Acidosis refers to a physiological condition in which the PH of arterial blood falls below the normal level of 7.35 in human beings while alkalosis occurs when the arterial blood PH is above 7.45(Grogono, 2006). It is important to maintain the PH of the blood as body proteins are usually sensitive to changes and only work optimally at a narrow range. The kidneys and the lungs are responsible for the maintenance of the blood PH between 7.35 to 7.45 to prevent any derangement (Grogono, 2006). In this regard, both conditions are divided into Respiratory and Metabolic categories based on their causation factors.
The clinical manifestations of metabolic alkalosis include myalgia, muscle spasms and weakness due to low levels of potassium ions in the blood (Grogono, 2006). It may also cause tetany due to hypocalcemia due to increased binding of free calcium to albumin when the PH of blood increases. Acidosis on the other hand, manifests in the Central Nervous system with symptoms such as confusion, headache, tiredness and dizziness, flapping tremor, and may lead to coma if not controlled (Morris & Low, 2008).
Respiratory alkalosis is caused by increased ventilation which results in loss of Carbon Dioxide and increase in blood PH. Some of the conditions that lead to the alkalosis include liver cirrhosis, anxiety, intracerebral hemorrhage, sepsis, and the use of drugs such as salicylates and progesterone (Kildeberg, 2009). Metabolic alkalosis may be caused by loss of hydrochloric acid in the stomach through repeated vomiting or oral consumption of alkaline fluids. Other causes include hormonal disorders such as Cushings syndrome, use of drugs such as diuretics, chronic diarrhea, renal failure, and hypokalemia (Kildeberg, 2009).
Metabolic acidosis is caused by increased production of acidic products such as lactic acid by the body or inability of the kidneys to excrete excess acid leading to accumulation of acidic by-products of catabolism (Morris & Low, 2008). For instance, lactic acidosis may be caused by inadequate oxygen in the tissues due to hypoxemia or tissues hypo perfusion as a result of hypovolemic shock. Additionally, there is increased production of metabolic acids in Diabetic Ketoacidosis and Starvation. Consumption of acids from poisons such as methanol, high levels of iron in the blood, and reduced bicarbonate production may also lead to a metabolic acidosis (Morris & Low, 2008). Other factors of causation include the use of drugs such as azetolamide, Renal Tubular Acidosis, diarrhea, and uremia.
Respiratory acidosis is as a result of increased carbon dioxide in the blood due to poor ventilation. Most of the causes include pulmonary problems such as asthma, severe pneumonia, chronic bronchitis, or emphysema (Grogono, 2006). It can also be caused by head injuries and brain tumors, chest wall deformities, and drugs such as narcotics, anesthetics, or sedatives. Its difference from metabolic acidosis is that the bicarbonate level is usually normal or increased (Morris & Low, 2008).
Extremely high or low PH of blood may lead to coma or even death. Therefore, treatment of the acid-base derangements is required in inadequate compensatory mechanisms. Itprimarily aims at treating the underlying conditions. However, in cases such as severe metabolic acidosis, it may require neutralization with bicarbonate infusions (Morris & Low, 2008). For uncompensated respiratory acidosis, mechanical ventilation may control the condition. Severe alkalosis may require strategies such as volume expansion with normal saline, and potassium supplements to prevent hypokalemia (Kildeberg, 2009). Drugs suspected to be causing the derangement should also be withdrawn. In all these cases, the most important factor is the identification of the underlying causes of particular conditions mentioned above and controlling them to prevent further derangements.
Grogono, A. (2006). Acid-Base Balance (Out of Print). Mededportal Publications.
Kildeberg, P. (2009). Respiratory Compensation in Metabolic Alkalosis. Acta Medica Scandinavica, 174(4), 515-522.
Morris, C. & Low, J. (2008). Metabolic Acidosis in the Critically Ill: Part 2. Causes and Treatment. Anesthesia, 63(4),396-411.
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