EKG in the Chest Pain Patient
qR waves can develop instantly and are not indicative of a patient who will not benefit from lytics or PCI (J Am Coll Cardiol 1995;25:1084); should not be applicable to a QS pattern.
Jayroe JB, Spodick DH, Nikus K, et al. Differentiating ST elevation myocardial infarction and nonischemic causes of ST elevation by analyzing the presenting electrocardiogram. Am J Cardiol 2009;103:301-306. Take home is electrocardiography cardiologists were not that great either.
Use 15 lead-V8 mid scapular, V9 paraspinal, V4R
How to Measure QT Interval
If there is a q-wave, it is not early repol
If you want a rule, I derived one a few years ago (AJEM 23(3):279-287; May 2005). Comparing proven acute LAD occlusion to patients with proven old MI and diastolic dysfunction and ST elevation, I found that the T/QRS ratio in any one of leads V1-V4 was almost always higher than 0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude (V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22. The only acute MI’s missed by this rule had at least 6 hours since symptoms onset.
Measuring ST elevation: >1 mm measured .08 (2 boxes) from j point compared to T-P as baseline or PR to J Point in 2 contiguous leads.
<2mm elevation in leads V1-V4 is borderline but can definitely indicate MI
LAD First Diagonal Branch (D1)
The pattern of ST elevation in I and aVL and V2 (also usually with some ST depression in V3-V5) has been described as a “Midanterolateral MI” (see article below) due to occlusion of the first diagonal (branch of the LAD, also known as D1, or LADD1) artery. The D1 branches off from the LAD to the lateral wall and may also supply some of the anterior wall.
In this case, as time and ischemia progressed, this became a full anterolateral MI, but the infarct-related artery was indeed a very large LAD D1. It was rapidly treated and the maximum troponin was low, but there was an anterolateral wall motion abnormality on Echo.
Isolated mid-anterior myocardial infarction: a special electrocardiographic sub-type of acute myocardial infarction consisting of ST-elevation in non-consecutive leads and two different morphologic types of ST-depression
Sclarovsky S. International Journal of Cardiology. Volume 46, Issue 1, August 1994, Pages 37–47
We describe eight patients with a distinct electrocardiographic pattern of anterior wall myocardial infarction characterized by three main features: (1) a pattern of ‘transmural ischemia’ (ST-elevation with positive T-wave) in nonconsecutive leads: aVL and V2, and two different types of ST-depression; (2) a pattern of ‘true reciprocal changes’ (ST-depression and negative T-wave) in III and aVF; (3) a pattern of ‘sub-endocardial ischemia’ (ST-depression with positive T-wave) in V4–5, while ST in V3 was either isoelectric or depressed. We characterize the electrocardiographic features and correlate them with the echocardiographic, radionuclide, and angiographic data. All patients admitted to the coronary care unit from January 1990 to April 1992 with evolving acute myocardial infarction were evaluated prospectively. Patients whose admission electrocardiogram met the description above were included. The electrocardiographic evolution, echocardiographic, Technetium MIBI tomography, and coronary angiography are described. Of 471 patients with acute anterior wall myocardial infarction, admitted to the coronary care unit during the study period, eight patients met the inclusion criteria (1.7% of acute anterior wall myocardial infarction). Echocardiographyic studies revealed mid-anterior hypokinesis in two patients, anterior and apical hypokinesis in one, and no wall motion abnormality in four patients. Technetium MIBI tomography, done in five patients, was consistent with mid-anterior or mid-anterolateral infarction without involvement of the septum or apex. Coronary angiography, performed in seven patients, demonstrated significant obstruction of the first diagonal branch in all of the patients. In four patients, the diagonal occlusion was the only significant coronary lesion in the left coronary artery. Conclusion: Most of the anterior myocardial infarctions also involve the septal and apical regions. Anterior wall myocardial infarctions limited to the mid-anterior or mid-anterolateral wall, without apical or septal wall involvement are relatively rare. This study describes a special electrocardiographic form of anterior wall acute myocardial infarction. This distinct electrocardiographic pattern represents true mid-anterior wall myocardial infarction, caused by occlusion of a first diagonal branch of the left anterior descending coronary artery. The septal and apical regions are not involved because the blood supply via the left anterior descending artery is not interrupted.
[From Steve Smith EKG Blog]
Acute MI from LAD occlusion, or early repolarization?
