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Congestive Heart Failure

Definition
Congestive heart failure (CHF): a complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention, and reduced longevity.

Framingham Criteria
Table 1 FRAMINGHAM CRITERIA FOR CONGESTIVE HEART FAILURE Major Criteria Paroxysmal nocturnal dyspnea Neck vein distention Rales Radigraphic cardiomegaly Acute pulmonary edema S3 gallop Central venous pressure16 cm H20 Circulation time 25 sec Hepatojugular reflux Pulmonary edema, visceral congestion, or cardiomegaly at autopsy Wight loss 4.5 kg in 5 days in response to treatment of congestive heart failure Minor Criteria Bilateral ankle edema Nocturnal cough Dyspnea on ordinary exertion Hepatomegaly Pleural effusion Decrease in vital capacity by one third from maximal value recorded Tachycardia (rate 120 beats/min)

Diagnosis
Two major or one major and two minor criteria

Incidence and Prevalence


* Incidence: 4.6 million persons/USA, 550,000 new cases/year * Prevalence: 1-2% at age of 50 to 59 10% at age> 75 years

Table 2 Common causes of heart failure Prerlominant systolic failure Coronary artery disease Hypertension Dilated cardiomyopathy Idiopathic Toxic (alcohol, doxorubicin) Infection (Viral, parasitic, and others) Predominant diastolic failure Hypertension Hypertrophic cardiomyopathy Restrictive cardiomyopathy Amyloidosis Sarcoidosis Hemachromatosis Constrictive pericarditis High-output failure Chronic anemia Atrioventricular shunt Thyrotoxicosis

Right-vs Left-sided OF
Right-sided HF: generalized edema, ankle edema, congestive hepatomegaly, ascites, pleural effusion. Left-sided HF: pulmonary congestion or edemaSystolic vs Diastolic HF TABLE.3 SYSTOLIC VS. DIASTOLIC HEART FAILURE PARAMETERS Physical Examination Cardiomegaly S3 gallop S4gallop Mitral regurgitation Rales Edema Jugular venous distention Chest Roentgenogram Cardiomegaly Pulmonary congestion Electrocardiogram Left ventricular hypertrophy Q waves SYSTOLIC +++ +++ + +++ ++ +++ +++ DIASTOLIC + + +++ + ++ + +

+++ +++

+ +++

++ ++

++++ +

Low voltage Echocardiogram Left ventricular hypertophy Left ventricular dilation Left atrial enlargement Reduced ejection fraction

+++

++ ++ ++ ++++

++++ ++ -

Low-output vs High-output HF
High-output HF: thyrotoxicosis, A-V fistula, sepsis, anemia, beriberi, Paget's disease. Low-output HF: clinical evidence of systemic vasoconstriction with cold, pale and sometimes cyanotic extremities.

NYHA functional class


Class I-No limitation Class II-Slight limitation of physical activity Class III-marked limitation of physical activity Class IV-Inability to carryon any activity without discomfort

Prognosis
5-year mortality: 50% 1 year mortality in severe CHF: 30-40% 90% of deaths due to progressive heart failure and sudden cardiac death (due to VT/VF)

Mechanisms of Pharmacotherapy
Decrease preload Decrease afterload Increased contractility Decrease preload, decrease edem a, decrease sodi um and water retention, improve neurohumoral adaptations Standard, first-line and mainstay therapy Diuretics do not influence the natural history of chronic HE Effects on long-term mortality: unknown Aldosterone antagonist (aldactone): ~ 30% mortality (pittb et at. NEJM, 1999) Complications: hyperkalemia, hypomagnesemia, hyponatremia, metabolic alkalosis, hyperglycemia, hyperlipidemia, and hyperuricemia

Diuretics

Vasodilators

Venous vasodilator (Nitrate) Activate guanylate cyclase Long-term effects: improve exercise capacity, relieve symptoms, increase LVEF, and improve mortality with hyralazine (V-HeFfI&II) Arterial vasodilator (Hydralazine) Decrease afterload, increase Condiac output Long-term effects on mortality: not improved

