Description

• Respiratory alkalosis:
  • Elevated serum pH secondary to alveolar hyperventilation and decreased PaCO₂
  • Hyperventilation occurs through stimulation of 2 receptor types:
    • Central receptors – located in the brainstem and respond to decreased CSF pH
    • Chest receptors – located in aortic arch and respond to hypoxemia
  • Increased alveolar ventilation secondary to:
    • Disorders causing acidosis
    • Hypoxemia or
    • Nonphysiologic stimulation of those receptors by CNS or chest disorders
  • Rarely life threatening with pH typically <7.50
• Metabolic alkalosis:
  • Primary increase in serum HCO₃⁻ secondary to loss of H⁺ or gain of HCO₃⁻
  • Pathogenesis requires an initial process that generates the metabolic alkalosis with a secondary or overlapping process maintaining the alkalosis
• Generation occurs through one of the following mechanisms:
  • Gain of alkali through ingestion or infusion
  • Loss of H⁺ through the GI tract or kidneys
  • Shift of hydrogen ions into the intracellular space
  • Contraction of extracellular fluid (ECF) volume with loss of HCO₃⁻-poor fluids
• Renal maintenance is required to sustain a metabolic alkalosis secondary to the kidney's enormous ability to excrete HCO₃⁻. This occurs through the following:
  • Decreased GFR (renal failure, ECF depletion)
  • Elevated tubular reabsorption of HCO₃⁻ secondary to hypochloremia, hyperaldosteronism, hypokalemia, ECF depletion
• Mortality 45% if pH >7.55 and 80% if pH >7.65

Etiology

• Respiratory alkalosis:
  • CNS:
    • Hyperventilation syndrome
    • Pain
    • Anxiety/psychosis
    • Fever
    • Cerebrovascular accident (CVA)
    • CNS infection (meningitis, encephalitis)
    • CNS mass lesion (tumor, trauma)
  • Hypoxemia:
    • Altitude
    • Anemia
    • Shunt
  • Medications/drugs:
    • Progesterone
    • Methylxanthines
    • Salicylates
    • Catecholamines
    • Nicotine
  • Endocrine:
    • Hyperthyroidism
    • Pregnancy
  • Chest stimulation:
    • Pulmonary embolism
    • Pneumonia
    • Pneumothorax
  • Other:
    • Sepsis
    • Hepatic failure
    • Heat exhaustion
• Metabolic alkalosis:
  • Chloride depletion:
    • GI losses:
      • Vomiting
      • Nasogastric (NG) suctioning
      • High-output ileostomy loss
      • Chloride-losing diarrhea (villous adenoma)
    • Renal loss:
      • Diuretics (loop and thiazide)
      • Post (chronic) hypercapnia
      • Drug/medication (carbenicillin)
      • Gitelman syndrome (chloride wasting)
      • Low chloride intake
      • Bartter syndrome (chloride wasting)
  • HCO₃⁻ retention:
    • NaHCO₃ infusion
    • Blood transfusions
  • Mineralocorticoid excess:
    • Primary hyperaldosteronism
  • Other:
    • Milk alkali syndrome
    • Severe potassium depletion

Signs and Symptoms

• Signs and symptoms secondary to:
  • Arteriolar vasoconstriction
  • Hypocalcemia secondary to decreased ionized calcium from increased calcium binding to albumin
  • Associated hypokalemia
  • Underlying cause
• Weakness
• Seizures
• Altered mental status
• Tetany
• Chvostek sign
• Trousseau sign
• Arrhythmias
• Myalgias
• Carpal–pedal spasm
• Perioral tingling/numbness
• Hypoxemia
• Dehydration

Essential Workup

• Electrolytes:
  • Elevated HCO₃⁻ with metabolic alkalosis
  • Evaluate for hypokalemia and hypocalcemia
• BUN/creatinine:
  • Evaluate for renal failure or dehydration
• Blood gas (arterial/venous):
  • pH
  • PCO₂ decreased in respiratory alkalosis
  • PO₂ for hypoxemia
  • Venous vs. arterial blood gas
    • pH – good correlation within 0.03–0.04 units
    • PCO₂ – good correlation, although VBG may not correlate with severe shock
    • HCO₃ – good correlation
    • Base excess – good correlation
• Calculate compensation to identify mixed acid–base disorders:
  • Acute respiratory alkalosis:
    • HCO₃⁻ decreases secondary to intracellular shift and buffering within 10–20 min
    • Expected HCO₃⁻ decreased by 2 mEq/dL for each 10 mm Hg decrease in PCO₂
  • Chronic respiratory alkalosis:
    • HCO₃⁻ decreased secondary to renal secretion of HCO₃⁻
    • Requires 48–72 hr for maximal compensation
    • Expected HCO₃⁻ decreased by 5 mEq/dL for each 10 mm Hg decrease in PCO₂
    • If HCO₃⁻ greater than predicted, concomitant metabolic alkalosis
    • If HCO₃⁻ less than predicted, concomitant metabolic acidosis
  • Metabolic alkalosis:
    • Expected PCO₂ = 0.9 [HCO₃⁻] + 9
    • If PCO₂ greater than predicted, concomitant respiratory acidosis
    • If PCO₂ less than predicted, concomitant respiratory alkalosis
• Urine chloride:
  • Used to determine chloride depletion vs. nonchloride depletion causes of metabolic alkalosis:
    • UCl⁻ <10 mEq/L in chloride responsive metabolic alkalosis
    • UCl⁻ >30 mEq/L in nonchloride responsive metabolic alkalosis

