CARDIAC AND VASCULAR FUNCTION CURVES.

Figure Length-force relationships in intact heart: a Frank-Starling curve Optimal Length

Cardiac index for the human being (cardiac output per square meter of surface area) at different ages

Effect of Total Peripheral Resistance on the Long-Term Cardiac Output Level The long-term cardiac output level varies reciprocally with changes in total peripheral resistance. 4

The Heart Has Limits for the Cardiac Output That It Can Achieve! The plateau level of this normal cardiac output curve is about 13 L/min, 2.5 times the normal cardiac output of about 5 L/min. Factors That Can Cause Hypereffective Heart – Only two types of factors usually can make the heart a better pump than normal. They are (1) nervous stimulation and (2) hypertrophy of the heart muscle. Hypoeffective Heart – Any factor that decreases the heart’s ability to pump blood causes hypoeffectivity. Some of the factors that can do this are the following: – Coronary artery blockage, causing a “heart attack”, Inhibition of nervous excitation of the heart, Pathological factors that cause abnormal heart rhythm or rate of heartbeat, Valvular heart disease, Increased arterial pressure against which the heart must pump, such as in hypertension, Congenital heart disease, Myocarditis, Cardiac hypoxia 5 The fig. depicts the normal cardiac output curve, showing the cardiac output per minute at each level of right atrial pressure.

Starting at N, which represents a normal, resting individual: A = decreased performance due to a reduction in preloadA = decreased performance due to a reduction in preload B = increased performance due to an increased preload C represents an increased performance due almost entirely to increased contractility (close to the situation during exercise) Points C, D, and E represent different levels of performance due to changes in preload only; all three points have the same contractility.

Q Haemorrhage and volume overload: how does it affects preload, performance and contractility?

Vector I: consequences of a loss in preload, e.g., hemorrhage, venodilators (nitro- glycerin) Vector II: consequences of a loss in contractility, e.g., congestive heart failure Vector III: consequences of an acute increase in contractility Vector IV: consequences of an acute increase in preload, e.g., volume loading the individual going from the upright to the supine position

Vascular function curves Defines the changes in central venous pressure that are caused by changes in cardiac output. It is venous return creating a filling pressure and preload that normally determines cardiac output. The vascular function (venous return) curve depicts the relationship between blood flow through the vascular system (or venous return) and right atrial pressure.

cardiac failure What parameter is reduced in cardiac failure? cardiac contractility How the kidneys are involved in the compensatory mechanism to cardiac failure. Sympathetic NS acts on Beta-1 cells in the kidney to release renin secretion. This increases blood volume and induces venoconstriction

Q. How does cardiac failure affect CO and RAP? slight fall in CO Increase RAP

1.The figure below shows pressure volume loops for two situations. When compared with loop A, loop B demonstrates (A) Increased preload (B) Decreased preload (C) Increased contractility (D) Increased afterload (E) Decreased afterload