NURS 221 – PERFUSION

Comprehensive Study Guide

Pericarditis | Cardiomyopathy | CAD | MI | Dysrhythmias | Shock | GI Bleed

• NURS 221 – Week 2 – Winter 2026

 📋 SECTION 1: PERICARDITIS
Reference: Iggy pp. 716–717

Definition & Pathophysiology

Acute pericarditis is inflammation or alteration of the pericardium (the membrane surrounding the
heart). It can be acute or chronic; most cases are acute.

Types of Pericarditis
• Fibrous
• Serous
• Hemorrhagic
• Purulent
• Neoplastic

Causes
• Infection: bacteria, virus, fungi (usually respiratory)
• Post-MI syndrome (Dressler syndrome)
• Postpericardiotomy syndrome (post-cardiac surgery)
• Acute exacerbations of systemic connective tissue disease

Chronic Constrictive Pericarditis

Chronic inflammation causes fibrous thickening of the pericardium; rigid pericardium prevents
ventricular filling → cardiac failure.
• Causes: TB, radiation therapy, trauma, renal failure, metastatic cancer

Assessment Findings
Pain: Substernal/precordial — radiates to L neck, shoulder, back; grating and oppressive
Aggravated by: Breathing (esp. inspiration), coughing, swallowing, supine position
Relieved by: Sitting up and leaning slightly forward
Pericardial Friction Rub: Scratchy, high-pitched sound at left lower sternal border (use diaphragm of
stethoscope) — like a person shifting in a leather couch
ECG Changes: ST elevation (concave-up) in all leads; PR segment depression; A-fib common
Labs: Elevated WBC, fever; send blood culture & sensitivity
⚠️Watch for CARDIAC TAMPONADE — this is a medical emergency!

Proposed Diagnostic Criteria (need 2 of 4):

• Pericardial chest pain
• Pericardial friction rub
• New ST elevation or PR segment depression
• New or worsening pericardial effusion (fluid buildup)

Chronic Constrictive Pericarditis Signs:

• Signs of right-sided HF
• Elevated systemic venous pressure / JVD (jugular venous distension)
• Hepatic engorgement
 • Dependent edema
• Exertional fatigue, dyspnea
• Thickened pericardium visible on echo or CT

Cardiac Tamponade — Beck's Triad:

• Jugular venous distension (JVD) with clear lungs
• Muffled heart sounds
• Decreased cardiac output / hypotension
• Also: pulsus paradoxus >10 mmHg = sign of tamponade (detect by BP auscultation method)
• Avoid aspirin and anticoagulants — may increase risk of tamponade

Diagnostics & Labs

• Elevated WBC count
• Blood culture and sensitivity
• ECG: 12-lead to assess changes; may be on telemetry for continuous monitoring
• Echocardiogram: assess pericardial effusion

Interventions / Implementation
• Pain management: NSAIDs (first-line)
• Colchicine (anti-inflammatory): adjunct to NSAIDs to reduce symptoms and decrease recurrence
• Corticosteroids: if pain not relieved and no bacterial pericarditis
• Position: sit upright and lean slightly forward
• Bacterial pericarditis: antibiotics + pericardial drainage
• Uremic pericarditis: hemodialysis
• Malignancy-related: radiation or chemotherapy
• Chronic constrictive pericarditis: pericardiectomy (surgical removal of pericardial sac)
• Monitor for pericardial effusion → increased risk for cardiac tamponade
• Notify HCP immediately if tamponade is suspected
 ❤️ SECTION 2: CARDIOMYOPATHY
Reference: Iggy pp. 718–724 | Subacute or chronic disease of cardiac muscle inhibiting effective
pumping

Overview
All 3 types share a common problem: limited/ineffective cardiac output. The pump itself is not
functioning properly.

1. Dilated Cardiomyopathy (DCM) — Most Common

Damaged myofibrils and interference with myocardial metabolism. Heart grows (cardiomegaly),
myocardium stretches and thins, ventricles dilate, muscles become too weak to pump efficiently →
SYSTOLIC PUMP FAILURE.
Causes: Alcohol misuse, chemotherapy, infection, inflammation, poor nutrition, lead poisoning, Lyme's
disease
Symptoms: Dyspnea on exertion (DOE), decreased exercise capacity, fatigue, palpitations, syncope,
AMS, chest pain
Signs: Left-sided HF, dysrhythmias, emboli, cardiomegaly, S3 and S4 gallops
Diagnostics: X-ray shows enlarged heart; echocardiography, chest x-ray, radionuclide imaging, BNP
lab
HEART FAILURE NOTE: Body thinks BP is low (due to dilated ventricles) → activates RAAS to
hold fluid → shows signs of RIGHT AND LEFT sided HF

DCM Treatment (ABCD Meds + DRESS):

