1. DISEASES OF THE HEART K.V.BHARATHI

2. 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.

3. 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 1/3 rd of the IVS.

4. Anatomy

5. Heart-blood supply

6. Heart drives the circulation

7. Pathology 1)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.

9. 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

10. Causes of cardiac failure Hypertension Valve disease Lung disease Ischaemic heart disease Cardiomyopathy

12. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. 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.

19. Pathological changes As for causative condition + ventricular hypertrophy/dilatation. Pleural effusion. “Nutmeg” liver:Cardiac cirrhosis/sclerosis of liver.