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coronary artery dise

coronary artery

2-D ADVANTAGES IN CAD EVALUATION Performed immediately Determines location and extent of LV wall motion abnormalities
Estimates systolic and diastolic function Serial studies Assess LV function changes after infarct or reperfusion therapy
Complications identified ACUTE MYOCARDIAL ISCHEMIA Ischemia is a reversible imbalance in the myocardial oxygen demand-to-supply ratio Obstructed coronaries can usually still compensate for demands at rest
When narrowing exceeds 70% of cross sectional area blood flow can’t keep up with demands from: Exercise Pharmacologic interventions mental stress
ACUTE MYOCARDIAL ISCHEMIA Consequences I Coronary artery occlusion/obstruction Diastolic dysfunction Impaired relaxation and decreased compliance Increased LVEDP
ACUTE MYOCARDIAL ISCHEMIA Consequences II Decreased left ventricular ejection fraction Impaired systolic thickening Reduction of endocardial motion Dysynchronous contrac
ACUTE MYOCARDIAL ISCHEMIA Consequences III Consequences Possible LV dilatation Large infarctions More increase in LVEDP CHF develops Increased heart rate to compensate and maintain adequate cardiac output
WALL MOTION ABNORMALITIES Describing abnormality: Hypokinesis – an increase in systolic wall thickening <40% Akinesis – systolic wall thickening <10% Dyskinesis – present when wall moves outward during ventricular systole and has wall thinning
CLASSIFICATIONS MI’s divided into 3 categories: Subendocardial – involving only the inner layer of the myocardium Subepicardial – involving both inner and middle layers Transmural – extending through all three layers of the myocardial walls
EKG FINDINGS T wave inversion suggests ischemia Elevated ST segment represent acute MI Prominent peaked T waves show acute MI Pathologic Q waves show “old” MI May also see ventricular arrhythmias or other conduction defects
SYMPTOMS Physical examination May be normal if MI is uncomplicated Symptoms are usually the last thing to occur Chest pain SOB Nausea Vomiting May not occur at all
MYOCARDIAL INFARCTION LAB VALUES CK I AKA Total CK, creatine phosphokinase, CPK, creatine kinase Levels rise when muscle or heart cells are injured Levels begin to rise 4-6 hrs after MI Highest levels are 18-24hrs after Will return to normal 2-3 days
MYOCARDIAL INFARCTION LAB VALUES CK II Can also be seen w/ skeletal muscle damage If CK is high, a more specific test is needed
LAB VALUES I CK-MB AKA CK MB, CPK MB, creatine kinase-MB CK-MB helps differentiate between heart damage or damage to other muscles CK-MB can also tell Dr. if clot dissolving drugs are working
LAB VALUES CK-MB II Ck-MB to total CK index higher than 2.5-3 indicates high likelihood of heart muscle damage Some skeletal muscle injury can be severe enough to raise CK-MB levels
LAB VALUES Troponin AKA Tn1, TnT, Cardiac specific Troponin I and T Usually ordered along with other cardiac markers Troponin is starting to replace CK & CK-MB because it is more specific for heart injury
Troponin Troponin is elevated for longer period of time, 1-2 weeks after a heart attack Levels are not affected by damage to other muscles
2D DOPPLER EXAM Sonographer needs: Clinical history Prior cardiac events Cardiac murmurs Evidence of CHF Systolic BP Pulmonary artery cath info in CCU Hemodynamic info 12 lead EKG for presumed infarct location
IMPORTANT ECHO INFORMATION LV and RV size and function Wall motion abnormalities Valve integrity and regurgitation LV diastolic filling parameters
ECHO FINDINGS 2D evidence of wall motion abnormalities is always seen in transmural infarction Wall motion abnormalities may or may not be seen where ischemia occurs in the subendocardial myocardium
COMPLICATION OF MI Pericarditis Pericardial inflammation May or may not see effusion Dressler’s syndrome Delayed form of pericarditis 1-12 weeks post MI Recurrence is common Tamponade is rare
Symptoms of Dressler’s Fever Pleuropericardial pain Malaise Pericarditis Pleuritis
RV infarction Frequent complication of inferior MI Hemodynamic signs of RV infarction resemble those of cardiac tamponade
Mitral regurgitation Common complication of acute or recent MI papillary muscle rupture can occur and cause MR Flail leaflet seen Papillary muscle dysfunction may occur due to localized ischemia with underlying wall motion abnormality
LV aneurysm:I May form at the site of infarction Most commonly involved are anterior wall and apex Distortion of LV contour at end diastole and end systole Thrombus frequently forms
LV aneurysm:II “hinge point” demarcates the infarct zone and aneurysm formation from normal myocardium
LV thrombus after MI: Higher incidence with aneurysm formation Thrombus can spontaneously resolve, or resolve after anticoagulant therapy
LV pseudoaneurysm I Myocardial rupture contained by parietal pericardium True aneurysm involves myocardium Usually seen post recent MI
LV pseudoaneurysm II Can also be seen in the following cases: Cardiac trauma Myocarditis Infective endocarditis Cardiac surgery
LV PSEUDOANEURYSM III There is a likelihood of rupture common in these patients Small communicating neck creates a gradient Thrombus may extend into neck and increase the size
Differential diagnosis of LV PSEUDOANEURYSM Loculated pericardial effusion Pericardial cyst LV diverticulum
LV DIVERTICULOSIS A rare congenital cardiac malformation which may be confused w/ aneurysm Small circular echo free space arising from LV w/ all 3 layers intact Doppler may demonstrate low velocity, systolic-diastolic flow w/in the chamber
Ventricular septal rupture or VSD post MI: New systolic murmur accompanied by signs of hypoperfusion after acute MI Could be rupture or severe MR 2D, color flow, and Doppler are used together to detect rupture
LV free wall rupture: Predisposing factors Large MI Lateral or posterolateral Elderly patient Post MI hypertension No prior CAD
LV FREE WALL RUPTURE Seen within 48 hours of acute MI Rupture site is between the zone of necrotic and normal myocardial tissue Cardiac tamponade can develop This causes hypotension and bradycardia Survival is rare
Created by: 100001592513232