DISEASES OF THE HEART

K.V.BHARATHI

Agenda:• Normal heart.• Heart failure.• Congenital heart disease.• Ischemic heart disease.• Sudden cardiac death.• Hypertensive heart disease.• Valvular heart disease.• Cardiomyopathies.• Pericardial disease.• Tumors of the heart.• Cardiac transplantation.

The normal heart:• Weight:Approximately 250-300g in female,300-350g in

male.• RV free wall thickness:0.3-0.5 cm.• LV free wall thickness:1.3-1.5 cm.• Blood Supply:The coronary arteries--- Left anterior descending(LAD)supplies most of the

apex,the anterior wall of LV & anterior 2/3rds of the IVS. Left circumflex(LCx) supplies LV myocardium. Right coronary artery(RCA) supplies RV free wall &

posterior 1/3rd of the IVS.

Anatomy

Heart-blood supply

Heart drives the circulation

Pathology1) Failure of the pump-due to weak contraction

OR insufficient relaxation.2) Obstruction to flow-valvular lesions or lesions

that cause outflow obstruction.3) Regurgitant flow-incompetent valves,dilated

heart.4) Disorders of cardiac conduction-heart blocks &

arrhythmias.5) Disruption of circulatory system continuity-

dissection,trauma.

Cardiac failure• End result of many pathological processes• Leads to complex adaptive processes– Increased sympathetic tone– Antidiuretic hormone secretion– Increased renin-angiotensin activity– Increased cardiac muscle bulk

Causes of cardiac failure

• Hypertension• Valve disease• Lung disease• Ischaemic heart disease• Cardiomyopathy

Right and left heart failure

• Interrelated but can be distinct especially in early stages.

• Left – pulmonary congestion/oedema.• Right – systemic congestion ( jugulovenous

pressure), hepatomegaly.• “Congestive cardiac failure” (CCF) – both sides

of the heart show features of failure.

Cardiac output

• Usually decreased in cardiac failure• High output failure caused by:– Increased blood volume.– Anaemia (severe).– Cirrhosis (vasodilatation with decreased

peripheral resistance).– “Wet” Beri-beri.

Cardiac hypertrophy:pathophysiology & progression to failure

• Cardiac myocyte can hypertrophy but not undergo hyperplasia.

• Increased mechanical load causes hypertrophy.• Can weigh upto 400-800 g (2-3 times of normal).• Causes: Systemic hypertension. AS & AR. MR. Dilated / hypertrophic cardiomyopathy.

Pattern of hypertrophy reflects the nature of the stimulus!

• Pressure-overloaded ventricles show concentric hypertyrophy as in Hypertension & AS.

• LV shows increase in wall thickness with reduced cavity diameter.

• Volume-overload causes eccentric hypertrophy with an increase in both wall thickness & cavity diameter due to LV dilatation.

• The causes are MR,AR ,dilated cardiomyopathy.• Cardiac dysfunction follows both these types of

hypertrophy.

Morphology of left-sided failure:• Heart—Non-specific changes of hypertrophy & fibrosis in the

myocardium.The LA may be dilated & may contain thrombus.• Lungs—Pulmonary congestion with perivascular & interstitial

transudate,accumulation of oedema fluid in alveoli,hemosiderophages or “heart failure cells”.

• Kidneys—Decreased cardiac output causes a decrease in renal perfusion.This activates the Renin-Angotensin-Aldosterone system,which causes salt & water retention.

• Persisiting perfusion deficit can cause Pre-renal azotemia.

• Brain—Cerebral hypoxia with hypoxic encephalopathy.

Morphology of right-sided failure:• Usually a secondary consequence of left-sided failure.• Pure right-sided failure occurs with chronic severe pulmonary

hypertension:cor-pulmonale.• Liver & Portal system—congestive hepatomegaly with passive

congestion.• With long standing severe right-sided failure, central areas of the

hepatic lobule show fibrosis along with necrosis,creating so-called cardiac sclerosis or cardiac cirrhosis.

• Elevated portal pressure can cause congestive splenomegaly,with marked sinusoidal congestion.

• Transudate in the peritoneal cavity---Ascites.• Kidneys---Show congestion & can lead to Azotemia.• Brain---identical to left-sided failure.• Pleural & pericardial effusion.• Subcutaneous tissues---dependant edema, can lead to

generalized massive oedema:Anasarca.

Pathological changes• As for causative condition + ventricular

hypertrophy/dilatation.• Pleural effusion.• “Nutmeg” liver:Cardiac cirrhosis/sclerosis of

liver.