Acid Base Essay 1
The acid-base disturbance that Mr. Davis is suffering from is metabolic acidosis disturbance. This is because he has uncompensated acidosis which can result from chronic consumption of alcohol. It is a condition primarily characterized by reduction in the concentration of bicarbonate serum and subsequent reduction in the carbon dioxide partial pressure of the arteries. The disturbance occurs due to the too much body acid, so that the kidneys are not excreting enough of the acid from the body. This disturbance mostly causes rapid breathe, makes someone to feel very tired, which can also cause shock or even death. The disturbance can also explain through alcoholic ketoacidosis which result to high anion gap (Suki & Massry, 1990). These symptoms can be related with the sign shown by Mr. Davis. The reduction in bicarbonate resulted to uncompensated acidosis. The reduced arterial pressure means that there was reduction in oxygen intake which in turn leads to difficulty in breathing.
The consumption of excessive alcohol makes the patients to display abnormalities of acid-base balance and serum electrolytes. There is normally a vital interactions between the acid-base balance and potassium which normally involve alteration in the function of the kidney and the exchanges of trans cellular cation. Alcohol consumption causes the result to the imbalance which in turn makes the potassium to shift into the cells and out of the cells, a phenomenon referred to as “internal potassium balance”. In the metabolic acidosis, over half of surplus hydrogen ions are usually held within the cells. In such a situation, there is maintenance of electro neutrality partly by the intracellular potassium movement into the extracellular fluid (Westgard, 2011). Therefore, metabolic acidosis leads to the concentration of potassium which is elevated as compared to the total amount in the body. This in some cases may lead to overt hyperkalemia. If someone’s body is depleted of potassium because of gastrointestinal or urinary losses, the concentration of potassium plasma can be normal or reduced. If the academia is collected, there can be a relative increase in the concentration of potassium plasma. The shifting of intracellular potassium to extracellular can also lead to dehydration. However, a reduction in the pH level may not raise the concentration of potassium plasma if the alcoholic has ketoacidosis or lactic acidosis. Moreover, the loss of urinary potassium may happen in several ways. Metabolic alkalosis which may result from diuretic use can induce a potassium shift into the cells that lead to the potassium being secreted into the urine. Non-potassium-sparing diuretics therapy increases further excretion of by rising sodium delivery to the exchange sites for sodium – potassium. The increase in aldosterone plasma after consumption of excess alcohol can be relates rightly with increase in excretion of urinary potassium (Basavanthappa, 2003). The consumption of ethanol in particular leads to loss of excessive magnesium in the urine and this contributes to hypomagnesaemia development which impairs the re-absorption of potassium in renal tubular, enhancing the wastage of potassium, thus hypokalemia. In addition, excessive alcohol intake result to nutritional intake that is inadequate and it’s mostly associated with deficiencies of various minerals and vitamins. Also, adrenergic stimulation due to excessive activity of the sympathetic nervous system is associated with alcohol withdrawal. Since the stimulation of adrenergic results to enhanced potassium entry into the cells, the hyperactivity of the nervous system common in alcoholic may through this mechanism lead to hypokalemia development (Basavanthappa, 2003). This can explain the cases of imbalances in the level of potassium cellular.
The type of fluid imbalance that Mr. Dvais has is hypertonic or the condition of hypernatremia which is associated with intoxication of alcohol or subjects attributed to alcohol. This is because of the increased concentration of alcohol which is most of the time an indication of water loss rather than a gain in the amount of sodium in blood. This situation happens when the level of sodium in the blood is above 135 mEq/L as indicated in the lab results. This means that there is need for more water absorption to restore the balance sodium balance in the water. This scenario can also be associated with loss of sodium in through fluids. This imbalance leads to intracellular water loss and thus cellular shrinkage. In the case of severe alcohol intoxication, hypernatremia and hypokalemia may be experienced (Westgard, 2011). This may happen even where the level of potassium is normal.
At 19, Mr.Davis anion gap is high in relation to the normal gap which ranges from 8 to16 mEq/L. The large anion gap can be credited to the accumulation of acid in the body. When the hydrogen ions in the acid react with hydrogen carbonate, it leads less concentration in the body. The high anion gap shows that the there is a concentration of the acid in the body (Westgard, 2011). This can be associated with consistent consumption of alcohol which has the effect of increasing the acidity of the blood.
The renal system is not attempting to compensate for the acid-base balance since there is no indication that the kidneys reabsorbed the bicarbonates that was filtered since its levels remained below the normal range. Bicarbonate normally works as the main extracellular defense against fixed acids, and it is very necessary for the concentration of plasma to be guarded against any renal loss. The renal system would have re-compensated the acid-base balance through the two ways; filtered carbonate re-absorption and fixed acid excretion processes that include the secretion of hydrogen ions into the lumen by way of renal cells (Petralli, Nelson, & White, 2008). The respiratory system tried to restore the acid-base balance through the rapid and deep breath. The aim is to regulate the amount of carbon dioxide which partly increases the level of acidity in the blood. The brain regulates the carbon dioxide level though ventilation, a process where it controls the depth and speed of breathing. Through the controlled breathing, the respiratory system was attempting to compensate for the acid-base balance.
The low glucose level can be attributed to build up of lactic acid – the condition of lactic acidosis. The body cells release lactic acid since energy is required when the body does not have adequate oxygen. This can be attributed to the anaerobic metabolism which can be attributed to panic or body weakness (Westgard, 2011). Mr. Davis experience metabolic acidosis which resulted to the low glucose level. The high level of serum ketone can be attributed to the alcoholic ketoacidosis which is refers to metabolic acidosis. In addition the protein level in the urine test is abnormal due to the condition of lactic acidosis (Westgard, 2011). The patient might possibly experience encephalopathy but most likely, he is having severe kidney injury due to excessive consumption of alcohol and dehydration. These condition can also be attributed to little food intake.
References
Suki, W. N., & Massry, S. G. (1990). Therapy of Renal Diseases and Related Disorders. Boston, MA: Springer US. 239
Westgard, E. (2011). Clinical coach for fluid & electrolyte balance. Philadelphia: F.A. Davis Co. 251
Basavanthappa, B. T. (2003). Medical surgical nursing. New Delhi: Jaypee Brothers. 96-98
Petralli, G., Nelson, K., & White, C. (2008). Alcoholism: The cause & the cure ; the proven orthomolecular treatment and the 101 program bringing the most advanced holistic detox center to you. Burbank, Calif.: Alternative Approaches to end Alcohol Abuse (AAAA).105-107
