Acidosis and alkalosis

Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis. Many cardiopulmonary disorders manifest respiratory alkalosis in their early to intermediate stages, and the finding of normocapnia and hypoxemia in a patient with hyperventilation may herald the onset of rapid respiratory failure and should prompt an assessment to determine if the patient is becoming fatigued. Respiratory alkalosis is common during mechanical ventilation. The hyperventilation syndrome may be disabling.

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Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and HyperaIncreased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction of renin. Mineralocorticoid excess increases net acid excretion and may result in metabolic alkalosis, which may be worsened by associated K + deficiency. ECFV expansion from salt retention causes hypertension.

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The clinical features vary according to the severity and duration of the respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia. A rapid increase in Pa CO2 may cause anxiety, dyspnea, confusion, psychosis, and hallucinations and may progress to coma. Lesser degrees of dysfunction in chronic hypercapnia include sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis.

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Alkali Administration Chronic administration of alkali to individuals with normal renal function rarely, if ever, causes alkalosis. However, in patients with coexistent hemodynamic disturbances, alkalosis can develop because the normal capacity to excrete HCO3– may be exceeded or there may be enhanced reabsorption of HCO 3–. Such patients include those who receive HCO3– (PO or IV), acetate loads (parenteral hyperalimentation solutions), citrate loads (transfusions), or antacids plus cation-exchange resins (aluminum hydroxide and sodium polystyrene sulfonate). ...

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Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone system. For example, the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or that the hypertensive patient is receiving diuretics.

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Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated with systemic acidosis), urine pH is usually around 6 because metabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+, thus providing a urinary buffer that increases urine pH. Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA (Chap.

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Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other unidentified organic acids may contribute to the acidosis. Due to its low molecular weight (32 Da), an osmolar gap is usually present. Metabolic Acidosis: Treatment This is similar to that for ethylene glycol intoxication, including general supportive measures, fomepizole or ethanol administration, and hemodialysis.

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Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aerobic disorders (type B)—malignancies, nucleoside analogue reverse transcriptase inhibitors in HIV, diabetes mellitus, renal or hepatic failure, thiamine deficiency, severe infections (cholera, malaria), seizures, or drugs/toxins (biguanides, ethanol, methanol, propylene glycol, isoniazid, and fructose).

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Alcoholic Ketoacidosis: Treatment Extracellular fluid deficits almost always accompany AKA and should be repleted by IV administration of saline and glucose (5% dextrose in 0.9% NaCl). Hypophosphatemia, hypokalemia, and hypomagnesemia may coexist and should be corrected. Hypophosphatemia usually emerges 12–24 h after admission, may be exacerbated by glucose infusion, and, if severe, may induce rhabdomyolysis. Upper gastrointestinal hemorrhage, pancreatitis, and pneumonia may accompany this disorder. Drug- and Toxin-Induced Acidosis Salicylates (See also Chap.

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Metabolic Acidosis Metabolic 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.

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Approach to the Patient: Acid-Base Disorders A stepwise approach to the diagnosis of acid-base disorders follows (Table 48-3). Care should be taken when measuring blood gases to obtain the arterial blood sample without using excessive heparin. Blood for electrolytes and arterial blood gases should be drawn simultaneously prior to therapy, since an increase in [HCO3–] occurs with metabolic alkalosis and respiratory acidosis. Conversely, a decrease in [HCO3–] occurs in metabolic acidosis and respiratory alkalosis.

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Figure 48-1 Acid-base nomogram. Shown are the 90% confidence limits (range of values) of the normal respiratory and metabolic compensations for primary acidbase disturbances. (From DuBose, used with permission.) Mixed Acid-Base Disorders Mixed acid-base disorders—defined as independently coexisting disorders, not merely compensatory responses—are often seen in patients in critical care units and can lead to dangerous extremes of pH (Table 48-2).

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Harrison's Internal Medicine Chapter 48. Acidosis and Alkalosis Normal Acid-Base Homeostasis Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (PaCO2) by the central nervous system and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali.

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Table 48-1 Prediction of Compensatory Responses on Simple AcidBase Disturbances and Pattern of Changes Range of Values Disorder Prediction Compensation of pH HCO3– PaCO2 Metabolic PaCO2= (1.5 x Low Low Low acidosis HCO3-) + 8 ± 2 or PaCO2 will 1.25 mmHg per mmol/L in [HCO3-] or PaCO2 = [HCO3] + 15 Metabolic alkalosis PaCO2 will 0.75 mmHg per mmol/L in [HCO3-] High High High or PaCO2 will 6 mmHg per 10 mmol/L in [HCO3-] or PaCO2= [HCO3-] + 15 Respiratory alkalosis High Low Low Acute 0.2 [HCO3-] mmol/L will per mmHg in PaCO2 Chronic 0.

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Liddle's syndrome is a rare familial (autosomal dominant) disease characterized by hypertension, hypokalemic metabolic alkalosis, renal K + wasting, and suppressed renin and aldosterone secretion. Increased distal delivery of Na+ with a nonreabsorbable anion (not Cl–) enhances K+ secretion. Classically, this is seen with proximal (type 2)renal tubular acidosis (RTA) and vomiting, associated with bicarbonaturia. Diabetic ketoacidosis and toluene abuse (glue sniffing) can lead to increased delivery of β-hydroxybutyrate and hippurate, respectively, to the CCD and to renal K+ loss.

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Extrarenal Nonrenal causes of hypovolemia include fluid loss from the gastrointestinal tract, skin, and respiratory system and third-space accumulations (burns, pancreatitis, peritonitis). Approximately 9 L of fluid enters the gastrointestinal tract daily, 2 L by ingestion and 7 L by secretion. Almost 98% of this volume is reabsorbed so that fecal fluid loss is only 100–200 mL/d. Impaired gastrointestinal reabsorption or enhanced secretion leads to volume depletion.

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Adaptation to Hypoxia An important component of the respiratory response to hypoxia originates in special chemosensitive cells in the carotid and aortic bodies and in the respiratory center in the brainstem. The stimulation of these cells by hypoxia increases ventilation, with a loss of CO2, and can lead to respiratory alkalosis. When combined with the metabolic acidosis resulting from the production of lactic acid, the serum bicarbonate level declines (Chap. 48).

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