UNIVERSITY OF SÃO PAULO
School of Nursing
Department of Medical-Surgical Nursing
ENC0250 - NURSING IN ADULT AND ELDERLY HEALTH IN CRITICAL CARE
Acid-base imbalance
Prof. Paula C Nogueira
pcnogueira@[Link]
Objectives
To know and identify respiratory and/or metabolic acid-base imbalance
metabolic.
Interpret arterial blood gas test.
Associate the patient's clinical condition with the acid-base disorder presented and
discuss the nursing interventions.
Arterial gasometry
Arterial blood has high levels of oxygen. It circulates between the arteries and
pulmonary veins, obtaining chemical energy and nourishing the cells. It has a
coloration in a strong/vivid red tone, due to the higher pH caused by
high presence of O2.
A gasometry measures the pH and the levels of oxygen and carbon dioxide in the blood.
analyzes the effectiveness of gas exchange by the lungs. The verification of blood gases
is used to verify the body's acid-base balance directly
related to pulmonary and metabolic performance.
Provides the values that allow for the analysis of blood gases and acid-base balance.
base (metabolic and/or respiratory).
Basic concepts – acid and base
• Acid - substance that can donate H+ ions
• Base - alkaline substance that can receive H+ ions
The balance between acids and bases is part of the homeostasis of the internal environment, which
try to maintain the [H+].
Disorders in the EAB: deviations in [H+] in plasma - pH
The accumulation or lack of acids in the internal environment leads to important disorders in
biochemical reactions necessary for life.
Basic concepts - Concentration of H+ ions
• The Hydrogen ion (H+) is the main responsible for the acid-base balance of
organism.
• All acid-base imbalance results from a change in concentration of
hydrogen ion [H+no LEC.
• The concentration of H+ ions is expressed on a logarithmic scale, using the
pH measurement unit
• The pH is related to the true concentration of H+ (expressed in Eq/L)
• The pH is inversely proportional to the concentration of H+ → the more H+ ions
but the solution is more acidic.
pH Levels in Arterial Blood
6.8 6.8 – 7.34 7.35 – 7.45 7.46 – 7.80 7.80
The organism can withstand pH changes that fluctuate between 6.8 and 7.8.
Physiology of Acid-Base Metabolism
• The pulmonary and renal systems are responsible for the elimination of H.+ produced during the
cellular metabolism.
• The lungs are responsible for regulating serum levels of CO.2, product of
cellular metabolism (volatile acid) that, when dissolved in water, transforms into acid
carbonic (H2CO3).
• Controlled by the bulb, the lungs adjust ventilation in response to the amount of CO.2
in arterial blood.
• The kidneys excrete non-volatile acids and regulate the serum level of bicarbonate (HCO 3) for-
half of the tubular reabsorption of HCO3filtration and excretion, through the secretion of H+ ions.
• EAB disturbances can be caused by respiratory and metabolic changes.
• The decrease in blood pH is called ACIDEMIA, while the disorder that
The cause is called ACIDOSIS.
• In the same way, the increase in blood pH, ALKALOSIS, is caused by
disorder called ALKALOSIS.
• The organism uses mechanisms to control the acid-base balance of
blood.
The body uses blood buffer solutions to defend itself against sudden changes.
from acidity. A buffer acts chemically to minimize changes in pH.
The MOST important buffer of blood uses bicarbonate (a basic compound) that
finds in equilibrium with carbon dioxide (an acidic compound).
As MORE acid enters the bloodstream, more HCO3 and less CO2 are produced.
produced.
As more base enters the bloodstream, more carbon dioxide and less
Bicarbonate is produced. In both cases, the effect on pH is minimized.
