Determinants of myocardial performance after blunt chest trauma

Objective: This study investigates whether factors that determine myocardia l performance (preload, afterload, heart rate, and contractility) are alter ed after isolated unilateral pulmonary contusion. Methods: Catheters were placed in the carotid arteries, left ventricles, an d pulmonary arteries of anesthetized, ventilated (Fio(2) = 0.5) pigs (31.2 +/- 0.6 kg; n = 26), A unilateral, blunt injury to the right chest was deli vered with a captive bolt gun (n = 17) followed by tube thoracostomy. To co ntrol for anesthesia and instrumentation at Fio(2) of 0.5, one group receiv ed tube thoracostomy only (sham injury; n = 6), To control for effects of h ypoxia without chest injury, an additional sham-injury group (n = 3) was ve ntilated with Fio(2) of 0.12. To generate cardiac function (i.e., Starling) curves, lactated Ringer's solution was administered in three bolus infusio ns at serial time points; the slope of stroke index versus ventricular fill ing pressure defines cardiac contractility, Results: By 4 hours after pulmonary contusion, pulmonary vascular resistanc e, airway resistance, and dead space ventilation were increased, whereas Pa o(2) (72 +/- 6 mm Hg at Fio(2) = 0.5) and dynamic compliance were decreased (all p < 0.05). Despite profound lung injury, arterial blood pressure, hea rt rate, cardiac filling pressures, and output remained within the normal r ange, which is inconsistent with direct myocardial contusion. The slope of pulmonary capillary wedge pressure versus left ventricular end-diastolic pr essure (LVEDP) regression was reduced by more than 50% from baseline (p < 0 .05), but there was no significant change in the slope of the central venou s pressure versus LVEDP regression. By 4 hours after contusion, the slope o f the stroke index versus LVEDP curve was reduced by more than 80% from bas eline (p < 0.05). By the same time after sham injury with Fio(2) of 0.12 (P ao(2) < 50 mm Hg), the regression had decayed a similar amount, but there w as no change in the slope after sham injury with Fio(2) of 0.5 (Pao(2) > 20 0 mm Hg), Conclusion: After right-side pulmonary contusion, the most often used estim ate of cardiac preload (pulmonary capillary wedge pressure) does not accura tely estimate LVEDP, probably because of changes in the pulmonary circulati on or mechanics. Central venous pressure is a better estimate of filling pr essure, at least in these conditions, probably because it is not directly i nfluenced by the pulmonary dysfunction, Also, ventricular performance can b e impaired by depressed myocardial contractility and increased right ventri cular afterload even with normal left ventricular afterload and preload, It is thus conceivable that occult myocardial dysfunction after pulmonary con tusion could have a role in the progression to cardiorespiratory failure ev en without direct cardiac contusion.