{"id":5225,"date":"2011-06-16T01:52:32","date_gmt":"2011-06-16T01:52:32","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5225.htm\/"},"modified":"2011-10-01T15:45:38","modified_gmt":"2011-10-01T15:45:38","slug":"5225","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/fix\/5225.htm\/","title":{"rendered":"Excerpt’s from Steve Smith’s ECG Blog"},"content":{"rendered":"

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EMCrit.org | Emergency Department Critical Care – \t \t\tDr. \t\tSmith’s ECG Blog <\/a> \t\t<\/p>\n

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pseudo-normalization of T waves post-mi is actually a subacute \t\tphenomena (1-2 weeks) post-MI and the t-waves will be large and \t\thyperacute. It is an expected event for the t-waves to eventually become \t\tupright with normal sized t-waves, this is not pseudo-normalization.<\/p>\n

Inverted T-waves in aVL is similar to Wellen’s<\/p>\n

hypokalemia-prolonged QTc, U waves,<\/p>\n

First, you should know that when there is precordial ST depression \t\tdue to subendocardial ischemia, it is not necessarily due to anterior \t\twall ischemia. Data from stress testing shows that subendocardial \t\tischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, \t\taVF and V4-V6. But, again, this does not tell you which artery is \t\tinvolved. Second, ST depression in V1-V3, vs. V4-V6, is much more likely \t\tto be posterior than subendocardial ischemia. Third, patients at higher \t\trisk of NSTEMI (older, more risk factors, h\/o angiogram with multivessel \t\tdisease) are much more likely to have subendocardial disease (vs., for \t\tinstance, a younger smoker). Fourth, patients with reasons to have \t\tdemand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more \t\tlikely to have subendocardial ischemia (like in a stress test); those \t\twith posterior MI are much more likely to present with onset of chest \t\tpain and with normal vital signs. Fifth, look for tall R-waves in V1-V3 \t\t(the analog of Q-waves in other locations). Sixth, an upright T-wave is \t\tmuch more likely to represent posterior MI, but probably signifies \t\treperfusion of the artery rather than persistent occlusion. An inverted \t\tT-wave can be either subendocardial or posterior. Seventh, placement of \t\tposterior leads is very helpful. Take leads V4-V6 and place them at the \t\tlevel of the tip of the scapula, with V4 placed at the posterior \t\taxillary line (“V7”), V6 at paraspinal area (“V9”), and V5 (“V8”) \t\tbetween them. At lease 0.5 mm of ST elevation in 2 consecutive leads is \t\tvery accurate for posterior MI.<\/p>\n

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<\/span>ECGs gathered from around the country<\/span><\/h2>\n

<\/span> \t\t\t\t\t\t \t\t\t\t\t\tCircumflex Occlusion May be Subtle or Invisible on the \t\t\t\t\t\tECG<\/a><\/span><\/h3>\n

By Steve Smith <\/p>\n

\t\t\t\t\t\t \t\t\t\t\t\t \t\t\t\t\t\t\t\t \t\t\t\t\t\t\t\t\tCase 1<\/p>\n

\t\t\t\t\t\t\t\t\tBelow are 2 cases of circumflex or obtuse \t\t\t\t\t\t\t\t\tmarginal (branch of circumflex) occlusions \t\t\t\t\t\t\t\t\tshowing how subtle they may be:<\/p>\n

\t\t\t\t\t\t\t\t\tA 52 y.o. male presents because he “thought \t\t\t\t\t\t\t\t\the might be having a heart attack.” He \t\t\t\t\t\t\t\t\treports intermittent CP and SOB for 2-3 \t\t\t\t\t\t\t\t\tdays. Pain worsened and became sharper after \t\t\t\t\t\t\t\t\tlifting a bookcase up the stairs. He \t\t\t\t\t\t\t\t\tcontinued to have worsening pain and \t\t\t\t\t\t\t\t\tdiaphoresis, and associated left arm pain \t\t\t\t\t\t\t\t\tdown to the fingers. Pt. reports MI in 2001 \t\t\t\t\t\t\t\t\twith a stent placed in the “marginal” \t\t\t\t\t\t\t\t\tartery. Pain is similar, but associated with \t\t\t\t\t\t\t\t\tless SOB. Exam is unremarkable. Here is the \t\t\t\t\t\t\t\t\tEKG at 1810:<\/p>\n

