CCF BY DR MWEBAZA VICTOR (UGANDA) 2024.pptx

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1. DR. Mwebaza Victor JOEL MBChB Congestive Heart Failure CME STAB- BUGEMBE 12/4/2024 UGANDA

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3. Definition The condition in which an abnormality of cardiac structure or function is responsible for the inability of the heart to fill with or eject blood at a rate commensurate with the requirements of the metabolizing tissues.” [email protected] DR MWEBAZA VICTOR

4. Forms of Heart Failure Systolic versus Diastolic Low-output versus High-output Right-sided versus Left-sided Acute versus Chronic [email protected] DR MWEBAZA VICTOR

5. Systolic versus Diastolic Heart Failure Systolic Heart Failure = The principle abnormaility is the inability of the ventricle to contract normally and expel sufficient blood Diastolic Heart Failure = The principle abnormality is the inability of the ventricle to relax and fill normally [email protected] DR MWEBAZA VICTOR

6. Low-Output versus High-Output Heart Failure Low-Output Heart Failure = Occurs in patients with a primary abnormality in the heart’s ability to discharge enough blood/nutrients to the arterial system High-output Heart Failure = Occurs in patients with reduced systemic vascular resistance. Etiologies include hyperthyroidism, severe Anemia, AV fistula, pregnancy and beriberi [email protected] DR MWEBAZA VICTOR

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8. The Sympathetic Nervous System in Heart Failure Baroreceptor mediated increase in sympathetic tone in heart failure results in tachycardia, arterial and venous constriction Increased local and circulating concentrations of norepinephrine cause myocyte hypertrophy and apoptosis Via renal venoconstriction the sympathetic nervous system stimulates the renin-angiotensin-aldosterone system [email protected] DR MWEBAZA VICTOR

9. The Renin-Angiotensin-Aldosterone System in Heart Failure Angiotensin II promotes cardiac remodeling Angiotensin II causes arterial vasoconstriction increasing afterload Angiotensin increases aldosterone secretion and proximal tubular sodium transport Aldosterone also promotes cardiac remodeling [email protected] DR MWEBAZA VICTOR

10. Non-osmotic release of arginine vasopressin Activation of carotid baroreceptors results in sympathetic stimulation of the supraoptic and paraventricular nuclei in the hypothalamus which results in the release of vasopressin Vasopressin is an antidiuretic agent and causes free water retention [email protected] DR MWEBAZA VICTOR

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12. Etiologies of Heart Failure Hypertensive heart disease Ischemic Heart Disease Cardiomyopathies (dilated, hypertrophic, and restrictive. Pericardial disease (tamponade, constriction. Valvular Heart disease. Arrythmias High output causes [email protected] DR MWEBAZA VICTOR

13. Most Common Ppt factors Infection Arrhythmias Physical, Dietary, Fluid, Environmental, and Emotional Excesses Myocardial Infarction Pulmonary Embolism Anemia Thyrotoxicosis and Pregnancy Aggravation of Hypertension Rheumatic, Viral, or Other Forms of Myocarditis Infective Endocarditis [email protected] DR MWEBAZA VICTOR

14. Symptoms of CHF Dyspnea cough Orthopnea Paroxysmal Nocturnal Dyspnea Cheyne-Stokes respiration Fatigue and weakness Anorexia and nausea associated with abdominal pain and fullness Nocturia Confusion, difficulty in concentration, memory impairment, headache, insomnia, anxiety [email protected] DR MWEBAZA VICTOR

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16. Physical Findings Diminished pulse pressure Elevated diastolic arterial pressure JVD Positive abdominojugular reflex Audible 3rd and 4th heart sounds Pulsus alternans Pulmonary rales (at lung bases) Lower limb edema (presacral if bedridden pt) Hydrothorax and ascites Enlarged, tender, pulsating liver Jaundice (late finding) Cardiac cachexia Cold, pale extremities [email protected] DR MWEBAZA VICTOR

17. Framingham Criteria for Diagnosis of CHF Major Criteria ( CRAP-PINS) Cardiomegaly Rales Acute pulmonary edema PND Positive hepato Jugular reflex HJR Increased venous pressure Neck vein S3 gallop Minor Criteria ( Enehpvt) Extremity edema Night cough Exertional dyspnea Hepatomegaly Pleural effusion Vital capacity reduced by 1/3 from normal Tachycardia ≥120 bpm 1major+2minor=Dx [email protected] DR MWEBAZA VICTOR

