Alkalosis

Basics

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

Diagnosis

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

Lab
  • 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

Imaging
CXR:
  • May identify cardiomyopathy or CHF
  • Underlying pneumonia

Diagnostic Procedures/Other
ECG:
  • 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

Treatment

Initial Stabilization/Therapy

Airway, breathing, circulation (ABCs):
  • 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

Ongoing Care

Disposition

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

Discharge Criteria
Resolving or resolved alkalosis

Pearls and Pitfalls

  • Increased minute ventilation is the primary cause of respiratory alkalosis, characterized by decreased PaCO2 and increased pH:
    • Metabolic alkalosis is usually caused by an increase in HCO3, reabsorption secondary to volume, potassium, or Cl loss
    • Traditional thinking was alkalosis was divided into contraction and noncontraction alkalosis; however, new literature suggests it is really a chloride depletion or nonchloride depletion alkalosis resulting in the increase in the plasma HCO3 concentration
    • Clues to the presence of a mixed acid–base disorder are normal pH with abnormal PCO2 or HCO3, when the HCO3 and PCO2 move in opposite directions, or when the pH changes in the direction opposite that expected from a known primary disorder

Additional Reading

  • Ayers C, Dixon P. Simple acid-base tutorial. J Parenter Enteral Nutr. 2012;36(1):18–23.
  • Rice M, Ismail B, Pillow MT. Approach to metabolic acidosis in the emergency department. Emerg Med Clin North Am. 2014;32(2):403–420.
  • Robinson MT, Heffner AC. Acid base disorders. In: Adams J, ed. Emergency Medicine. Philadelphia, PA: Elsevier; 2012.
  • Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin North Am. 2014;32(2):453–463.

See Also

Acidosis

Authors

Matthew T. Robinson
Catherine D. Parker


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