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OVERVIEW OF TREATMENT OF CONGESTIVE HEART FAILURE. OVERVIEW . Background and Historical Perspective Determinants of Cardiac Output and Hemodynamic Intervention Newer Therapeutics . EVOLUTION IN CONCEPTS. Cardio-renal (pre 1970) : Digoxin, diuretics
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OVERVIEW • Background and Historical Perspective • Determinants of Cardiac Output and Hemodynamic Intervention • Newer Therapeutics
EVOLUTION IN CONCEPTS • Cardio-renal (pre 1970) : Digoxin, diuretics • Hemodynamic 1970’s and 1980’s: + Inotropics, VD • Neurohormonal 1990’s: RAS, SNS
DETERMINANTS OF CARDIAC PERFORMANCE • HEART RATE • CONTRACTILITY • PRELOAD VASODILATOR THERAPY • AFTERLOAD
RATE AFTERLOAD PRELOAD LV CONTRACTILITY
CO = SV x HR EF = CO
HEART RATE • COMPENSATORY RESPONSE • ATROPHINE • ISUPREL • PACER
CONTRACTILITY • Inherent property of the myocardium • Allows the heart to increase its extent and force of shortening independent of the Starling mechanism • Not directly measurable
CONTRACTILITY • DIGITALIS • DOBUTAMINE • DOPAMINE • ISUPREL • EPINEPHRINE • CALCIUM • GLUCAGON • AMIRANOME (Miliron)
STARLING’S LAW THE MORE A MYOCARDIAL FIBER IS STRETCHED DURING DIASTOLE, THE MORE IT WILL SHORTEN IN SYSTOLE IT WILL ALSO SHORTEN WITH GREATER FORCE
PRELOAD The length to which a cell is stretched prior. To the next contraction The volume or pressure generated in the ventricles at end-diastole Degree to which a cell is stretched in diastole (preload) force during systole
AFTERLOAD IMPEDANCE OF BLOOD FROM THE VENTRICLE Determined by: The volume and mass of blood ejected from the ventricle The compliance and total cross-sectional area of the vascular space into which the blood is ejected.
AFTERLOAD – RESISTANCE PROXIMAL IMPEDENCE
SYSTEMIC VASCULAR RESISTANCE SVR= (MAP-RAP) (80) CO MAP= MEAN ARTERIAL PRESSURE RAP= RIGHT ATRIAL PRESSURE CO= CARDIAC OUTPUT
BASIC HEMODYNAMIC PARARMETERS Preload = PCWP Afterload = SVR
1 2 4 3
1 2 4 3
Clinical Profile of Nesiritide • Vasodilation (venous > arterial) • Rapidly improves symptoms of congestion • Does not increase heart rate (decreases myocardial oxygen demand) • Is not proarrhythimic • Neurohormonal suppression (decreases aldosterone, endothelin-1) • Mild diuresis/natriuresis
Clinical Profile Nesiritide (cont.) • No evidence of tachyphylaxis • Symptomatic hyptension as low as 4% in the VMAC study • Dosing convenience (bolus plus standard-dose IV infusion
EVOLUTION IN CONCEPTS • Cardio-renal (pre 1970): Digoxin, diuretics • Hemodynamic 1970’s and 1980’s: + Inotropics, VD • Neurohormonal 1990’s: RAS, SNS
NEUROHORMONAL FACTORS IN HEART FAILURE PROGRESSION • Circulating (RAS, SNS) Abnormality in regional blood flow, renal sodium retention • Endothelin (ET-1, ET-2, ET-3) Vasoconstrictors • Natriuretic Peptide, (ANP) Vasodilators, suppresses RAS • Cytokines (TNF , Interleukin) Depresses contractility, anorexia and cachexia
Neurohormonal Intervention in Heart Failure Heart Failure Renin- angiotensin system Sympathetic nervous system ACE inhibition Beta Blockade
ACE INHIBITORs (ANGIOTENSIN CONVERTING ENZYMES INHIBITORS) ARBs (ANGIOTENSION RECEPTOR BLOCKERS)
BETA BLOCKERs ALPHA AND BETA BLOCKERs
Effect of Carvedilol on Left Ventricular Ejection Fraction P<.001 Patients receiving diuretics, ACE inhibitors, digoxin; follow-up 6 months; placebo (n=84), carvedilol (n=261). Mulitcenter Oral Carvedilol Heart Failure Assessment Adapted from Bristow et al. Circulation. 1996;94:2807-2816. P<.05 vs placebo.
CLINICAL ASSESSMENT Warm vs. Cold (Perfusion)- Pulse Pressure Dry vs. Wet (Congestion)- Jugular Venus Pressure
NEWER THERAPEUTICS • Biventricular Pacing • EECP • Measurement of BNP levels