Robert E. Dutton

Detrimental effects of removing end-expiratory pressure prior to endotracheal extubation.

Patients recovering from acute respiratory insufficiency are usually not extubated until they can ventilate adequately while breathing spontaneously at ambient end-expiratory pressure (T-tube). It is hypothesized that this period of T-tube breathing might be detrimental to gas exchange since the endotracheal tube abolishes the expiratory retard produced by the glottis and thereby inhibits the patients ability to maintain adequate functional residual capacity (FRC). To test this hypothesis, pulmonary function of 17 patients was compared during T-tube breathing and Continuous Positive Airway Pressure (CPAP) and after extubation. Intrapulmonary shunt was higher (p less than 0.05) and arterial PO2 and FRC were lower (p less than 0.05) during T-tube breathing than during CPAP or after extubation. In contrast, shunt, PaO2 and FRC were similar during CPAP and after extubation. Furthermore, after extubation there was an increase (p less than 0.05) in mean expiratory airway pressure as compared to T-tube breathing. A comparison of patients extubated from T-tube with patients extubated from CPAP showed no difference in postextubation shunt, PaO2 or FRC. These data suggest that endotracheal intubation should be accompanied by low levels of CPAP and that patients should be extubated directly from CPAP. The practice of placing patients in T-tube prior to extubation should be abandoned as unnecessary and potentially harmful.

Chemoreceptor influence on pulmonary blood flow during unilateral hypox1a in dogs

Dogs anesthetized with 30 mg/kg pentobarbital were artificially respired after differential cannulation of the main stem bronchi. Following median sternotomy, blood flow was monitored by electromagnetic flow probes on the left pulmonary artery (QL) and on the pulmonary trunk or aorta, QT. Following 10 min of bilateral 100% O2, QL was 42.5 +/- 7% of QT. When 6% O2, was substituted as the gas mixture inspired by the left lung while the right lung remained on 100% O2, PaO2 was above 70 mm Hg and QL fell to 24.5 +/- 5% of QT. Room air was then used to ventilate the right lung while the left lung remained on 6% O2. This caused PaO2 to fall to 42.3 +/- 3 MM Hg and QL to rise to 38.3 +/- 6% QT. This increase in blood flow to the unilaterally hypoxic lung during systemic hypoxemia did not occur in dogs after peripheral chemoreceptor denervation. Therefore, interference with the local response to alveolar hypoxia during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

Pulmonary wedge catheterization during positive end-expiratory pressure ventilation in the dog.

In ten supine anesthetized dogs, recordings of left atrial (LA) and pulmonary-artery wedge (PW) pressures were simultaneously obtained at several levels of positive end-expiratory pressure (PEEP) ventilation with the thorax either open or closed. Lateral roentgenograms were taken to determine the relative vertical positions of the LA and PW catheter tips. When the wedge catheter tip was vertically above the left atrial catheter tip, mean PW followed airway pressure at PEEP of more than 5 cm H2O. For PEEP 5 cm H2O or less, and for PW catheter tip positions vertically below the LA catheter tip at all levels of PEEP, mean wedge catheter pressure was close to left atrial pressure. Thus, it appears that LA pressure can best be estimated by PW catheter positions vertically below the left atrium during positive end-expiratory pressure ventilation.

Hypertonic mannitol in the therapy of the acute respiratory distress syndrome.

Increased pulmonary artery pressure, an increase in pulmonary vascular resistance and an increase in physiologic dead space are consistent findings in patients with post-traumatic respiratory distress. Since mannitol has been shown to decrease renal vascular resistance following trauma, the effect of a bolus injection of 100 ml of 25% solution of this drug on pulmonary hemodynamics and physiologic dead space was investigated in 11 patients who had suffered multiple trauma. Five minutes after the injection, pulmonary vascular resistance fell (p less than .01), cardiac index increased (p less than .001) and physiologic dead space decreased (p less than .05). In contrast, the administration of 40 mg of furosemide produced no significant change in any of these parameters. Mannitol rapidly equilibrates in the extracellular space and exerts an osmotic effect across cell membranes. We postulate that the beneficial response to mannitol on the pulmonary vascular resistance and the improved perfusion of ventilated regions of the lung is due to a reduction in cell swelling and is not explainable by its diuretic effect. Improvement in the distribution of perfusion of pulmonary blood flow by mannitol may be a useful aid in the treatment of the post-traumatic form of the respiratory distress syndrome.

