Pulmonology · Acid-Base Disorders
The facts most likely to be tested
Respiratory alkalosis is defined by a primary decrease in PaCO2 resulting in an elevated arterial pH (>7.45).
The most common etiology of respiratory alkalosis is alveolar hyperventilation secondary to anxiety, panic attacks, or hypoxia.
Acute respiratory alkalosis causes a compensatory decrease in serum bicarbonate of approximately 2 mEq/L for every 10 mmHg drop in PaCO2.
Chronic respiratory alkalosis leads to a more robust renal compensation via decreased bicarbonate reabsorption in the proximal tubule.
Patients often present with perioral paresthesias, carpopedal spasm, and lightheadedness due to decreased ionized calcium levels.
Salicylate toxicity is a classic board-tested cause that presents with a mixed respiratory alkalosis and high anion gap metabolic acidosis.
Management of respiratory alkalosis focuses on treating the underlying cause rather than the use of paper bag rebreathing, which is no longer recommended.
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A 24-year-old female is brought to the emergency department after an episode of intense emotional distress. She complains of tingling in her fingers and around her mouth and feels like she cannot catch her breath. Physical examination reveals tachypnea and involuntary flexion of the wrists when the blood pressure cuff is inflated. Arterial blood gas shows a pH of 7.52, PaCO2 of 28 mmHg, and HCO3 of 22 mEq/L.
What is the most likely underlying mechanism for this patient's symptoms?
Decreased ionized calcium secondary to respiratory alkalosis
The patient's hyperventilation caused a primary respiratory alkalosis, which increases the binding of calcium to albumin, leading to symptomatic hypocalcemia (Trousseau sign) and paresthesias.
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Etiology / Epidemiology
Caused by alveolar hyperventilation leading to decreased PaCO2. Common in anxiety, pulmonary embolism, and high altitude.
Clinical Manifestations
Presents with circumoral paresthesias, carpopedal spasm, and lightheadedness. Often associated with hypocalcemia symptoms.
Diagnosis
Confirmed via Arterial Blood Gas (ABG) showing pH > 7.45 and PaCO2 < 35 mmHg.
Treatment
Treat the underlying cause. Avoid paper bag rebreathing due to hypoxia risk.
Prognosis
Generally excellent if the underlying trigger is corrected. Monitor for seizures if pH rises rapidly.
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Epidemiology & Etiology
Respiratory alkalosis is the most common acid-base disturbance in hospitalized patients. Primary drivers include anxiety/panic attacks, salicylate toxicity (early phase), and mechanical ventilation over-ventilation. High altitude exposure triggers compensatory hyperventilation due to low ambient oxygen.
Pertinent Anatomy
The medulla oblongata contains central chemoreceptors sensitive to pH changes in the cerebrospinal fluid. Peripheral chemoreceptors in the carotid bodies respond to low PaO2, driving the respiratory rate increase. This feedback loop is the primary mechanism for CO2 washout.
Pathophysiology
Hyperventilation causes excessive CO2 expiration, shifting the carbonic acid equilibrium to the left. This reduces H+ concentration, raising the serum pH. Acute compensation involves intracellular buffering, while chronic compensation involves renal bicarbonate excretion to normalize pH.
Clinical Manifestations
Patients often report lightheadedness and circumoral paresthesias. Severe cases manifest as carpopedal spasm (Trousseau sign) due to decreased ionized calcium. Seizures and cardiac arrhythmias may occur in extreme alkalemia. Always rule out pulmonary embolism in patients with unexplained tachypnea.
Diagnosis
The Arterial Blood Gas (ABG) is the gold standard diagnostic test. Findings include pH > 7.45 and PaCO2 < 35 mmHg. In chronic cases, the serum bicarbonate will be low (< 22 mEq/L) as the kidneys compensate.
Treatment
Management focuses on the underlying etiology (e.g., anxiolytics for panic, oxygen for hypoxia). Do not use paper bag rebreathing as it can cause dangerous hypoxemia. If on mechanical ventilation, decrease respiratory rate or tidal volume. Use sedation only if the patient is severely agitated.
Prognosis
Prognosis is excellent once the precipitating factor is resolved. Rapid correction of chronic respiratory alkalosis can lead to metabolic acidosis; monitor electrolytes closely. Watch for hypokalemia as H+ shifts out of cells.
Differential Diagnosis
Salicylate toxicity: associated with high anion gap metabolic acidosis later
Pulmonary embolism: sudden onset dyspnea and tachycardia
Panic disorder: normal oxygen saturation and clear lung exam
High altitude: history of recent ascent to >8,000 feet
Sepsis: early hyperventilation phase before metabolic acidosis develops