Acidosis etiologies

Convincing data in lactic acidosis is lacking D Manage underlying etiology... 

The principal function of the circulatory system is to supply oxygen and vital metabolic substrates to cells throughout the body, as well as removal of metabolic waste products. Circulatory shock is a life-threatening condition whereby this principal function is compromised. When circulatory shock is caused by a severe loss of blood volume or body water it is called hypovolemic shock, the focus of this chapter. Regardless of etiology, the most distinctive manifestations of hypovolemic shock are arterial hypotension and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic... 

It is important to realize that the serum HCO, concentration may be affected by the presence of unmeasured endogenous acids (lactic acidosis or ketoacidosis). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO, for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this transaction, the loss of serum HC03 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important for identifying the etiology of the acid-base disorder. The concept of the increased anion gap will be applied later in the case studies section. 

Respiratory acidosis is characterized by a reduced arterial pH, a primary increase in the arterial PaC02 and, when present for sufficient time, a compensatory rise in the HCOf concentration. Because increased C02 is a potent respiratory stimulus, respiratory acidosis represents ventilatory failure or impaired central control of ventilation as opposed to an increase in C02 production. As such, most patients will have hypoxemia in addition to hypercapnia. The most common etiologies of respiratory acidosis are listed in Table 25-6. 

Husain K, Mirza MA, Matin MA. 1987. Convulsions as the etiology of lactic acidosis in acute diazinon... 

In combination with other antiretroviral agents, stavudine has caused fatal lactic acidosis in some patients. It is also associated with motor weakness in which case it should be discontinued. Peripheral neuropathy is the most common toxicity associated with stavudine, which is more prevalent at high doses (4mg/kg per day). Neuropathy in these patients generally is associated with numbness, tingling or pain in feet or hands. Patients treated with the combination of stavudine and didanosine may also exhibit liver function abnormalities (hepatic steatosis) and pancreatitis. It may also be associated with the etiology of HIV lipodystrophy syndrome. 

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