Pulmonary injury depresses cardiac systolic function through Starling mechanism.
To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.
D000818:Animals; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D001810:Blood Volume; D003326:Coronary Circulation; D003971:Diastole; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000473:pathology; D008171:Lung Diseases / Q000473:pathology / Q000503:physiopathology*; D009200:Myocardial Contraction; D013599:Systole