Potassium bicarbonate is preferred when correcting hypokalemia associated with metabolic acidosis. Convulsions lead to lactic acidosis, hyperthermia and rhabdomyolysis. This propagates tissue ischemia and worsens lactic acidosis. Adverse effects include hyponatremia and volume depletion leading to metabolic acidosis. Ethanol increases production of uric acid by increasing production of lactic acid, hence lactic acidosis. If these homeostats are compromised, then a respiratory acidosis, or a respiratory alkalosis will occur. Heart failure with lactic acidosis syndrome has been observed. Buffer solutions are used to correct acidosis or alkalosis. Arterial Blood gases may show a mild hyperchloremic metabolic acidosis. The clinician must protect the patient against hypotension, kidney failure, acidosis, hyperkalemia and hypocalcemia. Effects include alcoholic intoxication and high anion gap metabolic acidosis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. However, sodium bicarbonate is not recommended for a person with lactic acidosis secondary to hypoperfusion. The loss of bicarbonate results in type 2 or proximal renal tubular acidosis. Cell stress could be due to infection, injury, ischemia, hypoxia, acidosis and complement lysis.