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Management of heart failure for medical students.pptx
- 1. Management of Heart Failure Dr.Abdullah Rahmanzai July 7, 2024
- 2. Definition of heartfailure HF is 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.
- 3. Types of heartfailure Heart failure may be right-sided or left-sided (or both) Preserved LV systolic function and diastolic dysfunction, or both EF: EF <40%: HF with reduced EF (HFrEF) EF 41%–49%: HF with borderline EF EF >50%: HF with preserved EF (HFpEF) HF with improved EF
- 4. Causes of HF CAD with resulting MI (ischemic cardiomyopathy) Systemic hypertension Cardiomyopathy(dilated, alcoholic, viral myocarditis, idiopathic….) Infiltrative diseases (hemochromatosis, sarcoidosis, amyloidosis, etc) metabolic disorders, cardio toxins, medication toxicity. Valvular heart diseases atrial arrhythmias aging and related myocardial stiffening hypertrophic r restrictive cardiomyopathy diabetes, and pericardial disease
- 5. stages Stage A:includes patients at risk for developing heart failure Stage B: includes patients who have structural heart disease but no current or previously recognized symptoms Stages C : include patients with clinical symptoms of heart failure Stages D: relatively small group of patients who have become refractory to the usual therapies
- 6. NYHA classification classI : (asymptomatic) class II: (symptomatic with moderate activity) Class III: (symptomatic with mild activity) class IV: (symptomatic at rest)
- 7. Clinical manifestation Symptoms Dyspnea Cough Nocturia fatigue exercise intolerance Edema loss of appetite Nausea
- 8. Clinical manifestation (Signs) Hepatic enlargement hepatojugular reflux Ascites Peripheral pitting edema parasternal lift diminished S1 S3 &S4 gallop Murmurs Cachectic or cyanotic Tachycardia Hypotension reduced pulse pressure cold extremities Diaphoresis Neck vein distention Crackles Sign of Pleural effusions Expiratory wheezing and rhonchi
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- 11. Treatment of HF A. Correction of Reversible Cause B. Pharmacologic Treatment C. Non pharmacologic Treatment
- 12. Aims of treatmentof HF control of congestion Stabilization of heart rate and blood pressure efforts at improving exercise tolerance Treat comorbidities like hypertension, diabetes, and arrhythmias. relieving symptoms Improving functional status preventing death and hospitalization
- 13. Treatments Heart FailureWith Preserved EF (HFpEF>40%) or chronic systolic heart failure Heart Failure With Reduced LVEF (HFrEF <40%) Acute heart failure & pulmonary edema Cardiogenic shock
- 14. Heart Failure WithPreserved EF (HFpEF>40%) A. Correction of Reversible Cause Hypertension pericardial disease atrial tachycardias B. Pharmacologic Treatment Diuretic therapy Inhibitors of the renin-angiotensin-aldosterone system FDA approved ARNIs SGLT2 inhibitors in all patients with HFpEF C. Non pharmacologic Treatment (ICD and resynchronizationdevice treatments do not have a role in patients with preserved EF)
- 16. Heart Failure WithReduced LVEF (HFrEF <40%) A. Correction of Reversible Cause B. Pharmacologic Treatment C. Non pharmacologic Treatment
- 17. Correction of ReversibleCause in HFrEF Valvular lesions Myocardial ischemia Uncontrolled hypertension arrhythmias (especially persistent tachycardias) alcohol- or drug-induced myocardial depression hypothyroidism Intracardiac shunts
- 18. Pharmacologic Treatment HFrEF 1. Diuretic therapy 2. Inhibitors of the renin–angiotensin–aldosterone system ARNIs ACE inh, ARBs 3. Beta-blockers 4. Digitalis glycosides 5. Nitrates and hydralazine 6. Ivabradine 7.SGLT2 inhibitors 8. Anticoagulation 9. Antiarrhythmic therapy 10. Statin therapy
- 19. B-BLOCKERS NYHA classII–IV symptoms. LVEF, exercise tolerance, and functional class 2–3 months of therapy is required to observe significant effects on LV function, but reduction of cardiac arrhythmia and incidence of sudden cardiac death (SCD) may occur much earlier β-Blockers should be instituted at a low dose and titrated with careful attention to blood pressure and heart rate. experience volume retention and worsening HF symptoms that typically respond to transient increases in diuretic therapy. The survival benefit of β-blockers is proportional to the heart rate reduction achieved Carvedilol Metoprolol succinate Bisoprolol
- 20. ARNIs, ACE-I, ARBs First line, Sacubitril-Valsartan 24/26 BID, 97/103 BID Adverse effects Kidney injury Wash-out
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- 22. Digoxin increase myocardialcontractility decrease rates of HF hospitalizations without improving overall narrow therapeutic index, usual daily dose is 0.125–0.25 mg and should be decreased in patients with renal insufficiency. Discontinuation of digoxin in patients who are stable on a regimen of digoxin, diuretics, and an ACE inhibitor may result in clinical deterioration Drug interactions with digoxin are common and may lead to toxicity. Agents that may increase levels include erythromycin, tetracycline, quinidine, verapamil, flecainide, and amiodarone. Electrolyte abnormalities (particularly hypokalemia), hypoxemia, hypothyroidism, renal insufficiency, and volume depletion may also exacerbate toxicity. Digoxin is not dialyzable, and toxicity is only treatable by the administration of digoxin immune Fab
