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.

Authors

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