physiological details.
- School-age children: Concrete explanation about their condition
- Pre-adolescents and adolescents: Detailed description to understand the defect.
- All ages: Encourage expression of feelings about the diagnosis.

Parental Role:
- Develop a supportive relationship with the healthcare team.
- Manage child's illness daily, monitor the illness, give meds, go to appointments, and communicate with caregivers.
 - Partnership based on mutual trust and respect is important
- Good communication among family, cardiologists, and primary care providers is essential.
- Recognize symptoms of cardiac conditions and signs of worsening status.
- Understand symptoms of HF and when to contact HCPs
- Keep an information sheet with the child's medical details for emergencies and other caregivers.
Therapeutic Management:
- Knowledge of surgery, procedures, medications, and lifestyle's role in health
Helping the Family Manage - Parents should know the importance of correct medication administration and storage
the Illness at Home - Have a discussion with the cardiologist about regular exercise and activity level
Nutrition:
- Importance of good nutrition for children with congenital heart disease (CHD).
- Breastfeeding support and high-calorie formulas for infants.
- Dietitian consultation for feeding challenges and providing high-nutrient food choices.
Immunization:
- Follow immunization guidelines, possibly modified around illness or surgery.
- RSV vaccine for certain infants and children during RSV season.
Developmental Concerns:
- Risk of developmental delays d/t various factors (genetics, preoperative, intraoperative, and postoperative conditions)
- Watch for learning disabilities or attention deficit disorders in early school years, especially after surgeries involving
cardiopulmonary bypass.
- Recent improvements in surgery techniques may enhance outcomes.

Preprocedure Preparation Goals:

- Reduce anxiety.
- Improve child's ability to assist with procedures.
- Enhance recovery.
- Develop trust with caregivers.
- Improve long-term emotional and behavioural adjustments after procedures.
Factors to Consider in Planning Preparation:
- Child's cognitive development.
- Previous hospital experiences.
Preparing the Child and - Child's temperament and coping style.
Family for Invasive - Timing of preparation.
Procedures - Involvement of parents.
Beneficial Preparation Strategies:
- Combine information-giving and coping skills training.
- Techniques include breathing exercises, distraction, guided imagery, or behavioural interventions.
Preoperative and Pre-catheterization Workups:
- Typically outpatient for elective procedures.
- Children admitted in the morning of the procedure.
Topics to Include in Preparation:
- Information on environment, equipment, and procedures.
- Sensory experiences in CCU or catheterization lab.
 - Coping strategies tailored to different age groups.
- Familiar objects for young children.
- Headphones and favourite music for older children.
- Simple coping techniques during painful procedures.
- Comforting aspects of the environment
Parental Involvement:
- Assuring child that parents will be present when child wakes up.
- Encourage parents to accompany child as far as possible to OR

- Observe VS
Providing Postoperative - Maintain respiratory status
Care - Monitor fluids
- Provide rest and progressive activity
- Provide comfort and emotional support

- Discharge planning for cardiac surgery should start during admission.

- Assess parents' adjustment to the child's health changes.
- Newborns may require additional screening tests and immunizations.
Planning for Discharge and - Provide verbal and written instructions on:
- Medication, nutrition, activity restrictions.
Home Care
- Subacute bacterial endocarditis, wound care.
- Signs of infection or complications.
- Long-term follow-up for growth and development.
- Consider referrals to community agencies for assistance.
- Provide clear instructions on when to seek medical care and how to contact healthcare providers.
- Arrange follow-up with cardiologist and primary care provider before discharge.
- Give parents a summary of the child's medical condition, medications, and HCPs for emergencies.
- Consider appropriate identification (e.g., MedicAlert) for children with specific medical needs.
- Surgical correction may not fully repair complex anomalies → repeat procedures may be needed
- Long-term prognosis can be uncertain, requiring ongoing medical follow-up and emotional support

Congenital Heart Disease: Therapeutic Management

*Same as HF*
(look below)
Outline a care plan for an infant or child with heart failure.
Digitalis glycosides (digoxin) → improve contractility → ↑ CO, ↓ heart size, ↓ venous pressure, relief of edema,
enhanced myocardial function
- Given PO or IV in divided doses over 24hrs, and then a maintenance dose is given BID
- Adverse effects: dysrhythmias
ACE inhibitors (e.g. enalapril, lisinopril) → blocks conversion of angiotensin I to angiotensin II → vasodilation → ↓
Improve cardiac function
SVR and PVR → ↓ BP and ↓ afterload → easier for heart to pump blood → enhanced myocardial function
(↑ contractility and ↓ afterload) - ACE inhibitors also ↓ aldosterone secretion → ↓ preload and ↓ fluid retention → ↓ risk for hypokalemia
- Adverse effects: hypotension, cough, renal dysfunction
ϐ-blockers​​(e.g. carvedilol) → blocks α and β receptors → ↓ HR, ↓ BP, vasodilation
- Adverse effects: dizziness, headache, hypotension
Cardiac Resynchronization Therapy (CRT) - already used for adults, and it is now starting to be used for pediatric
patients too

Removal accumulated fluid and - Diuretics (e.g. furosemide [Lasix], thiazides) → eliminate excess water and salt to prevent re-accumulation
sodium (↓ preload) - Fluid restriction → may be needed in acute stages of HF, but should be done carefully
- Sodium restriction → used less often

Minimize metabolic needs to help lessen workload on the heart by:

- Provide a neutral thermal environment → prevents cold stress in newborn
↓ Cardiac demands - Treat any existing infections
- ↓ the effort of
- breathing (place infant in semi-Fowler’s position)
- Use meds to sedate an irritable child
- Provide for rest and ↓ environmental stimuli

Improve tissue oxygenation and ↓ - Supplemental cool, humidified O2 → ↑ amount of O2 available during inspiration
O2 consumption - Everything that was already listed will also help with oxygenation
Describe the care for a child who has hypoxia.
- Nasal flaring is the first sign of respiratory failure
- Polycythemia
Manifestations - ↑ RBC → ↑ O2-carrying capacity of the blood
- Can lead to anemia if there isn’t enough iron available to form hemoglobin
- Leads to ↑ blood viscosity
- Clubbing >180
- Thickening and flattening of the tips of the finger and toes d/t chronic tissue hypoxemia + polycythemia
- Hypercyanotic spells - uncontrollable crying irritability hyperpnea cyanosis or pallor
- Leads to acute cyanosis and hyperpnea (fast, deep breathing) d/t right-to-left shunting
- Needs immediate assessment since it can lead to cerebral hypoxia

Hypoxia test:
Diagnostics - Place infant in 100% O2 environment, where blood parameters are monitored
- PaO2 ≥ 100mmHg → lung disease
- PaO2 < 100mmHg → cardiac disease

- IV prostaglandin E1 alprostadil → vasodilation and smooth muscle relaxation → ↑ dilation and patency of ductus
arteriosus
Therapeutic Management - Knee-chest position → ↓ venous return from the legs, ↑ SVR → more blood diverted into pulmonary artery
- SC or IV Morphine → ↓ infundibular spasm
- Hydration → will keep HCT and blood viscosity within normal limits and will ↓ risk of CVA IV fluids
- Monitor temperature - want to avoid bacteremia, which can lead to bacterial endocarditis
- Other techniques: Pulmonary hygiene, chest physiotherapy, administration of antibiotics, use of O2
 WEEK 3 - PERFUSION
[Link]
[Link]
Review the conduction system of the heart
Cardiac Cycle & Cardiac Conduction System

1: the SA node fires action potentials to the AV node and both atria. The SA
node fires 60-100x/min.

2: the AV node sends the signal down the AV bundle (Bundle of His). The AV
node fires 40-60x/min.

3: the AV bundle splits into the L and R bundle branches. The bundle branches
fire 20-40x/min.

4: Purkinje fibers send action potentials throughout the ventricles, to initiate

another action potential there. The purkinje fibers fire 20-40x/min.

1: the SA node fires an action potential. This happens during atrial

depolarization.

2: the AV node fires an action potential.

3: the signal passes through the AV bundles.

4: the signal passes through the L and R bundle branches.

5: the AV valves shut.

6: the signal passes through the purkinje fibers. This happens during ventricular
depolarization/ atrial repolarization. Note: during a heart attack, ventricular
depolarization appears downwards.

7: ventricular repolarization occurs.

8: the semilunar (SL) valves shut.

Explain nervous control of the heart.
NS Regulation of Heart:
- Originates in the cardiovascular center (CV) in medulla oblongata
- Receives input from sensory receptors and higher brain centers
- Directs SNS and PNS output to the heart

Anticipatory Increase in Heart Rate:

- Limbic system sends impulses to the CV center
- Proprioceptors send ↑ impulses at activity onset
- Other receptors (i.e. chemoreceptors and baroreceptors) also provide input

Sympathetic Stimulation:
- Sympathetic neurons extend from medulla to spinal cord
- Norepinephrine release speeds up SA and AV node firing
- ↑es contractility via enhanced Ca2+ entry.
- Maximal stimulation can increase HR to 200 bpm.

Parasympathetic Stimulation:
- Via right and left vagus nerves
- Releases acetylcholine → slows down HR via SA and AV node inhibition

Balancing Stimulation:
- At rest, PNS stimulation is dominant
- Resting HR is usually lower than SA node rate.
- Maximal PNS stimulation can slow HR to 20-30 bpm (or even momentarily stop it)

Explain how to calculate heart rate from an ECG.

Calculating HR from an ECG

Rule of 300: Rule of 1500:

Count the large squares between the 2 QRS complexes, and divide by 300 Count the small squares between the 2 QRS complexes, and divide by 1500
- 300 ÷ # of large squares - 1500 ÷ # of small squares
Identify the clinical characteristics and electrocardiographic (ECG) patterns of normal sinus rhythm, atrial fibrillation, sinus bradycardia,
sinus tachycardia, ventricular tachycardia, ventricular fibrillation.
ECG Patterns ECG Characteristics Clinical Associations

P wave: depolarization of the atria

- Passage of an electrical impulse
through the atria → atria contract
PR interval: the electrical impulse spread
through the atria, the AV node, the bundle of
Normal Sinus
His, and the Purkinje fibres
Rhythm QRS complex: depolarization of the ventricles
→ ventricles will contract
- Represents duration of depolarization
ST segment: the time between ventricular
depolarization and repolarization
T wave: repolarization of the ventricles
QT interval: total time for
depolarization/repolarization of ventricles

HR: < 60bpm - Seen in athletes, during sleep,

Sinus Rhythm: regular neurogenic shock, & ↑ ICP
Bradycardia Other characteristics: - Certain meds: ϐ-blockers​​, Ca2+
- PR interval is normal channel blockers
- QRS complex has normal shape and - Disease states: hypothyroidism, ↑
duration ICP, inferior wall MI

HR: > 100bpm - Seen in pain/injury, exercise, anxiety,

Rhythm: regular hpovolemia, hemorrhage,
Sinus Other characteristics: hypoglycemia
Tachycardia - PR interval is normal - Certain meds: caffeine, atropine,
- QRS complex has normal shape and E/NE, etc.
duration - Disease states: MI, HF, hyperthyroid

HR: atrial rate ≃ 300-650bpm, ventricular rate - Seen in thyrotoxicosis, caffeine use,
≃ 50-180bpm alcohol intoxication, electrolyte
Atrial Rhythm: irregular imbalance, stress, & cardiac surgery
Fibrillation Other characteristics: - Disease states: CAD, rheumatic
- P waves are replaced by chaotic, heart disease, cardiomyopathy, HTN,
fibrillatory waves HF & pericarditis
- Ventricular rhythm is irregular
- PR interval is not measurable
- QRS complex has normal shape and
duration
 HR: ventricular rate ≃ 150-250bpm - Can be seen in those without any
Rhythm: regular cardiac history
Monomorphic Other characteristics: - Disease states: MI, CAD, significant
Ventricular - QRS complexes are the same size, electrolyte imbalance,
shape, and duration cardiomyopathy, mitral valve prolapse,
Tachycardia
- However, QRS complex is long QT syndrome, digitalis toxicity, &
distorted, and duration is CNS disorders
longer than 0.12 seconds
- ST-T wave goes in the opposite
direction compared to the QRS
complex
- R-R interval can be regular or
irregular
- P wave is buried in QRS complex

HR: ventricular rate ≃ 150-250bpm

Rhythm: regular
Polymorphic Other characteristics:
Ventricular - QRS complexes gradually change
back and forth
Tachycardia
- Prolonged QT interval
(Torsades de - ST-T wave goes in the opposite
points) direction compared to the QRS
complex
- R-R interval can be regular or
irregular
- P wave is buried in QRS complex

HR: not measurable - Seen during cardiac pacing, cardiac

Rhythm: irregular and chaotic catheterization, fibrinolytic therapy,
Ventricular Other characteristics: hyperkalemia, hypoxemia, acidosis,
Fibrillation - P wave is not detectable accidental electric shock, & drug
- PR and QRS intervals are not toxicity
measurable - Disease states: acute MI, myocardial
ischemia, CAD, & cardiomyopathy
Describe the nursing and interprofessional management of patients with common dysrhythmias and ECG changes associated with ACS.
Dysrhythmias: Nursing & Interprofessional Management

Dysrhythmias Nursing & Interprofessional Management

- If bradycardia is d/t certain medications, the meds might need to be reduced or stopped
Sinus Bradycardia - If pt is symptomatic: administer atropine (anticholinergic)
- If atropine doesn’t work, pt may need:
- Pacemaker therapy, or
- Epinephrine or dopamine infusions

Treat underlying cause

Sinus Tachycardia - E.g. if pt is tachy d/t pain, treat the pain
If clinically stable:
- Vagal maneuvers can be used
Meds:
- ϐ-blockers​​(e.g. metoprolol), adenosine, calcium channel blockers (e.g. diltiazem)
- They will ↓ HR and ↓ myocardial O2 consumption
If clinically unstable:
- Synchronized cardioversion to restore regular heart rhythm

Goals of Treatment:
- ↓ ventricular response to <100/minute
- Prevent cerebral embolic events
Priority:
- Ventricular rate control
- Meds used: calcium channel blockers (e.g. diltiazem), β blockers (e.g. metoprolol)
Conversion:
- Used to convert Afib to normal sinus rhythm
Atrial Fibrillation - Considered for some patients (e.g. reduced exercise tolerance, contraindications to warfarin)
- Meds for conversion: procainamide, ibutilide (Corvert), amiodarone, vernakalant
- For unstable patients with LV dysfunction or HF: use amiodarone or direct current (DC) cardioversion
- If Afib lasts >48 hours, anticoagulation therapy with warfarin or NOAC (Xarelto) is given for 3–4 weeks before
cardioversion
- Anticoagulation continues for several weeks post-cardioversion to prevent stroke
- Transesophageal echocardiogram (TEE) may be used to rule out atrial clots
Long-term Management if cardioversion or medications don’t work:
- Long-term anticoagulation therapy
- Regular follow-up to assess need for long-term anti-thrombotic or antiarrhythmic therapy
Alternative Treatments:
- Used for drug-refractory cases or those avoiding long-term anticoagulation
- E.g. Radiofrequency ablation destroy heart tissue, causing arrhythmia
 Hemodynamically Stable with Preserved LV Function:
- Use IV amiodarone or lidocaine
Monomorphic Ventricular Hemodynamically Unstable or Poor LV Function:
Tachycardia - Start with IV amiodarone
- Follow with cardioversion if medication does not work
VT Without Pulse:
- Same as ventricular fibrillation.
- Start with CPR and rapid defibrillation.
- Administer epinephrine if defibrillation is unsuccessful.

Polymorphic Ventricular Normal Baseline QT Interval:

Tachycardia - Use β blockers, amiodarone or sotalol (K+ channel blocker)
(Torsades de points) - Cardioversion if medication does not work
Prolonged Baseline QT Interval:
- Use IV magnesium and anti-tachycardia pacing
- Discontinue medications that prolong QT interval (i.e. amiodarone, procainamide)
- Cardioversion if rhythm does not convert.

- Assess ABCs
Ventricular Fibrillation - If no pulse is found, CPR and ACLS needs to be started right away
- Will need to use defibrillation and medication therapy with it
- Meds: epinephrine, amiodarone, lidocaine
 WEEK 4 - ELIMINATION
[Link]
[Link]

Explain the structure and function of the renal system including kidneys
The Anatomy of a Kidney

1: renal cortex: makes up the outer layer of the kidney. Contains nephrons, and forms urine.

2: renal pyramid: found in the renal medulla (the deeper layer of the kidney). Mostly contains collecting
tubules. Transports urine.

3: renal column: space between renal pyramids.

4: minor calyx: where urine flows from the nephron

5: major calyx: where the urine flows from the minor calyx

6: renal pelvis: where the urine flows from the major calyx

7: ureter: where the urine flows from the renal pelvis, and travels to the urinary bladder
Describe the mechanisms for regulating renal blood flow.
At rest:
- Minimal SNS stimulation → renal blood vessels are dilated → ↓ GFR ?? (Dilated so shouldn’t it be increase GFR and
filtration?)→ ↓ filtration
- This allowed for lots of urine formation
Neural Regulation
Moderate SNS Stimulation:
- Afferent and efferent arterioles will equally constrict → ↓ renal blood flow to glomerulus → ↓ GFR → ↓ filtration

Extreme SNS Stimulation:

- ↑ vasoconstriction of afferent arterioles → ↓ hydrostatic pressure → ↓ GFR → ↓ filtration → ↓ urine output

Atrial Natriuretic Peptide → ↓ BP

Hormonal Regulation - Relaxation of glomerular mesangial cells → dilation of afferent arterioles + constriction of efferent arterioles → ↑ GFR
→ ↑ filtration

Angiotensin II → ↑ BP
- ↑ vasoconstriction of afferent/efferent arterioles → ↓ GFR → ↓ filtration

Explain the value of urine-specific gravity in evaluating renal function.

Urine-Specific Gravity

- It tells you how concentrated urine is

- E.g. if the urine specific gravity is low, the urine is dilute (diLute urine = Low gravity)
- The urine-specific gravity will tell you about hydration and tubular function

Explain the concept of the glomerular filtration rate.

Glomerular Filtration Rate (GFR)

Rate at which fluid is pushed through the glomeruli of both your kidneys
Definition: - E.g. if GFR = 150-180 L/day, that means that your kidneys are filtering out ~150-180L from your body. But you don’t urinate
out that much. You only urinate out a small portion of it.

Alterations in GFR: ↑ GFR → fluid will pass through tubules to quickly → important substances will get filtered out
↓ GFR → not enough removal of waste products → accumulation of waste products → affects CNS
Explain the value of serum creatinine and blood urea nitrogen levels in evaluating renal function.
Creatinine Blood Urea Nitrogen (BUN)

What is it? Product of muscle & protein metabolism Product of protein metabolism

- They assess renal function

What does it look at? - If these levels are elevated, it means that these waste products are not being excreted out in the urine.
- This indicates impaired renal function
- As creatinine and BUN ↑, GFR ↓, and kidney function ↓

Describe the normal metabolism of creatinine and identify the normal creatinine clearance rate.
Creatinine Metabolism Protein & muscle metabolism → creatinine production → creatinine is excreted by kidneys

Creatinine Clearance Rate: 1.42-2.25mL/sec (85-135mL/min)

Differentiate between acute kidney injury and chronic kidney disease.

Acute Kidney Injury (AKI) Chronic Kidney Disease (CKD)

Onset Sudden Gradual, often over many years

Most Common Cause Acute tubular necrosis Diabetic nephropathy

Diagnostics Acute ↓ in urine output, ↑ serum creatinine, or both GFR < 60mL/min/1.73m2 for > 3 months, kidney damage for > 3
months, or both

Reversibility Potentially Progressive and irreversible

Mortality Highly (~60%) 19-24% (patients on dialysis)

Primary Cause of Infection Cardiovascular disease d/t their immunosuppression

Death
Identify criteria used in the classification of AKI using the acronym RIFLE (risk, injury, failure, loss, end-stage kidney disease).
AKI: RIFLE

Stage 1 - Risk
- Creatinine ↑ by x1.5
- GFR ↓ by > 25%
- Urine output < 0.5mL/kg/hr in 6 hours

Stage 2 - Injury
- Creatinine ↑ by x2
- GFR ↓ by > 50%
- Urine output < 0.5mL/kg/hr in 12 hours

Stage 3 - Failure
- Creatinine ↑ by x3
- GFR ↓ by > 75%
- Creatinine > 4mg/100mL (acute rise) OR ≤ 0.5mg/100mL per day
- Urine output < 0.3mL/kg/hr in 24 hours OR anuria for 24hrs

Stage 4 - Loss
- Complete loss of renal function for > 4 weeks

Stage 5 - End-stage renal disease

Describe the clinical course of acute kidney injury.
Clinical Course of an AKI

- ↑ creatinine
Initiation Phase - ↑ BUN
- ↓ urine output

Urinary changes (pt can be nonoliguric, oliguric, or anuric)

- Normal urine specific gravity, high Na+ concentration, urine osmolality ~300mmol/kg
- Urine sediments: RBCs, WBCs, casts, proteinuria
Fluid volume excess
- Can lead to distended neck veins, bounding pulse, edema, HTN
- Can eventually lead to HF, pulmonary edema, pericardial and pleural effusions
Metabolic acidosis
- Kidneys cannot make ammonia, which is needed to excrete H+ ions and other acidic waste products
Maintenance Phase - Bicarb gets used up while the body tries to compensate for the accumulation of H+ ions
Sodium balance
Lasts days to weeks - Normal or below-normal levels of serum Na+ d/t ↑ urinary excretion of Na+
Potassium excess d/t impaired ability to excrete K+
- ECG will show tall peaked T waves, widening of the QRS complex, & ST depression
Hematological disorders
- Anemia
- Uremia → ↓ platelet adhesiveness → bleeding
Calcium deficit and phosphate excess
- Functioning kidneys are needed to activate vitamin D (so that the GI tract can absorb calcium)
- But since the kidneys don’t work → vitamin D cannot be activated → ↓ calcium absorption
- Hypocalcemia → PTH is released to trigger bone demineralization to release Ca → phosphate is
released from the bones too → ↑ phosphate but cannot be excreted d/t impaired kidney function
Waste product accumulation
- ↑ urea (product of protein metabolism from ammonia) and creatinine (product of muscle metabolism)
Neurological disorders
- Fatigue, difficulty concentrating
- Seizures, stupor, coma

- Return of BUN, creatinine, and GFR

- Nephrons are not fully functional → high urine volume d/t osmotic diuresis and inability to concentrate urine
- Patients can experience hypovolemia and hypotension from fluid losses
Recovery Phase - Diuretic phase → can lead to fluid & electrolyte abnormalities
- Diuretic phase lasts 1–3 weeks
- Monitor for hyponatremia, hypokalemia, and dehydration
- Acid-base, electrolyte, and waste product values normalize towards the end
- Major improvements occur in the first 1–2 weeks, but renal function may take up to 12 months to stabilize.
- Older patients are less likely to recover full kidney function.
Explain the interprofessional care and nursing management of patients with acute kidney injury.
AKI: Diagnostics

Diagnostic Study What do you see on there?

Urine Sediment (abundant cells, casts, or proteins)

- Suggest intrarenal disorders
- May be normal in prerenal and postrenal AKI
Urine Osmolality, Sodium Content, Specific Gravity:
Urinalysis - Help differentiate types of AKI
Hematuria, Pyuria, Crystals:
- May be seen with postrenal AKI

Renal Ultrasound - Provides anatomical and functional information

Renal Scan - Assesses renal blood flow and collecting system integrity

CT scan - Identifies lesions, masses, and obstructions

AKI: Interprofessional Care

Primary goals of AKI treatment:

- Eliminate the cause.
- Manage signs and symptoms.
- Prevent complications during kidney recovery.
Initial steps:
- Ensure sufficient intravascular volume and cardiac output for kidney perfusion.
- Use crystalloids
- Administer diuretics (loop diuretics like furosemide or osmotic diuretics like mannitol) to prevent volume overload, if not oliguric.
Fluid management:
- Monitor fluid intake during the oliguric phase.
- Calculate permitted fluid intake: previous 24-hour losses + 600 mL for insensible losses.
Hyperkalemia management:
- Treat elevated potassium to prevent life-threatening cardiac dysrhythmias.
- Use insulin and salbutamol to shift potassium into cells temporarily.
- Use calcium gluconate to stabilize the myocardium.
- Remove potassium using cation exchange resins (sodium polystyrene sulfonate) or dialysis.
Indications for RRT:
- Volume overload, compromising cardiac/pulmonary status
- Elevated potassium levels
 - Metabolic acidosis (serum bicarbonate <15 mmol/L)
- BUN level >43 mmol/L
- Significant change in mental status
- Pericarditis, pericardial effusion, or cardiac tamponade
RRT options:
- Peritoneal dialysis (PD) is rarely used
- Intermittent hemodialysis (HD) and continuous renal replacement therapy (CRRT) are effective
- HD for rapid changes, CRRT for continuous treatment.
Nutritional therapy:
- Provide 25-35 kcal/kg/day.
- Protein dosage: 1.5-2.5 g/kg/day based on AKI stage and RRT requirement
- Consult a renal dietitian for complex nutritional needs
- Regulate potassium and sodium according to plasma levels
- Increase dietary fat intake to 30-40% of total calories.
- Use enteral nutrition if possible, parenteral nutrition (PN) if GI tract is not functional.
- Use concentrated PN formulas to minimize fluid volume.