• Symptomatic treatment of HF
• A — ACE Inhibitors (e.g., Lisinopril [-pril]) — vasodilator
• B — Beta Blockers (e.g., Atenolol [-lol]) — ↓ workload of heart
• C — Calcium Channel Blockers (e.g., Nifedipine, Diltiazem, Verapamil)
• D — Digoxin (cardiac glycoside) — improve contractility
• D — Diuretics (loop or thiazide: Furosemide & HCTZ) — reduce fluid overload
• Vasodilators, dysrhythmia control, heart transplant
• DRESS: Diet (low Na/low fat), Rest periods, Exercise, Stop smoking/alcohol, Stress reduction

2. Hypertrophic Cardiomyopathy (HCM) — Most Deadly

Asymmetric ventricular hypertrophy and disarray of myocardial fibers. Heart walls become thick, stiff,
and non-compliant → can obstruct aortic valve → SUDDEN DEATH.
Mechanism: LV hypertrophy → stiff LV → impaired diastolic filling; obstruction in LV outflow tract;
mitral valve structural abnormalities; hypertrophied septum → ↓ stroke volume (SV) and cardiac output
(CO)
Causes: Genetics (usually diagnosed in childhood)
Symptoms: Often ASYMPTOMATIC; exertional dyspnea, angina, syncope, chest pain at rest NOT
relieved by nitrates, fatigue
Signs: Mild cardiomegaly, S4 gallop, HF, ventricular dysrhythmias
Risk: High incidence of ventricular dysrhythmias can cause SUDDEN DEATH
Diagnostics: Echo shows septal wall thickening
HCM Treatment:
• B — Beta Blockers (e.g., carvedilol) | C — Calcium Channel Blockers (e.g., verapamil)
• Surgery: Ventricular septal myectomy (excise portion of hypertrophied septum — long-term
improvement)
• Percutaneous alcohol septal ablation: absolute alcohol → small septal infarction → remodeling →
reduced obstruction
• ICD (implantable cardioverter/defibrillator) may be used
• Conversion of A-fib if present
• Encourage genetic counseling, screening 1st-degree relatives, and echos before age 12

⚠️NEVER GIVE THE 3 D's in HCM (will WORSEN obstruction):

• NO Digoxin
• NO Dilators (nitro)
• NO Diuretics

⚠️AVOID STRENUOUS ACTIVITY in HCM:

• Intense exercise
• Sudden position changes
• Bearing down (Valsalva maneuver)
• Avoid alcohol and dehydration

3. Restrictive Cardiomyopathy — Rarest

Stiff (not necessarily thick) ventricles restrict filling during diastole → REFILLING ISSUES. Heart
muscle becomes stiff and hard like a rock.
Causes: Genetics (amyloidosis, sarcoidosis), radiation exposure
Symptoms: Hypotension, fatigue, dyspnea at rest, orthopnea — similar to left or right HF
Diagnostics: Normal echo & x-ray (NO cardiomegaly)
Treatment: Treat underlying cause; heart transplant; decrease radiation exposure
Prognosis: POOR — heart muscle too hard & stiff for most medications to have positive effect

Heart Transplant
Indications:
• Severe DCM (primary recommendation)
• May be considered for restrictive cardiomyopathy
• End-stage heart disease due to CAD, valvular disease, or congenital heart disease

Candidate Criteria:
• Life expectancy < 1 year
• Age generally < 65 years
• NYHA Class III or IV
• Normal or only slightly increased pulmonary vascular resistance
• Absence of active infection
• Stable psychosocial status
• No evidence of current drug or alcohol misuse
Operation Details:
• Donor must have comparable body weight and ABO compatibility; must be within 6 hrs of
procurement
• Bicaval technique: anastomosis at superior and inferior vena cava
• Orthotopic technique: anastomosis between donor and recipient atria → remnant of SA node; 2
unrelated P waves on ECG

Post-Op Care:
• Watch for occult bleeding into pericardial sac with potential for tamponade
• Transplanted heart NOT connected to autonomic nervous system → unresponsive to vagal
stimulation
• May cause pronounced orthostatic hypotension in immediate post-op phase
• Early post-op: isoproterenol titrated to support HR and CO
• Atropine, digoxin, and carotid sinus pressure are NOT used (do not have usual effects)
• Some pts require permanent pacemaker (rate responsive to activity level)
• Lifelong combination immunosuppressants required

Signs of Heart Transplant Rejection (BOX 29.13):

• Shortness of breath
• Fatigue
• Fluid gain (edema, increased weight)
• Abdominal bloating
• New bradycardia
• Hypotension
• Atrial fibrillation or flutter
• Decreased activity tolerance
• Decreased ejection fraction (late sign)
 ⚡ SECTION 3: CARDIAC DYSRHYTHMIAS
References: Iggy pp. 669–675 (Sinus & Atrial), pp. 679–685 (Ventricular)
Definition: Abnormal heart beat pattern (rate and/or rhythm) — can be emergencies requiring
immediate identification and intervention.