Airway Function in Sarcoidosis: Smokers versus Nonsmokers

Pulmonary function was measured in 24 sarcoidosis patients, 17 nonsmokers and 7 smokers. 12 (4 smokers) had evidence of small airway disease and 6 patients (3 smokers) had evidence of large airway disease. A significantly greater proportion of smokers had an increased closing volume, and closing volume appears to be the most sensitive test for small airway disease in sarcoidosis. However, 3 patients with normal closing volumes had evidence of small airway disease by forced expiratory flow rates or frequency dependence of compliance. We conclude that there is a high incidence of small airway disease in patients with sarcoidosis. There also appears to be a synergism between sarcoidosis and smoking that leads to a significant degree of hyperinflation of the lung.

Pulmonary Function in Diffuse Sarcoidosis

Respiratory function was studied in 44 cases of sarcoidosis. Patients were classified into several groups depending on radiological findings. There was little correlation between functional abnormality and radiological change until advanced parenchymal infiltration occurred. The most common findings were lowered forced vital capacity, total lung capacity, diffusing capacity, and dynamic compliance. Significant correlations were found between diffusing capacity and forced vital capacity, diffusing capacity and total lung capacity, and between arterial oxygen tension and forced expiratory volume in 1 sec. There were no significant correlations between diffusing capacity and arterial oxygen tension or between diffusing capacity and dynamic compliance. Evidence of diffuse expiratory airway obstruction in 13 sarcoid patients who did not smoke is assumed to be due to peri-bronchiolar peripheral airway involvement

Carbon dioxide versus H ion as a chemoreceptor stimulus

Abstract The carotid chemoreceptor increases its discharge with increases in CO 2 and H ion though the CO 2 response may be greater than that attributed to concomitant pH changes alone. We attempted to study this increased CO 2 responsiveness. However, in 9 of 10 single fibers studied, once a 20–40 min equilibration period elapsed, the response to CO 2 -dependent H ion increases was comparable to increases due to acid infusion. Thus, we conclude that H ion changes alone can completely account for chemoreceptor CO 2 stimulation.

Effect of chemorceptor denervation on the pulmonary vascular response to atelectasis

Six dogs anesthetized with 30 mg/kg pentobarbital were ventilated after differential cannulation of the main stem bronchi. Following sternotomy, blood flow was monitored by electromagnetic flow probes on the left pulmonary artery (QL) and on the pulmonary trunk or aorta (QT). Following 10 min of bilateral 100% O2, QL was 37.4 +/- 5.8% of QT. When left lung atelectasis was induced while the right lung remained on 100% O2, PaO2 remained above 75 mm Hg and QL fell to 26.1 +/- 5.0% of QT. However, when the right lung was ventilated with room air while the left lung remained atelectatic, PaO2 fell to 50.0 +/- 2.6 mm Hg and QL rose to 36.7 +/- 6.2% of QT. Six dogs which had undergone peripheral chemoreceptor denervation prior to these experiments showed a similar decrease in perfusion of the atelectatic left lung when the right lung was ventilated with 100% O2, but did not increase blood flow to the atelectatic lung during systemic hypoxemia. Thus, the increased blood flow to the atelectatic lung which occurs during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

Non-random chemoreceptor activity during superfusion in vitro

As a means of probing the chemotransducer, impulse sequences from in vitro, superfused sinus nerve-carotid body preparations were analyzed for departures from randomness. Twelve of 17 spike trains showed interval histograms that did not differ significantly from exponential. Thus these sequences resembled a Poisson (random) process with respect to time-independence of probability of occurrence of an event. However, 5 spike trains departed significantly from the exponential distribution forcing rejection of the Poisson model in these cases. Furthermore, mean interval vs standard deviation analysis revealed a significant positive correlation among intervals. These data suggest that the carotid body impulse generator possesses an intrinsic regularity and that the Poisson model does not accurately describe the in vitro sinus nerve interspike interval sequence.

Dynamic Model of Ventilatory Response to Changes in Po 2 at the Carotid Body Chemoreceptors

Much of the recent work evaluating the role of the carotid body chemoreceptors in the control of ventilation has involved the application of transient stimuli. The response of ventilation to a sustained step decrease in Po 2 from 90 mm Hg to 32 mm Hg of blood perfusing the carotid bodies of dogs indicated an abrupt increase in ventilation to nearly the final steady-state levels. The similarity of this response to the classic linear second-order system response prompted the investigation of a mathematical model that could be used to simulate the ventilatory control loop. It has been determined that the response of the ventilatory system of the dog to step, ramp, pulse, and pulse train inputs of hypoxia can be simulated with good accuracy by a nonlinear closed-loop feedback system that contains linear second-order dynamics. The input to this system is proportional to the magnitude and the rate of change of Po 2 at the carotid bodies.