Transcript DISEASES OF THE HEART

DISEASES OF THE HEART
K.V.BHARATHI
Agenda:
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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
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 continuitydissection,trauma.
Cardiac failure
• End result of many pathological processes
• Leads to complex adaptive processes
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Increased sympathetic tone
Antidiuretic hormone secretion
Increased renin-angiotensin activity
Increased cardiac muscle bulk
Causes of cardiac failure
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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 socalled 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.