AKI: Nursing Management

Nursing Assessment: look out for…

- Monitor VS
- CV: peripheral edema, neck vein distention, S3 or gallop, murmurs, or pericardial friction rub, dysrhythmias (ECG),
- GI: ins/outs, urine (colour, glucose, blood, sediments, specific gravity)
- Skin: colour, bruising, oral mucosa (check for dehydration & inflammation)
- Respiratory: auscultate the lungs (look for crackles, wheezing, or diminished lung sounds)
- For dialysis (renal replacement therapy, RRT): assess the access site for inflammation
- Neuro: mental status, LOC
- Assess lab results & diagnostic tests

Nursing Diagnoses:
- Potential diagnoses: - Potential complications:
- Potential for infections d/t changes in skin integrity - Dysrhythmias d/t electrolyte imbalances
- Excess fluid volume d/t ↑ fluid intake & fluid retention
- Fatigue d/t malnutrition & physical deconditioning
- Anxiety d/t uncertainty of prognosis
Planning/ Goals of care:
- Completely recover without any loss of kidney function
- Maintain normal fluid & electrolyte balance
- Have ↓ anxiety
- Understand and adhere to the treatment plans and follow-up care
Nursing Implementation:
Health Promotion Acute Intervention Ambulatory & Home Care
Prevention strategies: - Provide holistic care, addressing both - Good nutrition, rest, and activity are
- Identify and monitor high-risk populations physical and emotional needs. important for recovery
- Control intake of nephrotoxic meds and - Educate pt and family on the systemic - Dietary restrictions should be tailored to
exposure to industrial chemicals. impact of renal failure kidney function
- Prevent long episodes of hypotension and - Accurate ins/outs recording and daily - Regular follow-up and evaluation of renal
hypovolemia weight measurement. function are necessary
Important practices: - Monitor for signs of hypervolemia (oliguric - Nurses should educate pts on s/s of
- Monitor of fluid & electrolyte balance phase) and hypovolemia (diuretic phase) recurrent kidney disease
- Assess and record extra-renal fluid losses and watch for K+ and Na+ disturbances. - Preventative measures for AKI recurrence
(vomiting, diarrhea, hemorrhage). - Use aseptic technique and protect the pt should be emphasized
- Replace significant fluid losses to prevent from infectious people - Long-term convalescence (3-12 months)
ischemic tubular damage. - Look out for local and systemic infection can cause psychosocial & financial issues
- Avoid aggressive diuretic therapy in signs - Nurses should refer pts for counselling if
patients with fluid overload to maintain - Antibiotic use requires careful needed.
renal blood flow consideration of type, dosage, & frequency - If kidneys do not recover, pts might need
Special considerations: d/t kidneys' role in drug excretion chronic dialysis or a future transplantation
- For patients with renal insufficiency, - Nephrotoxic meds should be avoided.
diabetes, or older age undergoing - Skincare and pressure injury prevention
diagnostic studies with IV contrast media: are important d/t the pt's likelihood of
○ Ensure enough hydration before edema and ↓ muscle tone.
and after the test. - Mouth care is essential to prevent
○ Use acetylcysteine to protect the stomatitis caused by ammonia in saliva,
kidneys irritating mucous membranes.
Patients on nephrotoxic meds:
- Use nephrotoxic meds in the smallest
effective doses for the shortest periods.
- Caution against misuse of OTC
analgesics, especially NSAIDs
- Be aware of risks r/t ACE inhibitors in renal
insufficiency (↓ perfusion pressure and
hyperkalemia).

Evaluation:
- Expected outcomes:
- Regain and maintain normal fluid and electrolyte balance
- Adhere to the treatment regimen
- Experience no infectious complications
- Have complete recovery
Define chronic kidney disease and delineate the five stages of chronic kidney disease based on the glomerular filtration rate.
CKD: Stages
CKD: progressive, irreversible destruction of the nephrons in both kidneys

Stage 1 Kidney function with normal or ↑ GFR ↓

- GFR ≥ 90 mL/min/1.73m2

What actions should be taken?

- Diagnose and treat any comorbid conditions
- Reduce risk of CV disease

Stage 2 Kidney damage with mild ↓ in GFR

- GFR ≃ 60-89 mL/min/1.73m2

What actions should be taken?

- Determine an estimate of the patient’s CKD progression

Stage 3 Moderate ↓ in GFR

- GFR ≃ 30 - 59 mL/min/1.73m2

What actions should be taken?

- Assess and treat any complications

Stage 4 Severe ↓ in GFR

- GFR ≃ 15 - 29 mL/min/1.73m2

What actions should be taken?

- Prepare for renal replacement therapy (RRT)

Stage 5 End-stage renal disease (ESRD)

- Advanced kidney disease
- GFR < 15 mL/min/1.73m2

What actions should be taken?

- Some form of RRT will be needed during this time (i.e. peritoneal dialysis, hemodialysis, kidney transplant)
Identify risk factors that contribute to the development of chronic kidney disease.
CKD: Risk Factors

- The patient’s condition and age

- Cause of CKD
- Adequacy of medical follow-up

Summarize the significance of cardiovascular disease in individuals with chronic kidney disease.
CKD and Cardiovascular Disease

- There are high morbidity and mortality rates d/t CV disease in patients with CKD
- CKD worsens outcomes of CVD outcomes → many pts die from CV disease before reaching CKD stage 5
- HTN is the most common CV issue
- HTN is worsened with CKD d/t sodium retention and ↑ extracellular fluid volume.
- ↑ renin production can contribute to HTN.
- HTN accelerates atherosclerosis, causes intrarenal arterial spasm, and leads to LV hypertrophy and HF
- Left ventricular hypertrophy can cause HF and pulmonary edema
- HTN also causes retinopathy, encephalopathy, and nephropathy
- Long-standing HTN and ↑ triglycerides contribute to CV complications (e.g. MI, stroke)
- DM is a major risk factor for vascular conditions
- ↓ coronary artery perfusion, hyperkalemia, hypocalcemia → Cardiac dysrhythmia
- Uremic pericarditis can develop → pericardial effusion and cardiac tamponade
- Manifestations: indicated by a friction rub, chest pain, and low-grade fever.

Explain the interprofessional care and related nursing management of the patient with chronic kidney disease.
CKD: Interprofessional Care

Medication therapy:
- Control via diet and meds
- Use non-pharm management for K+ levels > 5.5 mmol/L
- Use pharm intervention for K+ levels ≥ 6.0 mmol/L
Hyperkalemia - ECG is recommended to check for cardiac dysrhythmias
- ECG changes to look out for: peaked T waves, widened QRS complexes
- Dialysis may be needed for life-threatening dysrhythmias
- Use IV glucose and insulin or β2-adrenergic agonists to push K+ into the cells
- Cation exchange resins (Kayexalate) → ↓ K+ levels.
- Monitor for Na+ and water retention with cation exchange resins
 HTN Nondiabetic CKD:
- Target BP: <140/90 mmHg
- Initial therapy if proteinuria is present: ACE inhibitors (ramipril, enalaprl) or ARBs (irbesartan, losartan)
- Additional therapy: thiazide or loop diuretics for volume overload
Diabetic CKD:
- Target BP: <130/80 mmHg
- ACE inhibitors (ramipril, enalaprl) or ARBs (irbesartan, losartan)
- Other antihypertensives: dihydropyridine calcium channel blockers (nifedipine, thiazide diuretics, amlodipine)
Renovascular disease + CKD:
- Cautious use of ACE inhibitors and ARBs because they can further ↑ risk of AKI

Limit phosphorus
- Dietary limitations
- Calcium-based phosphate binders are given → they bind phosphate for excretion in stool
- The issue is that giving Ca2+-based binders when phosphate levels are ↑ causes formation of
calcium-phosphate deposits
- Instead, give Sevelamer (Renagel) - phosphate binder that does NOT have calcium or aluminum in it
CKD-Mineral and Bone - Phosphate binders should be taken with each meal.
Disorder - Common side effect: constipation.
Aluminum and Magnesium:
- Avoid aluminum preparations d/t risks of dementia (aluminum toxicity) and bone disease (osteomalacia)
- Use Mg2+-containing antacids (Maalon, Mylanta) in moderation because Mg2+ relies on kidneys for excretion
Hypocalcemia:
- GI tract may not absorb Ca2+ without vitamin D.
- If hypocalcemia persists, administer Calcitriol (active form of vitamin D)
- Lower phosphate levels before giving calcium or vitamin D to avoid soft tissue calcification
Calcimimetics:
- Cinacalcet (Sensipar) may be used to lower PTH levels and may cause hypocalcemia
Severe Renal Osteodystrophy:
- Subtotal or total parathyroidectomy may be needed
- Parathyroid tissue may be transplanted into the forearm.

Erythropoiesis-stimulating agents (ESAs)

Anemia - Are effective but take 2-3 weeks to significantly increase Hgb levels.
- ESAs improve exercise tolerance and QoL
- Common adverse effect: HTN d/t hemodynamic changes

Dyslipidemia - Use statins in pts with stages 1-3 CKD

- Many meds are excreted by the kidneys → impaired kidney function can lead to medication accumulation & toxicity
- Medication doses and administration frequency need to be adjusted based on kidney function and dialysis status
 Complications of - Critical meds to monitor: digoxin, oral glycemic agents (e.g., metformin, glyburide), antibiotics, and opioids (e.g.,
Medication Therapy hydromorphone, morphine).
- Pt should avoid NSAIDs because they worsen renal hypoperfusion and cause interstitial nephritis
- Tylenol is a safer option for pain relief

Nutritional therapy:
- Protein is restricted because protein metabolism produces urea, which won’t end up being excreted by the kidneys
- Moderate protein restriction needed for patients not on dialysis, with creatinine clearance < 25 mL/min.
Protein restriction - Low-protein diet needed for severe renal insufficiency to avoid malnutrition.
- PD patients need higher protein intake due to protein loss in dialysate

- Fluid intake is based on urine output and fluid balance

Sodium & fluid restriction - Fluids are not restricted for non-dialysis patients
- Diuretics and low-sodium diet manage fluid retention
- Fluid restrictions for HD patients based on urine output and weight gain between dialysis sessions
- Avoid high-sodium foods and most salt substitutes (contain potassium chloride)

- K+ restriction depends on kidney function.

Potassium restriction - Some PD patients may not need potassium restrictions.
- Avoid high- K+ foods (e.g. oranges, bananas, tomatoes, beans)

Phosphate restriction - CKD affects calcium, phosphorus, and vitamin D homeostasis

- Avoid high-phosphate foods (e.g. dairy products)
- Can also give calcium acetate to lower phosphate levels
 CKD: Nursing Management

Nursing Assessment:
- Pt’s Hx of renal disease and family Hx of renal disease.
- Assess long-term health conditions that can lead to CKD (HTN, DM, recurrent UTIs, lupus)
- Review current and past use of medications d/t potential nephrotoxicity
- Assess pt’s dietary habits and evaluate recent weight changes

Diagnoses & Planning:

Potential Diagnoses: Goals of Care:
- Excess fluid volume d/t ↑ fluid intake - Demonstrate knowledge and ability to adhere to therapeutic regimen
- Potential for electrolyte imbalance r/t excessive fluid volume - Participate in decision-making for the plan of care & future treatments
- Inadequate nutrition: less than body requirements d/t insufficient - Demonstrate effective coping strategies
dietary intake (restricted intake of nutrients, N/V, anorexia, stomatitis) - Continue with ADLs within physiological limitations

Nursing Implementation
Health Promotion Care Considerations for CKD in Stages 4 & 5 Ambulatory & Home Care
- Identify individuals at risk for CKD - Educate pt and family on diet, meds, - When RRT is required, options include HD,
- Regularly check creatinine, BUN, urinalysis follow-up care. PD, or transplantation
- Check for microalbuminuria in pt with DM - Daily weight checks, BP monitoring, - Early teaching and discussion about RRT
- Report changes in urine appearance, identify signs of fluid overload or ↑ K+ (stage 3) for informed decision-making.
frequency, or volume - Strict dietary adherence + regular dietitian - Clear explanation of dialysis and transplant
- Monitor renal function if prescribed consults processes
nephrotoxic medications - Avoid certain OTC medications, NSAIDs, - Transplantation remains an option even if
- Delay CKD progression and ↓ CV risk: natural/herbal preparations dialysis is chosen
glycemic control, BP control, lifestyle - Discontinue ACE inhibitors if contributing - Re-transplantation is possible if kidneys fail
modifications, smoking cessation to hyperkalemia or ↓ GFR.
 WEEK 5 - INFLAMMATION
[Link]

Structure and function of the liver and spleen.

Normal Liver Normal Spleen
 Functions of the liver: Functions of the spleen:
- Produces bile salts to break down fats - Red pulp:
- Filters ammonia, toxins, drugs, alcohol, and pathogens, and eliminates - Removes ruptured, worn out, or defective blood cells and
bilirubin platelets via macrophages
- Stores carbs (as glycogen), vitamins, and minerals (e.g. iron) - Stores platelets (up to a third of the body’s supply)
- Metabolizes lipids (e.g. cholesterol metabolism) - Produces blood cells (hemopoiesis) during fetal life
- Produces plasma proteins (e.g. albumin) and lipoproteins (HDLs + - White pulp:
LDLs), and even transports lipoproteins - T cells and B cells carry out immune functions (similar to lymph
- Maintains the portal vein immune system nodes)
- Spleen macrophages destroy blood-borne pathogens via
phagocytosis

Describe the physiologic basis for portal hypertension and relate it to the development of ascites, esophageal varices, and splenomegaly.
Explain the consequences of splenomegaly.
Ascites
Patho:
- Portal hypertension → ↑ pressure in peritoneal capillaries

Esophageal Varices
 Thin, dilated veins in the distal esophagus
Patho:
- Portal hypertension → portosystemic shunting of blood → development of collateral
vessels → esophageal varices
Manifestations/Consequence(s):
- Slow chronic bleeding → anemia, melena
- Rupture → hematemesis (mortality 30-60%)

Splenomegaly
Enlarged spleen
Patho:
- Portal hypertension → ↑ pressure in splenic vein → ↑ formed elements to spleen →
splenomegaly
Consequence(s):
- The longer a framed element stayed in the spleen, the more likely it is that it’ll be recycled.
- ↑ formed elements to spleen → ↓ RBCs → anemia → fatigue
- ↑ formed elements to spleen → ↓ WBCs → ↑ infections
- ↑ formed elements to spleen → ↓ platelets → ↑ bleeding time

Hepatic Encephalopathy
Patho:
- Portal hypertension → portosystemic shunting of blood → shunting of ammonia & toxins
into general circulation → hepatic encephalopathy
*Look at table above for all other information

Caput Medusae
Patho:
- Portal hypertension → portosystemic shunting of blood → ↑ pressure in collateral vessels
→ caput medusae

Explain the etiology, pathophysiology, manifestations, interprofessional care, and nursing management of acute liver failure with
rationales.
 Acute Liver Failure: Etiology

Cause How does it cause ALF?

Combination of Tylenol + alcohol (most common)

Drugs: They disrupt important intracellular processes, or may cause a buildup of toxic
Alcohol use disorder, isoniazid, antibiotics, sulpha-containing medications, metabolic products
anticonvulsants

Viral hepatitis I mean it’s literally a viral infection that affects the liver soooo

Mushroom poisoning Fungi called Amanita phalloides has really strong toxins that destroy the
process of protein synthesis

Acute Liver Failure: Pathophysiology

fulminant hepatic failure → Rapid deterioration of liver function → encephalopathy and coagulopathy for ~ 8–26 weeks

Acute Liver Failure: Manifestations

Manifestation Why it Occurs

Changes in cognitive function Caused by hepatic encephalopathy

Jaundice ↓ ability of the liver to excrete bilirubin

Coagulation abnormalities ↓ synthesis of clotting factors

Encephalopathy Accumulation of ammonia, leading to neurotoxic effects

Acute Liver Failure: Complications

 Complication Why it Occurs

Cerebral edema Maybe due to systemic inflammation ??

Renal failure Caused by hepatorenal syndrome

Hypoglycemia The liver normally stores glycogen. But since the liver doesn’t work, the
glycogen will be used up instead of saved for later

Metabolic acidosis Liver failure disrupts the metabolism of lactate and other acids, leading to their
buildup in the blood and causing metabolic acidosis

Sepsis Caused by ↓ WBC count, leading to ↑ chance of infection

Multiorgan failure

Acute Liver Failure: Diagnostics

Diagnostic Study What do you see on there?

Lab Studies ↑ bilirubin, prolonged PT, ↑ AST, ↑ ALT, hypoglycemia

Liver Biopsy Identifies coagulopathy, hepatitis, metastatic liver disease, or infiltrative liver disease

Doppler U/S, CT scan, MRI Will look at liver size/contour, presence of ascites or tumours, & patency of blood vessels

Acute Liver Failure: Nursing & Interprofessional Care

- Begin planning for transfer to a transplantation center for pts with grade 1 or 2 encephalopathy d/t risk of rapid deterioration
- It’s very important to frequently monitor the pt’s cognitive status frequently
- Regularly check for ↑ ICP (d/t cerebral edema)
- Keep HOB elevated 30°
- Avoid sedatives and benzodiazepines d/t their impact on mental status and encephalopathy risk
- Minimize pt stimulation and avoid Valsalva movements
- Protect renal function - maintain fluid balance, avoid nephrotoxic agents, and immediately treat infections
- Also involves monitoring hemodynamics and renal function, glucose, electrolytes, and acid–base status
- Maintain seizure precautions - pad bedrails and observe the pt closely to prevent injuries
- If the pt has an NG tube: remember that NG tubes can cause bleeding by irritating the nasal and esophageal mucosa
Explain the etiology, pathophysiology, clinical manifestations, interprofessional care, and nursing management of cirrhosis.
 Cirrhosis: Etiology

- Alcoholism
- Causes cell necrosis and fatty infiltration in the liver
- Chronic liver disease
- Chronic viral hepatitis, non-alcoholic fatty liver disease (NAFLD), alcohol-associated liver disease (ALD), autoimmune liver diseases
- Nutrition-related causes:
- Extreme dieting, malabsorption, obesity
- Environmental factors
- Genetics
- *Cardiac cirrhosis: hepatic conditions caused by long-standing, severe, right-sided heart failure*

Cirrhosis: Pathophysiology

Inflammation of the liver → liver tries to repair itself → extensive fibrosis/scarring and regenerative nodules → permanent liver distortion → ↓ liver function
**cirrhosis is the final stage of chronic liver failure**

Compensated Cirrhosis: Manifestations

Manifestation Why it Occurs

Abdominal pain (dull, heavy feeling in the RUQ or epigastrum) Swelling and stretching of the liver capsule, spasm of the biliary ducts,
intermittent vascular spasms, or a combo of these

Anorexia Poor digestion r/t ↓ bile production leads to lack of appetite

Dyspepsia Indigestion may be r/t ↓ bile production

N/V

Weakness, fatigue

Muscle loss Anorexia causes the body to turn to muscle breakdown for energy

Slight weight loss Probably r/t anorexia and muscle loss

Hepatomegaly, or shrunken liver Caused by inflammation, fibrosis, and fatty infiltration

Splenomegaly Caused by portal hypertension, which leads to blood backing up into the spleen
 Decompensated Cirrhosis: Manifestations

Manifestation Why it Occurs

Jaundice ↓ ability of the liver to excrete bilirubin

Skin lesions (spider angiomas, palmar erythema) ↑ circulating estrogen d/t liver’s inability to metabolize steroid hormones

Thrombocytopenia Platelet sequestration in the spleen, and ↓ thrombopoietin production in the liver

Leukopenia

Anemia Inadequate RBC production and survival, poor diet, poor absorptoin of folic acid, bleeding from varices

Coagulation disorders The liver cannot produce prothrombin and other coagulation factors that are needed for blood clotting

(1) Gynecomastia, impotence + ↓ libido, loss of axillary/pubic hair, and testicular atrophy occur d/t ↑
estrogen accumulation since the liver cannot metabolize it
Endocrine disturbances
(2) Hyperaldosteronism, Na+ & water retention, and potassium loss occur d/t the liver’s inability to
metabolize aldosterone.

(3) Amenorrhea (younger women) and vaginal bleeding (older women) also occur.

Peripheral neuropathy (numbness, pain, etc) Dietary deficiency of thiamine, folic acid, and cobalamin (vitamin B12)
 Cirrhosis: Complications

Manifestation Why it Occurs

Portal Hypertension Impaired blood flow through portal & hepatic veins leads to ↑ venous pressure to the portal circulation.
This leads to formation of “collateral circulation” (alternative circulatory pathways in the lower esophagus)

Caput Medusae & Esophageal Varices Collateral veins that are found close to systemic circulation form gastric varices (caput medusae) and
esophageal varices

(1) ↑ portal venous pressure causes proteins to shift from blood vessels to larger lymphatic spaces. When
the lymphatic system cannot carry excess water and protein, they leak into the peritoneal cavity
Ascites (2) liver’s inability to make albumin leads to hypoalbuminemia. This leads to ↓ colloidal oncotic pressure
(3) hyperaldosteronism as a compensatory mechanism d/t portal hypertension

Hepatic Encephalopathy Neurotoxic effects of ammonia, abnormal neurotransmission, astrocyte swelling, inflammatory cytokines.
Hallmark feature: asterixis (flapping tremors)

Fetor Hepaticus Accumulation of by-products that the liver cannot degrade leads to a musty, sweet odoured breath

Hepatorenal Syndrome ↓ renal blood flow & GFR d/t arterial vasodilation in splanchic (GI) circulation leads to renal failure
occurs without precipitating factors, kidney injury, and a normal renal U/S

Cirrhosis: Diagnostics

Diagnostic Study What do you see on there?

Liver biopsy Will identify cell changes

Non-invasive fibrosis markers Predicts liver fibrosis

Liver function test ↑ AST, ALP, ALT, GGT d/t excess release from damaged liver cells & bile ducts

↓ serum protein, ↓ albumin, ↑ bilirubin, ↑ globulin

Other lab test ↓ cholesterol d/t fat metabolism abnormalities
Prolonged PT or INR
 Cirrhosis: Interprofessional Care

Ascites
Low Sodium Diet - Should be limited to 2g/day; more stringent restrictions are not recommended
- Fluid restriction is usually unnecessary unless severe hyponatremia occurs
- Balance of fluid and electrolytes should be monitored and controlled
- Albumin infusions help maintain intravascular volume and adequate urinary output

Diuretics - Aldosterone antagonists (e.g. Spironolactone) are preferred d/t ↑ aldosterone in cirrhosis
- Combination therapy with loop diuretics (e.g. furosemide) and aldosterone antagonists (e.g. spironolactone) is
most effective

Paracentesis - Involves withdrawing fluid for diagnostic or therapeutic purposes (especially when diuretic therapy fails)
- Provides temporary relief for symptoms such as pain or breathing difficulty
- Make sure that the pt empties their bladder before the procedure
- Obtain consent from the pt
- Position client in upright position (or in semi-fowler’s position if pt is in bed
- The client's blood pressure should be monitored during the procedure
- Immediate interventions are needed if the pt has increased abdo pain (indicates diaphragmatic, liver, or spleen
perforation and may be life-threatening)

TIPS - TIPS procedure is considered for those with portal hypertension unresponsive to diuretics

Esophageal and Gastric Varices

Prevention of Bleeding - All cirrhosis patients should have upper endoscopy
- Risk factors for bleeding: Variceal size, wall thickness, liver dysfunction

Medications - Avoid: alcohol, aspirin (ASA), NSAIDs

- Prophylaxis to ↓ bleeding risk: non-selective β-blockers (e.g. propranolol)
- Will ↓ CO and constrict splanchic vessels → ↓ portal venous pressure
- Octreotide (Sandostatin), or vasopressin
- They will lead to vasoconstriction of splanchic arterial bed → ↓ portal blood flow → ↓ portal HTN
- If giving vasopressin, administer nitroglycerin with it to ↓ adverse effects

Managing Acute Bleeding - Manage airway, start IV therapy, possibly administer blood products
- Perform endoscopic examination for Dx
- Treatment: combination of drug therapy + endoscopic therapy.

Endoscopic Therapies - Sclerotherapy: Injection of sclerosing agent into varices to clot the distended/swollen veins
- Ligation: Putting a rubber band around the base of varices
 Balloon Tamponade - This is an option when endoscopy is not able to control the acute esophageal or gastric variceal hemorrhage
- Involves mechanical compression of the varices using different balloons (e.g., Sengstaken-Blakemore).

Supportive Measures - Administer dresh-frozen plasma, PRBCs, vitamin K, PPIs (e.g. Pantoloc), lactulose, and antibiotics
- Lactulose is given to prevent hepatic encephalopathy
- Antibiotics (e.g. norfloxacin) are given to prevent bacterial translocation into peritoneal cavity

Shunting - TIPS: Redirects portal blood flow, allows for adequate liver perfusion, reduces portal pressure.
- Surgical Shunts: used in emergencies (e.g. portacaval and distal splenorenal shunts)

Hepatic Encephalopathy
Lactulose - It will trap and expel ammonia via its laxative effect
- Route of administration: Oral, enema, or nasogastric (NG) tube.

Antibiotics - Rifaximin (Zaxine) is the antibiotic that is used if lactulose alone is ineffective
- It reduces ammonia-producing bacteria.

- Regular BMs are important to prevent ammonia buildup

Other Considerations - Prevention: treat precipitating causes
- GI bleeds, infections, electrolyte disorders, acid-base imbalance, constipation, lactulose
non-adherence or under-dosing

Nutritional Therapy
- Remember that malnutrition is often a driver for encephalopathy
- Enteral formulas with branched-chain amino acids (good for muscle metabolism) are needed for those with alcohol-related cirrhosis
- E.g. beef, chicken, whey, soy, tuna
- Na+ restriction is very important for patients with ascites and edema (no-added-sodium diet)
- Salt substitutes are discouraged d/t potassium chloride content
- Eat a high-carb diet
 Cirrhosis: Nursing Management

Nursing Assessment:
Subjective Objective

- Ask about PMHx (severe R-sided HF, chronic alcohol use disorder, - General - Fever, cachexia, muscle wasting
hepatitis, chronic biliary obstruction/infection) - Integumentary - jaundice (skin/sclera), petechiae, ecchymosis, spider
- Ask about meds (adverse reactions to any meds, use of ASA, angiomas, palmar erythema, alopecia, clubbing, peripheral edema
NSAIDs, Tylenol, or anticoagulants) - Respiratory - shallow, rapid respirations, epistaxis
- Ask about symptoms: - GI - abdo distension, ascites, palpable liver and spleen, hematemesis;
- Weakness, fatigue, difficulty with concentration black/tarry stools, hemorrhoids, fetor hepaticus
- Change in sleep–wake pattern - Neuro - confusion, asterixis
- Anorexia, muscle loss - Reproductive - gynecomastia and testicular atrophy (men), erectile
- Gum bleeding dysfunction (men), loss of libido (men & women), amenorrhea or
- Yellow sclera or skin; pruritis; easy bruising heavy menstrual bleeding (women)
- Dull pain in right upper quadrant or epigastric region - Possible findings - Anemia, thrombocytopenia, leukopenia, ↓
- Erectile dysfunction; amenorrhea albumin, abnormal LFTs, ↑ INR, ↑ bilirubin, abnormal abdo U/S or MRI

Nursing Diagnoses & Planning:

Potential Diagnoses: Goals of Care:
- Inadequate nutrition d/t insufficient dietary intake - Have a relief of discomfort
- ↓ tissue integrity d/t moisture & pressure over bony prominences - Have minimal to no complications
- Excess fluid volume d/t compensatory regulatory mechanisms (portal - Maintain a lifestyle as close to their usual one as possible
HTN and hyperaldosteronism)
- Inadequate health maintenance d/t ineffective coping (alcohol use)
Implementation:
- Prevention & early treatment should focus on eliminating primary cause
Health Promotion - Address alcohol use disorder through pharm and non-pharm interventions
- Urge pt to avoid drinking alcohol
- Encourage adequate nutrition

Conserve strength while maintaining muscle strength/tone:

- Provide rest periods, encourage activities as tolerated
- Adjust activity and rest schedule based on clinical improvement.
Nutrition:
- Small, frequent meals and snacks (give preferred foods, but explain dietary restrictions to pt and caregivers)
Acute Intervention Jaundice:
- Manage pruritus with meds (cholestryamine, hydroxyzine, gapapentin, rifampin) and other measures (baking soda,
control temperature, moisturizing bath oils/lotions, etc.)
 - Note urine (dark brown) and stool (grey/tan) color changes
Edema and Ascites:
- Monitor ins/outs, daily weight, extremities, and abdominal girth.
- Assess for dyspnea
- Use semi-Fowler’s or Fowler’s position
Monitor Labs:
- Monitor electrolytes - watch for signs of fluid and electrolyte imbalance
- Monitor for bleeding tendencies, anemia, and infection
Bleeding Varices:
- Watch for hematemesis and melena;
- Manage airway, assist with sclerotherapy, ligation, or balloon tamponade
- Monitor for complications of balloon tamponade
Hepatic Encephalopathy:
- Assess neuro status frequently
- Prevent constipation

Ambulatory & Home Care - Avoid use of ASA, NSAIDs, and aminoglycosides to prevent bleeding, edema, and renal complications
- Avoid sleeping pills or sedatives with codeine to prevent encephalopathy
- Follow a low-sodium diet
- Major lifestyle changes may be required, especially if alcohol use is the cause.
- Educate pt on signs of liver decompensation and where to seek medical attention
 WEEK 6 - GAS EXCHANGE/ PERFUSION
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Review shock in BSCN 3001 Weeks 5 and 6, especially obstructive shock.

