Classification of Congential Heart Diseases and cyanotic heart disease
DISEASES OF THE HEART
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DISEASES OF THE HEART
K.V.BHARATHI
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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.
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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.
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Anatomy
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Heart-blood supply
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Heart drives the circulation
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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.
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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
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Causes of cardiac failure
• Hypertension• Valve disease• Lung disease• Ischaemic heart disease• Cardiomyopathy
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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.
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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.
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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.
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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.
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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.
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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.
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Pathological changes• As for causative condition + ventricular
hypertrophy/dilatation.• Pleural effusion.• “Nutmeg” liver:Cardiac cirrhosis/sclerosis of
liver.
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