Therefore, HCO3 is in equilibrium with dissolved CO2 in the plasma and behaves-
as a buffer system
Mechanism to maintain pH level in the blood
The bicarbonate/carbonic acid buffer system is the main mechanism of
extracellular pH control:
Eliminates or reabsorbs HCO3- by the kidneys
Exhales or retains CO2 - through the lungs
Normal homeostatic mechanisms serve to maintain excretion.
appropriate CO2 uptake by the lungs and non-volatile acids by the kidneys - The lung
excretes more than 10,000 mEq of carbonic acid per day compared to less
of 100 mEq of fixed acids by the kidney.
The kidneys have a certain capacity to alter the amount of acid or
BASE that is excreted, but usually this process takes several days.
Mechanism of CONTROL of blood pH - excretion of CO2.
CO2 is an important byproduct of oxygen metabolism and, consequently, is
constantly produced by the cells. The blood transports carbon dioxide to the
lungs, where it is exhaled.
The respiratory control centers located in the brain regulate the amount of carbon dioxide
carbon dioxide that is expelled through the control of the speed and depth of breathing.
the serum concentration of carbon dioxide decreases, blood becomes more basic.
the serum concentration of carbon dioxide increases → blood becomes more acidic.
Through the adjustment of the speed and depth of breathing, the control centers
the respiratory system and the lungs are able to regulate blood pH minute by minute.
Mechanism of respiratory regulation of pH, by
means of the variation of CO2 elimination
Acid / Base Balance Disorders - disorders of the system
respiratory or metabolic
Basic line of reasoning - diagnosis
pH = RIM responsible for the concentration of HCO3 –
LUNG responsible for the concentration of CO2
WHILE
The lung to maintain THE RIM maintain
the concentration of CO2 the concentration of HCO3 -
The pH WILL BE
MAINTAINED
Margotto, PR ESCS/ SES/DF
• The characterization of any disorder basically requires three variables: pH, pCO2
and HCO3
• Primary alterations in bicarbonate (HCO3) concentration are called
metabolic disturbances result from abnormalities in base content.
• Primary changes in napCO2 are called respiratory disturbances, and are
resulting from disorders in pulmonary ventilation.
• A primary disorder in bicarbonate concentration results in a change
compensatory in pCO2.
• In a similar way, a primary change in pCO2 determines a renal response.
that alters the concentration of HCO3 in the ECF.
• Compensation always occurs in the same direction as the primary disturbance, for example, if the
bicarbonate concentration decreases due to metabolic acidosis, the compensation
respiratory manifests as a decrease in pCO2 (hyperventilation)
• In mild disturbances, the compensatory responses are sufficient to maintain the pH at
limits of normality.
• The complete normalization of acid-base balance depends on the reversal of the abnormality.
clinic that caused the imbalance and enough time for the mechanisms
homeostatic mechanisms normalize hydrogen concentrations in the internal environment.
ACID-BASE IMBALANCES
Metabolic acidosis
Deficit and excess
dabase
Metabolic alkalosis bicarbonate
Respiratory alkalosis
Deficit and excess
dioxide of
Respiratory acidosis. carbon
Differential diagnosis of disorders
acid - bases
• The disturbances that start with an ↑ or ↓ of CO2 are called respiratory.
• Disorders that start with an ↑ or ↓ of HCO3 are called metabolic.
• There are four fundamental types of acid-base imbalance.
Respiratory acidosis
Metabolic acidosis
Respiratory alkalosis
Metabolic alkalosis
Classification of acid-base disorders
Respiratory acidosis is caused by a decrease in
ventilation and ↑pCO2
Metabolic acidosis results from a decrease in concentration of
HCO3 no LEC
Respiratory Alkalosis is caused by an increase in
ventilation and ↓pCO2
Metabolic Alkalosis is caused by increased concentration
deHCO3no LEC
In the face of an acid-base disorder
• it is always important to seek the etiological diagnosis,
in order for the therapeutic approach to be directed towards
basic cause. There are some clinical data and
laboratory tests that can assist in the diagnosis of
acid-base disturbance
• 1. History and physical examination;
• 2. Gasometric data (pH, PCO2the HCO3) -
Analysis of arterial blood gas
Normal values of arterial gases
•pH–7,35 a 7,45
• pO2–80 to 100 mmHg
pCO2–35 to 45 mmHg
HCO3–22 to 26 mEq/L
• Oxygen saturation 95 to 98%
• Base excess (BE) –2.5 to +2.5 mEq/L
pH - determine whether acidosis or alkalosis is present. Normal pH does not necessarily indicate
absence of an acid-base disturbance depends on the degree of compensation.
