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Published byRoland Randolf Harper Modified over 9 years ago
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By:Dawit Ayele(MD,Internist)
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“Heart (or cardiac) failure is the pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure.” - Eugene Braunwald “Congestive heart failure (CHF) represents 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” - Milton Packer
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Burden of CHF is staggering 5 million in US (1.5% of all adults) 500,000 cases annually In the elderly 6-10% prevalence 80% hospitalized with HF 250,000 death/year attributable to CHF $38 billion (5.4% of healthcare cost)
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◦ Coronary artery disease- ◦ HTN--both ◦ Valvular heart disease (especially aorta and mitral disease)--chronic ◦ Congenital ◦ Alcohol-- ◦ Diabetes— ◦ Cardiomyopathies
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Infection Arrhythmia Physical,Fluid,Dietary,Env’tal,Emotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumatic,viral or other myocarditis..
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SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART FAILURE BACKWARD VERSUS FORWARD HEART FAILURE
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1. Syndrome of decrease exercise tolerance 2. Syndrome of fluid retention 3. No symptoms but incidental discovery of LV dysfunction
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Major Criteria Orthopnea/PND Venous distension Rales Cardiomegaly Acute pulm edema Elevated JVP HJR Circ time >25s Minor Criteria Ankle edema Night cough Exertional dyspnea Hepatomegaly Pleural effusion Tachycardia (>120) Decrease VC Weight loss with CHF tx Framingham Criteria
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Class I: Symptoms with more than ordinary activity Class II: Symptoms with ordinary activity Class III: Symptoms with minimal activity Class IIIa: No dyspnea at rest Class IIIb: Recent dyspnea at rest Class IV: Symptoms at rest
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At Risk for Heart Failure: STAGE A High risk for developing HF STAGE B Asymptomatic LV dysfunction Heart Failure: STAGE C Past or current symptoms of HF STAGE D End-stage HF
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Designed to emphasize preventability of HF Designed to recognize the progressive nature of LV dysfunction
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◦ COMPLEMENT, DO NOT REPLACE NYHA CLASSES NYHA Classes - shift back/forth in individual patient (in response to Rx and/or progression of disease) Stages - progress in one direction due to cardiac remodeling
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◦ Occurs when the left ventricle fails as an effective forward pump ◦ back pressure of blood into the pulmonary circulation ◦ pulmonary edema ◦ Cannot eject all of the blood delivered from the right heart. ◦ Left atrial pressure rises increased pressure in the pulmonary veins and capillaries ◦ When pressure becomes too high, the fluid portion of the blood is forced into the alveoli. ◦ decreased oxygenation capacity of the lungs ◦ AMI common with LVF, suspect
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◦ Severe resp. distress– Evidenced by orthopnea, dyspnea Hx of paroxysmal nocturnal dyspnea. ◦ Severe apprehension, agitation, confusion— Resulting from hypoxia Feels like he/she is smothering ◦ Cyanosis— ◦ Diaphoresis— Results from sympathetic stimulation ◦ Pulmonary congestion Often present Rales—especially at the bases. Rhonchi—associated with fluid in the larger airways indicative of severe failure Wheezes—response to airway spasm
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◦ Jugular Venous Distention— not directly related to LVF. Comes from back pressure building from right heart into venous circulation ◦ Vital Signs— Significant increase in sympathetic discharge to compensate. BP—elevated Pulse rate—elevated to compensate for decreased stroke volume. Respirations—rapid and labored
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◦ Neurohormonal system ◦ Renin-angiotensin-aldosterone system ◦ Ventricular hypertrophy
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Myocardial Disease LV DysfunctionImpedance VasoconstrictionNeurohormonal Activation LV Remodeling Vascular Remodeling Preload Renal Blood Flow Na Retention
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◦ Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys Aldosterone is released increase in Na+ retention water retention Preload increases Worsening failure
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◦ Long term compensatory mechanism ◦ Increases in size due to increase in work load ie skeletal muscle
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Principles:thorough Hx & P/E Supplemental investigations especially:BNP,ECG,Echocardiography,CXR Management:(1) general measures; (2) correction of the underlying cause; (3) removal of the precipitating cause; (4) prevention of deterioration of cardiac function; and (5) control of the congestive HF state
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Control Volume Slow Disease Progression Diuretic RAAS Inhibition RAAS Inhibition Beta-Blockade Treat residual symptoms Treat residual symptoms DIGOXIN + SPIRONOLACTONE Am J Cardiol 1999;83(suppl 2A):9A-38A
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