By Steve Smith
3 hours of chest pain. Is it STEMI or is it normal (or early repolarization)? This looks quite normal, with only moderate ST elevation, upward concavity, good R-wave amplitude, no ST depression or T-wave inversion. But one characteristic makes it unlikely to be normal: the computerized QTc is 455 milliseconds. In a study of early repolarization (ER) (n=167) near completion, only 2 of 167 (2%) cases of ER had a QTc > 455. The mean QTc was 394, compared to 420 for MI (n=125) from LAD occlusion. Conversely, only 4% of LAD occlusion, vs. 40% of ER, had a QTc For a reason unknown to me, this ECG cannot be clicked on and enlarged. Try clicking here and then going to image 11 of 12: http://picasaweb.google.com/smith253/DrSmithSECGBlog?authkey=RN1TG4WLAJA#5286371879749456434 Note that now there are tiny Q-waves in V2-V4, making this unequivocally diagnostic of acute STEMI. These subtle Q-waves were not appreciated, but the clinicians were astute and ordered a stat echocardiogram, which confirmed anterior wall motion abnormality. The patient was taken to the cath lab and had a 100% LAD occlusion.After reperfusion, the patients baseline ST-T complex was revealed. This is probably what they would have looked like prior to the LAD occlusion: For those who want some more detail on differentiating ER from MI, see below:Also useful was the mean (from V2-V4) R-wave amplitude, at a cutoff of 5 mm, with values less than 5 mm likely to represent MI. Interestingly, mean ST elevation (no matter how it was measured) was not as good a differentiator as the mean R-wave amplitude, but if mean R-wave was less than 5 mm OR the mean ST elevation (V2-V4, as measured at the J-point, STEJ) was greater than or equal to 2 mm, then it was very likely to be MI and very unlikely to be ER.Even better was a formula derived with logistic regression, which also included the QTc : (1.553 x mean STEJ in mm) + (0.0546 x computerized QTc in milliseconds) – (0.3813 x mean RA in mm)If the value of the formula is greater than or equal to 21, it is MI (Sens, spec, & accuracy of 92%, 79%, and 85%); if less, then ER.For the first ECG, STEJ = 1.17, QTc = 455, and Mean R = 11.5, so: (1.553 x 1.17) + (0.0546 x 455) – ( 0.3813 x 11.5) = 22.27 (>21). 22.27 is very close to 21, further illustrating that this EKG is very difficult.
Most recent publication validating his approach was just published in the Annals
([1.196 x STsegment elevation 60 ms after the J point in lead V3 in mm][0.059 x QTc in ms]–[0.326 x R-wave amplitude in lead V4 in mm]) is greater than 23.4 predicted STEMI and if less than or equal to 23.4, it predicted early repolarization in both groups, with overall sensitivity, specificity, and accuracy of 86% (95% confidence interval [CI] 79, 91), 91% (95% CI 85, 95), and 88% (95% CI 84, 92), respectively, with positive likelihood ratio 9.2 (95% CI 8.5 to 10) and negative likelihood ratio 0.1 (95% CI 0.08 to 0.3). (Ann Emerg Med 2012;60:45)
Reciprocal ST depressions
make any st elevation much more likely to represent AMI. From reflections of infarcted area or ischemia.
Hyperacute T Waves
hyperkalemia or ami (often broad based and asymmetric as opposed to t of hyper-k which is symmetric and needle-like)
PVCs should have discordant ST, if concordant, suspect AMI
V3: Almost any
V4: If more than 1 mm deep or larger than Q in V5 or > .02 sec wide (0.5 mm)
aVL: >.04 sec or >50% amplitude of the QRS
III: Q wave >0.04 sec, depth in this lead is not important
R waves should increase in amplitude from V1-V4, if not abnormal R wave progression
Rs should be >3mm by V3
Abnormal Q waves usually develop within 8 to 12 up to 24 to 48 hours after the onset of symptoms. Abnormal Q waves are at least 30 msec wide and 0.20 mV deep in at least two leads from the combinations listed.
According to the new criteria, an abnormal Q wave was any Q wave in leads V1 to V3 or a Q wave 30 msec in leads I, II, aVL, aVF, or V4 to V6; the Q wave must be present in any two contiguous leads and 1 mm in depth. (See “Diagnosis of an acute myocardial infarction”).
