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 1 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 kidneys 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:
- Medications/drugs:
- Progesterone
- Methylxanthines
- Salicylates
- Catecholamines
- Nicotine
- Endocrine:
- Chest stimulation:
- Pulmonary embolism
- Pneumonia
- Pneumothorax
- Other:
- Sepsis
- Hepatic failure
- Heat exhaustion
- Metabolic alkalosis:
- GI loss of H+:
- Vomiting
- Nasogastric (NG) suctioning
- Bulimia
- Antacid therapy
- Chloride-losing diarrhea (villous adenoma)
- Renal loss:
- Diuretics (loop and thiazide)
- Post (chronic) hypercapnia
- Mineralocorticoid excess
- Hyperaldosteronism
- Drug/medication (carbenicillin)
- Glucocorticoid excess (Cushing disease)
- Gitelman syndrome
- Hypercalcemia
- Milk-alkali syndrome
- Low chloride intake
- Bartter syndrome
- Intracellular H+ shift:
- Contraction alkalosis:
- Diuretics
- Sweat loss in CF
- Gastric losses
- HCO3- retention:
- NaHCO3 infusion
- Blood transfusions
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 versus 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:
- More accurate marker than urine Na+ for patients volume status:
- UCl- <20 mEq/L in volume depletion
- UCl- >40 mEq/L in euvolemia or edematous states
- Useful in therapy for determining saline-responsive vs. saline-resistant causes of metabolic alkalosis
Diagnosis Tests & 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/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:
- Saline responsive (urine Cl- <20 mEq/dL):
- Loss of gastric secretions
- Chloride-losing diarrhea
- Diuretics
- Post (chronic) hypercapnia
- CF
- Saline resistant:
- 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 saline-responsive or saline-resistant causes:
- Urine chloride <20 mEq/L indicates volume depletion:
- Rehydration with 0.9% saline lowers serum HCO3- by increasing renal HCO3- excretion
- Saline-responsive causes are associated with volume depletion.
- Urine chloride >20 mEq/L indicates saline-resistant etiology. Treat underlying disorder:
- Potassium supplementation in hypokalemic states
- Antagonism of aldosterone with spironolactone
- Acetazolamide to increase renal HCO3- excretion in edematous states
- Other:
- Infusion of dilute HCl in severe cases of metabolic alkalosis
- 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: 2% 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 or IM initial dose
- Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or 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/h 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
- 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.
- Contraction alkalosis can result from extracellular volume reduction, with a consequent 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.
- Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. 2006;(suppl 9):S86-S96.
- Laski ME, Sabatini S. Metabolic alkalosis, bedside and bench. Semin Nephrol. 2006;26(6):404-421.
- Middleton P, Kely AM, Brown J, et al. Agreement between arterial and central venous values of pH, bicarbonate, base excess and lactate. Emerg Med J. 2006;23(8):622-624.
- Robinson MT, Heffner AC. Acid base disorders. In: Adams J, ed. Emergency Medicine. Philadelphia, PA: Elsevier; 2012.
Codes
ICD9
- 276.3 Alkalosis
- 276.4 Mixed acid-base balance disorder
ICD10
- E87.3 Alkalosis
- E87.4 Mixed disorder of acid-base balance
SNOMED
- 21420006 Alkalosis (disorder)
- 111378004 Respiratory alkalosis