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RESPIRATORY CENTER DRIVE

Classic techniques for assessment of respiratory drive have measured ventilatory output (i.e., minute ventilation [V̇E]) as a function of varying levels of elevated PaCO₂ (i.e., hypercapnic ventilatory response) or decreased levels of PaO₂ (i.e., hypoxic ventilatory response). However, these techniques are difficult to implement in clinical situations. Nevertheless, assessment of the respiratory drive is particularly important in clinical evaluation of the effects of anesthetic agents on the respiratory system and particularly in the process of weaning patients from mechanical ventilation. Of the various causes of respiratory failure, including pulmonary mechanical abnormalities and impairment of respiratory gas exchange, depressed ventilatory drive is probably the most common cause of failure to wean after general anesthesia.

Partitioning the respiratory waveform into inspiratory and expiratory components can provide further information. Mean inspiratory flow (i.e., tidal volume/inspiratory time) is an index of respiratory drive.^[191] However, it is possible for a patient to have a high respiratory drive but not be able to translate that drive into respiratory output because of impaired ventilatory mechanics.

A low ventilation rate is conventionally considered to be a reasonable indicator of respiratory depression caused by anesthetic agents, particularly narcotics. Although parenteral narcotics usually slow the ventilation rate, several investigators have demonstrated in patients and normal volunteers that narcotic-induced ventilatory depression can manifest as a reduction in tidal volume, with little change in respiratory rate.^{[192] [193] [194] [195]} In a clinical series, one patient with a PaCO₂ of 95 mm Hg had a respiratory rate of 12 breaths/min.^[195] The published evidence indicates that apnea is not reliably predicted by bradypnea, and severe respiratory depression can exist in patients with acceptable respiratory rates.

A more sophisticated measure of respiratory drive is the maximum negative inspiratory airway pressure obtained 100 msec after a temporary occlusion of the airway (P₁₀₀ or P_0.1 ) in a spontaneously breathing patient. Periodic transient airway occlusion that occurs in this way is not appreciably noticed by the patient. Chemosensitivity, determined in volunteers by CO₂ responsiveness, is not significantly affected by intermittent (every 30 seconds) P₁₀₀ maneuvers.^[196] The normal value for P₁₀₀ during resting ventilation is 1 to 2 cm H₂ O. P₁₀₀ is a useful index of respiratory drive, requiring no voluntary effort on the part of the subject and being minimally affected by changes in respiratory mechanics. The technique is well described by Milic-Emili and associates.^[197]

Under anesthesia, P₁₀₀ is depressed,^[198] but the effect of anesthesia depends highly on PaCO₂ , such that P₁₀₀ at high PaCO₂ values is increased, even under anesthesia. In acute respiratory failure due to other causes, P₁₀₀ is generally elevated. Herrera and colleagues^[199] and Sassoon and coworkers^[200] observed values of P₁₀₀ above 6 cm H₂ O and 4.2 cm H₂ O, respectively, during T-tube trials to be correlated to lack of success in weaning. Using similar threshold values, P₁₀₀ can be used as a guide to the discontinuation of mechanical ventilation after general anesthesia.^[201] Montgomery and associates^[202] found a similar relationship but reported a better prediction of weaning successes using the P₁₀₀ response after breathing of 3% CO₂ (P₁₀₀ H). The mean P₁₀₀ H/P₁₀₀ ratio was 2.04 in seven successful weaning attempts and 1.17 in seven failures.