PO2-expresses the effectiveness of oxygen exchange between the alveoli and the pulmonary capillaries, and
depends directly on the partial pressure of oxygen in the alveolus (PaO2), of the capacity to
pulmonary diffusion of this gas. Changes in these factors are causes of variations in PaO.2.
• Under normal conditions, 97% of O2transported from the lungs to the tissues are carried by the
hemoglobin, inside the red blood cells, and the rest is dissolved in the plasma water and
of cells. APaO2refers to the O2dissolved in plasma and is measured in mmHg.
• Saturation of O2from hemoglobin to arterial sg (SatO2given the proportion of O2linked to
hemoglobin.
• A SatO2normal that reaches the left atrium is 98% → good indicator of availability
total of O2for the cells.
PCO2– respiratory component that is assessed by the amount of carbonic acid (H2CO3)
existing in the arterial system. The H2CO3exists almost completely in the form of carbon dioxide (CO2)2) e
water (H2O). Its quantity can therefore be determined by the partial pressure of carbon dioxide.
carbon dioxide in arterial blood (PaCO2)2).
• PaCO2 - the partial pressure of CO2 in arterial blood expresses the effectiveness of alveolar ventilation.
being practically the same as the CO2alveolar, given the great diffusibility of this gas:
• ↑PCO2hypoventilation → retention of CO2 in the blood → insufficient elimination of CO2 in the
pulmonary alveoli.
• PCO2 –hyperventilation→excessive elimination of CO2 from the blood→hyperventilation
pulmonary.
HCO3- - changes in [HCO3] in plasma trigger acid-base imbalances due to
distúrbios metabólicos. Existe em equilíbrio com o ácido carbônico para regular o pH.
HCO3- - When there is an excess of free H+ ions, the bicarbonate ion combines with hydrogen in
excess forms carbonic acid (H2CO3), which decomposes into CO2 and H2O. The excess of
CO2 is eliminated by the respiratory mechanism, and H2O by the kidneys.
Base Excess (BE) - accompanies metabolic disorders
• If the BE is positive and greater than +2.5mEq/l, it means there is an increase in the total of
bases, that is, the organism is retaining bases, due to primary metabolic disorder or
compensatory.
• If the BE is negative and less than -2.5 mEq/l, it means there is a decrease in bases, or
thus, the organism lost bases due to a primary metabolic disorder or
compensatory.
• The BE does not change in acute respiratory disturbances, as there is not enough time for a response.
renal compensatory.
Respiratory Acidosis
Pathophysiology Any sudden decrease in ventilation resulting in the accumulation of CO2.
alveolar hypoventilation
Hypoventilation → hypercapnia (PCO2 > 45 mmHg)
Etiology Respiratory center depression (sedatives)
Injury to the respiratory center (TBI, tumor)
Thoracic traumas
Pneumonias/ atelectasis
Accumulation of secretion/ EAP
PCR
Organic Response Increased renal reabsorption of HCO3-
Clinical picture Cyanosis, arterial hypertension, tachycardia, shallow breaths,
drowsiness, mental confusion, coma
Supplementary data ↓pO2, ↓pH, pCO2 ↑; HCO3nlou ↑
Treatment Correction of ventilation (hyperventilation)
Gradual decrease of PaCO2
Respiratory Acidosis - Laboratory Tests
pH < 7.35
PCO² > 45 mm Hg
• PO² < 80 mm Hg
• Sat O² < 98%
(if compensated)
•HCO³ > 26 mEq/l
Respiratory Acidosis
• Respiratory acidosis is the excessive acidity of the blood caused by an accumulation of carbon dioxide.
in the blood due to poor lung function or slow breathing. The speed and the
breathing depth controls the concentration of carbon dioxide in the blood.
