Why is hypokalemia alkalosis

The lungs change the alkalinity of your blood by allowing more or less carbon dioxide to escape as you breathe. The kidneys also play a role by controlling the elimination of bicarbonate ions. Treatment for metabolic alkalosis depends on whether your alkalosis is chloride-responsive or chloride-resistant.

It also depends on the underlying cause of the alkalosis. If you have only a mild chloride-responsive alkalosis, you may only need to make an adjustment in your diet, such as increasing your intake of salt sodium chloride. The chloride ions will make your blood more acidic and reduce the alkalosis.

If your doctor determines your alkalosis needs immediate attention, they may give you an IV intravenous drip containing a saline solution sodium chloride.

An IV is an almost painless procedure. It involves inserting a small needle into a vein in your arm. The needle is connected by a tube to a sterile bag containing salt dissolved in water. This is usually done in a hospital setting. If you have chloride-resistant alkalosis, your body may be depleted of potassium. Your doctor will instead look for ways to increase potassium. Metabolic alkalosis may not show any symptoms.

People with this type of alkalosis more often complain of the underlying conditions that are causing it. These can include:. Our body produces carbon dioxide when we convert the food we eat into energy in our cells. The red blood cells in our veins take up the carbon dioxide and carry it to our lungs to be exhaled. When the carbon dioxide gas mixes with the water in the blood, it forms a mild acid, called carbonic acid. The carbonic acid then breaks apart into the bicarbonate ion and hydrogen.

Bicarbonate ions are alkaline. By changing the rate of breathing, we can raise or lower the concentration of alkaline bicarbonate ions that are retained in our blood.

The body does this automatically in the process called respiratory compensation. The kidneys can help combat alkalosis by increasing the excretion of bicarbonate ions through the urine.

Loss of stomach acids. 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.

Specific treatments are required for chloride-resistant metabolic alkalosis. Patients with cirrhosis and congestive heart failure pose challenges in management as a low urinary Cl — would usually imply saline infusion for the correction of metabolic alkalosis.

This is not well tolerated in these patients since they have an excess of total body salt and water. Acetazolamide carbonic anhydrase inhibitor causes bicarbonaturia in patients with adequate renal function. Hypokalemia may worsen, however, with its use. Caution is warranted as it may cause hemolysis. Titration should be done to bring arterial pH to approximately 7. Hemodialysis using low HCO 3 — bath and high Cl — bath can be performed.

Gastrointestinal losses from vomiting and nasogastric suction lead to proton loss that triggers metabolic alkalosis. Chloride is actively transported from the parietal cell into the lumen and sodium ions are absorbed. This generates a negative potential of to millivolts in the canaliculus. The diffusion potential causes potassium to move into the canalicular lumen. Protons required for this reaction are generated from water breakdown.

The hydroxyl group generated combines with CO 2 and forms HCO 3 — which exits the parietal cell across the basolateral membrane. This mechanism is illustrated in Figure 1. GI losses increase gastric pH which triggers more proton secretion by gastric parietal cells resulting in further proton loss and ECF HCO 3 — addition.

This may be the reason why certain lower GI losses present with metabolic alkalosis villous adenomas or congenital chloridorrhea. They induced CDMA by gastric aspiration or diuretics. Sodium phosphate replacement worsened metabolic alkalosis when compared to KCl replacement in such patients. In CDMA, this transporter is activated aiding in bicarbonaturia. CDMA is not always accompanied by volume contraction as in the case in heart failure or cirrhotics with mixed acid-base disorders.

In such clinical scenarios, Cl — repletion is not possible. Acetazolamide can be used to increase renal HCO 3 — excretion if metabolic alkalosis is severe. To understand the physiology of renin and aldosterone in maintaining metabolic alkalosis, one first needs to review renal HCO 3 — excretion. Carbonic anhydrase CA is an important zinc metalloenzyme involved in the reabsorption of HCO 3 — in kidney.

It catalyzes the following reaction:. CA inhibition markedly reduces trans-epithelial HCO 3 — reabsorption. In the distal nephron, final regulation of acid excretion occurs.

Five to ten percent of remaining HCO 3 — is absorbed in this segment. The major functions of different parts of the distal nephron are shown in Figure 3. Mineralocorticoids are important determinants of net acid excretion.

Both result in increased HCO 3 — resorption and maintain metabolic alkalosis. Volume depletion can maintain metabolic alkalosis as high angiotensin II levels increases HCO 3 — reclamation. Patients with hypertension and easily provoked hypokalemia with urine electrolytes consistent with kaliuresis raises a suspicion of primary aldosteronism.

There is accompanied metabolic alkalosis and hypomagnesemia on laboratory examination, with the absence of peripheral edema on physical exam. Many patients have resistant hypertension that is difficult to control.

One can develop a stepwise approach to diagnose primary hyperaldosteronism. Step 2: To screen for primary aldosteronism, spironolactone and eplerenone must be stopped for 6 weeks prior to checking plasma aldosterone concentration PAC and plasma renin activity PRA.

However, most of these drugs are reasonable to continue for the first screen. It is drawn in the early morning to stimulate renin production diurnal pattern. October On the relationship between potassium and acid-base balance.

Acid-base and potassium homeostasis. Seminars in Nephrology ; Read more about acid-base: Acid-base disturbance in COPD Acid-base and electrolyte disorders in CKD — a review article Acid-base disturbance in diabetes Acid-base changes during resuscitation from out-of-hospital cardiac arrest.

Disclaimer May contain information that is not supported by performance and intended use claims of Radiometer's products. Chris Higgins has a master's degree in medical biochemistry and he has twenty years experience of work in clinical laboratories.

Acid-base balance ». Metabolic alkalosis develops when your body loses too much acid or gains too much base. This can be attributed to:. This can be due to prolonged vomiting or sweating.

Hypokalemic alkalosis occurs when your body lacks the normal amount of the mineral potassium. You normally get potassium from your food, but not eating enough of it is rarely the cause of a potassium deficiency.

Kidney disease, excessive sweating, and diarrhea are just a few ways you can lose too much potassium. Potassium is essential to the proper functioning of the:. These symptoms could lead to shock or coma. Call or go to the nearest emergency room if you experience any of these symptoms:. The symptoms of alkalosis mimic symptoms of other conditions.

Make an appointment with your doctor to get evaluated. They will likely order tests that will rule out other conditions. Common tests include:. A blood pH above 7. Your doctor may also want to measure the carbon dioxide and oxygen levels in your blood to rule out respiratory issues.