Cardiovascular disturbances in chronic respiratory insufficiency.
The mechanical factors by which chronic respiratory insufficiency may influence right and left ventricular performance during both spontaneous and mechanical ventilation are reviewed. During a spontaneous inspiration the right heart distends because of increased inflow and increased pulmonary vascular resistance. This decreases the effective left ventricular compliance, through ventricular interdependence, reducing the gradient for pulmonary venous return. The inspiratory decrease in pleural pressure also effectively increases the impedance to left ventricular ejection. An inspiratory increase in abdominal pressure further increases the left ventricular afterload. These factors combine to impair left ventricular performance. During intermittent positive pressure ventilation, left ventricular stroke volume increases early in inspiration. This increased inspiratory flow cannot be attributed to a phase lag in the right heart output reaching the left heart chambers because, even with a constant pulmonary arterial inflow, aortic flow increases during inspiration. Several factors may act in concert to improve left ventricular performance, despite the adverse effects of intermittent positive pressure ventilation on the right ventricle. These include (1) a decrease in right heart volume, increasing left ventricular compliance and hence the gradient for pulmonary venous return; (2) anterograde emptying of the alveolar capillary bed with lung inflation; (3) the increase in pleural pressure decreasing impedance to left ventricular emptying; and (4) physical compression of the heart by the lungs.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002318:Cardiovascular Diseases / Q000150:complications*; D002908:Chronic Disease; D003326:Coronary Circulation; D004285:Dogs; D006321:Heart / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D007385:Intermittent Positive-Pressure Ventilation; D008168:Lung / Q000503:physiopathology; D010496:Pericardium / Q000503:physiopathology; D011311:Pressoreceptors / Q000503:physiopathology; D012119:Respiration; D012131:Respiratory Insufficiency / Q000150:complications*; D013997:Time Factors