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:
    • Defined by arterial pH >7.45 and HCO3− >30 mmol/L
    • Primary increase in serum HCO3– are secondary to loss of H+, increase of HCO3– production or decrease in HCO3− excretion
      • Gain of alkali through ingestion or infusion
      • Loss of H+ through the GI tract or kidneys
      • Intracellular shift of H+
      • Contraction of extracellular fluid (ECF) volume with loss of HCO3−
    • A constant impairment of renal regulation of HCO3− must be present for metabolic alkalosis to persist
  • Renal maintenance is required to sustain a metabolic alkalosis secondary to the kidney’s enormous ability to excrete HCO3–. This occurs through:
    • Decreased glomerular filtration rate (GFR) (renal failure, ECF depletion)
    • Elevated tubular reabsorption of HCO3– secondary to hypochloremia, hyperaldosteronism, hypokalemia, ECF depletion
  • Mortality of 45% if pH >7.55 and 80% if pH >7.65

Etiology

  • Respiratory alkalosis:
    • CNS:
      • Hyperventilation syndrome
      • Pain
      • Anxiety/psychosis
      • Fever
      • Increased intracranial pressure
    • Hypoxemia:
      • Altitude
      • Anemia
      • Ventilation-perfusion mismatch
    • Medications/drugs:
      • Progesterone
      • Methylxanthines
      • Salicylates
      • Catecholamines
      • Nicotine
      • Caffeine
    • Endocrine:
      • Hyperthyroidism
      • Pregnancy
    • Pulmonary:
      • Pulmonary embolism
      • Pneumonia
      • Pneumothorax
      • Asthma
      • Iatrogenic secondary to mechanical ventilation
    • Other:
      • Sepsis
      • Hepatic failure
      • Heat exhaustion
  • Metabolic alkalosis:
    • Chloride depletion:
      • GI losses:
        • Vomiting
        • Nasogastric (NG) suctioning
        • High-output ileostomy loss
        • Chloride-losing diarrhea
      • Renal loss:
        • Diuretics (loop and thiazide)
        • Post (chronic) hypercapnia
        • Drug/medication (carbenicillin)
        • Gitelman and Bartter syndrome
        • Low chloride intake
    • 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
    • Hypokalemia
    • Hypomagnesemia
    • Underlying cause
  • Altered mental status
  • Arrhythmias
  • Carpal–pedal spasm
  • Chvostek sign
  • Dehydration
  • Hypoxemia
  • Myalgias
  • Perioral tingling/numbness
  • Seizures
  • Tetany
  • Trousseau sign
  • Weakness

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 >7.45
    • PCO2 decreased in respiratory alkalosis
    • PO2 for hypoxemia
    • Venous vs. arterial blood gas:
      • pH – venous pH is 0.003–0.004 less than arterial pH
      • 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:
    • Examination of the urine chloride allows etiologies to be divided into chloride depletion or nonchloride depletion alkalosis:
      • UCl– <20 mEq/L in chloride responsive metabolic alkalosis
      • UCl– >20 mEq/L in chloride nonresponsive metabolic alkalosis
  • Mineralocorticoid assessment:
    • Plasma renin, aldosterone, cortisol levels

Diagnostic Tests And Interpretation

Lab

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

Imaging

CXR:

  • May identify cardiomyopathy or CHF
  • Underlying pneumonia

Diagnostic Procedures/Surgery

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:
      • Vomiting
      • Loss of gastric secretions/NG suctioning
      • Laxative use
      • Villous adenoma
      • Congenital chloridorrhea
      • Diuretics
      • Post (chronic) hypercapnia
      • CF
      • Bartter or Gitelman syndrome
    • Chloride nonresponsive:
      • Primary hyperaldosteronism
      • Rental artery stenosis
      • Renin-secreting tumor
      • Cushing syndrome
      • Exogenous mineralocorticoids or glucocorticoids
      • Liddle syndrome
    • Other:
      • Hypokalemia
      • 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 and respiratory failure
  • 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:
    • Urine chloride <20 mEq/L indicates chloride depletion etiology. Assess hydration status to determine therapy
      • Euvolemic/volume overload state: treat with potassium chloride infusion
      • Hypovolemic state: treat with 0.9% NaCl
    • Urine chloride >20 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 or H2 blocker 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

Follow-Up

Disposition

Admission Criteria

  • ICU admission if:
    • pH >7.55 or altered mental status
    • Dysrhythmias
    • Severe electrolyte abnormalities
    • Hemodynamic instability
  • Admit if coexisting medical illness require further management

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:
    • Normal pH with abnormal PCO2 or HCO3–
    • HCO3– and PCO2 move in opposite directions
    • pH changes in the direction opposite that expected from a known primary disorder

Additional Readings

  1. Arena A, Miller E. Respiratory Acid-Base Disorders. Emerg Med Clin North Am. 2023;41(4):863–875.  [PMID:37758429]
  2. Ayers C, Dixon P. Simple acid-base tutorial. J Parenter Enteral Nutr. 2012;36(1):18–23.
  3. Lents S, Ackil D. Metabolic -Acid Base Disorders. Emerg Med Clin North Am. 2023;41(4):849–862.
  4. Rice M, Ismail B, Pillow MT. Approach to metabolic acidosis in the emergency department. Emerg Med Clin North Am. 2014;32(2):403–420.  [PMID:24766940]
  5. Robinson MT, Heffner AC. Acid base disorders. In: Adams J, ed. Emergency Medicine. Elsevier; 2012.
  6. Soifer JT, Kim HT. Approach to metabolic alkalosis. Emerg Med Clin North Am. 2014;32(2):453–463.  [PMID:24766943]

See Also (Topic, Algorithm, Electronic Media Element)

Acidosis

Authors

Matthew T. Robinson

Catherine D. Parker

Tarrin K. Casey