\t\t\t\t\t\t\t\t\t\"\"<\/a>There \t\t\t\t\t\t\t\t\tis subtle ST elevation in II, III, and aVF. \t\t\t\t\t\t\t\t\tIt is not 1 mm. There is no reciprocal ST \t\t\t\t\t\t\t\t\tdepression or T-wave inversion in aVL, so \t\t\t\t\t\t\t\t\tthe diagnosis of acute inferior MI is \t\t\t\t\t\t\t\t\tdifficult to make by the ECG. There are, \t\t\t\t\t\t\t\t\thowever, Q-waves in II, III, and aVF. These \t\t\t\t\t\t\t\t\tcould be due to old or acute MI. There is no \t\t\t\t\t\t\t\t\tST depression in the precordial leads, or \t\t\t\t\t\t\t\t\tsignificant ST elevation in the lateral \t\t\t\t\t\t\t\t\tleads, any of which would have supported the \t\t\t\t\t\t\t\t\tdiagnosis of inferior MI. This is a \t\t\t\t\t\t\t\t\tnon-diagnostic ECG. A repeat ECG 1 hour \t\t\t\t\t\t\t\t\tlater is subtly changed, with some evolving \t\t\t\t\t\t\t\t\tT-wave inversion best seen in V5 and V6.<\/p>\n

\t\t\t\t\t\t\t\t\t\"\"<\/a>
\t\t\t\t\t\t\t\t\tA stat echocardiogram would have helped to \t\t\t\t\t\t\t\t\tmake this diagnosis and facilitate timely \t\t\t\t\t\t\t\t\treperfusion. Angiography and PCI were \t\t\t\t\t\t\t\t\tundertake 8 hours after the initial ECG and \t\t\t\t\t\t\t\t\tshowed a completely occluded OM-1. Echo \t\t\t\t\t\t\t\t\trevealed inferior-posterior wall motion \t\t\t\t\t\t\t\t\tabnormality and troponin peaked at 100!<\/p>\n

\t\t\t\t\t\t\t\t\tIt is not unusual for occlusions of the \t\t\t\t\t\t\t\t\tcircumflex or its branches to show little on \t\t\t\t\t\t\t\t\tthe ECG even though they represent a large \t\t\t\t\t\t\t\t\tamount of ischemic myocardium at risk for \t\t\t\t\t\t\t\t\tcomplete infarction. The circumflex \t\t\t\t\t\t\t\t\tterritory is known as being \t\t\t\t\t\t\t\t\t“electrocardiographically silent”.<\/p>\n

\t\t\t\t\t\t\t\t\tHow can you make the diagnosis? First, this \t\t\t\t\t\t\t\t\tpatient had a known stent in the “marginal” \t\t\t\t\t\t\t\t\tartery and thought he was having a heart \t\t\t\t\t\t\t\t\tattack. In such a situation, when you know \t\t\t\t\t\t\t\t\tthat the circumflex is the likely culprit \t\t\t\t\t\t\t\t\tartery, you may suspect that an MI will not \t\t\t\t\t\t\t\t\tbe obvious on the ECG. In this case the ECG \t\t\t\t\t\t\t\t\twas very suspicious for MI, but not \t\t\t\t\t\t\t\t\tdiagnostic. Therefore, additional diagnostic \t\t\t\t\t\t\t\t\ttesting is warranted. Possibilities include: \t\t\t\t\t\t\t\t\tserial ECGs (which were done but still \t\t\t\t\t\t\t\t\tnondiagnostic), stat echocardiogram, or \t\t\t\t\t\t\t\t\tposterior \t\t\t\t\t\t\t\t\tECG. Use of the \t\t\t\t\t\t\t\t\tPRIME ECG \t\t\t\t\t\t\t\t\t80 lead body surface mapping shows \t\t\t\t\t\t\t\t\tgreat potential for improving diagnosis in \t\t\t\t\t\t\t\t\tsuch cases.<\/p>\n

\t\t\t\t\t\t\t\t\tBy definition, this is a non-STEMI because \t\t\t\t\t\t\t\t\tthere is not 1 mm of ST elevation in 2 \t\t\t\t\t\t\t\t\tconsecutive leads. However, ST elevation is \t\t\t\t\t\t\t\t\tonly an imperfect surrogate for complete \t\t\t\t\t\t\t\t\tacute persistent occlusion of an epicardial \t\t\t\t\t\t\t\t\tcoronary artery without collateral \t\t\t\t\t\t\t\t\tcirculation. It is neither fully sensitive \t\t\t\t\t\t\t\t\tnor specific. Even though the patient’s ECG \t\t\t\t\t\t\t\t\tdid not meet criteria for STEMI, he had all \t\t\t\t\t\t\t\t\tthe pathology of a STEMI.<\/p>\n

Case 2<\/p>\n

\t\t\t\t\t\t\t\t\tA 38 year old male with h\/o smoking only c\/o \t\t\t\t\t\t\t\t\ta few hours of severe substernal chest pain; \t\t\t\t\t\t\t\t\the thinks he is having a heart attack. The \t\t\t\t\t\t\t\t\tpain is very nitroglycerine responsive. The \t\t\t\t\t\t\t\t\tfirst ECG with pain (unavailable) showed T \t\t\t\t\t\t\t\t\twave flattening in V2 and V3. After \t\t\t\t\t\t\t\t\tresolution of pain with sublingual \t\t\t\t\t\t\t\t\tnitroglycerine, the second ECG was changed \t\t\t\t\t\t\t\t\tto near normal:<\/p>\n

\t\t\t\t\t\t\t\t\t\"\"<\/a>There \t\t\t\t\t\t\t\t\tare nondiagnostic T abnormalities in I and \t\t\t\t\t\t\t\t\taVL, but little to suggest ischemia except \t\t\t\t\t\t\t\t\tthat the precordial T waves are normalized. \t\t\t\t\t\t\t\t\tI was suspicious of LAD disease.<\/p>\n

\t\t\t\t\t\t\t\t\t73 minutes later, the patient developed pain \t\t\t\t\t\t\t\t\tagain:<\/p>\n

\t\t\t\t\t\t\t\t\t\"\"<\/a>
\t\t\t\t\t\t\t\t\tThe precordial T-waves are again flattened, \t\t\t\t\t\t\t\t\twithout any other abnormality. \t\t\t\t\t\t\t\t\tNitroglycerine
\t\t\t\t\t\t\t\t\tagain eventually resolved the pain, and the \t\t\t\t\t\t\t\t\tfollowing ECG was recorded at 2234:<\/p>\n

\t\t\t\t\t\t\t\t\t\"\"<\/a> \t\t\t\t\t\t\t\t\tNow the ECG is more normal appearing than \t\t\t\t\t\t\t\t\tever.<\/p>\n

\t\t\t\t\t\t\t\t\tThe troponin returned at 0.81 ng\/ml, so the \t\t\t\t\t\t\t\t\tpatient was started on heparin and \t\t\t\t\t\t\t\t\teptifibatide, in addition to IV \t\t\t\t\t\t\t\t\tnitroglycerine and Metoprolol (and, of \t\t\t\t\t\t\t\t\tcourse, aspirin).<\/p>\n

\t\t\t\t\t\t\t\t\tHis angiogram the next day revealed a 100% \t\t\t\t\t\t\t\t\tmid dominant circumflex occlusion that \t\t\t\t\t\t\t\t\tsupplied the inferior and posterior walls. \t\t\t\t\t\t\t\t\tThere was a large LAD that collaterally \t\t\t\t\t\t\t\t\tsupplied some of the inferior wall. Echo \t\t\t\t\t\t\t\t\tshowed an inferior-posterior wall motion \t\t\t\t\t\t\t\t\tabnormality. The troponin peaked at only 13, \t\t\t\t\t\t\t\t\tprobably because of the collateral \t\t\t\t\t\t\t\t\tcirculation from the LAD.<\/p>\n

\t\t\t\t\t\t\t\t\tHow could we have gotten him to angiography \t\t\t\t\t\t\t\t\tand PCI faster? Patients with objective \t\t\t\t\t\t\t\t\tevidence of acute coronary syndrome \t\t\t\t\t\t\t\t\t(positive troponin or ECG) AND \t\t\t\t\t\t\t\t\tuncontrollable pain should get emergent PCI \t\t\t\t\t\t\t\t\teven if they do not have ST elevation. This \t\t\t\t\t\t\t\t\tpatient did become pain free on maximal \t\t\t\t\t\t\t\t\tmedical therapy, so PCI was not indicated.<\/p>\n

\t\t\t\t\t\t\t\t\tFortunately, his MI was not large by \t\t\t\t\t\t\t\t\tbiomarkers. Although he had a wall motion \t\t\t\t\t\t\t\t\tabnormality, this may go away over time. \t\t\t\t\t\t\t\t\t\t \t\t\t\t\t\t\t\t \t\t\t\t\t\t\t\t \t\t\t\t\t\t\t \t\t\t\t\t\t \t\t\t\t\t\t\t \t\t\t\t\t\t \t\t\t\t\t\t\t<\/p>\n