Category Overview
• SINUS — controlled by SA node in right atrium
• ATRIAL — impulse generation from atrial tissues
• VENTRICULAR — increased irritability of ventricular cells
• AV HEART BLOCKS — conduction delays between atria and ventricles

Sinus Dysrhythmias
Sinus Tachycardia
• Mechanism: SNS stimulation or vagal/parasympathetic inhibition → increased HR
• Causes: physical activity, anxiety, pain, stress, fever, anemia, hypoxemia, hyperthyroidism, epi,
atropine, caffeine, alcohol, nicotine, cocaine, aminophylline, thyroid meds; compensation for
decreased CO/BP (dehydration, hypovolemic shock, MI, infection, HF)
• Effect: Initially ↑ CO and BP; sustained ↑ HR → ↓ coronary perfusion time, ↓ diastolic filling time, ↓
coronary perfusion pressure, ↑ myocardial O2 demand
• Care: Treat underlying cause; bed rest if hypotensive/weak; avoid caffeine, alcohol, nicotine; stress
management

Sinus Bradycardia
• Mechanism: Excessive vagal/parasympathetic stimulation → decreased HR
• Causes: carotid sinus massage, vomiting, suctioning, Valsalva maneuvers, ocular pressure, pain,
hypoxia, inferior wall MI, beta blockers, calcium channel blockers, digoxin, Lyme disease,
electrolyte imbalances, neurologic disorders, hypothyroidism
• Effect: ↑ coronary perfusion time, may ↓ coronary perfusion pressure, ↓ myocardial O2 demand
• Athletes may have hypereffective heart with strong SV and low HR → normal CO (not pathologic)
• Assessment: syncope, dizziness/weakness, confusion, hypotension, diaphoresis, SOB, chest pain
• Interventions: ID & treat cause → IV atropine + fluids + O2 if sat <94%
• Beta blocker overdose suspected → glucagon may increase HR and BP
• If HR does not increase → prepare for pacing

Pacing Options:
• Transcutaneous pacing: 2 large external electrodes; emergency use; may be painful →
pain/sedation meds
• Transvenous pacing: bridge to permanent pacemaker; wire threaded to RV via subclavian or
femoral vein
• Permanent pacemaker: if treatment fails to restore NSR

Pacemaker Patient Teaching (BOX 28.3):

• Avoid strong electromagnetic fields (magnets, telecom transmitters) — may cause malfunction;
MRI usually contraindicated
• Carry pacemaker ID card; wear medical alert bracelet
• Take pulse 1 full minute daily at same time; record in diary
 • Know rate at which pacemaker is set
• No tight clothing over generator; no pressure over generator
• Inform all HCPs about pacemaker
• Report: difficulty breathing, dizziness, fainting, chest pain, weight gain, prolonged hiccupping
• Avoid arc welding equipment; stay away from transmitter towers
• If symptoms near a device, move 5-10 feet away; pulse should return to normal
• Avoid sudden jerky movements for 8 weeks (pacemaker to settle)
• No lifting arm over head or >10 lbs for 4 weeks (if surgical site near shoulder)
• Encourage arm movement to prevent shoulder stiffness

Pacemaker Complications:
• Pericardial effusion
• Pericardial tamponade
• Diaphragmatic pacing

Pacemaker Failures:
Failure to Capture: Appropriately timed pacer spikes NOT followed by P (dual) or QRS (single) waves
Failure to Sense: Pacer spikes in inappropriate locations relative to native conduction; spikes may
appear in native conduction refractory periods
Failure to Pace: Absence of pacer spikes where expected; commonly caused by oversensing

Atrial Dysrhythmias
Premature Atrial Complexes (PAC)
• Atrial tissues irritable → fires ectopic impulse before it is due
• Causes: stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, epinephrine,
sympathomimetics, amphetamines, digoxin, anesthetic agents, MI, hypermetabolic states,
electrolyte imbalance, atrial stretch (CHF, valvular disease, pulmonary HTN, cor pulmonale)
• May be asymptomatic or have palpitations
• Treatment: treat cause; avoid stress and triggers; may need antidysrhythmic drugs
• ECG: Premature P wave before it's due; the following QRS is identical to sinus beats

Supraventricular Tachycardia (SVT)

• Rapid stimulation of atrial tissues: 100–280 bpm; P waves may not be visible
• Caused by reentry mechanism — one impulse circulates repeatedly through atrial pathway,
restimulating atrial tissue
• Assess: palpitations, chest pain, weakness, fatigue, SOB, nervousness, anxiety, hypotension,
syncope, angina, HF, cardiogenic shock
• Treatment: radiofrequency catheter ablation; vagal maneuvers may help (bearing down, carotid
sinus massage)

Atrial Fibrillation (A-Fib)

