low-output heart failure –systolic heart failure (hfref): –decreased left ventricular ejection...

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  • Low-Output Heart Failure Systolic Heart Failure (HFREF): Decreased Left ventricular ejection fraction Diastolic Heart Failure (HFPEF): Elevated Left and Right ventricular end-diastolic pressures Normal LVEF High-Output Heart Failure Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism, beri-beri, carcinoid, anemia Often have normal cardiac output Right-Ventricular Failure Seen with pulmonary hypertension, large RV infarctions.
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  • Causes of Low-Output Heart Failure Systolic Dysfunction Coronary Artery Disease Idiopathic dilated cardiomyopathy (DCM) 50% idiopathic (at least 25% familial) 9 % myocarditis (viral) tachycardia, peripartum, hypertension, HIV, connective tissue disease, substance abuse (alcohol), doxorubicin/herceptin Hypertension Valvular Heart Disease Diastolic Dysfunction Hypertension Coronary artery disease Hypertrophic obstructive cardiomyopathy (HCM) Restrictive cardiomyopathy
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  • (Mal)adaptation-hemodynamic
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  • ( Mal) adaptation-neurohormonal Activation of the sympathetic nervous system Vasoconstriction/increased afterload Tolerance Arhythmogenic
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  • Activation of renin-angiotensin system Na resorption Vasoconstriction Apoptosis/fibrosis
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  • Antidiuretic hormone Proinflammatory cytokines TNFalpha IL-6
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  • Clinical Presentation of Heart Failure Due to excess fluid accumulation: Dyspnea (most sensitive symptom) Edema Hepatic congestion Ascites Orthopnea, Paroxysmal Nocturnal Dyspnea (PND) Due to reduction in cardiac ouput: Fatigue (especially with exertion) Weakness
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  • S3 gallop Low sensitivity, but highly specific Cool, pale, cyanotic extremities Have sinus tachycardia, diaphoresis and peripheral vasoconstriction Crackles or decreased breath sounds at bases (effusions) on lung exam Elevated jugular venous pressure Lower extremity edema Ascites Hepatomegaly Splenomegaly Displaced PMI Apical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement>
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  • Lab Analysis in Heart Failure CBC Since anemia can exacerbate heart failure Serum electrolytes and creatinine before starting high dose diuretics Fasting Blood glucose To evaluate for possible diabetes mellitus Thyroid function tests Since thyrotoxicosis can result in A. Fib, and hypothyroidism can results in HF. Iron studies To screen for hereditary hemochromatosis as cause of heart failure. ANA To evaluate for possible lupus Viral studies If viral mycocarditis suspected
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  • Laboratory Analysis (cont.) BNP With chronic heart failure, atrial mycotes secrete increase amounts of atrial natriuretic peptide (ANP) and brain natriuretic pepetide (BNP) in response to high atrial and ventricular filling pressures Usually is > 400 pg/mL in patients with dyspnea due to heart failure.
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  • Chest X-ray in Heart Failure Cardiomegaly Cephalization of the pulmonary vessels Kerley B-lines Pleural effusions
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  • Cardiomegaly
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  • Pulmonary Edema due to Heart Failure
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  • Kerley B lines
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  • Cardiac Testing in Heart Failure Electrocardiogram: May show specific cause of heart failure: Ischemic heart disease Dilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular block Amyloidosis: pseudo-infarction pattern Idiopathic dilated cardiomyopathy: LVH Echocardiogram: Left ventricular ejection fraction Structural/valvular abnormalities
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  • Further Cardiac Testing in Heart Failure Coronary arteriography Should be performed in patients presenting with heart failure who have angina or significant ischemia Reasonable in patients who have chest pain that may or may not be cardiac in origin, in whom cardiac anatomy is not known, and in patients with known or suspected coronary artery disease who do not have angina. Measure cardiac output, degree of left ventricular dysfunction, and left ventricular end-diastolic pressure.
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  • Further testing in Heart Failure Endomyocardial biopsy Not frequently used Amyloidosis, giant-cell myocarditis
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  • Classification of Heart Failure ACCF/AHA Stages of HFNYHA Functional Classification A At high risk for HF but without structural heart disease or symptoms of HF. None B Structural heart disease but without signs or symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. C Structural heart disease with prior or current symptoms of HF. I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. DRefractory HF requiring specialized interventions.
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  • Aggravating Factors Medications New heart disease Myocardial ischemia Medications New heart disease Myocardial ischemia Endocarditis Obesity Hypertension Physical activity Dietary excess Endocarditis Obesity Hypertension Physical activity Dietary excess Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism
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  • Heart Failure and Myocardial Ischemia Coronary HD is the cause of 2/3 of HF Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia Segmental wall motion abnormalities are not specific if ischemia Angina coronary angio and revascularization Angina coronary angio and revascularization No angina No angina Search for ischemia and viability in all ? Search for ischemia and viability in all ? Coronary angiography in all ? Coronary angiography in all ?
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  • VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ ACE-i. Mechanism of Action A.C.E.
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  • ACE-I. Clinical Effects Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival
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  • Mortality Reduction with ACE-i StudyACE-iClinical Seting CONSENSUSEnalaprilCHF SOLVD treatment EnalaprilCHF AIRERamiprilCHF Vheft-IIEnalaprilCHF TRACETrandolaprilCHF / LVD SAVECaptoprilLVD SMILEZofenoprilHigh risk HOPERamiprilHigh risk
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  • Placebo Enalapril 12 11 10 9 9 8 8 7 7 6 6 5 5 Probabiility of Death Probabiility of Death Months 0.1 0.8 0 0 0.2 0.3 0.7 0.4 0.5 0.6 p< 0.001 p< 0.002 CONSENSUS N Engl J Med 1987;316:1429 CONSENSUS N Engl J Med 1987;316:1429 4 4 3 3 2 2 1 1 0 0 ACE-i
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  • Mortality, % Mortality, % 4 4 SAVE N Engl J Med 1992;327:669 SAVE N Engl J Med 1992;327:669 Years 30 20 10 0 0 1 1 2 2 3 3 Placebo Captopril 0 0 n=1115 n=1116 p=0.019 -19% n = 2231 3 - 16 days post AMI EF < 40 12.5 --- 150 mg / day n = 2231 3 - 16 days post AMI EF < 40 12.5 --- 150 mg / day Asymptomatic ventricular dysfunction post MI Asymptomatic ventricular dysfunction post MI ACE-i
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  • Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups ACE-i. Indications AHA / ACC HF guidelines 2001 ESC HF guidelines 2001
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  • ACE-i. Practical Use Start with very low doseStart with very low dose Increase dose if well toleratedIncrease dose if well tolerated Renal function & serum K + after 1-2 wRenal function & serum K + after 1-2 w Avoid fluid retention / hypovolemia (diuretic use)Avoid fluid retention / hypovolemia (diuretic use) Dose NOT determined by symptomsDose NOT determined by symptoms
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  • ACE-i. Dose (mg) InitialMaximum InitialMaximum Captopril 6.25 / 8h 50 / 8h Enalapril 2.5 / 12 h 10 to 20 / 12h Fosinopril 5 to 10 / day 40 / day Lisinopril 2.5 to 5.0 / day 20 to 40 / day Quinapril 10 / 12 h40 / 12 h Ramipril 1.25 to 2.5 / day 10 / day AHA / ACC HF guidelines 2001
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  • ACE-I. Adverse Effects Hypotension (1st dose effect) Hypotension (1st dose effect) Worsening renal function Worsening renal function Hyperkalemia Hyperkalemia Cough Cough Angioedema Angioedema Rash, ageusia, neutropenia, Rash, ageusia, neutropenia,
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  • ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension
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