Heart Failure Treatment Concepts

Treatment of Heart Failure

• Chronic heart failure (CHF) is a condition where the heart struggles to pump enough blood to supply the body's tissues and organs with oxygen and nutrients.
• The body attempts to compensate for this failure through mechanisms like cardiac muscle hypertrophy (enlarging heart chambers) and structural remodeling.
• The sympathetic nervous system and kidneys also play a crucial role in these compensatory responses.

Compensatory Responses

• Sympathetic activation releases norepinephrine and epinephrine, causing vasoconstriction, increased heart rate, and stronger myocardial contractions.
• The kidneys release renin, initiating a cascade that ultimately leads to angiotensin II production.
• Angiotensin II is a powerful vasoconstrictor, stimulating aldosterone release and ADH (antidiuretic hormone) for water retention.
• This renin-angiotensin-aldosterone (RAA) mechanism increases blood volume and pressure as a response to the heart failure.

Treatment of CHF

• Treatments have shifted from cardiac glycosides (digitalis) to vasodilators.
• Vasodilators decrease the workload on the heart by dilating blood vessels.
  • Decrease preload: Dilating veins
  • Decrease afterload: Dilating arteries
• Diuretics help eliminate excess sodium and water, reducing edema and congestion.
• Beta-blockers reduce heart rate and sympathetic activation.
• Digoxin is a second-line drug that increases myocardial stimulation.

Diuretic therapy for CHF

• Diuretics are essential for CHF treatment.
• Thiazides, loop diuretics, and potassium-sparing diuretics are utilized.
• The main effect is the elimination of excess sodium and water from the body.
• Thiazides and loop diuretics decrease preload and afterload
• Adverse effects include nausea, hypotension, hypokalemia, hyperuricemia, and hyperglycemia.
• Potassium-sparing diuretics can cause hyperkalemia

Vasodilator Treatment of CHF

• Vasodilators relax blood vessels, decreasing resistance.
• This allows for more efficient blood pumping by the heart.
• Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are common types of vasodilators in the treatment of CHF.
• Vasodilators lower peripheral resistance and blood pressure This decreases cardiac workload and oxygen consumption

Arterial Dilators

• Hydralazine is a drug that produces arterial vasodilation and reduces afterload.
• It involves nitric oxide (NO) production for relaxation of arteriolar smooth muscles.

Venodilators

• Nitrates (e.g., nitroglycerin, isosorbide dinitrate) primarily lead to venodilation, especially of larger veins and the vena cava.
• Reduces venous return, preload, and cardiac workload.

Balanced Vasodilators

• ACE inhibitors and angiotensin receptor blockers (ARBs) are balanced vasodilators.
• Inhibit angiotensin II’s effects, preventing vasoconstriction and reducing aldosterone/ADH release.
  • Decrease afterload, decreased preload

ACE Inhibitors

• Inhibit ACE, reducing angiotensin II formation, thus promoting vasodilation and sodium/water excretion.
• Also increase bradykinin levels.

Angiotensin Receptor Blockers (ARBs)

• Block angiotensin II receptors, preventing its actions.
• Promoting vasodilation, sodium, and water excretion.
• Do not affect bradykinin.

Adverse Effects of ACEIs and ARBs

• Adverse effects include headache, dizziness, hypotension, hyperkalemia, and GI disturbances.
• ACEIs can cause a dry cough and allergic reactions.

Other Drugs that Increase Myocardial Contraction

• Dopamine, dobutamine (Dobutrex), amrinone, and milrinone are used to increase myocardial contractility.
  • Used in acute cases and initially until better stabilization.

Cardiac Glycosides

• Digoxin is a cardiac glycoside that enhances myocardial contractility without increasing oxygen consumption.
• Slows heart rate and AV conduction.
• Has beneficial effects on kidney function.
• Causes decreased preload and afterload

Use of Adrenergic Receptor Blockers in CHF

• Beta-blockers block beta-receptors in the heart, reducing heart rate and contractility.
• Beta-blockers can enhance cardiac efficiency because of excessive activation of sympathetic nervous system that causes tachycardia.
• Reduces renin release from juxtaglomerular cells, causing less vasoconstriction and sodium/water retention.

Mechanism of Action of Digoxin

• Inhibits Na+/K+ATPase, leading to increased intracellular sodium and calcium.
• Increases calcium and contractility of cardiac muscle cells.

Pharmacokinetics of Digoxin

• Digoxin's effects are influenced by electrolyte levels (hypokalemia, hyperkalemia, hypercalcemia) affecting the effectiveness.
• Administration and dosage adjustments are critical for a therapeutic action.

Adverse and Toxic Effects of Digoxin

• Digoxin toxicity can lead to cardiac arrhythmias.
• Overdose symptoms include nausea, vomiting, headache, visual disturbance, and rashes.
• Digoxin-specific antibody fragments antidote for overdose.

Drug Interactions

• Other drugs (antacids, laxatives, etc.) can interfere with digoxin’s absorption.
• Certain drugs (e.g., antiarrhythmics, calcium channel blockers) can alter digoxin's effects and increase toxicity.
• Diuretics (thiazides and loop) cause hypokalemia, increasing digoxin toxicity.

This quiz delves into the mechanisms and treatments related to chronic heart failure (CHF). It covers compensatory responses of the body, including the roles of the sympathetic nervous system and the kidneys in heart failure management. Test your understanding of these critical physiological processes!