Inferior Wall MI
Five Criteria to differentiate between RCA and L Circumflex
ST segment elevation in I=LCx
ST segment more elevated in II than III=LCx
ST segment elevation in aVR=RCA, depression >1 mm=LCX
ST elevation in V4R=RCA, depression=LCx
ST elevation in V1 with ST depression in V2, Depression in both=LCx
(Chest 122:1, 2002, p.134)
Be extremely wary of labeling STE in the inferior leads as benign. Even with concave up morphology, this can represent AMI. BER is not normally seen in this leads in isolation.
Steve Smith’s group showed if there is AVL depression, then it is NEVER BER in inferior leads (Bischof J. Thompson RP. Tikkanen J. Porthan K. Huikuri H. Salomaa V. Smith SW. ST-segment depression in lead aVL differentiates benign ST elevation from inferior Acute STEMI. ACEP Research Forum 2012. Annals of Emergency Medicine 60(4 Suppl):S8-S9; October 2012.)
Right Ventricular MI
Robalino et al. found that STE greater than 1 mm in V4R has 100% sensitivity, 87% specificity, and 92% predictive accuracy in detecting acute infarction of the RV resulting from occlusion of the right coronary artery above its first ventricular branch. Has higher mortality and morbidity than inferior MI alone.
If inferior wall MI, if the greatest st elevation is in III, consider right-sided. also st elev in V1
any new ST elevation in the lateral leads should be intervened or lysed as often there will not be >1 mm elevation., also since sometimes aVL will be the only lead affected, there is not the normal requirement of two contiguous leads.
Posterior Wall MI
From descending RCA or L circumflex, so suspect in inferior or lateral wall MI
ST Seg depression in V1-V3, or Prominent Positive T
R/S ratio >1 in lead V2
V7-V9 c > 1 mm ST elevation
The precordial ST depression of PMI has a relatively horizontal morphology rather than downsloping ST depression, which is more suggestive of of anterior ischemia. Most PMIs occur in the presence of inferior or lateral MI (Am J EM, 10/07, pg. 966).
Up to 0.5 mm is within normal limits, but any amount in even one lead >/= 0.5 is abnormal and very sensitive and specific for posterior STEMI (Matetzky S. et al. JACC 1998;31:506-511. Matetzky S et al. JACC 1999;34:748-753. Taha B et al. J Electrocardiol 1998;31(Suppl):178-9. Wung SF et al. Am J Cardiol 2001;87:970-974;A4. (From Dr. Smith’s Blog)
From Dr. Smith:
from Dr. Smith’s ECG Blog by Steve Smith There are many studies that indirectly reveal that the percent of STEMIs that are isolated posterior is between 3 and 11% (about 8%). More recently, a substudy of the recent TRITON-TIMI 38 trial comparing Prasugrel to Clopidogrel for ACS enrolled 13,608 patients; 1198 had isolated ST depression in V1-V6. Of these, 314 (26%) had occlusion (TIMI 0 or 1 flow) of the infarct-related artery (i.e., STEMI).There were 3534 other STEMIs in this study, not including the 314 with ST depression only (posterior STEMI). Add these 314 to the 3534 and you have 314/3848 (8.1%) of STEMI have pure isolated posterior STEMI. This conforms with the previous smaller studies. Moreover, the cath was done a median of 29.4 hours after presentation, so this does not account for those arteries that spontaneously reperfused (about 25% of STEMI will reperfuse with antiplatelet and antithrombotic therapy alone within one day — old data). Thus, there were probably even more occluded arteries.Only 14/314 (4.5%) were interpreted by the investigator as STEMI. None of the patients with an occluded artery had an ECG to PCI time <6 hours.This is not a “rare” event. (From Stephen Smith EKG Blog)The 12-lead ECG, without the posterior leads, is so clearly due to posterior STEMI that in spite of negative posterior leads, I was certain that this was posterolateral STEMI because:
1) nothing else causes ST depression in II, III, aVF and in right precordial leads greater than left precordial leads
2) high pretest probability for STEMI (chest pain followed by cardiac arrest)
–Nearly half of all ventricular fib arrests are due to STEMI
–MI is nearly certain if arrest preceded by chest pain
–Non STEMI can of course also cause ventricular fibrillation, but not nearly as commonly.
