Chapter 048. Acidosis and Alkalosis (Part 13)

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. Headaches and other signs that mimic raised intracranial pressure, such as papilledema, abnormal reflexes, and focal muscle weakness, are due to vasoconstriction secondary to loss of the...
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Chapter 048. Acidosis and Alkalosis (Part 13) Chapter 048. Acidosis and Alkalosis (Part 13) The clinical features vary according to the severity and duration of therespiratory acidosis, the underlying disease, and whether there is accompanyinghypoxemia. A rapid increase in Pa CO2 may cause anxiety, dyspnea, confusion,psychosis, and hallucinations and may progress to coma. Lesser degrees ofdysfunction in chronic hypercapnia include sleep disturbances, loss of memory,daytime somnolence, personality changes, impairment of coordination, and motordisturbances such as tremor, myoclonic jerks, and asterixis. Headaches and othersigns that mimic raised intracranial pressure, such as papilledema, abnormalreflexes, and focal muscle weakness, are due to vasoconstriction secondary to lossof the vasodilator effects of CO2. Depression of the respiratory center by a variety of drugs, injury, or diseasecan produce respiratory acidosis. This may occur acutely with general anesthetics,sedatives, and head trauma or chronically with sedatives, alcohol, intracranialtumors, and the syndromes of sleep-disordered breathing, including the primaryalveolar and obesity-hypoventilation syndromes (Chaps. 258 and 259).Abnormalities or disease in the motor neurons, neuromuscular junction, andskeletal muscle can cause hypoventilation via respiratory muscle fatigue.Mechanical ventilation, when not properly adjusted and supervised, may result inrespiratory acidosis, particularly if CO2 production suddenly rises (because offever, agitation, sepsis, or overfeeding) or alveolar ventilation falls because ofworsening pulmonary function. High levels of positive end-expiratory pressure inthe presence of reduced cardiac output may cause hypercapnia as a result of largeincreases in alveolar dead space (Chap. 246). Permissive hypercapnia is beingused with increasing frequency because of studies suggesting lower mortality ratesthan with conventional mechanical ventilation, especially with severe centralnervous system or heart disease. The potential beneficial effects of permissivehypercapnia may be mitigated by correction of the acidemia by administration ofNaHCO3. Acute hypercapnia follows sudden occlusion of the upper airway orgeneralized bronchospasm as in severe asthma, anaphylaxis, inhalational burn, ortoxin injury. Chronic hypercapnia and respiratory acidosis occur in end-stageobstructive lung disease. Restrictive disorders involving both the chest wall andthe lungs can cause respiratory acidosis because the high metabolic cost ofrespiration causes ventilatory muscle fatigue. Advanced stages of intrapulmonaryand extrapulmonary restrictive defects present as chronic respiratory acidosis. The diagnosis of respiratory acidosis requires, by definition, themeasurement of PaCO2 and arterial pH. A detailed history and physicalexamination often indicate the cause. Pulmonary function studies (Chap. 246),including spirometry, diffusion capacity for carbon monoxide, lung volumes, andarterial PaCO2 and O2 saturation, usually make it possible to determine ifrespiratory acidosis is secondary to lung disease. The workup for nonpulmonarycauses should include a detailed drug history, measurement of hematocrit, andassessment of upper airway, chest wall, pleura, and neuromuscular function. Respiratory Acidosis: Treatment The management of respiratory acidosis depends on its severity and rate ofonset. Acute respiratory acidosis can be life threatening, and measures to reversethe underlying cause should be undertaken simultaneously with restoration ofadequate alveolar ventilation. This may necessitate tracheal intubation and assistedmechanical ventilation. Oxygen administration should be titrated carefully inpatients with severe obstructive pulmonary disease and chronic CO 2 retention whoare breathing spontaneously (Chap. 254). When oxygen is used injudiciously,these patients may experience progression of the respiratory acidosis. Aggressiveand rapid correction of hypercapnia should be avoided, because the falling Pa CO2may provoke the same complications noted with acute respiratory alkalosis (i.e.,cardiac arrhythmias, reduced cerebral perfusion, and seizures). The Pa CO2 shouldbe lowered gradually in chronic respiratory acidosis, aiming to restore the Pa CO2 tobaseline levels and to provide sufficient Cl– and K+ to enhance the renal excretionof HCO3–. Chronic respiratory acidosis is frequently difficult to correct, but measuresaimed at improving lung function (Chap. 254) can help some patients and forestallfurther deterioration in most. Respiratory Alkalosis Alveolar hyperventilation decreases PaCO2 and increases the HCO3–/PaCO2ratio, thus increasing pH (Table 48-7). Nonbicarbonate cellular buffers respond byconsuming HCO3–. Hypocapnia develops when a sufficiently strong ventilatorystimulus causes CO2 output in the lungs to exceed its metabolic production bytissues. Plasma pH and [HCO3–] appear to vary proportionately with PaCO2 over arange from 40–15 mmHg. The relationship between arterial [H+] concentrationand PaCO2 is ~0.7 mmol/L per mmHg (or 0.01 pH unit/mmHg), and that for plasma[HCO3–] is 0.2 mmol/L per mmHg. Hypocapnia sustained for >2–6 h is furthercompensated by a decrease in renal ammonium and titratable acid excretion and areduction in filtered HCO3– reabsorption. Full renal adaptation to respiratoryalkalosis may take several days and requires normal volume status and renalfunction. The kidneys appear to respond directly to the lowered Pa CO2 rather thanto alkalosis per se. In chronic respiratory alkalosis a 1-mmHg fall in PaCO2 causesa 0.4- to 0.5-mmol/L drop in [HCO3–] and a 0.3-mmol/L fall (or 0.003 rise i ...