Congestive Heart Failure

Larissa Bornikova, MDLarissa Bornikova, MD

July, 2006July, 2006

Objectives

• To review the basic pathophysiological To review the basic pathophysiological mechanisms of congestive heart failuremechanisms of congestive heart failure

• To review a diagnostic approach to the To review a diagnostic approach to the patient with suspected HF and initial work patient with suspected HF and initial work up of newly diagnosed HF.up of newly diagnosed HF.

• To summarize characteristics of diastolic To summarize characteristics of diastolic heart failureheart failure

• To outline management strategies for CHF To outline management strategies for CHF

Definition

• Heart failure is a clinical Heart failure is a clinical syndromesyndrome not a disease. not a disease.

• Clinically defined as the inability of the heart at the normal Clinically defined as the inability of the heart at the normal filling pressures to maintain an output adequate to meet the filling pressures to maintain an output adequate to meet the metabolic demands of the body.metabolic demands of the body.

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 More Medicare dollars are spent for diagnosis and

treatment of heart failure than for any other single treatment of heart failure than for any other single diagnosis.diagnosis.

The most common causes of CHF

Remember that CHF is a syndrome, so always look for an Remember that CHF is a syndrome, so always look for an underlying cause!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

EtiologyWHO Classification of Heart Failure EtiologiesWHO Classification of Heart Failure Etiologies

1.1. Dilated Cardiomyopathy (about 20-25% of cases are familial)Dilated Cardiomyopathy (about 20-25% of cases are familial)2.2. Hypertrophic Cardiomyopathy (e.g. IHSS, HOCM)Hypertrophic Cardiomyopathy (e.g. IHSS, HOCM)3.3. Restrictive Cardiomyopathy (infiltrating diseases)Restrictive Cardiomyopathy (infiltrating diseases)4.4. Arrhythmogenic Right Ventricular CardiomyopathyArrhythmogenic Right Ventricular Cardiomyopathy5.5. Unclassifiable Cardiomyopathies (fibroelastosis, mitochondrial)Unclassifiable Cardiomyopathies (fibroelastosis, mitochondrial)6.6. Specific Cardiomyopathies (ischemic, hypertensive, valvular Specific Cardiomyopathies (ischemic, hypertensive, valvular

obstruction/insufficiency, myocarditis, endocarditis, Chaga’s obstruction/insufficiency, myocarditis, endocarditis, Chaga’s disease, HIV, adenovirus, CMV, Enterovirus).disease, HIV, adenovirus, CMV, Enterovirus).

7.7. Metabolic (thyrotoxicosis, hypothyroidism, pheochromocytoma, Metabolic (thyrotoxicosis, hypothyroidism, pheochromocytoma, hemochromatosis, glycogen storage diseases, diabetes, hemochromatosis, glycogen storage diseases, diabetes, kwarshiokor, beriberi, starvation, amyloidosis, Familial kwarshiokor, beriberi, starvation, amyloidosis, Familial Mediterrenian Fever, etc.)Mediterrenian Fever, etc.)

8.8. General system disease (alcohol, anthracyclines, radiation, SLE, General system disease (alcohol, anthracyclines, radiation, SLE, PAN, scleroderma, dermatomyositis, sarcoidosis, muscular PAN, scleroderma, dermatomyositis, sarcoidosis, muscular dystrophies, neuromuscular disorders, peripartum cardiomyopathy, dystrophies, neuromuscular disorders, peripartum cardiomyopathy, etc.)etc.)

Pathophysiological mechanisms of CHF

• Multiple compensatory responses over the long-term Multiple compensatory responses over the long-term become deleterious.become deleterious.

