Myocardial function in the critically ill: factors influencing left and right ventricular performance in patients with sepsis and trauma.
Myocardial performance in critically ill patients is primarily responsive to the need to supply O2 to the periphery. An increase in CO is the common finding in an acute illness characterized by an increase in systemic VO2 (for example, sepsis and trauma), since acute variations in flow are the most efficacious mode of augmenting systemic O2t to match the VO2. The lower systemic VO2 of a patient with an acute cardiac illness explains why the CO in this disease is not as elevated as that found in the acutely ill patient with sepsis or trauma. Endogenous compensatory mechanisms used to vary flow according to the need for O2t include heart rate, ventricular preload, contractility, and afterload. An increase in LV contractility and a reduction in afterload facilitate LV stroke volume, hence O2t. Conversely, pulmonary hypertension may result in a restriction of LV preload if RV pump failure ensues. Other factors relevant to the care of the critically ill that will decrease LV preload--and thus reduce the heart's left-sided adaptation to maintain O2t--include the presence of underlying cardiac disease, which will limit any necessary increase in contractility, and the use of PEEP, which will restrict venous return to the RV. Therapeutic intervention is required when O2t does not balance systemic VO2 and arterial lactate levels rise. The use of resuscitative fluid to improve flow by the Frank-Starling (preload) mechanism may be limited by the compliance properties of either ventricle, but it is a reasonable first choice, with guidelines for administration determined by the PCWP, which influences fluid flux across the pulmonary microvascular exchanging membrane. Vasodilators may be used to increase CO by reducing impedance to ventricular ejection; they may also improve LV compliance, thereby allowing the administration of more fluid (that is, increasing preload) without an untoward rise in the PCWP. If vasodilators are without effect or are potentially dangerous because of concomitant hypotension, inotropic support to increase O2t is required. A brief summary of interventional pharmacologic support in acute illness is depicted in Figure 8.
D000208:Acute Disease; D000222:Adaptation, Physiological; D001424:Bacterial Infections / Q000378:metabolism / Q000503:physiopathology*; D001794:Blood Pressure; D002302:Cardiac Output; D006321:Heart / Q000503:physiopathology*; D006331:Heart Diseases / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D006333:Heart Failure / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D012151:Resuscitation; D014947:Wounds and Injuries / Q000378:metabolism / Q000503:physiopathology*
D010100:Oxygen