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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.