Doctor123.org

Alkalosis, Emergency Medicine

Basics

Description

- Increased alveolar ventilation secondary to: - Disorders causing acidosis - Hypoxemia or - Nonphysiologic stimulation of those receptors by CNS or chest disorders

- 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)

- Intracellular H+ shift: - Contraction alkalosis: - Diuretics - Sweat loss in CF - Gastric losses

- Signs and symptoms secondary to: - Arteriolar vasoconstriction - Hypocalcemia secondary to decreased ionized calcium from increased calcium binding to albumin - Associated hypokalemia - Underlying cause

- 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

- 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

- Metabolic alkalosis: - Saline responsive (urine Cl- <20 mEq/dL): - Loss of gastric secretions - Chloride-losing diarrhea - Diuretics - Post (chronic) hypercapnia - CF

- Respiratory alkalosis: - Treat underlying disorder. - Rarely life threatening - Sedation/anxiolytics for anxiety, psychosis, or drug overdose - Rebreathing mask bag for hyperventilation syndrome (used cautiously)

- 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.

- ICU admission if: - pH >7.55 or altered mental status - Dysrhythmias - Severe electrolyte abnormalities - Hemodynamic instability

  • Respiratory alkalosis:Elevated serum pH secondary to alveolar hyperventilation and decreased PaCO2Hyperventilation occurs through stimulation of 2 receptor types:Central receptors-located in the brainstem and respond to decreased CSF pHChest receptors-located in aortic arch and respond to hypoxemiaIncreased alveolar ventilation secondary to:Disorders causing acidosisHypoxemia orNonphysiologic stimulation of those receptors by CNS or chest disordersRarely 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 infusionLoss of H+ through the GI tract or kidneysShift of hydrogen ions into the intracellular spaceContraction 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 syndromePainAnxiety/psychosisFeverCerebrovascular accident (CVA)CNS infection (meningitis, encephalitis)CNS mass lesion (tumor, trauma)Hypoxemia:Medications/drugs:ProgesteroneMethylxanthinesSalicylatesCatecholaminesNicotineEndocrine:Chest stimulation:Pulmonary embolismPneumoniaPneumothoraxOther:SepsisHepatic failureHeat exhaustion
  • Metabolic alkalosis:GI loss of H+:VomitingNasogastric (NG) suctioningBulimiaAntacid therapyChloride-losing diarrhea (villous adenoma)Renal loss:Diuretics (loop and thiazide)Post (chronic) hypercapniaMineralocorticoid excessHyperaldosteronismDrug/medication (carbenicillin)Glucocorticoid excess (Cushing disease)Gitelman syndromeHypercalcemiaMilk-alkali syndromeLow chloride intakeBartter syndromeIntracellular H+ shift:Contraction alkalosis:DiureticsSweat loss in CFGastric lossesHCO3- retention:NaHCO3 infusionBlood transfusions

Diagnosis

Signs and Symptoms

  • Signs and symptoms secondary to:Arteriolar vasoconstrictionHypocalcemia secondary to decreased ionized calcium from increased calcium binding to albuminAssociated hypokalemiaUnderlying 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 alkalosisEvaluate for hypokalemia and hypocalcemia.
  • BUN/creatinine:Evaluate for renal failure or dehydration.
  • Blood gas (arterial/venous):pHPCO2 decreased in respiratory alkalosisPO2 for hypoxemiaVenous versus arterial blood gaspH-good correlation within 0.03-0.04 unitspCO2-good correlation, although VBG may not correlate with severe shockHCO3-good correlationBase 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 compensationExpected HCO3- decreased by 5 mEq/dL for each 10 mm Hg decrease in PCO2.If HCO3- greater than predicted, concomitant metabolic alkalosisIf HCO3- less than predicted, concomitant metabolic acidosisMetabolic alkalosis:Expected PCO2 = 0.9 [HCO3-] + 9If PCO2 greater than predicted, concomitant respiratory acidosisIf 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 depletionUCl- >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 sepsisLFT for hepatic failureAspirin levelUrine toxicology screenUrine diuretics screen (bulimia)Urine diuretic screen (surreptitious diuretic abuse)Renin levelCortisol levelAldosterone levelTSH, T4d-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 secretionsChloride-losing diarrheaDiureticsPost (chronic) hypercapniaCFSaline resistant:HyperaldosteronismCushing syndromeBartter syndromeExogenous mineralocorticoids or glucocorticoidsGitelman syndromeHypokalemiaHypomagnesemiaMilk-alkali syndromeExogenous alkali infusion/ingestionBlood 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 threateningSedation/anxiolytics for anxiety, psychosis, or drug overdoseRebreathing 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- excretionSaline-responsive causes are associated with volume depletion.Urine chloride >20 mEq/L indicates saline-resistant etiology. Treat underlying disorder:Potassium supplementation in hypokalemic statesAntagonism of aldosterone with spironolactoneAcetazolamide to increase renal HCO3- excretion in edematous statesOther:Infusion of dilute HCl in severe cases of metabolic alkalosisAntiemetics for vomitingProton pump inhibitors for patients with NG suctionFollow 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 statusDysrhythmiasSevere electrolyte abnormalitiesHemodynamic 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