ACE inhibitors
Inhibition of ACE, inactivate bradykinin prostaglandin, aldosterone, catecholamine. Improve symptoms, increase exercise tolerance, prolong life, progressive LV enlargement after MI, delay onset of symptoms and frequency of hospitalization. ACE! reduce the risk of asymptomatic HF to symptomatic HF ACEI attenuate CHF-induce atrial remodeling and fibrosis, reduce AF promotion Complications: renal function impairment (bilateral renal a. stenosis), hyperkalemia or cough Angiotensin II antagonist Similar hemodynamic effects as ACEI except did notbradykinin AT1 in all vascular tissue, liver and largely in the heart. ARBs (valsartan) improved SIS, HF Fc, EF, quality of life, but not mortality; ACEI + ARB: more complete block of angiotensin II Improve ventricular function, relieve symptoms and prolong life. Carvedilol improve morbidity and mortality in severe CHF. Possible mechanisms: Up regulati on of B- receptors, myocardi al protecti on, improve ability of noradrenergic sympathetic nerves, decrease NE, decrease RAS, vasopressi nand endothelin, antiarrhythmic effects, increase Coronary blood flow, prevent hypertrophy and remodeling, antioxidant and antiapoptosis effect

Carvedilol

Inotropic agents
Increase contractility, given intravenously for short-term support in decompensated HF Digitalis improve morbidity (relieve symptoms, decrease hospitalization) but not mortality. Calcium channel blocker (CCB) Not recommended for the treatment of CHF due to their negative inotropic effects

Non-pharmacologic therapy

Cardiac resynchronization: signi ficant eli ni cal improvement in severe HF CPAP: improve clinical function and maybe the prognosis and survival with CHF Volume reduction surgery:improve hemodynamics and functional capacity Heart transplantation

TREATMENT
SYSTOLIC HEAR FAILURE Reversal/Limitation of Primary Process Assess for suitability for surgical or percutaneous revascularization and aggressive lipid control. Treat hypertension Diabetes: aggressive glycemic control In valvular or congenital heart disease, consider possibility of surgical repair.

Figure1. Pharmacologic strategy in treating heart failure: first-line therapies Medical Management First-Line Stepwise Therapy of CHF 1. Start ACE inhibitor and titrate to target dose. a. Monitor RUN, Cr, and K as well as BP response 2. Add diuretic (e.g., furosemide) for symptoms of fluid retention.

3. Start beta blocker once ACE inhibitor reaches target dose 4. Digoxin is added for NYHA class 2 to 4 patients for symptom relief. 5. Spironolactone: for patient with class3 to 4 CHF if creatinine in normal and no Medical Management First-Line Stepwise Therapy of CHF 1. Start ACE inhibitor and titrate to target dose. a. Monitor BUN, Cr, and K as well as BP response 2. Add diuretic (e.g., furosemide) for symptoms of fluid retention. 3. Start beta blocker once ACE inhibitor reaches target dose 4. Digoxin is added for NYHA class 2 to 4 patients for symptom relief. 5. Spironolactone: for patient with class 3 to 4 CHF if creatinine in normal and no hyperkalemia Second-Line Therapies for Selected Patients 1. Angioensin receptor blocker (ARB) a. If patient cannot tolerate ACE inhibitor because of cough or other nonrenal adverse effect. 2. Nitrate-hydralazine combination 3. Calcium-channel blockers a. Amlodipine or Felodipine can be added if there is coexisting hypertension or angina. Third-Line therapies for Patients Refractory to Conventional Thera pies 1. Intravenous inotropes 2. Biventricular pacing a. For patients with class 3 to 4 heart failure 3. Continuous positive airway pressure (CPAP) a. For patients with central sleep apnea and Cheyne-Stokes breathing. 4. Cardiac transplantation a. Major indications: LVEF < 20% i. ii. NYHA class 3 or 4+ Exercise capacity: oxygen consumption (V02max) < 14 mL/kg/min iii. iv. Is the patient psychologically capable of handing the demanding transplant regimen. b. Contraindications i. Significant comorbid conditions ii. Pulmonary hypertension not reversible with medication.

DIASTOLIC HEART FAILURE

DIAGNOSIS The diagnosis of definite diastolic heart failure is based on all three cri teria a. History and physical showing definitive evidence of CHF b. Noninvasive imaging showing normal LVEF systolic function c. Cardiac catheterization evidence of LV diastolic dysfunction Echocardiography can provide additional information on the severity of diastolic dysfunction TREATMENT Step 1: Diuretics Step 2: Beta blocker or ACE inhibitor Step 3: Calcium-channel blockers

HIGH OUTPUT HEART FAILURE


Anemia Hyperthyroidism Large and significant Left to Right shunt including congenital heart disease, artificial AV fistula

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