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Why the Heart Fails and How the Body Compensates

1Cardiac Output and the Determinants of Pump Performance2What Heart Failure Is and Why the Pump Fails3The Frank-Starling Response: Using Preload to Defend Output4Sympathetic Activation: Raising Rate and Contractility5The Renin-Angiotensin-Aldosterone System: Defending Volume and Pressure6Cardiac Remodeling: When Compensation Becomes the Disease
Sympathetic Activation: Raising Rate and Contractility

The Baroreceptor Reflex in Reduced Cardiac Output

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Follow the signal from the arterial wall to the heart and vessels. The baroreceptors in the carotid sinus and aortic arch are stretch sensors; when the arteries are well filled, they fire steadily and hold the vasomotor center in the medulla under inhibition. As cardiac output falls, arterial stretch decreases, baroreceptor firing drops, and that inhibition is released. Sympathetic outflow rises while vagal tone to the heart falls. Watch the four targets as they respond: the sinoatrial node accelerates, ventricular contractility increases, arterioles narrow and raise resistance, and veins narrow to reduce their capacitance. Notice that the trigger is reduced effective arterial filling, not necessarily a low total blood volume — a failing pump can make a normal or even expanded volume register as inadequate.
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Arterial baroreceptors are stretch-sensitive nerve endings in the carotid sinus and aortic arch that fire in proportion to the stretch of the arterial wall. Their firing rate is therefore a continuous report of how well the arterial tree is filled and how high the arterial pressure is. When cardiac output falls, arterial pressure and arterial wall stretch decrease, and baroreceptor firing falls.

The baroreceptors tonically inhibit the vasomotor center in the medulla. A fall in their firing removes that inhibition, so sympathetic outflow to the heart and blood vessels increases while parasympathetic (vagal) outflow to the heart decreases. The result is a coordinated set of effects: the sinoatrial node fires faster, raising heart rate; ventricular contractility increases; arterioles constrict, raising systemic vascular resistance and therefore afterload; and veins constrict, reducing venous capacitance and supporting venous return.

The reflex is fast, operating within seconds, and it is graded: the larger the fall in effective circulating volume, the larger the sympathetic response. In heart failure the trigger is not always a low absolute blood pressure. Reduced effective circulating volume — the portion of blood volume that is actually perfusing tissues under adequate pressure — can be sensed as inadequate even when total body fluid is expanded, because a weak pump and dilated vascular bed reduce the effective arterial filling.

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