Pathophysiological mechanisms of CHF

CARDIAC ABNORMALITIESCARDIAC ABNORMALITIES• Frank-Starling MechanismFrank-Starling Mechanism• Compensatory hypertrophyCompensatory hypertrophy• Ventricular remodelingVentricular remodeling• Coronary arteriesCoronary arteries• Mitral regurgitationMitral regurgitation• ArrhythmiasArrhythmias

OTHER MECHANISMSOTHER MECHANISMS• Redistribution of cardiac Redistribution of cardiac

outputoutput

NEUROHORMONALNEUROHORMONAL• Renin-angiotensin-Renin-angiotensin-

aldosterone systemaldosterone system• Sympathetic nervous systemSympathetic nervous system• Natriuretic peptidesNatriuretic peptides• Vasodilator peptidesVasodilator peptides• CytokinesCytokines• Matrix MetalloproteinasesMatrix Metalloproteinases

Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018

Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure (Panel B)

Evaluation of the patient with suspected CHF:

• Establish diagnosisEstablish diagnosis

• Determine the etiologyDetermine the etiology

• Assess acuity and severityAssess acuity and severity

Clinical Manifestations of CHF

SYMPTOMSSYMPTOMS• Fluid overloadFluid overload• DyspneaDyspnea• OrthopneaOrthopnea• Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea• Cardiac asthmaCardiac asthma• Cheyne-Stokes Respiration Cheyne-Stokes Respiration

(aka cyclic respiration)(aka cyclic respiration)• Fatigue, weaknessFatigue, weakness• Exercise intoleranceExercise intolerance• Decreased urine outputDecreased urine output• ConfusionConfusion• LethargyLethargy• NocturiaNocturia• AnorexiaAnorexia

PHYSICAL SIGNSPHYSICAL SIGNS• RalesRales• TachycardiaTachycardia• Displaced PMIDisplaced PMI• S3 (ventricular gallop)S3 (ventricular gallop)• S4 (atrial gallop)S4 (atrial gallop)• Pulmonary HTN (loud P2)Pulmonary HTN (loud P2)• Neck vein distentionNeck vein distention• Hepatic enlargementHepatic enlargement• Peripheral edemaPeripheral edema• AscitesAscites• Pleural effusionPleural effusion• Cardiac CachexiaCardiac Cachexia• JaundiceJaundice• Skin cold and clammySkin cold and clammy• Pulsus alternansPulsus alternans

Fun facts

sensitivitysensitivity specificityspecificity

Dyspnea on exertionDyspnea on exertion 100 %100 % 17%17%

OrthopneaOrthopnea 22%22% 74%74%

PNDPND 39%39% 80%80%

Peripheral edema Peripheral edema 49%49% 47%47%

Based on study of 259 patients referred for echocardiographyBased on study of 259 patients referred for echocardiography

Diagnosis of HF

• CHF should be suspected on the basis of clinical CHF should be suspected on the basis of clinical presentation and radiographic findings.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 Depressed ventricular EF should be confirmed with echocardiography, radionucleotide ventriculography, or echocardiography, radionucleotide ventriculography, or cardiac catheterization with left ventriculography.cardiac catheterization with left ventriculography.

Diastolic Heart Failure

• Diagnosis is based on the finding of typical symptoms and signs of 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 heart failure in a patient who has a normal LVEF and no valvular abnormalities on echocardiography. abnormalities on echocardiography.

• Diagnostic findings on echocardiogram: Diagnostic findings on echocardiogram: - normal EF- normal EF- no evidence of acute MR, AR, or constrictive pericarditis - no evidence of acute MR, AR, or constrictive pericarditis

- abnormal relaxation pattern as evidenced by abnormal E/A - abnormal relaxation pattern as evidenced by abnormal E/A ratio ratio in mild diastolic dysfunction, or by Doppler assessment of in mild diastolic dysfunction, or by Doppler assessment of flow flow into the LA, or by tissue Doppler imaging.into the LA, or by tissue Doppler imaging.

• Insufficient data from randomized trials to assess the effects of various Insufficient data from randomized trials to assess the effects of various treatment modalities.treatment modalities.

Aurigemma G and Gaasch W. N Engl J Med 2004;351:1097-1105

Patterns of Left Ventricular Diastolic Filling as Shown by Standard Doppler Echocardiography

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

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 History/physical examination to identify disorders and behaviors that

might cause or accelerate the development of progression of HF.might cause or accelerate the development of progression of HF.

