| Alkalosis | |
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| Specialty | Endocrinology  |
Alkalosis is the result of a process reducinghydrogen ion concentration ofarterialblood plasma (alkalemia). In contrast toacidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher). Alkalosis is usually divided into the categories ofrespiratory alkalosis andmetabolic alkalosis or a combined respiratory/metabolic alkalosis.[1]
Metabolic alkalosis is usually accompanied bylow blood potassium concentration, causing, e.g., muscular weakness,muscle pain, and muscle cramps (from disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles).
It may also causelow blood calcium concentration. As the blood pH increases, bloodtransport proteins, such asalbumin, become more ionized into anions. This causes the free calcium present in blood to bind more strongly with albumin. It may causetetany in severe cases. .
Respiratory alkalosis is caused byhyperventilation,[2] resulting in a loss ofcarbon dioxide. Compensatory mechanisms for this include release of hydrogen ion from tissue buffers and excretion ofbicarbonate in the kidneys, both of which lower bloodpH.[3] Hyperventilation-induced alkalosis can be seen in several deadlycentral nervous system diseases such asstrokes orRett syndrome.[2]
InMcArdle disease (glycogen storage disease type V), the inability to utilize muscle glycogen leads to a shortage of ATP during exercise and subsequent exercise-induced prematuremuscle fatigue, muscle cramps, muscle pain (myalgia), inappropriate rapid heart rate response to exercise (tachycardia), rapid depletion ofphosphocreatine, insufficient ATP production, increased ADP and AMP, increased rise in venous ammonia (from thepurine nucleotide cycle), increased epinephrine (adrenaline), increased plasma free fatty acids (lipolysis), increased venous pH (alkalosis), rapid (tachypnea) and commonly (approx. 50%) also heavy breathing (hyperpnea), that is exercisehyperventilation.[4][5][6][7][8][9] During exercise, due to the inability to utilize muscle glycogen as a substrate for ATP synthesis, plasma lactate does not significantly rise (and may fall below) compared to resting levels; consequently, McArdle disease individuals do not experience lactic acidosis.[7] The rise in venous pH (alkalosis), may be due to increased ammonia production,[10] increased epinephrine, and/or increased oxygen demand for oxidative phosphorylation of blood borne substrates (free fatty acids and blood glucose).[8][6]
Metabolic alkalosis can be caused by repeated vomiting,[2] resulting in a loss ofhydrochloric acid in the stomach contents. Severedehydration, and the consumption ofalkali,[3] are other causes. It can also be caused by administration of diuretics[2] and endocrine disorders such asCushing's syndrome. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increaseserum carbon dioxide,[2] a condition leaning toward respiratoryacidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and vice versa, a delicate balance is created between these two conditions.
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