CHF Pathophysiology

S S Gambbhir Hamdard

Human Heart
2 Pumps in series Left & Right To Provide Adequate Blood to tissues Venous to Lungs Arterial to all other organsincl. Coronary
S=90-140 mm Hg D= 4-12 mm Hg EDP=Av. 5 mm Hg EDV=Normal 50 ml

S=15-30 mm Hg D= 0-5 mm Hg

Pathophysiology of CHF
Heart Failure defined as FAILURE of C.O. to MEET DEMANDS DECREASED CARDIAC OUTPUT (C.O.=S.V. x H.R.) INCREASED DEMAND Thyrotoxicosis Anemia Beri Beri

Pathophysiology of CHF
STROKE VOLUME depends on Extrinsic Factors

Intrinsic Contractility

Venous (PRE-LOAD)

Arteriolar (AFTER-LOAD)

Pathophysiology of CHF
1. PRE-LOAD: Defined as LOAD on Heart created by VOLUME of Blood entering the VENTRICLES during DIASTOLE (& this volume must be ejected during NEXT SYSTOLE) MORE the BLOOD entering MORE the STRETCH of the Ventricular Muscle more Ventricular Volume EDP Work Stroke Volume (within Physiological Limits Frank Starlings Law) Excess Pre-Load (e.g.Valve defects) HEART FAILURE VENODILATORS PRE-LOAD RELIEVE CHF

Pathophysiology of CHF
2. AFTER-LOAD: Defined as LOAD on the Contracting Ventricle exerted due to RESISTANCE in ARTERIOLES against which HEART HAS TO PUSH Blood during Systole (i.e. Peripheral Resistance PR) MORE the PR MORE the WORK-load on the HEART can be Handled only within Physiological Limits (by a gradual Myocardial Hypertrophy) Excess After-Load (e.g. Hypertension, Arteriosclerosis) HEART FAILURE ARTERIO-DILATORS Pre-Load Relieve CHF

Pathophysiology of CHF
3. CONTRACTILITY of Heart:
Defined as CAPACITY of Heart to GENERATE FORCE to Handle NORMAL PRE - & AFTER-LOAD Respond to the INCREASED PRE-LOAD Overcome the INCREASED AFTER-LOAD
 Initially VENTRICULAR HYPERTROPHY* within Limits Compensatory in Contractility  Later FAILURE (CARDIAC DILATATION*) *(REMODELLING)

Decreased Contractility Can not handle normal Preload & Afterload INCREASE C.O. OF FAILING HEART ( CONTRACTILITY WITHOUT INCREASING O2 CONSUMPTION)

CHF - involves many Organs / Processes

Defective Excitation-Contraction of myosytes Suppressed Baro-Receptor Reflexes Sympathetic Nervous System Over-activity (Compensatory) Renal Hypoperfusion & Renin-Angiotensin System Overactivity Some other Peptides (ANP, etc) Cardiac Cell Death (APOPTOSIS)

DECREASED CARDIAC OUTPUT CAROTID SINUS (Baro-receptor) Firing LESS INHIBITORY IMPULSES SYMPATHETIC DISCHARGE

RENAL BLOOD FLOW RENIN RELEASE ANGIOTENSIN II

REMODELLING CARDIAC Dilatation

Heart Force of PRE-Load AFTERRate ) Load Contraction (Veno

INITIALLY Compensatory in LV Ejection Fraction LATER Decompen. Stage in LV Ejection Fraction

HyperEj. Fract. trophy

(Arteriolar Constrict)

Opposes

CHF

BACKWARD FAILURE EFFECTS

VENOUS PRESSURE CONGESTION

FORWARD FAILURE EFFECTS FATIGUE

Sympath Activity HR PR

C. O. B. P. RENAL FLOW

LUNGS Creps Dyspnea

LIVER Enlarged Palpable

Less Urine

Renin AngT-II ALDOSTERONE Na , 2O Retenti n

Capillary Filtration

EDEMA

MYOCARDIAL YPERTROP Y CARDIAC DILATATION

REMODELLING

HEART FAILURE can be Acute: Myocardial Infarction (MI) Acute Myocarditis (e.g. Viral) Chronic: as in Arteriosclerosis Hypertension Valvular Defects Congenital Heart Defects Myopathies

Stages of CHF (N.Y. Heart Association): 1. Minimal Dyspnea after Mild Exertion 2. Dyspnea on Walking on Flat 3. Dyspnea on getting in/out of BED 4. Dyspnea while LYING IN BED

THERAPEUTIC GOALS : A. C.O. (Relieve Smptoms); B. SURVIVAL A. INCREASE C.O.: 1. Increase Contractility (Inotropic Drugs) CARDIOTONIC GLYCOSIDES - Digoxin ADRENERGIC INOTROPES Dobutamine PDE III Inhibitors Amrinone, Milrinone 2. Decrease Cardiac Load Body Fluid (Pre- / After-Load): Diuretics Pre-Load (Veno-dilators): Nitrites/Nitrates After-Load (Arteriolar-dilators): Ca+++ Channel Blockers Nifedipine K+ Channel Openers Nicorandil Pre- & After-Load ACE , AT1-Blockers B. INCREASE SURVIVAL: -blockers, ACE , etc.