Alkalosis

Alkalosis refers to a condition reducing hydrogen ion concentration of arterial blood plasma (alkalemia) through the loss of acids or retention of bicarbonate. Generally alkalosis is said to occur when pH of the blood exceeds 7.45. The opposite condition is acidosis.

More specifically, alkalosis can refer to:

• Respiratory alkalosis
• Metabolic alkalosis

The main cause of respiratory alkalosis is hyperventilation, resulting in a loss of carbon dioxide. Compensatory mechanisms for this would include increased dissociation of the carbonic acid buffering intermediate into hydrogen ions, and the related consumption of bicarbonate, both of which would lower blood pH.

Metabolic alkalosis can be caused by prolonged vomitting, resulting in a loss of hydrochloric acid with the stomach content. Severe dehydration, and the consumption of alkali are other causes. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase serum carbon dioxide, a condition leaning toward respiratory acidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and visa versa, a delicate balance is created between these two conditions.

• Administration of citrates
• After respiratory acidosis
• Alkali therapy for stomach problems
• Bartter’s Syndrome
• Conn syndrome
• Cushing’s Syndrome
• Cystic Fibrosis
• Diarrhea
• Gastric juice drainage
• Hepatic coma
• Hyperemesis gravidarum
• Milk Alkali Syndrome
• Mineralcorticoid therapy
• Overcorrection of acidosis with bicarbonates
• Renal potassium loss
• Vomiting

It is thought that metabolic [alkalosis] is the result of the shift of hydrogen ions intracellularly, reduced blood volume, loss of gastric acid, and extracellular volume expansion.

• Electrolyte imbalance like hypokalemia causes a shift of hydrogen ions intracellular caused defect of protons and an increase in bicarbonate ion concentration. ^[1]

• Volume depletion results in reduced glomerular filtration rate. This stimulates the production of Angiotensin II, sympathetic nervous system activation, and aldosterone secretion.
• The sympathetic nervous system and angiotensin II causes increased absorption of sodium in proximal convoluted tubules via sodium hydrogen exchange.
• Aldosterone acts primarily on the principal cells of the late distal convoluted tubule and collecting ducts. It causes sodium and water retention in exchange for potassium and hydrogen ions secretion. The loop and thiazide diuretics also act by similar mechanisms of action.^[2]

• The hydrogen ions are primarily secreted in large amounts in the gastric juice. The hydrogen ions are secreted via active transport mediated by hydrogen potassium ATPase pump. Excessive vomiting causes loss of a large amount of gastric juice with depletion of hydrogen and chloride from the body.

• Primary hyperaldosteronism (Conn’s syndrome) causes increased sodium reabsorption with the resultant increase in extracellular volume. The patient may be hypertensive or normotensive. The hypokalemia caused by the action of aldosterone causes increased reabsorption of sodium bicarbonate in the proximal convoluted tubule with a worsening of metabolic alkalosis.

• It is thought that the respiratory alkalosis is the result of hyperventilation. The causes of hyperventilation can be due to increased stimulation of the medullary respiratory center, low oxygen tension in blood, lung pathologies, and iatrogenic. The stimulation of the respiratory center occurs due to stroke, head injury, metabolic disease like hyperthyroidism, emotional stress, panic attack, and side effect of medications like aspirin. The low oxygen tension in the blood causes stimulation of the respiratory center resulting in hyperventilation and hypocapnia. The acute attack of asthma, COPD, pulmonary embolism can cause tachypnea with increase loss of carbon dioxide.

• The prevalence of alkalosis ranges from 32,727 to 80,000 per 100,000 in hospitalized patients with an acid-base metabolic disorder. ^[3][4]
• The prevalence of alkalosis is approximately 44,046 per 100,000 in acute heart failure patients. ^[5]

Differential diagnosis of metabolic alkalosis is as follow:

Differential diagnosis of respiratory alkalosis is as follow: