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  • Cardiac pump dysfunction may be due to ventricular dysfunction, compression by surrounding structures (eg, cardiac tamponade), increased afterload, valvular dysfunction, or abnormal heart rate and rhythm.

  • Ventricular dysfunction may be due to decreased systolic contractility or increased diastolic stiffness and may involve right or left ventricles.

  • Systemic vascular factors controlling venous return, and their interaction with cardiac pump function, must be considered to identify and treat causes of inadequate cardiac output.

  • Myocardial ischemia, relative to demand, is the most common acute reversible contributor to decreased 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; mechanical ventricular assist devices and extracorporeal membrane oxygenation (ECMO); and cardiac transplantation.

  • Point-of-care ultrasound (POCUS) provides key initial information and allows subsequent monitoring of therapeutic effects. It can be supplemented by a subsequent comprehensive echocardiographic exam for additional information.


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. 36) 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. 36) and mechanisms for ventricular dysfunction in the context of other diseases (see Chaps. 23, 31, 34, 35, 37, and 65).


Decreased 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 focuses on right and left ventricular dysfunction because cardiac tamponade is discussed in Chap. 39, pulmonary embolism in Chap. 38, valvular dysfunction in Chap. 40, and arrhythmias in Chap. 35. 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 both right and left ventricular dysfunction 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. 33-1). How can one rapidly determine the presence of ventricular dysfunction, distinguish between right and left ventricular dysfunction, and then identify the specific cause? Point-of-care ultrasound (POCUS) plays ...

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