CHF -Pathophysiology

S S Gambbhir

Hamdard

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

S=90-140 mm HgD= 4-12 mm HgEDP=Av. 5 mm HgEDV=Normal 50 ml

Human Heart•2 Pumps – in series Left & Right•To Provide Adequate Blood to tissues

Venous to Lungs

Arterial to all other organs- incl. Coronary

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 CHF1. 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 Starling’s Law)

☞Excess Pre-Load (e.g.Valve defects) HEART FAILURE ☞VENODILATORS PRE-LOAD RELIEVE CHF

Pathophysiology of CHF2. 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

CHF - involves many Organs / ProcessesDefective 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

RENAL BLOOD FLOW CAROTID SINUS(Baro-receptor) Firing

LESS INHIBITORY IMPULSES RENIN RELEASE

ANGIOTENSIN II SYMPATHETIC

DISCHARGE

Heart Rate

Force of Contraction

PRE-Load (Veno )

REMODELLING CARDIAC

Hyper-trophy

Dilat-ation

INITIALLY Compensatory in LV Ejection Fraction

LATER Decompen. Stage in LV Ejection Fraction

Ej. Fract. Opposes

CHF

AFTER-Load (Arteriolar Constrict)

FORWARD FAILURE EFFECTS

BACKWARD FAILURE EFFECTS

C. O.

RENAL FLOW

VENOUS PRESSURE

LUNGS• Creps• Dyspnea

LIVER•Enlarged•Palpable Less Urine

Capillary Filtration EDEMA

Sympath Activity

• HR• PR

CONGESTION B. P.

FATIGUE

Renin AngT-II

ALDO-STERONE

Na2 , H2O Retention

MYOCARDIAL HYPERTROPHY CARDIAC DILATATION

REMODELLING

HEART FAILURE can be –• Acute: Myocardial Infarction (MI)

Acute Myocarditis (e.g. Viral)• Chronic: as in Arteriosclerosis

HypertensionValvular Defects

Congenital Heart DefectsMyopathies

•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