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exce4rcise is always better, more physiologic than vsoliation, gives
additional info 9excercise tolerance, liming symtoms), but must wait
2-6 wks post MI, and shoudn't do it if pt has a left bundle or if has
a pacemaker or may get a false pos
pharm: (*all vasoldialtors adenosine, regeadnosine and persantine
cause diffuse hyperemia)
*adenosine - like persantine but done in a few seconds, short acting,
safe post MI (even 48 hrs post MI), use for + troponins or when pt
can't walk
*regeadenosine - slightly longer acting than adenosine, slightly
increases the BP/HR, don't do if pt has a left bundle or a pacemaker,
or if there is renal insufficiency (since excreted that way), or on
old patient's since there is no data on that
*persantine - longer acting, cheap, but must give aminophaline. is
safe post MI (even 48 hrs post MI)
dobutamine - use least, has + ionotroypy(contracts more) and +
chronotropy (speeds up heart), weak vasodilator though, only use if pt
has severe asthma since the others can cause be bad if severe asthma.
used more in echo stress where you must see the ionotropy. used s/p
heart transplant (dobut stress echo).
usually you do excercise first, if can't then go to regadenosine, if
can't then go to adenosine (or possibly persantine), if can't then go
to dobutamine (i.e. if there is severe asthma)
at Columbia they used to always do thalim rest (longer T1/2 but
increased radiation,cand can bring back necxt day for redistribution)
followed by mibi stress (best combination for work flow).
thalium has better extraction fraction (80%), Tc is 60%, Tetraphos is
58%. the best is water (O15) 100%, F18 is close tot that.
Dr. Einstein always tries ALARA, uses mibi only- single low dose
stress with 10 mci(not below 8, as FDA doesn't approve), and don't do
rest if normal...if need a rest, wait (3 hrs from 1st dose, but often
only wait 2-3) and do at least 3x the 1st dose (i.e. 10 vs 30 mci).
kids get a 2 day mibi stress rest since they will get 2 low doses.
only prone the stress. skinny males (not females), but prone females
for the breasts. don't prone the rest or whll be there all day!. you
breath more on stress than on rest so diaphram is more of a problem.
if you get a problem on prone, just repeat the study.
ACC-AHA guidelines, 50-70% brightness-mild defect, 30-50 is mod, less
than 30 is severe, 0 is 0
small is less than 2 segments on the qps(quantitative perfusion
scan?), moderate is 2-5 segments, large is more than 5 segments.
don't worry aobut LHR
TID is abnl is greater than 1.2, the EDV of LV dilates with ischemia
so the ratio of stress to rest will be greater than 1.. indicates
severe ischemia
other signs of sever ischemia is:
-if there is lung uptake i.e.more than 40 or 50 % of the myocardial activity
-if there is significant RV uptake
if there is post ischemic stunning, meaning the EF dropped on stress
rather than increased.
I AVR V1 V4
II AVL V2 V5
II avF V3 V6
I and AVL are lateral
ignore avR
II, III and avF are inf
V1 and V2 are septal
V4 and V4 are anterior
V5 and V6 are anterolateral
a fixed dilated EF less than 40%, consider revascularizing only if
viable (i.e hybernating) can tell with a 24 hr thalium or mri or pet
viability
attenuate correct if fat pt's or to get calcium score.
(all courtesy of Tamim Nazif)
, the referring physicians should be informed that BP meds such as vasodilators,
B-blockers, calcium channel blockers, and nitrates should be withheld prior exam,
however, ACE-inhibitors and diuretics are ok to continue. Diabetic patients taking
insulin should remain NPO but take 1/2 of their morning dose of insulin, and can
always be given additional insulin if they are found to be hyperglycemic.
Check out the last point of this section on artifacts from a handout I had
Artifacts related to non-coronary disease.
* Left bundle-branch block (LBBB). This conduction abnormality
produces apparent septal hypoperfusion that can be either reversible
or fixed, lowering the specificity of the study for detection of
ischemic heart disease. In gated studies, however, the septal wall
usually exhibits paradoxical motion but with preserved thickening,
aiding in the differential diagnosis.
* Left ventricular hypertrophy. It can cause localized hot spots
with relative hypoactivity of remote areas, and other myocardial
non-homogeneities.
* Long membranous /short muscular septum. It can produce false
impression of hypoperfused basal septum.
* Apical thinning. This can be either a normal physiological
variant or an artifact produced by varying spatial resolution of the
acquired images (higher at the apex because of detector proximity). It
usually simulates a fixed defect and can be differentiated from scar
by gating since myocardial thickening and wall motion will be
preserved.
* The eleven / seven o'clock defect. More frequent at
anterior-septal region (11 o'clock) in short-axis tomograms, this
pseudo-defect probably represents attenuation by the right ventricle
since it usually lies, together with the 7 o'clock defect, close to
the insertion points of the right ventricular wall. Again, gated SPECT
can aid in diagnosis.