Give a concise account of the compensatory responses of the cardiovascular system to heart failure.

Outline:

·        Causes

·        Acute responses:

- baroreceptor reflex

- chemoreceptor reflex

·        Chronic responses: renin-angiotensin-aldosterone

·        Recovery phase

Essay:

            Cardiac failure refers to the failure of the heart to pump enough blood to satisfy the needs of the body. Cardiac failure may be manifest by a decrease in cardiac output and/or damming of the blood in the veins behind the left or right side of the body. The causes of cardiac failure include myocardiac infarction due to occlusion of one of the coronary arteries, damage to heart valves, external pressure around the heart and vitamin B deficiency.

            When cardiac output falls precariously low, the baroreceptor, chemoreceptor and CNS ischemic reflexes are activated. The sympathetics become strongly stimulated within a few seconds, and the parasympathetics become reciprocally inhibited at the same time. Sympathetic stimulation increases the rate of firing of the SA and AV nodes and increase the strength of myocardial contraction. This makes the heart a stronger and faster pump which elevates the cardiac output. Sympathetic stimulation also increases the tendency of venous return because it increases the tone of most of the blood vessels of the circulation, especially the veins, raising the mean systemic filling pressure to twice above normal. As more blood fills the right atrium, the pumping force is increased due to the intrinsic Frank-Starling mechanism, helping the heart to pump still larger quantities of blood.

            After the first few minutes of an acute heart attack, a prolonged secondary state begins, characterized mainly by retention of fluid by the kidneys. The reduced renal blood flow and sympathetic stimulation on the renal arterioles leads to increased renin production and release by the juxtaglomerular cells. Renin cleaves angiotensinogen to angiotensin I which is converted to the active hormone angiotensin II by the angiotensin-converting enzyme. Angiotensin II is a potent vasoconstrictor itself and it acts on the renal tubules to increase NaCI reabsorption. It stimulates the synthesis and release of ADH by the posterior pituitary. ADH increases the permeability of the collecting ducts to water by insertion of water channels in the apical membrane and this helps the body to conserve water and hence body volume. Angiotensin causes thirst by an action on the subfornical organ and ingestion of fluids helps restore the ECF volume. The increases in circulating angiotensin II and ACTH levels increase aldosterone secretion. Aldosterone causes the retention of sodium, which helps reexpand the blood volume. The increased blood volume increases the venous return by increasing the mean systemic filling pressure, which increases the pressure gradient for causing flow of blood toward the heart and distends the veins, which reduces the venous resistance and thereby allows increased ease of flow of blood to the heart. If the heart is not too greatly damaged, this increased tendency for venous return can often fully compensate for the heart’s diminished pumping ability and return the cardiac output back to normal. When cardiac output is normal, increased secretion of atrial natriuretic peptide reverses all the actions of angiotensin II and aldosterone, preventing continual retention of fluid.

            After infarction of the heart, a new collateral blood supply begins to penetrate the peripheral portions of the infarcted area, often causing much of the muscle in the fringe areas to become functional again. Also, the undamaged musculature hypertrophies, in this way offsetting much of the cardiac damage. With the compensatory mechanisms elevating the cardiac output back to near normal, the heart ordinarily recovers rapidly during the first few days and weeks and achieves most of its final state of recovery within 5 to 7 weeks, although some recovery continues for months.