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Hypercalcemia and vitamin D excess increases proximal renal HCO 3 — reabsorption. Vomiting and some forms of chloride-containing diarrhea cause proton loss and subsequent HCO 3 — generation.
ECF volume contraction and hypokalemia maintain metabolic alkalosis once it has been initiated. In the process a gain in HCO 3 — with each proton secreted occurs, causing metabolic alkalosis.
The process is maintained in the presence of activation of the renin-angiotensin-aldosterone system which increases both proximal and distal nephron bicarbonate reabsorption. Hence, this condition is different from alkalosis induced by diuretics, which is sensitive to effects of dietary NaCl intake.
Chronic diuretic use would lead to metabolic alkalosis, particularly on a low NaCl diet. Hypokalemia adds to net acid excretion and increases ammoniagenesis perpetuating the severity of metabolic alkalosis. Factors that act to maintain a sustained metabolic alkalosis are further discussed below. Hypokalemia causes a decline in intracellular pH in renal tubular epithelial cells resulting in increased proximal tubular HCO 3 — reabsorption.
Renal ammoniagenesis is increased and net acid excretion by the kidneys is increased. These pathophysiologic processes perpetuate metabolic alkalosis.
This is the most common scenario seen in clinical practice. Volume depleted patients excrete less HCO 3 — than volume replete or volume expanded patients. Volume depletion decreases GFR and results in stimulation of the renin-angiotensin-aldosterone axis. Increased catecholamines and angiotensin II levels increase HCO 3 — absorption in proximal and distal nephron. Increased angiotensin II or aldosterone activity increases net acid excretion in the distal nephron. Hence, pure mineralocorticoid excess causes metabolic alkalosis that is different from gastric or diuretic induced alkalosis due to a volume expanded state.
This limits renal capacity to excrete a bicarbonate load. Primary aldosteronism, Cushing syndrome or licorice ingestion present with this abnormality. This condition is not commonly encountered in clinical practice. It does not play a major role in sustaining chronic metabolic alkalosis in common clinical practice. The majority of metabolic alkalosis episodes are mild and self-limiting.
Systemic alkalosis lowers the threshold for arrhythmia especially by decreasing ionized calcium levels. It causes vasoconstriction in various systemic vascular beds and manifests with masquerading CNS and peripheral nervous system symptoms.
Patients have increased predisposition for seizures and metabolic encephalopathy due to hypocalcemia. Many patients have accompanying hypokalemia and present with muscular cramps.
Hypoxemia is never clinically severe. Tissue delivery of oxygen is reduced due to the greater oxygen affinity of hemoglobin. As a result, it facilitates anaerobic respiration with a slight increase in lactate production and high anion gap commonly seen in severe metabolic alkalosis.
Albumin has higher electronegativity with increased arterial pH adding to the elevated anion gap. Digitalis toxicity is increased in alkalemic patients due to concomitant hypocalcemia and hypokalemia. Metabolic alkalosis is first noticed by the clinician when HCO 3 — is elevated on serum chemistries. Note that patients on dialysis without renal function develop metabolic alkalosis only from alkali load and do not demonstrate elevated HCO 3 — with elevations in PaCO 2.
Arterial blood gas ABG analysis can differentiate between these two conditions. Sometimes, chronic obstructive pulmonary disease COPD patients on diuretics can have mixed acid-base disturbances.
Some examples are as follows:. COPD can cause an elevation of bicarbonate due to CO 2 retention and diuretics can cause contraction alkalosis: pH — 7.
Typically, bicarbonate rises 0. Cirrhotics on diuretics can have respiratory alkalosis and metabolic alkalosis: pH — 7. Typically, pure respiratory alkalosis would cause a decline in HCO 3 — 0. Uremic patients with vomiting can have combined metabolic acidosis and metabolic alkalosis: pH — 7. A patient with chronic alcohol abuse that has been vomiting may have: pH — 7. If this patient develops ketoacidosis, pH may drop to 7.
You should take a careful history and physical exam in order to provide clues into initiating and maintenance factors for metabolic alkalosis. Table I. Medication use especially diuretics, laxative use and alkali intake, as well as ingestion of licorice. Family history should be sought regarding hypertension and electrolyte abnormalities to suggest inherited disorders such as Bartter and Liddle syndromes.
GI symptoms of vomiting or diarrhea can explain metabolic alkalosis. Certain villous adenomas may be chloride secreting. Other diseases: obstructive sleep apnea, cirrhosis, COPD, cystic fibrosis also can be associated with mixed acid-base disturbances. One must also be cognizant of blood transfusions. On physical examination it is very important to assess hypertension, signs of Cushing syndrome, volume status and other co-morbid conditions as mentioned in Table I.