Obstructive Shock (↓ CO, not d/t heart issues)

Causes Valvular stenosis, pulmonary embolism, tension pneumothorax, pleural effusion, cardiac tamponade, etc.

We know that SV and afterload are inversely proportional. So, as afterload, ↑es, SV ↓es. With a higher afterload, the
Pathophysiology harder it is for the ventricles to pump blood out.
E.g. ↑ RV afterload:
- PE is present → blood cannot move from RV, into the pulmonary vasculature → ↓ blood flow → ↓ CO
E.g. ↑ LV afterload:
- Aortic stenosis → blood cannot move from LV into systemic circulation

We also know that SV is proportional to preload. So, the higher the preload, the higher the SV.
E.g. pneumothorax → lungs push on vena cava → ↓ venous return → ↓ preload → ↓ SV → ↓ CO
E.g. cardiac tamponade → ↑ pressure on the heart → ventricles cannot fill → ↓ preload → ↓ SV → ↓ CO

Clinical Presentations - Muffled heart sounds

- Elevated lactic acid levels
- Jugular vein distention

Nursing Management Treat based on cause -

- In general: vasopressors to ↑ inotropic action (contractility of the heart), isotonic fluids, give O2
- If caused by cardiac tamponade, perform a pericardiocentesis
- If caused by PE, give heparin, thrombolytics, etc.
 Common Traumatic Chest Injuries and Mechanisms of Injury

Mechanism of Injury Common Related Injury

Blunt Trauma

Blunt steering-wheel injury to chest Rib fractures, flail chest, pneumothorax, hemopneumothorax, cardiac
contusion, pulmonary contusion, cardiac tamponade, great vessels tears

Shoulder-harness seat belt injury Fractured clavicle, dislocated shoulder, rib fractures, pulmonary contusion,
pericardial contusion, cardiac tamponade

Crush injury (e.g. heavy equipment, crushing thorax) Pneumothorax and hemopneumothorax, flail chest, great vessel tears and
rupture, ↓ blood return to the heart with ↓ CO

Penetrating Trauma

Gunshot or stab wound to chest Open pneumothorax, tension pneumothorax, hemopneumothorax, cardiac
tamponade, esophageal damage, tracheal tear, great vessel tears
Identify the common mechanisms of injuries, clinical manifestations, interprofessional care and nursing management, with rationales, of
patient experiencing different types of pneumothoraxes, fractured ribs, and flail chest.
Pneumothorax: Mechanisms of Injury (Causes)

- Rupture of small blebs on the visceral pleural space

- Blebs: air-filled alveolar dilations < 1cm in diameter, on the edge of the lung at the apex of the upper lobe
Closed Pneumothorax or superior segment of the lower lobe
- Can be seen in underweight smokers, or in those with COPD
- Injury to the lungs from mechanical ventilation
- Injury to the lungs from insertion of a subclavian catheter
- Perforation of the esophagus
- Injury to the lungs from broken ribs

Open Pneumothorax Air enters the pleural space through an opening in the chest wall
- Stab or gunshot wound
- Surgical thoracotomies

Tension Pneumothorax Pneumothorax with rapid accumulation of air in the pleural space, causing severely high intrapleural pressures with
resultant tension on the heart and great vessels
- Open or closed pneumothorax
- Open chest wound
- Mechanical ventilation
- Clamps or blocked chest tubes

Hemothorax Accumulation of blood in the intrapleural space

- Chest trauma
- Lung malignancy
- Complications of anticoagulants
- Pulmonary embolus
- Tearing of pleural adhesions

Chylothorax Presence of lymphatic fluid in the pleural space d/t a leak in the thoracic duct
- Trauma, surgical procedures, malignancy
- Disrupted thoracic duct
 Pneumothorax: Manifestations

Manifestation Why it Occurs

↓ movement of involved chest wall Lungs cannot expand when air is trapped inside

Diminished or absent breath sounds on affected side Since there is a lack of air entering/leaving the lungs, there are diminished
breath sounds.

Hyper-resonance to percussion Hyper-resonance occurs when there is too much air filled in an organ/region

Respiratory distress The collapsed lung d/t the pneumothorax cannot allow blood to become
(rapid shallow respirations, dyspnea, air hungry, ↓ O2 sat) oxygenated, → ↓ ventilation and perfusion

Hypotension (only in tension pneumothorax) Accumulation of air can put pressure on the heart, making it harder for the heart
to pump

Mediastinal displacement (trachea shifts to unaffected side) All the tension from the pneumothorax puts pressure on the trachea, and shifts
it to the unaffected side.

Pneumothorax: Diagnostics

Diagnostic Study What do you see on there?

Chest XR Presence of air or fluid in the pleural space

Pneumothorax: Interprofessional Care

- Treatment depends on severity and underlying disease

- Most common & definitive treatment: chest tube insertion connected to water-seal drainage
- No treatment is needed if the patient is stable and pneumothorax is minimal
- Use a large-bore needle to aspirate minimal air/fluid
- Heimlich valve can be used to evacuate air from the pleural space
- Repeated spontaneous pneumothorax may require surgical treatment
- Partial pleurectomy, stapling, or pleurodesis
 Fractured Ribs

Etiology:
- Rib fractures are the most common chest injury d/t trauma
- Ribs 5-10 are most frequently fractured d/t less muscle protection

Manifestations:
- Pain at the injury site, especially during inspiration
- Leads to shallow breathing and splinting the affected area
- Splintered or displaced fractures can damage the pleura and lungs
- Shallow breathing may cause atelectasis

Treatments:
- Goal of treatment: ↓ pain to allow for adequate breathing & chest expansion
- Intercostal nerve blocks with local anesthesia can provide temporary pain relief
- Opioids should be used carefully d/t potential respiratory depression
- NSAIDs help with pain, deep breathing, and coughing
- Strapping the chest or using binders is discouraged because you want to avoid ↓ing lung expansion and preventing atelectasis.

Patient Education:
- Focus on deep breathing, coughing, incentive spirometry, and pain management
 Flail Chest

Etiology:
- Multiple rib fractures → leading to instability of the chest wall
Patho:
- Multiple rib fractures → instability of the chest wall d/t loss of structural integrity → chest wall cannot maintain proper ventilation → flail segment moves
paradoxically → impairs lung ventilation in the injured area
- Paradoxical movement: the affected part of the chest will move in the opposite direction compared to the rest of the chest. So during inhalation,
instead of expanding outwards, the affected part of the chest will move inwards. And during exhalation, instead of moving inwards, the affected
part of the chest will move outwards.
Manifestations:
- Pain
- Potential lung injury
- Can worsen breathing patterns and cause hypoxemia
- Unconscious patient:
- Rapid, shallow breaths
- Tachycardia
- Conscious patient:
- Initial sign: chest wall splinting
- Poor air movement
- Asymmetrical thorax motion
Diagnostics:
- Palpation - rib crepitus grinding sound
- Chest radiography
- ABGs assessment
Treatment:
- Goal of treatment: re-expand the lung and ensure oxygenation
- Pt may need short-term mechanical ventilation.
- Ensure adequate ventilation, humidified oxygen, crystalloid IV fluids, and pain management
Describe the purpose of chest tubes, the methods of action, and related nursing responsibilities in the care of a patient with a chest tube.
Chest Tubes

Purpose - Remove air and fluid from pleural space

- Restore normal intrapleural pressure for lung re-expansion

Chest Tube Insertion Can be done in ER, bedside, or OR

- In OR, it’s inserted via thoracotomy incision
- In ER/bedside, pt is positioned sitting or lying with affected side elevated

Pleural Drainage Three Compartments:

- Collection Chamber: Receives fluid and air from chest cavity
- Fluid stays and air vents to the second compartment
- Water-Seal Chamber: Contains 2 cm of water acting as a one-way valve
- Prevents backflow of air
- Initial bubbling indicates pneumothorax evacuation
- Tidalling indicates pleural pressure changes
- Air leak → continued bubbling
- Suction Control Chamber: Applies controlled suction
- Uses water or dry system
- Regulates suction depth
- Excess pressure is relieved through bubbling

Heimlich Valves:
- Used to evacuate air
- Used in emergency transport and home care

Small Chest Tubes (Pigtail Catheters):

- Less traumatic
- Not suitable for trauma or blood drainage
- Risks: kinking, occlusion, or dislodgement
- Caution is needed with pts on mechanical ventilator d/t risk of tension pneumothorax

Nursing Responsibilities - Routine milking/stripping of chest tubes is no longer recommended d/t risk of high intrapleural pressure and
pleural tissue damage
- Clamping for more than a few seconds should only be done to assess pt tolerance before tube removal
- Ensure that the chest tube dressing is right and intact
- Administer prescribed analgesic
- Check around the chest tube insertion side for crepitus (which indicated air leakage)
- Add fluid to the suction control chamber as needed
- Chest for air bubbling in the water seal chamber
- Palpate the skin to detect subcutaneous emphysema
- Place the chest tube drainage system below the chest
 Complications
- Chest tube malposition (most common complication)
- Nurse should:
- Check for tidalling in the water-seal chamber
- Listen to breath sounds
- Measure the amount of fluid drainage
- Re-expansion pulmonary edema d/t rapid lung expansion or evacuation of large pleural fluid volumes
- Vasovagal response with symptomatic hypotension d/t too-rapid fluid removal.
- Infection at the skin site
- Pneumonia d/t lack of deep breaths, not using an incentive spirometer, and splinting on the affected side.
- Frozen shoulder d/t lack of ROM exercises

Explain the types of chest surgery and appropriate preoperative and postoperative care.
Indications Preoperative Care Postoperative Care

- Baseline data on respiratory and

CV systems before surgery
Thoracotomy Hiatal hernia repair, open-heart surgery, (thorough assessment needed)
esophageal surgery, tracheal resection, - Perform diagnostic studies:
aortic aneurysm repair pulmonary function, chest
radiography, ECG, ABGs, BUN,
serum creatinine, blood glucose, Idk I don’t have access to it, but the rest
serum electrolytes, CBC is the same as regular post-op care
- Pre-op teaching - deep breathing anyways
exercises, incentive spirometry,
Video-Associated pain management, incision
Thorasoscopic Surgery Lung biopsy, lobectomy, resection of
nodules, repair of fistulas splinting using a pillow, purpose Thank you from Jp.
(VATS) of chest tubes & their connection
to water-sealed drainage
systems
- Teach ROM exercises for the
surgical side
- Reassure pt about the lung's
functional reserve and ability to
Lobectomy Lung cancer, bronchiectasis, TB, maintain adequate oxygenation
emphysematous bullae, benign lung even after partial removal
tumours, fungal infections
 WEEK 8 - GAS EXCHANGE/ PERFUSION
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Explain the expected anatomical and physiological adaptations to pregnancy in the gravid patient.
Pregnancy: Hormonal Changes

Hormone Changes Associated Signs + Symptoms

hCG hCG will ↑ until 9–10 weeks N/V, fatigue

(earliest biomarker of pregnancy) Abnormally high hCG → multiple gestation
Decreasing/ slowly increasing → miscarriage

Causes fat to deposit over maternal abdomen, back, upper Excess salivation, nasal congestion, epistaxis,
thighs. gingivitis
Estrogen Promotes enlargement of uterus, genitals, breasts.
Relaxes pelvic ligaments + joints.
↑ water + Na+ retention.
↑ vascularity.

Maintains pregnancy via uterine muscle relaxation (prevents Constipation, heartburn, flatulence
Progesterone contractions).
Stimulates uterine growth.
Causes fat to deposit over maternal abdomen, back, upper
thighs.

Oxytocin Stimulates uterine contractions. L+D at the end of pregnancy

Prolactin Prepares the breasts for lactation. Production of colostrum (white-yellow pre-milk)
 Pregnancy: Reproductive Changes

Organ Changes

Changes in shape: at conception, the uterus looks like an upside down pear.
- Then, it looks like a sphere during the second trimester.
- As the fetus grows, the uterus looks more oval

Changes in size: Uterus becomes bigger.

- Uterine bruit (because of ↑ dilation, vascularity, hypertrophy)
Uterus - The uterus is the size of an egg at 7 weeks, an orange at 10 weeks, and a grapefruit at 12 weeks

Changes in position: overtime, the uterus moves out of the pelvis, and into the abdominal cavity
- Fundal height can tell you the position of the uterus
- Around 22–24 weeks, you can palpate the uterus by the umbilicus.
- When the pregnancy reaches full term, you can palpate the uterus by the xyphoid process

Friability: ↑ sensitivity of the cervix → ↑ bleeding after sex or cervical exam

Goodell sign, chadwick sign, hegar sign

Cervix - Cervical softening, blueish mucus membranes, softening of uterine isthmus (respectively)

After birth, the cervix becomes more oval (whether lacerations occur or not)

The cervix becomes more vascular, and tends to bleed more easily

Placenta The placenta helps deliver oxygen and nutrients from the mother to the fetus

Leukorrhea: white mucus discharge with musty smell

Vagina pH of vaginal secretions become more acidic

- But even with this, there is still an ↑ in yeast infections

Formation of a mucus plug

 Pregnancy: Breast Changes

Changes in: Associated Signs + Symptoms of Pregnancy

Breast Become enlarged + areola darkens → ↑ stretch marks around outer area of the breasts

↑ sensitivity/tenderness by 6 weeks (prickling sensation, fullness/heaviness of breasts)

Blood vessels under the breasts become more visible

Breasts become softer and looser because there’s more glandular tissue present

Discharge Colostrum is secreted during the second trimester

- White-yellow pre-milk produced at 16+ weeks (breasts are ready for lactation by week 16)

Pregnancy: Skin Changes

Changes Associated Signs + Symptoms of Pregnancy

Striae Gravidarum Stretch marks (most common during second half of pregnancy)

Linea Nigra Hormone-induced hyperpigmentation, moving down the midline

- Appears around 3 months during the first pregnancy
- In 2nd or later pregnancies, it shows up much earlier

Chloasma Blotchy, brownish hyperpigmentation around the cheeks, nose, and forehead
- Sun exposure makes them more noticeable
- Fades after birth
- Can recur with more pregnancies or oral contraceptives

Spider Nevi (Vascular Spiders) Tiny, branched pulsating end-arterioles

- Found on neck, thorax, face, and arms
- Caused by ↑ estrogen → ↑ blood flow to skin
- Disappears within first 3 months postpartum
 Pregnancy: Cardiac Changes

Changes Associated Signs + Symptoms of Pregnancy

↑ cardiac volume + output The fetus is growing → ↑ metabolic demands → ↑ blood volume → hypertrophy
- CO increases from 30% → 50% (by 32 weeks)

↑ pulse by 15-20bpm (by 32 weeks)

↑ pulse - Helps meet ↑ O2 demands

Palpitations, murmurs, and arrhythmias may be present

↑ systolic BP during first trimester, and ↓ systolic BP during second trimester

↑/↓ diastolic BP
↓ diastolic BP throughout 1st and 2nd trimester, and levels off by the time pregnancy reaches full term

Supine hypotensive syndrome ↓ BP when you lay on your back because the uterus presses on the vena cava
- Happens during the second half of pregnancy
- The mom should lay on her side instead

↑ blood volume ↑ by 40-50%

- It’s a protective mechanism after delivery
- Helps take away waste products

↑ RBCs Linked to ↑ blood volume

↑ WBCs Peaks during 3rd trimester

↑ Blood clotting ↑ risk of thromboembolic disease

- Caused by ↑ clotting factors, and ↓ coagulation inhibitors

Physiologic Anemia Caused by ↑ blood volume, but not enough RBCs

- This is because plasma production is faster than RBC production
 Pregnancy: Respiratory Changes

Changes Associated Signs + Symptoms of Pregnancy

↑/unchanged Respiratory Rate Caused by ↑ progesterone and ↑ basal metabolic rate (BMR)

Elevated Diaphragm Growing uterus puts pressure on diaphragm, causing it to rise

- Chest breathing replaces abdominal breathing

Costal angle ↑, and lower rib cage flares out

↑ Chest Expansion Transverse diameter ↑

**total lung capacity does NOT change

↑ O2 consumption ↑ by 20-40% above non-pregnant levels

- Caused by ↑ basal metabolic rate (BMR)

Shortness of Breath (SOB) More intense closer to the end of the pregnancy

Changes in Acid-Base Balance ↑ progesterone → respiratory centre to become more sensitive

Causes PaCO2 and bicarbonate to ↓, and causes pH to slightly ↑

↑ estrogen → URT becomes more vascular

Nasal Congestion/Epistaxis
Causes edema and hyperemia in the nose, pharynx, larynx, trachea, bronchi

Leads to sinus stiffness, epistaxis (nosebleed), voice change, increased inflammatory responses
 Pregnancy: Urinary Changes

Changes Associated Signs + Symptoms of Pregnancy

Renal pelvis + ureters dilate

- Later on in pregnancy, renal pelvis + ureters dilate more on the right side than on the left
Structural Changes
Bladder is located by the true pelvis during the second trimester

↑ Frequency ↑ bladder sensitivity → ↑ frequency (early in pregnancy)

Bladder compression → ↑ frequency (closer to term)

↑ Bladder Capacity Structural changes → urinary stasis → ↑ infections because MOs will stay in the body

Glycosuria Caused by impaired tubular resorption of glucose

Edema Pooling of fluid, usually in the legs, during latter parts of pregnancy
- Causes ↓ in renal blood flow and GFR

Proteinuria ↑ urinary excretion of protein + albumin (mostly after 20 weeks)

Proteinuria > 300mg/day or albuminuria > 30mg/day is abnormal

 Pregnancy: Gastrointestinal (GI) Changes

Changes Associated Signs + Symptoms of Pregnancy

Pica: cravings for things that are not food (dirt, ice, starch, etc.)
- Can be a concern for nurses because it can cause an imbalanced diet, or the pt may eat something unsafe
- Associated with iron-deficiency anemia and poor weight gain
Appetite
↑ hCG → N/V is common (morning sickness)
- Occurs around 4 weeks, and lasts until the end of the 1st trimester

Gums look red, swollen, bleed easily, etc., because of ↑ estrogen

- Nursing intervention: have the pt use a softer toothbrush
Mouth
↑ risk of gingivitis + periodontis

Some may experience ptyalism (excessive salivation)

Colon is displaced

↑ progesterone → slower emptying time of stomach + reverse peristalsis → pyrosis (heartburn)

Esophagus, Stomach, Intestines
↑ progesterone → ↑ water reabsorption → constipation
- If hemorrhoids are present during constipation, they can bleed
- Hemorrhoids would be caused by ↑ venous pressure

↓ muscle tone → gallbladder is distended

Gallbladder
Bile becomes thicker, ↑ emptying time

↑ progesterone → hypercholesterolemia → gall stone formation

There are only minor changes in liver function

Liver ↓ serum albumin levels and protein levels

Intrahepatic cholestasis (bile retention + accumulation) occurs later in pregnancy

Abdominal Discomfort Growing uterus → intra-abdominal changes → ↑ venous pressure → pelvic pressure, bowel distention + cramping,
uterine contractions, flatulence, round ligament tension
 Pregnancy: Neuro-Musculoskeletal (N-MSK) Changes

Changes Associated Signs + Symptoms of Pregnancy

Stooped shoulder stance → lordosis → acroesthesia (numbness + tingling in hands)

Centre of gravity is shifted forwards → lordosis

Postural Changes - Encourage the patient to maintain good posture to help ↓ strain on the back

Abdominal distention → pelvis tilts forward, ↓ abdominal muscle tone, ↑ weight-bearing

↑ peripheral joint flexibility as pregnancy progresses

Relaxation of Pelvic Joints ↑ elasticity of tissue +mobility of pelvic joints → waddling gait

Third trimester: rectus abdominis muscles separate → abdomen sticks out

- Muscles will regain tone after birth

Umbilicus either flattens, or sticks out

Edema of peripheral nerves → CTS during last trimester

Carpal Tunnel Syndrome (CTS) Causes burning or tingling sensation, pain in the hand radiating to elbow
- Dominant hand is affected the most

Symptoms slowly disappear after pregnancy

Surgery might be needed

Differentiate gestational hypertension, chronic hypertension, and other hypertension.

- Hypertension in Pregnancy (HDP)
- Non-severe HTN
- Systolic BP ≥ 140mmHg and/or diastolic BP ≥ 90mmHg
- Should be taken at two separate measurements at least 15 mins apart
- Prevention:
- Antihypertensives
- BP goal: diastolic BP of ~85mmHg to ↓ risk of severe HTN
- Severe HTN
- Systolic BP ≥ 160mmHg and/or diastolic BP ≥ 110mmHg
- Should be taken at two separate measurements at least 15 mins apart
- The higher the BP, the greater the risk of adverse perinatal outcomes
 Gestational Hypertension Chronic Hypertension Transient Hypertension

Definition: HTN that appears for the first time at or Definition: HTN that either, predates the Definition: elevated BP d/t environmental stimuli
beyond 20 weeks’ gestation, in the absence of pregnancy, or appears before 20 weeks’ gestation
proteinuria and without changes in blood work

White Coat Hypertension Masked Hypertension Pre-eclampsia / Eclampsia

Definition: BP that is elevated in the doctor’s office Definition: BP that is consistently normal in the **Look below**
(≥140/90), but is normal outside of it (<135/85) doctor’s office (<140/90), but is consistently higher
outside of it (≥135/85)

Explain the etiology, pathophysiology, clinical manifestations, interprofessional care, and nursing management of preeclampsia and
eclampsia with rationales.
Preeclampsia: What is it?

Definition: a hypertensive disorder accompanied by new-onset proteinuria and, potentially, other end-organ dysfunction
- It’s a multisystem, vasospastic disease process involving a ↓ in organ perfusion
- It’s characterized by the presence of HTN and proteinura
- It has a clinical continuum from mild to severe

- In pre-eclampsia, the vessels are abnormally thick-walled and muscular and have higher resistance
- Pre-eclampsia → a distinctive lesion called acute atherosis → greater occurrence of placental infarcts
- There is a ↓ in placental perfusion → hypoxia → several pathophysiological abnormalities (especially endothelial damage)
- Many of these pathophysiological changes of pre-eclampsia occur before clinical symptoms develop

Preeclampsia: Pathophysiology

The pathophysiology of pre-eclampsia reflects alterations in the normal adaptations of pregnancy

- Normal physiological adaptations to pregnancy include ↑ blood plasma volume, vasodilation, ↓ systemic vascular resistance, ↑ CO, and ↓ colloid osmotic
pressure.

- Main pathogenic factor is poor perfusion d/t vasospasm, NOT an ↑ in BP. Arteriolar vasospasm → VERY small diameter of blood vessels → disrupted
blood flow to all organs, ↑ BP
- Vessels are abnormally thick-walled and muscular and have higher resistance
- Presence of pre-eclampsia → a distinctive lesion called acute atherosis → greater occurrence of placental infarcts
- There is a ↓ in placental perfusion → hypoxia → several pathophysiological abnormalities (especially endothelial damage)
- Many of these pathophysiological changes of pre-eclampsia occur before clinical symptoms develop
 Preeclampsia: Etiology

Risk Factors
- Nuliparity - Pre-eclampsia in previous pregnancy
- Age > 40 years - Poor outcome in previous pregnancy
- Pregnancy with assisted reproductive technology - Chronic HTN
- Interpregnancy interval > 7 years - Renal disease
- Family Hx of pre-eclampsia - T1DM
- Obesity/gestational DM - Antiphospholipid antibody syndrome
- Multifetal gestation - Factor V Leidon mutation
Causes:
- Abnormal prostaglandin action
- Endothelial cell dysfunction
- Coagulation abnormalities
- Vasoconstrictor tone
- Dietary deficiencies or excess

Preeclampsia: Manifestations

Manifestation Why it Occurs

Edema around the face and extremities As endothelial cells become damaged, permeability of blood vessels changes.
So as water leaks out of the vessels & into the interstitial space, swelling will ↑

HTN

Proteinuria As endothelial cells become damaged, protein will be able able to leak through
the blood vessels, into the urine

SOB Occurs d/t the fluid leaking into the lungs

Weight gain Occurs d/t ↑ water weight

Neuro changes: blurred vision, headache, irritability, etc. Occurs d/t edema/swelling of the brain, which will cause CNS changes

RUQ pain Occurs d/t poor perfusion to the liver

Hyperreflexia Occurs d/t neuro changes. It shows that the pt is at greater risk for seizures
 Preeclampsia: Diagnostics/Criteria

Presence of gestational or chronic HTN + new-onset proteinuria

- There may also be presence of other organ dysfunctions
- E.g. acute kidney or liver dysfunction; neurological complications (seizures, blindness, stroke, or severe headaches)
- There will be ↑ BUN, ↑ creatinine, and ↓ urine output because as endothelial cells become damaged, fluid will leak out, which will ↓
perfusion to the kidneys and other organs
- E.g. hematological complications (thrombocytopenia, disseminated intravascular coagulation (DIC), or hemolysis)
- Proteinuria: concentration of 0.03 g/L or more in at least 2 random urine specimens collected at least 6 hrs apart where there is no evidence of a UTI
- In a 24hr specimen, proteinuria is defined as a concentration > 0.3 g/L per 24 hrs
 Preeclampsia: Interprofessional Care

**Treatment must occur in the hospital, to ↓ risk of complications to the pregnant pt, or risk of intrauterine fetal morbidity and mortality r/t uteroplacental
insufficiency and placental abruption

Preeclampsia: Nursing Management

Nursing Assessment:
- Important for establishing a baseline and for monitoring subtle changes throughout the pregnancy
Blood Pressure Assessment - BP is affected by pt’s position and measurement techniques (so you want to make sure that you’re being consistent)

- Biceps and patellar reflexes, and the ankle clonus are assessed
Deep Tendon Reflexes (DTRs) - This is very important for pts on magnesium sulphate
- ↓ or absent DTRs indicate magnesium toxicity
- Calcium gluconate is an antidote for magnesium sulphate toxicity

- Can be done through a non-stress test (NST), contraction stress test (CST), biophysical profile (BPP),
and serial ultrasonography
Fetal Health Surveillance - Fetal HR is assessed for baseline rate, variability, and presence of accelerations
- Abnormal baseline rate, ↓ or absent variability, or late decelerations are indications of fetal stress in the
intrauterine environment
- Should also assess pt’s uterine tone, tenderness, and for any vaginal bleeding

Implementation:
- Strict bed rest is not recommended, but some reduced activity would be helpful when trying to ↓ BP,
promote fetal growth, and and improve amniotic fluid levels
Activity Restriction - Adverse physiological outcomes r/t bed rest: cardiovascular deconditioning, diuresis with accompanying fluid
loss/electrolyte loss/weight loss, muscle atrophy, psychological stress
- Prolonged bed rest can ↑ risk of thrombophlebitis.

