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Congestive Heart Failure Larissa Bornikova, MD July, 2006.

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Presentation on theme: "Congestive Heart Failure Larissa Bornikova, MD July, 2006."— Presentation transcript:

1 Congestive Heart Failure Larissa Bornikova, MD July, 2006

2 Objectives To review the basic pathophysiological mechanisms of congestive heart failureTo review the basic pathophysiological mechanisms of congestive heart failure To review a diagnostic approach to the patient with suspected HF and initial work up of newly diagnosed HF.To review a diagnostic approach to the patient with suspected HF and initial work up of newly diagnosed HF. To summarize characteristics of diastolic heart failureTo summarize characteristics of diastolic heart failure To outline management strategies for CHFTo outline management strategies for CHF

3 Definition Heart failure is a clinical syndrome not a disease.Heart failure is a clinical syndrome not a disease. Clinically defined as the inability of the heart at the normal filling pressures to maintain an output adequate to meet the metabolic demands of the body.Clinically defined as the inability of the heart at the normal filling pressures to maintain an output adequate to meet the metabolic demands of the body.

4 Epidemiology 5 million Americans have heart failure5 million Americans have heart failure 500,000 new cases of symptomatic heart failure annually500,000 new cases of symptomatic heart failure annually 20% of hospital admissions among persons older than 6520% of hospital admissions among persons older than 65 45% annual mortality in severe symptomatic heart failure45% annual mortality in severe symptomatic heart failure More Medicare dollars are spent for diagnosis and treatment of heart failure than for any other single diagnosis.More Medicare dollars are spent for diagnosis and treatment of heart failure than for any other single diagnosis.

5 The most common causes of CHF Remember that CHF is a syndrome, so always look for an underlying cause! Ischemic heart disease ~ 40 percent Dilated cardiomyopathy ~ 30 percent Primary valvular heart disease ~ 15 percent Hypertensive heart disease ~ 10 percent Other ~ 5 percent

6 Etiology WHO Classification of Heart Failure Etiologies 1.Dilated Cardiomyopathy (about 20-25% of cases are familial) 2.Hypertrophic Cardiomyopathy (e.g. IHSS, HOCM) 3.Restrictive Cardiomyopathy (infiltrating diseases) 4.Arrhythmogenic Right Ventricular Cardiomyopathy 5.Unclassifiable Cardiomyopathies (fibroelastosis, mitochondrial) 6.Specific Cardiomyopathies (ischemic, hypertensive, valvular obstruction/insufficiency, myocarditis, endocarditis, Chaga’s disease, HIV, adenovirus, CMV, Enterovirus). 7.Metabolic (thyrotoxicosis, hypothyroidism, pheochromocytoma, hemochromatosis, glycogen storage diseases, diabetes, kwarshiokor, beriberi, starvation, amyloidosis, Familial Mediterrenian Fever, etc.) 8.General system disease (alcohol, anthracyclines, radiation, SLE, PAN, scleroderma, dermatomyositis, sarcoidosis, muscular dystrophies, neuromuscular disorders, peripartum cardiomyopathy, etc.)

7 Pathophysiological mechanisms of CHF Multiple compensatory responses over the long-term become deleterious.Multiple compensatory responses over the long-term become deleterious.

8 Pathophysiological mechanisms of CHF CARDIAC ABNORMALITIES Frank-Starling MechanismFrank-Starling Mechanism Compensatory hypertrophyCompensatory hypertrophy Ventricular remodelingVentricular remodeling Coronary arteriesCoronary arteries Mitral regurgitationMitral regurgitation ArrhythmiasArrhythmias OTHER MECHANISMS Redistribution of cardiac outputRedistribution of cardiac output NEUROHORMONAL Renin-angiotensin- aldosterone system Sympathetic nervous system Natriuretic peptides Vasodilator peptides Cytokines Matrix Metalloproteinases

9 Jessup M and Brozena S. N Engl J Med 2003;348: Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure (Panel B)

10 Evaluation of the patient with suspected CHF: Establish diagnosisEstablish diagnosis Determine the etiologyDetermine the etiology Assess acuity and severityAssess acuity and severity

11 Clinical Manifestations of CHFSYMPTOMS Fluid overloadFluid overload DyspneaDyspnea OrthopneaOrthopnea Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea Cardiac asthmaCardiac asthma Cheyne-Stokes Respiration (aka cyclic respiration)Cheyne-Stokes Respiration (aka cyclic respiration) Fatigue, weaknessFatigue, weakness Exercise intoleranceExercise intolerance Decreased urine outputDecreased urine output ConfusionConfusion LethargyLethargy NocturiaNocturia AnorexiaAnorexia PHYSICAL SIGNS Rales Tachycardia Displaced PMI S3 (ventricular gallop) S4 (atrial gallop) Pulmonary HTN (loud P2) Neck vein distention Hepatic enlargement Peripheral edema Ascites Pleural effusion Cardiac Cachexia Jaundice Skin cold and clammy Pulsus alternans

12 Fun facts sensitivityspecificity Dyspnea on exertion100 %17% Orthopnea22%74% PND39%80% Peripheral edema 49%47% Based on study of 259 patients referred for echocardiography

13 Diagnosis of HF CHF should be suspected on the basis of clinical presentation and radiographic findings.CHF should be suspected on the basis of clinical presentation and radiographic findings. It’s a clinical diagnosis. There is no diagnostic test!It’s a clinical diagnosis. There is no diagnostic test! Depressed ventricular EF should be confirmed with echocardiography, radionucleotide ventriculography, or cardiac catheterization with left ventriculography.Depressed ventricular EF should be confirmed with echocardiography, radionucleotide ventriculography, or cardiac catheterization with left ventriculography.