An orthostatic decrease in blood pressure and increase in heart rate, sunken eye balls, decreased skin turgor and thirst are signs of ECF volume depletion. Cushing syndrome would be suggested by signs of hypercortisolism such as moon facies, buffalo hump, striae and hypertension.
After taking a detailed history and performing a physical examination, one should next order laboratory studies. One should start with serum chemistries including calcium, magnesium and phosphorus levels.
Low chloride and low potassium levels are common occurrences in patients with metabolic alkalosis. One should look for an anion gap as a small anion gap can be seen in severe metabolic alkalosis for reasons discussed earlier. High calcium levels should point towards milk alkali syndrome or hypercalcemia from other causes.
Magnesium depletion may be seen with diuretic use or renal tubular magnesium wasting. Low phosphorus concentration could be present in patients recovering from diabetic ketoacidosis or starvation ketoacidosis. Arterial blood gases may be obtained to rule out mixed disorders and chronic respiratory acidosis. You should look at the urinalysis to assess urinary pH. Alkaline urine would be an appropriate response from the kidneys trying to excrete excess HCO 3 —.
Volume depleted patients would have urine with high specific gravity. Finally, urine electrolytes are extremely helpful in differentiating a wide range of disorders.
Hypertension with hypokalemia can be seen in the hypertensive patient on diuretics or patients with primary aldosteronism state. Table II depicts some common causes of metabolic alkalosis. If one is dealing with chloride-resistant metabolic alkalosis in a patient with hypertension, plasma hormone levels can aid in establishing a diagnosis. This will be discussed in detail in another section.
Some hypothetical examples of serum and urine electrolytes in different conditions are as follows:. An adrenal adenoma or bilateral adrenal hyperplasia cause increased production of aldosterone. Increased mineralocorticoid activity is a main mechanism for initiating and maintaining metabolic alkalosis. In some families, glucocorticoid remediable aldosteronism occurs due to a genetic defect in the aldosterone synthase gene. There is a family history of difficult to control hypertension that is amenable to steroid therapy.
It can be diagnosed by the presence of elevated OH-cortisol and oxocortisol in urine. One can differentiate primary aldosteronism from other chloride-resistant metabolic alkaloses based on renin and aldosterone levels Table III. Bartter syndrome presents in childhood without hypertension.
It results from various abnormalities that impair NaCl reabsorption in the thick ascending limb. NaCl delivery to the distal nephron is increased, the renin-angiotensin-aldosterone system is activated and hypokalemic metabolic alkalosis that is chloride resistant occurs. Gitelman syndrome presents in adults and is more common than Bartter syndrome. It is caused by mutations in the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule. Surreptitious diuretic use should always be considered and screening for diuretics in urine should be part of the work up.
Liddle syndrome is a rare autosomal dominant disease resulting from mutations in the epithelial sodium channel in collecting duct. Severe hypertension is often present. Glucocorticoid remediable aldosteronism GRA is an autosomal dominant disorder presenting similarly to primary aldosteronism with volume dependent hypertension and hypokalemic metabolic alkalosis.
Apparent mineralocorticoid excess AME mimics licorice ingestion. Hypertension responds to thiazides and spironolactone. One should treat the underlying mechanism that initiates and maintains metabolic alkalosis. Chloride-sensitive metabolic alkalosis responds to volume resuscitation and restoration of ECF potassium. As a recently published review makes clear, all the above may well be true, but it represents a gross oversimplification of the complex ways in which disorders of acid-base affect potassium metabolism and disorders of potassium affect acid-base balance.
The review begins with an account of potassium homeostasis with particular detailed attention to the renal handling of potassium and regulation of potassium excretion in urine. This discussion includes detail of the many cellular mechanisms of potassium reabsorption and secretion throughout the renal tubule and collecting duct that ensure, despite significant variation in dietary intake, that plasma potassium remains within narrow, normal limits.
There follows discussion of the ways in which acid-base disturbances affect these renal cellular mechanisms of potassium handling. For example, it is revealed that acidosis decreases potassium secretion in the distal renal tubule directly by effect on potassium secretory channels and indirectly by increasing ammonia production.
The clinical consequences of the physiological relation between acid-base and potassium homeostasis are addressed under three headings: Hyperkalemia in Acidosis; Hypokalemia with Alkalosis; and Hypokalemia with Acidosis.
Among the topics discussed under these headings is the important revelation that a variety of mechanisms account for the hyperkalemia in acidosis. So that for example, the mechanisms for the hyperkalemia associated with diabetic ketoacidosis differ from the mechanisms of the hyperkalemia associated with lactic acidosis. This review article, which is one of eleven contained in the May issue of Seminars in Nephrology all devoted to different aspects of potassium homeostasis, provides much detail of an aspect of acid-base pathophysiology that often receives minimal explanation in medical texts.
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