{"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":"
\ufeff <\/p>\n
EMCrit.org | Emergency Department Critical Care – \t \t\tDr. \t\tSmith’s ECG Blog <\/a> \t\t<\/p>\n 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 \u00a0<\/p>\n \u00a0<\/p>\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\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\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 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\tThis patient is 38 years old with \t\t\t\t\t\t\t\t\thyperlipidemia. He was at the gym when he \t\t\t\t\t\t\t\t\thad the onset of chest pain. EMS was \t\t\t\t\t\t\t\t\tactivated and recorded the following ECG \t\t\t\t\t\t\t\t\t(scanned from a prehospital ECG, so the \t\t\t\t\t\t\t\t\tquality is not perfect):<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>Notice \t\t\t\t\t\t\t\t\tthe small Q wave in V1 followed by a very \t\t\t\t\t\t\t\t\tlarge R-wave, with a prolonged QRS. There is \t\t\t\t\t\t\t\t\ta wide S-wave in V6. Thus, there is right \t\t\t\t\t\t\t\t\tbundle branch block, which should never \t\t\t\t\t\t\t\t\t(unlike Left BBB) have any ST elevation. But \t\t\t\t\t\t\t\t\there there is a large degree of ST elevation \t\t\t\t\t\t\t\t\tin V2-V6, I, and aVL. RBBB in acute STEMI \t\t\t\t\t\t\t\t\thas a very high mortality. <\/p>\n \t\t\t\t\t\t\t\t\tThe paramedics activated the cath lab from \t\t\t\t\t\t\t\t\tthe field.<\/p>\n \t\t\t\t\t\t\t\t\tThe patient had 2 ventricular fibrillation \t\t\t\t\t\t\t\t\tarrests during transport, but was \t\t\t\t\t\t\t\t\timmediately defibrillated both times, and \t\t\t\t\t\t\t\t\twas awake in the ED, when the following ECG \t\t\t\t\t\t\t\t\twas recorded:<\/p>\n \t\t\t\t\t\t\t\t\t<\/a> \t\t\t\t\t\t\t\t\tAngiography revealed a very tight LAD \t\t\t\t\t\t\t\t\tstenosis with some flow (confirming the \t\t\t\t\t\t\t\t\treperfusion that we see on the ECG). A stent \t\t\t\t\t\t\t\t\twas placed, and the patient had an excellent \t\t\t\t\t\t\t\t\toutcome with no wall motion abnormality.<\/p>\n Learning \t\t\t\t\t\t\t\t\tpoint: the prehospital ECG is \t\t\t\t\t\t\t\t\tcritical, as was early prehospital cath lab \t\t\t\t\t\t\t\t\tactivation. Were it not for this prehospital \t\t\t\t\t\t\t\t\tECG and the cardiac arrest, the diagnosis \t\t\t\t\t\t\t\t\tmay have been significantly delayed. Had \t\t\t\t\t\t\t\t\tthis happened, the artery may have \t\t\t\t\t\t\t\t\tre-occluded prior to angiography, with \t\t\t\t\t\t\t\t\tresultant recurrent cardiac arrest and\/or \t\t\t\t\t\t\t\t\tshock and death. \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 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\tHere is a case of an 89 year old woman who \t\t\t\t\t\t\t\t\thad syncope but no chest pain or shortness \t\t\t\t\t\t\t\t\tof breath. Her initial EKG (#1) shows some \t\t\t\t\t\t\t\t\tnondiagnostic ST depression in V4-V6, \t\t\t\t\t\t\t\t\tprobably due to LVH. She has a troponin of \t\t\t\t\t\t\t\t\t0.13 ng\/ml (ref range up to 0.09).<\/p>\n (#1)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a> (#2)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a><\/p>\n \t\t\t\t\t\t\t\t\tThe patient returned with another episode of \t\t\t\t\t\t\t\t\tsyncope 15 days later. She had no other \t\t\t\t\t\t\t\t\tsymptom except weakness; none whatsoever. \t\t\t\t\t\t\t\t\tShe had the following EKG at 0700:<\/p>\n \t\t\t\t\t\t\t\t\t(#3)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>Here \t\t\t\t\t\t\t\t\tthere is 4 \t\t\t\t\t\t\t\t\tmm of ST elevation that can only be \t\t\t\t\t\t\t\t\tdue to myocardial ischemia. If there is any \t\t\t\t\t\t\t\t\tdoubt, then the presence of \t\t\t\t\t\t\t\t\tnew ST \t\t\t\t\t\t\t\t\televation and T inversion in I and aVL \t\t\t\t\t\t\t\t\tshould erase that. If there is still any \t\t\t\t\t\t\t\t\tdoubt, the \t\t\t\t\t\t\t\t\tloss of R-wave amplitude in V2 and V3 \t\t\t\t\t\t\t\t\tshould erase that as well. The inversion of \t\t\t\t\t\t\t\t\tthe T wave in aVL and V2 suggests an open \t\t\t\t\t\t\t\t\tartery. However, this is a very strange \t\t\t\t\t\t\t\t\tlooking Wellens’ T wave because of the \t\t\t\t\t\t\t\t\tmarked ST elevation.<\/p>\n \t\t\t\t\t\t\t\t\tThe treating physician contacted the \t\t\t\t\t\t\t\t\tcardiologist immediately, but the \t\t\t\t\t\t\t\t\tcardiologist was not convinced, mostly \t\t\t\t\t\t\t\t\tbecause of the minimal symptoms and partly \t\t\t\t\t\t\t\t\tbecause it is not the classic morphology of \t\t\t\t\t\t\t\t\tanterior STEMI due to persistently occluded \t\t\t\t\t\t\t\t\tLAD, which should have upright T waves.<\/p>\n \t\t\t\t\t\t\t\t\tSo they recorded another EKG at 0720:<\/p>\n \t\t\t\t\t\t\t\t\t(#4)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a> \t\t\t\t\t\t\t\t\tAnother EKG was done at 0739:<\/p>\n (#5)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a> \t\t\t\t\t\t\t\t\tFortunately, the physicians were attentive \t\t\t\t\t\t\t\t\tand kept ordering frequent serial EKGs.<\/p>\n Learning \t\t\t\t\t\t\t\t\tpoint: some EKGs represent STEMI no matter \t\t\t\t\t\t\t\t\twhat the symptoms, until proven otherwise by \t\t\t\t\t\t\t\t\tangiography. \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 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\tBelow are several examples of hyperacute T \t\t\t\t\t\t\t\t\twaves.<\/p>\n Case 1 (Hyperacute \t\t\t\t\t\t\t\t\tT waves with ST depression–LAD occlusion).<\/p>\n \t\t\t\t\t\t\t\t\tThe following is a perfect example of \t\t\t\t\t\t\t\t\tAnterior MI with LAD occlusion but WITHOUT \t\t\t\t\t\t\t\t\tany ST elevation. This is seen commonly, but \t\t\t\t\t\t\t\t\tonly recently reported on by de Winter, \t\t\t\t\t\t\t\t\tVerouden, Wilde, and Wellens’ in a long \t\t\t\t\t\t\t\t\tletter to the New England Journal (NEJM \t\t\t\t\t\t\t\t\t359(19):2071-2073; Nov. 6, 2008).<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>The \t\t\t\t\t\t\t\t\tauthors reported this morphology in 2% of \t\t\t\t\t\t\t\t\tLAD occlusions. The morphology is as \t\t\t\t\t\t\t\t\tfollows: 1-3 mm of upsloping ST depression \t\t\t\t\t\t\t\t\tin leads V1 to V6 that continues into tall, \t\t\t\t\t\t\t\t\tpositive symmetrical T waves, with normal \t\t\t\t\t\t\t\t\tQRS and loss of R-wave progression and with \t\t\t\t\t\t\t\t\t1-2 mm ST elevation in aVR. Interestingly, \t\t\t\t\t\t\t\t\tthey found that this was not a transient \t\t\t\t\t\t\t\t\tfeature that later progressed to ST \t\t\t\t\t\t\t\t\televation, but that it remained static until \t\t\t\t\t\t\t\t\tangiography up to 50 minutes after the \t\t\t\t\t\t\t\t\tinitial ECG. The mean time from symptom \t\t\t\t\t\t\t\t\tonset was 90 minutes. K levels were normal. \t\t\t\t\t\t\t\t\tMI was very large as measured by high CK-MB.