Ischemic Heart disease Flashcards
(24 cards)
Angina pectoris Etiology
atherosclerosis
coronary artery spasm (drugs, idiopathic)
aortic valve dysfunction
Angina pectoris Pathogenesis
occurs when cardiac work and 02 demand exceeds blood supply
conversition of aerobic to anerobic metobalism: hypoxic metabolites accumylate
Coronary flow reserve
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
Angina pectoris Clinical presentation
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
Angina pectoris diagnosis
EKG, ECHO
graded stress test is gold standard
graded stress test absolute contraindication
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
determinants of 02 demand
rate
contractility
preload
unstable angina clinical presentation
increasing intensity, duration, frequency of angina
sx at rest
unstable angina pathogenesis
rupture of plaques lead to thrombi
unstable angina prognossi
50% will have MI within 6 months
prinzmetal/variant angina incidence
more common in women
prinzmetal/variant angina clinical presentation
substernal squeezing at the same time each day
often wakes them up at night
SOB
palpitations
prinzmetal/variant angina etiology
coronary vasospasm of unknown origin
Acute MI cllinical presentation
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
Acute MI ETIOLOGY
90% have plaque rupture leading to thrombosis
Acute MI pathogenesis
ischemic necrosis (more than 20 min)
anterior infarcts
occlusion of LCA, larger
“widow maker”
v3,v4
inferior infarcts
RCA
AVF, ii, iii
Acute MI diagnostic
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
Acute MI complications
> 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
Acute MI enzymes labs
troponin: 3-6 hrs , peak: 24-48 hrs , lasts: 10 days
CKMB: 6-10 hrs , peak: 24 hrs, lasts 48-72 hrs
cardiogenic shock
sustained hypertension: systolic BP <90 more than 30 min
evidence of hypoperfusion in tissue in spite of normal LV fillin pressure
PCWP in cardiogenic vs hypovolemic shock
cardio: elevated(>18)
hypovolemic: decreaased
what type of murmur is seen in acute MI and when does it show up
apical systolic blowing murmur
2-3 days post MI