- Similar diet recommendations as other pregnant women

Diet - Not recommended: high-protein, low-sodium diet
- Recommended: adequate fluid intake, limit caffeine intake, adequate fibre intake,

- If the patient’s condition requires intensive monitoring, they may need care in a CCU for hemodynamic
monitoring
- If pre-eclampsia with severe features is diagnosed, birth is warranted regardless of gestational age
- For pregnant patients at risk of giving birth prior to 35 weeks’ gestation, corticosteroids (betamethasone)
 should be given to promote fetal lung maturation.

Assessments:
- CNS: Monitor for signs of neurological complications
- CV System: Regularly check BP and HR, assess hemoglobin O2 sat
Hospital care - Respiratory System: Auscultate breath sounds for crackles or diminished sounds (they indicate
pulmonary edema)
- Renal System:
○ Insert indwelling urinary catheter to measure urinary output
○ Monitor renal function and effectiveness of therapy
○ Be mindful of the risk of UTIs in stable antepartum patients

Baseline Laboratory Assessments:

- Liver Function Tests: AST, ALT, lactate dehydrogenase (LDH), and bilirubin.
- CBC: Includes platelet count.
- Coagulation Profile: Includes fibrinogen to assess for disseminated intravascular coagulation (DIC).
- Electrolytes: To assess renal function

Fetal Assessment:
- Uterine Activity: Vaginal examination for cervical changes.
- Abdominal Palpation: Check uterine tonicity, fetal size, activity, and position.
- Fetal Surveillance: Non-Stress Test (NST) and Biophysical Profile (BPP) to monitor for potential hypoxia.
- Electronic Fetal Monitoring: Initiate at least once a day

- Goal of care: prrevent/control convulsions (eclamptic seizures)

- It’s administered as a secondary infusion ("piggyback") to a primary line
- Rarely given through IM route d/t poor absorption control, pain, and risk of tissue necrosis
- After the loading dose, there may be a transient lowering of the arterial BP secondary to relaxation of smooth muscle.
- MoA: Interferes with ACh release → ↓ neuromuscular irritability, ↓ cardiac conduction, ↓ CNS irritability
Magnesium Sulphate - Monitoring:
- Monitor maternal kidney Function and urine output
- Diuresis indicates improved kidney perfusion but can signal impending renal failure if clinical
status worsens
- Magnesium Toxicity is rare at 1g/hr (monitor symptoms & Mg2+ levels)
- Serum Creatinine Levels: Monitored as a risk factor for toxicity
- Common Adverse Effects: Lethargy, warmth, headache, nausea.
- Early Signs of Toxicity: Vomiting, respiratory distress, hypotension, flushing, muscle weakness, ↓
reflexes, slurred speech
 - Goals of care: prevent left ventricular failure and cerebral hemorrhage, ↓ BP without excessive/rapid ↓(to
avoid affecting uteroplacental perfusion)
Controlling Blood Pressure - Preferred medication: labetalol
- Alternatives: nifedipine, methyldopa, hydralazine, other β-blockers (acebutolol, metoprolol,
pindolol, propranolol)

Immediate Care Goals:

- Ensure Airway Patency
- Document: time, duration, and description of convulsions; note any urinary or fecal incontinence.
Immediate Care for Eclampsia - Administer Magnesium Sulphate for prevention of recurrent seizures.
- Alternative Medications: Phenytoin or benzodiazepines if magnesium sulphate is contraindicated
- Monitor Fetus for adverse effects
Post-Seizure Care:
- Hygiene Assistance - gown change, oral care with a soft toothbrush
- Evaluate uterine activity, cervical status, & fetal status post-seizure
- Control seizure activity and BP, then assess the need for immediate delivery based on the pt's condition
Post-Stabilization Care:
- Aspiration Risk: Leading cause of maternal morbidity and mortality.
- Anticipate CXR and ABGs to check for aspiration

- After birth, symptoms of pre-eclampsia and eclampsia will resolve within 48hrs
- But postpartum pt should still be monitored from days 3-6 after giving birth
- Diuresis within 24-48hrs indicates that the problem is resolving
Ongoing Assessments:
- Vital Signs, ins/outs, reflexes and LOC
- Monitor uterine tone and lochia flow for abnormalities.
- Continue magnesium sulphate infusion for 24 hrs for seizure prophylaxis. Assess as needed until
Postpartum Care medication is discontinued.
Postpartum Care and Medications:
- Use Oxytocin or Prostaglandin products for bleeding control
- Avoid ergot products (e.g., ergonovine, methylergonovine) d/t blood pressure-raising effects.
- Headache Management: Assess affect, consciousness, BP, pulse, and respiratory status before
administering analgesics
- Use narcotics and CNS depressants with caution, d/t potentiation by magnesium sulphate.
- Pts using antihypertensive meds during pregnancy can go back to using them after birth as well
Postpartum Recovery Considerations:
- Nurse should assist and monitor for weakness, dizziness, SOB, and muscle soreness.
- Consider thromboprophylaxis with LMWH for pts with HTN or pre-eclampsia, C-section, or significant
postpartum hemorrhage
Emotional and Psychological Support:
- Monitor and support emotional well-being. Encourage involvement in newborn care as desired.
- Address concerns, especially if the infant is premature or in the NICU
 - Let the pt and family discuss their experiences and concerns
- Assist the family with dealing with unfavorable outcomes and grief

- Even if pts have a normal BP in future pregnancies, there is a higher risk of:
- Preterm birth, small-for-gestational-age infant, perinatal death
Counselling during preconception visits:
Future Health Care - Review previous pregnancy Hx and prognosis for upcoming pregnancy
- Encourage weight loss and ↑ physical activity.
- Assess and control chronic medical conditions (e.g. DM, HTN)
- Review and modify current medications if necessary
- Likely recommended low-dose aspirin, especially if previous pregnancy was complicated by pre-eclampsia
Long-term health risk:
- Pts with a Hx of pre-eclampsia have ↑ risk of chronic HTN and CV disease

Describe HELLP syndrome, including appropriate nursing actions with rationales.

HELLP Syndrome: What is it?

HELLP syndrome is severe pre-eclampsia + abnormalities in laboratory blood results:

- Hemolysis (H)
- Elevated Liver enzymes (EL)
- Low Platelets (LP)

HELLP Syndrome: Pathophysiology

Arteriolar vasospasm and adherence of platelets in blood vessels → RBCs become damaged as they pass through narrow blood vessels → RBCs become
hemolyzed → ↓ RBC, ↓ platelet count, hyperbilirubinemia.

Endothelial cell dysfunction with fibrin deposits in the liver → impaired liver function → hemorrhagic necrosis, ↑ liver enzymes (d/t hepatic tissue damage)

HELLP Syndrome: Manifestations

Manifestations: Why it Occurs

Malaise Occurs for several days

Epigastric or RUQ pain Occurs d/t hepatic ischemia

 N/V Probably caused by liver dysfunction

Renal failure Occurs d/t ↓ renal blood flow

Pulmonary edema

Ruptured liver hematoma

DIC Occurs d/t ↓ platelets

Placental abruption

HELLP Syndrome: Diagnostics

Diagnostic Study What do you see on there?

CBC Platelet count < 100×109/L

Liver Function Test ↑ AST and ALT

PT/PTT normal

Coagulation Factor Assay normal

Uterine Artery Doppler Velocimetry Will determine patients at risk for pre-eclampsia during their first or second
trimester, so that they can be started on low-dose aspirin

HELLP Syndrome: Management

Intervention Rationale

Salt restriction Will help manage HTN

Zinc, magnesium, fish oil, or vitamin C & E supplements

Diuretics or other antihypertensives Will help manage HTN

Heparin or low-dose aspirin Helps manage pre-eclampsia, which will ↓ risk of severe HELLP syndrome
Discuss the diagnosis and management of disseminated intravascular coagulation (DIC) with rationales.
DIC: Causes

- Placental abruption
- Retained dead fetus syndrome
- Amniotic fluid embolus
- Pre-eclampsia
- HELLP syndrome
- Gram-negative or gram-positive sepsis

DIC: Diagnostics

Diagnostic Study What do you see on there?

CBC ↓ platelets

Coagulation Panel ↓ PT/PTT prolong?

Factor Assays ↓ factor V, ↓ factor VIII

Fibrinogen Level ↓ fibrinogen

Fibrin Degradation Products Test (including D-dimer) ↑ fibrin degradation products, ↑ D-dimer

Peripheral Blood Smear Fragmented RBCs

DIC: Collaborative Care

Intervention Rationale

Correct underlying cause You want to to treat pre-eclampsia, eclampsia, or severe infection. Or you may
want to remove a placental abruption or dead fetus.

Volume expansion Will help maintain BP and perfusion to vital organs

Rapid replacement of blood products and clotting factors Will help replenish all the blood cells products that are lost in DIC

Optimization of oxygenation Will help prevent hypoxemia r/t bleeding

Achieve normal body temperature

 Vitamin K administration Will help synthesize clotting factors

Recombinant activated factor VIIa

Fibrinogen concentrate

Hemostatic agents

DIC: Nursing Interventions

Intervention Rationale

- Assess for signs of bleeding (e.g., petechiae, oozing from injection

sites, hematuria, hemoptysis)
Monitoring and Assessment - Monitor for complications from blood/blood products administration
- Cardiac and hemodynamic monitoring
- Protect patient from injury
- Monitor urinary output (goal: ≥ 30 mL/hr) using indwelling catheter
- Frequent assessment of VS
- Continuous electronic fetal monitoring if DIC develops before birth
- Maintain pt in a side-lying tilt to maximize uterine blood flow

Oxygen Administration - Administer O2 through a tight-fitting rebreathing mask at 8-10 L/min or

per protocol/order

Maintaining Normothermia - Use forced-air warming systems (e.g., Bair Hugger)

- Utilize warmed blankets and fluid warmers as needed

Emotional Support - Offer explanations about care

- Provide emotional support to the patient and their family
 WEEK 9 - GAS EXCHANGE/ PERFUSION
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Compare/contrast placenta previa & placental abruption in terms of signs and symptoms, complications, and management with rationales.
Placenta Previa: What is it?

In placenta previa, the placenta is implanted in the lower uterine segment such that it completely or partially covers the cervix or is close enough to the cervix to
cause bleeding when the cervix dilates or the lower uterine segment effaces

Placenta Previa: Manifestations

Manifestation Why it Occurs

Painless, bright red vaginal bleeding Occurs d/t stretching and thinning of the lower uterine segment, which causes
disruption of placental blood vessels that occurs with

Normal vital signs VS will be normal d/t compensatory mechanisms of pregnancy (and because up to
40% of blood volume can be lost without showing signs of shock)

Soft, relaxed, nontender uterus with normal tone

Greater fundal height than expected The presenting part of the fetus usually remains high because the placenta occupies
the lower uterine segment

Fetal malpresentation (breech, transverse, or oblique lie) Occurs d/t the abnormally presented placenta
 Placenta Previa: Complications

Complication Why it Occurs

Maternal complication: hemorrhage Pt in labour → cervix dilates → disrupted placental attachment → bleeding

Maternal complication: abnormal placental attachment

Fetal complication: preterm birth

Fetal complication: intrauterine growth restriction (IUGR) There may be inadequate nutrients and oxygen to the fetus → ↓ fetal growth

Placenta Previa: Diagnosis

Diagnostic What it will show

Transabdominal Ultrasound Placenta will be located in the lower uterine segment

Transvaginal Sonography (TVS) The placenta is classified as a “complete placenta previa” if it completely covers
the internal cervical os
If the edge of the placenta is 2.5 cm or closer to the internal cervical os, it’s
called “marginal placenta previa”
 Placenta Previa: Collaborative Care

Intervention Rationale

Criteria: < 36 weeks gestation, not in labour, minimal/no bleeding

Rationale: will help the fetus grow in utero
Additional info:
Expectant Management (↓ activity, close observation) - U/S will be done every 2 weeks.
- NST or BPP will be done for fetal surveillance.
- B/W will be done to check Hgb, Hct, and coagulation values.
- Antepartum steroids (i.e. betamethasone) will be given to promote fetal
lung maturity if pt is < 34w gestation.

Home Care Criteria: varies between primary perinatal providers.

Additional info:
- Pt must have close supervision by family/friends at home
- Pt should avoid intercourse, douching, and use of enemas

Active Management Criteria: ≥ 36 weeks gestation, excessive bleeding

Additional info:
- C-section needed immediately
- Monitor maternal VS to look out for changes in BP, ↑ HR, changes in
LOC, and oliguria
- Explain all procedures, and support person should be present with pt
- Contact hospital chaplain service if pt and family want spiritual care
 Placental Abruption: What is it?

“Placental abruption” is the detachment of a part of, or all of, the placenta from its implantation site.

Placental Abruption: Manifestations

Manifestation Why it Occurs

Partial or complete separation of the placenta I mean, it’s literally in the name

Couvelaire uterus Occurs because ​extensive myometrial bleeding damages the uterine muscle. So,
(ecchymotic, purplish & copper-coloured uterus, and loss of contractility) blood can accumulate between the separated placenta and the uterine wall

Dark red, vaginal bleeding It’s probably dark red d/t venous blood pooling

Abdominal pain Pain will be mild to severe, and will be localized over one region of the uterus,
or diffuse over the uterus with a boardlike abdomen

Uterine tenderness Uterine tenderness will be mild-to-severe.

Contractions

Maternal hypovolemia

Coaguloapathy
 Placental Abruption: Complications

Complication Why it Occurs

Hemorrhage Caused by severe abruption

Hypovolemic shock Caused by severe abruption

Hypofibrinogenemia Caused by severe abruption

Thrombocytopenia Caused by severe abruption

Couvelaire uterus

DIC

Infection

Renal failure Caused by ischemia

Pituitary necrosis Caused by ischemia

IUGR

Oligohydramnios (↓ amniotic fluid volume for gestational age)

Preterm birth

Hypoxemia

Stillbirth
**light pink = maternal complication; darker pink = fetal complication
 Placental Abruption: Diagnosis

Diagnostic Study What do you see on there?

Ultrasound (used to rule out placenta previa) May be able to see a retroplacental mass.

Physical examination Abdominal pain, uterine tenderness, contraction, ↑ fundal height over time

Electronic fetal heart monitor Loss of variability and late decelerations, uterine tachysystole

Clotting studies Coagulopathy

Placental Abruption: Collaborative Care

Intervention Rationale

Hospitalization & close monitoring This is done for mild placental abruption. Expectant management is
implemented if the fetus is < 36 weeks of gestation, and not in distress.

Fetal monitoring Fetal HR needs to be intermittently monitored, and NST and BPP needs to be
done until the fetus is more mature.

Immediate birth Immediate delivery is needed if the pt is deteriorating.

Rho(D) immunoglobulin Will be given to Rh negative pts if fetal-to-maternal hemorrhage occurs, and the
fetal blood is Rh positive.

In-dwelling catheter Used in order to assess urine output (which indicates maternal perfusion)

Fluid volume (or blood products) replacement May be needed to correct any coagulation defects
Identify causes, signs and symptoms, possible complications, and medical and nursing management of postpartum hemorrhage.
Postpartum Hemorrhage: Causes

Tone: Uterine Atony (marked hypotonia) Trauma

Uterus fails to contract after birth, leading to bleeding - Lacerations of the birth canal
- Over-distended uterus (large fetus, multiple fetuses, hydramnios, - Trauma during labour and birth—forceps-assisted birth,
distension of clots) vacuum-assisted birth, Caesarean birth
- Anaesthesia and analgesia - conduction anaesthesia - Ruptured uterus
- Previous history of uterine atony - Inversion of the uterus
- High parity - Manual removal of a retained placenta
- Prolonged labour, oxytocin-induced labour - Pelvic hematomas
- Magnesium sulphate administration during labour or postpartum period
- Chorioamnionitis Tissue
- Uterine subinvolution - Retained placental fragments
- Obesity - Placenta accreta, increta, percreta
- Placental abruption
Thrombin - Placenta previa
Can result from conditions like pre-eclampsia, severe infections, or fetal demise
- Coagulation disorders
- Immune thrombocytpenic purpura (ITP), von Willebrand disease
(vWD), DIC

Postpartum Hemorrhage: Manifestations

Manifestation Why it Occurs

Persistent perineal, vaginal, or rectal pain, pressure Occurs d/t vulvar hematoma

Minimal pain, initial symptoms can be signs of shock Retroperitoneal hematoma

Prolonged lochial discharge, foul odour, pain, fever, irregular or excessive D/t subinvolution of the uterus (delayed return of the enlarged uterus to normal
bleeding, and sometimes hemorrhage size and function)

Presence of a palpable mass through the dilated cervix Occurs d/t incomplete inversion of the uterus

Presence of mass in the vagina Occurs d/t a complete inversion of the uterus, since the lining of the fundus
crosses through the cervical os

A large, red, rounded mass protrudes 20-30 cm outside the introitus Occurs d/t a prolapsed inversion of the uterus
 Postpartum Hemorrhage: Collaborative Care

Intervention Rationale

- Accurately quantify blood loss (e.g. weigh perineal pads)

- During excess blood loss, evaluate uterine contractility and amount of bleeding
Early Recognition & Treatment - If the uterus is hypotonic, try to ↑ contractility with uterine massage and uterotonic medications
- If the uterus is firm but bleeding continues, identify & treat the bleeding source through
visual/manual inspection and lab studies

Active Management during Third Stage of Labor:

- Administer IM or IV oxytocin after delivery
- Consider delayed cord clamping, gentle cord traction, and immediate fundal massage
- IV infusion of oxytocin after complete birth
- If placenta delivery exceeds 30 minutes, PPH risk will ↑
Management of Uterine Atony:
- Provide firm massage of the uterine fundus
Medical Management - Remove clots
- Eliminate bladder distension
- Continuously administer 10–40 units of IV oxytocin in 1000mL of RL or NS
- If unresponsive to oxytocin, use additional uterotonic medications
- Misoprostol, Methylergonovine, Carboprost
Other Treatments Options:
- Administer crystalloid solutions or blood products to restore intravascular volume
- Provide O2 via NRB mask to enhance cellular O2 delivery
- Monitor bladder status
- Use indwelling catheter to keep bladder empty and monitor urine output
- Conduct lab studies (CBC, platelet count, coagulation studies, blood type, antibody screen)
Management of Persistent Bleeding:
- Perform bimanual compression by an obstetrical HCP
- Conduct manual exploration for retained placental fragments
- If needed, pursue surgical management (uterine tamponade, bilateral ligation of internal iliac artery,
compression suturing, or hysterectomy)
 Postpartum Hemorrhage: Nursing Management

Nursing Assessment & Interventions:

- Be vigilant for symptoms of hemorrhage and hypovolemic shock
- Use noninvasive monitoring for circulatory status
- Frequently monitor VS and encourage bladder emptying
- Interventions should align with the cause of PPH

Patient and Family Communication:

- Provide explanations about interventions and the need for quick action to ↓ anxiety

Post-Stabilization and Discharge:

- Prepare for discharge with instructions similar to standard postpartum care, plus additional considerations:
- Expect and manage fatigue
- Limit physical activity
- ↑ dietary iron and protein, and use iron supplements to rebuild RBC volume.
- Arrange assistance for newborn care and household activities until strength is regained
- Address potential delayed lactogenesis, insufficient milk production, or perinatal mood disorders
- Refer to home care follow-up or community resources as needed
 WEEK 10 - HORMONE REGULATION
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Addison’s Disease Cushing’s Syndrome SIADH Diabetes Insipidus

Prepare a concept map or table summarizing the concept of hormone regulation.
Hormones & Hormone Regulation

What are hormones? How many types of Hormones are chemical messages found in the blood, and they have specific effects depending on target cells
hormones are there?

What do they do? Synthesis of new molecules, change membrane permeability, activate/deactivate enzymes, stimulate
reproduction

How do they work? Hormones affect cells with specific receptors, and they’re constantly self-regulated
- There are about 2000 – 10,000 receptors per target cell

Lipid-soluble (fat-based) hormones are transported via fenestrated endothelium (sinusoids), which allow the
hormones to pass through into and out of the bloodstream
How are they transported? - Exception: water-soluble (protein-based) hormones require receptor-mediated transcytosis to get
out of blood
Most hormones are secreted in little bursts, and they circulate for a short amount of time. But their effects stay for
minutes to hours.

How are they regulated? Negative Feedback:

Once the desired effects occur, the pathway that caused the effect would shut down. The hormone would also be
inactivated by the liver and excreted by the kidneys.
Review the structure and function of the pituitary gland.
Pituitary Gland

Anterior Pituitary Gland Posterior Pituitary Gland

Another name for the gland: Adenohypophysis Neurohypophysis

Growth hormone - Stimulates liver, muscle, cartilage, bone, and Oxytocin - Stimulates contraction of smooth muscle cells of uterus
other tissues to synthesize and secrete insulin-like growth factors → during childbirth; stimulates contraction of myoepithelial cells in
promotes growth of body tissues. GH acts directly on target cells to mammary glands to cause milk ejection.
enhance lipolysis and ↓ glucose uptake. Antidiuretic hormone (ADH) - Conserves body water by ↓ing
Thyroid-stimulating hormone (TSH) - Simulates synthesis urine volume; ↓ water loss through perspiration; raises blood
and secretion of thyroid hormones by thyroid gland. pressure by constricting arterioles.
Follicle-stimulating hormone (FSH) - In females, initiates
Hormones produced: development of oocytes and induces ovarian secretion of estrogens.
In males, stimulates testes to produce sperm.
Leutinizing hormone - In females, stimulates secretion of
estrogens and progesterone, ovulation, and formation of corpus
luteum. In males, stimulates testes to produce testosterone.
Prolactin - Together with other hormones, promotes milk
production by mammary glands
Adrenocorticotropic hormone (ACTH) - Stimulates secretion
of glucocorticoids (mainly cortisol) by suprarenal cortex.
Melanocyte-stimulating hormone (MSH) - When present in
excess, can cause darkening of skin
Review the structure and function of the adrenal cortex.

- The adrenal cortex produces corticosteroids

- Mineralocorticoids - i.e. aldosterone
- Glucocorticoids (steroids that affect glucose metabolism) - i.e. cortisol
- Androgens (male and female sex hormones)

Explain the adverse effects of corticosteroid therapy.

Hypertension Latent Tuberculosis
- Caused by vasopressive effects of hormones - Caused by suppression of inflammation
- Will greatly reduce resistance to other infections and cancers

Describe the pathophysiology and clinical manifestations of an imbalance of hormones produced by the adrenal cortex as well as the
interprofessional care and nursing management of affected patients.
Adrenal Insufficiency/Addison’s Disease: Cause(s)

- Primary cause: ↓ supply of glucocorticoids (e.g. cortisol), mineralocorticoids (e.g. aldosterone), and androgens (e.g. testosterone)
- Most common in industrialized nations, d/t autoimmune adrenalitis (especially in white women)
- Associated with ↑ levels of 21-hydroxylase antibodies (which destroys adrenal tissue)
- Often part of polyglandular autoimmune syndrome
- Other global causes: TB, infarction, fungal infections (e.g., histoplasmosis), AIDS, metastatic cancer
- Iatrogenic causes: adrenal hemorrhage (often d/t anticoagulant therapy), antineoplastic chemotherapy, ketoconazole therapy for AIDS, bilateral
adrenalectomy
- Secondary cause: lack of pituitary ACTH secretion
- Mineralocorticoid levels are usually normal, but levels of glucocorticoids and androgens are low
- Caused by pituitary disease or suppression of the HPA axis (e.g. from exogenous corticosteroids)
 Adrenal Insufficiency/Addison’s Disease: Pathophysiology

- Autoimmune/idiopathic destruction → insufficiency to produce + secrete adrenocortical hormones

- If it affects all layers of the adrenal cortex, then aldosterone and androgen levels will also be low
- 90% of cortex is destroyed before manifestations occur

Adrenal Insufficiency/Addison’s Disease: Manifestations

Manifestation Why it Occurs

Progressive weakness, Fatigue Probably d/t low cortisol levels

Anorexia, Weight loss

Nausea, Diarrhea

Skin hyperpigmentation ↓ negative feedback leads to low corticosteroid levels. This causes an ↑ in the
**only seen in Addison’s disease, not secondary adrenal insufficiency** secretion of β-lipotropin (which contains MSH). This leads to hyperpigmentation
in sun-exposed areas of the skin, pressure points, joints, and skin creases.

Orthostatic hypotension

Pain: Headache, Joint pain, Abdominal pain

Salt craving Probably d/t low aldosterone levels

Adrenal Insufficiency/Addison’s Disease: Complication

Adrenal Crisis (Addisonian crisis)

Why it Occurs Caused by insufficient adrenocortical hormones, or a sudden sharp ↓ in these hormones.

Triggers Stress, sudden withdrawal of corticosteroid hormone therapy, adrenal surgery, sudden pituitary gland destruction.

Manifestations Symptoms of glucocorticoid and mineralocorticoid deficiency: hypotension (can lead to shock), tachycardia,
dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion.
GI symptoms: severe vomiting, diarrhea, abdominal pain.
General: pain in the lower back and legs.

Treatment Circulatory collapse r/t adrenal insufficiency is unresponsive to usual treatment (vasopressors, fluid replacement)
 Adrenal Insufficiency/Addison’s Disease: Diagnostics

Diagnostic Study What do you see on there?

ACTH Stimulation Test Subnormal cortisol levels, or cortisol levels fail to rise above basal levels

Urinalysis Low free cortisol levels, low aldosterone levels

Serum electrolyte levels Hyperkalemia, hypochloremia, hyponatremia

CBC Anemia

Blood glucose Hypoglycemia

BUN ↑ BUN

Adrenal Insufficiency/Addison’s Disease: Interprofessional Care

Treatment Rationale

Hydrocortisone has both, mineralocorticoid and glucocorticoid properties.