Normally, when carbon dioxide accumulates, blood pH drops and the blood becomes
acid.
• Respiratory acidosis occurs when the lungs do not adequately eliminate carbon dioxide.
carbon. This can occur in diseases that severely affect the lungs.
Nursing Diagnoses
NANDA 2018 - 2020
Nursing Interventions
Promotion of acid-base balance and prevention of complications resulting from elevated serum levels of pCO2
higher than desired
• Obtain blood sample for arterial blood gas analysis
• Monitor arterial blood gas levels
• Monitor hemodynamic status
• Monitor breathing pattern
• Provide oxygen therapy/VM/NIV
• Position the patient and facilitate breathing
• Monitor the determinants of oxygen supply to the tissues (Sat O2)
• Monitor neurological state (level of consciousness and confusion)
• Maintain clear access IV
WHEN TO INTERVENE?
Respiratory acidosis
•The treatment of respiratory acidosis should be directed at the underlying cause of
disturbance. According to the situation, it will include all or some of the measures below:
1. Ventilatory support (mechanical ventilation, when indicated);
2. Bronchodilators (mainly in cases of bronchial hyperreactivity).
Respiratory Alkalosis
Pathophysiology Caused by hyperventilation
Etiology Pain, Anxiety
altitude changes
Mechanical ventilation
CNS injuries, tumors
Organic Response Increased renal excretion of HCO3-
Clinical picture Hyperventilation, dizziness, syncope, confusion
Additional data ↑pH, ↓pCO2; HCO3 normal ↓
Treatment Correction of ventilation (slowing of the respiratory rate): sedatives;
breathing in a paper bag can help with the VM frequency.
increase the concentration of CO2 in the blood, as the individual inhales
again the CO2 after exhaling it. With the increase of
carbon dioxide concentration, the symptoms of hyperventilation improve and,
Consequently, the anxiety decreases and the crisis ceases.
Non-pharmaceutical interventions for reducing anxiety.
Respiratory Alkalosis - Laboratory Tests
> pH 7.45
PCO² < 35 mmHg
• PO²normal
• Oxygen saturation normal
HCO³ < 22 mEq/l(if compensated)
Respiratory Alkalosis
• Respiratory alkalosis is a condition in which the blood is alkaline because the
rapid or deep breathing leads to a low concentration of carbon dioxide
carbon dioxide in the blood. Hyperventilation (rapid and deep breathing) causes a
excessive elimination of carbon dioxide from the blood.
• The MOST common cause of hyperventilation and consequently of alkalosis
respiratory is anxiety. Other causes of respiratory alkalosis are pain, and
inadequate VM parameters.
Nursing Interventions
Promotion of acid-base balance and prevention of complications resulting from serum levels of
pCO2 lower than desired
• Obtain blood sample for arterial gasometry
• Monitor arterial gasometry levels
• Monitor hemodynamic status
• Monitor respiratory pattern
• Position the patient and facilitate breathing
• Reduce oxygen consumption and minimize hyperventilation (comfort, positioning)
• Promover redução do estresse
• Maintain clear access IV
Metabolic Acidosis
Pathophysiology Increased base excretion (HCO3-) -↓ primary HCO3;
Increase in production, accumulation or decrease in excretion of
acids.
Etiology Diabetic ketoacidosis
Lactic acidosis (caused by poor perfusion or hypoxia) - shock
TGI losses (ileostomy)
Organic Response Hyperventilation; increased elimination of CO2
Clinical picture The discreet is asymptomatic.