<\/p>\n Case 2 (Hyperacute \t\t\t\t\t\t\t\t\tT waves present AFTER ST elevation is \t\t\t\t\t\t\t\t\tresolving).<\/p>\n \t\t\t\t\t\t\t\t\tThis is the EKG of a previously healthy 40 \t\t\t\t\t\t\t\t\tyear old man with one hour of chest pain and \t\t\t\t\t\t\t\t\tprofound weakness and sense of “doom”. He \t\t\t\t\t\t\t\t\thas a history of HTN, smoking, and family \t\t\t\t\t\t\t\t\thistory. Vital signs and exam were normal.<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>This \t\t\t\t\t\t\t\t\tECG show large symmetric T waves, best \t\t\t\t\t\t\t\t\tdistinguished from those of early \t\t\t\t\t\t\t\t\trepolarization by the absence of large \t\t\t\t\t\t\t\t\tR-waves (in this case, the R-wave amplitude \t\t\t\t\t\t\t\t\tis very small). It also helps that there is \t\t\t\t\t\t\t\t\tinferior ST depression. There is some \t\t\t\t\t\t\t\t\tborderline ST elevation in leads V2 and V3. \t\t\t\t\t\t\t\t\tSimilar to case 1, there is ST depression in \t\t\t\t\t\t\t\t\tleads V4-V6. This should be recognized as an \t\t\t\t\t\t\t\t\tEKG diagnostic for LAD occlusion.<\/p>\n \t\t\t\t\t\t\t\t\tA prehospital EKG had been done and is shown \t\t\t\t\t\t\t\t\tbelow (but has very poor quality)<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>This \t\t\t\t\t\t\t\t\tshows much ST elevation in anterior leads \t\t\t\t\t\t\t\t\tand illustrates an underrecognized \t\t\t\t\t\t\t\t\tphenomenon: hyperacute T waves are not only \t\t\t\t\t\t\t\t\tpresent early after occlusion, as the STEMI \t\t\t\t\t\t\t\t\tis developing, but also after the ST segment \t\t\t\t\t\t\t\t\televates AND they are present early after \t\t\t\t\t\t\t\t\treperfusion as the ST segments are falling. \t\t\t\t\t\t\t\t\tThey may be the only remaining clue to a \t\t\t\t\t\t\t\t\treperfused LAD occlusion.<\/p>\n Case 3 (Hyperacute \t\t\t\t\t\t\t\t\tT waves misdiagnosed as Hyperkalemia).<\/p>\n \t\t\t\t\t\t\t\t\t49 yo man with 1 week of stuttering chest \t\t\t\t\t\t\t\t\tburning and tightness for 1-2 hours. Today \t\t\t\t\t\t\t\t\tthe discomfort is associated with multiple \t\t\t\t\t\t\t\t\tepisodes of vomiting and it is unremittant. \t\t\t\t\t\t\t\t\tThe following EKG was obtained and \t\t\t\t\t\t\t\t\thyperkalemia was diagnosed. The patient was \t\t\t\t\t\t\t\t\ttreated with Calcium, Insulin, D50, and \t\t\t\t\t\t\t\t\tbicarbonate, with no change in the ECG. A \t\t\t\t\t\t\t\t\tbedside ultrasound revealed a possible \t\t\t\t\t\t\t\t\tanterior wall motion abnormality. The K \t\t\t\t\t\t\t\t\treturned at 2.9 mEq\/L. There was an LAD \t\t\t\t\t\t\t\t\tocclusion that was opened and stented.<\/p>\n \t\t\t\t\t\t\t\t\t<\/a>These \t\t\t\t\t\t\t\t\tT waves are NOT typical for hyperK. They are \t\t\t\t\t\t\t\t\t“fat” and wide, with a blunt peak and poor \t\t\t\t\t\t\t\t\tR-wave progression (especially V3). The \t\t\t\t\t\t\t\t\tT-waves of hyperkalemia are peaked and \t\t\t\t\t\t\t\t\ttented. See below:<\/p>\n \t\t\t\t\t\t\t\t\t<\/a> \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 \u00a0<\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n By Steve Smith <\/p>\n \t\t \t\t\tCase 1.<\/p>\n \t\t\tThis is a 44 yo male with h\/o HTN, CABG at age 34, and 2 drug \t\t\teluting stents to the first diagonal graft 3 months prior. He \t\t\tpresented at 1810 with chest pain 5 days after stopping clopidogrel \t\t\t(on the instructions of another physician). The following ECG (#1) \t\t\twas recorded, with ECG #2 as his baseline.<\/p>\n \t\t\t#1, presenting ECG \t\t\tThe differential diagnosis is subendocardial ischemia with probably \t\t\tNSTEMI vs. posterior STEMI. By ECG \t\t\talone, posterior MI is more likely because of maximal ST depression \t\t\tin right, as opposed to left, precordial leads. However, \t\t\tgiven the history of severe 3 vessel coronary disease it is prudent \t\t\tto start with medical management, then observe for resolution of \t\t\tpain, but to also obtain an immediate echocardiogram to ascertain \t\t\twhich wall is involved. If pain or ECG findings do not resolve, or \t\t\tif there is posterior wall motion abnormality, then immediate \t\t\tangiography with PCI is indicated.<\/p>\n \t\t\tIn this case, maximal medical therapy was undertaken with Aspirin, \t\t\tclopidogrel, heparin, eptifibatide, metoprolol, and IV nitroglycerin \t\t\tand the patient was admitted to the CCU with cardiology consulted \t\t\timmediately. Chest pain resolved and angiogram was not done until \t\t\tthe next day. It showed a 100% re-occluded SVG stent to D1; thrombus \t\t\twas suctioned out. Echo confirmed posterior wall motion abnormality. \t\t\tMax troponin was 47.<\/p>\n Case 2.<\/p>\n \t\t\t54 yo female with h\/o smoking, DM, HTN, c\/o chest pain for 3 hours, \t\t\tsubsternal radiating to both shoulders. She has an initial ECG which \t\t\tshows diffuse ST depression and she was treated for NSTEMI. She \t\t\tdeveloped some pulmonary edema after metoprolol. ECG #2 was \t\t\trecorded:<\/p>\n \t\t\t<\/a>ST \t\t\tdepression is maximal from V2 to V4. This is due to posterior STEMI \t\t\tuntil proven otherwise. Unfortunately, it was treated as an NSTEMI \t\t\tfor 2.5 hours until an echocardiogram showed a posterior wall motion \t\t\tabnormality. Cath revealed a 100% occluded circumflex. This was \t\t\topened and stented, with the convalescent ECG below, which shows \t\t\tlarge upright posterior reperfusion T waves with a long QT.<\/p>\n \t\t\t<\/a><\/p>\n \t\t\tHow can such delay be avoided? By recording posterior leads V7-V9, \t\t\tat the level of the tip of the scapula and at the posterior axillary \t\t\tline (V7), a position midway between this and the spine (V8), and a \t\t\tparaspinal lead (V9). Also, obtaining a stat echo. Most of all, \t\t\trecognize this ECG pattern as being by far more likely to be \t\t\tposterior STEMI than due to subendocardial ischemia, which has \t\t\tmaximum ST depression in leads V4-V6.