Cardiac pump dysfunction may be due to ventricular dysfunction, compression by surrounding structures (eg, cardiac tamponade), increased afterload, valvular dysfunction, and/or abnormal heart rate and rhythm.
Ventricular dysfunction may be due to decreased systolic contractility and/or increased diastolic stiffness and may involve right and/or left ventricles.
Systemic vascular factors controlling venous return, and their interaction with cardiac pump function, must be considered in order to identify and treat causes of inadequate cardiac output.
Myocardial ischemia, relative to demand, is the most common acute reversible contributor to depressed contractility but exogenous toxins and drugs (β-blockers, Ca2+ channel blockers, etc), a myocardial inflammatory response (due to ischemia-reperfusion, sepsis, etc), hypoxemia, acidosis, ionized hypocalcemia and other electrolyte abnormalities, and hypo- and hyperthermia also contribute.
Management of acute-on-chronic heart failure progressively includes oxygen; optimizing preload with diuretics, morphine, and nitrates or fluid infusion for hypovolemia; afterload reduction (including positive pressure ventilation); increasing contractility using catecholamines or phosphodiesterase inhibitors; antiarrhythmic drugs and resynchronization using biventricular pacing; intra-aortic balloon counterpulsation, ventricular assist and ECMO devices; and cardiac transplantation.
This chapter emphasizes how critical illness disturbs ventricular function and the systemic factors governing venous return. This does not diminish the possibility that occult ischemic heart disease (see Chap. 37) might be unmasked by the stress imposed by multisystem organ failure or its diverse treatments. To avoid redundancy, I refer liberally to other chapters in this book that discuss ischemic heart disease (Chap. 37) and mechanisms for ventricular dysfunction in the context of other diseases (see Chaps. 25, 26, 33, 36, 38, and 64).
ASSESSMENT OF CARDIAC DYSFUNCTION
Depressed cardiac pump function may be due to (1) right and/or left ventricular dysfunction, (2) external compression (eg, cardiac tamponade), (3) excessively elevated right or left ventricular afterload, (4) valvular dysfunction, and (5) abnormal heart rate or rhythm. This chapter focus on right and left ventricular dysfunction because cardiac tamponade is discussed in Chap. 40, pulmonary embolism in Chap. 38, valvular dysfunction in Chap. 41, and arrhythmias in Chap. 36. Yet in every case one should consider the role of the pericardium, lungs and other surrounding structures, right- and left-ventricular afterloads, valvular function, and heart rate and rhythm. For right and left ventricular dysfunction both decreased systolic contractility (a shift down and to the right of the end-systolic pressure-volume relation [ESPVR]) and increased diastolic stiffness (a shift up and to the left of the diastolic pressure-volume relation) must be considered (Fig. 35-1). How can one determine the presence of ventricular dysfunction, distinguish between right and left ventricular dysfunction, and then identify the specific cause?
Left ventricular pressure-volume relations, A. The continuous thick lines represent a single cardiac cycle as a pressure-volume loop. During diastole, the ventricle fills along a diastolic pressure-volume relation (1). At the onset of systole, left ventricular pressure rises with no change in volume (2). When ...
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