Hyperpnea (Kussmaul breathing); hypotension, lethargy,
mental confusion, polydipsia and polyuria, coma.
Additional data ↓pH, PCO2 normal ↓; HCO3 ↓
Treatment Correction of the cause of the disorder; administration of NaHCO3.
Metabolic Acidosis - Laboratory Tests
•pH < 7,35
•PCO² < 35 mmHg (if compensated)
• PO² normal or increased (with deep and rapid breaths)
• SatO² normal
HCO3 < 22 mEq/l
Metabolic acidosis
• Metabolic acidosis is the excessive acidity of the blood characterized by a
abnormally low concentration of bicarbonate in the blood. When the pH
blood falls, breathing becomes deeper and faster as the
the organism tries to rid the blood of excess acid by reducing the amount of
carbon dioxide. Finally, the kidneys also try to compensate by excreting more.
acid in the urine. However, both mechanisms can be overcome when the
the body continues to produce excessive acid, which results in severe acidosis and,
ultimately, the coma.
Nursing Diagnoses
NANDA 2018 - 2020
Nursing Interventions
Promotion of acid-base balance and prevention of complications resulting from serum levels of HCO3
less than desired
• Keep access IV open
• Obtain a blood sample for arterial blood gas analysis
• Monitor arterial blood gas levels and electrolytes
• Monitor hemodynamic status (CVP)
• Monitor respiratory pattern
• Position the patient and facilitate breathing
• Monitor determinants of oxygen supply to tissues (Sat O2)
• Monitor blood glucose levels (for cases of diabetic ketoacidosis)
Metabolic Alkalosis
Pathophysiology Caused by the increase in serum bicarbonate (retention or addition
of bases); loss of acids
Etiology TGI losses (vomiting, open CNG) – loss of fixed acids
Diarrhea–hypokalemia (K+ interferes with H+ secretion and ↑ the
reabsorption of HCO3
Excessive intake of bases (NaHCO3)
Organic Response Hypoventilation for CO2 retention
Clinical picture Nonspecific. Paresthesias; tetany; cramps; orthostatic hypotension
(due to volume depletion); tachycardia; arrhythmias.
Additional data pH↑; PCO2nlou ↑ ; HCO3↑
Treatment Volume correction with 0.9% NaCl solutions and potassium replacement.
Acetazolamide (BIC excreting diuretic) for patients with
water restriction.
METABOLIC ALKALOSIS _ Laboratory tests
•pH > 7,45
• PCO² > 45 mm Hg (if compensated)
• Normal PO²
• Normal O² saturation
HCO³ > 26 mEq/l
METABOLIC ALKALOSIS
• Metabolic alkalosis is a condition in which the blood is alkaline due to a concentration
abnormally HIGH bicarbonate. Metabolic alkalosis occurs when the body loses acid in
excess. For example, there is a considerable loss of gastric acid during periods of
prolonged vomiting or by gastric catheter (AS is sometimes done in hospitals,
especially after abdominal surgeries). In rare cases, metabolic alkalosis occurs in a
individual who ingested an excessive amount of alkaline substances (e.g., bicarbonate of
sodium). Additionally, metabolic alkalosis can occur when there is excessive loss of sodium or
Potassium affects the kidneys' ability to regulate the acid-base balance of the blood.
