Topic: Acid-Base Balance
Next Unit: Respiratory Acidosis
14 minute read
Metabolic Alkalosis--a condition in which the body produces too much bicarbonate, raising to pH to a level above normal.
Causes of Metabolic Alkalosis
- Loss of hydrogen ions from the gastrointestinal tract (loss of gastric secretions) or in the urine.
- Hydrogen ion movement into cells, which increases bicarbonate.
- Increased serum bicarbonate concentration from alkali administration.
- Extracellular fluid volume contraction around a relatively constant amount of extracellular bicarbonate, as with dehydration.
Most patients with normal volume and adequate renal function can excrete excess bicarbonate in the urine. For metabolic alkalosis to persist, there must be enough kidney dysfunction to reduce the excretion of excess bicarbonate into the urine.
Loss of gastric secretions or H+ ions in the urine: the most common causes of metabolic alkalosis.
Gastric contents usually have a high concentration of hydrogen chloride. In the intestines, the hydrogen and bicarbonate ions combine to form carbonic acid and water, and the secreted chloride, sodium, and potassium ions are reabsorbed into the systemic circulation.
With vomiting or nasogastric tube suction, HCl is removed from the body, so it doesn't reach the duodenum--subsequent secretion of bicarbonate into the more distal gastrointestinal lumen is not neutralized.
Note: diarrhea, on the other hand, loses mainly alkali, causing metabolic acidosis:
- N&V causes alkalosis;
- diarrhea causes acidosis.
Diuretics that block sodium chloride reabsorption (thiazides and loop diuretics) increase urine chloride concentration but then the concentration falls when the diuretic effect has dissipated. This can cause wide swings in the urine chloride concentration from day to day, and this back-and-forth can only be caused by diuretic use.
Gastrointestinal and renal hydrogen loss is usually accompanied by the loss of chloride and potassium, resulting in hypochloremia and hypokalemia.
CAVEAT: Blowing off too much CO2, as in hyperventilation, is respiratory alkalosis. When there is not enough CO2 in the blood, the body uses bicarb to compensate for the lack of respiratory acid. (Metabolic compensation of a respiratory alkalosis.)
Chloride-responsive and Chloride-unresponsive Metabolic Alkalosis
Metabolic alkalosis can be either chloride-responsive or -resistant:
Chloride-responsive: involves loss or excess secretion of Cl; it typically corrects with IV administration of NaCl-containing fluid.
Chloride-responsive metabolic alkalosis can be caused by
- vomiting (which causes the loss of hydrochloric acid (HCl), causing the kidneys to retain sodium, leading to alkalosis),
- congenital chloride diarrhea (causes alkalosis instead of normal acidic response),
- dehydration that causes contraction alkalosis (triggering the renin-angiotensin-aldosterone system to stimulate reabsorption of sodium and water in the kidneys, while causing the kidneys to excrete hydrogen ions and retain bicarbonate—causing alkalosis),
- loop diuretics and thiazides, and
- posthypercapnia (hypoventilation causes hypercapnia and its associated respiratory acidosis--that is reversed by the kidneys but with excess bicarbonate release, seen after the carbon dioxide levels from hypoventilation return to base line, thus causing alkalosis.)
Chloride-unresponsive: (AKA "chloride-resistant") alkalosis does not correct with NaCl-containing fluids, and typically involves severe magnesium and/or potassium deficiency or mineralocorticoid excess.
Chloride-resistant metabolic alkalosis can be caused by retention of bicarbonate:
- the shift of hydrogen ions into the intracellular space (as in hypokalemia--low K+) or
- an excess of bicarbonate or antacid medications (milk-alkali syndrome),
- hyperaldosteronism (mineralocorticoid excess).
Renal loss of hydrogen ions caused by excess aldosterone increasing the activity of a sodium-hydrogen exchange in the kidney, increasing the retention of sodium ions, and pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume, and the loss of hydrogen ions causes metabolic alkalosis.
Signs and symptoms related DIRECTLY to metabolic alkalosis are uncommon.
On the other hand, while direct symptoms from metabolic alkalosis are uncommon, respiratory alkalosis causes a cluster of symptoms called Hyperventilation syndrome: dyspnea, dizziness, chest pain, paresthesias, palpitations, and carpopedal spasm.
Signs and Symptoms that do present are related to the underlying cause of the alkalosis. For example, dehydration that causes metabolic alkalosis can cause
- muscle cramping (prolonged muscle spasms and/or twitching, hand tremor),
- cardiac arrhythmias
- bradypnea (to retain carbon dioxide),
- nausea, and
- numbness, .
In severe cases,
- difficulty breathing,
More severe alkalemia increases protein binding of ionized calcium (Ca++), leading to hypocalcemia and subsequent headache, lethargy, and neuromuscular excitability, sometimes with delirium, tetany, and seizures.
Alkalemia also lowers threshold for anginal symptoms and arrhythmias. Concomitant hypokalemia (low K+) may cause weakness.
The most common causes of metabolic alkalosis are
- vomiting or nasogastric suction and
- diuretic therapy.
These are usually apparent from the history. Besides vomiting and diuretics, taking too much alkali by self-administering too much antacid can cause the "milk-alkali syndrome."
- laxative abuse,
- DKA Kussmaul respiration (deep and fast breathing--the body is trying to compensate for its metabolic acidosis by producing a respiratory alkalosis on purpose.);
Treatment of metabolic alkalosis is based on treating the cause and includes:
- medications (acetazolamide--promotes NaCl and NaHCO3 loss),
- hydrochloric acid (HCl) infusion,
- treating symptoms; and by
- treating it via its respiratory connection: decrease rate and depth of ventilations. (Calm them down or stop bagging so fast. and their CO2 will climb, which is the "respiratory acid.")
In the field, your most likely exposure to metabolic alkalosis will be via severe nausea and vomiting, dehydration (contraction alkalosis), milk-alkali syndrome, overcompensation for a triggering hypoventilation (COPD), and misuse of diuretics. Therefore, your role is in support which includes maintenance of ABC (airway, breathing, circulation), IV access, and comfort measures during transport.