Ischemic Heart Disease Flashcards

1
Q

Def of ischemic HD and 5 basis of perfusion imablance

A

Effects on cardiac fxn and structure due to insuff O2 delivery via coronary arteires

Athero - most common
Spasm - with or without atherosclerosis
Systemic hypotension
Aortic valve dz - syphilitic ostial stenosis

Kawasaki - rare, coronary arteritis with thomboroiss and aneurysms in children/teens with circulating antiendothelial ABs ….IVIG

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2
Q

Coronary anatomy

A

RCA goes around back to supply post LV

Circumflex is lateral

LADA is anterior

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3
Q

Risk factors for CAD and effects

A

HTN, cigs, hyperlip, DM

Affects mostly the proximal portion of epicardial branches

NArrowing commonly involves 2 or more branches

Narrowing >75% affects distal flow

Collaterals expand to compensate

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4
Q

Angina pectoris

A

Typical AP of paroxysmal chest pain worse with exertion and relieved by rest…inc demand in setting of fixed suplply

Ischemic injury is reversilbe and accompanied by ECG changes…deteriorates ot unstable AP

Atypical angina - pain at rest and spont reduction in supply in absnece of inc demand..probabyl due to transient coronary artery stenosis from a spasm

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5
Q

MI

A

Zone of irreversible injury…commonly setting of severe atheroscelrotic narrowing of 2 or more branches

Coagulative necrosis

Hemorrhage into vulnerable plaque, erosion of vulnerable laque with luminal thrombosis, coronary spasm…udden atherothrombosis

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6
Q

CHF
Sudden death
Arrhythmias

A

Extensive muscle loss and scarring

Initil presentation in about 30% of cases

V tach
Vfib
Afib

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7
Q

Lab findings in MI

A

ECG changes - Q waves…loss of R waves ST segment elevation, ventricular arrhythmias, heart block

ST elevation/non-STEMI
Q wave or non Q wav

CK-MB, troponin or CRP

Leukocytosis and ESR

Myocardial perfusion scans…maps areas of loss of blood flow

ECHo - zone of akeiniesia, dyskinesia of LV or IV septum

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8
Q

Transmural vs. nontransmural

A

Trnasmural MI - Larger/full thickness…Q wave and ST elevation due to complete loss

Non - small and subendocardial myocardial zonal necrosis….non Q wave, non STEMI, shorter and incomplete loss of coronary artery

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9
Q

How does non-STEMI become STEMI

A

Non-Q wave to Q wave

From Subendocardial to myocardial necrosis to full thickness myocardian lnecoriss

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10
Q

Gross morphologic changes

A

18-24 - pallor
24-72 - pallor iwth hyperemia
3-7 days - hyperemic border iwth central yellowing
10-21 days - max yellow and soft iwth vasc margins
7 weeks - white fibrosis

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11
Q

Microscopic changes

A

1-3 - wave myocard fibers
2-3 - staining defect
4-12 - coag necrosis with bands
18-24 - continuning coag
24-72 - loss of nuclei and striations with neutrophilic infiltrate
3-7 days - macrophge and mononuclear infiltration being
10-21 days - fibrovascular response wth grnaulation
7 weeks - fibrosis

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12
Q

Comps of MI

A

Hospital mortality

CHF, a fib, thrombus in atrial appendages

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13
Q

CHF

A

Pulm congesiton and edema

Elevated RA and venous pressure

Hepatosplenomegaly

Peripheral edema

Pleural effusion, ascites, pericardial effusion

DOE/PND, wt gain, DVT, PE

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14
Q

Dressler’s syndrome

A

2 weeks

Fibrinous pericarditis

Chest pain, fever, and friction rub

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15
Q

CABG

A

Spahenous vein bypass graft…connect aorta to distal coronary arteries

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16
Q

VBG

A

Worry about neointima developing atheroscelrosis and stenosis

17
Q

Stent placement or PTA

A

Site of isolated coronary artery is distended with inflatbale catheter…retrograde throug hthe femoral artery

Stent comps are intimal reocclusion or late thrombosis…could also get thrombotic occlusion

18
Q

Homo FH

A

LDLR dual gene mutation is greatest known risk of fatal atheroscelrosis of any cause