Nursing Interventions
Promotion of acid-base balance and prevention of complications resulting from serum levels of
HCO3 higher than desired
Maintain clear access IV
Monitor arterial blood gas levels
Monitor hemodynamic status of intake and elimination
Monitor respiratory pattern
Obtain a blood sample for arterial blood gas analysis
Monitor determinants of oxygen supply to tissues (SaO2)
Interpretation of arterial blood gas
Start by looking at each number individually and classify them (decide if the
value is high, low or normal
STEP 1–Check the pH
pH < 7.35 = the primary disorder is acidosis
pH > 7.45 = the primary disorder is alkalosis
STEP 2 - Determine if the primary disorder is a result of a
metabolic or respiratory process
Interpretation of arterial blood gas
STEP 3–Check HCO3- and PCO2:
↑PCO2 results in respiratory acidosis
↓PCO2 results in respiratory alkalosis
↑HCO3- results in metabolic alkalosis
↓HCO3- results in metabolic acidosis
STEP 4–Analyze if the compensation is appropriate
Alterations of the acid-base balance
Conditions pH HCO3 pCO2 Typical Causes
Acidosis Low Low Normal or Ketoacidosis
metabolic decreased diabetic;
lactic acidosis
Alkalosis High Alto Normal or vomit
metabolic increased
3. Acidosis Low Normal or High Ailments
respiratory increased pulmonary
obstructive
chronicles
4. Alkalosis High Normal or low Low Sharp pain,
respiratory anxiety
In summary: Interpretation of gasometry
[Link] of pH
When the pH is increased Alkalosis
When the pH is decreased Acidosis
normal pH equilibrium or disturbance that has already been compensated
2. Interpretation of the type of disorder
pCO2 respiratory disturbance
HCO3 metabolic disorder
pCO2 and HCO3 altered in opposite directions - mixed disorder
3. Determine the extent of compensation
Look at the respiratory and metabolic system that does not match the pH for
determine if it is outside of its normal limit, in the effort to correct the disturbance
Clinical Approach
In the face of the clinical picture of:
• Changes in respiratory pattern
• Hemodynamic changes
• Altered states of consciousness
• Changes in kidney function
• Abnormal losses through the TGI and annexes
• Severe infections
Suspect acid-base disorder
BLOOD SAMPLE COLLECTION
ARTERIAL
The analysis of arterial gases is a
method aimed at evaluating the
oxygenation conditions of the client
and the position of the blood gases
The analysis of arterial blood gas
(GA) is a rule in the findings
initials of clients who
we experiment with disorders
respiratory
An analysis of
arterial blood gas
assesses as
effectively the lungs
they are making the exchange
of O2 and CO2–
determines as
concentrations of O2 and
CO2, just like the
acidity of the blood.
indicates how the lungs and
rings are interacting
between themselves, to maintain
normal blood pH
(acid-base equilibrium).
Normal Values
•pH–7,35 a 7,45
PaO2 – 80 to 100 mmHg
PaCO2–35 to 45 mmHg
•HCO3–22 a 26 mEq/L
•SatO2–95 to 98%
Base excess -2.5 to +2.5 mEq/L
Purpose of the Technique
Collect arterial blood to obtain a
evaluation of acid-base changes of
patient
Material
1 syringe of 3 or 5 ml
disposable needle 25x7 or 30x8
cotton with 70% alcohol
Heparin if necessary
syringe obliterator
procedure gloves
lining/waterproof
The Technique
The arterial blood sample is obtained through arterial puncture.
insert a sterile needle (connected to a heparinized syringe)
["radial","brachial","femoral","pedal"]
The radial artery is the most commonly used because it is quickly
accessible, easily tangible, and not associated with such severe
complications.
The analysis of GA
Interpretation of GA
Like in any other laboratory test, interpret the
analysis of GA considering the patient's clinical state.
Errors can occur just like in any other exam.
laboratorial. An incorrect technique or improper handling
the material can affect the results.
Procedures
1 - Preparation of the Collection for GA
Explain the objective of
procedure and how it is
made to the patients and
companions. Give them time
to ask questions and
express concerns.
Procedures
Angle to puncture the
artery
Radial
Brachial
Femoral
•Pediosa
Procedures
Perform antisepsis with alcohol
70%
Insert the needle until the
the artery should be punctured
Allow the syringe to fill.
with 2 ml of arterial blood
Procedures
Immediately after
remove the needle from
artery. compress
firmly the place of
punctured by at least
five minutes.
