Dr Jayanta Bhattacharya explains Heart mechanisms

How does it really work?

Heart Failure and Mechanism Behind It

Physicians have long believed that the erythrocyte sedimentation rate is low in patients with congestive heart failure, but this concept is based on a misinterpretation of the results in a single report published in 1936.  But more recent data – 1991 onwards – indicate that the erythrocyte sedimentation rate is correlated with the severity of illness in patients with chronic heart failure. Because of its lack of discriminatory power, however, the test is of limited value in the clinical management of this disorder. Evolution to terrestrial life meant leaving behind the sea and its continuous source of salt and water. Water on land, when available, was fresh, and therefore adaptation to land necessitated the development of mechanisms to preserve salinity. An internal source of salinity is provided by extracellular fluid. Each arterial pulse of blood to exchange vessels of the microcirculation represents an onrushing saline tide that maintains a dynamic equilibrium with extracellular fluid. Animals living on land had to become capable of preserving their internal environment, including maintaining osmotic balance and salinity under a wide range of conditions over which they had little control. Kidneys became responsible for regulating the balance of salt and water by conserving both during periods of deprivation and excreting dilute urine when water consumption was high.

Normal regulation of salt and water homeostasis in mammals involves various sensors and controls operating in a negative-feedback loop. These include sensors of renal perfusion and tubular sodium delivery present within the kidney and effector hormones elaborated by endocrine organs. Key among them are renin, released by the juxtaglomerular cells lining afferent renal arterioles and neighboring macula densa cells of the distal tubule, and aldosterone produced by the adrenal glands. Renin cleaves four amino acids from circulating angiotensinogen, the angiotensin-peptide precursor produced by the liver, to form angiotensin I, a biologically inert decapeptide. Angiotensin-converting enzyme, which is bound to the plasma membrane of endothelial cells, cleaves two amino acids from angiotensin I to form angiotensin II. Angiotensin II has several important actions integral to maintaining circulatory homeostasis, including promoting the constriction of the arterioles within the renal and systemic circulations and the reabsorption of sodium in proximal segments of the nephron. It also stimulates the adrenal cortex to secrete aldosterone, which promotes the reabsorption of sodium (in exchange for potassium) in distal segments of the nephron and in the colon and the salivary and sweat glands. From a teleologic perspective, the evolution of the renin-angiotensin–aldosterone system was a delayed event necessitated by periods of salt deprivation or the loss of salt and water and the need to retain them.

For a healthy heart, we have to keep these factors in mind.

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