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IHD
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INTRODUCTIONIschemic heart disease also designated
as coronary artery disease refers to a group of closely related syndromes caused by an imbalance between myocardial oxygen demand and blood supply.
ETIOLOGYThe most common cause of imbalance
between need and supply of oxygen is atherosclerotic narrowing of the coronary arteries producing ischemia.
RISK FACTORS FOR ATHEROSCLEROSIS
Fixed Risk FactorsAgeMale SexFamily History
MODIFIABLE RISK FACTORS
STRONG ASSOCIATIONHyperlipidemiaHypertensionCigarette SmokingDiabetes Mellitus
OTHER ASSOCIATIONS
ObesityLack of exerciseHeavy alcoholismDietary factorsOral contraceptivesGoutHigh level of coagulation factor vii &
fibrinogenAnxiety & depression
PATHOGENESIS
Defective Oxygen DeliveryIncreased Oxygen DemandIHD becomes symptomatic when there is 75% or more reduction of the lumen of one or more coronary arteries by atherosclerotic plaque.
Superimposed Lesions Acute changes in plaque morphology
Local platelet aggregation Coronary artery spasm Coronary artery thrombosis
CLASSIFICATION OF IHD
Stable anginaUnstable anginaMyocardial infarctionSudden cardiac death
WHAT IS ANGINA?
Angina is a clinical syndrome characterized by intermittent chest pain caused by reversible myocardial ischemia.
The pain is usually substernal or precordial radiating to the shoulder and arm or to the jaw.
It lasts for several minutes.
TYPES OF ANGINA
STABLE ANGINAVARIANT ANGINA
UNSTABLE ANGINA
STABLE ANGINAIt occurs due to increased myocardial
oxygen demand during exertion in a patient of narrow coronary arteries.
VARIANT ANGINAIt occurs at rest and produced by the
reduction of the myocardial blood supply due to coronary artery spasm.
UNSTABLE ANGINAIn this type of angina, frequency, severity
and duration of episodes are progressively increased. It occurs at rest due to thrombus formation and coronary artery spasm.
DIFFERENCE B/W STABLE & UNSTABLE ANGINA
STABLE ANGINA
Due to fixed stenosis
Demand-led ischemia
Related to effort
Symptoms over long term
UNSTABLE ANGINA
Due to dynamic stenosis
Supply-led ischemia
Symptoms at rest
Symptoms over short term
INVESTIGATIONS
ECGETTThallium scanCT AngiographyEchocardiography Coronary Angiography
ECG
During pain ECG showsST –segment depression with or without T
wave inversion that reverses after ischemia disappears.
Elevation of ST segment in variant angina.The resting ECG may be normal b/w
attacks however it may show old MI, heart block or left ventricular hypertrophy.
ETT
When history is suggestive of angina but ECG normal ETT is performed for diagnosis.
Positive test is one in which ST segment is depressed by 1 mm.
MYOCARDIAL INFARCTION
INTRODUCTION•MI is death or necrosis of myocardial cells.
Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted.
ETIOLOGY Commonly caused due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, in the wall of an artery. The resulting ischaemia and hypoxia, if left untreated for a sufficient period, can cause damage and or death (infarction) of heart muscle tissue.
ETIOPATHOGENESIS1. Mechanism of MI i) Diminished coronary blood flow ii) Increased myocardial demand iii) Cardiac hypertrophy without se of
coronary blood flow
2. Role of Platelets - rupture of atherosclerotic plaque exposes
subendothelial collagen to platelets - aggregation, activation, release of platelets
3. Complicated Plaques i) Superimposed coronary thrombosis ii) Intramural haemorrhage
4. Non-atherosclerotic causes - coronary vasospasm - arteritis - embolism - thrombotic diseases - trauma
5. Transmural versus subendocardial infarcts
Transmural infarcts- involve full thickness of
ventricular wall subendocardial (laminar) infarcts- affecting inner subendocardial one-third to one-half.
Classical symptoms of acute myocardial
infarction
Sudden chest pain Shortness of breath Nausea Vomiting Palpitations Sweating Anxiety
Risk factors for myocardial infarction
1. Older age 2. Sex (males) 3. Tobacco smoking 4. Hypercholesterolemia 5. Diabetes 6. Hypertension 7. Obesity 8. Stress
Pathological Changes
Vary according to the age of the infarct
Most infarcts occur singly (very less multifocal), 4-10 cm size
Most often in left ventricle
Subendocardial infarcts produce less well-defined infarcts gross changes than the transmural infarcts.
CLINICAL DIAGNOSIS
Clinical diagnosis is based on Symptoms ECG changesElevation of specific serum enzymes
SYMPTOMS
Onset is sudden with severe constricting, crushing, burning substernal or precordial pain that radiates to the left shoulder and arm or jaw.
Pain is accompanied by sweating, nausea, vomiting or dyspnea.
Cardiogenic shock.
ECG Changes
ST Segment elevation, follwed by abnormal new Q waves and inverted T wave.
Serum EnzymesCreatinine phosphokinaseLactic dehydrogenaseCardiac troponin I & Troponin T.
CHRONIC ISCHEMIC HEART DISEASE
Chronic IHD some times called ischemic cardiomyopathy is used to describe the development of progressive CHF.
It is characterized by multifocal areas of myocardial atrophy and fibrosis secondary to slowly developing coronary atherosclerosis leading to dilatation of cardiac chambers.
CLINICAL FEATURES
Usually it remains asymptomatic and progressively CHF develops.
Cardiac arrhythmias may occur when scarring involves conduction system.
Angina, MI
TYPES OF HEART FAILURE
ACUTE HEART FAILURE CHRONIC HEART FAILURE RIGHT AND LEFT HEART FAILURE CONGESTIVE HEART FAILURE FARWARD HEART FAILURE BACKWARD HEART FAILURE CARDIAC ARREST
ACUTE HEART FAILURE
Sudden onset of heart failure without previous symptoms of ischemia or MI.
CHRONIC HEART FAILURE
Gradual onset of heart failure with symptoms of ischemia or MI.
CONGESTIVE CARDIAC FAILURE
Bi ventricular heart failure.
CARDIAC ARREST
Complete cessation of heart function.
Conductive system of heart completely block.