Chapter 048. Acidosis and Alkalosis (Part 5)

Metabolic AcidosisMetabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids (as in renal failure). Metabolic acidosis has profound effects on the respiratory, cardiac, and nervous systems. The fall in blood pH is accompanied by a characteristic increase in ventilation, especially the tidal volume (Kussmaul respiration). Intrinsic cardiac contractility may be depressed, but inotropic function can be normal because of catecholamine release. Both peripheral arterial vasodilation and central venoconstriction can be present; the decrease in central and pulmonary vascular compliance predisposes...
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Chapter 048. Acidosis and Alkalosis (Part 5) Chapter 048. Acidosis and Alkalosis (Part 5) Metabolic Acidosis Metabolic acidosis can occur because of an increase in endogenous acidproduction (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), oraccumulation of endogenous acids (as in renal failure). Metabolic acidosis hasprofound effects on the respiratory, cardiac, and nervous systems. The fall inblood pH is accompanied by a characteristic increase in ventilation, especially thetidal volume (Kussmaul respiration). Intrinsic cardiac contractility may bedepressed, but inotropic function can be normal because of catecholamine release.Both peripheral arterial vasodilation and central venoconstriction can be present;the decrease in central and pulmonary vascular compliance predisposes topulmonary edema with even minimal volume overload. Central nervous systemfunction is depressed, with headache, lethargy, stupor, and, in some cases, evencoma. Glucose intolerance may also occur. There are two major categories of clinical metabolic acidosis: high-AG andnormal-AG, or hyperchloremic acidosis (Table 48-3 and Table 48-4). Table 48-4 Causes of High-Anion-Gap Metabolic Acidosis Lactic acidosis Toxins Ketoacidosis Ethylene glycol Diabetic Methanol Alcoholic Salicylates Starvation Propylene glycol Pyroglutamic acid Renal failure (acute and chronic) Metabolic Acidosis: Treatment Treatment of metabolic acidosis with alkali should be reserved for severeacidemia except when the patient has no potential HCO3– in plasma. Potential[HCO3–] can be estimated from the increment (∆) in the AG (∆AG = patients AG– 10). It must be determined if the acid anion in plasma is metabolizable (i.e., β-hydroxybutyrate, acetoacetate, and lactate) or nonmetabolizable (anions thataccumulate in chronic renal failure and after toxin ingestion). The latter requiresreturn of renal function to replenish the [HCO3–] deficit, a slow and oftenunpredictable process. Consequently, patients with a normal AG acidosis(hyperchloremic acidosis), a slightly elevated AG (mixed hyperchloremic and AGacidosis), or an AG attributable to a nonmetabolizable anion in the face of renalfailure should receive alkali therapy, either PO (NaHCO3 or Shohls solution) orIV (NaHCO3), in an amount necessary to slowly increase the plasma [HCO3–] intothe 20–22 mmol/L range. Controversy exists, however, in regard to the use of alkali in patients with apure AG acidosis owing to accumulation of a metabolizable organic acid anion(ketoacidosis or lactic acidosis). In general, severe acidosis (pH < 7.20) warrantsthe IV administration of 50–100 meq of NaHCO3, over 30–45 min, during theinitial 1–2 h of therapy. Provision of such modest quantities of alkali in thissituation seems to provide an added measure of safety, but it is essential tomonitor plasma electrolytes during the course of therapy, since the [K +] maydecline as pH rises. The goal is to increase the [HCO 3–] to 10 meq/L and the pH to7.15, not to increase these values to normal. High-Anion-Gap Acidoses Approach to the Patient: High-Anion-Gap Acidoses There are four principal causes of a high-AG acidosis: (1) lactic acidosis,(2) ketoacidosis, (3) ingested toxins, and (4) acute and chronic renal failure (Table48-4). Initial screening to differentiate the high-AG acidoses should include (1) aprobe of the history for evidence of drug and toxin ingestion and measurement ofarterial blood gas to detect coexistent respiratory alkalosis (salicylates); (2)determination of whether diabetes mellitus is present (diabetic ketoacidosis); (3) asearch for evidence of alcoholism or increased levels of β-hydroxybutyrate(alcoholic ketoacidosis); (4) observation for clinical signs of uremia anddetermination of the blood urea nitrogen (BUN) and creatinine (uremic acidosis);(5) inspection of the urine for oxalate crystals (ethylene glycol); and (6)recognition of the numerous clinical settings in which lactate levels may beincreased (hypotension, shock, cardiac failure, leukemia, cancer, and drug or toxiningestion).