Circulatory effects of deep inspirations, blocked expirations and positive pressure inflations at equal transpulmonary pressures in conscious dogs.
1. Circulatory effects of deep inspirations, blocked expirations and constant endotracheal positive pressure inflations were studied in six conscious dogs under comparable geometries of the pulmonary vascular bed, i.e. at equal transpulmonary pressures (around 10.2 cm H(2)O) and similar lung volumes.2. In order to characterize these effects, we measured beat-by-beat left and right ventricular ejections, pulmonary arterial, left atrial and aortic mean transmural pressures, and concomitant intrathoracic and tracheal pressures. Changes in pulmonary-left heart blood volume were also computed.3. During inspiration when intrathoracic pressure became more negative, there was a slight increase in right ventricular output (+15%; P < 0.1) and always a net decrease in left ventricular output (-25%; P < 0.01) despite a significant increase in mean transmural left atrial pressure (+3 cm H(2)O, i.e. +40%; P < 0.005). It is concluded that the more negative intrathoracic pressure increases the left ventricular outflow impedance and that an inspiratory increase in pulmonary vascular capacity cannot explain the observed reduction in left ventricular output since this reduction occurs together with an increase in left ventricular filling pressure.4. During blocked expiration when intrathoracic pressure was positive, decreases in right ventricular output (-17%; P < 0.05) and in pulmonary-left heart blood volume (-12 ml.; P < 0.05) were observed while right ventricular outflow impedance increased. After an initial augmentation in left ventricular output (despite a concomitant progressive decrease in mean transmural left atrial pressure), left ventricular output also decreased (-17%; P < 0.05). Such circulatory changes were similar but less marked than those observed under constant positive pressure inflations. These observations suggest that the decrease in venous return (and consequently in right ventricular output) following the increase in intrathoracic pressure is the leading factor which overshadows the augmentation in left ventricular output associated with the simultaneous decrease in left ventricular outflow impedance.5. Similar experiments performed on two additional dogs in acute conditions showed the same circulatory effects before and after pharmacological blockade. These observations therefore confirm that mechanical factors play a leading part during these respiratory manoeuvres.
D000818:Animals; D001013:Aorta, Thoracic; D001285:Atropine / Q000494:pharmacology; D001775:Blood Circulation; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D002306:Cardiac Volume; D004285:Dogs; D006339:Heart Rate; D010643:Phenoxybenzamine / Q000494:pharmacology; D011175:Positive-Pressure Respiration; D011312:Pressure; D011433:Propranolol / Q000494:pharmacology; D011651:Pulmonary Artery; D011652:Pulmonary Circulation; D012119:Respiration / Q000187:drug effects; D013909:Thorax; D014655:Vascular Resistance; D016276:Ventricular Function
D010643:Phenoxybenzamine; D001285:Atropine; D011433:Propranolol