18. New York Heart Association Functional Classification Class I: symptomatic only with greater than ordinary activity Class II: symptomatic with ordinary activity Class III: symptomatic with minimal activity Class IV: symptomatic at rest [email protected] DR MWEBAZA VICTOR

19. Diagnostic studies Chest Xray = Cardiomegaly, pulmonary vascular congestion, pleural effusions, Kerley B lines ECG = Will aid in evaluating for ischemia, or structural changes in heart,arrythmias,chamber enlargement. Echocardiogram = Will aid in determining underlying etiology and severity of ventricular systolic and/or diastolic dysfunction. Labs : BUN, Cr, Na, abnormal LFTs, CBC, cardiac enzymes. [email protected] DR MWEBAZA VICTOR

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21. Overview of drugs used in congestive heart failure Mx: Reduce symptom Reduce motality Reduice hospitalization Pharmacologica l Diuretics (loop, thiazides, potassium-sparing) Angiotensin-Converting Enzyme (ACE) Inhibitors/ARBs OR Hydralazine + Nitrates Beta blockers Digoxin [email protected] DR MWEBAZA VICTOR

22. Diuretics Avoid overtreatment: Hypovolemia  CO  impaired renal function  weakness and lethargy Thiazide Diuretics Reduce reabsorption of Na+ and Cl- in distal convoluted tubule (H2O follows salt) Watch out for K+ depletion and metabolic alkalosis Use by themselves for mild HF or in combination w/ other drugs for severe HF Loop Diuretics Reversibly inhibit reabsorption of Na+, K+, and Cl- in the thick ascending loop of Henle. Metabolic alkalosis and hypokalemia Useful for all forms of HF Potassium-Sparing Diuretics Block exchange between Na+ and both K+ and H+ in distal tubules and cortical collecting ducts  Na+ diuresis and K+ retention Weak, not good as sole agents [email protected] DR MWEBAZA VICTOR

23. Thiazide and Loop diuretics provide symptomatic relief but there is no known mortality benefit Spironolactone does have a mortality benefit although it is a weak diuretic; In RALES trial published in NEJM in 1999 a 30% decrease in mortality was noted in Class III or IV heart failure [email protected] DR MWEBAZA VICTOR

24. ACE Inhibitors Chronic activation of renin-angiotensin-aldosterone system in HF causes: Ventricular remodeling Further deterioration of cardiac function Potentially fatal arrhythmias ACEI Produce vasodilation (limit angiotensin II-mediated vasoconstriction) aldosterone  sodium retension Inhibit degredation of bradykinins  bradykinin levels  synthesis of prostaglandins and NO Careful: may induce hypotension! Start slowly. Watch for azotemia, K+, cough, angioedema [email protected] DR MWEBAZA VICTOR

25. notice If a patient can not tolerate an ACE-I or ARB secondary to azotemia, hyperkalemia or cough hydralazine + nitrates should be used as a 25% decrease in mortality was shown with these drugs in the V-HeFT trial published in the NEJM . Arteriodilators (e.g. hydralazine   afterload Venodilators (e.g. nitrates)   preload Combination of these  maximal benefit [email protected] DR MWEBAZA VICTOR

26. Beta-Blockers CHF  chronically catecholamines and sympathetic nervous system  progressive myocaridal damage   LV function and LV dilation -blockers  EF (will transiently )  LV size and mass Contraindicated in decompensated CHF [email protected] DR MWEBAZA VICTOR

27. Metoprolol bisoprolol and carvedilol have been shown to improve survival in patients with heart failure. Carvedilol also is an alpha receptor blocker and thus causes mild vasodilation. It is the most studied drug and preferred B blocker in heart failure patients. Must be titrated very carefully and is contraindicated in decompensated CHF [email protected] DR MWEBAZA VICTOR

28. Digoxin Increases myocardial contractility No mortality benefit but decreases hospital admissions for CHF No use in diastolic heart failure, hypertophic cardiomyopathy Prefered in systolic HF [email protected] DR MWEBAZA VICTOR

29. Inotropic agent Electrophysiologic effects: enhanced cardiac parasympathetic tone  delayed AV conduction and sinus node automaticity intracellular Ca+ and Na+ may myocyte excitability and  ventricular arrhythmias Reduces symptoms and hospitalizations but not mortality Check blood levels after 7-14 days and monitor for digoxin toxicity [email protected] DR MWEBAZA VICTOR

30. REVIEW Discuss pathogenesis of ascites in ccf Clinical presentation of left heart failure Action of digoxin and its symptoms of toxicity Management of acute heart failure Contraindications of ACEI Outline management of heart failure. [email protected] DR MWEBAZA VICTOR