Hydrocortisone Replacement therapy During situations r/t physiological stress, glucocorticoid dosage needs to ↑ to
prevent addisonian crisis. Mineralocorticoid replacement with fludrocortisone
acetate is given daily, along with ↑ salt in diet

Aggressive Management for Addisonian Crisis: Treatment is directed towards shock management and high-dose
hydrocortisone replacement. Give LOTS of 0.9% NS and 5% dextrose to
reverse hypotension and electrolyte imbalances until BP is back to normal.
 Adrenal Insufficiency/Addison’s Disease: Nursing Management

Acute Intervention:
- Hospitalization (for diagnosis, acute crisis, or other health problem):
- Immediate treatment should be done while diagnostic tests are being performed (serum cortisol, ACTH, aldosterone, renin, and serum chemistry)
- Treatment for Adrenal crisis:
- IV hydrocortisone STAT for adrenal crisis
- Start 1-3L of 0.9% NS or 5% dextrose in 0.9% NS to correct hypoglycemia, fluid volume deficit, and Na+ and K+ imbalances within 12–24 hrs
based on volume status, lab values, & urinary output.
- Avoid hypotonic IV 0.45% NS to prevent worsening hyponatremia
- Treatment for Chronic Adrenal Insufficiency:
- Management should focus on adhering to glucocorticoid regimens, and maintaining fluid and electrolyte balance
- Obtain full Hx of medications to see which ones might interact with corticosteroids (e.g. hypoglycemics, cardiac glycosides, oral contraceptives,
anticoagulants, NSAIDs)

Ambulatory and Home Care:

- Long-term management:
- Glucocorticoids are usually given in divided doses (⅔ in the morning and ⅓ in the afternoon)
- Mineralocorticoids are given once daily (preferably in the morning)
- Stress Management:
- Extra medication and techniques are needed for stress management (both physical and emotional)
- Doses of corticosteroids are usually doubled in situations of minor stress (e.g., a respiratory infection, dental work) and tripled in
situations of major stress (e.g., divorce, loss of parent)

Patient and Caregiver Teaching:

- The following information should be included when teaching the patient and caregiver about management of Addison’s disease:
- Symptoms of overdosage and underdosage
- Conditions necessitating ↑ medication (e.g. trauma, infection, surgery, emotional crisis)
- Course of action to take in regard to changes in medication
- ↑ in dose of corticosteroid
- Administration of large dose of IM corticosteroid, including demonstration and return demonstration
- Consultation with HCP
- Prevention of infection and need for prompt and vigorous treatment of existing infections
- Need for lifelong replacement therapy, lifelong medical supervision, & medical identification device
- Fall prevention
- Adverse effects of corticosteroid therapy and prevention techniques
- Special instruction for patients who are diabetic, and management of blood glucose when taking corticosteroids
 Cushing’s Syndrome: Cause(s)

- ACTH-secreting pituitary tumour (Cushing’s disease)

- Cortisol-secreting neoplasm within the adrenal cortex (either carcinoma or adenoma)
- Excess secretion of ACTH from carcinoma of the lung or other malignant growth outside the pituitary or adrenal glands
- Prolonged administration of high doses of corticosteroids

Cushing’s Syndrome: Pathophysiology

1. Anterior pituitary tumour → ↑ ACTH → ↑ cortisol (1o hypercortisolism)

2. Adrenal cortex tumour → ↑ cortisol → ↓ ACTH (2o hypercortisolism)
3. Paraneoplastic syndrome (lung cancer) → enlarged adrenal cortex → ↑ cortisol
4. Iatrogenic (cortisol meds for arthritis + lupus) → no cortisol secretion (most common)

Cushing’s Syndrome: Manifestations

Manifestation Why it Occurs

Weight gain Will mostly occur in the trunk, face, and cervical area d/t the accumulation of
adipose tissue in these areas. Can also be caused by sodium and water
retention d/t cortisol’s mineralocorticoid effects

Hyperglycemia Occurs d/t cortisol-induced insulin resistance and ↑ liver gluconeogenesis

Protein-wasting Caused by catabolic effects of cortisol on peripheral tissue. Leads to muscle

weakness, osteoporosis, bone fractures, and back pain.

Skin changes Catabolic processes will cause the skin to become weaker and thinner, which
will bruise more easily. This will also lead to delayed wound healing.

Mood disturbances Irritability, anxiety, euphoria, insomnia, irrationality, and sometimes psychosis
might also occur. Why does it happen? No clue

Hypertension Caused by excess mineralocorticoids, causing fluid retention.

Adrenal androgen excess Causes acne, masculinization in women, feminization in men, menstrual
disorders, hirsutism in women, gynecomastia, and erectile dysfunction in men
**Clinical signs indicative of Cushing's syndrome include centripetal obesity, moon facies (fullness of the face), purplish red striae (on the abdomen, breasts, and
butt), hirsutism, menstrual disorders, hypertension, and unexplained hypokalemia.
 Cushing’s Syndrome: Diagnostics

Diagnostic Study What do you see on there?

24-hour urine free cortisol excretion Elevated cortisol

late-night/bedtime salivary cortisol levels Elevated cortisol levels indicate Cushing’s syndrome

1mg overnight dexamethasone suppression test normally see ↓ in cortisol but high cortisol if they have cushing’s

Physical Exam Observe for symptoms (often the first indication of Cushing’s syndrome)

CT, MRI Will scan for the adrenals and pituitary

Monitor ACTH levels High or normal levels indicate ACTH-dependent Cushing’s syndrome. Low
levels indicate adrenal adrenal or exogenous causes.

CBC, U/A, blood sugar, electrolytes Granulocytosis, lymphopenia, eosinopenia, hyperglycemia, glycosuria,
hypercalciuria
**The cortisol tests (first 3 rows) can be false positive in people who: exercise to capacity, experience depression, experience acute stress and significant weight
loss, and misuse alcohol.

Cushing’s Syndrome: Interprofessional Care

Underlying Cause Treatment & Rationale

Pituitary adenoma Radiation therapy

- Used if surgical outcomes are not optimal, or if pt is at high risk of surgical complications
Trans-sphenoidal resection
- Surgical removal of the tumour

Adrenocortical adenoma, carcinoma, Adrenalectomy (open or laparoscopic)

or hyperplasia - Laparoscopic method is appropriate, unless the pt is known to have a malignant adrenal tumour
Medication therapy
- Goal is to inhibit adrenal function
- Mitotane (Lysodren)
- Will suppress cortisol production, alter peripheral metabolism of cortisol, and will ↓ plasma and
urine corticosteroid levels
- Ketoconazole (Nizoral)
- Will inhibit cortisol synthesis
 Ectopic ACTH-secreting tumour Treatment of the underlying tumour
- Can be done via surgery or radiation

Exogenous corticosteroid therapy 3 options for treatment:

- Gradually discontinue corticosteroid therapy
- This will help avoid life-threatening adrenal insufficiency
- Reduce corticosteroid dose
- Convert to an alternate-day regimen
- Twice the daily dose of a shorter-acting corticosteroid is taken every other morning, to minimize
suppression of growth, altered appearance, and the HPA-axis

Cushing’s Syndrome’s: Nursing Management

Nursing Assessment:
Subjective Objective

- Ask about PMHx (pituitary tumour, adrenal/pancreatic/pulmonary - General - centripetal (truncal) obesity, supraclavicular fat pads,
neoplasms, GI bleeding, frequent infections) buffalo hump, moon facies
- Ask about meds (use of corticosteroids) - Integumentary - facial plethora; hirsutism of body and face, thinning
- Ask about symptoms of head hair; thin, friable skin; acne; petechiae; purpura;
- Amenorrhea, erectile dysfunction, ↓ libido hyperpigmentation; purplish red striae on breasts, buttocks, and
- Anxiety, mood disturbances, emotional lability, psychosis abdomen; edema of lower extremities
- Headache; back, joint, bone, and rib pain - Cardiovascular - HTN
- Insomnia, poor sleep quality - Musculoskeletal - muscle wasting, thin extremities, awkward gait
- Malaise, weakness, fatigue, poor concentration/memory - Reproductive - gynecomastia testicular atrophy (in men); enlarged
- Negative feelings regarding changes in personal appearance clitoris (in women)
- Polyuria - Possible findings - hypokalemia, hyperglycemia, dyslipidemia;
- Prolonged wound healing, easy bruising polycythemia, granulocytosis, lymphocytopenia, eosinopenia; ↑
- Weight gain, anorexia plasma cortisol level; high/low/normal ACTH levels; abnormal result of
dexamethasone suppression test; ↑ urine free cortisol &
17-ketosteroids; glycosuria, hypercalciuria; osteoporosis

Nursing Diagnoses & Planning:

Potential Diagnoses: Goals of Care:
- Potential for infection resulting from insufficient knowledge to avoid - Experience relief of symptoms
exposure to pathogens (suppression of immune system) - Avoid serious complications
- Potential for overweight as demonstrated by energy expenditure below - Maintain a positive self-image
energy intake based on standard assessment (↑ appetite, high caloric - Actively participate in the therapeutic plan
content of foods, inactivity)
- Disrupted body image resulting from alteration in self-perception (change
 in appearance)
- Disrupted skin integrity resulting from chemical injury agent (excess
corticosteroids)
Implementation:
- Identify pts at risk for Cushing’s syndrome.
Health Promotion - Long-term use of exogenous cortisol will increase risk of developing Cushing’s syndrome
- Educate pts about medication use and monitoring adverse effects

- Focus on daily assessment of hormone/drug toxicity and complications (e.g., cardiovascular disease, diabetes,
infection)
- Monitor vital signs, daily weight, and glucose levels
- Assess for signs of infection (pain, loss of function, purulent drainage) and thromboembolic events (sudden chest
pain, dyspnea, tachypnea)
- Provide emotional support for distress d/t physical changes
- Reassure that physical changes and emotional lability will resolve with normalized hormone levels
- If treatment involves surgical removal of pituitary adenoma, pre-op and post-op care is very important
Acute Intervention - Pre-operative care:
- Optimize physical condition before surgery (control hypertension and hyperglycemia, correct
hypokalemia, high-protein meal plan)
- Pre-op teaching includes anticipated post-op care (NG tube, urinary catheter, IV therapy, central
venous pressure monitoring, leg compression devices)
- Post-operative care:
- Monitor and report significant changes in BP, RR, or HR
- Monitor ins/outs
- High doses of corticosteroids are given during/after surgery. So, monitor for infection and delays
in wound healing
- Assess morning urine cortisol levels to determine effectiveness of surgery
- Watch for signs of acute adrenal insufficiency (vomiting, increased weakness, dehydration,
hypotension).
- Maintain bed rest until BP stabilizes

- Discharge instructions focus on lack of endogenous corticosteroids and inability to react to stress
- Consider referral for a visiting nurse
- Wear medical alert bracelets and carry medical ID
Ambulatory and Home Care - Avoid extreme temperatures, infections, and emotional disturbances
- Adjust corticosteroid replacement therapy based on stress levels; consult with HCP for dosage changes
- Contact HCP if weakness, fainting, fever, or N/V occur.
- Expect many months to adjust hormone dose satisfactorily; some may need lifetime replacement therapy
Describe the pathophysiology and clinical manifestations relating to an imbalance of hormones produced by the posterior pituitary gland
as well as the interprofessional care and nursing management of patients with this imbalance.
SIADH: Causes

- ↑ ADH production, despite normal or low plasma osmolality

- “Low osmolality” means that everything in the plasma is more diluted. This should technically cause the body to ↓ ADH so that less water is
retained in the body. But instead, with SIADH, there is more ADH being produced, causing more water to be retained in the body.
- ~75% of causes are caused by ectopic production of ADH by tumour cells
- E.g. small cell carcinoma of lungs (paraneoplastic syndrome)
- SIADH can sometimes be the first indication of cancer
 SIADH: Manifestations

Manifestation Why it Occurs

↑ extracellular fluid volume Excess ADH leads to ↑ permeability of distal tubules and collecting ducts, as
well as reabsorption of water into circulation

↓ plasma osmolality Excess ADH leads to ↑ permeability of distal tubules and collecting ducts, as
well as reabsorption of water into circulation

↑ glomerular filtration rate (GFR) Excess ADH leads to ↑ permeability of distal tubules and collecting ducts, as
well as reabsorption of water into circulation

Dilutional hyponatremia Excess ADH leads to ↑ permeability of distal tubules and collecting ducts, as
(manifestations of hyponatremia will appear as levels drop below 120mmol/L) well as reabsorption of water into circulation

Fluid retention ↑ ADH production

Hypochloremia ↑ intravascular volume → everything is diluted

↑ body weight Fluid builds up in the body

Lethargy, anorexia, confusion, headaches, seizures, coma As plasma osmolality and serum sodium levels decline, cerebral edema occurs

SIADH: Diagnostics

Diagnostic Study What do you see on there?

Na+ levels Hyponatremia (Na+ < 134mmol/L), in addition to low serum osmolality
(<280mmol/kg) and USG > 1.005

Urine osmolality high

Serum osmolality low Serum osmolality <285mmol/kg

 SIADH: Interprofessional Care

Treatment Rationale

Discontinue drugs that stimulate ADH release Because you wanna ↓ the release of ADH? Duh

Hypertonic saline (3-5%) Administer if hyponatremia is severe (Na+ < 120mmol/L), with presence of
neurological symptoms. This will bring up Na+ levels.

Fluid restriction This is done if symptoms are mild and Na+ > 125mmol/L, the pt should restrict
between 800-1000mL/day to gradually ↓ weight and ↑ Na+ levels.
If hyponatremia is severe, pt can only restrict up to 500mL/day.

Furosemide (Lasix) Administer if Na+ levels ≥ 125mmol/L, to promote diuresis without losing Na+

Potassium, calcium, and magnesium supplements Will help offset electrolyte losses associated with diuretic therapy

Administer vasopressin receptor antagonist (i.e. Tolvaptan (Samsca)) Treats euvolemic hyponatremia. Can be administered to patients who cannot
tolerate water restriction guidelines, since it will still help dilute the urine

SIADH: Nursing Management

Nursing Assessment:
- Daily weight measurements - Monitoring of heart and lung sounds
- Frequent measurement of urine specific gravity - Monitoring of LOC
- Frequent measurement of intake (oral and parenteral) and output - Observation for signs of hyponatremia (e.g. ↓ neurological function,
- Frequent measurement of vital signs seizures, N/V, muscle cramping)
Management:
- Frequent oral hygiene - Provision of support for patient and significant others regarding
- Frequent turning, positioning, and ROM exercise (if pt is bedridden) diagnosis and any mental status changes
- Position HOB flat or ≤ 10° to enhance venous return to heart, and ↑left - Restricting total fluid intake to no more than 1000mL/day (including
atrial filling pressure → ↓ ADH release that taken with medications)
- Protect from injury (e.g. assist with ambulation, bed alarm) d/t - Seizure precautions
potential alterations in mental status
Self Management for Chronic SIADH:
- Self manage fluid restriction (800-1000mL/day)
- Eat ice chips or sugarless gum to help ↓ thirst
- Plan out fluid intake to align with social occasions
- Have well-diluted sodium and potassium supplements with meals to prevent GI irritation or damage
- Be aware of symptoms of fluid and electrolyte imbalances so that pt can monitor progress during treatment
 Diabetes Insipidus (DI): What is it?

Group of conditions associated with ↓ ADH production or secretion, along with ↓ renal response to ADH d/t injury to the neurohypophyseal system
Pathophysiology:
↓ ADH → ↓ water reabsborption in renal tubules and ↓ intravascular fluid volume → ↓ ability to concentrate urine → ↑ urinary output, hypernatremia, dehydration

Diabetes Insipidus: 3 Forms of DI

Nephrogenic DI Central (Neurogenic) DI Primary DI (most common)

- ↓ response to ADH (by renal tubules due to - ↓ ADH secretion - Excessive water intake
lesions) - Causes: brain tumours, aneurysms, - Causes: structural lesion in the thirst centre,
- Causes: kidney infections, uropathies thrombosis, infection, head injury psychological disorder

Diabetes Insipidus: Manifestations

Manifestation Why it Occurs

Polyuria (↑ urination) 5-20L/day will be lost d/t ↑ production of dilute urine. It will have a very low
specific gravity (<1.005), and urine osmolality (low) will be < 100mmol/kg

Polydipsia (↑ thirst) Caused by large amount of urine loss

Nocturia Urine production continue to occur at night, leading to nocturia

Fatigue/ Generalized weakness Caused by nocturia, since they would not be able to sleep through the night

high serum osmolality Will be high d/t hypernatremia that is caused by pure water loss from kidneys.
This can lead to CNS manifestations (irritability, mental dullness, coma)

Fluid volume deficit Seen in patients whose fluid intake cannot balance urinary losses

Central (neurogenic) DI occurs after excess fluid loss (e.g. Intracranial surgery). There are 3 phases:
1. Acute phase
a. Abrupt onset of polyuria
2. Interphase
a. Urine volume normalizes
3. Permanent (?) phase
a. Occurs 10-14 days post-op, and central (neurogenic) DI becomes permanent
 Diabetes Insipidus: Diagnostics

Diagnostic Study What do you see on there?

Water deprivation test If a pt has central DI, their urinary osmolality will ↑ significantly after
vasopressin (ADH) is given. If a pt has nephrogenic DI, they will have no
response to vasopressin

Diabetes Insipidus: Interprofessional Care

Treatment Rationale

Hormone replacement (for central DI) Hormone replacement is needed because of the lack of ADH
(i.e. desmopressin acetate [DDAVP], or vasopressin) production/secretion. DDAVP can be given PO, IV, SC, or as nasal spray. Not
helpful for nephrogenic DI since the kidney won’t be able to respond to the ADH

Fluid replacement - Hypotonic saline (0.45% NS) Given to pt with acute DI to help replace urinary output

Carbamazepine (Tegretol) Will help ↑ ADH release and enhance ADH effects on the kidney

Low Na+ diet (for nephrogenic DI) Limit Na+ intake to no more than 3g/day will help ↓ urine output

Thiazide diuretics (for nephrogenic DI) Will help slow down the GFR so that the kidneys can increase proximal Na+ and
water reabsorption in the loop of Henle and distal tubules.

Indomethacin (Indocin) This medication is an NSAID, which will help ↑ renal responsiveness to ADH. It
is administered when a low-sodium diet and thiazides are not effective.
 Diabetes Insipidus: Nursing Management

Goals of Care:
- Early detection of polyuria, nocturia, and polydipsia
- Maintenance of adequate hydration
- Patient teaching regarding nutrition (i.e. low-sodium and protein diet) and pharmacological management

Management:
- Fluid replacement (PO or IV) - Monitor BP, HR, urine output, and urine specific gravity (should be
- Monitor serum glucose levels if IV glucose solutions are used, done hourly for acute pt)
because hyperglycemia and glycosuria can lead to osmotic diuresis → - Monitor LOC and signs of acute dehydration, by assessing alertness,
↑ fluid volume deficit response to stimuli,
- Monitor ins/outs
Pharmacological Management:
- Desmopressin - will ↓ nocturia and control diuresis during the day
- Make sure to monitor pt for weight gain, headaches, restlessness, and signs of hyponatremia and water intoxication
- Call physician STAT if pt develops ↑ urine volume with low specific gravity

Management - Chronic DI
- Pt will need long-term ADH replacement (i.e. DDAVP)
- Headache, nausea, and other signs of hyponatremia indicate overdosage
- Failure to improve indicates underdosage
- There needs to be close follow-up of lab studies
 WEEK 11 - GAS EXCHANGE/ PERFUSION
[Link]
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Describe the oxygen hemoglobin dissociation curve, and explain the reasons and significance of a shift to the left or right in the curve.
Shift to the LEFT:
- Indicates that blood picks up O2 more readily in the lungs, but delivers
O2 less readily to the tissues
- This means that Hb has a higher affinity to O2
- Seen in alkalosis, hypothermia, and ↓ PaCO2

Treatment:
- Give more O2 to compensate for the lack of O2 that gets delivered to
the tissues

Shift to the RIGHT:

- Indicates that blood picks up O2 less readily in the lungs, but delivers
O2 more readily to the tissues
- This means that Hb has a lower affinity to O2
- Seen in acidosis, hyperthermia, and ↑ PaCO2

Review gas exchange and the factors that affect it.

Factors that Affect Gas Exchange: Ventilation, Perfusion, Transport

Factors that cause ventilation issues

Spinal cord injuries (C2-C3)
- The phrenic nerve stimulates the diaphragm → therefore, you need an intact spinal cord
Neuromuscular disorders
- NM disorders affect how your intercostal muscles work
Muscle weakness
Rib fractures
- With rib fractures, you cannot breathe deeply because it causes pain → ↓ ventilation
Ventilation Obstruction
Process of inhaling oxygen - Cystic fibrosis (CS), chronic bronchitis, form body (FB), allergic reaction, epiglottitis)
into the lungs and exhaling Narrowed airways (asthma, allergic reactions, COPD)
carbon dioxide from the lungs Alveoli issues
 - Can be affected by negative pressure, ↓ surfactant, etc.
- Can be caused by:
○ Pneumonia
○ Pulmonary edema (can be caused by MI)
○ ARDS (extension of respiratory failure + sepsis) → affects the alveoli membrane
Pneumothorax (can be caused by rib fractures)
- Loss of negative pressure → lung collapses
Hemopneumothorax
- There are both blood and air in the lungs → pleural effusion
Empyema
Problem with the brainstem
- Specifically, issues with the medulla oblongata and/or pons will affect respiration
- Brainstem also have chemoreceptors, so it'll affect blood pH in the brain

Factors that cause perfusion issues

Perfusion Fluid volume deficit (FVD)
Refers to the ability of blood Emboli
to transport Vessel narrowing
oxygen-containing - With vessel narrowing, the distance between alveoli and blood vessels ↑es.
hemoglobin to cells and Vasoconstriction
return carbon
dioxide-containing
Prematurity
hemoglobin to the alveoli - Their lungs aren't fully developed yet. So, the distance between alveoli and blood vessels is much larger, which means that
the O2 needs to travel further to reach the blood

Factors that cause transportation issues

Hemoglobin issues
- Anemia
- Sickle cell: RBCs cannot travel because of the shape of the cells
Transport Fetal hemoglobin
Refers to the availability of - It has a high affinity for oxygen.
hemoglobin and its ability to - The turnover time is 20–30 days (on avg), while for adults, the turnover time is about 120 days.
carry O2 from alveoli → cells - When the baby is born, 80-90% of the baby's body is fetal hemoglobin. The body needs to make adult hemoglobin, but the
for metabolism, and to carry fetal hemoglobin is being turned over too quickly (this is what causes hyperbilirubinemia in babies).
CO2 (via cellular metabolism)
from cells → alveoli to be
Hemorrhage
eliminated Carbon monoxide (CO)
- Its affinity for hemoglobin is way higher than oxygen's affinity for hemoglobin (Hb).
- So, when CO binds to Hb, it won't let go.
- The patient's O2 sat will show 100% Hb is still bound to something (the system just can't tell that Hb is bound to CO instead
of O2).
- Since there's no O2 bound to Hb, O2 won't be able to travel to your tissues.
Explain the difference between hypoxia and hypercapnia and the clinical manifestations of both across the lifespan.
Hypoxia Hypercapnia

Definition: PaO2 is very low → signs/symptoms of inadequate oxygenation Definition: presence of too much CO2 in the blood (PaCO2 > 45mmHg)
- Causes anaerobic metabolism to occur → ↑ lactic acid → metabolic
acidosis → cell death Manifestations:
- Dyspnea
Manifestations: - ↓ RR or ↑ rate with shallow respirations
- ↑ HR - Bounding pulse
- ↓ RR or ↑ rate with shallow respirations - Dysrhythmias
- ↑ CO - Hypertension
- Tripod position - Tachycardia
- Pursed lips - ↓ Deep tendon reflexes
- Angina, dysrhythmias - Muscle weakness
- One-word or two-word dyspnea - Tremor, seizures (late)
- Only 2–3 words can be said before pausing to breathe - Pursed-lip breathing
- Inspiratory-to-expiratory ratio will change (from 1:2 to 1:3)
- Retraction of intercostal spaces or supraclavicular area
- Paradoxical breathing (severe hypoxia)

Explain how age-related differences impact gas exchange.

- Have enough surfactant to prevent alveoli from collapsing after every exhalation
Full Term Newborns & Infants - Obligate nose breathers until ~ 3 months
- Struggle to breathe if their nose is blocked
- Newborns have irregular respiratory pattern (brief pauses between breaths)

- ↓ strength of respiratory muscles → ↓ maximal inspiratory/expiratory force → weak cough

Older Adults - Alveoli are less elastic & more fibrous → ↓ diffusion across alveolar-capillary membrane → dyspnea
- ↓ erythrocytes → ↑ risk of anemia
Explain the structure of cardiac muscle tissue and cardiac conduction system.
Cardiac Cycle & Cardiac Conduction System

1: the SA node fires action potentials to the AV node and both atria. The SA
node fires 60-100x/min.

2: the AV node sends the signal down the AV bundle (Bundle of His). The AV
node fires 40-60x/min.

3: the AV bundle splits into the L and R bundle branches. The bundle branches
fire 20-40x/min.

4: Purkinje fibers send action potentials throughout the ventricles, to initiate

another action potential there. The purkinje fibers fire 20-40x/min.

1: the SA node fires an action potential. This happens during atrial

depolarization.

2: the AV node fires an action potential.

3: the signal passes through the AV bundles.

4: the signal passes through the L and R bundle branches.

5: the AV valves shut.

6: the signal passes through the Purkinje fibres. This happens during
ventricular depolarization/ atrial repolarization. Note: during a heart attack,
ventricular depolarization shows down.

7: ventricular repolarization occurs.

8: the semilunar (SL) valves shut.

Explain coronary circulation and how the coronary arteries are perfused.
Coronary Vessels

How a coronary artery delivers blood into deeper layers of the

myocardium:

If there’s too much tension in the tissue, the coronary arteries will constrict.
This would minimize blood flow. So, for efficient blood flow, you need enough
time in diastole to nourish those heart cells.

If there is any obstruction of blood flow, then the superior cells will be the only
ones getting any nutrients. This means that if there is an obstruction, the first
cells to die off will be the ones closest to the myocardium.

1: if there’s too much tension in the tissue, the coronary arteries would
constrict, which would minimize blood flow. So, for efficient blood flow, you
need enough time in diastole to nourish the heart cells.

2: if there is any obstruction to blood flow, then the cells that are superior will
be the only ones getting any nutrients.

3: following what was stated above, if there’s an obstruction to blood flow, then
the first cells to die off will be the ones closest to the myocardium.
Review which area of the heart each of the main coronary arteries supply.
Branches of the Left Coronary Artery Branches of the Right Coronary Artery

CIRCUMFLEX BRANCH MARGINAL BRANCH POSTERIOR INTERVENTRICULAR

ANTERIOR INTERVENTRICULAR
BRANCH BRANCH

Supplies BOTH ventricles Supplies L atrium & L ventricle Supplies R ventricle Supplies BOTH ventricles

Left coronary artery, supplies left side of the heart + R ventricle Right coronary artery, supplies right side of the heart + L ventricle

Explain how age-related differences impact perfusion.

Infants & Adolescents Older Adults

- Size of infant’s heart is large in relation to total body size - They have stiffening and thickening of myocardial tissue
- Newborns have lower systolic BP d/t weaker left ventricle (strengthens - ↓ elasticity of arterial walls
within first 6 weeks) - Heart valves become fibrose
- Systolic BP reaches adult level after puberty - ↓ CO, ↓ SV, ↑ BP, orthostatic hypotension, lower extremity edema
- Heart size will ↑ during puberty → ↑ BP, ↓ HR
Describe the pathophysiology, types, clinical manifestations, interprofessional care and nursing management of patients HF.
Heart Failure (HF): What is it?