• History of current and past use of alcohol, illicit drugs, current or past History of current and past use of alcohol, illicit drugs, current or past standard or “alternative therapies”, and chemotherapy drugs should be standard or “alternative therapies”, and chemotherapy drugs should be obtained from the patients presenting with HF.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, Physical examination should include assessment of volume status, orthostatic blood pressure changes, measurement of weight and height, orthostatic blood pressure changes, measurement of weight and height, and BMI..and BMI..

Remember that CHF is a syndrome, so look for the underlying cause.Remember that CHF is a syndrome, so look for the underlying cause.

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 CXR (cardiomegaly, Kerley B-lines, pleural effusions, pulmonary

edema)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 Echocardiogram with Doppler (LV and RV function/mass/wall

thickness, LVEDV, LA size, E/A ratio, valvular disease) thickness, LVEDV, LA size, E/A ratio, valvular disease) • Coronary angiography if applicableCoronary angiography if applicable

*** Based on clinical scenario/suspicion, may also consider *** Based on clinical scenario/suspicion, may also consider plasma BNPplasma BNP, iron studies, ANA, , iron studies, ANA, serologies for SLE, evaluation for pheochromocytoma, viral serologies and antimyosin serologies for SLE, evaluation for pheochromocytoma, viral serologies and antimyosin Ab, thiamine, carnitine, selenium, genetic testing (not class I).Ab, thiamine, carnitine, selenium, genetic testing (not class I).

Evaluation of the patient with suspected CHF:

Role of BNP • Low BNP level has a good negative predictive value to exclude CHF Low BNP level has a good negative predictive value to exclude CHF

as a primary diagnosis in dyspneic patients who present to the as a primary diagnosis in dyspneic patients who present to the Emergency Department. (Emergency Department. (N Engl J Med 2002; 327; 161N Engl J Med 2002; 327; 161))

• BNP levels correlate with the severity of HFBNP levels correlate with the severity of HF

• BNP levels predict survival BNP levels predict survival

New York Heart Association classification of heart failure.

Focuses on symptomsFocuses on symptoms

Class I: Class I: No limitation of physical activity.No limitation of physical activity.Class II: Class II: Slight limitation with ordinary exertion.Slight limitation with ordinary exertion.Class III:Class III: Marked limitation with less than ordinary exertion.Marked limitation with less than ordinary exertion.Class IV: Class IV: Symptoms are present at rest.Symptoms are present at rest.

ACC/AHA ClassificationACC/AHA ClassificationEmphasizes evolution and progression of heart failure.Emphasizes evolution and progression of heart failure.

Class A:Class A: At risk for CHF, but heart is structurally normal.At risk for CHF, but heart is structurally normal.Class B:Class B: Structural abnormality of the heart, never had symptomsStructural abnormality of the heart, never had symptomsClass C:Class C: Structural abnormality; current or previous symptoms.Structural abnormality; current or previous symptoms.Class D:Class D: End-stage symptoms; refractory to standard treatment.End-stage symptoms; refractory to standard treatment.

Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018

Management of Heart Failure

1.1. General measuresGeneral measures

2.2. Correct underlying causeCorrect underlying cause

3.3. Remove precipitating causeRemove precipitating cause

4.4. Prevention of deterioration of Prevention of deterioration of cardiac functioncardiac function

5.5. Control of congestive HF Control of congestive HF statestate

Nonpharmacologic therapy

• Exercise training for stable HF patients increased exercise capacity, Exercise training for stable HF patients increased exercise capacity, decreased hospitalization rate, increased quality of life, decreased decreased hospitalization rate, increased quality of life, decreased symptoms. symptoms.

