BASICS
- A disruption of acid–base homeostasis producing decreased H+ concentration, which is reflected by alkalemia (increased blood pH) and high plasma HCO3–
- Normal plasma HCO3– concentration is ≅24 mEq/L
- Normal blood pH ranges from 7.35 to 7.45
- Hypoventilation should increase CO2 concentrations to lower pH; however, respiratory compensation is limited once hypoxemia develops
- The kidney normally is capable of responding to a high pH by excreting HCO3– into the urine. Metabolic alkalosis persists only when renal excretion of HCO3– is impaired or reabsorption is enhanced
- Excessive loss of H+, retention of HCO3–, and contraction of extracellular fluid volume without loss of HCO3– (i.e. contraction alkalosis) are the common mechanisms that initiate metabolic alkalosis
- Respiratory
- Chemoreceptors sense high pH in blood or cerebrospinal fluid and depress ventilation to decrease removal of CO2
- Cardiovascular
- Cardiac arrhythmias
- Arteriolar vasoconstriction
- Decreased coronary and cerebral blood flow caused by vasoconstriction
- Metabolic
- Increased affinity of O2–hemoglobin binding, which inhibits release of O2 to the tissues
- Decreased ionized Ca2+ concentration
- Renal
- The kidney responds to high pH by excreting HCO3–
- Gastrointestinal loss of H+ and Cl– is seen with gastric reflux that occurs with anterior enteritis and ileus
- Salivary loss of Cl– (e.g. ptyalism, dysphagia, esophageal trauma/obstruction)
- Cl– loss is seen with excessive sweating (e.g. endurance event) and diuretic therapy (furosemide). Equine sweat contains large amounts of Cl– and K+; fluid loss can be extreme with moderate intensity exercise, especially in warm, humid conditions
- K+ depletion is associated with anorexia, renal failure, and diuretic therapy (acetazolamide)
- Iatrogenic HCO3– therapy in racehorses
- Hypoalbuminemia since proteins are weak acids
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS