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ekg by SMITH reminders/tips
Terms in this set (54)
1-heart REpolarizes from epicardium to endocardium and leaves what type of deflection (+ or -) for the T wave in a healthy heart?
2.) in an ischemic heart?
3.)What do peaked T waves indicate
btw...this shit is confusing. important to just get the patterns down though.
1-positive...although this is over all confusion, just think that your electrodes are on the skin and are thus closer to the epicardium than the endocardium...therefore, from the electrodes point of view, the heart it REpolarizing AWAY from the electrode and is thus registered as a positive deflection.
2.) negative deflection because repolarization of the epicardium is greatly delayed by ischemia leading to a reversal of the vector (subendocardium to subepicardium)
3.) indicates ischemia as well but not quite as bad as inverted T waves. Peaked T waves are caused by subendocardial ischemia that is not effecting the subepicardium yet (because the subendocardium is further from blood supply). Thus, the subendocardium, at any point in time compared to a normal heart, is much more negative (outside of cell) than the subepicardium which further increases the positive deflection that is normally seen.
**note that the above pattern holds true for the anterior, lateraly, and inferior leads. It is the opposite for posterior leads which will show upright T waves in leads V1-2 during transmural posterior MI (makes sense because the subendocardium of the posterior side of the heart is actually closer to the electrodes than the subepicardium of the posterior wall!...so in an infarcted posterior wall, you would have repolarization AWAY from the anteriorly placed skin electrodes and would get a positive deflection...note that) That being, said, if you put on posterior electrodes, the rules would be followed as with the other leads....
ST depression vs elevation?
Depression indicates subendocardial injury whereas elevation indicates transmural (subepicardial) injury. Note that it is actually a shift of the baseline and not of the ST segment itself. so..."ST elevation" is actually when the baseline is depressed and visa versa. You can recall this by thinking of it the same way as the previous notecard...If the subEPIcardium is effected, repolarization will occur from endocardium to epicardium towards the electrodes and thus the baseline will be depressed (much like T waves were inverted) giving the appearence of ST elevation...and visa versa.
Does ST depression indicate specific areas of involvment?
yes, it indicates specific areas of subendocardial involvement...note that it can also indicate STEMI in the case of posterior infarction since it is detected in the anterior leads.
T/F: Q waves only occur after STEMI
I think this is true...however, Q waves do NOT ALWAYS occur even after STEMI. Also, by the time Q waves appear, it is generally thought that the damage has already been done (infarct complete) and reperfusion therapy is in question as to whether or not it will help.
what are the characteristics of a type 1A ekg? (the "o shit" ekg)
-ST elevation of 2mm in precordial leads or 1mm in limb leads in 2 consecutive leads.
-no confounding factors such as LVH, LBBB, pericarditis, or early repolarization.
What are "significant ST depressions"
What are some insignificant (not indicative of ischemia) ST depressions and T wave inversions?
ST depressions less than 1mm or T waves that are flat or less than 1mm of inversion
What is a possible explanation for ST elevations with T wave inversions?
This indicates spontaneous reperfusion...I think of it as the ST elevation (which is actually baseline depression) as covering up the "would be" T wave inversion...as reperfusion occurs, the baseline raises to normal and reveals T wave inversions. **whether or not this is what is actually happening, I have no idea and its just how I remember it.
What are some approximate percentages of the types of EKG's seen in acute MI?
-45% type 1A
-30% type 2 (these are NSTEMIs...with signs of ST depression or T wave inversion) note that type 2 ekg's also include unstable angina but in my question I was asking for EKG types of acute MI.
-20% type 3 (things like "insignificant" ST changes or T wave inversions...or Qwaves which usually indicates old infarct or LVH)
-6% type 4 (normal EKGs!) so you still have to be weary of patients with a good story or cardiac history that have a normal ekg.
idea behind Q wave formation?
develop after complete occlusion without reperfusion...thus usually after STEMI. The idea is that initial depolarization of the ventricle occurs everywhere except in the direction of that infarcted muscle...thus, a negative Q wave develops. 86% of STEMI patients that do not get reperfusion will develop Q waves. Interestingly, in patients with AMI that only had ST depression 29% percent develop Q waves which tells you this person may have had STEMI but the EKG didn't show it as described in the next note card. Also, 24% of those with AMI and no ST changes, will develop Q waves. Q waves resolve in months-years. Thus, there does not have to be transmural INFARCTION. That being said, Q waves are most likely to occur with complete occlusion without reperfusion leading to transmural infarction.
T/F: All complete occlusions will show up as STEMI on an EKG?
F: if there is intermittent occlusion or reperfusion of the area before an EKG is taken, then a future EKG will not show the STEMI
Why can EKG's be innacurate at times? just read the answer...
It is just a snap shot...it does not account for changes in the patients heart with time such as new occlusion or spontaneous reperfusion and it does not account for individual anatomy which may have better collateral circulation. This is why 2 patients with the same blockage could have different EKG results...ex: complete occlusion may be STEMI in one patient but justST depression in another thanks to great collateral. They both need urgent revascularization but patient number 1 will be the one to get it.
Statistics of patients with AMI who only have atypical symptoms (N/V, abdominal pain, arm/jaw/hand pain, dizziness, hyperglycemia difficult to control in diabetics)....
42% over 75yrs and 75% over 85yrs do not have chest pain. Also, 35% of STEMI patients over 65yrs do NOT have chest pain! So really be on the look out for elderly patients and have a low threshold for getting an ekg!
ways to limit delay in diagnosis of AMI:
-do NOT hesitate to get EKG in elderly patient with atypical symptoms
-serial EKGs in patients with minor changes or "less worrisome" changes such as ST depression or T wave inversions
-learn how to interpret type 1b and 1c EKGs!
what are serial ekg's?
-EKG's taken 15min apart!
**if very high suspicion, you can put them on continuous ST segment monitoring
What are the only 2 meds that take priority over thrombolytic therapy AND PCI in a patient in need of such intervention?
ASA and sublinual nitroglycerin! note that nitro can someitmes abort the MI itself thanks to the decreased preload and stress on the heart.
**If PCI (not thrombolytic therapy), then you should give Heparin and GP IIB/IIA inhibitors before.
-IV nitroglycerin should never delay reperfusion therapy unless uncontrollable HTN or CHF.
1.) What is the best indicator for spontaneous reperfusion?
2.) What are requirements of ST changes that allow you to abort reperfusion therapy?
1-resolution of ST segment elevation (NOT resoloution of patient symptoms...so if they are feeling better, you must get a repeat EKG)
2.) either 25-50% resolution of ST segment elevation (this means that even if ST elevation is resolving but only by 20%...you still need to reperfuse!) OR terminal T wave inversion. **Once you suspend therapy, you need to monitor making sure ST elevation resolves by 50% and then continuously monitor them on the floor.
****what are pseudonormalized T waves?
These are upright T waves in the limb leads that actually support re-occlusion in the setting of AMI. Think...normally T waves are upright but with ischemia can become inverted. However, when this mild ischemia turns into occlusion, the baseline becomes depressed (ST elevation) and the previously inverted T wave becomes/appear as upright again thus indicating occlusion or re-occlusion. Also, recall that reperfusion of an occluded vessel will cause T waves to go from upright (pseudonormalized) to inverted as the baseline rises to normal again (resolution of ST elevation).
*Note that this T wave stuff is reversed when looking at the anterior leads in the setting of POSTERIOR infarction. Recall that
-What is the best inferior lead for detecting inferior AMI?
-T/F: inferior infarction with ST depression in lead III will practically always have reciprocal change in lead AVL?
-Describe the ekg changes in pericarditis
-T (unless there is concurrent lateral AMI with ST elevation)
-diffuse inflammation leads to diffuse repolarization abnormalities and thus diffuse ST elevation. There will NOT be reciprocal changes. (so NO reciprocal AVL ST depression like in inferior AMI)
Most sensitive lead for lateral AMI?
T/F: Leads V1-V4 are placed opposite the posterior wall and thus are useful in detecting posterior wall AMI?
T (also recall that AVL is most opposite lead III and is thus best at picking up reciprocal changes from an inferior infarct)
What are some indications of Right ventricular infarct?
-ST elevation in V1 on normal ekg or V2R in right sided ekg. **In the presence of posterior MI where you would suspect reciprocal depression in the anteriorleads, the sight of ST elevation in V1 should definitely make you think RV infarct!
