Active and passive respiratory mechanics in anesthetized dogs.

In six spontaneously breathing anesthetized dogs (pentobarbital sodium, 30 mg/kg) airflow, volume, and tracheal and esophageal pressures were measured. The active and passive mechanical properties of the total respiratory system, lung, and chest wall were calculated. The average passive values of respiratory system, lung, and chest wall elastances amounted to, respectively, 50.1, 32.3, and 17.7 cmH2O X l-1. Resistive pressure-vs.-flow relationships for the relaxed respiratory system, lung, and chest wall were also determined; a linear relationship was found for the former (the total passive intrinsic resistance averaged 4.1 cmH2O X l-1 X s), whereas power functions best described the others: the pulmonary pressure-flow relationship exhibited an upward concavity, which for the chest wall presented an upward convexity. The average active elastance and resistance of the respiratory system were, respectively, 64.0 cmH2O X l-1 and 5.4 cmH2O X l-1 X s. The greater active impedance reflects pressure losses due to force-length and force-velocity properties of the inspiratory muscles and those due to distortion of the respiratory system from its relaxed configuration.

Immediate response to resistive loading in anesthetized humans.

In eight spontaneously breathing anesthetized subjects (halothane: approximately 1 minimal alveolar concn; 70% N2O-30% O2), we determined 1) the inspiratory driving pressure by analysis of the pressure developed at the airway opening (Poao) during inspiratory efforts against airways occluded at end expiration; 2) the active inspiratory impedance; and 3) the immediate (first loaded breath) response to added inspiratory resistive loads (delta R). Based on these data we made model predictions of the immediate tidal volume response to delta R. Such predictions closely fitted the experimental results. The present investigation indicates that 1) in halothane-anesthetized humans the shape of the Poao wave differs from that in anesthetized animals, 2) the immediate response to delta R is not associated with appreciable changes in intensity, shape, and timing of inspiratory neural drive but depends mainly on intrinsic (nonneural) mechanisms; 3) the flow-dependent resistance of endotracheal tubes must be taken into account in studies dealing with increased neuromuscular drive in intubated subjects; and 4) in anesthetized humans Poao reflects the driving pressure available to produce the breathing movements.

Respiratory and acid-base parameters during salicylic intoxication in dogs.

This paper examines the mechanism responsible for hyperventilation and accompanying respiratory alkalosis during acute salicylism. Sodium salicylate (250 mg/kg) was administered to 8 spontaneously breathing anesthetized dogs (alpha-chloralose, 50 mg/kg, and urethane, 500 mg/kg, iv). The trachea was sectioned and connected to a pneumotachograph. A catheter was placed in the cisterna magna for sampling cerebrospinal fluid (CSF) and a femoral artery was cannulated for blood sampling and pressure determinations. Once the cardiorespiratory steady-state was obtained, air flow, tidal volume, arterial pressure, ECG and rectal temperature were measured for baseline control. The measurements were repeated 8 times during 100 min after salicylate infusion. Simultaneous determinations of CSF and plasma salicylate showed that plasmatic levels were maximal just after infusion, diminishing with time. CSF concentration increased gradually as the salicylate diffused through the blood-brain barrier. Minute ventilation increased to more than 600% of control values and was maximal between 60-100 min after salicylate infusion. Respiratory alkalosis and hyperthermia (up to 40.3 degrees C) followed the time-course of hyperventilation. Only a small part of hyperventilation can be attributed to the temperature increase. A high correlation coefficient (r = 0.974) was obtained by regression analysis of the values for ventilation and CSF salicylate. We conclude that the central action of salicylate is much more important for increasing ventilation than effects related to oxidative phosphorylation uncoupling.

Volume-time profile during relaxed expiration in the normal dog.

Airway opening pressure, esophageal pressure, and flow were obtained during relaxed expirations in two normal anesthetized paralyzed dogs. The signal-to-noise ratio in the flow signals was greatly increased by averaging 10 different signals obtained with the same lung inflation volume. Numerical integration of an averaged flow signal then yielded the time course of the volume of the respiratory system above functional residual capacity (the elastic equilibrium volume). Comparison of volume signals obtained with different inflation volumes suggests that the resistance of the respiratory system increases with flow. The flow-volume and semilog volume curves show that expiration is induced by two apparently separate mechanisms: one causes emptying of most of the expired volume over a time interval of much less than 1 s, whereas the other contributes a relatively small amount to the expired volume over a significantly longer time (greater than or equal to 1 s). We postulate the first mechanism to be due to that of the respiratory system behaving like a single unit, with an elastance that is slightly volume dependent, emptying through a single airway which has a resistance that increases with flow. From the nature of airway opening pressure and esophageal pressure measured after occlusion in midexpiration, we conclude that the second mechanism is due to the viscoelastic properties (i.e., creep) of the respiratory system. The properties are manifest mainly in the chest wall.