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Transcript
Systolic and Diastolic Heart Failure Cardiology Devision Othmane Taha Heart Failure It is not a disease ! • complex clinical syndrome • caused by any structural or functional cardiac disorder which damages the ventricular systolic and/or diastolic function. EHO Taha 2014 Facts on Heart Failure • • • • 22 million cases world wide 10 millions in Europe 5 millions in USA 300.000 in Hungary EHO Taha 2014 Facts on Heart Failure One of the leading causes of death. 50% readmission rate within 6 months. 5-year mortality is 50% > 50% of the patients with severe heart failure die within a year EHO Taha 2014 Types of Heart Failure Left versus right HF Systolic versus diastolic HF High-output versus low-output HF Acute versus chronic HF EHO Taha 2014 Systolic dysfunction Decrease in myocardial contractility Cannot pump enough amount of blood into the circulation Reduction in the ejection fraction: EF<50 % EHO Taha 2014 Systolic Heart Failure (SHF) Etiologies: CAD Most common cause (65%) Reversible Revascularization can markedly improve outcomes Primary heart disease Dilated cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy. EHO Taha 2014 Systolic Heart Failure (SHF) Secondary heart disease Hypertension, Alcoholic/toxin-induced cardiomyopathy, Infections (virus, bacteria, ..etc.) Endocrine (hyperthyroidism, hypothyroidism, pheochromocytoma) - Valvular HD - Congenital HD - Pulmonary hypertension - Peripartum cardiomyopathy - Tachycardia mediated cardiomyopathy EHO Taha 2014 Pathophysiology of SHF • Myocardial ischema Ischemia Stunning Hibernation Necrosis systolic dysfunction EHO Taha 2014 Pathophysiology of SHF • Myocardial apoptosis triggers - oxidative stress - overstrain of myocytes - tumor necrosis factor (TNF-α) apoptosis (cell fragmentation) systolic dysfunction EHO Taha 2014 Pathophysiology of SHF • Ventricular remodeling Cell death other cells remodeling - cellular dilation, hypertrophy - extracellular fibrosis start: helps compensation later: helps the progression of HF Systolic dysfunction EHO Taha 2014 Pathophysiology of SHF • Sympathetic activity Early heamodynamic changes of HF baroreceptor activation vasomotor center activation progression of HF sympathetic activity ↑ parasympathetic activity ↓ vasoconstriction preload ↑ afterload ↑ tacycardia EHO Taha 2014 Pathophysiology of SHF • Activation of renin-angiotensin-aldosterone system Sympathetic activation and renal hypoperfusion Renin-angiotensin ↑- vasoconstriction - afterload and preload ↑ - hypertrophy (remodeling) Aldosterone ↑ - preload ↑ - fibrosis (remodeling) progression of HF EHO Taha 2014 • Imbalance between vasoconstrictors and vasodilators Vasoconstrictors Vasodilators Arginin-vasopressin system Endothelium 1 ANP, BNP NO Brdykinin rostaglandin Predominantly vasoconstrictive in HF Progression of HF EHO Taha 2014 Symptoms of SHF Shortness of breath Tender abdomen with loss of appetite Swelling of feets and legs cough Chronic lack of energy Increased urination at night Difficulty sleeping at night due to breathing problems Confusion and/or impaired memory EHO Taha 2014 Physical sings • • • • • • Displaced apex 3rd heart sound (Gallop rhythm) JVP ↑ (distended JV) Crackle (crepitation) Fast pulse Peripheral edema EHO Taha 2014 Staging NYHA: NewYork Heart Association Symptoms, functional status ABCD: (ACC/AHA) Structural changes EHO Taha 2014 NYHA Stages NYHA I: ordinary physical activity does not cause symptoms, NYHA II: comfortable at rest, but ordinary physical activity results symptoms, NYHA III: comfortable at rest, but less than ordinary activity causes symptoms, NYHA IV: symptoms at rest. EHO Taha 2014 ABCD Stages Stage A: risk factors for HF, but normal ventricular function, no symptoms Stage B: ventricular dysfunction (systolic/diastolic), but no symptoms Stage C: ventricular dysfunction and mild symptoms Stage D: ventricular dysfunction and severe symptoms EHO Taha 2014 Staging A, B NYHA I. C NYHA II-III. D NYHA IV. EHO Taha 2014 Diagnosis Medical history, physical status, Volume status (fluid retention), Laboratory tests: col, HDL col, LDL col, trig., Hgb, Htk, TSH , T3, T4, renal function, liver function, electrolytes. ECG, chest X-ray, Echocardiography. EHO Taha 2014 M- mode Ejection fraction EHO Taha 2014 Systolic dysfunction if EF< 50% EHO Taha 2014 • To achieve improvement in symptoms : • To achieve improvement in survival: • Diuretics • Digoxin • Oral nitrates plus hydralazine • ACE inhibitors • ß blockers • Angiotensin