-V5 and V6 are most opposite the RV wall and thus pick up reciprocal changes the best. ***note that V5-V6 also can sometimes show reciprocal changes for septal infarct.
reciprocal changes for lateral MI?
reciprocal changes form anterior MI?
both have reciprocal changes in the inferior leads...just think that MI's suck and shit tends to go "down"
type 3 ekgs can include unchanging or old T wave inversions of less than 1mm and/or ST depressions of 1mm. Type 2 ekgs would include the T wave or ST depressions typical of UA/NSTEMI ( new or evolving, especially if >1mm but don't have to be...if they are new or evolving)
important distinction...recall that other type 3 ekgs would be those with changes non-diagnostic of AMI. ex: Q waves, LVH
Is it ever necessary to perform repeat ekgs on type 4 ekg's?
yes...if clinical suspicion is still high. even type 4 can evolve into type 1
treatment for type 3 ekg?
If you still have clinical suspicion of MI, then do serial ekg's (q15min for 1hr).
Also, these patients are candidates for PCI but not thrombolytics so if you have a type 3 ekg patient who is very unstable then you should call cath lab.
what is the ekg finding in Wellen's syndrome and what does it signify?
Terminal T wave inversion in the anterior leads and it means severe LAD stenosis. So the T wave literally looks like a wave (biphasic is how I would describe it otherwise)
How long do Q waves and inverted T waves last after an MI, respectively?
Q waves: months to years
Inverted T waves: weeks to months
progression of Q, T, and ST waves/segments in coronary occlusion withOUT reperfusion
Hyperacute T waves (minutes-hours), ST elevation (minutes-12hours), Q waves (1-12hrs), T wave inversion (within 3 days), ST normalization (within 3 days but always after T wave inversion...unlike in pericarditis in which ST resolves before T wave inversion occurs)
-recall that the inverted T waves return to normal in weeks-months while Q waves resolve within months to years.
*note that WITH reperfusion, the T waves invert and the ST segments normalize much more quickly. The T waves often become biphasic for a while before completely inverting. Q waves may be less likely to develop or be less pronounced.
list some characteristics of the ST segment in benign early repolarization
-highest in V2-V4, up to 3mm
-ST segment is concave up (smiley face...no worries)
-T waves are tall, but never much taller than the R wave...as opposed to hyperacute T waves which are significantly taller than R wave
-NOT seen in AVL
-less commonly found in patients over 55
***that being said, this can sometimes trick you and be an anterior MI...so always look at previous ekg's and look for reciprocal changes in the inferior leads which would indicate AMI.
What are some different morphologies of elevated ST segments and which are most worrisome?
-flat...most common with anterior MI
-convex up (sad face...least common but always bad as in AMI)
-concave up (happy face...although this is the second most common seen overall in AMI, it is also the one that is most likely to be benign and of no significance)
differential for ST elevation?
AMI, pericarditis, benign early repol, LBB, LVH, LV aneurysm, hyperkalemia, critically ill patients with intracranial pathology like SAH
T/F: Reciprocal ST depression occurs in leads that register the opposite ekg view from the leads near the infarcted area.
Which leads detect reciprocal changes best for posterior MI?
T/F: Inferior AMI may actually be better detected by ST depression in AVL than ST elevation in lead III
T/F: If there aren't any reciprocal changes, then there is not an AMI
F...reciprocal changes tend to mean that the infarct is larger/worse and has better potential for thrombolytic therapy but still....
T/F: In inferolateral AMIs, the ST segment in I and AVL can be elevated, depressed, or isoelectric?
T...combination of elevation from lateral MI and reciprocal depression from inferior MI. Thus, in a patient with ekg signs of inferior MI and a normal AVL...think possible inferolateral MI (circumflex a.)
What are some ST segment findings with LVH and LV aneurysm?
-other findings in LV aneurysm?
findings similar to inferior MI...ST elevation in III with reciprocal depression in AVL
-other findings include QS waves and Qr waves
what are some distinguishing factors of inferolateral MI and pericarditis?
-reciprocal depression in AVL as well as ST depression being greatest in III supports AMI. Also, no ST elevation in the anterior leads supports that its MI and not pericarditis.
What are 2 possible interpretations of terminal T wave inversion (biphasic)?
reperfused myocardium OR an MI that is late in its course...recall that from a previous notecard that in an MI that is not reperfused, T wave inversion will occur within 3 days.
*thus, this complicates thrombolytic decision
Causes of ST depression?