14 Diastolic Heart Failure Diagnosis is based on the finding of typical symptoms and signs of heart failure in a patient who has a normal LVEF and no valvular abnormalities on echocardiography.Diagnosis is based on the finding of typical symptoms and signs of heart failure in a patient who has a normal LVEF and no valvular abnormalities on echocardiography. Diagnostic findings on echocardiogram:Diagnostic findings on echocardiogram: - normal EF - no evidence of acute MR, AR, or constrictive pericarditis - abnormal relaxation pattern as evidenced by abnormal E/A ratio in mild diastolic dysfunction, or by Doppler assessment of flow into the LA, or by tissue Doppler imaging. Insufficient data from randomized trials to assess the effects of various treatment modalities.Insufficient data from randomized trials to assess the effects of various treatment modalities.

15 Aurigemma G and Gaasch W. N Engl J Med 2004;351: Patterns of Left Ventricular Diastolic Filling as Shown by Standard Doppler Echocardiography

16 Evaluation of the patient with suspected CHF: Mechanisms to consider Systolic vs. diastolicSystolic vs. diastolic Low-output vs. high-outputLow-output vs. high-output Acute vs. chronicAcute vs. chronic Right-sided vs. left-sidedRight-sided vs. left-sided Backward vs. forwardBackward vs. forward

17 Evaluation of the patient with CHF: establish etiology and assess acuity/severity. ACC/AHA guidelines (class I) History/physical examination to identify disorders and behaviors that might cause or accelerate the development of progression of HF.History/physical examination to identify disorders and behaviors that might cause or accelerate the development of progression of HF. History of current and past use of alcohol, illicit drugs, current or past standard or “alternative therapies”, and chemotherapy drugs should be obtained from the patients presenting with HF.History of current and past use of alcohol, illicit drugs, current or past standard or “alternative therapies”, and chemotherapy drugs should be obtained from the patients presenting with HF. Assessment of the patient’s ability to perform ADLs.Assessment of the patient’s ability to perform ADLs. Physical examination should include assessment of volume status, orthostatic blood pressure changes, measurement of weight and height, and BMI..Physical examination should include assessment of volume status, orthostatic blood pressure changes, measurement of weight and height, and BMI.. Remember that CHF is a syndrome, so look for the underlying cause.

18 Initial evaluation of the patient with CHF: Etiological approach. ACC/AHA guidelines (class I) CBCCBC Serum electrolytes, BUN and creatinineSerum electrolytes, BUN and creatinine LFTsLFTs Fasting blood glucoseFasting blood glucose Lipid profileLipid profile TSHTSH UrinalysisUrinalysis CXR (cardiomegaly, Kerley B-lines, pleural effusions, pulmonary edema)CXR (cardiomegaly, Kerley B-lines, pleural effusions, pulmonary edema) EKG (assess for evidence of ischemia, LVH, a fib)EKG (assess for evidence of ischemia, LVH, a fib) Echocardiogram with Doppler (LV and RV function/mass/wall thickness, LVEDV, LA size, E/A ratio, valvular disease)Echocardiogram with Doppler (LV and RV function/mass/wall thickness, LVEDV, LA size, E/A ratio, valvular disease) Coronary angiography if applicableCoronary angiography if applicable *** Based on clinical scenario/suspicion, may also consider plasma BNP, iron studies, ANA, serologies for SLE, evaluation for pheochromocytoma, viral serologies and antimyosin Ab, thiamine, carnitine, selenium, genetic testing (not class I).

19 Evaluation of the patient with suspected CHF: Role of BNP Low BNP level has a good negative predictive value to exclude CHF as a primary diagnosis in dyspneic patients who present to the Emergency Department. ( N Engl J Med 2002; 327; 161 )Low BNP level has a good negative predictive value to exclude CHF as a primary diagnosis in dyspneic patients who present to the Emergency Department. ( N Engl J Med 2002; 327; 161 ) BNP levels correlate with the severity of HFBNP levels correlate with the severity of HF BNP levels predict survivalBNP levels predict survival

20 New York Heart Association classification of heart failure. Focuses on symptoms Class I: No limitation of physical activity. Class II: Slight limitation with ordinary exertion. Class III:Marked limitation with less than ordinary exertion. Class IV: Symptoms are present at rest. ACC/AHA Classification Emphasizes evolution and progression of heart failure. Class A:At risk for CHF, but heart is structurally normal. Class B:Structural abnormality of the heart, never had symptoms Class C:Structural abnormality; current or previous symptoms. Class D:End-stage symptoms; refractory to standard treatment.

21 Jessup M and Brozena S. N Engl J Med 2003;348: Management of Heart Failure 1.General measures 2.Correct underlying cause 3.Remove precipitating cause 4.Prevention of deterioration of cardiac function 5.Control of congestive HF state

22 Nonpharmacologic therapy Exercise training for stable HF patients increased exercise capacity, decreased hospitalization rate, increased quality of life, decreased symptoms.Exercise training for stable HF patients increased exercise capacity, decreased hospitalization rate, increased quality of life, decreased symptoms. Weight loss in obese patientsWeight loss in obese patients Dietary Na restriction (≤ 2 g/day)Dietary Na restriction (≤ 2 g/day) Fluid and free water restriction (≤ 1.5 L/day) especially if hyponatremicFluid and free water restriction (≤ 1.5 L/day) especially if hyponatremic Minimize medications known to have deleterious effects on heart failure (negative inotrops, NSAIDs, over-the-counter stimulants)Minimize medications known to have deleterious effects on heart failure (negative inotrops, NSAIDs, over-the-counter stimulants) OxygenOxygen Fluid removal (dialysis, thoracentesis, paracentesis)Fluid removal (dialysis, thoracentesis, paracentesis)

23 Jessup M and Brozena S. N Engl J Med 2003;348: Stages of Heart Failure and Treatment Options for Systolic Heart Failure

24 Pharmacologic therapy  diuretics  ** / digoxin  ** / spironolactone / spironolactone / beta-blockers /? / beta-blockers /? ACE I → ARB → Hydralazine/nitrates ACE I → ARB → Hydralazine/nitrates NYHA ClassIII IIIIV ** no change in mortality

25 Drugs to avoid in HF patients NSAIDs. Induce systemic vasoconstriction, counteract ACE inhibitors, blunt effects of diuretics.NSAIDs. Induce systemic vasoconstriction, counteract ACE inhibitors, blunt effects of diuretics. Thiazolidinediones. Contribute to fluid retention. Should be avoided in severe (class III-IV) failure.Thiazolidinediones. Contribute to fluid retention. Should be avoided in severe (class III-IV) failure. Metformin. Increased (but small) risk of lactic acidosis.Metformin. Increased (but small) risk of lactic acidosis. Cilostazole. (PDE inhibitor). Increases mortality.Cilostazole. (PDE inhibitor). Increases mortality. Calcium channel blockers (avoid Verapamil and Diltiazem). Trials with amlodipine and felodipine showed a neutral effect on mortality. V-HeFT trial. Circulation 1997; 96; 856.Calcium channel blockers (avoid Verapamil and Diltiazem). Trials with amlodipine and felodipine showed a neutral effect on mortality. V-HeFT trial. Circulation 1997; 96; 856.

26 Treatment of HF exacerbation: Parenteral agents IV VasodilatorsIV Vasodilators - Nitroglycerine - Nitroprusside - Recombinant BNP (nesiritide) IV Inotropic agentsIV Inotropic agents - Dopamine - Dobutamine - PDE inhibitors (amrinone, milrinone) IV DiureticsIV Diuretics - Furosemide - Bumetanide

27 Other management considerations Anticoagulation. No RCT. Warfarin therapy may be considered in the absence of contraindications for patients who are in sinus rhythm and have EF <30%.Anticoagulation. No RCT. Warfarin therapy may be considered in the absence of contraindications for patients who are in sinus rhythm and have EF <30%. Ventricular resynchronization therapy. Survival benefit in patients with NYHA class III-IV HF despite optimal medical therapy, who are in sinus rhythm, have EF ≤35%, and a prolonged QRS ( ≥120 msec). CARE-HF and COMPANION trial.Ventricular resynchronization therapy. Survival benefit in patients with NYHA class III-IV HF despite optimal medical therapy, who are in sinus rhythm, have EF ≤35%, and a prolonged QRS ( ≥120 msec). CARE-HF and COMPANION trial. ICD. Based on the SCD- HeFT trial. Significant benefit in NYHA class II - III HF and EF ≤35%. Class IV patients have not been studied.ICD. Based on the SCD- HeFT trial. Significant benefit in NYHA class II - III HF and EF ≤35%. Class IV patients have not been studied. Mechanical circulatory support.Mechanical circulatory support. Cardiac transplantation.Cardiac transplantation.

28 References Jessup M, Brozena S. Heart Failure. N Engl J Med 2003; 348: 2007 – 18.Jessup M, Brozena S. Heart Failure. N Engl J Med 2003; 348: 2007 – 18. Aurigemma GP, Gaasch WH. Diastolic Heart Failure. N Engl J Med 2004; 351: 1097 – 105.Aurigemma GP, Gaasch WH. Diastolic Heart Failure. N Engl J Med 2004; 351: 1097 – 105. Hunt SA, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. Circulation 2005; 112.Hunt SA, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. Circulation 2005; 112. Harrison’s Principles of Internal Medicine, 16 th editionHarrison’s Principles of Internal Medicine, 16 th edition UpToDateUpToDate


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