By:Dawit Ayele(MD,Internist)
“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
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)
◦ Coronary artery disease- ◦ HTN--both ◦ Valvular heart disease (especially aorta and mitral disease)--chronic ◦ Congenital ◦ Alcohol-- ◦ Diabetes— ◦ Cardiomyopathies
Infection Arrhythmia Physical,Fluid,Dietary,Env’tal,Emotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumatic,viral or other myocarditis..
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
1. Syndrome of decrease exercise tolerance 2. Syndrome of fluid retention 3. No symptoms but incidental discovery of LV dysfunction
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
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
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
Designed to emphasize preventability of HF Designed to recognize the progressive nature of LV dysfunction
◦ 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
◦ 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
◦ 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
◦ 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
◦ Neurohormonal system ◦ Renin-angiotensin-aldosterone system ◦ Ventricular hypertrophy
Myocardial Disease LV DysfunctionImpedance VasoconstrictionNeurohormonal Activation LV Remodeling Vascular Remodeling Preload Renal Blood Flow Na Retention
◦ 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
◦ Long term compensatory mechanism ◦ Increases in size due to increase in work load ie skeletal muscle
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
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