receptor blockers (ARB’s) • Aldosterone antagonists EHO Taha 2014 ß blockers • Reduction in all mortality • Use in stable patients • Titrate slowly Medication Starting Dose Target Dose Bisoprolol 1.25mg 10mg Carvedilol 3.125mg 25mg Metoprolol 12.5-25mg 200mg EHO Taha 2014 ACE inhibitors • reduction in all mortality • Titrate slowly • Monitor creatinin and potassium Medication Starting Dose Target Dose Enalapril 2X2.5mg 2X 10-20 mg Lisinopril 1X2.5-5 mg 1X 20-35mg Ramipril 1X 2.5 mg 2X 5mg EHO Taha 2014 Aldosterone Antagonists • Spironolactone – Decreases all cause mortality • Eplerenone – Decreases CV mortality Monitor renal function !! Medication spironolactone eplerenone Starting Dose Target Dose 12.5-25mg 25-50 mg 25 mg 50 mg EHO Taha 2014 Angiotensin receptor blocker • If ACE inhibitor is intolerable • Reduce all mortality • Monitor the renal function Medication Candesartan Valsartan Starting Dose Target Dose 1X 4-8 mg 1X 32 mg 2X40 mg 2X160 mg EHO Taha 2014 Digoxin May improve symptoms, Does not reduce mortality, Beneficial in AF, Reduced hospital admission due to heart failure, Should not be used in ischemic cardiomyopathy EHO Taha 2014 Some Practical Tips Diuretics : Intravenous for 48-72 hours in acute decompensation, then change to oral. ß blocker to be initiated when lungs are ‘Dry’ (“Start low and go slow” ). First dose of ACEI /ARB (small dose) usually at night. EHO Taha 2014 Management summary Stage Sypmtomatic NYHA I. -------- survival ACEI ß blockers NYHA II. If fluid retention Diuretics ACEI ß blockers NYHA III. Diuretics+ digoxin ACEI + ß blockers + Spironolactone NYHA IV. Diuretics+ Digoxin + pos. inotropic ACEI + ß blockers + Spironolactone EHO Taha 2014 Diet Patients maintain a low-salt diet (3-6 g /day) in order to minimize fluid overload. EHO Taha 2014 Activity Until decompensation is resolved, patients should be placed on complete bed rest. This is necessary to reduce myocardial oxygen demand EHO Taha 2014 The myocardium is unable to relax adequatly, Elevated filling pressures but inadequate ventricular filling, No reduction in systolic function : EF> 50% EHO Taha 2014 Pathophysiology Relaxation ability ↓ inadequate ventricular filling filling pressure ↑ stroke volume ↓ atrial pressure ↑ , dilated atrium Cardiac output ↓ Pulmonary congestion EHO Taha 2014 Diastolic HF Inadequate treatment of hypertension, Diabetes cardiomyopathy, Infiltrative disorders (amyloid) Storage disorders Obstructive sleep apnea Restrictive cardiomyopathy, Concentric LV hypertrophy Ischemic heart disease EHO Taha 2014 Predisposing factors Obesity Older age Female gender EHO Taha 2014 Same stages NYHA I-IV. A,B,C,D. Same symptoms • dyspnea • Edema • Decreased activity EHO Taha 2014 Systolic vs diastolic HF Characteristic Diastolic HF Systolic HF Symptomps (e.g. dyspnea) yes yes Cong. status (e.g. edema) yes yes Neurohormonal activation yes yes decreased decreased Clinical fearutes Exercise Exercise capacity EHO Taha 2014 Systolic vs diastolic HF Characteristic Diastolic HF Systolic HF normal decreased LV mass increased increased Relative wall thickness increased decreased normal increased End diastolic pressure increased increased Lift atrial size increased increased LV stracture and function Ejection fraction End diastolic volume EHO Taha 2014 Summary The clinical features of diastolic heart failure are similar to those of systolic heart failure but lift ventricular structure and function are distinctly different. EHO Taha 2014 Diagnosis Medical history, physical status, Volume status (fluid retention), Laboratory tests: col, HDL col, LDL col, trig., Hgb, Htk, TSH , T3, T4, renal function, liver function, electrolytes. ECG, chest X-ray, Echocardiography. EHO Taha 2014 Mitral inflow (PW) EHO Taha 2014 Tissue Doppler Index Ea Aa Sa EHO Taha 2014 E/Ea E/Ea < 8 normal 8 ≥ E/Ea ≤ 15 BNP > 200 pg/ml E/Ea > 15 Diastolic heart failure EHO Taha 2014 Is it important to distinguish DHF from SHF? Incidence: up to 50% of all heart failure 5-year mortality 56% less diagnosed less treated While the prognosis of SHF improved in the last two decades, the prognosis of DHF did not. The treatment of DHF is different from SHF. EHO Taha 2014 Management of DHF Managing etiologies (HT, DM, ischemia) Diuretics (edema, pulmonary congestion) Positive lusitropic medication: -ß blockers, -Calcium channel blockers (non-dihydrpyridine) EHO Taha 2014 Home message Beside systolic dysfunction the diastolic dysfunction also causes HF and related symptoms. EHO Taha 2014 TAHNK YOU EHO Taha 2014
