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Heart failure
The document discusses heart failure, including its definition, causes, pathophysiology, clinical features, investigations, therapeutic objectives, and treatment options. Heart failure results from impaired ventricular filling or ejection and causes symptoms like dyspnea and fatigue. It can be caused by systolic or diastolic dysfunction from various structural heart diseases. Treatment aims to improve symptoms and prolong survival through lifestyle changes, medications like diuretics, ACE inhibitors, beta-blockers, and devices or procedures for advanced cases. Digoxin is also used to improve symptoms in some heart failure patients.
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Heart failure
- 1. Heart Failure Dr. PravinPrasad MBBS, MD Clinical Pharmacology Assistant Professor, Department of Clinical Pharmacology Maharajganj Medical Campus, Kathmandu 8 June 2020 (26 Jestha 2077), Monday
- 2. By the endof this discussion, B. Pharm 2nd year students will be able to: Define the term Heart failure List the factors involved in the development of heart failure Explain the pathophysiology of heart failure Outline the clinical features of heart failure Elaborate the therapeutic objectives and options for heart failure Justify the pharmacotherapy of heart failure
- 3. Introduction Heart Failure: A complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales. Includes: Heart failure with reduced Ejection fraction (HFrEF)- systolic HF Heart failure with preserved Ejection fraction (HFpEF)- diastolic HF Acute decompensated heart failure Advanced heart failure
- 4. Etiology Systolic dysfunction(decreased contractility) Reduction in muscle mass (e.g., myocardial infarction) Dilated cardiomyopathies Ventricular hypertrophy Pressure overload (e.g., systemic or pulmonary hypertension, and aortic or pulmonic valve stenosis) Volume overload (e.g., valvular regurgitation, shunts, and high-output states) Diastolic dysfunction (restriction in ventricular filling) Increased ventricular stiffness Ventricular hypertrophy Infiltrative myocardial diseases (e.g., amyloidosis, sarcoidosis, and endomyocardial fibrosis) Myocardial ischemia and infarction Mitral or tricuspid valve stenosis Pericardial disease (e.g., pericarditis and pericardial tamponade)
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- 7. Investigations To establishthe nature and severity of the underlying heart disease and detect any complications: Serum urea, creatinine and electrolytes, haemoglobin, thyroid function, ECG, chest X-ray Brain natriuretic peptide (BNP): risk assessment Echocardiography: Determine the aetiology Detect unsuspected valvular heart disease Identify patients who will benefit from long-term drug therapy, e.g. ACE inhibitors (see below)
- 8. Therapeutic Objectives Toimprove symptoms To prolong survival
- 9. Therapeutic Options GeneralInformation and advice Non-pharmacologic therapy Pharmacologic therapy Referral • Education • Explanation of nature of disease, treatment and self-help strategies • Diet • Cessation of alcohol and smoking • Regular moderate aerobic exercise within limits of symptoms • Enhanced External Counterpulsation • Vaccination • Consider influenza and pneumococcal vaccination
- 10. Therapeutic Options GeneralInformation and advice Non-pharmacologic therapy Pharmacologic therapy Referral • Implantable cardiac defibrillators and resynchronization therapy • Coronary revascularization • Heart Transplantation • Ventricular Assist Devices
- 11. Therapeutic Options GeneralInformation and advice Non-pharmacologic therapy Pharmacologic therapy Referral • Renocentric Therapy model • Diuretics • Haemodynamic Therapy model • Vasodilators (arteriolar, venous) • Digoxin • Inotropes • Disease modifying therapy • Renin-Angiotensin Aldosterone System Blockers
- 12. Pharmacotherapy of HeartFailure Relief of congestive/low output symptoms Arrest/reversal of disease progression and prolongation of survival Inotropic drugs: Angiotensin Converting Enzyme inhibitors (ACE-inhibitors), Angiotensin Receptor Blockers (ARBs) Digoxin, Dobutamine, Dopamine, Amrinone/Milrinone Diuretics: Furosemide, Thiazides β- blockers RAS inhibitors: ACE inhibitors, ARBs Aldosterone Antagonists: Vasodilators: Spironolactone, Eplerenone Hydralazine, Nitrate, Nitroprusside β- blockers: Metoprolol, Bisoprolol, Carvedilol,
- 13. Diuretics in HeartFailure Chronic heart failure: Loop diuretics (Furosemide); Thiazide in mild cases To control symptomatic oedema and dyspnoea in patients with heart failure Spironolactone improves survival in patients with cardiac failure and counters diuretic-induced hypokalaemia Monitor for hyperkalaemia Acute heart failure: Intravenous furosemide ( repeated boluses or infusion) To correct acute pulmonary oedema
- 14. Angiotensin Converting Enzyme Inhibitorsin HF Patients with HF have overactive RAAS system Consequently most likely to benefit from an ACEI in the long term Improves survival Start with small bedtime dose Gradually increased to one that improves symptoms (and survival) Better response in Caucasian patients Preferred due to greater experience and cost considerations
