Respiratory Acidosis

Respiratory acidosis is defined by alveolar hypoventilation and is diagnosed when the P co2 is greater then the expected value. Acute respiratory acidosis may have origins such as increased CO2 production (high-glucose diet) and abnormal gas exchange (e.g., pneumonia). Final common path is inadequate ventilation.

Inadequate minute ventilation is most frequently due to head trauma, chest trauma, or disease or excess sedation. The chronic hypoventilation seen in extremely obese patients is often referred to as the pickwickian syndrome, after an obese character in Charles Dickens' Pickwick Papers. Patients with severe COPD have increased dead space and frequently also have a decreased minute ventilation.

In general, a rise in the Pco2 stimulates the respiratory center to increase respiratory rate and minute ventilation. However, if the arterial P co2 chronically exceeds 60 to 70 mmHg, as may occur in 5 to 10 percent of patients with severe emphysema, the respiratory acidosis may depress the respiratory center. Under such circumstances, the stimulus for ventilation is provided primarily by hypoxemia acting on chemoreceptors in the carotid and aortic bodies. Giving oxygen could take away the main stimulus to breathe, causing the Pco2 to rise abruptly to extremely dangerous levels. Consequently, one should not administer oxygen to patients with COPD without carefully watching for the development of apnea or hypoventilation.

Evaluation of ventilation requires attention to several important clinical issues. First, the ventilation that would be expected based on assessment of the respiratory rate and depth should be compared to the actual ventilation of the patient (i.e., P co2). A "normal" Pco2 of 40 mmHg in a tachypneic, dyspneic patient probably reflects significant ventilatory insufficiency. Second, the impact of respiratory acidosis on PA o2 in such a patient may be considerable. The alveolar gas equation suggests that if inspired oxygen concentration and respiratory quotient do not vary, increases in P co2 will result in reductions in PAo2.

The relationship of Pco2 to hydrogen ion concentration in acute respiratory acidosis is suggested by the Kassirer-Bleich equation:

Each 1-mmHg increase in Pco2 results in a 1-mmol increase in [H+]. Across the linear portion of the pH-hydrogen ion concentration relationship, then, each 1-mmHg increase in Pco2 should theoretically produce a 0.01-unit decrease in pH. The actual relationship between changes in P co2 (up to values of 90 mmHg) and changes in

[H+] determined in normal humans is about 8:10, as shown in Eq (7). Thus, a 10-mmHg increment in Pco2 produces an 8-mmol increase in hydrogen ion concentration, with little change in bicarbonate concentration (usually 1 meq/dL) or urinary acid excretion. 19 If the [H+] is higher or lower than that suggested by the change in the Pco2, a mixed disorder is present.

The adaptation to chronic respiratory acidosis is complex. Over time, chronic elevation of P co2 results in a reduction in the sensitivity of carotid sinus sensitivity to hypercapnia; ventilatory drive is then controlled by Pa co2. The acidosis results in significant increases in renal bicarbonate generation and avid reclamation of filtered bicarbonate. The relationship between [H +] and [HCO3-] in chronic respiratory acidosis at steady state, derived from studies in humans, is shown in Eq (9).

It is rarely certain during a given clinical encounter whether a patient has an acute respiratory acidosis, a chronic respiratory acidosis, or an acute exacerbation of chronic COPD. Evaluation of the acid-base status in such circumstances does not require "baseline" arterial blood gas values. Instead, the change in hydrogen ion concentration is compared with the change in Pco2. If this ratio is 0.3, the patient has a chronic respiratory acidosis; if it is 0.8, the patient has an acute respiratory acidosis. States resulting in other ratios suggest a mixed acid-base disturbance, as shown in T.ab!ei21-5.

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TABLE 21-5 Evaluation of Acid-Base Status in Respiratory Acidosis

Treatment of respiratory acidosis is primarily designed to improve alveolar ventilation. In general, if the minute ventilation is doubled, the P co2 will be reduced by 50 percent. In patients with COPD, bronchodilators such as aminophylline or various sympathomimetic agents such as isoproterenol or adrenalin, together with careful administration of small amounts of oxygen, may substantially improve ventilation. However, ventilating assistance may be required in some patients who do not respond adequately to lesser measures, particularly if the pH falls below 7.25 to 7.30. Unfortunately, it may be extremely difficult to extubate such patients later.

In patients with a chronic respiratory acidosis, reduction of the P co2 should generally proceed slowly. The minute ventilation for a 70-kg person is normally about 6 L/min, and in COPD patients it may be less than 4 L/min. In a patient with COPD and severe hypercarbia, it may be wise to start treatment with a minute ventilation of about 5 L/min and then gradually increase it according to the clinical response and changes in P co2.

Rapid correction of a chronic respiratory acidosis can cause sudden development of a severe combined metabolic and respiratory alkalosis with resulting dysrhythmias. A rapid rise in pH can cause an abrupt fall in ionized calcium. The resulting ionic hypocalcemia can then cause dangerous dysrhythmias or seizures. In patients with a chronic respiratory acidosis, the arterial P co2 should not be reduced by more than 5.0 meq/h.

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