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Questions and Answers
What is a potential terminal manifestation if a condition remains untreated?
What is a potential terminal manifestation if a condition remains untreated?
Which underlying condition would likely cause respiratory alkalosis due to hyperventilation?
Which underlying condition would likely cause respiratory alkalosis due to hyperventilation?
How does the body compensate for acute respiratory alkalosis?
How does the body compensate for acute respiratory alkalosis?
What might cerebral vasoconstriction lead to during acute respiratory alkalosis?
What might cerebral vasoconstriction lead to during acute respiratory alkalosis?
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What is a common treatment for the underlying disorder associated with respiratory acidosis?
What is a common treatment for the underlying disorder associated with respiratory acidosis?
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What is a primary cause of metabolic alkalosis?
What is a primary cause of metabolic alkalosis?
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Which of the following is NOT a common treatment option for metabolic alkalosis?
Which of the following is NOT a common treatment option for metabolic alkalosis?
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What mechanism is responsible for the body's response to acute respiratory acidosis?
What mechanism is responsible for the body's response to acute respiratory acidosis?
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In which condition would hypoventilation commonly cause respiratory acidosis?
In which condition would hypoventilation commonly cause respiratory acidosis?
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Which of the following best describes chronic respiratory acidosis?
Which of the following best describes chronic respiratory acidosis?
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What is the expected bicarbonate increase in chronic respiratory acidosis due to changes in PCO2?
What is the expected bicarbonate increase in chronic respiratory acidosis due to changes in PCO2?
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Which symptom is primarily associated with severe acute respiratory acidosis?
Which symptom is primarily associated with severe acute respiratory acidosis?
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Which renal condition contributes to the maintenance of metabolic alkalosis?
Which renal condition contributes to the maintenance of metabolic alkalosis?
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What common drug type is associated with causing respiratory acidosis through respiratory depression?
What common drug type is associated with causing respiratory acidosis through respiratory depression?
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Which of the following best identifies a consequence of hypoventilation?
Which of the following best identifies a consequence of hypoventilation?
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What is the primary reason for adjusting the normal anion gap in this patient?
What is the primary reason for adjusting the normal anion gap in this patient?
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What is the calculated normal anion gap for this patient before adjustment?
What is the calculated normal anion gap for this patient before adjustment?
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In which scenario is adjunctive sodium bicarbonate therapy indicated?
In which scenario is adjunctive sodium bicarbonate therapy indicated?
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What is the maximum pH level that sodium bicarbonate therapy aims to raise the arterial pH to in cases of acute severe metabolic acidosis?
What is the maximum pH level that sodium bicarbonate therapy aims to raise the arterial pH to in cases of acute severe metabolic acidosis?
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Which of the following conditions is least likely to require sodium bicarbonate therapy?
Which of the following conditions is least likely to require sodium bicarbonate therapy?
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What potential risk is associated with correcting plasma [HCO3−] entirely when using sodium bicarbonate?
What potential risk is associated with correcting plasma [HCO3−] entirely when using sodium bicarbonate?
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What adjustment is made to the normal anion gap for this patient due to albumin deficiency?
What adjustment is made to the normal anion gap for this patient due to albumin deficiency?
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What does a low bicarb level and low PCO2 suggest about the patient's condition?
What does a low bicarb level and low PCO2 suggest about the patient's condition?
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What does the anion gap represent?
What does the anion gap represent?
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What would happen to the anion gap if HCl is added to plasma?
What would happen to the anion gap if HCl is added to plasma?
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What is the calculated formula for the anion gap?
What is the calculated formula for the anion gap?
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In which scenario does the anion gap increase?
In which scenario does the anion gap increase?
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How should the anion gap be adjusted in critically ill patients with hypoalbuminemia?
How should the anion gap be adjusted in critically ill patients with hypoalbuminemia?
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In the case of a patient with a calculated AG of 11 mEq/L and a serum albumin of 2.4 g/dL, what would the adjusted AG be?
In the case of a patient with a calculated AG of 11 mEq/L and a serum albumin of 2.4 g/dL, what would the adjusted AG be?
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If a patient has a higher concentration of unmeasured cations, what condition may they exhibit?
If a patient has a higher concentration of unmeasured cations, what condition may they exhibit?
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Which of the following is a characteristic of hyperchloremic acidosis?
Which of the following is a characteristic of hyperchloremic acidosis?
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Which component is NOT essential in establishing the etiology of an acid-base disturbance?
Which component is NOT essential in establishing the etiology of an acid-base disturbance?
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What is the primary compensatory mechanism during metabolic acidosis?
What is the primary compensatory mechanism during metabolic acidosis?