- 23. α-Adrenergic receptorantagonists have not been shown to improve survival in HF, and hypertensive patients treated with doxazosin as firstline therapy are at increased risk of developing HF. Calcium channel blockers have no favorable effects on mortality in HFrEF. Dihydropyridine calcium channel blockers such as amlodipine may be used in hypertensive HF patients already on maximal guidelinedirected medical therapy; however, these agents do not improve mortality Nondihydropyridine calcium channel blockers should be avoided in HFrEF because their negative inotropic effects may potentiate worsening HF
- 24. Loop diuretics(furosemide, torsemide, bumetanide, ethacrynic acid) should be used in patients who require significant diuresis and in those with markedly decreased renal function. Furosemide reduces preload acutely by causing direct venodilation when administered intravenously, making it useful for managing severe HF or acute pulmonary edema Use of loop diuretics may be complicated by hyperuricemia, hypocalcemia, ototoxicity, rash, and vasculitis. Furosemide, torsemide, and bumetanide are sulfa derivatives and may rarely cause drug reactions in sulfa-sensitive patients; ethacrynic acid can be used in such patients. Dose equivalence of oral loop diuretics is approximately 50 mg ethacrynic acid = 40 mg furosemide = 20 mg torsemide = 1 mg bumetanide
- 26. We typicallyadd each drug sequentially, rather than all at once, to allow for identification of the source of any adverse effect or intolerance. (ie, ARNI, beta blocker, MRA, and, finally, SGLT2 inhibitor). However, patient characteristics (potassium, blood pressure, HF severity) can allow for a different sequence of therapy, and some experts advocate for initiation of more than one drug at the same time. Adding an agent before dose optimization – We start additional agents prior to maximizing the dose of any given primary therapy for HFrEF unless there is a clinical need to increase the dose of a RAAS inhibitor, beta blocker, or MRA (eg, uncontrolled hypertension, rate control for atrial fibrillation). Time course for initiation – The primary therapies for HFrEF should be started over the shortest time course possible but in a manner that allows for assessment of the tolerance of each agent. In general, we start each of the primary agents for the treatment of HFrEF within two to three months of initiating therapy. (See 'Time course for initiation' above.) Duration of therapy – Pharmacologic therapy for treatment of HFrEF is generally continued indefinitely, even in patients with recovery of systolic function
- 28. ANTI-COAGULATION, ANTI-PLATELETS Routineanticoagulation is not recommended in HF patients in the absence of AF, prior thromboembolism, or a prior cardioembolic source use of the CHADS2 or CHADS2-VASc risk score is recommended for determining when to use anticoagulant therapies. novel anticoagulants dabigatran, rivaroxaban, and apixaban have been shown to be effective in HF patients with nonvalvular AF. insufficient data to support the routine use of aspirin in patients with HF who do not have coronary disease or atherosclerosis.
- 29. Non pharmacologic Treatmentin HFrEF Coronary revascularization Implantable cardioverter defibrillators (ICDs) Biventricular pacing (resynchronization), CRT Case management, diet, and exercise training Cardiac transplantation Palliative care
- 30. Implantable cardioverter defibrillators(ICDs) SCD: 6-9 times more often in HF, leading cause of death symptomatic or asymptomatic arrhythmias EF of 35% or less. Recive at least 3-6 months of GDMT chronic heart failure LV systolic dysfunction who are receiving contemporary heart failure treatments
- 32. Biventricular pacing (resynchronization) Improve quality of life, reduce risk of death systolic dysfunction + abnormal intraventricular conduction wide QRS complexes left bundle branch block EF of 35% or less Non-ischemic cardiomyopathy class II, III, and ambulatory class IV heart failure
- 34. Coronary revascularization Reduceischemia and may improve systolic dysfunction Since underlying CAD is the cause of heart failure LVEF of 35% or less CABG Good 10 year survival rates
- 35. Case management, diet,and exercise training Home monitoring of weight adjustment of diuretics salt restriction (2–2.5 g sodium or 5–6 g salt per day) Fluid restriction (<1.5 L/ day) Abstinence from alcohol and smoking cessation Exercise training Weight loss
- 36. HFrEF NYHA class I–IV (StageC) ACEI or ARB AND GDMT beta-blocker; diuretics as needed (COR I) CRT or CRT- D2 (COR I) NYHA class II–IV, provided est. CrCI > 30 mL/min and K+ < 5.0 mEq/L NYHA class II–III HF Adequate BP on ACEI or ARB1; No C/I to ARB or sacubitril NYHA class III–IV, in black patients NYHA class II–III, LVEF≤ 35%; (caveat: >1 ysurvival, > 40 d post Ml) NYHA class II–IV, LVEF ≤ 35%, NSR and QRS ≥150 msec with LBBB pattern NYHA class II–III,NSR, heart rate ≥ 70 bpm on maximally tolerated dose beta-blocker Aldosterone antagonist (COR I) Discontinue ACEI or ARB; initiate ARNI (COR I) Hydral-Nitrates (COR I) ICD (COR I) lvabradine (COR lla) Refractory NYHA class III-IV (Stage D) Palliative care2 (COR I) Transplant2 (COR I) LVAD2 (COR IIa) Investigationa l studies3 Symptoms improved Step 1 Establish Dx of HFrEF; assess volume; initiate GDMT Step 2 Consider the following patient scenarios Step 3 Implement indicated GDMT. Choices are not mutually exclusive, and no order is inferred Step 4 Reassess symptoms Step 5 Consider additional therapy
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