Secondary: LVH, RVH, LBBB, RBBB, hypokalemia, WPW, tachycardia, digitalis use. *note that abnormalities in depolarization (ex: LBBB or LVH) can cause ST depression as just mentioned.
T/F: TRANSIENT changes in ST depression and T wave inversion usually indicate UA/NSTEMI?
*other indicators of UA/NSTEMIA compared to complete occlusion include flat or downsloping ST segments as well as no reciprocal ST elevation.
What are some ST or T wave findings that suggest anterior ischemia compared to posterior MI?
suggestive of anterior ischemia: if V1-6 anterior leads all have ST and T waves changes (as opposed to just V2-V3), if QRS returns to baseline before gradual downsloaping ST depression (as opposed to deep ST depression), and also if the T wave is inverted symmetrically (compared to biphasic appearence)
1.) Findings in RVH?
1.) R axis deviation, deep S waves in V5-6, very large and wide R wave in V1
**pg 54/62 of Smith's book has a fantastic example of RVH that looks very scary as if it could be posterolateral AMI...however, with a previous ekg that had the same findings as well as RVH, the abnormalities including ST depressions and T wave inversions were able to be attributed to RVH.
T/F: RV AMI usually occurs concurrently with inferior AMI?
1.) What is the normal axis of T waves?
2.) What are some leads where T wave inversion is often normal?
3.) In what lead is T wave inversion always abnormal
1.) down and to the left of the heart (same as QRS axis)
2.) V1 is most commonly negative (inverted). In order of decreasing normality, V2-V4 can also be inverted...but do not count on that being a "normal" finding.
3.) I (assuming the QRS is normal), V5 and V6
*leads III, AVL, and AVF can sometimes be negative
...just think of the axis and it helps you understand these findings. ex: lead V5 detects lateral things and since that is in the direction of the normal T wave axis, it should always be upright.
What does minimal ST elevation with T wave inversion indicate?
reperfusion of an occluded vessel...so dangerous.
*recall that ST depression does NOT occur during the course of an MI withOUT reperfusion...this means that if you see ST depression and T wave inversion at the same time then it is likely UA/NSTEMI and not complete occlusion.
T/F: T wave inversion is not seen in early total occlusion?
T...recall that the series of events is hyperacute T waves, ST elevation, Q waves, and then you get the T wave inversion. Thus, if you see T wave inversion it is either UA/NSTEMI sometimes with ST depression findings but not ST elevation...or its a late occlusion, especially supported if you see Q waves, ST elevation, or deep QS waves.
***the big thing to remember is that ST depression is NOT part of the series when looking at complete occlusion. so although ST depression can mean ischemia, it is not the "o shit" complete occlusion ischemia.
What is Wellens syndrome and what is the treatment
-Wellens is spontaneous reperfusion of a coronary artery that often results in terminal T-wave inversion called type A (sometimes complete deep symmetric inversion though called type B). It was originally described in the anterior leads thus indicating severe LAD obstruction with reperfusion...but can actually be seen in all leads.
-treatment is medical therapy, continuous ST segment monitoring, and if re-occlusion occurs (very common...indicated by pseudonormalization of the T wave...returning to upright position) then immediate PCI or thrombolysis.
T/F: Cardioversion is a cause of ST depression...often widespread?
T...that being said, perform serial ekg's as this depression should resolve. if it doesn't, consider other etiologies such as posterior MI
Is there such thing as reciprocal ST elevation? If so, when can it be seen?
Yes...reciprocal ST elevation can be seen in the lateral leads in the setting of posterior MI with ST depression in the anterior leads (usually V2-3)
what is the sensitivity of ekg for STEMI?
62%...meaning that with computer algorithms that use current "criteria" for MI, you really can't safely rule out AMI and the necessity for PCI/thrombolytics
T/F: when determining degree of ST elevation, you should actually base it off of the CHANGE from a previous ekg the patient may have?
T...this helps in ssituations of "borderline" st elevation
Info on hyperacute T wave appearence?
-starts off as ST segment becoming an oblique upslopingline
-disproportionately large compared to qrs...so if low voltage qrs, the hyperacute T wave may be small but isbig in proportion
-concave up (but not nearly as much as T waves seen with early repolarization) and wide...broad hump (early repol T waves would be narrower at the tip)
-often have j point depression...making it appearas though the T wave begins below the isoelectric line
-qt interval prolonged
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