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What symptom is NOT typically associated with acute metabolic acidosis?
What symptom is NOT typically associated with acute metabolic acidosis?
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Chronic metabolic acidosis can lead to which of the following musculoskeletal problems?
Chronic metabolic acidosis can lead to which of the following musculoskeletal problems?
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Which of the following factors could lead to a secondary decrease in HCO3-?
Which of the following factors could lead to a secondary decrease in HCO3-?
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What type of metabolic acidosis is characterized by an increase in the anion gap?
What type of metabolic acidosis is characterized by an increase in the anion gap?
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Which of the following best describes the pathology of metabolic acidosis?
Which of the following best describes the pathology of metabolic acidosis?
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Which clinical condition does metabolic acidosis NOT typically result in?
Which clinical condition does metabolic acidosis NOT typically result in?
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What is a potential result of impaired renal function in metabolic acidosis?
What is a potential result of impaired renal function in metabolic acidosis?
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In the context of acid-base balance, what does the body need to maintain to ensure electrical neutrality?
In the context of acid-base balance, what does the body need to maintain to ensure electrical neutrality?
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Study Notes
Acid-Base Disturbances Etiology and Treatment
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To establish the cause of an acid-base disturbance, a comprehensive assessment is necessary, encompassing:
- Clinical history
- Recent medications
- Physical examination findings
- Arterial blood gas (ABG) analysis
- Serum electrolytes
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Frequent monitoring of the patient’s response to treatment is crucial, often necessitating an arterial line to minimize discomfort from repeated ABG collections.
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The underlying disease process must be identified and addressed for effective treatment of acid-base disturbances, as supportive therapy only manages pH and electrolytes while the root cause persists.
Metabolic Acidosis
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Metabolic acidosis: Characterized by a decrease in serum bicarbonate (HCO3-) and a compensatory decrease in partial pressure of carbon dioxide (PCO2) through hyperventilation.
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Symptoms:
- Cardiovascular: Ventricular arrhythmias, reduced cardiac contractility, pulmonary edema, systemic hypotension.
- Musculoskeletal: Impaired growth, rickets, osteomalacia, osteopenia (chronic acidosis).
- Neurologic: Lethargy progressing to coma, severity correlated with pH derangement.
- Respiratory: Dyspnea, respiratory fatigue, respiratory failure due to marked increases in minute ventilation.
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Pathophysiology:
- Buffering: Consumption of HCO3- due to exogenous acid.
- Organic acid accumulation: Metabolic disturbances lead to accumulation of organic acids like lactate or ketoacids.
- Endogenous acid accumulation: Impaired renal function results in accumulation of endogenous acids such as phosphates and sulfates.
- HCO3- loss: Bicarbonate-rich fluid losses through diarrhea, biliary drainage, or pancreatic fistula.
- Dilutional acidosis: Rapid administration of non-alkali containing IV fluids.
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Classification:
- Increased anion gap metabolic acidosis: Anions of acid added are not chloride.
- Normal anion gap metabolic acidosis: Chloride is the primary anion added.
Anion Gap
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Anion gap: Represents the difference between unmeasured anions and unmeasured cations in the extracellular fluid.
- Anion gap = [Na+] - ([Cl-] + [HCO3-])
- Normal range: 6 to 12 mEq/L
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Normal anion gap: Addition of HCl results in hyperchloremic acidosis, as the decrease in HCO3- is balanced by an increase in Cl-.
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Increased anion gap: When an acid with an anion other than chloride is added (e.g., lactate, beta-hydroxybutyrate), the decrease in HCO3- is not matched by an increase in Cl-, leading to an elevation in the anion gap.
Adjusted Anion Gap
- In critically ill patients with hypoalbuminemia, the anion gap should be adjusted:
- Adjusted AG = AG + 2.5 × (normal albumin - measured albumin in g/dL)
- Normal albumin concentration: 4.4 g/dL
Metabolic Acidosis Treatment
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Primary cause correction: Address the underlying cause of metabolic acidosis.
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Sodium bicarbonate (NaHCO3) administration:
- Indicated in cases of severe acidemia (pH < 7.15) and renal dysfunction preventing adequate bicarbonate regeneration.
- May not be necessary in metabolic acidosis resulting from lactic acidosis and ketoacidosis, which generally resolves with targeted therapy.
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Considerations for NaHCO3 use:
- Avoid complete correction of plasma HCO3- to prevent:
- Volume overload
- Hypernatremia
- Hyperosmolarity
- Overshoot alkalemia
- Hypocalcemia
- Hypokalemia
- Avoid complete correction of plasma HCO3- to prevent:
Metabolic Alkalosis
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Metabolic alkalosis: Characterized by an increase in serum bicarbonate (HCO3-).