Post-puncture intervention
The biggest complication of arterial puncture is the
arterial blood extravasation at the site of
puncture for the adjacent tissues.
Squeeze firmly on
artery for at least 5
minutes
Subsequent Care
•Register if the patient is
in VM, and the amount of O2.
Transport the sample
immediately (process it
in 15 minutes)
Factors that affect the results
The non-immersion of the sample in •The storage of the sample to the
container with dry ice can ambient temperature accelerates the
result in a DECREASE in pH and of the drop in pH
PO2
Extended period of time
•The non-expulsion of HEPARIN from between the collection and the examination may
syringe before collection of result in a reduction of pH
sample may result in reduction
do pH, PCO2 PO2
Factors that affect the results
If the patient receives oxygen during the arterial puncture, record it.
flow or the percentage of oxygen in the order form of
laboratory. percentage of inspired oxygen;
1. respiratory rate of the individual and the ventilator,
2. current volume provided by the fan;
3. any other relevant information.
Allen test video and arterial blood collection
Allen test
[Link]
IAI–invasive arterial pressure
Venous gasometry x Arterial gasometry
The main difference is the partial pressure of oxygen which is lower in venous blood.
that half of the arterial blood. Venous blood, therefore, should not be used
in the assessment of oxygenation. Arterial blood gas analysis evaluates ventilatory parameters.
The other parameters - pH, PCO2, and HCO3 - have similar values in the blood.
venous and arterial. Arterial blood gas analysis is usually chosen because it presents a
more complete result, allowing for a more complex analysis.
Venous gasometry is performed as a second option when the collection in the artery is not possible.
it is possible, being done through vein collection.
Clinical Case - COVID-19
•ID: DD, masculino, 25 anos, natural e procedente de São Paulo- SP.
•Queixa principal: “Falta de ar” há 3 dias.
HDA: Patient with complaints of fatigue and progressive dyspnea for 3 days, now at
minimal efforts. Reports dry cough and fever not measured during the period. Denies others.
associated complaints. Denies contact with people showing similar symptoms.
Physical examination:
•Dados vitais: PA: 120/70mmHg; FC: 120bpm; FR: 15mpm; SatO2: 93%; Temp: 38,2°C
General: REG, flushed, hydrated, acyanotic, and non-icteric.
•AR: MV with diffuse and discrete expiratory wheezes.
•ACV: Tachycardic, BRNF in 2T without murmurs. ABD: without changes.
•EXT: well perfused, without edema.
Neurological: no apparent focal deficits.
Clinical Case - COVID-19
Complementary tests for suspected covid-19
Chest tomography:
Multiple opacities with a consolidative appearance, predominantly subpleural and
multilobar commitment, showing areas with ground-glass attenuation in
adjacent parenchyma, suggestive of pulmonary inflammatory/infectious process,
not being able to rule out the possibility of infection by SARS-CoV-2 in the face of
clinical context.
SARS-CoV-2 uses receptors of the angiotensin-converting enzyme 2 (ACE2)
to enter the lung cells, causing manifestations that vary from a
mild to critical spectrum, which may lead to Severe Acute Respiratory Syndrome (SARS) and to
obituary.
Caso Clínico–COVID-19
Complementary exams for suspected covid-19
Laboratories:
•Hb: 12,1 / Leucograma: 12.300 sem desvio (vr: 4.500 a 11.000/mm³) / Plaquetas:
156mil (vr: 150 a 450 mil)/ PCR: 1,2 (vr: 0,3mg/dl)
Arterial gasometry:↓ pH 7,32 / pO2: 82 / ↑ pCO2: 48 / HCO3: 24 / SatO2: 91% /
1. What is the acid-base disorder?
Respiratory acidosis
Is there compensation?
No, because the HCO3 is normal; it should be increased to compensate.
Patient progressed with desaturation (88-90%), with increasing need for oxygen
supplementary, with orotracheal intubation and ICU vacancy indicated. Patient transferred
to the ICU. After 5 days, received a positive RT-PCR for SARS-CoV-2.