Diagnostic Tests and Interpretation

• Glucose
• Ionized calcium
• Magnesium level
• Urine pregnancy
• Additional labs to evaluate underlying cause:
  • CBC, blood cultures for sepsis
  • LFT for hepatic failure
  • Aspirin level
  • Urine toxicology screen
  • Urine diuretics screen (bulimia)
  • Urine diuretic screen (surreptitious diuretic abuse)
  • Renin level
  • Cortisol level
  • Aldosterone level
  • TSH, T4
  • D-dimer

• May identify cardiomyopathy or CHF
• Underlying pneumonia

• May identify regional wall motion abnormalities or valvular dysfunction
• Evaluate for conduction disturbances

Differential Diagnosis

• Respiratory alkalosis:
  • It is essential to rule out organic disease prior to diagnosing hyperventilation syndrome or anxiety states
• Metabolic alkalosis:
  • Chloride responsive (urine Cl⁻ <10 mEq/dL):
    • Loss of gastric secretions
    • Chloride-losing diarrhea
    • Diuretics
    • Post (chronic) hypercapnia
    • CF
  • Chloride nonresponsive:
    • Hyperaldosteronism
    • Cushing syndrome
    • Bartter syndrome
    • Exogenous mineralocorticoids or glucocorticoids
    • Gitelman syndrome
    • Hypokalemia
    • Hypomagnesemia
    • Milk–alkali syndrome
    • Exogenous alkali infusion/ingestion
    • Blood transfusions

Initial Stabilization/Therapy

• Early intubation and airway control for altered mental status
• IV, oxygen, and cardiac monitor
• Naloxone, D₅₀W (or Accu-Chek), and thiamine for altered mental status

Ed Treatment/Procedures

• Respiratory alkalosis:
  • Treat underlying disorder
  • Rarely life threatening
  • Sedation/anxiolytics for anxiety, psychosis, or drug overdose
  • Rebreathing mask bag for hyperventilation syndrome (used cautiously)
• Metabolic alkalosis: Examination of the urine chloride allows etiologies to be divided into chloride depletion or nonchloride depletion alkalosis:
  • Urine chloride <10 mEq/L indicates chloride depletion:
    • Assess hydration status to determine therapy
    • Euvolemia/volume overload state treat with potassium chloride infusion
    • Hypovolemia treat with 0.9% saline lowers serum HCO₃⁻ by increasing renal HCO₃⁻ excretion
  • Urine chloride >30 mEq/L indicates nonchloride depletion etiology. Treat underlying disorder:
    • Potassium supplementation in hypokalemic states
    • Antagonism of aldosterone with spironolactone
    • Acetazolamide enhances renal HCO₃⁻ excretion in edematous states
  • Other:
    • Antiemetics for vomiting
    • Proton pump inhibitors for patients with NG suction
    • Follow ventilatory status closely
    • Correct electrolyte abnormalities
    • Consider hemodialysis for severe electrolyte abnormalities

Medication

• Dextrose: D₅₀W 1 amp (50 mL or 25 g; peds: 25% dextrose and water 2–4 mL/kg) IV
• KCl (K-Dur, Gen-K, Klor-Con): 20–120 mEq PO daily
• Naloxone: 2 mg (peds: 0.1 mg/kg) IV/IM initial dose
• Thiamine (vitamin B₁): 100 mg (peds: 50 mg) IV/IM
• 0.1–0.2 N HCl (100–200 mEq/L): Infuse over 24–48 hr at a rate not faster than 0.2 mmol/kg/hr and through a central line to prevent sclerosing vein

Disposition

• ICU admission if:
  • pH >7.55 or altered mental status
  • Dysrhythmias
  • Severe electrolyte abnormalities
  • Hemodynamic instability
• Coexisting medical illness requiring admission

See Also

Acidosis