An academic note on terminology of posterior MI: Bayes de Luna determined by MRI that what was thought to be posterior MI as manifested by enlarged R-waves in V1-V3 is really “lateral.” One Society changed the terminology; here is the article:
Sinus rhythm with a slightly prolonged QRS, but not bundle branch block. There is ST depression in V2-V4, maximal in V3. There is also ST depression in II, III, and aVF. This should always alert to ST elevation in aVL, and, sure enough, aVL has minimal ST elevation.
This is diagnostic of posterolateral STEMI. When precordial ST depression is maximal in V1-V3, in contrast to V4-V6, then posterior infarct is the usual etiology. As stated many times in this blog, high lateral STEMI may show itself primarily through “inferior” reciprocal ST depression. On the contrary, with ST depression in II, III, aVF and also in precordial leads but maximal in V4-V6, then subendocardial ischemia is fairly certain, often accompanied by ST elevation in aVR. In such cases (not this one!), the “inferior” ST depression is not reciprocal to ST elevation. A consulting cardiologist requested posterior leads, but these showed no ST elevation (not shown). Nevertheless, the patient was taken to the cath lab and found to have a 100% acutely occluded obtuse marginal off the circumflex supplying the posterior and lateral walls.
Left Main Disease
Left main = ST-depression = 1 mm in 6 or more leads
Lead aVRwith ST-elevation=1mm
ST-elevation in lead aVR =V1
st elevations are highest in V2-V3 (can be seen in V1 and V4 as well, sometimes inferior) usually <3.5 mm
are upwardly concave
show j-point elevation
rarely occur with low voltage QRS are rarely greater than 1 mm in the lateral precordium (V5, V6)
seldom >2mm in pts >45 y/o
are not seen in aVL
STE c widespread distribution. Notching or slurring of the qrs (J wave, fishhook appearance)
Symmetric, concordant large t waves
Not BER actually MI
Steve Smith’s Annals Article
Wide S in I, aVL, and/or V6
Delayed intrinsicoid deflection >40-50 ms
RSR’ in V1 with the r prime>r or qR
V1-V6 usually with STE and T wave depressions which are discordant, if concordant, suspect AMI
Measure QRS duration in a lead where it is clear, use this to find the ST segment in other leads, compare this to the TP segment
Mattu-V1-3 should have st depression, the rest should be isoelectric
Left axis deviation
Deep S in the inferior leads
Small Q waves in I and aVL, small R in II, III, aVF
Late intrinsicoid deflection in aVL
Increased QRS Voltage in the limb leads
No ST elevation
If seen with RBBB then it is a bifasicular block
Right Axis Deviation
Narrow Q in inferior leads
Narrow R in aVL followed by a wide S
No ST elevation
Best article for the next three: Emerg Med Clin N Am 2005;23:999
wide, monophasic R in I, avL, V5 and V6
Delayed Intrinsicoid Deflection in V5-6 >40 ms
rS or QS in V1
Discordant ST deviation and T wave inversion
The Sgarbossa Clinical Decision Rule for the ECG Diagnosis of AMI with LBBB. The electrocardiographic criteria suggesting a diagnosis of AMI according to Sgarbossa et al include the following:
A, STE elevation greater than 1 millimeter, which is concordant with the QRS complex (score of 5);
B, STD greater than 1 millimeter in leads V1 , V2 , or V3 (score of 3); and
C, STE greater than 5 millimeters, which is discordant with the QRS complex (score of 2).
A total score of 3 or more suggests that the patient is likely experiencing an acute infarction based on the electrocardiographic criteria. With a score less than 3, the electrocardiographic diagnosis is less assured, requiring additional evaluation.
lack of association between LBBB and AMI (AJEM 2009;27:916)
Most patients with possible MI with new or presumably new LBBB do not have MI. Concordant ECG changes were an important predictor of MI and death. Current guidelines regarding early reperfusion therapy for patients with LBBB should be reconsidered. (Am Heart J 2011;161:698-704.)
usually right paced producing LBBB. Appropriate discordance to terminal portion of the QRS (ie. If terminal portion positive, should get st depressions.)