• Rapid impulses from atria → chaotic rate; rhythm typically irregular
• Patient at risk for CLOTTING: PE or VTE
• Causes: HTN, HF, CAD, genetic mutations, prior ischemic stroke, TIA, DM, obesity,
hyperthyroidism, CKD, alcohol misuse, mitral valve disease
• Signs: irregular pulse; poor perfusion (fatigue, weakness, SOB, dizziness, anxiety, syncope,
palpitations, CP, hypotension)
A-Fib Classification:
• Paroxysmal: converts within 7 days
• Persistent: longer than 7 days
• Long-standing persistent: more than 12 months
• Permanent
• Nonvalvular

A-Fib Treatment:
• Antidysrhythmic drugs: CCB, amiodarone, beta blockers, digoxin
• Long-term anticoagulant therapy: dabigatran, apixaban
• Reversal for dabigatran = idarucizumab (S/E: hypokalemia, confusion, constipation, fever,
pneumonia)
• Teach pts to AVOID: excessive vitamin K, ginger, ginseng, goldenseal, Ginkgo biloba, St. John's
wort

Ventricular Dysrhythmias
Junctional vs. Idioventricular Rhythms
Junctional: 40–60 bpm from AV nodes; Narrow QRS <0.12; Inverted/irregular P waves (or absent)
Idioventricular: 20–40 bpm from ventricles; Wide QRS >0.12; No P waves

Premature Ventricular Complexes (PVC)

• Increased irritability of ventricular cells
• QRS: unifocal/uniform (same shape) OR multifocal/multiform (different shape)
• Repetitive rhythms: bigeminy, trigeminy, quadrigeminy
• 2 sequential PVCs = pair/couplet; 3+ PVCs = nonsustained ventricular tachycardia (NSVT)
• Frequency increases with age; can be insignificant
• Can occur with MI, chronic HF, COPD, anemia, hypokalemia, hypomagnesemia
• Causes: sympathomimetic agents, anesthesia drugs, stress, nicotine, caffeine, alcohol, infection,
surgery
• May be asymptomatic OR: palpitations, chest discomfort, diminished/absent peripheral pulses
• Treatment: treat underlying cause; electrolyte replacement; beta blockers if excessive

Ventricular Tachycardia (VT / V-Tach)

• Repetitive firing of ectopic ventricular beat: 140–180+ bpm
• Mechanism: increased automaticity OR reentry mechanism
• Can be intermittent or sustained (>15–30 seconds)
• Causes: ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular
heart disease, HF, drug toxicity (steroids), hypotension, cocaine, inhalants
• ACLS: elective cardioversion for stable VT
• If pt on digoxin → withhold up to 48 hrs before cardioversion
• Oral antidysrhythmic to prevent future occurrences
• Persistent VT → radiofrequency catheter ablation
• Unstable VT treated the same as VF

Ventricular Fibrillation (VF / V-Fib) — Life-Threatening

• Electrical chaos in ventricles; consumes large amounts of O2
 • NO CO or pulse = no cerebral, myocardial, or systemic perfusion = FATAL IN 3–5 MINUTES
• Causes: CAD, MI, hypokalemia, hypomagnesemia, hemorrhage, drug therapy, rapid SVT, shock,
surgery, trauma
• Assessment: faint, LOC, pulseless, apneic, no BP, heart sounds absent → respiratory/metabolic
acidosis, seizures, fixed and dilated pupils, cold/mottled skin, DEATH
• Treatment: CPR + defibrillate per ACLS; epi after 2 min CPR after first shock; mag sulfate for
refractory VT/VF or torsades de pointes

AV Heart Blocks
1st Degree: PR interval > 0.2 seconds (1 big box); 'R is far from P'
2nd Degree Type I (Wenckebach/Mobitz I): PR interval progressively gets longer then a QRS
complex is dropped; 'Longer, longer, longer, drop'
2nd Degree Type II (Mobitz II): Dropped QRS complexes (can be 2:1, 3:1, etc.); fixed PR interval; 'If
some P's don't get through'
3rd Degree (Complete): P and QRS do not agree — no relationship between P waves and QRS
complexes; 'If P's and Q's don't agree'

Nursing Care for Dysrhythmias (BOX 28.4)

• Evaluate patient immediately for life-threatening dysrhythmia or hemodynamic deterioration
• Assess for: angina, hypotension, heart failure, decreased cerebral and renal perfusion
• Consider: hypoxia, drug toxicity, electrolyte imbalances, HF, MI when taking history
• Teach: generic and trade names of antidysrhythmic drugs, dosage, side effects, instructions
• Teach: how to take pulse and report significant changes
• Avoid caffeine, stop smoking, drink alcohol only in moderation, follow prescribed diet
 🫀 SECTION 4: CORONARY ARTERY DISEASE &
MYOCARDIAL INFARCTION
Reference: Iggy pp. 781–806

