These deficiencies can be treated with intravenous fluids or, in mild cases, with a diet adjustment. Some cases of alkalosis are caused by serious underlying heart, kidney, or liver conditions. While the alkalosis can often be reversed in the short term, the underlying condition has to be treated for a lasting cure.
Your body works constantly to carefully control the pH of blood and other fluids. The right pH levels are needed for good health. Learn what your…. If your lungs or kidneys are…. Despite its acidic pH, some people say lemon juice has alkalizing effects in the body. This article takes a look at the science behind this claim. What is alkaline water, and why is it being raved about in the health industry? Learn more about what it is and its effect on your body. Multiple tests can analyze metabolism.
Most need blood drawn, but some can be ordered online and done at home. Here are 2. This simple, at-home test can introduce you to your metabolic hormones. Health Conditions Discover Plan Connect. Mental Health. Metabolic Alkalosis. Medically reviewed by Deborah Weatherspoon, Ph. Treatment of metabolic alkalosis. Symptoms of metabolic alkalosis. How the body compensates for metabolic alkalosis. Causes of metabolic alkalosis.
Diagnosis of metabolic alkalosis. Metabolic alkalosis with hypochloremia. This site uses Akismet to reduce spam. Learn how your comment data is processed. O2, monitoring and observation avoid hyperventilation as this worsens the alkalaemia. Critical Care Compendium. Chris Nickson. His one great achievement is being the father of two amazing children.
Leave a Reply Cancel reply. We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits. In case of sale of your personal information, you may opt out by using the link Do not sell my personal information. Cookies Policy. The kidney plays a crucial role in maintaining HCO 3 —. Most often, the kidneys can excrete excess HCO 3 — and bicarbonaturia occurs.
Factors that facilitate bicarbonaturia are adequate extracellular fluid ECF volume, dietary salt intake, potassium balance and appropriate mineralocorticoid activity. In order for metabolic alkalosis to be maintained the kidneys ability to excrete excess bicarbonate must be impaired, most commonly as a result of ECF volume contraction.
Patients can present with either simple or mixed acid-base disturbances. The evaluation of a patient with suspected metabolic alkalosis on a set of arterial blood gases involves four simple steps:. Step 1: Assess the arterial pH and identify the primary disturbance. An elevated serum HCO 3 — could be the result of metabolic alkalosis or may represent compensation for respiratory acidosis. The arterial pH will be elevated in the former and low in the latter.
Compensation attempts to return arterial pH to normal but does not quite get there. Step 2: Assess whether compensation is appropriate. If compensation is not appropriate the change in PaCO 2 is either higher or lower than expected then a superimposed respiratory acidosis PaCO 2 higher than expected or alkalosis PaCO 2 lower than expected is present.
Step 3: Assess the anion gap. This will help identify whether an elevated anion gap acidosis is also present. One needs to keep in mind, however, that a slight increase in the anion gap is often seen in the patient with severe metabolic alkalosis due to changes in the net anion charge and increased production of organic acids. Step 4: If the anion gap is elevated, compare the increase in the anion gap to the decline in HCO 3 —.
The increase in anion gap should roughly match the decline in HCO 3 —. If the decrease in HCO 3 — is much larger than the increase in the anion gap this suggests that both an anion gap and non-anion gap metabolic acidosis are present. Some clinical scenarios where mixed disturbances can occur are in the patient with renal failure and vomiting or the patient with diabetic ketoacidosis and vomiting.
Step 5: Remember a caveat to laboratory data interpretation. With severe metabolic alkalosis, one should rely on measurements of arterial pH and PaCO 2 to calculate serum bicarbonate concentration. Similarly, large amounts of HCO 3 — precursors might be administered during massive blood transfusion or plasmapheresis. A lesser degree of alkalosis is observed when blood anticoagulated with citrate dextrose A formula ACD-A is used. There is a rising incidence of milk-alkali syndrome especially in women taking calcium supplements for osteoporosis.
It presents with nephrocalcinosis, declining renal function and metabolic alkalosis. In some Asian countries, betel nut chewing can cause this problem due to excessive calcium ingestion. 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. Videos Figures Images Quizzes Symptoms. Symptoms and Signs. Key Points. Acid-Base Regulation and Disorders.
Test your knowledge. Secondary adrenal insufficiency is adrenal hypofunction due to lack of adrenocorticotropic hormone ACTH. Most of the symptoms and signs of this condition are similar to those of Addison disease. Which of the following symptoms and signs is present in patients with secondary adrenal insufficiency but not in patients with Addison disease?
More Content. Metabolic Alkalosis By James L. Click here for Patient Education. Acid loss. Diuretic use. Bicarbonate excess.
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