HF is a syndrome involving impaired cardiac pumping or filling, or both.

HF is characterized by ventricular dysfunction, ↓ exercise tolerance, diminished QoL, and shortened life expectancy.
Patients with any type of HF have ↓ SBP, ↓ CO, poor renal perfusion, poor exercise tolerance, and ventricular dysrhythmias.

Heart Failure (HF): Types

Left-Sided HF Right-Sided HF

- Most common - Right-sided HF is mostly caused by left-sided HF

- Caused by LV dysfunction - Left-sided HF → pulmonary congestion & pulmonary HTN →
- Leads to backflow of blood through the LA and into the pulmonary right-sided hypertrophy & right-sided HF
veins → ↑ pulmonary pressure → fluid leaks from pulmonary capillary - Can also be caused by cor pulmonale (RV dilation & hypertrophy) or
bed into interstitium & alveoli → pulmonary congestion, pulmonary right ventricular infarction
edema, pink/frothy sputum - Leads to backflow of blood into the RA and venous circulation (SVC &
IVC) →venous congestion → peripheral edema, hepatomegaly,
splenomegaly, vascular congestion of GI tract, JVD

Heart Failure (HF): Pathophysiology

Heart Failure with ↓ Ejection Fraction (HFrEF)

- Most common form of HF
- Caused by heart’s inability to pump blood properly
- Patho: Impaired contractile function (e.g. myocardial ischemia), ↑ afterload (e.g., HTN), cardiomyopathy, and mechanical abnormalities (e.g., valvular
heart disease) → LV loses ability to create enough pressure to eject blood forward → ↓ LV ejection fraction (normal: > 55%; HFrEF: ≤ 40%)

Heart Failure with Preserved Ejection Fraction (HFpEF)

- Caused by ventricles’ inability to relax and fill during diastole
- ↓ filling of the ventricles → ↓ SV and CO
- Patho: LV hypertrophy from HTN (most common), myocardial ischemia, valve disease (e.g. aortic, mitral), cardiomyopathy → poorly compliant ventricles
→ high filling pressures & ↓ filling of the ventricles → venous engorgement in pulmonary and systemic vascular systems

Heart Failure with Mid-Range Ejection Fraction (HFmEF)

- Ejection fraction will be between 41% and 49%

Mixed Heart Failure

- Dilated cardiomyopathy → dilated LV walls cannot relax and fill properly → poor ejection fraction (< 35%), high pulmonary pressures, biventricular failure
(both ventricles might be dilated and have poor filling & emptying capacity)
 Heart Failure (HF): Compensatory Mechanisms

SNS Activation Neurohormonal Responses

- This is the first mechanism triggered by low CO RAAS system
- Least effective - ↓ CO → ↓ renal perfusion → kidneys release renin → renin converts
- Inadequate SV and CO → ↑ SNS activation → ↑ catecholamines angiotensinogen to angiotensin I → angiotensin I is converted into
(E/NE) → ↑ HR, ↑ myocardial contractility, peripheral angiotensin II via angiotensin-converting enzyme (ACE) → angiotensin
vasoconstriction → temporary ↑ in CO II causes: (1) aldosterone to be released from the adrenal cortex →
Consequence sodium & H2O retention, (2) ↑ peripheral vasoconstriction → ↑ BP
- The ↑ in HR and contractility will ↑ the failing heart’s workload and need Vasopressin
for O2, and the vasoconstriction will cause an ↑ in preload, which will - ↓ CO → ↓ cerebral perfusion pressure (CPP) → posterior pituitary
also ↑ venous return (while the heart is already volume overloaded) secretes ADH → ↑ water reabsorption in kidneys → water retention →
↑ blood volume (even though heart is already volume overloaded)
Contribution to HF
- Catecholamines, ADH, and angiotensin II stimulate production of
endothelin (vasoconstrictor) → further arterial vasoconstriction & ↑
myocardial contractility and hypertrophy
- Cardiac injury → release of TNF & interleukin-1 (IL-1) → hypertrophy,
contractile dysfunction, cell death → ↓ heart function

Ventricular Dilation Ventricular Hypertrophy

- ↑ pressure in heart chambers → muscle fibers of the heart stretch → ↑ - Hypertrophy will develop slowly
contractions → ↑ CO - Hypertrophy → ↑ contractile power of heart muscles → ↑ CO and
Consequence maintenance of tissue perfusion
- This mechanism will eventually cause the elastic elements of heart Consequence
muscles to become overstretched, and they won’t be able to contract - Hypertrophic muscle tissue will eventually have poor contractility and
properly any longer → CO will be diminished will need more O2 to work, and coronary circulation will become poor
- This will cause the heart to become prone to dysrhythmias
 Heart Failure (HF): Counter-regulatory Mechanisms

Natriuretic Peptides (atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP))
- These are hormones produced by the heart muscle
- ANP is released from the atria in order to ↑ blood volume to the heart
- BNP is released from the ventricles in order to ↑ blood volume to the heart

Renal effects of ANP & BNP:

- ↑ GFR and diuresis
- Excretion of sodium (natriuresis)

Cardiovascular effects of ANP & BNP:

- Vasodilation
- ↓ BP

Hormonal effects of ANP & BNP:

- Inhibition of aldosterone and renin secretion (which will then prevent sodium and H2O retention)
- Interference with ADH release

Heart Failure (HF): Etiology

Risk Factors
- Coronary artery disease (CAD) - Diabetes mellitus
- HTN

Primary Causes of Acute HF:

- Acute MI - Hypertensive crisis
- Dysrhythmia - Rupture of papillary muscle
- Pulmonary embolus - Myocarditis
- Thyrotoxicosis - Bacterial endocarditis

Primary Causes of Chronic HF:

- CAD - Pulmonary disease
- HTN - Cardiomyopathy
- Rheumatic heart disease - Anemia
- Congenital heart disease - Bacterial endocarditis
- Ventricular septal defect - Valvular disorders
Precipitating Causes of HF:
- Anemia - Myocarditis
- ↓ O2-carrying capacity of the blood → ↑ in CO to meet tissue - ↑ HR, ↓ CO, acute right and left ventricular failure
demands - Pulmonary embolism
- Infection - ↑ Pulmonary pressure and ↑ pressure on the RV, leading to
- ↑ O2 demands of tissues → ↑ CO right ventricular hypertrophy and failure
- Thyrotoxicosis - Pulmonary disease
- Changes in tissue metabolic rate; ↑ HR & workload of the - ↑ Pulmonary pressure and ↑ pressure on the RV, leading to
heart right ventricular hypertrophy and failure (same as above)
- Hypothyroidism - Paget’s disease
- Indirectly predisposes pt to ↑ atherosclerosis; severe - ↑ Workload of the heart by ↑ vascular bed in skeletal muscle
hypothyroidism will ↓ myocardial contractility - Nutritional deficiencies
- Dysrhythmias - Will ↓ myocardial muscle mass and myocardial contractility,
- May ↓ CO, ↑ workload & O2 requirements of myocardial tissue which will ↓ cardiac function
- Bacterial endocarditis - Hypervolemia
- Infection: ↑ metabolic demands and O2 requirements - ↑ Preload, causing volume load on the RV
- Valvular dysfunction: causes stenosis and regurgitation

Heart Failure (HF): Manifestations

Manifestation Why it Occurs

Caused by acute LV failure secondary to acute myocardial ischemia.

Will cause manifestations, such as anxiety, pallor, possible cyanosis,
Pulmonary edema (diagram below) cold/clammy skin, tachycardia, ↑/↓ BP, severe dyspnea, RR > 30, orthopnea,
coughing with frothy, blood/tinged sputum. Auscultation will show crackles,
wheeze, and rhonchi.

Caused by ↑ venous pressure, which causes the pulmonary vascular system to

↓ lung compliance become filled with fluid. This causes the lungs to become less compliant, and
there's ↑ pressure in the small airways.

Tachypnea, SOB Caused by ↓ lung compliance and ↑ lymphatic flow to help maintain constant
volume of pulmonary extravascular fluid

Interstitial edema Occurs as pulmonary venous pressure continues to ↑, causing more fluid to
leak into interstitial space compared to how much lymphatic vessels can drain

Alveolar edema, worsening ABGs (↑ PaCO2, ↓ PaO2) Occurs as pulmonary pressure continues to ↑, since it causes more fluid to
move into the alveoli and airways
 Chronic Heart Failure (HF): Manifestations

Manifestation Why it Occurs

Fatigue Occurs d/t ↓ CO, impaired perfusion to vital organs, ↓ tissue oxygenation, &
anemia (r/t poor nutrition, renal disease, or meds)

Dyspnea, orthopnea Caused by ↑ pulmonary pressure r/t interstitial & pulmonary edema

Paroxysmal nocturnal dyspnea Caused by reabsorption of fluid from dependent body areas when the pt is flat

Cough Starts off as a dry, nonproductive cough

Tachycardia Failing ventricles (diminished CO) will trigger the SNS, which will ↑ HR

Edema Occurs in dependent body areas (peripheral edema), liver (hepatomegaly),

abdominal cavity (ascites), and lungs (pulmonary edema, pleural effusion).

Occurs d/t ↓ CO, which causes impaired renal perfusion and ↓ urinary output.
Nocturia But when the pt lies down, cardiac workload will ↓ and fluid moves from the
interstitial space to circulation, causing ↑ renal perfusion & diuresis.

The skin will appear dusky d/t ↑ tissue capillary oxygenation extraction
Skin changes (idk what this even means lol)
Lower extremities will appear shiny and swollen with ↓ hair growth.

Hemosiderin staining Caused by chronic swelling in the lower extremities

(brown/brawny areas covering the ankles & lower legs)

Behavioural changes Occurs d/t poor gas exchange and/or co-existing psychological disorders
(restlessness, confusion, ↓ attention span/memory) (depression, anxiety)

Chest pain Caused by ↓ coronary artery perfusion r/t ↓ CO and ↑ myocardial work

Weight gain will occur d/t fluid retention. The pt may eventually experience
Weight changes cardiac cachexia (muscle metabolism) with muscle wasting and fat loss, but
this will be masked by all the edema.

Heart Failure (HF): Complications

Manifestation Why it Occurs

Transudative pleural effusion Caused by ↑ pressure in blood vessels or low albumin levels, causing fluid to leak into the pleural space

Dysrhythmias Caused by enlargement of the atria and ventricles, which can change normal electrical pathways. Often
can lead to A-fib, V-tach, or V-fib

Left ventricular thrombus Caused by enlargement of the LV and ↓ CO, which together, lead to ↑ chance of thrombus formation

Hepatomegaly Occurs d/t RV failure, which causes the venous system to become backed [Link] will cause liver lobules
to become congested with venous blood (can eventually lead to cirrhosis)

Renal failure Caused by ↓ CO, which results in ↓ renal perfusion and renal insufficiency

Heart Failure: Diagnostics

Diagnostic Study What do you see on there?

Echocardiogram, CXR Will not confirm diagnosis, but will contribute to diagnosis

Measurement of ejection fraction Will differentiate between HFrEF and HFpEF

Measurement of BNP or N-terminal-pro-BNP The higher the levels, the greater the degree of LV dysfunction
 Chronic Heart Failure: Interprofessional Care

Referral to Multidisciplinary - Recommended for pts with newly diagnosed HF, and pts at greater risk for development of HF
Clinics or Specialist Care

Oxygen
- It’s normal to see lower SPO2 in someone with HF because blood isn’t properly oxygenated in the lungs
- If SPO2 < 90%, supplementary O2 will be needed

Non-pharmacological Therapies Self-Management Teaching

- Teach the pt and caregivers about avoiding risks for decompensation, and detecting early manifestations

Exercise & Activity

- Pts with stable chronic HF should be given regular activity/exercise periods
- Can be provided by cardiac rehabilitation program

Cardiac Resynchronization Therapy (CRT)

- Beventricular pacing and cardiac resynchronization therapy are used for pts with HF who:
Devices - Are receiving maximum medical therapy
- Have class III or IV symptoms
- Have a widened QRS interval
- This will coordinate contractility of the RV and LV, which will improve LV performance and CO
- Will also improve pt’s exercise capacity and ↓ overall symptoms

Implantable Cardioverter-Defibrillator (ICD)

- ICD should be combined with CRT for pts with HF who:
- Have functional class II or III HF
- Are on optimal medical therapy
- Have an ejection fraction < 35%

Mechanical Circulatory Support

- Intra-aortic balloon pump can be used for short-term support of acute decompensation
- Not good for long-term use d/t limitations of bed rest, infection, and vascular complications
- Extracorporeal membrane oxygenation can be used for critically ill HF patients, who are also being assessed for
more advanced therapies (e.g. ventricular assist device (VAD))

Cardiac Transplantation - Treatment of choice for pts with end-stage HF

- Only preferred for small number of pts, since there’s a lack of donor hearts

Advance Care - Goal of care for a pt with end-stage HF, should be directed towards guideline-driven therapies
- Includes goal setting according to pt’s preferences, and planning for end-of-life
 Diuretics
- Will help move edematous fluid, ↓ pulmonary venous pressure, and ↓ preload
- This will then ↓ blood volume returning to the heart → improved cardiac function
- Thiazide diuretics - first choice to treat edema r/t HF, and to control HTN
- Promoted sodium and water excretion
- Loop diuretics (e.g. Lasix) - promotes sodium, chloride, and water excretion
- Adverse effects: hypokalemia, ototoxicity, possible allergic reaction
Medication Therapy
ACE Inhibitors (e.g. ramipril, enalapril)
- ACE is needed to convert angiotensin I into angiotensin II
- Blocking ACE will, in turn, ↓ angiotensin II levels → ↓ aldosterone levels (since angiotensin II normally causes
aldosterone to be released)
- Adverse effects: symptomatic hypotension, chronic cough, renal insufficiency
- Give pt ARBs if they cannot tolerate ACE inhibitors d/t angioedema or cough

Neprilysin Inhibitors
- Can be combined with an ARB
- Will block the enzyme that degrades natriuretic peptides

β-Adrenergic Blockers (β-blockers)

- E.g. carvedilol, metoprolol
- Will directly block the negative effects of the SNS on the failing heart
- Adverse effects: edema, hypotension, fatigue, asthma exacerbation, bradycardia

Mineralocorticoid Receptor Antagonists

- E.g. Spironolactone (a K+-sparing diuretic), Eplerenone (Inspra)
- Promotes sodium and water excretion, but blocks potassium excretion by blocking aldosterone activity

Inotropic Medications
- Used to improve cardiac contractility in order to ↑ CO, ↓ LV diastolic pressure, and ↓ SVR
- Most commonly used: dobutamine, milrinone
- Sympathomimetic agents (β-Adrenergic agonists)
- E.d. dopamine, dobutamine, epinephrine, NE (levophed)
- Used for short-term treatment of acute exacerbations of HF
- Phosphodiesterase inhibitors
- E.g. milrinone
- Will improve cardiac contractility, ↑ CO, promote peripheral vasodilation, and ↓ SVR
- Vasodilator medications
- Will ↓ symptoms of dyspnea in HFrEF

Nutritional Therapy - Stick to a low-sodium diet

- Pt should weigh themselves at the same time every day to monitor fluid retention
 Acute Decompensated Heart Failure (HF): Nursing Management

Decreasing Intravascular Volume

- Loop diuretics (e.g. Lasix) - will ↓ intravascular volume very quickly, and will ↓ venous return
- Since less blood will return to the LA (which goes to the LV), there will be a ↓ in preload. This will let the LV pump more efficiency → ↑ CO

Decreasing Venous Return

- ↓ venous return (preload) → ↓ blood returning to LV during diastole
- Put pt in high-fowler’s position with feet either horizontal or dangling, so that blood stays in the lower extremities
- IV Nitroglycerin - it will ↓ preload and dilate coronary arteries → ↑ coronary artery circulation → ↓ circulatory volume
- It can also ↓ afterload when used in high doses
- Can also ↑ myocardial O2 supply
- Lasix will also ↓ venous return (I talked about it right above this section)

Decreasing Afterload
- Afterload: resistance that the LV needs to pump blood against (it’s basically the amount of work it takes for the LV to eject blood into systemic circulation)
- LV filling and SVR determine afterload
- ↓ afterload → improved CO and ↓ pulmonary congestion

Improving Oxygenation & Gas Exchange

- IV morphine → ↓ preload and afterload, ↓ myocardial O2 demands
- Supplementary O2 can be given if SPO2 falls < 90%
- If pt has severe pulmonary edema, they may need BiPAP or intubation and mechanical ventilation

Improving Cardiac Function

- Positive inotropic therapy may be needed if diuretics, morphine sulphate, and vasodilators don’t help
- E.g. dobutamine, milrinone - they will ↑ myocardial contractility without ↑ing O2 consumption, will ↑ peripheral vasodilation, and ↓ afterload
- Pt will need constant hemodynamics monitoring
- Put in a pulmonary artery catheter for this pt
- Make sure to measure CO, pulmonary artery pressure, and pulmonary artery occlusive pressure once this catheter is in
- Ideal pulmonary artery occlusive pressure: 14-18mmHg

Reducing Anxiety
- IV morphine will act as a sedative
 Heart Failure (HF): Nursing Management

Nursing Assessment:
Subjective Objective

- Ask about cultural & psychosocial Hx: (availability of caregivers, - Integumentary - cool/diaphoretic skin, cyanosis/pallor, peripheral
living situation, pets at home, smoking, alcohol, illicit drug use, edema (right-sided HF)
advance directives if available) - Respiratory - tachypnea, crackles particularly at the bases, rhonchi,
- Ask about PMHx (CAD, MI, HTN, cardiomyopathy, valvular or wheezes; frothy, blood-tinged sputum
congenital heart disease, DM, thyroid/lung disease, irregular HR) - Cardiovascular - tachycardia, S3, S4, murmurs, PMI displaced
- Ask about meds (cardiac meds, diuretics, estrogens, corticosteroids, inferiorly and posteriorly, JVD
NSAIDs, OTC meds, herbal supplements) - GI - abdominal distension, hepatosplenomegaly, ascites
- Ask about symptoms: - Neuro - restlessness, confusion, ↓ attention or memory
- Fatigue, depression, anxiety - Possible findings - altered electrolytes levels (especially Na+ and
- N/V, anorexia, stomach bloating K+), ↑ BUN, ↑ BNP or NT–pro-BNP, ↑ creatinine, ↑ LFT results,
- Weight gain, ankle swelling, nocturia, ↓ daytime urine output cardiomegaly, pulmonary congestion, and interstitial pulmonary
- Dyspnea, orthopnea, cough edema on CXR, echocardiogram showing ↑ chamber size and ↓ wall
- Chest pain or heaviness, palpitations, dizziness, fainting motion, ECG showing atrial & ventricular enlargement; ↓ SPO2
- RUQ pain, abdominal discomfort, constipation
- Behavioural changes, visual changes

Nursing Diagnoses:
- ↓ gas exchange - Excess fluid volume
- Caused by ↑ preload and alveolar-capillary membrane - Caused by excessive fluid intake & excessive sodium intake
changes - ↓ stamina
- Inadequate gas exchange - Caused by imbalance between O2 supply/demand
- Caused by altered contractility, altered preload, altered SV, or
a combo of these
Implementation:
Health Promotion - Treatment or control of underlying heart disease is important to prevent HF
- Early & continued treatment of HTN will help prevent HF
- Manage hyperlipidemia in people with CAD, with diet, exercise, and meds

Acute Intervention - Acute decompensation may need to be treated in a CCU

Ambulatory & Home Care - Teach pt and caregivers how to recognize symptoms of decompensation
- Pt needs to know that they should continue to take HF meds for the rest of their lives
- Recommend community care services
Describe the pathophysiology, types, and clinical manifestations of hypertensive crisis and interprofessional care and nursing
management of patients with rationales.
Hypertensive Crisis: What is it?

It’s a severe and abrupt ↑ in BP.

Defined as DBP > 120-130mmHg (but the rate at which it rises is more important)
Can be caused by HTN (whether the pt did not stick to meds, or was under-medicated), cocaine, crack, amphetamines, phencyclidine (PCP), LSD.
HTN r/t drug use can be complicated by drug-induced seizures, stroke, MI, or encephalopathy.

Hypertensive Crisis: Types

Hypertensive Emergency Hypertensive Urgency

- Develops over hours to days - Develops over days to weeks

- BP will be very elevated, WITH signs of acute target-organ damage - BP will be very elevated, WITHOUT signs of target-organ damage
(especially damage to the CNS)
- E.g. hypertensive encephalopathy, intracranial or subarachnoid
hemorrhage, acute LV failure with pulmonary edema, MI, renal failure,
and dissecting aortic aneurysm

Hypertensive Crisis: Manifestations

Manifestation Why it Occurs

Hypertensive encephalopathy Occurs d/t cerebral edema and spasms of the cerebral vessels.
Leads to headache, N/V, seizures, confusion, stupor, coma, blurred vision, and transient blindness

Renal insufficiency Can range from minor to complete renal shutdown

Rapid cardiac decompensation Can range from unstable angina to infarction and pulmonary edema (causing chest pain and dyspnea).
Pt may experience chest pain, back pain, diaphoresis, and loss of pulses in an extremity d/t aortic dissection.
 Hypertensive Crisis: Nursing & Interprofessional Management

Treatment Rationale

↓ MAP by 10-20% in the first 1-2hrs, and gradual ↓ for the next 24hrs

Vasodilators Will cause arterial vasodilation, which will ↓ SVR and BP

(e.g. sodium nitroprusside, nitroglycerin, diazoxide, hydralazine hydrochloride)

Adrenergic inhibitors Will cause peripheral vasodilation (↓ SVR and BP)

(e.g. phentolamine mesylate, labetalol, esmolol hydrochloride)

ACE inhibitors Will inhibit ACE, which will ↓ conversion of angiotensin I to angiotensin II. This
(e.g. enalapril) will ↓ aldosterone levels (aldosterone normally causes Na+ & H2O retention)

Continuous BP monitoring An arterial line or an automated BP monitoring machine may be needed if IV

meds are given, since the quicker onset of action can cause BP do ↓ faster.

Continuous ECG monitoring This is done to monitor for cardiac dysrhythmias

Hourly measurement of urinary output This is done to assess pt’s renal function

Frequent neuro checks Pt should be assessed for LOC, pupillary size & reaction, movement of
extremities, and reaction to stimuli, as a way to monitor changes in condition
 WEEK 12 - GAS EXCHANGE/ PERFUSION
[Link]
[Link]
[Link]

Differentiate between bronchial and pulmonary circulation of the respiratory system.

Bronchial Circulation Pulmonary Circulation

Origin Thoracic aorta Pulmonary artery

Distributes blood to the conducting airways and the

Function supportive structures of the lungs. It also warms and Involved in the function of gas exchange by the lungs
humidifies incoming air

Pathway Thoracic aorta → bronchial arteries → bronchi & lung RA → RV → pulmonary trunk → R/L pulmonary arteries →
structures → bronchial veins → vena cava & pulmonary veins lung capillaries → pulmonary veins → LA

Type of Blood Deoxygenated blood Deoxygenated blood from RA to lungs; oxygenated blood
(oxygenated/deoxygenated) (since it’s not involved in gas exchange) from lungs to LA

- Does not participate in gas exchange - Can undergo angiogenesis and can develop collateral
Unique features - Creates a physiological shunt (slightly deoxygenated circulation during a pulmonary embolism
blood entering LV because the bronchial circulation - Only part of circulation where arteries carry
will enter the LA through pulmonary veins) deoxygenated blood & veins carry oxygenated blood

Explain the etiology, pathophysiology, clinical manifestations, interprofessional care, and nursing management of pulmonary hypertension
and cor pulmonale with rationales.
Pulmonary HTN: What is it?

Pulmonary HTN refers to ↑ pulmonary pressure d/t ↑ pulmonary vascular resistance through small arteries and arterioles.

Pulmonary HTN: Types

Primary Pulmonary HTN (PPH) Secondary Pulmonary HTN (SPH)

Mean Pulmonary Arterial Pressure > 25mmHg at rest, or > 30mmHg during Primary disease causes a chronic ↑ in pulmonary artery pressures
exercise
 Pulmonary HTN: Etiology

Primary Pulmonary HTN (PPH) Secondary Pulmonary HTN (SPH)

- Unknown cause - Parenchymal lung disease

- Linked to fenfluramine - Left ventricular dysfunction
- Genetic component - Intracardiac shunts
- More common in women - Chronic pulmonary thromboembolism
- Systemic connective tissue disease

Pulmonary HTN: Pathophysiology

Primary Pulmonary HTN (PPH) Secondary Pulmonary HTN (SPH)

Cause: Anatomical changes:

Deficient release of vasodilators from the pulmonary epithelium Primary disease → (1) loss of capillaries d/t alveolar wall damage (e.g. COPD),
(2) stiffening of pulmonary vasculature (e.g. pulmonary fibrosis connective
When vasoactive mediators are released, they cause vasoconstriction → tissue disorder), (3) obstructed blood flow (e.g. chronic emboli) → ↑ resistance
release of growth factors → remodelling (vessel wall thickening) → sustained ↑
in pulmonary pressures Vascular changes:
Primary disease characterized by hypoxia → ↑ PVR → localized
vasoconstriction, shunting of blood away from poorly ventilated alveoli

Pulmonary HTN: Manifestations

Primary Pulmonary HTN (PPH) Secondary Pulmonary HTN (SPH)

Dyspnea on exertion (progresses to dyspnea at rest) Dyspnea

Fatigue Fatigue

Exertional chest pain Lethargy

Dizziness chest pain

Exertional syncope Right ventricular hypertrophy

Right ventricular failure

 Pulmonary HTN: Diagnostics

Diagnostic Study What do you see on there?

CXR Enlarged central pulmonary arteries & clear lung fields

Echocardiogram Right ventricular hypertrophy

ECG

CT scan Will measure pulmonary artery pressure

Cardiac catheterization Will measure pulmonary artery pressure

Pulmonary HTN: Interprofessional Care

Primary Pulmonary HTN (PPH) Secondary Pulmonary HTN (SPH)

- No cure - Treat the underlying disorder/condition

- Diuretics - will ↓ dyspnea and peripheral edema, and it might help ↓ - Treatment of SPH is similar to that of PPH
right ventricular volume overload.
- Anticoagulation therapy - recommended for pts with severe
pulmonary HTN
- Will prevent in situ thrombus formation and venous thrombosis
- Vasodilators - will ↓ right ventricular overload by dilating pulmonary
vessels and reversing remodelling
- E.g. calcium-channel blockers (nifedipine, diltiazem)
- Synthetic prostacyclins - promotes pulmonary vasodilation & ↓ PVR
- Recommended for pts that are unresponsive to calcium
channel blockers
- E.g. bosentan (PO), treprostinil (SC), epoprostenol (IV)
- Surgical interventions - atrial septostomy, pulmonary
thromboendarterectomy, lung transplantation
 Cor Pulmonale: What is it?

“Cor Pulmonale” refers to hypertrophy of the right side of the heart, with or without HF, d/t pulmonary HTN.
Commonly caused by diseases of the lung/thorax (e.g. COPD) or changes in pulmonary circulation.

