Author:
Matthew T.Robinson
Catherine D.Parker
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:
- Medications/drugs:
- Endocrine:
- 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 & 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:
- 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
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
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
- AyersC, DixonP. Simple acid-base tutorial . J Parenter Enteral Nutr. 2012;36(1):18-23.
- RiceM, IsmailB, PillowMT. Approach to metabolic acidosis in the emergency department . Emerg Med Clin North Am. 2014;32(2):403-420.
- RobinsonMT, HeffnerAC. Acid base disorders. In: AdamsJ, ed. Emergency Medicine. Philadelphia, PA: Elsevier; 2012.
- SoiferJT, KimHT. Approach to metabolic alkalosis . Emerg Med Clin North Am. 2014;32(2):453-463.
See Also (Topic, Algorithm, Electronic Media Element)
Acidosis