T waves should also be discordant
QRS must be less than 120 ms in isolated LVH
R in I + S in III >25 mm
R in aVL > 11 mm
R in aVF >20 mm
S in aVR >14 mm
R in V5 or V6 > 25 mm
R in V5 or V6 plus S in V1 >35 mm
Largest R plus Largest S >45 mm
poor r wave progression, discordant changes
right to mid precordium should have discordant ST elev
Lateral leads usually have st depression and t-wave inversion
Stage I-STE Stage II-resolution
Stage III-T wave inversion
Stage IV-return to normal
Pr seg depression. None in AVR, best seen in V5, V6 and inf leads
no reciprocal changes may be seen
MI or Pericarditis? (EMEDHome) Distinguishing between acute MI and acute pericarditis can, at times, be challenging. In myocardial infarction caused by occlusive thrombus, ST-segment elevations are typically convex in shape and occur in a localized anatomical distribution; widespread ST-segment elevations across the precordial and limb leads, as well as upward concave ST segments and PR-segment depression is highly characteristic of pericarditis. On occasion, however, the EKG may not be completely classic for MI or pericarditis. The clinician should be aware that the ratio of the ST-segment elevation (in millimeters) to T-wave amplitude (in millimeters) in excess of 0.24 in lead V6 strongly supports the diagnosis of pericarditis and this finding has been shown to reliably distinguish pericarditis from other repolarization abnormalities (1,2).References: (1) Lewis GD, et al. Case records of the Massachusetts General Hospital. Case 8-2007. A 48-year-old man with chest pain followed by cardiac arrest N Engl J Med 2007;356: 1153-62. (2) Ginzton LE, Laks MM. The differential diagnosis of acute pericarditis from the normal variant: new electrocardiographic criteria Circulation 1982;65:1004-1009.
Left Ventricular Aneurysm
Bulges outwards during systole and diastole. Gives persistent STE
most common in V1-V3
always <4 mm
relatively static when compared to old ekgs
should have deep Qs in the same leads
deep t wave inversion
Prominent U waves
(Bundle of Kent)-Short PRI, Wide QRS, Delta wave
angina with t-wave inversion from V2-V4
Wellens’ Syndrome (from EMEDhome.com)The Emergency Physician must be familiar with the characteristic changes of Wellens’ Syndrome, first described in 1982 and recognized to represent a critical stenosis of the proximal left anterior descending artery. This entity is manifested by characteristic biphasic or inverted T waves in V2 and V3 and is a marker for a critical stenosis high in the left anterior descending artery. Patients exhibiting Wellens’ T-wave changes are at a high risk for the development of an extensive anterior wall MI. This is a subgroup of patients who do poorly with conservative management, even though initially they seem to respond well to treatment. Two variants of the Wellens’ Syndrome exist. The figure below is from the original paper published by Wellens and colleagues.
click to enlargeReprinted with permission from de Zwaan C, Bar FW, Janssen JH, et .al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J 1989; 117: pg. 731On the right, is the more common, more dramatic variant manifested by deeply inverted T waves often extending to leads V4 and V5. On the left, is the less common pattern which is much more subtle. This is the pattern exhibited on the EKG of the previous page, and the one often underappreciated by clinicians. The T waves have a characteristic upsloping then sharply downsloping pattern leading to a symmetric T-wave inversion in leads V2 and V3 (and on occasion V4). Wellens’ changes are not uncommon. In the original description, of 145 consecutive patients admitted with unstable angina, 18% exhibited this pattern (1). The EKG abnormalities – the mechanism of which remains unclear -usually occur when the patient is pain-free and when other evidence of ischemia or unstable angina may be absent. The importance for the Emergency Physician is to recognize that the patient exhibiting Wellens’ changes is at high risk and should undergo urgent angiography as exercise stress tests are relatively contraindicated in the presence of left-main lesions. It is incumbent upon the Emergency Physician to avoid the following pitfalls when confronted with this entity: • Discharge the patient home for follow up after “ruling out” for a myocardial infarction in a short stay/observation unit. The patient should undergo timely aniography and a strong case can be made that this should be done upon recognition of the changes, not at a later date given the high risk for development of an extensive anterior MI. • Arrange for exercise stress test for evaluation of the patient’s coronary arteries. Although such evaluation is usually done by a cardiologist, the increased use of observation units often places this responsibility in the hands of the EP. Again, exercise stress testing is relatively contraindicated. These patients fare poorly with medical management and often require surgical intervention. • Interpret the T-wave changes as “non-specific ST-T changes” and not appreciate that the patient is at high risk.