<\/p>\n Case 3.<\/p>\n \t\t\tHere is a case of a 66 yo male with a history of CAD who presents \t\t\twith 1.5 hours of chest pain and is stable.<\/p>\n \t\t\t<\/a>There \t\t\tis ST depression maximal in, again, V2-V4. The vast majority of \t\t\tposterior STEMI is not isolated, but rather concurrent with inferior \t\t\tand\/or lateral involvement. In this case there is subtle ST elevtion \t\t\tin the inferior leads, not noticed by the treating physicians. \t\t\tCompare these ST segments with those of the post reperfusion ECG \t\t\tbelow:<\/p>\n \t\t\t<\/a> The T-wave in posterior STEMI<\/p>\n \t\t\tNotice also that in the first (pre-reperfusion) ECG of case 3, the T \t\t\twave is not upright as in previous cases. Some authors claim that \t\t\tthe T wave must be upright for posterior STEMI. Evidence for this is \t\t\tlacking. In fact, an upright T wave probably indicates reperfusion \t\t\tof the posterior STEMI, whereas an inverted T wave is the analog of \t\t\ta hyperacute T wave (still occluded) but recorded from the opposite \t\t\tside. Either can be present in posterior STEMI, depending on the \t\t\tstate of microvascular perfusion due to recanalization or to \t\t\tcollateral circulation. \t\t \t<\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \t \t\tThis is a 46 yo male with acute onset of chest pain, in distress, who \t\tcalled the ambulance. He arrived and had this ECG recorded at 0118 AM:<\/p>\n \t\t<\/a> \t\t(In this case, the limb leads are suggestive of ischemia as well, with \t\tsome subtle ST depression inferiorly, suggesting pending ST elevation in \t\taVL due to lateral MI from proximal LAD occlusion.)<\/p>\n \t\tI have developed a decision rule to differentiate Anterior STEMI from \t\tBER in patients who present to the ED with chest pain. These rules only \t\tapply when the DDx is Anterior MI vs. \t\tBER. A simple rule is the R-wave \t\trule, which depends on the fact that, in BER, the R-wave is always well \t\tdeveloped:<\/p>\n \t\tIf the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is \t\talmost certainly MI. If greater than 5 mm, it is probably BER. A cutoff \t\tof 5 mm gives a sensitivity for MI of about 70%, but a specificity of \t\tgreater than 95%.<\/p>\n \t\tA more complex rule was derived using logistic regression, and involves \t\t2 other variables: mean ST elevation at the J point (STEJ) from V2-V4, \t\tand computer measured QT-c (Bazett method). This relies on the findings \t\tthat the mean ST elevation was higher in the MI group, and the mean QTc \t\tin BER is short (mean = 390 ms).<\/p>\n \t\tIf the formula: (1.553 x mean STEJ) + (.0546 x QTc in ms) – (0.3813 x \t\tmean RA) is > 21, vs. less than or equal to 21, then it represents MI \t\twith high sensitivity and specificity.<\/p>\n \t\tIn this case, the values are (1.553 x 1.0) + (.0546 x 420) – (.3813 x \t\t1.17) = 1.553 + 22.93 – 0.3813 = 24.1<\/p>\n \t\tThus, the rule predicts that this is anterior MI.<\/p>\n \t\tThe clinicians were suspicious of MI, so they were smart to obtain \t\tserial ECGs. They obtained the second ECG at 0143:<\/p>\n \t\t<\/a>This \t\tshows unequivocal straightening \t\tof the ST segments, compared to the first ECG. This ST straightening \t\tresults in T waves which are \t\tfattened and “hyperacute”. This \t\tis diagnostic of anterior STEMI.<\/p>\n \t\tHe had a 100% proimal thrombotic LAD occlusion with TIMI-0 flow. It was \t\topened and stented.<\/p>\n \t\tThe followup ECG gives an idea of what this patient’s T-waves looked \t\tlike before his occlusion:<\/p>\n \t\t<\/a> \t\t \t\t \t \t \t\t \t\t\tPosted by Steve \t\t\tSmith at \t\t\t \t\t\t8:09 AM<\/a> \t\t\t \t\t\t \t\t\t \t\t\t<\/a> \t\t\t \t\t\t<\/a> \t\t\t \t\t \t\t\t \t\t \t\t\t \t\t\t \t\t\t\t\tReactions:\u00a0 \t\t\t\t\t \t\t\t\t\t \t\t\t\t\t \t\t\t\t \t \t \t<\/p>\n Dr. Smith –<\/p>\n \t\tYou wrote:<\/p>\n \t\t“If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is \t\thighly unlikely to be BER. If greater than 5 mm, it is probably MI. A \t\tcutoff of 5 mm gives a sensitivity for MI of about 70%, but a \t\tspecificity of greater than 95%.”<\/p>\n \t\tIs this a typo? <\/p>\n \t\tIf the R-wave amplitude is greater than 5 mm, then it’s probably MI? Or \t\tdid you mean to say that it’s probably BER?<\/p>\n \t\tI have two cases of anterior STEMI vs. BER, and in both cases, it turned \t\tout to be anterior STEMI.<\/p>\n \t\tIn the \t\t \t\tfirst<\/a> case, the mean R-wave amplitude in V2-V4 is less than 5 mm.<\/p>\n \t\tIn the \t\t \t\tsecond<\/a> case, the mean R-wave amplitude in V2-V4 is greater than 5 \t\tmm.<\/p>\n \t\tWould it be safe to say that the second case shows anterior STEMI in the \t\tpresence of BER?<\/p>\n \t\tThanks for another great teaching point!<\/p>\n<\/dd>\n<\/dl>\n \u00a0<\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \t \t \t \t\tCase 1. \t\tClassic anterior LV aneurysm morphology \t\t(Persistent ST elevation after previous MI).<\/p>\n \t\t<\/a>This \t\t46 yo male presented with chest pain. There is 1 mm of ST elevation in \t\tV1-V3, but there are large QS-waves preceding the STE. Such QS waves are \t\thighly suggestive of old transmural MI, with subsequent akinesis or \t\tdyskinesis of the anterior wall. Acute MI, if early in its course (first \t\t6 hours, at least), always has tall T-waves in addition to ST elevation.<\/p>\n \t\tThere is one retrospective study (Smith SW. American Journal of \t\tEmergency Medicine 23(3):279-287, May 2005) showing that the T\/QRS ratio \t\tis significantly greater in acute anterior STEMI than in old anterior MI \t\twith persistent ST Elevation. The best criterion for differentiating was \t\tthe sum of STE in V1-V4 divided by the sum of the QRS’s in V1-V4 \t\t(TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4). If this value was \t\t<0.22,>0.36, then it is likely to be acute STEMI.<\/p>\n \t\tT-waves in aneurysm may be upright or inverted, but in neither case \t\tshould they have high voltage. [Deep inversions suggest very recent \t\tNSTEMI (e.g., Wellens’). Tall T-waves suggest acute STEMI.]<\/p>\n \t\tThe above ECG has a summed ratio of 0.05 and is clearly NOT an acute \t\tSTEMI. It is important to know that only about 70%-80% of patients with \t\tthe ECG morphology of “LV aneurysm” actually have an LV aneurysm, as \t\tdefined by echocardiographic dyskinesis. “LV aneurysm” is far less \t\tcommon in this era of reperfusion, in which STEMI is not allowed to \t\tprogress to full infarction (also known as “transmural” infarction, an \t\told but useful term). The patient above had akinesis and had formerly \t\thad a mural thrombus, which is a common complication of an immobile wall \t\twhich also may have post-infarction inflammation.<\/p>\n \t\tThis patient ruled out for MI with negative troponins.<\/p>\n Case 2. \t\tExaggeration of persistent STE after \t\told MI by tachycardia<\/p>\n \t\tThis 65 yo male presented with dyspnea but no CP. The lungs sound wet. \t\tThe ECG is shown.<\/p>\n \t\t<\/a>There \t\tis quite a bit of ST elevation in the anterior leads, but it is preceded \t\tby very deep QS waves suggestive of old MI. Previous MI can have \t\tpersistent ST elevation, and just like in Left Bundle Branch block and \t\tother entities, ST elevation may be \t\texaggerated in states of tachycardia. Therefore, the T-wave to \t\tQRS ratio may also be exaggerated. Here the formula TV1+TV2+TV3+TV4 \t\tdivided by QRSV1+QRSV2+QRSV3+QRSV4 = 0.27, substantially > 0.22, and \t\twould indicate acute STEMI. But one must be suspicous of a false \t\tpositive in the presence of extreme tachycardia such as this. Also \t\targuing against STEMI is the fact that there is no single T\/QRS ratio \t\t(V1-V4) > 0.36.<\/p>\n \t\tThe difficult decision is this: is this an old MI with exaggerated \t\tpersistent STE due to tachycardia, or is it an old MI with a new STEMI \t\tsuperimposed? Given that the BNP was > 5000 and the patient had no chest \t\tpain, and the high likelihood that such a morphology represented the \t\tformer (not the latter) diagnosis, the patient was not set up for \t\tangiogram and reperfusion.<\/p>\n \t\tA previous ECG was found and is shown:<\/p>\n \t\t<\/a>It \t\tis evident that there previously was classic LV aneurysm morphology, but \t\twith much less ST elevation. The ratio here is 0.05. A previous echo had \t\tshown severe decreased LVF with an akinetic anterior wall.<\/p>\n \t\tClinicians correctly interpreted the first ECG as exaggeration of ST \t\televation of old MI due to tachycardia, stress, and exacerbation of CHF. \t\tTreatment of CHF resulted in a slowing heart rate. Follow up confirmed \t\tall troponins negative and resolution of ST elevation when the heart \t\trate came down. <\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \t \t \t \t\tThis is a 58 year old male with 40 minutes of chest pain of acute onset. \t\tHe called 911 and paramedics recorded a prehospital 12 lead ECG which \t\tshowed a clear inferior STEMI (not shown, tracing could not be found). \t\tHe was given aspirin and sublingual nitroglycerine, which improved his \t\tpain. The cath lab was activated by the paramedics. On arrival, the \t\tfollowing ECG was recorded.<\/p>\n \t\t<\/a>There \t\tis 0.5 mm of ST elevation in inferior leads II, III, and aVF. In \t\taddition, the T-waves in II, III, and aVF are very large, significantly \t\tlarger than normal in both height and width. To diagnose inferior MI, \t\tthere must always be reciprocal ST depression or T-wave inversion or \t\tboth in lead aVL. This is \t\tpresent here.<\/p>\n \t\tHyperacute T-waves can be present early, before the ST segment elevates, \t\tbut they can also be present as ST elevation is resolving from \t\tspontaneous reperfusion.<\/p>\n \t\tIn this case the diagnosis was clear due to the prehospital ECG. But \t\tsuppose there had been no prehospital ECG? Or if the first ECG had \t\tlooked like this? Suppose the ST segments were on the way up rather than \t\ton the way down. Would you have diagnosed this? This identical ECG could \t\tbe all the evidence you might have.<\/p>\n \t\tIf you find yourself in this diagnostic dilemma and you are uncertain of \t\tthe diagnosis, remember that you can use serial ECGs, old ECGs, and \t\timmediate echocardiography to help in the diagnosis. <\/p>\n <\/p>\n \t\t \t\t \t\t \t\t \t\t \t\t\tfrom \t\t\t \t\t\tDr. Smith’s ECG Blog<\/a> by \t\t\tSteve Smith \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\tI had a very good question regarding the post on \t\t\t\t\t\tposterior STEMI, and I wanted to be sure that the answer \t\t\t\t\t\tgets attention:<\/p>\n smallville said…<\/p>\n While your blog does an \t\t\t\t\t\texcellent job of highlighting posterior STEMIs that were \t\t\t\t\t\tmistaken, are there any solid criteria to help provide a \t\t\t\t\t\tDDx between anterior or subendocardial ischemia and \t\t\t\t\t\tposterior STEMI? Will posterior ST alteration always be \t\t\t\t\t\tlimited to v2-v4?<\/p>\n \t\t\t\t\t\tThis is a very good question, and not easily answered \t\t\t\t\t\tbecause there is very little solid research on this.<\/p>\n \t\t\t\t\t\tFirst, you should know that when there is precordial ST \t\t\t\t\t\tdepression due to subendocardial ischemia, it is not \t\t\t\t\t\tnecessarily due to anterior wall ischemia. Data from \t\t\t\t\t\tstress testing shows that subendocardial ischemia DOES \t\t\t\t\t\tNOT LOCALIZE on the ECG, and usually is in leads II, \t\t\t\t\t\tIII, aVF and V4-V6. But, again, this does not tell you \t\t\t\t\t\twhich artery is involved.<\/p>\n \t\t\t\t\t\tSecond, ST depression in V1-V3, vs. V4-V6, is much more \t\t\t\t\t\tlikely to be posterior than subendocardial ischemia.<\/p>\n \t\t\t\t\t\tThird, patients at higher risk of NSTEMI (older, more \t\t\t\t\t\trisk factors, h\/o angiogram with multivessel disease) \t\t\t\t\t\tare much more likely to have subendocardial disease \t\t\t\t\t\t(vs., for instance, a younger smoker).<\/p>\n \t\t\t\t\t\tFourth, patients with reasons to have demand ischemia \t\t\t\t\t\t(tachycardia, sepsis, GI Bleed, etc.) are much more \t\t\t\t\t\tlikely to have subendocardial ischemia (like in a stress \t\t\t\t\t\ttest); those with posterior MI are much more likely to \t\t\t\t\t\tpresent with onset of chest pain and with normal vital \t\t\t\t\t\tsigns.<\/p>\n \t\t\t\t\t\tFifth, look for tall R-waves in V1-V3 (the analog of \t\t\t\t\t\tQ-waves in other locations).<\/p>\n \t\t\t\t\t\tSixth, an upright T-wave is much more likely to \t\t\t\t\t\trepresent posterior MI, but probably signifies \t\t\t\t\t\treperfusion of the artery rather than persistent \t\t\t\t\t\tocclusion. An inverted T-wave can be either \t\t\t\t\t\tsubendocardial or posterior.<\/p>\n \t\t\t\t\t\tSeventh, placement of posterior leads is very helpful. \t\t\t\t\t\tTake leads V4-V6 and place them at the level of the tip \t\t\t\t\t\tof the scapula, with V4 placed at the posterior axillary \t\t\t\t\t\tline (“V7”), V6 at paraspinal area (“V9”), and V5 (“V8”) \t\t\t\t\t\tbetween them. At lease 0.5 mm of ST elevation in 2 \t\t\t\t\t\tconsecutive leads is very accurate for posterior MI.<\/p>\n References on posterior \t\t\t\t\t\tleads:<\/p>\n \t\t\t\t\t\t1) Matetzky S et al. Acute myocardial infarction with \t\t\t\t\t\tisolated ST-segment elevation in posterio chest leads \t\t\t\t\t\tV7-V9: “hidden” ST -segment elevation revealing acute \t\t\t\t\t\tposterior infarction. JACC 1999;34:748-53 \t\t\t\t\t\t \t\t\t\t\t\t \t\t\t\t\t\t \t\t\t\t\t\t\tThis 64 year old woman presented intoxicated with \t\t\t\t\t\t\tnausea and vomiting and epigastric pain, with no \t\t\t\t\t\t\tchest pain. She has a history of a stent, but \t\t\t\t\t\t\tunknown in which artery. She stopped taking \t\t\t\t\t\t\tclopidogrel 2 weeks ago because she ran out.<\/p>\n \t\t\t\t\t\t\t<\/a> \t\t\t\t\t\t\tA troponin returned elevated, and a repeat ECG was \t\t\t\t\t\t\trecorded:<\/p>\n \t\t\t\t\t\t\t<\/a>Now \t\t\t\t\t\t\tthe inferior T-waves have become mostly upright, in \t\t\t\t\t\t\tthis case biphasic. There is some ST elevation, but \t\t\t\t\t\t\tit is not quite 1 mm in two consecutive leads. There \t\t\t\t\t\t\tis new ST elevation in lead V1, which in this \t\t\t\t\t\t\tcontext is diagnostic of right ventricular STEMI.<\/p>\n \t\t\t\t\t\t\tThis phenomenon is called “pseudonormalization of \t\t\t\t\t\t\tT-waves” because normal T-waves are upright (same \t\t\t\t\t\t\taxis as QRS), but become inverted in non-STEMI that \t\t\t\t\t\t\tis reperfused. They become deceptively upright (not \t\t\t\t\t\t\tnormal, but “pseudo” normal) when the artery \t\t\t\t\t\t\tre-occludes. Thus, where reperfusion of the \t\t\t\t\t\t\tinfarct-related artery (IRA) leads to T-wave \t\t\t\t\t\t\tinversion, if inverted leads become suddenly \t\t\t\t\t\t\tupright, this is diagnostic of \t\t\t\t\t\t\tre-occlusion \t\t\t\t\t\t\tof the IRA.<\/p>\n \t\t\t\t\t\t\tThere is nothing magical about 1 mm of ST elevation. \t\t\t\t\t\t\tST elevation is used as a very imperfect surrogate \t\t\t\t\t\t\tfor coronary occlusion. Coronary occlusion that does \t\t\t\t\t\t\tnot spontaneously reperfuse or is not compensated \t\t\t\t\t\t\tfor by collateral circulation will quickly lead to \t\t\t\t\t\t\tirreversible myocardial loss. Reperfusion therapy is \t\t\t\t\t\t\tindicated for occlusion, even when there is not 1 mm \t\t\t\t\t\t\tof STE in 2 consecutive leads. However, the \t\t\t\t\t\t\tspecificity of the ECG for occlusion becomes less as \t\t\t\t\t\t\tthe STE is less. So expertise in interpreting the \t\t\t\t\t\t\tECG is particularly important for these cases.<\/p>\n \t\t\t\t\t\t\tIn this case, it was clear that there was a very \t\t\t\t\t\t\tunstable thrombus in the RCA or circ, and that if it \t\t\t\t\t\t\twas not 100% occlusive, it was very nearly so.<\/p>\n \t\t\t\t\t\t\tThe cath lab was activated, a 100% proximal RCA \t\t\t\t\t\t\tstent thrombosis was seen and the artery was opened.<\/p>\n \t\t\t\t\t\t\tThis also illustrates how chest pain or even \t\t\t\t\t\t\tdiscomfort may be completely absent in STEMI. Below \t\t\t\t\t\t\tis the post-cath ECG, showing T-waves are now \t\t\t\t\t\t\tinverted again (indicating reperfusion).<\/p>\n \t\t\t\t\t\t\t<\/a> \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\tPosted by \t\t\t\t\t\t\t\tSteve Smith \t\t\t\t\t\t\t\tat \t\t\t\t\t\t\t\t \t\t\t\t\t\t\t\t \t\t\t\t\t\t\t\t7:36 AM<\/a> \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<\/a> \t\t\t\t\t\t \t\t\t\t\t \t\t\t\t \t\t\t \t\t \t <\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \tThis 51 yo male presented with Chest pain.<\/p>\n \t<\/a> \tDeep and widespread ST depression is associated with very high mortality \tbecause it signifies severe ischemia usually of LAD or left main origin.<\/p>\n \tThis patient was treated with nitroglycerine, ASA, and heparin. His pain \tdiminished substantially but did not go away altogether. An ED ultrasound \tshowed an anterior, apical, and septal wall motion abnormality. Repeat ECG \tshowed most of the ST depression resolved (but not all).<\/p>\n \tThere is no ST elevation, no evidence of occlusion that will cause imminent \tnecrosis of a myocardial wall. But there is evidence of a very unstable \tatherosclerotic plaque that could completely thrombose at any moment. Also, \this ongoing pain signified ongoing ischemia, which is an indication for \timmediate angiography and PCI. Therefore he was taken emergently (in the \tevening) to the cath lab. There was a severe ostial LAD thrombosis that was \tvery close to the left main.<\/p>\n \tHe went for emergent bypass that evening and had a good outcome.<\/p>\n \tST elevation in aVR is often thought to represent left main occlusion. \tHowever, it really just signifies widespread and diffuse subendocardial \tischemia which could be due to left main or 3-vessel disease, or severe \tproximal LAD disease. Left Main occlusion generally causes rapid death; most \twho survive left main ACS have some flow and thus often have widespread ST \tdepression.<\/p>\n \tThink of aVR as (-)aVR. (-)aVR is 180 degrees opposite aVR and thus is \tbetween leads I and II. Thus, if I and II have ST depression, the (-) aVR \tmust have ST depression, and (+) aVR must have ST elevation. <\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \tA 53 year old male with no previous cardiac history presented with sudden \tsubsternal chest pain with tingling of bilateral arms and dyspnea.<\/p>\n \tthis is the first ECG at 1559:<\/p>\n \t<\/a>There \tis very subtle and < 1 mm ST elevation in II, III, and aVF. The T-waves in \tthese inferior leads are much larger than normal, with almost the same \tvoltage as the QRS, and are “fat”. These are hyperacute T waves. Just as \timportantly, there is minimal reciprocal ST depression in aVL, with T wave \tinversion. This is diagnostic for inferior STEMI, even though it doesn’t \tmeet the arbitrary criteria of 1 mm ST elevation in 2 consecutive leads.<\/p>\n \tThe cath lab was activated and a distal RCA thrombus with TIMI-0 flow was \tseen. For technical reasons, it could not be opened. An ECG was repeated, \tshowing the development of the inferior MI without reperfusion:<\/p>\n \t<\/a> \t \t \t \t\tPosted by Steve S <\/p>\n \u00a0<\/p>\n \tA 32 year old male presented with a 4 day history of dyspnea, cough, \tpalpitations, and chest pain. He had an ECG done immediately (shown above). \tThis showed anterior T wave inversions, a QTc of 431, and also T inversion \tin lead III. There is sinus tachycardia and an S1Q3T3. This is all highly \tsuspicous for pulmonary embolism. \t \t. \t \tOxygen saturation was 95%, there were some end expiratory wheezes. D dimer \twas 3000. A CT pulmonary angio confirmed large central PE. \t \t. \t \tKosuge et al. (Am J Cardiol 2007;99:817-821) compared patients with ACS and \tPE who had precordial T wave inversions in V1-V4. They found that in this \tselect population, negative T waves were observed in only 15 of patient with \tACS compared with 88% of patients with Acute PE. \t \t. \t \tIt is tempting to diagnose Wellens’ syndrome with anterior T wave \tinversions, but Wellens’ T waves simply look different, should have a longer \tQTc, generally don’t extend out to V6, and, most importantly, don’t have T \tinversion in lead III. \t \t. \t \tOf course the clinical scenario is most important. <\/p>\n <\/a><\/p>\n <\/p>\n This 70 year old woman with a history of left bundle branch block presented with 10 hours of dyspnea.<\/p>\n Notice there is QRS widening with a wide upright R wave in lead V6. That the QRS is not similar to V6 in leads I and aVL makes this an atypical LBBB. Nevertheless,, the same rules of concordance and discordance apply: the ST-T complex should go the opposite, or discordant, direction of the majority of the QRS.<\/p>\n Notice there is concordant ST elevation in inferior leads.<\/p>\n In addition, there is less discordant ST elevation in leads V1–V3 than is normal for LBBB. A normal amount of discordant ST elevation almost always produces an ST to S ratio of less than 0.20. The mean of normal LBBB is 0.09 to 0.11, but ratios of 0.07 to 0.15 may be seen. Thus, with a 26 mm S-wave in V2, the minimum amount of normal ST elevation is 26 x 0.07 or 1.8 mm. However, there is only 1 mm of ST elevation in V1 because of relative<\/em><\/strong> ST depression in leads V1 to V3.<\/p>\n This is infero–posterior STEMI in the context of old atypical LBBB.<\/p>\n \u00a0<\/p>\n <\/a><\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \tfrom \t \tDr. Smith’s ECG Blog<\/a> by \tSteve Smith \t \t \t\t \t\t\t \t\t\t\tFor this topic, see also this post: \t\t\t\t \t\t\t\thttp:\/\/hqmeded-ecg.blogspot.com\/2009\/01\/st-depression-limited-to-inferior-leads.html<\/a><\/p>\n \t\t\t\tThis 72 yo male with h\/o HTN, hyperlipidemia, and CAD, and h\/o \t\t\t\t4-vessel CABG 17 years prior presented with 8 hours of \t\t\t\tsubsternal chest pain radiating to upper back.<\/p>\n \t\t\t\tHere is his initial ECG:<\/p>\n \t\t\t\t<\/a> \u00a0<\/p>\n A 56 yo f with h\/o HTN and hypercholesterolemia called EMS from home after onset of L chest pain radiating to the left arm. Before EMS arrived, she had “seizure activity” and became unresponsive. She was defibrillated successfully from ventricular fibrillation and developed a perfusing rhythm. She was intubated. She arrived comatose and in cardiogenic shock and the following ECG was recorded.<\/p>\n <\/p>\n <\/a>There is a bradycardic rhythm of uncertain etiology, possibly a sinus pause with escape, and occasional PVCs.<\/p>\n There is ST elevation in II, III, and aVF, but also ST elevation in V1, but also in V2 and V3. This is diagnostic of Right ventricular MI. RVMI that has ST elevation in V1 all the way to V3 is referred to as “pseudoanteroseptal MI,” and is distinguished from LAD anterior MI by the inferior ST elevation (although a “wraparound” LAD can do this) and by the fact that there is more ST elevation in V1 than in V4. That this is an RVMI is confirmed with the following right sided ECG:<\/p>\n <\/a> She was bradycardic and hypotensive. Normal saline bolus was given, with improvement in BP. . She underwent therapeutic hypothermia, and emerged from coma. There was a comment with a couple inaccurate statements:<\/p>\n 1) “In RVMI, you normally see STE in lead III higher than II, and normally you’d see ST depression in V1-V3…”<\/p>\n RVMI is always a result of RCA occlusion, and it is true that STE in lead III is usually higher than in lead II in RCA (as opposed to circumflex) occlusion, as seen here.<\/p>\n ST depression in V1-V3 is only present if the RCA has branches to the posterior wall, which happens < 50% of the time.<\/p>\n When there is concomitant RVMI and posterior MI, ST segment in V1 may be either elevated or depressed, depending on which dominates.<\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \t \t \tfrom\u00a0Dr. \tSmith’s ECG Blog<\/a>\u00a0by\u00a0Steve \tSmith \tA 74 yo f with ESRD on dialysis and h\/o CAD bumped her access fistula and \tbegan to bleed profusely. She had a prehospital BP of 60, pulse 70, and this \tremained the same in the ED. The bleeding was controlled. She was \tasymptomatic. Hgb was 10 and fluids were given, and the BP rose to 80 \tsystolic. An ECG was recorded (below, 1st ECG):<\/p>\n \t<\/a>\u00a0This \tshows sinus rhythm with LVH and typical LVH repolarization abnormalities, \twith no evidence of acute ischemia. QTc = 440 ms. \t\t \t\t<\/a>\u00a0. \t\t\t \t\t\t<\/a>\u00a0. There is 2-3 mm of ST elevation in leads V2-V4, and also ST elevation in V5, V6, I, II, and aVL. However, the ST elevation in anterior leads looks very much like early repolarization. I have derived and validated a 3 part rule to differentiate early repol from acute LAD occlusion (paper submitted). If 2 of the following 3 questions are answered “yes”, then it is MI with an accuracy of about 85%: 1) is the QTc > 392 ms? (here, yes) 2) Is the ST elevation at 60 ms after the J-point in lead V4 > 2mm (here, yes) 3) Is the R-wave in V4 < 13 mm (here, no). So by this rule, the ECG leans toward acute LAD occlusion. <\/p>\n \u00a0<\/p>\n \u00a0<\/p>\n \t \t \tAn 80 yo male presented with chest pain.<\/p>\n \t<\/a> \t.<\/span>\u00a0<\/span><\/h2>\n
<\/span>\u00a0<\/span><\/h2>\n
<\/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
\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\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\n
<\/span> \t\t\t\t\t\t \t\t\t\t\t\tRight Bundle Branch Block with Acute ST Elevation Seen \t\t\t\t\t\tBest on Prehospital ECG<\/a><\/span><\/h3>\n
\t\t\t\t\t\t\t\t\tThe ST elevation has mostly resolved on this \t\t\t\t\t\t\t\t\tECG, and were it not for the arrest and the \t\t\t\t\t\t\t\t\tprehospital ECG, this would not be a slam \t\t\t\t\t\t\t\t\tdunk diagnosis. There is still ST elevation \t\t\t\t\t\t\t\t\tin I and aVL, but it is subtle. There are \t\t\t\t\t\t\t\t\tabnormal T waves in V2-V4, with \t\t\t\t\t\t\t\t\tstraightening of the ST segment which is \t\t\t\t\t\t\t\t\ttypical of hyperacute T waves.<\/p>\n\n
<\/span> \t\t\t\t\t\t \t\t\t\t\t\tElderly With No Symptoms, Wellens’s Thus Overlooked, \t\t\t\t\t\tThen ST Elevation Doubted<\/a><\/span><\/h3>\n
\t\t\t\t\t\t\t\t\tShe is admitted, her trop peaks at 0.23, her \t\t\t\t\t\t\t\t\tnext day EKG done 8 hours later is shown \t\t\t\t\t\t\t\t\tbelow (#2) \t\t\t\t\t\t\t\t\tand shows some terminal T inversion in V3, \t\t\t\t\t\t\t\t\tconsistent with the positive trop and \t\t\t\t\t\t\t\t\tsuggesting tight LAD occlusion but open \t\t\t\t\t\t\t\t\tartery (T inversions are “reperfusion T \t\t\t\t\t\t\t\t\twaves; an inverted T wave is a sign of an \t\t\t\t\t\t\t\t\topen artery and an upright T wave is a sign \t\t\t\t\t\t\t\t\tof occlusion or re-occlusion). Echo the next \t\t\t\t\t\t\t\t\tday is normal. She is diagnosed with “demand \t\t\t\t\t\t\t\t\tischemia” and discharged home.<\/p>\n
\t\t\t\t\t\t\t\t\tNow the ST elevation is unmistakable, even \t\t\t\t\t\t\t\t\twith the persistently inverted T waves. But \t\t\t\t\t\t\t\t\tbecause the patient was asymptomatic, the \t\t\t\t\t\t\t\t\tcath lab was not yet activated. A bedside \t\t\t\t\t\t\t\t\techo suggested anterior wall motion \t\t\t\t\t\t\t\t\tabnormality.<\/p>\n
\t\t\t\t\t\t\t\t\tThis shows even more ST elevation. The \t\t\t\t\t\t\t\t\tpatient was still asymptomatic. An initial \t\t\t\t\t\t\t\t\ttroponin returned at 12 ng\/ml. The cath lab \t\t\t\t\t\t\t\t\twas activated. There was a ruptured plaque \t\t\t\t\t\t\t\t\twith thrombus in the LAD, with some flow \t\t\t\t\t\t\t\t\tstill (accounting for the inverted T waves).<\/p>\n\n
<\/span> \t\t\t\t\t\t \t\t\t\t\t\tHyperacute T waves<\/a><\/span><\/h3>\n
<\/span> Pure (Isolated) Posterior STEMI — not so rare, but often ignored!<\/a><\/span><\/h3>\n
\t\t\t<\/a>#2, \t\t\tbaseline from 3 months prior
\t\t\t<\/a>#1 \t\t\tshows new marked ST depression in V2 and V3.<\/p>\n
\t\t\tThe patient had rapid PCI of a 100% acutely thrombotically occluded \t\t\tmid circumflex which was opened and stented. There was 3 vessel \t\t\tdisease.<\/p>\n<\/span> Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)???<\/a><\/span><\/h3>\n
\t\tThere is 1 mm of ST elevation in V2 and V3, so this meets the criteria \t\tfor reperfusion by the ACC\/AHA guidelines. Unfortunately, the majority \t\tof patients who meet such “criteria” do not have MI. The most common \t\treason for ST elevation is early repolarization.<\/p>\n3 comments: <\/h4>\n
\n
<\/span>Wednesday, August 26, 2009<\/span><\/h2>\n
<\/span> \t \tPersistent ST elevation after previous MI, otherwise known as “LV aneurysm” \tmorphology<\/a> <\/span><\/h3>\n
<\/span>Wednesday, August 26, 2009<\/span><\/h2>\n
<\/span> \t \tInferior Hyperacute T-waves<\/a> <\/span><\/h3>\n
<\/span> \t\t \t\tComment on Posterior STEMI<\/a><\/span><\/h2>\n
\t\t\t\t\t\t2) Matetzky S et al. Significance of ST segment \t\t\t\t\t\televations in posterior chest leads (V7-V9) in patients \t\t\t\t\t\twith acute inferior myocardial infarction: application \t\t\t\t\t\tfor thrombolytic therapy. JACC 1998;31 506-11.
\t\t\t\t\t\t3) Wung SF et al. New electrocardiographic criteria for \t\t\t\t\t\tposterior wall acute myocardial ischemia validated by a \t\t\t\t\t\tpercutaneous transluminal coronary angioplasty model of \t\t\t\t\t\tacute myocardial infarction. Am J Cardiol 2001;87:970-4; \t\t\t\t\t\tA4.<\/p>\n<\/span> \t\t\t\t\t\t \t\t\t\t\t\tPseudonormalization of T waves, Coronary occlusion \t\t\t\t\t\twithout 1 mm ST elevation<\/a> <\/span><\/h3>\n
\t\t\t\t\t\t\tNotice there is deep symmetric T inversions in \t\t\t\t\t\t\tinferior leads, and a large upright T wave in aVL. \t\t\t\t\t\t\tThere is also some T inversion laterally. This is \t\t\t\t\t\t\tall suggestive of inferior (and lateral?) Non-STEMI, \t\t\t\t\t\t\tdue to reperfused RCA or circ. Inverted T waves are \t\t\t\t\t\t\talso known as “reperfusion” T-waves. If they are in \t\t\t\t\t\t\tthe anterior leads, they are often referred to as “Wellens’ \t\t\t\t\t\t\tT-waves.”<\/p>\n<\/span> Deep and widespread ST depression signifies high risk coronary lesion<\/a> <\/span><\/h3>\n
\tThere is ST depression, greater than 3 mm in some leads<\/strong>, in \tI-III, aVF, and V3-V6. aVR also has ST elevation.<\/p>\n
\n<\/span> Coronary occlusion need not have 1 mm ST elevation; often it does not<\/a> <\/span><\/h3>\n
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\n<\/span> Inferior ST depression in ACS is reciprocal to ST elevation in aVL<\/a><\/span><\/h2>\n
\t\t\t\t\tNotice there is ST segment depression in II, III, and aVF. \t\t\t\t\tThe QRS is normal, so any ST segment abnormality cannot be \t\t\t\t\tblamed on the QRS (i.e., ST depression is “primary”, not \t\t\t\t\t“secondary,” and the ddx of this is ischemia, hypokalemia, \t\t\t\t\tdigoxin, and normal variant). The ST depression is somewhat \t\t\t\t\t“scooped” in appearance, suggesting hypoK or digoxin, but \t\t\t\t\tthe QTc is 423 ms, so hypokalemia is unlikely (usually > 450 \t\t\t\t\tms) and the patient was not taking Digoxin. \t\t\t\t
\t\t\t\t \t\t\t\t \t\t\t\t\tST depression of subendocardial ischemia does not \t\t\t\t\t“localize”. That is to say, for example, that “inferior” ST \t\t\t\t\tdepression does not represent inferior subendocardial \t\t\t\t\tischemia. When there is inferior ST depression from \t\t\t\t\tischemia, it is invariably reciprocal<\/strong> to ST \t\t\t\t\televation in aVL (i.e., the high lateral wall). So if we \t\t\t\t\tlook at aVL, there is indeed some ST elevation, about 0.5 \t\t\t\t\tmm. This is actually a significant amount of ST elevation \t\t\t\t\tbecause the R-wave is only 2 mm, and this is common in aVL. \t\t\t\t