• Weight loss in obese patients Weight loss in obese patients • Dietary Na restriction (Dietary Na restriction (≤ 2 g/day)≤ 2 g/day)• Fluid and free water restriction (≤ 1.5 L/day) especially if Fluid and free water restriction (≤ 1.5 L/day) especially if

hyponatremichyponatremic• Minimize medications known to have deleterious effects on heart Minimize medications known to have deleterious effects on heart

failure (negative inotrops, NSAIDs, over-the-counter stimulants)failure (negative inotrops, NSAIDs, over-the-counter stimulants)• Oxygen Oxygen • Fluid removal (dialysis, thoracentesis, paracentesis)Fluid removal (dialysis, thoracentesis, paracentesis)

Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018

Stages of Heart Failure and Treatment Options for Systolic Heart Failure

Pharmacologic therapy

- - - - - diuretics - - - -- - - - - diuretics - - - - ****/ digoxin - - - - - -/ digoxin - - - - - - ** ** / spironolactone/ spironolactone / beta-blockers // beta-blockers / ?? ACE I ACE I → ARB → Hydralazine/nitrates→ ARB → Hydralazine/nitrates

NYHA ClassNYHA Class II II II IIIIII IVIV

** ** no change in mortalityno change in mortality

Drugs to avoid in HF patients

• NSAIDs. Induce systemic vasoconstriction, counteract ACE NSAIDs. Induce systemic vasoconstriction, counteract ACE inhibitors, blunt effects of diuretics.inhibitors, blunt effects of diuretics.

• Thiazolidinediones. Contribute to fluid retention. Should be avoided in Thiazolidinediones. Contribute to fluid retention. Should be avoided in severe (class III-IV) failure.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 Calcium channel blockers (avoid Verapamil and Diltiazem). Trials with amlodipine and felodipine showed a neutral effect on mortality. with amlodipine and felodipine showed a neutral effect on mortality. V-HeFT trial. Circulation 1997; 96; 856.V-HeFT trial. Circulation 1997; 96; 856.

Treatment of HF exacerbation: Parenteral agents

• IV VasodilatorsIV Vasodilators- Nitroglycerine- Nitroglycerine- Nitroprusside- Nitroprusside- Recombinant BNP (nesiritide)- Recombinant BNP (nesiritide)

• IV Inotropic agentsIV Inotropic agents- Dopamine- Dopamine- Dobutamine- Dobutamine- PDE inhibitors (amrinone, milrinone)- PDE inhibitors (amrinone, milrinone)

• IV Diuretics IV Diuretics - Furosemide- Furosemide- Bumetanide- Bumetanide

Other management considerations

• AnticoagulationAnticoagulation. No RCT. Warfarin therapy may be considered in the . No RCT. Warfarin therapy may be considered in the absence of contraindications for patients who are in sinus rhythm and absence of contraindications for patients who are in sinus rhythm and have EF <30%. have EF <30%.

• Ventricular resynchronization therapyVentricular resynchronization therapy. Survival benefit in patients . Survival benefit in patients with NYHA class III-IV HF despite optimal medical therapy, who are with NYHA class III-IV HF despite optimal medical therapy, who are in sinus rhythm, have EF in sinus rhythm, have EF ≤≤35%, and a prolonged QRS ( 35%, and a prolonged QRS ( ≥≥120 msec).120 msec). CARE-HF and COMPANION trial.CARE-HF and COMPANION trial.

• ICDICD. Based on the . Based on the SCD- HeFTSCD- HeFT trial. Significant benefit in NYHA trial. Significant benefit in NYHA class II - III HF and EF class II - III HF and EF ≤≤35%. Class IV patients have not been 35%. Class IV patients have not been studied.studied.

• Mechanical circulatory support.Mechanical circulatory support.

• Cardiac transplantation.Cardiac transplantation.

References

• Jessup M, Brozena S. Heart Failure. N Engl J Med 2003; 348: 2007 – Jessup M, Brozena S. Heart Failure. N Engl J Med 2003; 348: 2007 – 18.18.

• Aurigemma GP, Gaasch WH. Diastolic Heart Failure. N Engl J Med Aurigemma GP, Gaasch WH. Diastolic Heart Failure. N Engl J Med 2004; 351: 1097 – 105.2004; 351: 1097 – 105.

• Hunt SA, et al. ACC/AHA 2005 Guideline Update for the Diagnosis Hunt SA, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. Circulation and Management of Chronic Heart Failure in the Adult. Circulation 2005; 112.2005; 112.

• Harrison’s Principles of Internal Medicine, 16Harrison’s Principles of Internal Medicine, 16 thth edition edition• UpToDateUpToDate