Below is an example of true Wellens’. Wellens’ occurs when an area of STEMI (which goes unrecorded by an EKG) gets reperfused. You’re seeing the after effects of an occlusion which is now reperfused. The T inversions are also called “reperfusion T waves” because they happen after therapeutic Reperfusion therapy for STEMI. In the case of Wellens’, there was no EKG recorded at the time of occlusion. The first EKG was only recorded after the perfusion restored itself spontaneously and the pain resolved. That is why EVERY PATIENT in the Wellens’ studies was pain free at the time of the EKG AND had either an open artery or collateral flow.
This is Wellens’ Type A (terminal T wave inversion). Type A will evolve into Type B (deep symmetric T wave inversion) over hours. If it does not evolve or resolve, it is not Wellens’. (Dr. Smith)
T-wave inversion of anterior infarction (Wellens’ syndrome) almost always has an upright T-wave in lead III. Also, anterior ischemia is unlikely to spare lead V4. (Stephen Smith’s EKG Blog)
New Wellens’ sign (NEJM 2008;359(19):2071)
we describe a new ECG patternwithout ST-segment elevation that signifies occlusion of theproximal left anterior descending coronary artery (LAD). Insteadof the signature ST-segment elevation, the ST segment showeda 1- to 3-mm upsloping ST-segment depression at the J pointin leads V1 to V6 that continued into tall, positive symmetricalT waves. The QRS complexes were usually not widened or wereonly slightly widened, and in some there was a loss of precordialR-wave progression. In most patients there was a 1- to 2-mmST-elevation in lead aVR (see Figure 1 for representative examplesof this ECG pattern). We recognized this characteristic ECGpattern in 30 of 1532 patients with anterior myocardial infarction(2.0%).
Loss of precordial T-wave balance
tall upright T in V1
diffuse tented T waves contrasted with the hyperacute Ts of AMI which are localized, bulky, wide
short QT interval when here is no QRS prolongation
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Mattu EKG Stuff
if st elev greater in avr than V1 think proximal left main disease or three vessel disease (Am Heart J;154:71)
ST-segment elevation greater than 1.5 mV worry about LMCA
Yamaji et al attempted to determine the ECG features of acute LMCA in the patient with ACS. The ECGs of 86 consecutive patients who experienced ACS were analyzed. Sixteen patients experienced LMCA obstruction, 46 patients experienced obstruction of the left anterior descending artery, and the final 24 patients were diagnosed with right coronary artery obstruction. In this study group, Yamaji noted the relationship between acute LMCA obstruction and ST-segment elevation greater than 0.05 mV in lead aVR. This electrocardiographic finding was present in 88% of patients with LMCA obstruction, as opposed to 43% of patients with left anterior descending obstruction, and 8% of patients with right coronary artery obstructions. From the study, the sensitivity of ST-segment elevation in lead aVR for predicting LMCA obstruction was determined to be 81% and the specificity to be 80%.
Statistical analysis of this finding revealed a sensitivity of 78%, a specificity of 86%, a positive predictive value of 57%, and a negative predictive value of 95%. This reasonably high sensitivity allows the clinician to “rule-in” LMCA in the ACS patient with lead aVR abnormality.
In addition to aiding in the diagnosis of LMCA involvement in patients presenting with acute coronary syndromes, the finding of ST-segment elevation in lead aVR also has prognostic significance. In his second study on the topic, Kosuge et al examined the admission ECGs and biochemical markers of 333 patients with diagnosed non-AMI acute coronary syndromes. Although Kosuge studied numerous ECG findings and a variety biochemical markers, only ST-segment elevation greater than 0.5 mm in lead aVR on the admission ECG and elevated troponin T levels were determined to be independent predictors of adverse clinical events at 90 days, with an odds ratio of 13.8 and 7.9, respectively. Patients with ST-segment elevation in lead aVR and elevated troponin T levels were also determined to have the highest rates of both LMCA or 3-vessel disease and 90-day adverse outcome (62% and 47%, respectively).
. Yamaji, K. Iwasaki and S. Kusachi et al., Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1), J Am Coll Cardiol 38 (2001), pp. 1348–1354.
 M. Kosuge, K. Kimura and T. Ishikawa et al., Predictors of left main or three-vessel disease in patients who have acute coronary syndromes with non–ST-segment elevation, Am J Cardiol 95 (2005), pp. 1366–1369.