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Causes:
- H+ loss: Gastrointestinal (GI) losses (e.g., nasogastric suctioning, vomiting), renal losses (e.g., diuretics, Cushing syndrome), and excessive alkali intake.
- Bicarbonate gain: Administration of bicarbonate, acetate, lactate, or citrate.
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Maintenance: Abnormal renal function prevents the kidneys from excreting excess bicarbonate.
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Mechanisms contributing to decreased HCO3- excretion: Hypovolemia, hypokalemia, mineralocorticoid excess.
Metabolic Alkalosis Treatment
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Address the underlying cause.
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Pharmacological interventions:
- Spironolactone, amiloride, or triamterene for endogenous mineralocorticoid excess.
- Surgery may be considered if pharmacological therapies are ineffective.
Respiratory Acidosis
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Respiratory acidosis: Characterized by an increase in partial pressure of carbon dioxide (PCO2) and compensatory increase in serum bicarbonate (HCO3-).
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Acute respiratory acidosis: Intracellular buffering leads to an increase in HCO3- proportional to the rise in PCO2.
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Chronic respiratory acidosis: New HCO3- generation due to increased ammonium excretion results in a greater increase in HCO3- compared to acute acidosis.
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Hypoventilation: The primary cause of increased PCO2, occurring with any interference in respiratory processes.
Causes of Respiratory Acidosis
- CNS disease: Central sleep apnea, intracranial hypertension, trauma, infection, tumors, drug-induced (e.g., aminoglycosides, anesthetics, β-blockers, hypnotics, narcotics, neuromuscular blocking agents, sedatives).
- Neuromuscular disease: Muscular dystrophy.
- Pulmonary disease: Lower airway obstruction, COPD, status asthmaticus, pneumonia, pneumonitis, pulmonary edema, restrictive lung disease, ascites, obesity, pleural effusion, smoke inhalation, upper airway obstruction, obstructive sleep apnea, inadequate mechanical ventilation.
- Other causes: Congestive heart failure.
Respiratory Acidosis Symptoms
- Neurologic abnormalities: Headache, blurred vision, restlessness, anxiety, tremors, asterixis, somnolence, delirium.
- Severe, acute respiratory acidosis can lead to:
- Peripheral vasodilation
- Hypotension
- Cardiac arrhythmias
Respiratory Acidosis Treatment
- Treat the underlying cause: Address the respiratory impairment.
- Oxygen therapy: Carefully initiated only if Pao2 is less than 50 mm Hg, as hypoxemia drives breathing rather than hypercarbia.
- Corticosteroids and bronchodilators: Reduce airway inflammation and resistance.
- Mechanical ventilation: If ventilation fails.
Respiratory Alkalosis
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Respiratory alkalosis: Characterized by a decrease in partial pressure of carbon dioxide (PCO2) and compensatory decrease in serum bicarbonate (HCO3-).
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Acute respiratory alkalosis: Intracellular buffering leads to a decrease in HCO3- proportional to the decrease in PCO2.
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Chronic respiratory alkalosis: Decreased HCO3- reabsorption and decreased ammonium excretion contribute to a greater decrease in HCO3- compared to acute alkalosis.
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Hyperventilation: The primary cause of decreased PCO2, frequently triggered by stressors such as anxiety, pain, and infection.
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Other causes: Hypoxemia, sepsis, liver failure, pulmonary embolism.
Respiratory Alkalosis Clinical Presentation
- Acute onset of hypocapnia: Cerebral vasoconstriction.
Respiratory Alkalosis Treatment
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Treat the underlying cause: Address the stressor or medical condition causing hyperventilation.
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In severe cases, re-breathing into a paper bag can increase PCO2 levels.
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Management of underlying conditions may be necessary, such as:
- Treatment of pain
- Anti-anxiety medications
- Correction of hypoxemia
- Management of sepsis or liver failure
Key Points
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Acid-base disturbances are common in clinical practice and can have significant implications for patient health.
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A thorough assessment is crucial to identify the underlying cause and tailor appropriate treatment.
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Treatment often involves addressing the primary cause and providing supportive therapy to manage pH and electrolytes, while carefully monitoring patient response.
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Understanding the mechanisms of acid-base balance and the different types of disturbances is essential for effective clinical management.
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Description
This quiz covers the etiology and treatment of acid-base disturbances, focusing on the assessment process and the importance of identifying underlying causes. It includes details on metabolic acidosis, symptoms, and management strategies, including monitoring techniques like arterial blood gas analysis.