Cor Pulmonale: Manifestations

Manifestation Why it Occurs

Dyspnea

Chronic productive cough

Wheezing

Retrosternal or substernal pain

Fatigue

Polycythemia, ↑ blood volume and viscosity Occurs d/t chronic hypoxemia

Symptoms of HF (if it accompanies cor pulmonale) Manifestations include: peripheral edema, weight gain, distended neck veins,
bounding pulse, enlarged liver

Cor Pulmonale: Diagnostics

Diagnostic Study What do you see on there?

Hx and physical exam

ECG

ABGs

Serum & urine electrolytes

CXR Enlarged RV and pulmonary artery

 Cor Pulmonale: Interprofessional Management

Treatment Rationale

Long-term low-flow O2 therapy Is used to correct hypoxemia and ↓ vasoconstriction in chronic states of
respiratory disorders

Correct fluid, electrolyte, and acid-base imbalances

Diuretics and low-sodium diet Will help ↓ plasma volume and workload on the heart

Bronchodilator therapy Used if the underlying respiratory condition is caused by an obstructive disorder

Digitalis Used if there is left-sided HF

For pulmonary HTN: Vasodilator therapy will ↓ RV overload by dilating pulmonary vessels and reversing remodelling

For pulmonary HTN: Calcium channel blockers

For pulmonary HTN: Anticoagulants Will prevent in situ thrombus formation and venous thrombosis

Theophylline Can be helpful d/t its weak inotropic effect on the heart

Lung transplantation Recommended if medical treatment fails

Continuous low-flow oxygen Needed during sleep and exercise for COPD pts

Small, frequent meals Needed for better activity and well-being for COPD pts
 WEEK 13 - MOBILITY
[Link]
[Link]

Review the structure, histology, blood and nerve supply of bone.

Blood Supply of Bone

- Periosteum: The outer membrane covering the bone, where blood vessels pass into the bone.

Key Structures
- Perforating Canals: Small canals that carry small arteries from the periosteum into the bone.
- Periosteal Arteries: Small arteries (accompanied by nerves), that enter the diaphysis through perforating canals & supply the osteonic canals of osteons
near the surface.
- Osteonic Canals: Channels in compact bone that contain blood vessels and nerves; connected by transverse canals.
- Nutrient Foramen: A hole in the compact bone where the nutrient artery enters the bone at an oblique angle.
- Nutrient Canal: A canal in the diaphysis that the nutrient artery passes through to reach the medullary cavity.
- Medullary Cavity: Central cavity of the bone where the nutrient artery divides into branches that supply the inner compact bone, spongy bone, and bone
marrow.

Specifics for Long Bones

- Nutrient Artery: A large artery that enters the diaphysis through the nutrient foramen, supplying the inner bone tissues.
 - Proximal & Distal Branches: The nutrient artery divides into these branches in the medullary cavity, extending toward each end of the bone

Arterial Supply to Long Bones

- Metaphyseal Arteries:
- Enter metaphyses of long bones.
- Supply red and yellow bone marrow and spongy bone in the metaphyses.
- Work with branches of the nutrient artery.
- Epiphyseal Arteries:
- Enter epiphyses of long bones.
- Supply red and yellow bone marrow and spongy bone in the epiphyses.
- Arise from arteries supplying the associated joint.
- Enter bone through perforating canals.

Venous Drainage from Long Bones

- Nutrient Veins:
- Accompany the nutrient artery.
- Exit through the diaphysis.
- Epiphyseal and Metaphyseal Veins:
- Accompany their respective arteries (epiphyseal arteries + veins; metaphyseal arteries + veins)
- Exit through the epiphyses and metaphyses.
- Periosteal Veins:
- Accompany periosteal arteries.
- Exit through the periosteum.

Nerve Supply to Bones

- Nerves in Periosteum:
- Accompany blood vessels supplying bones.
- Rich in sensory nerves, especially sensitive to tearing or tension.
- Pain associated with fractures, bone tumors, and bone marrow biopsies due to nerve sensitivity in the periosteum.
Review bone growth during infancy, childhood, and adolescence.

Growth in Length Growth in Thickness

Epiphyseal Plate and Bone Growth Bone Formation Process
- The epiphyseal plate is the only way the diaphysis can ↑ in length - Osteoprogenitor Cells: Differentiate into osteoblasts at the bone
- Chondrocyte Activity: surface in the osteogenic layer of the periosteum.
- Chondrocytes proliferate on the epiphyseal side. - Osteoblasts: Secrete collagen fibers and other organic molecules to
- New chondrocytes replace older ones destroyed by form bone extracellular matrix.
calcification. - Osteocytes: Form when osteoblasts become surrounded by the
- Cartilage on the diaphyseal side is replaced by bone,
extracellular matrix.
increasing bone length.
- Fracture Impact: Damage to the epiphyseal plate can result in shorter Formation of Bone Ridges and Tunnels
bone length due to accelerated closure and halted cartilage cell - Bone Ridges: Form on either side of a periosteal blood vessel as
division. osteoblasts secrete matrix.
Epiphyseal Plate Closure - Groove Formation: Ridges enlarge and create a groove for the blood
- Adolescence End: vessel.
- Females: Around age 18 - Tunnel Formation: Ridges eventually fold together and fuse, enclosing
- Males: Around age 21 the blood vessel in a tunnel.
- Epiphyseal cartilage stops dividing, bone replaces cartilage, - Periosteum to Endosteum: The former periosteum becomes the
forming the epiphyseal line. endosteum lining the new tunnel.
- Bone Growth Stop: Once the epiphyseal line appears, bone growth in Osteon Formation
length ceases. - Osteoblasts in Endosteum: Deposit bone extracellular matrix,
- Age Determination: forming new concentric bone lamellae.
- Open plate: Indicates youth. - Inward Growth: Lamellae formation proceeds inward toward the
- Partially/fully closed plate: Indicates older age. periosteal blood vessel, filling the tunnel.
- Closure occurs 1–2 years earlier in females - New Osteon: A new osteon is created as the tunnel is filled in.
Describe the remodelling of bone and relate to the fracture healing process.

Phase 1: hematoma formation Phase 2: fibrocartilaginous callus formation

- Bone fracture causes blood vessels in the bone and surrounding Formation of Procallus
tissues to tear. - New capillaries infiltrate the hematoma at the fracture site, organizing it
- Blood pools around the fracture site, forming a hematoma into granulation tissue called the “procallus”
- The hematoma is a source of signaling molecules that initiate
- Fibroblasts from the periosteum, endosteum, and red bone marrow
critical cellular events for healing
- The hematoma facilitates formation of a fibrin meshwork that seals the proliferate and invade the procallus.
fracture site Formation of Soft Callus
- The fibrin meshwork provides a framework for: - Fibroblasts produce a soft callus bridge that connects the bone
- Influx of inflammatory cells fragments
- Ingrowth of fibroblasts - The soft callus reaches max size by the end of the 2nd-3rd week
- Development of new capillary buds (blood vessels) - **The soft callus is not strong enough for weight-bearing
 Phase 3: bony callus formation Phase 4: remodelling

- Ossification: Conversion of fibrocartilaginous callus → bony callus - Osteoclasts gradually remove dead bone
- Osteogenic cells develop into osteoblasts (bone-building cells) near - Compact bone replaces spongy bone around the fracture's periphery
well-vascularized bone tissue (which produce spongy bone trabeculae) - Mineralized bone is reorganized along lines of mechanical stress
- The osteoblasts first deposit bone on the outer surface of the bone, - Excess material on the bone surface and within the medullary cavity is
away from the fracture site removed
- Bone formation progresses towards fracture site until a new bony - Compact bone is laid down to reconstruct the shaft
sheath covers the fibrocartilaginous callus - Final structure resembles the original bone, but a thickened area on the
- Fibrocartilage is gradually converted to spongy bone, forming the bony surface might remain as evidence of the healed fracture
callus
- Bony callus starts to calcify & is replaced by mature bone over time.
- Formation starts 3–4 weeks after injury and continues until a
firm bony union is formed months later
Differentiate among osteomyelitis due to spread from a contaminated wound, hematogenous osteomyelitis, and osteomyelitis due to
vascular insufficiency in terms of etiologies, manifestations, and treatment.
Osteomyelitis

Osteomyelitis d/t contaminated Hematogenous osteomyelitis Osteomyelitis d/t vascular

wound insufficiency

Etiology MO gains direct entry into the body through Infectious MO spreads from other sites of Leg or foot ulcers, pressure-related injuries
an open wound (e.g. fractures, penetrating infection in the body, through the blood (e.g.
wounds, surgery, etc.) ear, skin, sinus, teeth)

Manifestations Persistent or recurrent fever Chills Ingrown toenails

↑ pain at operative/trauma site Fever Cellulitis
Poor incisional healing Malaise Perforating foot ulcer
Continued wound drainage Pain on movement of affected extremity No pain d/t peripheral neuropathy
Wound separation Loss of movement
Joint pain, fever, cutaneous drainage (seen Local tenderness
in prosthetic joint infections) Redness & swelling

Treatment - Antibiotics (prophylactic before - Parenteral, followed by PO, - Debridement

surgery) antimicrobials - Antibiotics
- Placement of antimicrobial beads - Debridement - Hyperbaric O2 therapy
during infected hip arthroplasty or - Surgical drainage - Amputation
for wound infection after SCI - Rest and pain control (depends on
- Surgical decompression if pt’s symptoms)
antibiotics don’t work

Explain the functions of the various types of traction.

Explain the etiology, pathophysiology, clinical manifestations, and interprofessional care of soft tissue injuries, including strains; sprains;
dislocations; subluxations; bursitis; repetitive strain injury; carpal tunnel syndrome; and injuries to the rotator cuff, meniscus, and anterior
cruciate ligament.
Strains & Sprains

Strains Sprains

A stretching injury to a muscle, a muscle’s fascial sheath, or a Involves ligaments surrounding a joint.
Definition tendon. Resembles a strain, but the pain and swelling subside more
slowly.

First degree First-degree sprain (mild)

- Mildly or slightly pulled muscle - Involves tears in only a few fibers → mild tenderness
Second degree and minimal swelling
Classification - Moderate or moderately-torn muscle Second-degree sprain (moderate)
Third degree - Partial tearing of the ligament, with more swelling and
- Severely torn or ruptured muscle tenderness
Third-degree sprain (severe)
- A complete tearing of the ligament in association with
moderate to severe swelling

- Unusual muscle contraction Abnormal or excessive wrenching or twisting motion.

Etiology - Excessive forcible stretch Most commonly occurs in the ankle, knee, or wrists.
- Common in the leg (hamstrings), knee, wrist, back

- Pain aggravated by continued use - Pain aggravated by continued use

- Edema d/t local inflammatory response - Edema d/t local inflammatory response
Manifestations - ↓ funciton - ↓ funciton
- Bruising - Bruising
- Hemarthrosis (bleeding into a joint space/cavity) can
occur with very severe sprains (avulsion fracture)

Health Promotion
- Perform warm-up exercises before exercisin/vigorous activity, followed by stretching
- Strength, balance, and endurance exercises
- Strengthening exercises involve working against resistance
- Baalnce exercises help prevent falling
Nursing & Interprofessional - Endurance exercises should be started at a low effort
Management Acute Intervention - RICE Method
- Rest: stop activity and limit movement
- Ice: apply ice compress to the injured area
- Will help ↓ muscle s20–30pasms, inflammation, and edema
 - Should not exceed 20-30 mins, and should not be applied directly to the skin
- Compression: compress the involved extremity
- Use an elastic compression bandage
- Will prevent edema and encourage fluid return
- Elevation: elevate the extremity
- Elevate above heart level to mobilize excess fluid from the area
- Should also be elevated during sleep
- Provide analgesia if needed (e.g. NSAIDs)
- Use heat to help ↓ swelling and provide comfort AFTER 24-48hrs
- Should not exceed 20–30 mins
Ambulatory & Home Care
- Instruct pt to use ice and elevate extremity for 24-48hrs after injury
- Encourage use of mild analgesics

Dislocations & Subluxations

Definition - Disclocation: displacement or separation of the bone ends of a joint, with loss of articulation
- Subluxation: partial dislocation, where the bone ends in the joint are still in partial contact with each other

Etiology - Caused by large forces transmitted to the joint

- Most common: thumb, elbow, shoulder, hip, patella

Manifestations - Deformity
- Local pain
- Tenderness
- Loss of function of the injured part
- Swelling of the soft tisues in the region of the joint
Complications: open joint injuries, intra-articular fractured, avascular necrosis, damage to adjacent neurovascular tissue

- Realign the dislocated portion of the joint into its original anatomical position
Nursing & Interprofessional - Local reduction or conscious sedation
Management - Immobilization (bracing, splinting, taping, using a sling)
- Pain relief
- Gentle ROM exercises can be started is joint is stable and well-supported
 Repetitive Strain Injury (RSI)

Definition Refers to injuries caused by prolonged force or repetitive movements & awkawrd postures

- Unknown cause
Individuals at risk:
- Muicians, dancers
- Butchers, grocery clerks
Etiology - Those qho frequently use technology (i.e. smartphones)
- Competitive athletes, poorly trained athletes, etc.
Other risk factors:
- Poor posture & positioning
- Poor workspace ergonomics
- Badly designed workplace equipment
- Repetitive lifting of healthy workloads without sufficient msucle rest

- Pain
Manifestations - Weakness
- Numbness
- Impairmenet of motor function in the muscles, tendons, and nerves of the neck, shoulder, forearm,
and hand

- Identify the precipitating cause

Nursing & Interprofessional Management - Modify equipment or activity
- Pain management (heat/cold application, NSAIDs)
- Physiotherapy
- Lifestyle changes
 Carpal Tunnel Syndrome (CTS)

Definition CTS is a type of repetitive strain injury (RSI), which results in the compression of the median nerve

- Inflammation of a tendon (tenosynovitis)

- Neoplasm
Etiology - Rheumatoid arthritis (RA)
- Soft tissue masses (e.g. ganglia)
- Associated with hobbies or occupations that require continuous wrist movement
- E.g. musicians, painters, carpenters, computer operators

- Weakness (especially in the thumb)

- Burning pain (causalgia)
- Numbness or impaired sensation in the distribution of the median nerve
Manifestations - Clumsiness when performing fine hand movements
- Positive Tinel sign (tingling sensation in the distribution of the median nerve over the hand)
- How to test: tapp over the median nerve as it passes through the carpal tunnel
- Positive Phalen sign (tingling sensation in the distribution of the median nerve over the hand)
- How to test: let the wrist fall freely into maximum flexion and maintain position for > 60sec

Health Promotion
Nursing & Interprofessional Management - Educate pts, employees, and employers to identify risk factors
- Encourage wearing wrist splints to hold the wrist in slight extension → will ↓ pressure on the nerve
- Encourage workplace modifications, using special keyboard pads and mice, changing body
positions, and frequent breaks from work-related activities
Acute Intervention
- Wear a splint at night to keep the wrist in a neutral position (may also ↓ pain and numbness)
- Physiotherapy
- Corticosteroid injections
- Carpal tunnel release surgery
 Rotator Cuff Injury

- Rotator cuff: complex of 4 muscles (supraspinatus, infraspinatus, teres minor, subscapularis)

What is the rotator cuff? - These muscles stabilize the humeral head while helping with ROM of the shoulder joint, and
rotation of the humerus

- Degeneration r/t aging

- Repetitive stress (especially overhead arm motions)
Etiology - Injury to the shoulder while falling
- Falling onto an outstretched arm and hand
- A blow to the upper arm
- Heavy lifting
- Repetitive work motions

- Shoulder weakness
Manifestations - Pain (severe when arm is abducted)
- ↓ ROM

- Conservative therapy: rest, ice and heat, NSAIDs, corticosteroid injections into the joint, physiotherapy
Nursing & Interprofessional Management - Surgery (arthroscopy, acromioplasty/shoulder decompression)
- Post-op care:
- Sling or shoulder immobilizer
- Pendulum exercises and physiotherapy (post-op day 1)
- No lifting weights (for up to 6 months)

Anterior Cruciate Ligament (ACL) Injury

What is the ACL? - It’s a ligament found in the knee joint

Etiology - Noncontact injury (e.g. an athlete pivots, lands from a jump, or slows down when running)

- Positive Lever sign (slight flexion at knee joint)

Manifestations - How to test: place pt in supine position with knees fully extended. Place a fist under the tibial
tuberosity of the affected knee

- Conservative treatment: rest, ice, NSAIDs, elevation, and ambulation as tolerated with crutches
- Knee immobilizer or hinged knee brace
Nursing & Interprofessional Management - Physiotherapy
- Reconstructive surgery
- Post-op care:
- ROM exercises, use brace or immobilizer, physiotherapy
 Meniscus Injury

What are minisci? - Menisci: crescent-shaped pieces of fibrocartilage in the knee

- Associated with ligament sprains (common in athletes)

Etiology - E.g. basketball, football, socker, hockey
- Rotational stress when the knee is in varying degrees of flexion while the foot is planted or fixed
- Blow to the knee

- Localized tenderness
Manifestations - Pain
- Elicited by flexion, internal rotation, and then extension (McMurray test)
- Effusion

- Teach athletes to do warm-up activities

Nursing & Interprofessional Management - Examin acutely injured knee within 24hrs of the injury
- Initital care:
- Apply ice and immobilize the knee
- Partial weight bearing with crutches
- Use a knee brace or immobilizer during the first few days after injury
- Physiotherapy after acute pain has gone down
- Surgical repair or excision of part of the meniscus (via arthroscopy)
- Post-op care:
- Rehab with quads- and hamstring-stengthening exercises
- ROM exercises

Bursitis

Definition Inflammation of the bursa

- Repeated or excessive trauma

- Friction
Etiology - Gout
- RA
- Infection

- Warmth
Manifestations - Pain
- Swelling
- Limited ROM in the affected area
 - Determine cause
Nursing & Interprofessional Management - Rest
- Ice the area to help ↓ pain and inflammation
- Immobilize affected area with a cmpression dressing or a splint
- NSAIDs to ↓ pain and inflammation
- Aspiration of bursal fluid
- Intra-articular injection of corticosteroid therapy
- Surgical excision if bursal wall has thickened or has become septic

Compare closed reduction, cast immobilization, open reduction, and traction regarding purpose, complications, and nuEnsurersing
management.
Purpose Complications Nursing Management

Closed Reduction Nonsurgical, manual realignment of bone - Risk of misalignment if not - Once completed, immobilize pt to
fragments to restore position, length, and properly maintained maintain alignment during healing
alignment. - Monitor for alignment and
complications
- Educate pt about care and
immobilization

- Pressure sores from improper fit - proper application & padding

Cast Immobilization Stabilize the bone and joint above and - Compartment syndrome - Monitor for signs of compartment
below the fracture to allow healing - Skin irritation or breakdown syndrome & pressure sores
- Delayed bone healing if - Elevate extremity to ↓ edema
immobilization is inadequate - Educate pt on cast care

Open Reduction Surgical realignment of bone with internal - Possibility of infection - Monitor for infection at surgical
fixation (wires, screws, pins, etc.) to - Complications r/t anesthesia site
stabilize fractures - The effect(s) of pre-existing - If ORIF is performed, early ROM
medical conditions exercises with CPM machines is
indicated
- Educate pt about signs of
infection and post-op care

Traction - Skin breakdown - Regularly assess skin for

Provides a pulling force on a fractured - Delayed union or nonunion with breakdown in skin traction
extremity to attain realignment. skeletal traction - Maintain proper alignment and
Used for pain relief, joint space - Infection risk in skeletal traction. weight balance
expansion, or soft tissue healing. - Complications d/t prolonged - Monitor for infection
immobility (e.g., pressure ulcers, - Educate pt on maintaining traction
muscle atrophy) & monitoring for complications
Explain the early and late complications of fractures and fracture healing.
Complications of Fractures

General Info Interprofessional Care

Infection - There’s a high risk of infection in open fractures - Open fractures need surgical debridement
and soft tissue injuries - Extent of the soft tissue injury determines if the
- Prophylactic antibiotics may be needed to help wound will be closed up during surgery, or if it
prevent extended length of care and osteomyelitis needs repeated debridement, closed suction
drainage, or skin grafting
- Post-op care:
- IV antibiotics for at least 3 days

Compartment Syndrome - Caused by: (1) ↓ compartment size (e.g. - Regular neurovascular assessments are needed
restrictive dressings, casts, excessive traction, - Carefully assess location, quality, and intensity of
Swelling and ↑ pressure within a etc); (2) ↑ compartment contents d/t bleeding, the pain
compartment, compromising the function of edema, etc. - Assess urine output d/t possible muscle damage,
blood vessels, nerves, & tendons that run - Leads to ↓ perfusion, which is lower than the level which can lead to AKI
through that compartment
needed for viable tissue - Do not elevate extremity above heart level, since
- 6 Ps: (1) pain distal to the injury that is not it will show down arterial perfusion
relieved by opioids and pain on passive stretch of - Avoid cold compress - it can exacerbate
muscle travelling through the compartment; (2) ↑ compartment syndrome
pressure in the compartment; (3) paresthesia; (4) - May need to loosen or remove bandage around
pallor & coolness; (5) paralysis; (6) pulselessness the affected extremity
or absent peripheral pulses - Surgical decompression

- Veins of the lower extremities and the pelvis are - Prophylactic anticoagulants for at least 10–14
highly susceptible to thrombus formation after days
Venous Thromboembolism (VTE) fracture (especially hip fracture) - Wear compression stockings
- Limited mobility → inactivity of muscles that - Use sequential compression devices
normally assist in pumping venous blood - Dorsiflex and plantar flex fingers/toes of affected
returning from extremities → venous stasis extremity against resistance
- Perform ROM exercises on unaffected extremity

Fat Embolism Syndrome (FES) - Most common with fractures of long bones, ribs, - Investigate CNS involvement if pt has headache,
and pelvis memory loss, restlessness, confusion, or fever
Presence of systemic fat globules from - Manifestations occur within 24-48hrs post injury - Early & careful immobilization
fractures that are distributed into tissues and - Manifestations: signs of ARDS, changes in - Fluid resuscitation to prevent hypovolemic shock
organs after a traumatic skeletal injury mental status, ↑ temperature, restlessness, etc. - Replace blood loss
- FES can be differentiated from other conditions - Correct acidosis
 d/t the presence of petechiae around the neck, - Maintain SPO2
anterior chest wall, axilla, buccal membrane, and
eye conjunctiva, & continuous changes in LOC

Complications of Fracture Healing

Delayed Union - Fracture healing progresses more slowly than expected; healing eventually occurs

Nonunion - Fracture fails to heal properly despite treatment

- No radiographic evidence of callus formation

Malunion - Fracture heals in expected time but in unsatisfactory position, possibly resulting in deformity or dysfunction

Angulation - Fracture heals in abnormal position in relation to midline of structure (type of malunion)

Pseudoarthrosis - Type of non-union occurring at fracture site in which a false joint is formed with abnormal movement at site

Refracture - New fracture occurs at original fracture site

Myositis Ossificans - Deposition of Ca2+ in muscle tissue at the site of blunt muscle trauma, or repeated muscle injury

Describe the interprofessional and nursing management of patients with specific fractures.
Fractures: Nursing Management

Nursing Assessment:
Subjective Objective

- Ask about PMHx: Traumatic injury; long-term repetitive forces (stress - General - Apprehension, guarding of injured site
fracture); bone or systemic diseases, prolonged immobility - Integumentary - Skin lacerations, pallor and cool skin or bluish and
(pathological fracture), osteopenia, osteoporosis warm skin distal to injury; ecchymosis, hematoma, edema at site of
- Ask about meds: Corticosteroids (osteoporotic fractures), analgesics, fracture
hormone therapy, calcium supplementation - Cardiovascular - ↓ or absent pulse distal to injury, ↓ skin temperature,
- Ask about surgeries/other treatments: First aid treatment of delayed capillary refill
fracture, previous musculoskeletal surgeries - Neurlo - Paresthesias, ↓ sensation, hypersensation
- Ask about symptoms: - MSK - Restricted or lost function of affected part; local bony
- Loss of motion or weakness of affected part; muscle spasms deformities; abnormal angulation; shortening, rotation, or crepitation of
- Sudden/severe pain in affected area; numbness, tingling, loss affected part; muscle weakness
of sensation distal to injury; chronic pain that increases with - Possible findings - Identification and extent of fractures on XR, bone
 activity (stress fracture) scan, CT scan, or MRI

Neurovascular assessment:
- Peripheral vascular assessment
- Colour & temperature - pale & cool indicates arterial insufficiency; warm & cyanosis indicates poor venous return
- Capillary refill - blanking of the nail bed < 3 seconds indicates good arterial perfusion
- Peripheral pulses - compare rate and quality of pulses on both extremities
- Edema - pitting edema pay be present with injury
- Peripheral neurological assessment
- Sensation - stroking the plantar surface (sole) of the foot (any paresthesia? Hyperesthesia? paralysis?)
- Motor function - upper ext: abduction and adduction of the fingers, opposition of the fingers, and supination and pronation of the hand; lower
ext: dorsiflexion, plantar flexion
- Pain - assess location, quality, and intensity

Nursing Diagnoses & Goals of Care:

Potential Diagnoses: Goals of Care:
- Reduced mobility d/t joint stiffness and pain - Have healing with no associated complications
- Potential for peripheral neurovascular complications as demonstrated - Obtain satisfactory pain relief
by fracture (vascular insufficiency and nerve compression, mechanical - Achieve maximal rehabilitation potential
compression by traction, splints, or casts)
- Pain as a result of physical injury agent (edema, movement of bone
fragments, muscle spasms)
Implementation:
Health Promotion - Educate the public on safety precautions to prevent fractures (e.g., seat belts, helmets).
- Encourage regular exercise, especially for older adults, to maintain muscle strength and balance.
- Promote proper footwear and a safe living environment to reduce falls.
- Stress the importance of adequate calcium and vitamin D intake.

Pre-op Management:
- Prepare patients for surgery by informing them about immobilization devices and activity limitations.
- Reassure patients about pain management post-surgery.
Post-op Management:
Acute Intervention - Monitor vital signs and perform frequent neurovascular assessments.
- Ensure proper alignment and positioning to minimize pain and discomfort.
- Observe dressings or casts for signs of bleeding or drainage.
- Maintain wound drainage systems using aseptic technique
Other Measures:
- Prevent constipation with high fluid intake, activity, and a diet rich in fiber.
- Prevent renal calculi by promoting fluid intake to prevent hypercalcemia.
- Diminish cardiopulmonary deconditioning by encouraging gradual activity ↑es (e.g., sitting, standing).
 - Assess for orthostatic hypotension and VTE
Traction:
- Regularly inspect skin exposed to traction for pressure sores.
- Prevent hip external rotation with proper positioning.
- Inspect pin sites for infection and provide pin-site care with aseptic technique
- Encourage ROM exercises, deep-breathing exercises, and use of assistive devices.
- Assist with mobility training and use of assistive devices like crutches or walkers.
- Ensure proper technique in using assistive devices to prevent complications.