CAD / Coronary Heart Disease (CHD) Overview

Atherosclerosis → fatty plaque build-up in coronary arteries → narrowing → limits perfusion (cardiac
output) → decreases pumping capability. Can happen in any vascular space in and out of the heart.
Ischemia: Insufficient oxygen to tissue (reversible)
Infarction (Necrosis): Prolonged ischemia + decreased perfusion → permanent damage

Types of Coronary Disease

Chronic Stable Angina (CSA)
• Angina pectoris: chest pain from temporary lack of O2 to cardiac muscles
• Does NOT cause permanent damage
• Stable angina: chest discomfort with moderate to prolonged exertion; happens commonly but does
not severely limit activity
• Usually caused by fixed atherosclerotic plaque
• Tx: nitroglycerin / rest / drug therapy

Acute Coronary Syndrome (ACS)

• Unstable angina: chest pain at rest OR with exertion, causing severe activity limitation
◦ Increase in number of attacks and intensity of pressure
◦ Pressure may last longer than 15 min
◦ NOT relieved by nitro
◦ May show ST changes on 12-lead but NO changes in troponin
◦ Types of unstable angina:
▪ New-onset angina: first angina symptoms, usually after exertion
▪ Vasospastic angina: chest pain from coronary artery spasm, typically at rest
▪ Preinfarction angina: chest pain in days/weeks before an MI

Myocardial Infarction (MI)

• Myocardial tissue abruptly and severely deprived of oxygen
• Types: NSTEMI and STEMI
• 3 Zones of Infarction:
◦ Zone of Necrosis: initial area of infarction → abnormal Q wave on ECG
◦ Zone of Injury: tissue injured but not necrotic → ST elevation on ECG
◦ Zone of Ischemia: oxygen-deprived tissue → T-wave inversion on ECG
• Physical changes to heart occur ~6 hrs after infarction → reason for intervention within 4–6 hr of
symptom onset
• Epi and norepi released → ↑ HR, contractility, afterload → ↑ O2 demand → risk of life-threatening
ventricular dysrhythmias
• After MI: scar tissue forms at site → does NOT contract or conduct electricity → decreased CO /
HF + chronic ventricular dysrhythmias
STEMI vs NSTEMI
STEMI: ST elevation; 100% occlusion of coronary artery; rupture of fibrous atherosclerotic plaque →
platelet aggregation → thrombus; EMERGENCY — immediate reperfusion needed
NSTEMI: ST depression and/or T-wave inversion; initial troponin may be normal, elevates in 3–12 hr;
partial blockage; prompt attention — antiplatelets, anticoagulants, then early cath
NSTEMI Type 1: Plaque rupture or erosion causing occlusive or partially occlusive thrombus
NSTEMI Type 2: Imbalance between myocardial O2 supply and demand; often elevated troponin +
ECG changes WITHOUT typical ACS symptoms

Angina vs MI — Key Differences

Angina Pain: Substernal discomfort; radiates to left arm; precipitated by exertion/stress (or rest in
vasospastic); relieved by nitroglycerin or rest; lasts <15 min; few associated symptoms
MI Pain: Substernal chest/pressure radiating to L arm, jaw, back, shoulder, abdomen; occurs without
cause (often in morning); relieved only by opioids; lasts ≥30 min; many associated symptoms
MI Associated Sx: N/V, diaphoresis, dyspnea, fear/anxiety, dysrhythmias, fatigue, palpitations,
epigastric distress, anxiety, dizziness, disorientation, feeling 'short of breath'

Risk Factors
• Atherosclerosis
• Metabolic syndrome (diagnosed with 3 factors from table 32.1)
Prevention: Address modifiable risks; AED education to public

Assessment
• Full pain assessment: pressure, tightness, burning, or indigestion
• Pain from angina resolves when O2 is returned; pain from MI does NOT
• Assess BP, HR, ECG, temp
• Sinus tach with PVCs frequently occurs in first few hours after MI
• Temp may be increased from inflammation from myocardial necrosis
• Assess pulses and skin temp: weak pulses + cool diaphoretic skin = poor cardiac output
• Auscultate: S3 gallop (HF), crackles/wheezes (HF)

Diagnostics & Labs

• Labs: Troponin (T and I) — key cardiac marker; BNP
• Imaging: 12-lead ECG (within 10 min of chest pain report); Cardiac echo; CT angio with contrast;
Chest x-ray (rule out aortic dissection)
• Testing: Exercise tolerance test / stress test (physical or pharmacologic)
• Procedures: Cardiac catheterization to determine extent and location of blockages

Emergency Care — Acute Pain & Increasing Perfusion

For Acute Pain:
• Nitroglycerin (NTG): decreases O2 demand and dilates coronary arteries
• Morphine: decreases pain and O2 demand

Box 32.9 — Managing Chest Pain at Home:

