Respiratory and Metabolic Alkalosis

Alkalosis Overview - pH Up Party

• Alkalosis: Systemic increase in blood $pH > \textbf{7.45}$, indicating decreased hydrogen ion concentration ([H⁺]↓).
• Key physiological disturbances:
  • ↑ Neuromuscular excitability: Paresthesias, muscle cramps, carpopedal spasm, tetany.
  • Cerebral vasoconstriction: Dizziness, lightheadedness, confusion.
  • Cardiac effects: Potential for arrhythmias.
• Classified into Respiratory and Metabolic alkalosis.

⭐ Alkalosis ($pH > \textbf{7.45}$) can precipitate hypocalcemic tetany by decreasing ionized calcium and cause hypokalemia due to intracellular K+ shift.

Respiratory Alkalosis - Huffing & Puffing pH

• Definition: Primary ↓ $PCO_2$ (hypocapnia) leading to ↑ pH.
• Pathophysiology: Alveolar hyperventilation blows off $CO_2$.
• Lab Findings:
  • pH > 7.45
  • $PCO_2$ < 35 mmHg
  • $HCO_3^-$ ↓ (renal compensation: takes hours to days)
    • Acute: $HCO_3^-$ ↓ by 2 mEq/L for every 10 mmHg ↓ in $PCO_2$.
    • Chronic: $HCO_3^-$ ↓ by 4-5 mEq/L for every 10 mmHg ↓ in $PCO_2$.
• Causes: 📌 CHAMPS
  • CNS disorders (stroke, trauma)
  • Hypoxia (high altitude, pneumonia, PE)
  • Anxiety, pain, fever, ASA (Salicylates)
  • Mechanical ventilation (overventilation)
  • Progesterone (pregnancy), Pulmonary disease (restrictive)
  • Sepsis, Salicylates
• Clinical Features: Lightheadedness, dizziness, paresthesias (perioral, digital), carpopedal spasm, tetany (due to ↓ ionized $Ca^{2+}$), syncope, seizures.

⭐ Salicylate toxicity classically presents with a mixed acid-base disorder: primary respiratory alkalosis (due to direct stimulation of medullary respiratory center) and primary metabolic acidosis.

• Management: Treat underlying cause. Reassurance, rebreathing into a paper bag (for anxiety-induced hyperventilation). Adjust ventilator settings if iatrogenic.

Metabolic Alkalosis - Bicarb Bonanza

• Pathophysiology: Primary ↑ $[HCO_3^-]$ ($> \textbf{28 mEq/L}$), leading to ↑ pH ($> \textbf{7.45}$).

  • Compensation: Respiratory acidosis; $pCO_2$ ↑ by $\textbf{0.7 mmHg}$ for each $\textbf{1 mEq/L}$ ↑ in $[HCO_3^-]$ above 24 mEq/L.
  • Maximal compensation: $pCO_2$ rarely exceeds $\textbf{55 mmHg}$.

• Etiology & Management: Differentiated by urine chloride ($U_{Cl^-}$).

![Saline-responsive vs. saline-resistant metabolic alkalosis](https://ylbwdadhbcjolwylidja.supabase.co/storage/v1/object/public/notes/L1/Biochemistry_Acid-Base_and_Electrolyte_Balance_Respiratory_and_Metabolic_Alkalosis/3b904e48-4dfb-4d76-9b79-c3c56db26284.gif)

• Clinical Features: Often asymptomatic. Severe:
  • Hypokalemia effects: Weakness, arrhythmias.
  • ↓ Ionized $Ca^{2+}$: Tetany, paresthesias, seizures.
  • Compensatory hypoventilation.
• Diagnosis: ABG, serum electrolytes, urine $Cl^-$, $K^+$, $Na^+$.

  ⭐ Urine chloride is crucial in differentiating saline-responsive (< 15 mEq/L) from saline-resistant (> 20 mEq/L) metabolic alkalosis.

• Treatment Principles:
  • Address underlying cause.
  • Correct volume depletion (if present) with isotonic saline.
  • Replete $K^+$ if hypokalemic.
  • Severe cases ($pH > \textbf{7.6}$): Acetazolamide, HCl infusion (rare), dialysis.

Compensation & Mixed Disorders - Body's Balancing Act

Body attempts to normalize pH. Suspect mixed disorder if compensation is outside expected range.

• Respiratory Alkalosis (Primary ↓PaCO₂):
  • Metabolic Comp: Kidneys ↓ plasma [HCO₃⁻].
    • Acute: ↓10 PaCO₂ → ↓2 [HCO₃⁻].
    • Chronic: ↓10 PaCO₂ → ↓4-5 [HCO₃⁻].
• Metabolic Alkalosis (Primary ↑[HCO₃⁻]):
  • Respiratory Comp: Lungs ↑PaCO₂ (hypoventilation).
    • Expected PaCO₂: $\text{PaCO}_2 = (0.7 \times [HCO_3^-]) + 20 \text{ mmHg (range } \pm 5)$.

⭐ The PCO₂ in compensatory hypoventilation for metabolic alkalosis rarely rises above 55 mmHg due to the overriding stimulus of hypoxic drive.

High‑Yield Points - ⚡ Biggest Takeaways

• Respiratory alkalosis: Caused by hyperventilation (↓ PCO₂); e.g., hypoxia, anxiety, salicylates. Renal HCO₃⁻ excretion is compensatory.
• Metabolic alkalosis: ↑ HCO₃⁻. Key causes: vomiting/NG suction (saline-responsive, urine Cl⁻ < 10) or mineralocorticoid excess (saline-resistant, urine Cl⁻ > 20).
• Hypoventilation (↑ PCO₂) is the limited respiratory compensation for metabolic alkalosis.
• Hypokalemia often accompanies and worsens metabolic alkalosis.
• Tetany and paresthesias (↓ ionized Ca²⁺) can occur in severe respiratory alkalosis.