CAD: Diagnosis Flashcards
type II error
false negative
Target HR in stress test
85% of age predicted HR (220-age)
Rate Pressure Product
peak HR x SBP
measures myocardial workload
Sn and Sp of ETT
both around 70%
on ETT does ST elevation or depression localize ischemia?
ST elevation does
ECG changes prognostic on ETT
- max ST depression
- # leads involved
- time to ST shift
- recovery time
- inducible ventricular arrhythmias
Hemodynamic changes prognostic on ETT?
- peak HR (Chronotropic incompetence)
- BP (exercise induced hypotension)
- rate pressure product
what does exercise induced hypotension on ETT mean?
LM or 3VD
Are HOCM, high degree AVB, severe HTN absolute contraindications to ETT?
no
at what high BP do you stop a ETT?
250/115
absolute reasons to stop an ETT (7)
1- ischemia w/ SBP dec by 10mm Hg 2- mod-sev angina 3- CNS sxs 4- cyanosis/pallor 5- sustained VT 6- >1mm ST elev (other than V1 or aVR) 7- pt requests
which conditions obscure ST changes on ETT?
WPW PPM ST dep 1mm at rest LBBB LVH Dig
ST depression in which leads of an ETT don’t matter?
V1, aVR
ST Elevation on ETT
Should be in leads without Q waves
Transmural ischemia from coronary spasm or myocardial injury
Duke Treadmill Score
Exercise time (mins) - (5 x mm ST dep) - (4 x angina index)
Angina index
0- no CP
1- CP
2- CP stops exercise
type I errors = ?
false positives
Scores and corresponding mortality for Duke treadmill
Low risk > 5 (0.5%)
Intermediate risk +4 to -10 (.5-5%)
High risk < -11 (>5%)
HR reserve and chronotropic incompetence
HR Reserve = 220-age-resting hR
Chron. incomp is inability to inc HR by 80% of HR reserve
what is considered a low level of exercise?
HR<70% max HR
differences in SN/Sp b/w stress echo and nuclear
similar Sn
stress echo- higher Sn (fewer false +)
adenosine stress MOA
A2A receptor agonist–> 4x inc in coronary blood flow