• Keep fresh NTG available; at first indication → cease activity, sit or lie down
• Place 1 NTG tablet or spray under tongue; wait 5 min for relief
 • If no relief → call 911; while waiting for EMS, repeat NTG and wait 5 more min
• If still no relief → repeat and wait 5 more min
• Carry medical ID card or wear bracelet identifying heart condition
• Notify HCP if: HR <50 after arising, wheezing/difficulty breathing, weight gain ≥3 lb/week or 1–2 lb
overnight, persistent ↑ NTG use, dizziness/faintness/SOB with activity
• Call 911 if: chest discomfort not improved after 5 min or 1 sublingual NTG; extremely severe
chest/epigastric pain with weakness, N/V, or fainting

Increasing Perfusion — Drug Therapy:

• Antiplatelet: Aspirin (chew 4 baby aspirin = 325 mg at new-onset, call 911); Glycoprotein inhibitors
(prevent fibrinogen buildup)
• Anticoagulants
• Beta blockers (monitor HR, BP, LOC, CP)
• ACEIs, ARBs, CCBs
• Statins (cholesterol-lowering)
• Thrombolytic therapy (TPA, reteplase, tenecteplase) = CLOTBUSTER!
◦ For STEMI pts who cannot have timely PCI → goal: administer within 10 min
◦ NOT indicated for NSTEMI
◦ ABSOLUTE contraindications: prior intracranial hemorrhage, active bleeding, significant
trauma within 3 months
• O2 therapy: maintain SpO2 ≥90%

Managing Dysrhythmias:
• Treat when causing hemodynamic compromise, ↑ myocardial O2 requirements, or predispose to
lethal dysrhythmias
• Common post-MI dysrhythmias: bradycardia, 2nd degree AV blocks, PVCs, 3rd degree/bundle
branch block
• Pacemaker may need to be placed

CAD Procedures
PCI — Percutaneous Coronary Intervention
• Done in cath lab; initial coronary angiography to visualize clots
• Clot removed → balloon inflated at site → stent placed (expandable metal mesh to keep artery
patent)
• On heparin drip during procedure to prevent clots
• NOT used for complex cases; often used before CABG is considered
• After procedure: dual antiplatelet therapy (aspirin + platelet inhibitor)
• Post-care: monitor for infection and bleeding, pain management, vital signs, wound care

Laser Angioplasty & Atherectomy:

• Laser angioplasty: breaks clot with laser
• Atherectomy: excise or emulsify plaque; risk of restenosis

CABG — Coronary Artery Bypass Grafting

• Occluded arteries bypassed using patient's own blood vessels or grafts
• Indicated when CAD cannot be medically managed or disease has progressed extensively
• Most effective with good ventricular function and EF ≥50% (normal 50–70%)
 • Candidates: angina with >50% left main coronary artery occlusion unable to be stented; unstable
angina with severe 2-vessel or moderate 3-vessel disease; ischemia with HF; acute MI with
cardiogenic shock; small vessel disease where stents cannot be used
• Pre-op teaching: CHG shower, cough and deep breathing exercises, early ambulation
• Operation: general anesthesia + cardiopulmonary bypass (CPB)
◦ CPB: provides oxygenation, circulation, hypothermia during induced cardiac arrest; blood
diverted from heart → bypass machine → heparinized + oxygenated → returned via cannula
in aorta or femoral artery
◦ Core temp kept 95°F to normal; can use internal mammary artery, saphenous vein, or radial
artery
• Post-op: sterile technique for dressings; manage chest tubes; control pacemaker; hemodynamic
monitoring
• Complications: fluid/electrolyte imbalance, hypotension, hypothermia, HTN, bleeding, cardiac
tamponade, infection
• Measure chest tube drainage hourly; report drainage >150 mL/hr to surgeon
• Neuro status: q30–60 min, then q2–4 hr per policy

Activity for Pts with CAD (Box 32.8):

• Walk 400 ft three times daily; carry nitroglycerin; check pulse before, during, after exercise
• Stop activity if pulse increases >20 bpm, SOB, angina, or dizziness
• Avoid straining (lifting, push-ups, pull-ups, straining at bowel movements)
 ⚠️ SECTION 5: SHOCK
Reference: Iggy pp. 763–769 (Hypovolemic Shock)
Definition: Shock is a condition where the body doesn't get enough oxygen and blood flow to the
tissues.

