Alkalosis is a condition where the blood pH is elevated above the normal range of 7.35 to 7.45, indicating an abnormally high level of alkalinity. This imbalance, characterized by too much base or not enough acid, is categorized as either respiratory or metabolic. Contraction alkalosis is a specific type of metabolic alkalosis, involving a disruption of the chemical base bicarbonate in the body’s fluid systems. The condition is characterized by a significant reduction in the volume of the extracellular fluid, such as the fluid surrounding cells and in the bloodstream. This volume depletion drives the resulting increase in blood alkalinity.
The Physiological Mechanism
Contraction alkalosis begins with the loss of fluid that is poor in bicarbonate but rich in sodium and chloride. Since the total amount of bicarbonate remains stable, this fluid loss effectively concentrates the bicarbonate within the remaining, smaller volume of extracellular fluid. This concentration effect is the core mechanism of the condition.
The body registers this fluid loss as a reduction in effective circulating volume, signaling the kidney to initiate compensatory mechanisms to retain water and salt. The Renin-Angiotensin-Aldosterone System (RAAS) is activated, increasing levels of angiotensin II and aldosterone. Angiotensin II acts on the proximal tubule, stimulating the reabsorption of sodium, which is often paired with bicarbonate reabsorption, thereby worsening the alkalosis.
Aldosterone acts on the collecting ducts, promoting sodium reabsorption while simultaneously increasing the secretion of hydrogen and potassium ions into the urine. The loss of hydrogen ions directly raises the blood pH, contributing to the alkalosis. The accompanying loss of chloride ions also plays a significant role in maintaining the elevated bicarbonate level.
Chloride depletion makes it difficult for the kidney to excrete excess bicarbonate because chloride is needed for the specialized chloride-bicarbonate exchanger in the renal tubules. Without sufficient chloride, the kidney cannot effectively swap bicarbonate into the urine, forcing the body to retain the alkali. The combination of volume loss and renal retention mechanisms due to chloride and volume deficits allows the alkalosis to persist.
Common Causes of Volume Depletion
The primary triggers for contraction alkalosis involve processes causing a disproportionate loss of fluid and chloride. Diuretic medications are the most frequent cause observed in clinical practice, particularly loop diuretics (like furosemide) and thiazide diuretics. These drugs interfere with the kidney’s ability to reabsorb sodium and chloride, leading to a large output of salt and water in the urine.
The resulting volume loss activates the kidney’s attempt to conserve fluid, including mechanisms that inadvertently retain bicarbonate. Severe vomiting or gastric suctioning similarly leads to a direct loss of highly acidic gastric secretions, which are rich in hydrogen chloride. This loss of acid generates alkalosis, and the accompanying volume loss triggers the renal mechanisms that maintain the condition.
Gastrointestinal losses often include potassium loss, which further supports the kidney’s retention of bicarbonate. Another cause involves patients recovering from chronic hypercapnia, an elevated level of carbon dioxide in the blood. The body initially develops a compensatory metabolic alkalosis to balance the high acid load from the carbon dioxide.
When the respiratory issue is corrected, the carbon dioxide level drops rapidly, but the kidney’s ability to excrete the accumulated bicarbonate can be impaired. If volume depletion or chloride deficit is present, the existing metabolic alkalosis becomes maintained. This post-hypercapnic state is a distinct cause where the kidney is slow to eliminate the unnecessary bicarbonate, especially if the patient is volume-contracted.
Symptoms Diagnosis and Complications
Symptoms of contraction alkalosis are often vague and subtle, especially in mild cases. Patients may experience generalized muscle weakness, fatigue, muscle cramping, and irritability. Severe alkalosis can cause specific neurological signs, including numbness or tingling sensations (paresthesias), particularly around the mouth, hands, and feet.
Diagnosis begins by recognizing the clinical setting, such as a patient using high-dose diuretics or experiencing persistent vomiting. Laboratory testing confirms the acid-base disorder, starting with an arterial blood gas analysis showing an elevated blood pH and high plasma bicarbonate concentration. A basic electrolyte panel typically reveals hypokalemia (low serum potassium level), which commonly co-exists with this condition.
Hypochloremia (low chloride concentration in the blood) is a hallmark of contraction alkalosis and confirms the diagnosis. Measuring the chloride concentration in a urine sample helps determine if the cause is renal or extrarenal. If left uncorrected, severe alkalosis can lead to serious complications due to the profound impact of high pH on the body’s systems.
The reduced level of ionized calcium accompanying severe alkalosis can lead to tetany, characterized by prolonged, painful muscle spasms. Extremely high pH levels affect the central nervous system, potentially causing confusion, delirium, stupor, and seizures. The condition can also predispose a person to cardiac arrhythmias, which are dangerous disturbances in the heart’s electrical rhythm.
Treatment and Correction Strategies
The goal of treatment is to interrupt the cycle of volume depletion and bicarbonate retention. Since the alkalosis is maintained by fluid and chloride deficits, the primary intervention involves administering an intravenous solution containing sodium chloride (normal saline). This fluid replacement corrects the underlying volume deficit, which reduces the activity of the RAAS.
The infusion of chloride is important because it provides the necessary anion for the kidney to excrete the accumulated bicarbonate. Raising the chloride level prevents the kidney from being forced to reabsorb bicarbonate, restoring the normal function of the chloride-bicarbonate exchanger. Adequate chloride delivery effectively reverses the renal mechanism maintaining the high blood pH.
Because low potassium levels frequently accompany this alkalosis, potassium replacement is an integral part of the correction strategy. Potassium is often added to the intravenous saline solution to correct hypokalemia and normalize the acid-base balance. In severe or life-threatening cases where the blood pH is extremely high, direct administration of dilute acid, such as hydrochloric acid, may be necessary to rapidly restore balance.