Transcript Document 7465003

Congestive Heart Failure
Larissa Bornikova, MD
July, 2006
Objectives
• To 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 summarize characteristics of diastolic
heart failure
• To outline management strategies for CHF
Definition
• 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.
Epidemiology
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5 million Americans have heart failure
500,000 new cases of symptomatic heart failure annually
20% of hospital admissions among persons older than 65
45% 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.
The most common causes of CHF
Remember that CHF is a syndrome, so always look for an
underlying cause!
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Ischemic heart disease ~ 40 percent
Dilated cardiomyopathy ~ 30 percent
Primary valvular heart disease ~ 15 percent
Hypertensive heart disease ~ 10 percent
Other ~ 5 percent
Etiology
WHO Classification of Heart Failure Etiologies
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Dilated Cardiomyopathy (about 20-25% of cases are familial)
Hypertrophic Cardiomyopathy (e.g. IHSS, HOCM)
Restrictive Cardiomyopathy (infiltrating diseases)
Arrhythmogenic Right Ventricular Cardiomyopathy
Unclassifiable Cardiomyopathies (fibroelastosis, mitochondrial)
Specific Cardiomyopathies (ischemic, hypertensive, valvular
obstruction/insufficiency, myocarditis, endocarditis, Chaga’s
disease, HIV, adenovirus, CMV, Enterovirus).
Metabolic (thyrotoxicosis, hypothyroidism, pheochromocytoma,
hemochromatosis, glycogen storage diseases, diabetes, kwarshiokor,
beriberi, starvation, amyloidosis, Familial Mediterrenian Fever, etc.)
General system disease (alcohol, anthracyclines, radiation, SLE,
PAN, scleroderma, dermatomyositis, sarcoidosis, muscular
dystrophies, neuromuscular disorders, peripartum cardiomyopathy,
etc.)
Pathophysiological mechanisms of CHF
• Multiple compensatory responses over the long-term
become deleterious.
Pathophysiological mechanisms of CHF
CARDIAC ABNORMALITIES
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Frank-Starling Mechanism
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Compensatory hypertrophy
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Ventricular remodeling
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Coronary arteries
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Mitral regurgitation
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Arrhythmias
OTHER MECHANISMS
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Redistribution of cardiac
output
NEUROHORMONAL
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Renin-angiotensinaldosterone system
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Sympathetic nervous system
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Natriuretic peptides
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Vasodilator peptides
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Cytokines
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Matrix Metalloproteinases
Ventricular Remodeling after Infarction (Panel A) and in Diastolic and Systolic Heart Failure
(Panel B)
Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018
Evaluation of the patient with suspected CHF:
• Establish diagnosis
• Determine the etiology
• Assess acuity and severity
Clinical Manifestations of CHF
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SYMPTOMS
Fluid overload
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Cardiac asthma
Cheyne-Stokes Respiration (aka
cyclic respiration)
Fatigue, weakness
Exercise intolerance
Decreased urine output
Confusion
Lethargy
Nocturia
Anorexia
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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
Fun facts
Dyspnea on exertion
Orthopnea
PND
Peripheral edema
sensitivity
100 %
22%
39%
49%
specificity
17%
74%
80%
47%
Based on study of 259 patients referred for echocardiography
Diagnosis of HF
• CHF should be suspected on the basis of clinical
presentation and radiographic findings.
• 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.
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.
• 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.
Patterns of Left Ventricular Diastolic Filling as Shown by Standard Doppler Echocardiography
Aurigemma G and Gaasch W. N Engl J Med 2004;351:1097-1105
Evaluation of the patient with suspected CHF:
Mechanisms to consider
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Systolic vs. diastolic
Low-output vs. high-output
Acute vs. chronic
Right-sided vs. left-sided
Backward 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
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.
• 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..
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)
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CBC
Serum electrolytes, BUN and creatinine
LFTs
Fasting blood glucose
Lipid profile
TSH
Urinalysis
CXR (cardiomegaly, Kerley B-lines, pleural effusions, pulmonary
edema)
• 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)
• Coronary 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).
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)
• BNP levels correlate with the severity of HF
• BNP levels predict survival
New York Heart Association
classification of heart failure.
Focuses on symptoms
Class I:
Class II:
Class III:
Class IV:
No limitation of physical activity.
Slight limitation with ordinary exertion.
Marked limitation with less than ordinary exertion.
Symptoms are present at rest.
ACC/AHA Classification
Emphasizes evolution and progression of heart failure.
Class A:
Class B:
Class C:
Class D:
At risk for CHF, but heart is structurally normal.
Structural abnormality of the heart, never had symptoms
Structural abnormality; current or previous symptoms.
End-stage symptoms; refractory to standard treatment.
Management of Heart Failure
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Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018
General measures
Correct underlying cause
Remove precipitating cause
Prevention of deterioration of
cardiac function
Control of congestive HF
state
Nonpharmacologic therapy
• Exercise training for stable HF patients increased exercise capacity,
decreased hospitalization rate, increased quality of life, decreased
symptoms.
• Weight loss in obese patients
• Dietary Na restriction (≤ 2 g/day)
• Fluid 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)
• Oxygen
• Fluid removal (dialysis, thoracentesis, paracentesis)
Stages of Heart Failure and Treatment Options for Systolic Heart Failure
Jessup M and Brozena S. N Engl J Med 2003;348:2007-2018
Pharmacologic therapy
 - - - - - diuretics - - - - **
/ digoxin - - - - - - **
/ spironolactone
/ beta-blockers / ?
ACE I → ARB → Hydralazine/nitrates
NYHA Class
I
** no change in mortality
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IV
Drugs to avoid in HF patients
• 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.
• Metformin. Increased (but small) risk of lactic acidosis.
• 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.
Treatment of HF exacerbation:
Parenteral agents
• IV Vasodilators
- Nitroglycerine
- Nitroprusside
- Recombinant BNP (nesiritide)
• IV Inotropic agents
- Dopamine
- Dobutamine
- PDE inhibitors (amrinone, milrinone)
• IV Diuretics
- Furosemide
- Bumetanide
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%.
• 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.
• Mechanical circulatory support.
• Cardiac transplantation.
References
• 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.
• 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, 16th edition
• UpToDate