Heart failure syndrome is defined as the inability of the heart to deliver adequate blood to the body to meet end-organ metabolic needs and oxygenation at rest or during mild exercise. Myocardial dysfunction can be defined as systolic and/or diastolic, acute or chronic, compensated or uncompensated, or uni- or biventricular. Several counterregulatory mechanisms are activated depending on the duration of the heart failure. Neurohormonal reflexes such as sympathetic adrenergic system, renin-angiotensin cascade, and renal and peripheral alterations attempt to restore both cardiac output and end-tissue perfusion. An adequate stroke volume cannot be ejected from the left ventricle, which shifts the whole pressure-volume relationship to the right (systolic failure). Adequate filling cannot be realized due to diastolic stiffness, which shifts the diastolic pressure-volume curve upward without affecting the systolic pressure-volume curve (diastolic failure). Left ventricular heart failure is the dominant picture of heart failure syndrome, but the right heart can develop isolated failure as well. Biventricular failure is mostly an end-stage clinical situation of the heart failure syndrome. More recently, the rise in the incidence of right ventricular failure can be seen after the implantation of a left ventricular assist device. This chapter clarifies and presents pathophysiologic alterations in heart failure syndrome.
Part of the book: Cardiomyopathies