- 15. Angiotensin Receptor Blockersin HF Similar to those of ACEI apart from a lower incidence of some adverse effects, including, particularly, dry cough Possibly have additive effect when combined with ACEI
- 16. Beta blockers inHeart Failure Bisoprolol, Metoprolol, Carvedilol Beta-blockers are negative inotropes Helps by antagonizing counterregulatory sympathetic activation and improved survival Start with low dose and up-titrate the dose as tolerated
- 17. Vasodilators in Heartfailure Hydralazine and a long-acting nitrate Hydralazine reduces afterload Nitrate reduces preload Improves survival in African-American patients
- 18. Digoxin in HeartFailure A cardiac glycoside; source: Digitalis lanata Digitoxin (D. purpurea); Ouabain (Strophanthus gratus) Pharmacological Actions: Direct effect on myocardial contractility, electrophysiological properties Other effects: Vagomimetic action, altered sympathetic activity (due to direct CNS effects), reflex effects (altered haemodynamics) Myocardial contractility: Increased force of contraction Decreased Heart Rate Addition of digoxin to diuretics and ACEI reduces hospitalization and improves symptoms, without prolonging life
- 19. Digoxin: Mechanism ofAction → Selectively binds to extracellular face of the membrane associated Na+K+ ATPase of myocardial fibres and inhibits it → Progressive accumulation of Na+ intracellularly → Accumulation of Ca++ intracellularly → Taken up by Sarcoplasmic Reticulum → Augumented subsequent Ca++ transients → Increased force of contraction Slow and gradual response
- 20. Digoxin: Adverse Effects Extra-cardiac: GIT: nausea, vomiting, abdominal pain (gastric irritation, mesenteric vasoconstriction, CTZ stimulation) CNS: fatigue, malaise, headache, mental confusion, restlessness, hyperapnoea, disorientation, psychosis, visual disturbances Skin: rashes Endocrine: gynaecomastia Cardiac: Arrhythmias: all types Partial to complete A-V block
- 21. Digoxin: Adverse Effects Treatment: Stop further doses Extra-cardiac side effects (S/E): nothing more needed For tachy-arrhythmias: K+ supplementation for chronic use associated toxicity; K+ monitoring directed supplementation for acute ingestion For ventricular arrhythmias: Lidocaine For supraventricular arrhythmia: Propanolol For A-V block and bradycardia: atropine, cardiac pacing Digoxin antibody
- 22. Digoxin: Additional Points Precautions and Contraindications Hypokalemia Elderly, renal insufficiency, hepatic disease Myocardial ischaemia Thyrotoxicosis Myxoedema Ventricular tachycardia Partial A-V block Acute Myocarditis Wolff-Parkinson-White syndrome
- 23. Digoxin: Additional Points Interactions Diuretics Calcium Quinidine Adrenergic drugs Metoclopramide, sucralfate, antacids, neomycin, sulfasalazine: decreased absorption Atropinic drugs, TCA: increased absorption Propanolol, verapamil, diltiazem, disopyramide Succinylcholine
- 24. Digoxin: Uses CongestiveHeart Failure Standard treatment: ACE inhibitors, ARBs, β- blockers and diuretics Most effective in patients with dilated heart and low ejection fraction Stable clinical state: withdrawal can be attempted CHF with AF in need of ventricular rate control: continuous digoxin Cardiac arrhythmias: Atrial Fibrillation Atrial Flutter Paroxysmal Supraventricular Tachycardia (PSVT)
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Editor's Notes
- #10 Education • Explanation of nature of disease, treatment and self-help strategies Diet • Good general nutrition and weight reduction for the obese • Avoidance of high-salt foods and added salt, especially for patients with severe congestive heart failure Alcohol • Moderation or elimination of alcohol consumption. Alcohol induced cardiomyopathy requires abstinence Smoking • Cessation Exercise • Regular moderate aerobic exercise within limits of symptoms Vaccination • Consider influenza and pneumococcal vaccination
- #11 Education • Explanation of nature of disease, treatment and self-help strategies Diet • Good general nutrition and weight reduction for the obese • Avoidance of high-salt foods and added salt, especially for patients with severe congestive heart failure Alcohol • Moderation or elimination of alcohol consumption. Alcohol induced cardiomyopathy requires abstinence Smoking • Cessation Exercise • Regular moderate aerobic exercise within limits of symptoms Vaccination • Consider influenza and pneumococcal vaccination
- #12 Education • Explanation of nature of disease, treatment and self-help strategies Diet • Good general nutrition and weight reduction for the obese • Avoidance of high-salt foods and added salt, especially for patients with severe congestive heart failure Alcohol • Moderation or elimination of alcohol consumption. Alcohol induced cardiomyopathy requires abstinence Smoking • Cessation Exercise • Regular moderate aerobic exercise within limits of symptoms Vaccination • Consider influenza and pneumococcal vaccination