\t\t\t\t \t\t\t\t \t\t\t\t\tFurthermore, there is subtle ST depression in lead V3 (0.5 \t\t\t\t\tmm). There should NEVER be ST depression in leads V2 and V3, \t\t\t\t\tthere is usually some amount of ST elevation. 0.5 mm of ST \t\t\t\t\tdepression is likely to be 1.0-1.5 mm of relative<\/em> \t\t\t\t\tST depression. \t\t\t\t
\t\t\t\t \t\t\t\t \t\t\t\t\tA colleague showed me this and I said that, because there is \t\t\t\t\tST elevation in aVL and ST depression in V3, it is probably \t\t\t\t\tan obtuse marginal (OM) branch (of the circumflex) or \t\t\t\t\tnear-occlusion. \t\t\t\t
\t\t\t\t \t\t\t\t \t\t\t\t\tAppropriate management is to treat maximally for ischemia \t\t\t\t\twith ASA, heparin or enoxaparin (depending on institutional \t\t\t\t\tpreference), clopidogrel if institutionally acceptable and \t\t\t\t\tepitifibatide if not. If the pain does not<\/em><\/strong> \t\t\t\t\tresolve, go urgently to the cath lab. If the pain and ECG \t\t\t\t\tfindings resolve, then next day cath is acceptable. \t\t\t\t \t\t\t\t \t\t\t\t
\t\t\t\t\tThe patient had initial symptom control and was put in the \t\t\t\t\tICU, but symptoms recurred and were refractory, so he was \t\t\t\t\ttaken urgently to cath and was found to have ACS of the \t\t\t\t\tsaphenous vein graft to the obtuse marginal. This was \t\t\t\t\tstented, and flow was TIMI-III after the procedure. \t\t\t\t\tPre-procedure flow was not documented, but pain was resolved \t\t\t\t\tafterwards. Troponin I peaked at 8.5 ng\/ml. Post-procedure \t\t\t\t\tECG showed prominent T-wave inversion in aVL (analogous to \t\t\t\t\tWellens’ T-waves in the anterior leads). Notice the ST \t\t\t\t\tdepression in V3 is gone, but the ST elevation in aVL is \t\t\t\t\tmore pronounced, as is the reciprocal ST depression. \t\t\t\t
\t\t \t <\/p>\n
Now it can be seen that most of the precordial ST elevation is in V4R, much more than is present on the left side of the heart (V1R, which is equivalent to V2 on the left sided ECG.<\/p>\n
Pressors were required, and the patient was transported to the cath lab with a door to balloon time of 60 minutes, where a proximal dominant RCA occlusion was opened and stented.<\/p>\n
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She awoke and was discharged to home with no disability<\/p>\n\n
<\/span> Cardiac Arrest suddenly after blood loss, is it due to MI? Also, when the rhythm looks like torsade, it is usually not.<\/a><\/span><\/h2>\n
\t.
\tSuddenly she became bradycardic and lost pulses. CPR was begun. She was \tgiven atropine 1 mg, Epi 1 mg, and Calcium chloride 1 “amp”. Moments later, \tthis rhythm was recorded:<\/p>\n
\t\tThis shows polymorphic ventricular tachycardia or ventricular \t\tfibrillation. There appear to be “turning of the points,” but torsade de \t\tpointes can only be diagnosed in the presence of a long QT on the \t\tpreceding ECG. Polymorphic v tach\u00a0may<\/strong><\/em>\u00a0be \t\ttorsade, but we know this case is not because the previous QTc was 440 \t\tms. Torsade would be due to one set of circumstances (electrolytes, \t\tcongenital, drugs). More commonly, however this polymorphic v tach is\u00a0NOT<\/em><\/strong>\u00a0torsade; \t\tin fact, ventricular fibrillation looks like this as well. In the case \t\tof v fib or non-torsade polymorphic v tach, the most likely etiology is \t\tischemia. \t \t\t. \t \t\tSo this 12-lead was recorded:
\t\t.<\/p>\n
\t\t\tThis shows Left Bundle Branch Block (new), with concordant ST \t\t\televation in II, III, aVF, V5 and V6, and also concordant ST \t\t\tdepression in V2. This is diagnostic for transmural ischemia of the \t\t\tinfero-postero-lateral wall. This explains the cardiac arrest. \t\t \t\t\t. \t\t \t\t\tNotice also the PVC (1st complex in V1, V2 and V3). It shows \t\t\tdiscordant ST depression that is EXCESSIVELY discordant. Thus, it is \t\t\ta PVC complex that reveals posterior STEMI. \t\t \t\t\t. \t\t \t\t\tIs this transmural ischemia due to hypotension from fluid loss? \t\t\tUnlikely, because the previous ECG, taken after quite a period of \t\t\thypotension, showed no ischemia. \t\t \t\t\t. \t\t \t\t\tIs this due to ACS (plaque rupture with MI)? It seems unlikely only \t\t\tbecause it would be a coincidence. \t\t \t\t\t. \t\t \t\t\tThe bleeding from the fistula has stopped. It is controlled. There \t\t\tis no risk now that it will bleed if anticoagulants and antiplatelet \t\t\tagents are given. \t\t \t\t\t. \t\t \t\t\tThe patient should go immediately to the cath lab. \t\t \t\t\t. \t\t \t\t\tIt seemed incredible to the physicians caring for the patient that \t\t\tshe could be having an acute MI, and the LBBB confused them as well, \t\t\tso that there was some delay in cath lab activation, during which \t\t\ttime a much more obvious ECG was recorded and an echocardiogram \t\t\tconfirmed what an astute electrocardiographer would already know: \t\t\tthere were new wall motion abnormalities. \t\t \t\t\t. \t\t \t\t\tAt cath, an occluded circumflex was found and stented. \t <\/p>\n<\/span> Dr. Smith’s Rule to differentiate BER from LAD occlusion<\/span><\/h2>\n
<\/span> LAD occlusion in the setting of paced rhythm<\/a> <\/span><\/h3>\n
\t<\/a>There is clearly a ventricular paced rhythm. Normally in a paced rhythm, \tthe QRS is usually all negative from V1-V6 because the pacing wire is in the \tapex of the RV and thus all depolarization goes away from the apex.<\/p>\n
\tIn the above ECG, the QRS in V2 is positive and all others are negative, as \tin the patient’s previous ECG below. This implies some problem with lead \tplacement. Nevertheless, leads V1, V3, and V4 have excessively discordant ST \tsegments.
\t.
\tThough there is not a lot of data to support it, the ratio used for left \tbundle branch block seem to be applicable to paced rhythm. An ST\/S ratio in \tV1-V4 > 0.20 I believe to be quite specific for LAD occlusion. V2, though \tsuspect because of the positive QRS, has a concordant ST segment, which is \tdiagnostic of STEMI.<\/p>\n