【Pharmacology】Heart Failure

Heart failure

a chronic, progressive disorder in which the heart muscle is unable to pump enough blood to meet the body's needs.
upper chambers: atria
lower chambers: ventricles

squeeze and relax in turn to move blood through the body.

Content:

1. Blood flows
2. Heart failure
3. Sympathetic activation
4. Reference

1. Blood flows

Blood flows through the heart and lungs in four major steps

a. The oxygen-poor blood that has already circulated through the body is received by the right atrium, which in turn pumps it over to the right ventricle.

b. The right ventricle pumps the blood through the pulmonary artery into the lungs, where it picks up oxygen.

c. The pulmonary vein empties oxygen-rich blood, from the lungs into the left atrium, which in turn pumps it to the left ventricle.

d. The left ventricle pumps oxygenated blood through the aorta to the rest of the body.

Frank-Starling law of the heart

a basic physiological principle that describes how the heart is able to move blood through the body in a regulated way by pumping out as much blood as it receives.
increased filling of the ventricle, results in greatercontraction force, and thus a rise in the cardiac output.

2. Heart failure

Frank-Starling law of the heart fails

as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient.

can manifest itself as either systolic or diastolic dysfunction.

Systolic heart failure: the heart muscle becomes weak and cannot squeeze as much blood out.

Poor ventricular contractility leads to reduction in the amount of blood pumped out of the ventricle

also known as ejection fraction.

Normal ejection fraction: between 50 and 75%
heart failure: less than 40%

due to systolic dysfunction is typically associated with an ejection fraction

For this reason, the systolic heart failure is most commonly referred to as Heart Failure with Reduced Ejection Fraction (HFrEF).

Diastolic heart failure: the heart squeezes normally, but becomes stiff and cannot adequately relax to allow for normal ventricular filling.

Patients with diastolic heart failure have relatively normal ejection fraction

although stroke volume and cardiac output are reduced.

For this reason, diastolic failure is most commonly referred to as Heart Failure with Preserved Ejection Fraction (HFpEF).

3. Sympathetic activation

In order to counteract the effect of

falling cardiac output
reduced perfusion to vital organs

the body will try to compensate via two mechanisms

a. Increase in sympathetic nervous system activity

In the face of a reduced cardiac output,

the arterial baroreceptors located in the aortic arch and carotid sinus will sense changes in blood pressure
leading to the release of norepinephrine
stimulates beta-1 receptors located in the

SA node
myocardium
ventricular conduction system.

Stimulation of these receptors increases heart rate and cardiac contractility leading to greater stroke volume.

Cardiac output = heart rate × stroke volume

When heart rate and stroke volume increase, cardiac output will also increase to maintain adequate blood pressure and thereby perfusion to vital organs.

increased sympathetic nerve traffic to the kidney
activates alpha 1-adrenergic receptors located on juxtaglomerular cells
causing release renin

an enzyme responsible for regulation of blood pressure and volume

b. Activation of the renin angiotensin aldosterone system

Sympathetic nerves directly stimulating renin secretion via alpha 1 receptors
release of renin from the juxtaglomerular cells regulated by two other primary mechanisms

Renal vascular baroreceptors

stimulate renin secretion in response to low renal perfusion pressure

Macula densa cells of the distal nephron

stimulate renin secretion in response to fall in sodium chloride concentration.

once released into the blood,

renin acts upon a circulating substrate
primarily supplied by the liver called angiotensinogen to produce angiotensin I.
On passing through the pulmonary circulation,

angiotensin I is converted into angiotensin II by angiotensin-converting enzyme (ACE)
circulating angiotensin II exerts its action by binding to various receptors

most of its effects being mediated via angiotensin II type 1 receptor (AT1)

stimulation of AT1 receptors in the endothelium of systemic arterioles → vasoconstriction
stimulation of angiotensin receptors in the brain

→ pituitary to release antidiuretic hormone (ADH)
→ binds to specific vasopressin II receptors in the collecting ducts of the nehpron
→ promotes reabsorption of water back into the circulation

angiotensin receptors in the adrenal cortex

→ stimulate the release of aldosterone
→ binds to nuclear mineralocorticoid receptor within the cells of the distal tubule and the collecting duct
→ increases expression of genes that encode epithelial sodium channels and the sodium/potassium pump (Na/K ATPase)
→ promoting sodium and water reabsorption and potassium secretion
→ increase in plasma volume and blood pressure.

Activation of the renin angiotensin aldosterone system

Furthermore, vasoconstriction and fluid retention

elevates venous and capillary hydrostatic pressures
forcing additional fluid out of the blood into the tissue
edema, particularly in the feet and legs.

Increased peripheral resistance and greater blood volume

strain on the heart and accelerate the process of damage to the myocardium
structural cardiac remodeling

In the final attempt to maintain circulatory system homeostasis

the body will try to counterbalance overstimulation of the

renin angiotensin aldosterone system (RAAS)
sympathetic nervous system

by activating cardioprotective natriuretic peptides
In response to increased myocardial stretch and volume overload,

atria begin to secrete A-type natriuretic peptide (ANP)
ventricles begin to secrete B-type natriuretic peptide (BNP)

In response to increased levels of pro-inflammatory mediators resulting from cardiac injury,

vascular endothelial cells begin to secrete C-type natriuretic peptide (CNP).

Main role of these natriuretic peptides: counter the effects of volume overload and adrenergic activation by

stimulating sodium and water excretion
promoting myocardial relaxation
inhibiting cardiac hypertrophy and fibrosis
suppressing sympathetic outflow
stimulating vasodilation

However, in the end, even this counter response is not enough to save the failing heart.

As heart failure advances, further activation of the renin angiotensin aldosterone system and the sympathetic nervous system, ultimately overcomes the short-lived beneficial effects of the natriuretic peptides.

4. Reference

https://youtu.be/AJV1BsRnImA

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