Unsuspected right ventricular dysfunction in shock and sepsis.

Monitoring of ventricular function by central venous (CVP) and pulmonary wedge pressures (PCW) was compared with ejection fraction and end-diastolic volume (gated pool scan) in patients resuscitated from hypovolemic and septic shock. Sixteen patients were studied within 24 hours of resuscitation and all showed depressed right ventricular ejection (RVEF) and/or an increased end-diastolic volume (RVEDVI). Group I (eight patients, hypovolemia and sepsis) had low RVEF (mean, 0.30), high RVEDVI (mean 129.2 ml/m2), and nearly normal left ventricular function (LVEF 0.63 and LVEDVI 63.6 ml/m2), compared to angiographic normals (RVEF 0.52, RVEDVI 55.8 ml/m2; nL LVEF 0.59, LVEDVI 52.3 ml/m2). Group II (3 patients, all septic) had better RVEF (mean, 0.54) but high RVEDVI (mean, 121.1 ml/m2) with normal LVEF (mean, 0.67) and high LVEDVI (mean LVEDVI 107.2 ml/m2). Group III consisted of five patients (hypovolemia and sepsis) who had biventricular depression (RVEF 0.25 and LVEF 0.29) and elevated EDVI. The mortality rate for group I (25%) was significantly less than for groups II and III (100% and 80%, respectively), and could be correlated with failure to improve RV function. Follow-up studies in ten patients showed improvement in seven which correlated with increased RVEF and reduced RVEDVI. Comparing survivors to non-survivors showed no predictability on the basis of initial studies but a significantly larger RVEDVI and RV stroke work index in non-survivors' follow-up studies. No correlation could be made with left ventricular performance, and there were no correlations between PCWP and LVEDVI or CVP and RVEDVI. A significant negative correlation was seen between RVEF and pulmonary vascular resistance (r = -0.34, p less than 0.05). Both LVEDVI and RVEDVI were correlated significantly with cardiac index and with each other. RV dysfunction occurs after resuscitation of hypovolemia and sepsis without reliable alteration in filling pressure and is likely related to myocardial ischemia as well as increased pulmonary vascular resistance. Survival seems to depend on improvement in RV performance, which can be measured at the bedside by cardiac scintigraphy.