ischemic heart disease Flashcards

1
Q

a. Risk factors modifiable for ischemic heart disease

A

i. Age: Men>45, Women>55 (non-modifiable)
ii. Family history: CAD or stroke (non-modifiable)
iii. Lipid abnormalities: (modifiable)
1. LDL>160 mg/dL
2. HDL<35 mg/dL
iv. Smoking tobacco (modifiable)
v. HTN (modifiable)
vi. DM (controllable)

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2
Q

MCC of ischemic heart disease

A
atherosclerotic disease
 also arterial thrombi
 spasm
 and rarely coronary emboli
 myocardial oxygen demands are abnormally increased, as in severe ventricular hypertrophy due to hypertension or aortic stenosis
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3
Q

i. Scarring specific to arteries

A

a. Arteriosclerosis

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4
Q

i. Scarring of all vessels

A

b. Atherosclerosis

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5
Q

LAD

A

i. LAD: left anterior descending = anterior interventricular artery

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6
Q

Feeds the anterior portion of the left ventricle

A

LAD

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7
Q

Feeds the posterior and inferior part of left ventricle

A

RCA

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8
Q

Feeds the posterior third of the interventricular septum

A

b. RCA:

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9
Q

iii. Feeds the right bundle branch

A

LAD

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10
Q

iv. Feeds both SA and AV node

A

RCA

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11
Q

iv. Feeds the anterior division of left bundle

A

LAD

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12
Q

v. Feeds His bundle

A

rca

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13
Q

vi. Feeds the posterior division of left bundle

A

rca

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14
Q

coronary arteries fill during what portion of the cardiac cycle

A

a. Coronary vessels fill in diastole diastole b/c when the ventricle contracts the blood goes through the aortic valve to get to the aorta. Position of aortic valve during systole is open. The origin of the coronary artery is at the base of the aorta****

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15
Q

when does tachycardia decrease filling itme of the coronary arteries?

A

b. HR>180 decreases filling time of coronary arteries –> leading to ischemia

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16
Q

“causes of atherosclerosis”

A
  1. Cholesterol/TG (?) (cannot truly call it causative, can call it contributory)
  2. HTN
  3. Smoking
  4. Glycolated substances (byproduct of having high blood sugar is that they attach to everything and cause cardiovascular disease)í by product is ketones.
17
Q

why do we see arteriosclerosis in pts with DM

A

(byproduct of having high blood sugar is that they attach to everything and cause cardiovascular disease)í by product is ketones.

18
Q

lipid deposition in the wbc leads to

A

smooth muscle proliferation and fatty streaks that are asymptomatic and can be seen in early adolescence

19
Q

what are foam cells

A

macrophages that ingest fat

this happens in early formation of plauqe

20
Q

what is a fribromuscular plaque

A

muscle fibers and colesterol core this is seen in mature plaque formation

this occurs when proliferating smooth muscle cells and connective tissue become incorporated into plaQUE

“fibrous cap”

21
Q

Describe the formation of early plaque

A

LDL enters the endothelium in the fatty streak and is oxidized which attracts macrophages and smooth muscle cells to ingest harmful LDL –> become foam cells

the foam cells attract more macrophages fibroblasts and inflammatory cells

22
Q

why do you see most ischemic dz during exercise

A

because this leads to narrowing of the vessels and further occlusion of already occluded vessels

or increased demands where more blood is needed and the metabolic demands are not met

23
Q

all pts with CAS

A

d. All patients with coronary artery disease of any kind should receive drug therapy if their LDL >130 mg/dL with the goal of reducing it to <100mg/dL

24
Q

iv. ST segment depression indicates what

A

(subendocardial ischemia) w/ ischemia
1. ST segment elevation w/ infarction

nonSTEMI or stable angena

25
Q

i. Coronary artery spasm, typically with arterial stenosis

A

XVI. Prinzmetal variant angina (happens at rest)

26
Q

prinzmetal variant angina is typically seen in what population? at what time>

A

ii. Frequently occurs in women, and at night (12-8am)

27
Q

XVI. Prinzmetal variant angina is relieved with what tx

A

by nitroglycerin

28
Q

b. Lifestyle modification to lower risk factors for angina

A

i. Stop smoking
ii. Diet control
iii. Exercise as tolerated

29
Q

angina tx

A

: antiplatelets (ASA), B-blockers, CCB (vasodilator so help improve blood flow), nitrates (for symptomatic tx - nitroglycerin - short acting, potent vasodilator-SE -HYPOTENSION and HA), lipid control

30
Q

cause if unstable angina

A

i. Caused by nonocclusive thrombus in an area of coronary atherosclerosis
1. It is partially occlusive

31
Q

most common type of MI

what is the pathophysiology behind this

A

i. Transmural infarction (

Q wave infarction
1. Ischemic necrosis of >50% of myocardial wall

32
Q

what types of MI’s do we see

A

transmural and subednothelial

ii. Subendothelial infarction: non-Q wave infarction
1. Ischemic necrosis of <50% of myocardial wall

33
Q

how frequently do we see thrombosis in

LAD
RCA
LCA

A

a. LAD: 45%
b. RCA: 35%
c. LCA (left circumflex artery): 15%

34
Q
  • present with GI sx when having a heart attack and less classic sx
A

MI in women

35
Q

if ventricular wall ruptures you get

A

a. If Ventricular wall ruptures then you have cardiac tamponade

36
Q

sudden cardiac death is defined as

A

death within 1 hour of the onset of symptoms

i. Fatal cardiac arrhythmia (usually, VF)

37
Q

MCC of sudden cardiac death

A

i. Coronary artery disease (80%)
ii. Hypertrophic cardiomyopathy
iii. Mitral valve prolapse
iv. Aortic stenosis
v. Congenital heart abnormalities
vi. Myocarditis