Alkalosis

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List of terms related to Alkalosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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.

Classification

More specifically, alkalosis can refer to:

• Respiratory alkalosis
• Metabolic alkalosis

Causes

Common Causes

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.

Metabolic Alkalosis

• 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

Pathophysiology

Metabolic Alkalosis

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.

Shift of hydrogen ions intracellularly

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

Reduced Blood volume

• 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.

Loss of Gastric acid

• 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.

Extracellular volume expansion

• 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.

Respiratory 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.

Epidemiology and Demographics

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

Differential Diagnosis

Differential diagnosis of metabolic alkalosis is as follow:

Disease		Clinical						Paraclinical												Gold standard diagnosis	Other findings
		Symptoms			Signs			Lab data
								ABG			Chemistry					Enzyme	Renal function
		fatigability	Muscle weakness	Muscle paresthesia	Cardiac arrythmia	Hypotension	Dehydration	HCO3−	paCO2	O2	Cl−	K+	Na+	Ca+	Mg+	Renin	Bun	Cr	Urine Cl−
Vomiting		+	+	+	-	+	+	↑	↑	Nl	↓	↓	↑	Nl	Nl	↑	Nl to ↑	Nl	↓	Clinical manifestations	Not applicable
Nasogastric tube suction		+	+	+	-	+	+	↑	↑	Nl	↓	↓	↑	Nl	Nl	↑	Nl to ↑	Nl	↓	Clinical manifestations	GERD Pulmonary aspiration
Chronic laxative abuse		+	−	−	-	+	+	↑	↑	Nl	↓	↓	↓	↓	↓	↓	Nl to ↑	Nl	↓	Medication history	Abdominal cramps, large volume diarrhea
Villous adenoma		+	+	+	+	+	+	↑	↑	Nl	↓	↓	↓	↓	↓	↑	Nl to ↑	Nl	↑	Colonoscopy	Metabolic acidosis
Loop diuretics		+	±	-	-	+	−	↑	↑	Nl	↓	↓	↓	↓	↓	↑	↑	↑	↑	Medication history	Not applicable
Thiazide diuretics		+	±	-	-	+	−	↑	↑	Nl	↓	↓	↓	↑	↓	↑	↑	↑	↑	Medication history	Not applicable
Renal artery stenosis		−	+	+	+	↑	+	↑	↑	↓	↓	↑	↓	↑	Nl	↑	↑	↑	Nl	Clinical manifestations+ imaging	Chronic kidney disease Acute rise in Cr following ACEIs or ARBs
Liddle syndrome		−	−	−	−	↑	+	↑	↑	Nl	↓	↓↓	↓	Nl	↓	↑	Nl	Nl	Nl	Genetic testing	Not applicable
Cushing's syndrome		−	−	+	−	↑	+	↑	↑	Nl	↓	↑	↓	↑	Nl	↓	↑	↑	Nl	24−hour urinary cortisol excretion + low−dose dexamethasone suppression test	Obesity Lethargy Hirsutism Menstrual changes
Primary hyperaldosteronism		−	−	+	−	↑	+	↑	↑	Nl	↓	Nl to ↓	↓	↑	Nl	↓	↑	↑	Nl	Lab findings	Resistant HTN Aldosterone−producing adenomas Bilateral adrenal hyperplasia
Cystic fibrosis		−	+	−	+	↓	+	↑	↑	Nl	↓	↓	Nl	Nl	Nl	↑	Nl to ↑	Nl	↑	Genetic testing	Fatigue Persistent pulmonary infection Pancreatic insufficiency

Differential diagnosis of respiratory alkalosis is as follow:

Disease		Clinical						Paraclinical												Gold standard diagnosis	Other findings
		Symptoms			Signs
								ABG			CBC					Imaging	PFTs
		Dyspnea on exertion	Orthopnea	Cough	Chest pain	Agitation	loss of consciousness References Template:GoldBookRef