Types of Shock
Hypovolemic: Loss of fluid volume → decreased MAP → decreased RBC → slows blood flow →
decreases tissue perfusion
Cardiogenic: Heart muscle is unhealthy and pumping is impaired (direct pump failure; fluid volume not
affected)
Distributive: Blood volume NOT lost from body but distributed to interstitial tissues where it cannot
perfuse organs (includes neurogenic, anaphylactic, septic)
Obstructive: Cardiac function decreased by noncardiac factor (indirect pump failure); total body fluid
not affected, but central volume is decreased

Hypovolemic Shock Causes:

• Hemorrhage
• Trauma
• GI ulcer
• Surgery
• Inadequate clotting/hemophilia
• Liver disease
• Cancer therapy
• Anticoagulation therapy
• Dehydration
• Vomiting
• Diarrhea
• Heavy diaphoresis
• Diuretic therapy
• Nasogastric suction
• Arginine vasopressin deficiency (AVP-D)

Cardiogenic Shock Causes:

• Myocardial infarction
• Cardiac arrest
• Ventricular dysrhythmias
• Cardiomyopathies
• Myocardial degeneration
• Cardiac tamponade

Distributive Shock Causes:

• Neural-induced
• Pain
• Anesthesia
• Stress
• Spinal cord injury
 • Head trauma
• Chemical-induced
• Anaphylaxis
• Sepsis
• Capillary leak
• Burns
• Extensive trauma
• Liver impairment
• Hypoproteinemia
• Adrenal insufficiency

Obstructive Shock Causes:

• Cardiac tamponade
• Arterial stenosis
• Aortic dissection
• Pulmonary embolus
• Pulmonary hypertension
• Constrictive pericarditis
• Thoracic tumors
• Tension pneumothorax
• Increased intrathoracic pressure
• Inferior vena cava syndrome

Stages of Shock
Progresses through 4 stages when conditions remain uncorrected and poor perfusion continues:

1. Initial Stage:
• Decreased tissue perfusion
• Increased anaerobic metabolism → increased lactic acid and waste build-up
• MAP ↓ by less than 10 mmHg of baseline; ↑ HR, ↑ RR, ↑ diastolic pressure

2. Compensatory Stage:
• Neural: stimulates sympathetic system → systemic vascular constriction, coronary artery dilation, ↑
HR, ↑ myocardial contractility
• Kidneys: release renin, ADH, aldosterone → ↓ urine output, Na reabsorption, vessel constriction
• Lungs: decreased perfusion → ↑ RR and depth
• MAP ↓ 10–15 mmHg from baseline; tissue hypoxia, acidosis, ↓ UO, tachycardia, narrowing pulse
pressure, cool extremities, ↓ SpO2, altered mental status, cyanosis

3. Progressive Stage:
• Compensatory mechanisms continue but NO longer enough O2 to supply vital organs
• Vital organs become hypoxic; non-vital organs become anoxic or ischemic
• Sustained ↓ in MAP >20 mmHg; pt may feel 'pending doom'; cyanosis; 5–20% ↓ in SpO2; ↑ lactic
acid and potassium; weak pulse

4. Refractory Stage:
• Too much cell death and tissue damage — organ failure despite interventions ('circling the drain')
 • Massive release of toxic metabolites and enzymes → Multiple Organ Dysfunction Syndrome
(MODS)
• Rapid loss of consciousness; nonpalpable pulse; slow, shallow RR; unmeasurable SpO2

Assessment Findings — Hypovolemic Shock

Cardiovascular:
• Decreased cardiac output
• Increased pulse rate
• Thready pulse
• Decreased blood pressure
• Narrowed pulse pressure
• Postural hypotension
• Low central venous pressure
• Flat neck and hand veins in dependent positions
• Slow capillary refill in nail beds
• Diminished peripheral pulses

Respiratory:
• Increased respiratory rate
• Shallow depth of respirations
• Decreased PaCO2 initially then progressing to increased PaCO2
• Decreased PaO2
• Cyanosis especially around lips and nail beds

Neuromuscular (Early):
• Anxiety
• Restlessness
• Increased thirst

Neuromuscular (Late):
• Decreased CNS activity (lethargy to coma)
• Generalized muscle weakness
• Diminished or absent deep tendon reflexes
• Sluggish pupillary response to light

Kidney:
• Decreased urine output
• Increased specific gravity
• Sugar and acetone present in urine

Integumentary:
• Cool to cold
• Pale to mottled to cyanotic
• Moist, clammy
• Mouth dry, paste-like coating present
• Decreased capillary refill
GI:
• Decreased motility
• Diminished or absent bowel sounds
• Nausea and vomiting
• Constipation

Interventions — Hypovolemic Shock

Nursing Care:
• Strict I&O
• Daily weights
• Monitor changes in pulses, cap refill, vitals, LOC every 15 min

For the Patient in Hypovolemic Shock:

• Ensure patent airway
• Insert IV catheter or maintain established catheter; large-bore catheter suggested; if IVs cannot be
obtained → central venous catheter
• Correct hypoxemia: O2 to maintain SpO2 90–96%; supplemental O2 no longer recommended if
saturation is normal
• Elevate feet; keep head flat or elevated at no more than 30-degree angle
• Examine patient for overt bleeding; if present → apply direct pressure
• Administer drugs as prescribed; do NOT leave the patient

Fluid & Drug Therapy:

• Fluids: IV fluids (isotonic solutions), blood/platelets/plasma
• Vasoconstrictors: norepinephrine, epinephrine, dopamine, vasopressin, phenylephrine HCl
• Inotropes: epinephrine, dobutamine, milrinone
• Surgical: fix whatever is causing the hemorrhage