 M. Kosuge, K. Kimura and T. Ishikawa, Combined prognostic utility of ST segment in lead aVR and troponin T on admission in non-ST segment elevation acute coronary syndromes, Am J Cardiol 97 (2006), pp. 334–339.
Mattu on the use of aVR
ST ELEVATION IN aVR.
LMCA Stenosis Predictor?
aVR is the forgotten ECG lead – some even suggest we should call it an 11 lead ECG. ST segment elevation in aVR is often ignored as just being a reciprocal change but does it mean more than that?
The answer is yes, but it probably isn’t as much of a direct correlate with LMCA stenosis as the cardiologist is stating. Some quote a specificity of 98% when ST elevation in aVR is also present in aVL. However this figure seems to be from several deeply flawed papers with small numbers of highly selected non-emergency patients.
The largest study on ST elevation in aVR found it was associated with LMCA stenosis when compared to patients with ACS without elevation, but nowhere near as strongly as previously suggested (14.7% of patients with ? 1mm vs 5.1% without). When LMCA stenosis was combined with 3 vessel disease into a composite endpoint (ie: the traditional indications for CABG) it performed substantially better – 55.9% vs 26.1. It’s a good indicator, but certainly not a done deal.
One study of 775 consecutive patients with NSTEMI found in hospital mortality was 1.3% in those without ST elevation in aVR, compared with 19.4% in those with ? 1mm ST elevation.
However a subsequent much larger (and possibly definitive study) of 5064 patients from the GRACE registry suggests a much less startling , but still substantial difference in mortality (4.2 % vs 7.9%. p<0.03).
LMCA stenosis is bad – 70 % mortality without surgery / PTCA.
ST Elevation of more than 1mm in aVR in the setting of Acute Coronary syndrome is:
associated with left mainstem disease and 3 vessel disease.
suggests urgent angiography is necessary.
associated with an increase in mortality.
Probably not an indication for emergent angiography @ 3am unless the patient is not settling with standard medical therapy.
For another (opposing) view on aVR, as discussed in Cardiovascular Curveball #003, the brilliant and hugely influential Amal Mattu discusses aVR here.
Yan AT, Yan RT, Kennelly BM, Anderson FA Jr, Budaj A, et al.Relationship of ST elevation in lead aVR with angiographic findings and outcome in non–ST elevation acute coronary syndromes. Am Heart J. 2007 Jul;154(1):71-8. PMID: 17584554
Kosuge M, Kimura K, Ishikawa T, Ebina T, et al. Combined prognostic utility of ST segment in lead aVR and troponin T on admission in non-ST-segment elevation acute coronary syndromes. Am J Cardiol. 2006 Feb 1;97(3):334-9. PMID: 16442391
Kosuge M, Ebina T, Hibi K, Morita S, et al. Early, accurate, non-invasive predictors of left main or 3-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Circ J. 2009 Jun;73(6):1105-10. PMID: 19359810
S Kurisu, I Inoue, T Kawagoe, M Ishihara, et al. Electrocardiographic features in patients with acute myocardial infarction associated with left main coronary artery occlusion. Heart. 2004 Sep;90(9):1059-60. PMID: 15310704
Barrabés JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation. 2003 Aug 19;108(7):814-9. PMID: 12885742
Inferior with RBBB
Fishhook concAve high volt
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Mattu and Tabas USC Essentials Talks
Mattu & Tabas EKG Course
AVR elevation with st depressions= Left main diseaseMore specific if also AVL elevation as well, V1 elevation and AVR is greater > 1.5 mm
Camel Hump T wave Hypokalemia or buried p wave from Mobitz II
In order to be a LBBB Must have a monophasic R wave in I, V5, and V6
WellensV2 & V3 biphasic T wave, first up then down
RBBB May have depressions in V1-3 No st elevations
Causes of Wide Complexes
Causes of ST Elevations
Benign early Repol
Benign Early Repol
V3 or V4 fishhooking (aka Osbourne)
Predominant elevations in V1-V4
High Voltage (or LVH)
In both I and II, there must be a constant P to P interval
If not consider non-conducted PAC
V8 tip of scapula 5th ICS
V9 paraspinal 5th ICS
ST Depression Morphology
Flat/planar st segment depressions ~95% specific for ischemia
upsloping still concerning, ~20% are ischemia
downsloping is less concerning
_/ is normal U
can be adrenal
strain should only be lateral
Tall R waves downsloping
asymetric inverted t wave
Six Causes of ST Depression
2. Subendocardal MI
4. LVH with strain
5. Dig effect
T in V1> V6 think ischemia
Benign Early RepolarizationConcave upV1-V4No evolutionLVHfishhook V4rarely inferior
RBBB V1-V3 depressions rest of leads should be normal
Loss of precordial T-wave balance
The normal ECG has a flat or inverted T-wave in lead V1 (TV1). An upright TV1 should be considered abnormal, especially if it is “tall” and especially if it is new.An upright TV1 suggests significant underlying CAD and if new, may suggest acute ischemia. TV1 > TV6 is especially concerning. Of note, a new upright T-wave in V1 may precede other expected ischemic ECG changes.
