Blood Gas of the Week #23 – Metabolic Alkalosis Part 3: Clinical Implications and Management
Now that we have covered the generation and maintenance of a metabolic alkalosis, let’s talk about what happens to the body as a result of metabolic alkalosis. The most clinically relevant effects occur in the cardiovascular, respiratory, and central nervous systems. If you haven’t already read Metabolic Alkalosis Part 1 and Part 2, check them out first then come back here to finish up the discussion.
Cardiovascular and Respiratory Effects
Many of the effects of a severe metabolic alkalosis on the heart were studied in the 1960s using dogs and then extrapolated to humans – particularly convenient for small animal practitioners. Metabolic alkalosis alters coronary blood flow, glucose utilization, lactate and pyruvate utilization, is pro-arrhythmic, and reduces myocardial contractility. It also shifts the oxygen-hemoglobin dissociation curve to the left which impairs oxygen-offloading at the tissues. Because the compensatory response to a metabolic alkalosis is to decrease ventilation (compensatory respiratory acidosis), in severe cases hypoxemia may occur, further complicating the tissue oxygen status. Hypoventilating patients get small areas of atelectasis, and because the alkalosis impairs the normal hypoxic-pulmonary vasoconstriction reflex the hypoxemia is worsened by the ventilation-perfusion mismatch.
Central Nervous System Effects
In addition to the effects on the CNS as a result of the cardiovascular and respiratory effects above, metabolic alkalosis causes decreased cerebral blood flow and neuromuscular excitability. The patient may become confused, dysphoric, or obtunded. A low ionized calcium may occur in severe metabolic alkalosis (albumin gives up hydrogen ions and calcium binds to the albumin in place of hydrogen during alkalemia) further contributing to the neuromuscular excitability.
Treatment
As with most things the solution is to treat the underlying problem – eliminate the pyloric outflow obstruction, stop the diuretics, etc. To be successful we need to treat both the initiating process (if still present) and the maintaining process. This means in addition to eliminating then pyloric obstruction or stopping the diuretics, we need to correct hypokalemia, hypochloremia, etc (see metabolic alkalosis parts 1 & 2 for discussion of maintaining processes). So:
- Correct the initiating process (remove the pyloric outflow obstruction, stop the diuretics, etc)
- Correct the deficiencies that are preventing excretion of bicarbonate (give chloride, water, and potassium)
- Correct hypovolemia/expand the extracellular fluid compartmant – 0.9% saline, +/- KCl, +/- Mg++ (depending on serum potassium and magnesium respectively) will be the best fluid choice in most cases
- If the diagnosis isn’t obvious consider measuring urine chloride (low = probably have Cl- deficit and need to supplement chloride; high = probably have adrenocortical excess and probably need K+ replacement)
- Provide supportive care (antiemetics, pain control, oxygen supplementation, etc)
