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Explore anatomy, determinants of cardiac output, and drug therapy for heart failure in this lecture. Learn about preload, afterload, and contractility affecting cardiac output. Discover common drugs like diuretics, ACE inhibitors, and beta blockers. Understand left and right heart failure symptoms and the role of diuretics, ACE inhibitors, digitalis, and vasodilators in treatment.
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Drug acting on the Heart Heart failure
Lecture objectives At the end of the this lecture, the student will able to: • Describe basic anatomy of the heart. • List determinants factor of cardiac out put. • Describe main approach to the treatment of heart failure. • List the names of drug used to treat heart failure and hypertension
A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body. • It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent
Cardiac Physiology(remember this?) CO = SV x HR • HR: parasympathetic and sympathetic tone • SV: preload, afterload, contractility
70 ml 75 beat/min Cardiac Output • Volume of blood ejected per minute • Averages between 4-6L/min • CO = Stroke volume X heart rate =70 ml X 60 beats/min =4,200 ml/min
Preload • Degree of stretch of myocardial fibers • Determined by the volume of blood in left ventricle (LV) at end of diastole • Increased volume –> increased preload-> increased cardiac output (CO) • Decreased volume –> decreased preload –> decreased cardiac output (CO) • Compliance of myocardial cells also affects preload
More out • Factors on Cardiac Output • Preload: More in Preload cardiac output (Starling-Frank Mechanism)
Factors Which Increase Preload • IV fluids • Blood • Vasoconstriction Factors Which Decrease Preload • Diuretics • Dehydration • Hemorrhage • Vasodilation
Factors on Cardiac Output Afterload • Preload: • 2) Afterload: R afterload CO
Afterload • Related to arterial pressure or diameter of arteries • As pressure increases, resistance increases, afterload increases • As pressure decreases, resistance decreases, afterload decreases
Contractility • Force generated by the myocardium when it contracts – inotropic property • Ejection fraction (EF) - percentage of LV end-diastolic volume that is ejected with each contraction • EF - normally approximately 50-55%
Factors on Cardiac Output • Preload: • 2) Afterload: • 3) Contractility: contractility CO
Left Heart Failure - Dyspnea - Dec. exercise tolerance - Cough - Orthopnea - Pink, frothy sputum Left versus Right Failure Right Heart Failure - Dec. exercise tolerance - Edema - JVD - Hepatomegaly - Ascites
Five main drugs are used • Diuretics • ACE inhibitors • Positive isotropic drugs • Vasodilator • ß blockers
1) Diuretics • Drugs that accelerate the rate of urine formation. • Result: removal of sodium and water • They relive distention of the heart by reducing blood volume
Side Effects • Pre-renal azotemia • Skin rashes • Neutropenia • Thrombocytopenia • Hyperglycemia • ↑ Uric Acid • Hepatic dysfunction
More severe heart failure → loop diuretics • Lasix (20 – 320 mg QD), Furosemide • Bumex (Bumetanide 1-8mg) • Torsemide (20-200mg)
2) Inhibitors of renin-angiotensin- aldosterone system • Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important rolein the progression of the syndrome • Angiotensin converting enzyme inhibitors • Angiotensin receptors blockers • Spironolactone
Angiotensin Converting Enzyme Inhibitors • They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II → vasodilation and ↓ Na retention
Side effects of ACE inhibitors • Angioedema • Hypotension • Renal insuffiency • Rash • cough
3)Digitalis Glycosides (Digoxin, Digitoxin) • The role of digitalis has declined somewhat because of safety concern • Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant • Reduction in hospitalization • Reduction in symptoms of HF
Digitalis (cont.)Mechanism of Action • +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase → inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange • Arrhythmogenic effect
Digitalis Toxicity • Narrow therapeutic to toxic ratio • Non and cardiac manifestations • Anorexia, • Nausea, vomiting, • Headache, • Disorientation • Sinus bradycardia and arrest • A/V block (usually 2nd degree) • Atrial tachycardia with A/V Block • Development of junctional rhythm in patients with a fib
4) β Blockers • Has been traditionally contraindicated in pts with CHF • Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV function • In addition to improved LV function multiple studies show improved survival
Subdivisions of ANS • Parasympathetic – acetylcholine produces inhibitory response • Sympathetic – catecholamines stimulate • Increase heart rate – Beta 1 receptors • Dilate smooth muscles – Beta 2 receptors • Vasoconstrict vessels – Alpha receptors
5) Vasodilators • Reduction of afterload by arteriolar vasodilatation (hydralazin) reduce LVEDP, O2 consumption,improve myocardial perfusion, stroke volume and COP • Reduction of preload Byvenous dilation • ( Nitrate) ↓ the venous return ↓ the load on both ventricles. • Usually the maximum benefit is achieved by using agents with both action.
Positive inotropic agents • These are the drugs that improve myocardial contractility (β adrenergic agonists, dopaminergic agents, phosphodiesterase inhibitors), • dopamine, dobutamine, milrinone, amrinone • Several studies showed ↑ mortality with oral inotropic agents • So the only use for them now is in acute sittings as cardiogenic shock
Home work? • Write the nursing implication to the drug that treat HF? • Write two examples to each group of medication? thank you for listening