Cast Care:
- Perform frequent neurovascular assessments of the immobilized extremity.
- Educate patients about the importance of elevating the extremity and applying ice.
- Instruct patients on proper cast care, avoiding foreign objects inside the cast, and recognizing complications.
Ambulatory & Home Care Psychosocial Problems:
- Assist patients in transitioning to independence in ADLs.
- Provide emotional support and address concerns related to injury and rehabilitation
Ambulation:
- When the pt starts to ambulate, the nurse should know the pt’s weight-bearing status and the correct technique if
the patient is using an assistive device
- Weight-bearing ambulation occurs in different degrees:
- Non–weight-bearing ambulation (no weight on affected leg)
- Touch-down weight-bearing ambulation or toe-touch weight-bearing ambulation (contact with floor only for
balance; no weight on affected leg)
- Partial weight-bearing ambulation
- Weight bearing as tolerated (based on pt’s pain & tolerance)
- Full weight-bearing (no limitations)
Assistive devices:
- The decision about which device is appropriate for a patient involves weighing the need for maximum stability and
safety versus manoeuvrability (which is needed in small spaces)
- Use a transfer belt when learning to ambulate with injury
Counselling & Referrals:
- Educate caregivers on assisting with mobility and promoting daily activities.
- Evaluate patients for PTSD) and provide appropriate referrals

Evaluation:
- Expected outcomes:
- Report satisfactory relief of pain
- Demonstrate appropriate care of cast or immobilizer
- Experience no peripheral neurovascular complications
- Experience uncomplicated bone healing
 Colles Fracture

General Info - Colles fracture: fracture of the distal radius

- Common in people > 50yo with osteoporosis

Manifestations - Pain in the immediate area of injury

- Pronounced swelling
- Dorsal displacement of the distal fragment
- Complication: vascular insufficiency d/t edema

Interventions - Closed manipulation of the fracture

- Immobilization via splint or cast
- If bone is displaced, external fixation is needed
- Frequent neurovascular assessments needed

Fracture of the Humerus

General Info - Common among yound and middle-aged adults

Manifestations - Obvious displacement of the humerus shaft

- Shortened extremity
- Abnormal mobility
- Pain
- Complications: radial nerve injury, vascular injury to brachial artery d/t laceration, transection, or muscle spasm

Interventions - Treatment depends on location and displacement of the fracture

- Hanging arm cast
- Shoulder immobilizer
- Sling & swathe (type of immobilization that prevents glenohumeral movement)
- Make sure to elevate HOB when using this, so that gravity can help reduce the fracture
- Place absorbable composite dressing pads in the axilla - will protect the axilla, and will prevent skin maceration
- Skin or skeletal traction - used for reduction and immobilization
 Fracture of the Pelvis

General Info - Associated with the highest mortality rate

- Can cause more serious intra-abdominal injury
- I.e. paralytic ileus, hemorrhage, laceration of the urethra, the bladder, or the colon
- Can cause acute pelvic compartment syndrome

Manifestations - Local swelling, tenderness, deformity, unusual pelvic movement, ecchymosis

Interventions - Early immobilization - for stable, nondisplaced fractures

- Pelvic sling traction, skeletal traction, external fixation, open reduction, or combo of these methods
- All of these are used for more complex pelvic fractures
- ORIF for displaced fracture
- Assess bowel and urinary function, since pelvic fracture can damage internal organs

Hip Fracture

General Info - Common in older adults

- Hip fracture: fracture of the proximal third of the femar, which extends up to 5cm below the lesser trochanter
- Intracapsular fractures: fractures that occur within the hip joint capsule
- Capital fracture: fracture of the head of the femur
- Subcapital fracture: fracture just below the head of the femur
- Transcervical fracture: fracture of the neck of the femur

Manifestations - External rotation

- Muscle spasm
- Shortening of the affected extremity
- Severe pain and tenderness in the region of the fracture site

Interventions - Affected extremity needs to be immobilized until pt’s physical condition is stabilized and surgery can be performed
- Buck traction - will relieve painful muscle spasms for up to 24-48hrs
- Surgical options:
- Repair with internal fixation devices
- Replacement of part of the femur with prethesis (partial hip replacement)
- Total hip repalcement (involves both, the femur and the acetabulum)
 Femoral Shaft Fracture

General Info - Caused by severe direct force

- More common in young adults
- Can damage adjacent soft tissue structures
- Can cause lots of blood loss → hemorrhagic anemia
- Most common types of femoral shaft fractures: transverse, spiral, communited, oblique, and open

Manifestations - Marked deformity and angulation

- Shortening of the extremity
- Inability to move either the hip or the knee
- Pain
- Complications: fat embolism, nerve/vascular injury, problems r/t bone union, open fractuer, & soft tissue damage

Interventions - Stabilize the pt and immobilize the fracture

- Intramedullary nailing - metal rod is placed into the marrow canal of the femur (will keep bone in position)
- Internal fixation
- Post-op care:
- Gluteal and quads isometric exercises
- Non-weight-bearing activities with assistive device (e.g. crutches, walker, etc.)

Fracture of the Tibia

General Info - Stress fractures are common in the tibia

Manifestations - Complications: compartment syndrome, FES, conditions r/t bony union, possible infection r/t open fracture

Interventions - Closed reduction followed by immobilization with long leg cast (for closed fracture)
- ORIF with intramedullary rods, plate fixation, or external fixation (for complex fractures)
- Assess neurovascular status q2h during first 48hrs
 Stable Vertebral Fracture

General Info - Usually caused by MVCs, falls, diving, or other athletic injuries
- Stable fracture: fracture where the fracture/fragment is not likely to move or cause spinal cord damage
- Usually seen in the vertebral body of the spinal column in the lumbar region
- Less common in the cervical and thoracic resions
- Unstable fracture: fracture where the ligamentous structures are significantly disrupted, causing dislocation of the
vertebral structures → instability and injury to the spinal cord

Manifestations - Pain
- Tenderness in the affected region of the spine
- Sudden loss of function below the level of the fracture → SCI
- Kyphotic deformity - seen in stable compression fractures
- Dowager’s hummp (abnormal curvature of the thoracic spine) - seen in fracture r/t osteoporosis
- Lumbar lordosis (extreme inward curve) is also seen in fractures r/t osteoporosis
- Complication: fracture displacement

Interventions - Main medications

- Early mobilization and bracing
- Log rolling technique should be used when turning
- Vertebroplasty or kyphoplasty - used for vertebral compression fractures
- Pt needs to wear c-collar or halo vest if there’s a fracture in the cervical region

Facial Fracture

General Info - Can be caused by trauma (i.e. MVCs, assault, fall, etc.)
- Mandibular fractures
- Caused by trauma to the face or jaws
- Can be closed with no bone displacement, or it can involve loss of tissue and bone
- Can only be done for therapeutic purposes

Manifestations - Eye-globe rupture (possible if the eye is injured)

Interventions - Maintain patent airway

- Provide adequate ventilation
- Treat facial injury as if the pt has a cervical injury too, until proven otherwise
Describe the types of joint replacement surgery associated with arthritis and connective tissue.
Types of Joint Replacement Surgery

Description Common Areas of Surgery Indications Post-op Considerations

Synovectomy Removal of synovial membrane; Elbow, wrist, fingers, knee (less Rheumatoid arthritis Disease can still recurr.
Used for prophylaxis. common) Helps improve disease, pain,
Helps prevent inflammation into ROM, and weight-bearing
adjacent cartilage, ligaments,
and tendons

Osteotomy Removal or addition of a bone Cervical spine, hip, knee Hip osteoarthritis (OA), Similar to internal fixation
wedge to change alignment, ankylosing spondylitis
correct deformiy, & relieve pain

Debridement Removal of degenerative debris Shoulder, knee Osteoarthritis (OA) Outpatient procedure.
(loose bodies, osteophytes, joint Weight-bearing permitted after
debris, degenerated menisci) knee arthroscopy.

Arthroplasty Reconstruction or replacement Hip, knee, elbow, shoulder, OA, RA, avascular necrosis Post-op care varies by joint
of a joint to relieve pain, improve fingers, wrist, ankle, foot (AVN), congenital deformities or Emphasis on pain management,
ROM, and correct deformity. dislocations, etc. physiotherapy, and rehabilitation.

Arthrodesis Surgical fusion of a joint Wrist, ankle, cervical spine, Articular surfaces are too
lumbar spine, damanged or infected to allow
metatarsophalangeal (MTP) joint joint replacement. Or if
of the great toe reconstructive surgery fails.
Describe the preoperative and postoperative management of the patient having joint replacement surgery.
Preoperative Management Postoperative Management

Assessing risk factors: Neurovascular assessment:

- previous medical diagnoses (e.g. DM, thrombophlebitis), expectations, - This is done to monitor nerve function and circulatory status
pain tolerance, functional status, social support, home care needs Medication administration:
Infection control: - Anticoagulation therapy
- Ensure pt does not have infection or joint inflammation before surgery - Analgesia (e.g. epidural, intrathecal, femoral nerve block, PCA, IV/PO
Muscle strength and joint function assessment: opioids/NSAIDs)
- Assess upper extremity muscle strength and joint function, especially if - Parenteral antibiotics
lower extremity surgery is planned, to determine the need for assistive Early mobilization:
devices postoperatively. - Exercise affected joint and encourage ambulation ASAP to prevent
Pre-op physiotherapist consult: complications of immobility, enhance mobility, & build muscle strength
- Educate the patient and family about the expected hospital course, Thrombus prevention:
postoperative management, and the importance of physiotherapy to - Implement anticoagulation protocols
maximize prosthesis usefulness. - Start with warfarin on the day of surgery (continue for 3 weeks with
Patient education: regular INR checks) or LMWH (e.g. enoxaparin) post-op (continue for 2
- Prepare the patient for the reality of a prolonged recovery period; weeks without daily coagulation monitoring)
consider arranging conversations with individuals who have undergone Hospital:
similar surgeries - Typical hospital stay: 3 to 5 days
- Depends on the pt’s recovery progress and physio needs
 MEDS TO REMEMBER FOR SIM LAB:
Medication Indication Side Effects Notes

Ondansetron (zofran) N/V Might cause headache dose: 4mg?

Insulin Will ↓ amount of glucose in the liver Check glucose before giving insulin

Tylenol Pain or fever

Ceftriaxone Infection Nausea dose: 100mg?

Hydromorphone Pain Sleepiness (?) Do not give if BP is low

Sulfamethoxazole-trimethoprim Infection Nausea

Dimenhydrinate (Gravol) Motion sickness, nonproductive Drowsiness

cough, allergies, N/V, sedation, rhinitis

Toradol (ketorolac) Moderate to severe acute pain GI pain, nausea, dyspepsia, edema

Azithromycin Infection Nausea

Salbutamol (ventolin) Acute asthma, bronchitis, COPD Hyperglycemia, hypokalemia, - Hold breath for 5–10 seconds
tachycardia, insomnia, tremors after inhalation
- Wait ~1 min between puffs

Calcium Gluconate Hypocalcemia

Humulin R Insulin Diabetes, hyperglycemia Hypoglycemia It’s a short-acting insulin

Ibuprofen (Advil) MSK pain, soft tissue injuries Heartburn, abdo pain, GI bleed

Coumadin (warfarin) DVT, PE, AFib, MI, CVA thrombosis Hematuria, nausea, bleeding, etc. Vitamin K antagonist

Naloxone Opioid overdose Changes in BP, dysrhythmia, Anticipate N/V, diaphoresis, and
pulmonary edema agitation (withdrawal symptoms)

Glucagon Hypoglycemia Hyperglycemia dose: 1mg

Morphine Pain Sedation, constipation, N/V dose: 5mg?

Pantoprazole Gastritis, GERD, PUD Headache (not so often)

 Amiodarone

Diphenhydramine (Benadryl)

Albumin

Lactulose

Vitamin K

Hydroxyurea
 SIM LAB #1
SCENARIO 1: PE, MI
Jean Kelly is post-op (day 3) from a hemicolectomy. PMHx: CAD, COPD, high cholesterol, HTN, and T2DM. Her NG tube was taken out today. She is complaining of
chest pain.

Assessment:
- OPQRST for chest pain
- Vitals
- SPO2 will be low
- BP will be high
- Cardiovascular assessment
- Skin colour
- Cap refill
- Peripheral pulses
- Listen to heart sounds
- Respiratory assessment
- Check for nasal flaring and use of accessory muscles
- Check for pallor/cyanosis
- Auscultate the lungs
- Abdo assessment
- Assess surgical site (any redness? Any bleeding? Swelling? Heat? Foul odour?)
- Check lab values
- Check trop, BNP, D-Dimer
- Idk what else

Orders (SBAR):
- Ask for ECG and CXR
- Ask for nitroglycerin for chest pain
- If there is a PE, call the doctor back and ask for anticoagulants (warfarin)
- If the pt has an MI, ask for aspirin

Interventions:
- Put the pt in semi fowler’s position
- Administer anticoagulants (warfarin or aspirin, idk)
SCENARIO 2: ALLERGIC REACTION
Jean Kelly has pneumonia. She has SOB d/t her pneumonia. She got Tylenol and ceftriaxone 10 mins ago. She has acute onset of itchiness and hives all over the
face, neck, and arms.

Assessment:
- Check Vitals
- Subjective assessment
- Ask when their SOB started? Has it gotten worse?
- Ask if their throat is itchy? Check to see if their tongue is swollen.
- Respiratory assessment
- Check for nasal flaring and use of accessory muscles
- Check for pallor/cyanosis
- Auscultate the lungs
- Skin assessment
- Look for any hives
- Look for any redness
- Ask about any itchiness and where it is

Orders (SBAR):
- Ask for benadryl and ventolin
- Ask for ventolin if you hear wheezing

Interventions:
- Once you realize the pt is having an allergic reaction, you should discontinue the IV antibiotic right away (if it’s still running, but you can ask)
- Administer benadryl for itchiness and hives

SCENARIO 3: PNEUMONIA R/T UTI

Jean Kelly, 90yo, came in 2 days ago because of a UTI. PMHx: CVA (with right sided weakness), HTN, T2DM, high cholesterol. Jean Kelly is very lethargic, only
oriented x2. She also has NS running at 75ml/hr. When the nurse walks in, the pt is coughing.

Assessment:
- Check Vitals
- High BP, high HR, high RR, fever
- Neuro assessment
- GCS will still be the same
- Subjective assessment
- Ask about their cough
- Respiratory assessment
- Check for nasal flaring and use of accessory muscles - no
- Check for pallor - yes
- Auscultate the lungs - crackles on the right side

Orders (SBAR):
 - Ask for a CXR
- Ask for blood culture, and CBC
- Once the blood work comes back, you can ask for antibiotics - maybe ceftriaxone since it’s broad-spectrum

Interventions:
- Raise HOB
- Administer antibiotics
SCENARIO 4: OVERDOSE, ICP, HYPOGLYCEMIA
Jean Kelly is 80 something years old. She came into the ER after falling. She lost consciousness when she fell. Did a head CT and found a subdural hematoma, and
C-spine wasn’t affected. Her GCS was 15 when she came in. I don’t remember the PMHx, but maybe it was just HTN? She’s NPO since she might get surgery. And
she was given 2mg hydromorphone and 4mg zofran before you got report. When the nurse walks in, the pt doesn’t respond.

Assessment:
- Pinch her and make sure she’s alive
- She will only moan d/t the pain
- Check Vitals
- normal O2, BP 180/50 I think (widening pulse pressure), RR 10, pulse somewhere in the 40s, and normal temperature
- Neuro assessment
- PERRLA
- Right eye will respond to light, but the left eye won’t (it’ll stay constricted)
- This tells you that there may be an overdose, since pupils stay constricted, but who really knows
- GCS
- Check blood sugar

Orders (SBAR):
- If you see constricted pupils, you can call the doctor and tell them you need Narcan for an overdose
- If there’s no constricted pupils, tell the doctor that you think the bleeding may be spreading, causing an increase in ICP
- Ask for mannitol, and tell the doctor that the pt needs surgery right away
- Can also be r/t hypoglycemia. So if the BS is very low, then ask for 1mg glucagon

Interventions:
- If pt has an increase in ICP, make sure to elevate the HOB
- Administer whatever medication you asked for (probably narcan? Or mannitol? Or glucagon? idk)
 SIM LAB #2
SCENARIO 1: DYSRHYTHMIA
Jean Kelly came in and had a hemicolectomy 1 day ago. PMHx: MI (2 months ago with stent placement), HTN, T2DM, high cholesterol, and is a smoker. When the
nurse walks into her room, Jean Kelly is complaining of SOB. She’s then diagnosed with pneumonia.
Assessment:
- Vitals
- SPO2 88%
- Respiratory assessment
- Check for nasal flaring and use of accessory muscles
- Check for pallor/cyanosis
- Auscultate the lungs
- Cardiovascular assessment
- Skin colour
- Cap refill
- Skin temperature
- Peripheral pulses - bounding pulse
- Abdo assessment
- Assess surgical site (any signs of infection)

Orders (SBAR):
- Ask for ECG (it will show A-fib)
- Once you find out that the pt has A-fib, call the Dr. again and ask for amiodarone

Interventions:
- Elevate HOB right when the pt complains about SOB
- The doctor’s orders say that O2 should be kept above 89-93%, so you need to give supplementary O2
- Do this right when you notice the low SPO2
- Once you get the order for amiodarone, administer that

SCENARIO 2: HYPOVOLEMIA
Jean Kelly came in with a STEMI and went to the cath lab to get a PCI in the femoral artery (?). The patient is now in the hospital, and when the nurse walks in, the
pt is feeling dizzy (almost unconscious).

Assessments:
- Check VS - everything is normal, except RR is increased
- Check incision site for infection
- Any redness? Swelling? Heat around the area? Any bleeding/drainage?
- The site will be bleeding a lot
- In some scenarios, there was no bleeding
- Peripheral vascular assessment
 - Check peripheral pulses below the femoral incision site
- Cardiovascular assessment
- Skin colour
- Cap refill
- Skin temperature
- Listen to the heart sounds

Interventions:
- Since the dressing is all soaked, change the dressing

Orders (SBAR):
- Ask for a bolus of NS or a blood transfusion d/t all the blood loss
- Ask for an ECG

Evaluation:
- Re-check the VS
- Re-check the dressing

SCENARIO 3:
Jean Kelly came in 3 days ago with SOB, cough, and fever. She was diagnosed with pneumonia (bilaterally). PMHx: COPD, T2D, smoker, HTN. Her last set of VS
were: BP 130/88, HR 80, RR 28, 37.2, SPO2 93% on 50% venturi mas. Once the nurse walks in, the pt complains of SOB, saying that she “can’t breathe.” She
cannot talk much, only in short sentences.

Assessments:
- Since the pt cannot talk much, you don’t want to ask too many questions. Go straight to physical assessments
- Check O2 level
- Make sure that it’s at 50% just like you were told during report
- Check VS
- Check SPO2 first, then RR and then HR
- You can check BP and temperature, but they’re not as important right now.
- Respiratory assessment:
- Look for laboured breathing
- Look for deep or shallow breaths
- Look for accessory muscle use - yes there is
- Look for nasal flaring and retractions - yes there is
- Look for any cyanosis around the mouth - yes there is
- Auscultate the lungs - wheezing and crackles bilaterally
- Cardiovascular assessment:
- Cap refill - will be > 3 seconds
- Check skin colour and temperature - will be cool/pale
 Interventions:
- Dr’s order has Ventolin, so administer Ventolin (bronchodilator)
- This won’t work
- Venturi mask → max level won’t work → switch to NRB → that will not work either

Orders (SBAR):
- High-flow mask @ 100%
- Make sure you know that 100% is not a venturi mask. It’s a NRB mask → make sure to inflate the bag first!
- CXR
- Order ABGs again → labs from day before show partial uncompensated severe acidosis
- Ask the doctor to come assess the pt
- Contact RT and possibly CCRT

SCENARIO 4:
Jean Kelly came in complaining of nausea, vomiting and severe lower abdo pain x 1 day. She was then diagnosed with bowel perforation, and subsequently had a
hemicolectomy 1 day ago (so now she’s post op day 1). PMHx: COPD, T2D, smoker, HTN, dyslipidemia, had an MI 2 yrs prior with stent placement. When the nurse
walks in, the pt is complaining of SOB and a fluttering feeling in her chest.

Assessments:
- Check to see if the IV is still running - there should be KCl
- Check VS
- RR 36, SPO2 89% on RA, BP 140/85, HR 141, T 36.9
- Respiratory assessment
- Check for nasal flaring and use of accessory muscles - yes, laboured breathing
- Check for pallor/cyanosis - no
- No retractions → maybe it’s a cardiovascular issue, then?
- Cardiovascular assessment
- Pulse was irregular
- Check peripheral pulses
- Cap refill
- Skin colour/ temperature

Orders (SBAR):
- Tell the doctor that she’s in AFib (that’s what the monitor will show you)
- Say that the reason she’s having SOB is being the AFib is causing her CO to decrease. This AFib may be present d/t her Hx of MI (for some
people, she had a Hx of HF instead, so just say whatever your pt has)
- Ask for IV amiodarone, beta blocker (metoprolol) or calcium channel blocker (diltiazem)
- Ask for ECG and CXR
 SIM LAB #3
SCENARIO 1:
Jean Kelly, 69 yo, is diagnosed with liver failure. She has been experiencing SOB and abdominal pain for the past 3 days, which has been related to her ascites.
PMHx: cirrhosis, liver failure d/t alcoholism, HTN, current drinker, ongoing ascites. She just had a paracentesis, where 4L of fluid was removed. She was also given
1 dose of albumin and antibiotics by the previous nurse. Last set of vitals: BP 120/60, HR 66, RR 22, O2 95% RA.
Assessment:
- Vitals - BP 108/70, T 37.5, HR 82, RR 20, O2 94
- Abdo assessment
- Distension
- Neuro assessment
- Pt is confused → hepatic encephalopathy?
- GCS 13
- Edema - present in feet
- Weak arm/leg strength
- Pain assessment

Orders (SBAR):
- Lactulose 30mL BID
- Another set of blood work (CBC, PTT, INR, albumin, ammonia, lactate, etc.)

SCENARIO 2:
Jean Kelly, 69 yo, came in to the ER 3 days ago with decompensated liver failure, and was admitted with SOB and abdominal pain. She had a paracentesis, where
4L of fluid was removed. PMHx: HTN, alcohol abuse, ascites. Dx: bacterial peritonitis. She was started on antibiotics. She had a hypotensive episode the day
before, where her BP was 88/50. Then last night, her BP went back up to 110/68. But her most recent vitals are: BP 96/60, HR 88, RR 24, T 37.2, O2 94.
Assessment:
- Vitals
- BP 94/64, T 37.2, HR 90, O2 90 (went up to 92% at 2L)
- Respiratory assessment
- Bilateral crackles
- Abdo assessment
- Slight distension
- No redness/swelling at paracentesis site
- Neuro assessment
- Patient is alert/oriented, GCS 15
- Edema - present in feet
- Pain assessment - no pain
- Labs - hyperkalemia, hypernatremia, hyperchloremia, ↑creatinine, ↑ BUN

Orders (SBAR):
- Albumin 25% 100mL over 1hr
- ECG d/t hyperkalemia
SCENARIO 3: GI BLEED
Jean Kelly, 69 yo, came in to the ER with chest pain, epigastric pain, and believes that she may have an ulcer. PMHx: HTN, high cholesterol, chronic AFib. Home
medications: Norvasc, Coumadin, Simvastatin. The patient is currently NPO, since she will be getting an endoscopy done soon. Last set of vitals: BP 130/88, HR 82,
RR 20, O2 97.
Assessment:
- Vitals - BP 112/74, T 37, RR 22, HR 110, O2 98
- Pain assessment
- GI assessment
- Ask about last BM - what colour is the stool? It’ll be very dark
- Vascular assessment
- Pulses
- Abdo assessment
- Is it symmetrical? Flat? Rounded? Etc.
- Is it tender?
- Listen to bowel sounds
- Check lab values
- INR will be increased

Orders (SBAR):
- Ask for vitamin K

SCENARIO 4:
Jean Kelly (a child) came in with sickle cell anemia and is in lots of pain.

Assessments:
- Skin assessment
- Look for jaundice
- Look for pallor
- Cardiovascular assessment
- Pain assessment
- OPQRST
- Vitals
- Look for ↑ RR, fever, HTN
- Labs
- Look for ↓ Hgb and HCT
- Ask about medications
- Have they been consistent with meds? How many sickle cell crises have they experienced?

Interventions:

- Fluids to help thin out the blood

- IV morphine for pain
- Give Tylenol for fever
 - If pt has infection, give antibiotics - do sbar for it if not on the MAR
- Administer hydroxyurea to help increase production of fetal hemoglobin (HbF)

SIM LAB #4
SCENARIO 1:
Jean Kelly had a left lower lobectomy this morning. She came onto the unit with a chest tube placed at the 5th left intercostal space. She has supplementary O2 with
5L nasal prongs. PMHx: COPD, lung cancer (reason for lobectomy), DM, ↑ cholesterol, HTN. Her main concern right now is that she is having “trouble breathing”
with chest pain.

Assessments:
- OPQRST for trouble breathing
- OPQRST for chest pain
- Check VS
- RR was too high, SPO2 84%
- Respiratory assessment
- ↑ work of breathing
- Pt is pale, cyanotic
- Asymmetrical chest expansion
- Left lung sounds are diminished compared to right side
- Assess skin around the dressing of the chest tube
- Dress is dry and intact
- Assess chest tube drainage
- Bubbling is on and off (there may be a leak)

Interventions:
- Raise HOB and increase O2 to 6L when you notice that the SPO2 is really low
- Change NP to venturi mask @ max oxygenation (50% 8L “orange colour”)
- But you’ll see that there is no change in SPO2
- Look at the chest tube for the cause of the leak
- The connection between the chest tube and the tube connecting the machine was loose → re-tighten the connection

Orders (SBAR):
- Say EVERYTHING that is wrong
- Talk about the loose connection
- Ask for a CXR
- CXR showed a closed pneumothorax
SCENARIO 2:
A pregnant woman comes into the ER with high BP.

Assessments:
- Check VS
- Neuro assessment - you’re checking for any neuro complications r/t HTN
- Any headache? Any vision changes? GCS?
- Cardiovascular assessment
- Maybe check deep tendon reflexes d/t pre-eclampsia?
- Check blood work – is there high liver enzymes and low platelets?

Orders (SBAR):
- Ask for a U/A (since proteinuria is seen in pre-eclampsia)

Interventions:
- Admin antihypertensive medications (look at doctor's order)
- If pt has pre-eclampsia, maybe administer magnesium sulphate too?

Evaluation:
- Assess VS (esp BP & HR)
- Assess LOC
- Apply safety precautions (in case of seizure)

SCENARIO 3:
End-of-life care for individual. The pt is complaining about pain.

Assessments:
- Do NOT check VS

Orders (SBAR):
- Advocate for pain management → maybe changing the time to administer hydromorphone
- Give morphine
SCENARIO 4:
Patient was okay at first, and then they just coded?

Assessments:
- Assess ABCs
- Airway:
- Breathing:
- Circulation:

Interventions:
- CPR