Clinical Case
21-year-old patient with a history of diabetes mellitus arrives at the Emergency Department.
torpid, dehydrated, with increased frequency and depth of breathing. To
clinical examination notes ketone breath. Arterial gas analysis:↓ pH=7,10; ↓ pCO2=20
mmHg↓ HCO3= 15 mEq/L. Glicemia = 350mg/dl.
What acid-base disorder is presented?
Metabolic acidosis.
Is there a compensation process?
Yes, there is an attempt at compensation indicated by a low pCO2.
3. What is the likely cause of this disorder?
The probable cause of the disturbance is acute decompensation of Diabetes Mellitus, with
diabetic ketoacidosis frame. The body undergoes lipolysis due to the absence of insulin, and
releases fatty acids into the circulation, making the blood acidic.
Clinical Case
57-year-old obese patient is in the postoperative period of rectosigmoidectomy for tumor of
sigmoid. He remains bedridden in a horizontal position, headboard at 0 degrees. He is with a
ileostomy with drainage of 2,000 mL/24 hours of liquid stool. The blood gas analysis reveals:
pH=↓ 7.03↑pCO2=54 mmHg;↓HCO3=14 mEq/L.
1. What acid-base disturbance is presented? Justify.
Mixed acidosis (respiratory - increased PCO2 and metabolic - decreased HCO3).
Is there a compensation process? Justify.
No, because the disorder is mixed. Both systems are affected.
What is the likely cause of this disorder?
The cause of the metabolic disorder is the loss of intestinal bicarbonate through ileostomy.
The cause of the respiratory disturbance is alveolar hypoventilation due to compression.
diaphragmatic, caused by obesity and decreased pulmonary expandability due to
horizontal decubitus.
Clinical Case
70-year-old patient in post-operative period of abdominal surgery complains of cramps and
prostration. Upon detailed clinical examination, muscle tremors and drainage are observed.
elevated by the nasogastric catheter (2,000mL/24 h). Arterial blood gas:↑pH=7.62;
PCO2=40 mmHg; ↑HCO3=36 mEq/L.
1. What acid-base disorder is presented? Justify.
Metabolic alkalosis
2. Is there a compensation process? Justify.
No, because the pCO2 is normal.
3. What is the likely cause of this disorder?
When high drainage occurs through the gastric catheter, there is a large loss of acid.
hydrochloric, component of gastric juice. The loss of acid leads to alkalinity
blood.
Clinical Case
17-year-old patient arrives at the Emergency Room not speaking, presenting eye blinking and
respiratory rate of 50 incursions per minute. Arterial blood gas:↑pH=7,63;
↓pCO2=18 mmHg; HCO3=25 mEq/L.
1. What acid-base disorder is presented? Justify.
Respiratory alkalosis
2. Is there a compensation process? Justify.
No, because the HCO3 is normal.
3. What is the likely cause of this disorder?
The mechanism is hyperventilation, likely of emotional etiology, significantly increasing the
elimination of CO2 and reducing blood pCO2.
References
Mendes NT. Hydroelectrolytic imbalance and acid-base disorders. In: Cheregatti AL and Amorin CP.
Enfermagem em Unidade de Terapia Intensiva. Ed Martinari, 2 ed., São Paulo, 2010. Cap. 5, p. 138-149.
Miranda MPF. Disturbances in acid-base balance. In: Padilha et al (Eds). Nursing in ICUs: caring for
critical patient. São Paulo: Manole, 2010. Chap 32, p. 730-744.
Oliveira LB; Campanili TCGF. Laboratory tests in Intensive Care Unit. In: Lopes JL and Gengo RCG.
Interpretation of Laboratory Tests: A Practical Guide for Nurses and Nursing Students. Rio de
January: Golden Eagle. 2015. Cap17, p. 333-339.