Ischemic Heart disease

Question 1

Angina pectoris Etiology

Answer 1

atherosclerosis
coronary artery spasm (drugs, idiopathic)
aortic valve dysfunction

Question 2

Angina pectoris Pathogenesis

Answer 2

occurs when cardiac work and 02 demand exceeds blood supply

conversition of aerobic to anerobic metobalism: hypoxic metabolites accumylate

Question 3

Coronary flow reserve

Answer 3

how much blood to coronary A during stress

healthy heart: able to increse blood 4-6 times the resting blood flow
atherosclerotic heart: vastly diminshed capability to increase blood flow

Question 4

Angina pectoris Clinical presentation

Answer 4

substernal squeezing pressure
radiates to L arm, neck and jaw
better with rest and nitroglycerin

duration: 2-5 min
<10-15= no necrosis
more than 20= necrosis

brought on by: coldm large meal. exercise

Question 5

Angina pectoris diagnosis

Answer 5

EKG, ECHO

graded stress test is gold standard

Question 6

graded stress test absolute contraindication

Answer 6

unstable angina
arrthymia
recent MI
peri/myocarditis

when to stop:
drop in syst bp by >10 mmHg
chest pain
SOB
arrythmia develop
ST seg depression by >2mm

Question 7

determinants of 02 demand

Answer 7

rate
contractility
preload

Question 8

unstable angina clinical presentation

Answer 8

increasing intensity, duration, frequency of angina

sx at rest

Question 9

unstable angina pathogenesis

Answer 9

rupture of plaques lead to thrombi

Question 10

unstable angina prognossi

Answer 10

50% will have MI within 6 months

Question 11

prinzmetal/variant angina incidence

Answer 11

more common in women

Question 12

prinzmetal/variant angina clinical presentation

Answer 12

substernal squeezing at the same time each day
often wakes them up at night
SOB
palpitations

Question 13

prinzmetal/variant angina etiology

Answer 13

coronary vasospasm of unknown origin

Question 14

Acute MI cllinical presentation

Answer 14

pale, cool, clammy cyanosis possible
severe crushing pain
radiation ot neck, arm.jaw, back
N/V
loss of consiousness
diaphoris
2/3 have prodomal sx

Question 15

Acute MI ETIOLOGY

Answer 15

90% have plaque rupture leading to thrombosis

Question 16

Acute MI pathogenesis

Answer 16

ischemic necrosis (more than 20 min)

Question 17

anterior infarcts

Answer 17

occlusion of LCA, larger
“widow maker”

v3,v4

Question 18

inferior infarcts

Answer 18

RCA
AVF, ii, iii

Question 19

Acute MI diagnostic

Answer 19

thready pulse
systolic blowing murmur at heaart apex
abnormal, deep/wide Q wave: remains forever
ST elevation:90% specific , 45% sensitive : normal in 2 wks

Question 20

Acute MI complications

Answer 20

> 90% develop arryhtmia
50% of deaths occur within 3 hrs due to vfib
heart failure in 2/3
mitral valve insufficency
cardiogenic shock: 55% mortality

Question 21

Acute MI enzymes labs

Answer 21

troponin: 3-6 hrs , peak: 24-48 hrs , lasts: 10 days

CKMB: 6-10 hrs , peak: 24 hrs, lasts 48-72 hrs

Question 22

cardiogenic shock

Answer 22

sustained hypertension: systolic BP <90 more than 30 min
evidence of hypoperfusion in tissue in spite of normal LV fillin pressure

Question 23

PCWP in cardiogenic vs hypovolemic shock

Answer 23

cardio: elevated(>18)
hypovolemic: decreaased

Question 24

what type of murmur is seen in acute MI and when does it show up

Answer 24

apical systolic blowing murmur
2-3 days post MI