GCR: Heart Failure Disease Specific Site

HEART FAILURE
Clinical Overview

Epidemiology and Pathophysiology

Definition of Heart Failure:

"...a clinical syndrome or condition characterized by (1) signs and symptoms of intravascular and interstitial volume overload, including shortness of breath, rales, and edema, or (2) manifestations of inadequate tissue perfusion, such as fatigue or poor exercise tolerance which develops as a result of the inability of the heart to meet the metabolic requirements of the tissues at rest or exercise."⁴

In order to understand the pathophysiology of heart failure, a basic understanding of normal cardiac function is necessary.

The normal cardiac cycle is comprised of two main components, ventricular diastole (filling) and ventricular systole (contraction), and diseases which adversely affect either may lead to heart failure. Until recently, it was thought that decreased myocardial contractility, or systolic dysfunction was the only cause of heart failure. Although this etiology is still the major cause of heart failure, it has now been shown that diastolic dysfunction or stiffness of the ventricle is the cause in approximately 30% to 40% of patients.⁵

^{Stroke volume (SV)

the volume of blood ejected during systole

dependent on preload, afterload, and
contractility⁶

Heart rate (HR)

controlled by the autonomic nervous
system⁶

Cardiac output (CO)

the volume of blood pumped by the heart per unit of
time 60the product of heart rate (HR) and stroke volume
(SV)⁶

CO=HR x SV

Total peripheral resistance (TPR) or systemic
vascular resistance (SVR)

the resistance to blood flow exerted by the vascular
bed

commonly used clinically to approximate left
ventricular afterload⁶

Blood pressure (BP), or mean arterial pressure
(MAP)

the average blood pressure in the arterial tree
throughoutthe entire cardiac cycle

the product of cardiac output and total peripheral
resistance⁶

BP = CO x TPR}

Preload

definition: left ventricular end diastolic volume (LVEDV) - the amount of blood returned to the heart by the venous system including that in the pulmonary circulation.

As defined by the Frank-Starling mechanism, the ability of the heart to alter the force of contraction is dependent on changes in preload. As the myocardial fibers are stretched, the force of contraction is increased. Because the length of the fiber is determined primarily by the volume of blood in the ventricle, LVEDV is the primary determinant of preload.⁷

This graph depicts the Frank-Starling mechanism of compensation in CHF. The curves represent ventricular function in a normal subject and one with left ventricular dysfunction. Line N to A represents the initial reduction in cardiac output due to CHF. Line A to B represents the Frank-Starling mechanism of compensation; an increase in left ventricular end-diastolic pressure needed to maintain cardiac output. Notice that this point (B) puts the subject into the area of congestive symptoms such as dyspnea.

Afterload

the forces against which the left ventricle must work against to eject blood into the systemic circulation.
left ventricular afterload is approximated clinically by using SVR⁷

Contractility

intrinsic property of the heart muscle that gives it the ability to contract⁶

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