A number of physiologic mechanisms aid the heart when faced with an increased he

Question

A number of physiologic mechanisms aid the heart when faced with an increased hemodynamic burden and reduced cardiac output. These compensatory responses have both beneficial and detrimental effects. Of the compensatory responses listed below, discuss both the beneficial and detrimental effects these responses will have in a patient experiencing low cardiac output. Tachycardia & increased contractility (due to SNS activation) Increased preload (through sodium & water retention) Vasoconstriction

Explanation / Answer

Tachycardia is a condition of rapid but regular or irregular heartbeat which is not in proportion to the person's age and level of exertion or activity. In some cases, tachycardia may cause no symptoms or complications but if left untreated, it can disrupt normal heart function and lead to serious complications like heart failure and stroke.

But in a person with low cardiac output tachycardia may help n improving the rate of blood flow through the body. However, this can cause overexertion of the cardiac muscles which might lead to other serious complications of the heart.

Increased cardiac contractility due to SNS activation -- Contractility is the inherent strength of the heart's contraction during systole. The stroke volume will be greater if the contractility of the heart is greater.

An increase in sympathetic nerve stimulation to the heart increases its contractility. SNP can accelerate heart rate and widen the bronchial passage. On the other hand, it can constrict blood vessels which will increase the stress on the heart and increase blood pressure.

Increased preload due to sodium and water retention-- Activation of the renin-angiotensin-aldosterone [ RAAS ] system causes increased sodium retention by the kidneys which lead to reduced water loss through urine which in turn results in blood volume expansion.

Sodium and water excretion leads to decreased cardiac preload. Reduced heart rate, which increases ventricular filling time. Increased aortic pressure, which increases the afterload on the ventricles, reduces stroke volume by increasing end-systolic volume and leads to a secondary increase in ventricular preload. So, an increase in ventricular preload will increase the heart rate resulting n a forced increase n the cardiac output.

Vasoconstriction means a constriction or narrowing of the blood vessels due to which blood will face greater resistance n flowing through them. The heart will have to pump harder to push the blood through the narrowed blood vessels. As a result of this, the heart rate will increase and so will the arterial blood pressure. In the long run, this will have a detrimental effect on the heart leading to other complications of the heart.

Venous vasoconstriction leads to increased cardiac output by increasing the stroke volume [ venous blood return].

So, vasoconstriction will increase the heart rate but will put a lot of strain on the heart to increase the cardiac output.

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