Comprehensive Overview of Congestive Heart Failure: Anatomy, Pathophysiology, and Treatment

Comprehensive Overview of Congestive Heart Failure: Anatomy, Pathophysiology, and Treatment

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  Congestive heart failure Ms.Sakshi bajaj Global research institute of Pharmacy, Radaur, Yamuna Nagar
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  Anatomy of Heart •Normal heart weighs about 250-350 g in an adult. It is a two-sided pump having four chambers upper two atria(right and left) and the lower two ventricles (right and left). • The two atria are separated from each other by interatrial septum and the two ventricles are separated by an interventricular septum . • The atria are separated from the ventricles by an atrioventricular valves. • These are tricuspid on the right side and mitral valve on the left side. • Blood enters each side of the heart into the atrium and then enters into the ventricles across atrioventricular valves, the mitral valve on the left and tricuspid valves on the right.
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  • On theventricular side , these valves leaflets have strong fibrous cords called chordea tendineae which are attached to the inner suface of ventricular wall via papillary muscles. • The blood flows from ventricles through the semilunar valves namely pulmonary on the right side and aortic on the left side. • The right ventricles is thinner than the left ventricles. • The heart wall has three layers ( inner endocardium, 2. middle myocardium and outer pericardium
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  Blood supply toHeart • The heart is supplied by the right and left coronary arteries which arise directly from aorta . • The left coronary artery sullies the major part of heart. • The heart contracts at the ranging from 60-80 beats per minutes. • During systole ,the heart contracts and relexes during diastole. • The heart sounds are produced during opening and closing of cardiac valves and flow of blood through the cardiac chambers and the valves.
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  Heart failure Heart failure(HF) is a clinical syndrome in which the heart is unable to pump enough blood to meet the body's metabolic demands or can do so only at the expense of elevated ventricular filling pressures. It results from structural or functional abnormalities that impair ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction). Heart failure is a progressive condition associated with reduced cardiac output, activation of compensatory neurohormonal mechanisms, fluid retention, and congestion of the lungs and peripheral tissues.
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  Types of Heartfailure Depending on onset • Chronic heart failure : Heart failure is the common end stage of many forms of chronic heart disease. • It is characterized by gradual development of heart failure and systemic arterial pressure is well maintained but edema develops .Examples include valvular heart disease, hypertension. • Acute heart failure: It is characterized by sudden development of heart failure. Example myocardial infarction and rupture of a cardiac valves.
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  • Major causesinclude: • Hypertension: Chronic high blood pressure increases afterload, making the left ventricle work harder, eventually leading to hypertrophy and heart failure. • Coronary artery disease (Myocardial infarction): Reduced coronary blood flow causes ischemia and loss of functioning cardiac muscle. • Valvular heart disease: Stenosis or regurgitation produces pressure or volume overload. • Cardiomyopathy: Structural abnormalities weaken myocardial contractility. • Diabetes, toxins, infections, congenital disorders: Cause metabolic and structural damage to cardiac muscle. • Myocardial injury decreases the heart's pumping efficiency
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  Decreased Cardiac Output Asmyocardial function deteriorates: •Myocardial contractility decreases. •Ventricular filling may become impaired due to stiff ventricles. •Stroke volume decreases. •Consequently, cardiac output (CO = Stroke Volume × Heart Rate) falls. •Reduced cardiac output means less oxygen and nutrients reach vital organs.
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  Compensatory Mechanisms (InitiallyBeneficial) The body activates several neurohormonal systems to maintain blood pressure and tissue perfusion. A. Sympathetic Nervous System (SNS) Activation Reduced cardiac output stimulates baroreceptors, activating the sympathetic nervous system. This results in: •Increased norepinephrine release •Increased heart rate (tachycardia) •Increased myocardial contractility •Peripheral vasoconstriction Benefit Initially helps maintain blood pressure and cardiac output Long-term effect Persistent SNS activation increases myocardial oxygen demand and promotes ventricular remodeling
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  Renin-Angiotensin-Aldosterone System (RAAS) Reducedrenal perfusion stimulates renin secretion. Sequence: Renin ↑ → Angiotensin I → Angiotensin II → Aldosterone release Effects Angiotensin II •Potent vasoconstrictor •Increases afterload Aldosterone •Sodium retention •Water retention •Increased blood volume •Increased preload Initially these mechanisms improve cardiac output but eventually worsen heart failure.
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  Antidiuretic Hormone (ADH)Release Low blood pressure stimulates ADH secretion from the posterior pituitary. Effects •Increased water reabsorption in collecting ducts •Expanded plasma volume •Increased preload Excessive ADH contributes to edema and hyponatremia Result of Chronic Compensation (Maladaptive Changes) Long-term activation of SNS, RAAS, and ADH becomes harmful. Major consequences include: Persistent vasoconstriction Increased systemic vascular resistance Increased afterload Sodium and water retention Increased preload Fluid overload Pulmonary and peripheral edema Increased myocardial oxygen demand The heart works harder despite inadequate blood supply.
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  Cardiac Dysfunction The damagedheart undergoes structural and functional changes. Characteristics include: •Ventricular dilation •Reduced ejection fraction (HFrEF) •Impaired ventricular relaxation (HFpEF) •Reduced pumping efficiency Cardiac dysfunction leads directly to clinical heart failure. Congestive Heart Failure At this stage, the heart cannot pump enough blood to satisfy the metabolic needs of the body except at abnormally elevated filling pressures. Patients develop: Dyspnea Fatigue Exercise intolerance Fluid retention Reduced exercise capacity
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  Drug Class ExamplesMechanism of Action Clinical Benefits ACE Inhibitors (ACEIs) Enalapril, Ramipril, Lisinopril Inhibit conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion Reduce mortality, improve symptoms, prevent ventricular remodeling Angiotensin Receptor Blockers ARBs) Losartan, Valsartan, Candesartan Block AT1 receptors, preventing angiotensin II effects Alternative for ACEI intolerance; reduce mortality and hospitalization β-Blockers Carvedilol, Metoprolol Succinate, Bisoprolol Block β-adrenergic receptors, reducing heart rate and myocardial oxygen demand Improve ejection fraction, reduce mortality and arrhythmias Mineralocorticoid Receptor Antagonists (MRAs) Spironolactone, Eplerenone Block aldosterone receptors, reducing sodium retention and fibrosis Reduce mortality and ventricular remodeling Loop Diuretics Furosemide, Torsemide, Bumetanide Inhibit Na -K -2Cl ⁺ ⁺ ⁻ transporter in the loop of Henle Relieve pulmonary and peripheral edema; improve symptoms Thiazide Diuretics Metolazone, Hydrochlorothiazide Inhibit sodium reabsorption in distal convoluted tubule Added to loop diuretics in refractory edema Cardiac Glycoside Digoxin Inhibits Na /K -ATPase, ⁺ ⁺ increasing intracellular calcium and cardiac contractility Improves symptoms, reduces hospitalization, controls ventricular rate in atrial fibrillation Vasodilators Hydralazine + Isosorbide Dinitrate Arterial and venous vasodilation, reducing preload and afterload Alternative for ACEI/ARB intolerance; beneficial in selected patients