Cardiogenic Shock — Key Difference

Oxygen and blood NOT distributed to tissues outside of the heart due to dysfunction of the organ (the
pump). Unlike hypovolemic shock, the fluid volume is NOT affected — the problem is the heart's ability
to pump.
• Signs overlap with hypovolemic shock but treatment approach differs
• Treatment targets underlying cardiac pathology: inotropic support, revascularization, IABP
 🩸 SECTION 6: GI BLEED
Reference: Iggy pp. 1158–1160 | Managing Upper GI Bleeding

Overview
Assume an upper GI bleed is an EMERGENCY — significant risk for hypovolemic shock.

Key Symptoms of GI Bleeding

• Hematemesis (vomiting blood)
• Melena (black, tarry stools)
• Hematochezia (bright red blood in stool)
• Pallor (pale skin)
• Fatigue
• Dizziness
• Anemia
• Cramping
• Abdominal pain
• Shock

Interventions — Prioritized by ABCs

• A — Airway: oxygen, ventilatory support
• B — Breathing: monitor respiratory status
• C — Circulation: counter hypovolemia with isotonic solutions; 2 large-bore IVs
• Depending on severity: stabilize first → then monitor OR prep for surgery
• NG tube: assess return volume and characteristics; decompress GI system; prevent gastric dilation
• 72 hours after initiation → clamp NG tube and document volume/characteristics collected in ~30
min
• Medication: Proton pump inhibitors (PPIs)
• Endoscopic therapy and interventional radiologic procedures can aid in support

Monitoring & Trends

• Labs: H&H first (hemoglobin and hematocrit); ABG if critically ill; coagulation studies
• Vitals: including orthostatic vital signs
• I&O including NG tube output

Assessment for PUD Patient

GI/Cardiovascular:
• Vital signs including orthostatic
• Skin color
• Abdominal pain (location, severity, character, duration, precipitating factors, relief measures)
• Character, color, and consistency of stools
• Changes in bowel elimination pattern
• Hemoglobin and hematocrit
• Bowel sounds; palpate for areas of tenderness
Nutritional Status:
• Dietary patterns and habits
• Intake of caffeine and alcohol
• Relationship of food ingestion to symptoms

Patient Education:
• Symptoms to report to HCP
• Expected effects and side effects of medications
• Drugs to avoid such as NSAIDs
 📊 QUICK REFERENCE: MEDS & KEY FACTS
ABCD Medications
A — ACE Inhibitors: End in -pril (e.g., Lisinopril) — vasodilator, reduce afterload
B — Beta Blockers: End in -lol (e.g., Atenolol, Carvedilol) — ↓ HR and workload
C — Calcium Channel Blockers: End in -dipine, -zem, -amil (e.g., Nifedipine, Diltiazem, Verapamil)
D — Digoxin: Cardiac glycoside — improves contractility
D — Diuretics: Loop or Thiazide (Furosemide & HCTZ) — reduce fluid overload

DRESS (Lifestyle Modifications for DCM & HF)

D: Diet: low sodium and low fat
R: Rest Periods
E: Exercise
S: Stop Smoking & Alcohol
S: Stress Reduction

Cardiomyopathy Treatment Summary

DILATED (DCM) HYPERTROPHIC (HCM) RESTRICTIVE
Use ALL: ABCD Meds + B & C MEDS ONLY TREAT UNDERLYING
DRESS NEVER 3 D's! CAUSE
Diuretics OK No Digoxin Heart transplant
Digoxin OK No Dilators Decrease radiation
Vasodilators OK No Diuretics Poor prognosis
Heart transplant for severe Surgery: myectomy or alcohol
DCM ablation

Shock Stages Quick Reference

Stage MAP Key Signs
Change
Initial ↓ <10 mmHg ↑ HR, ↑ RR, ↑ diastolic, anaerobic metabolism
Compensatory ↓ 10–15 Tissue hypoxia, acidosis, ↓ UO, tachycardia, cool extremities, altered
mmHg mental status
Progressive ↓ >20 mmHg 'Pending doom', cyanosis, 5–20% ↓ SpO2, ↑ lactic acid + potassium,
weak pulse
Refractory Unmeasurable MODS, rapid LOC, nonpalpable pulse, slow shallow RR, death

CAD Prevention Highlights

• Quit smoking/vaping/tobacco
• Diet: saturated fats 5–6% of calories; avoid trans fats; cholesterol <200 mg/day; sodium <1500
mg/day
• Exercise: ≥40 min, 3–4 times/week; warm-up and cool-down included
• Have lipid levels checked regularly; statins if LDL elevated
• Manage diabetes, hypertension, and obesity
• Avoid severely restrictive/fad diets

NURS 221 Perfusion Study Guide — Good luck on your exam!