Early reciprocal changes in lead aVLIn an normal ECG, lead aVL exhibits an isoelectric ST-segment and an upright T-wave. An acute inferior MI is commonly associated with “reciprocal changes” which may include:
ST-segment downsloping in aVL
T-wave inversion in aVL
These reciprocal aVL changes can precede the development of inferior lead abnormalities and may be the first sign of acute inferior wall ischemia. Of note, both LBBB pattern and LVH may result in similar changes in aVL as a “normal variant”.
Clinical Pearl topic courtesy of Amal Mattu, MD
References:(1) Lin KB, et al. Predictive value of T-wave abnormalities at the time of emergency department presentation in patients with potential acute coronary syndromes Acad Emerg Med 2008;15: 537-43. (2) Wagner, GS Marriott’s Practical Electrocardiography, 11th ed. © 2008, Lippincott Williams & Wilkins.
Determining Vascular Dominance
Elevation II,III,avFRCAelevation III>IIavL depression > 1 mmst elevation V4R or V1Circelevation II>IIIElevation I, avL, V5-6Elevation V1-V3LMAElevation avR>V1Global depressionsProx LADst elevation V1 (>2.5 mm)New RBBB depressions II, III, avFDistal LADElevation II,III, avF
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What is Ischemic ST Elevation
discover from resus.me
Older men – 2mm in V2/V3 and 1mm everywhere elseYounger men – 2.5 mm in V2/V3 and 1mm everywhere elseWomen – 1.5 mm in V2/V3 and 1mm everywhere else
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Pearls from Smith
ACS and STEMI do not cause tachycardia unless there is cardiogenic shock. Are the lungs clear? Is the patient cool and pale? Then ACS (STEMI) might be primary; this might be cardiogenic shock. . More often, tachycardia with ST segment abnormalities (elevation or depression) is due to an underlying illness (PE, sepsis, hemorrhage, dehydration, hypoxia, respiratory failure, etc.). One must clearly rule out these processes before jumping on the ACS diagnosis. . One very useful adjunct is ultrasound: bedside ED echo of his heart revealed no wall motion abnormality and hyperdynamic function. Large volume fluid resuscitation was undertaken. The K returned at 6.9 mEq/L. The HCO3 was 8. Cr was 13.4. Even after 3 liters of fluid, his CVP was very low.
Regarding Q Waves in Acute MI
Q-waves in acute MI:1) QR-waves are common early in anterior MI. 2) QS-waves are uncommon early in anterior MI; they are common in late presentation.3) Q-waves are independently associated with worse outcomes (78% relative increase in 90-day mortality in Armstrong et al.)4) Q-waves alone do not necessarily imply irreversibly infarcted myocardium; they should not dissuade from reperfusion therapy.References:Armstrong PW et al. Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention. J Am Coll Cardiol 2009;53(17):1503-9.Raitt MH et al. Appearance of abnormal Q-waves early in the course of acute myocardial infarction: implications for efficacy of thrmoblytic therapy. J Am Coll Cardiol 1995;25(5):1084-8.
There is another more likely explanation of this T-wave inversion: “Cardiac Memory.” Cardiac Memory (CM) has been described for a couple decades. It is most common after termination of pacing and other etiologies of abnormal depolarization such as Left Bundle Branch Block. After resolution of the abnormal depolarization, there may be transiently inverted T-waves that last for hours to days (these T-waves are the heart’s “memory” of the previous abnormal conduction). This phenomenon is poorly understood, but involves “transient electrical remodeling.”
Shvilkin et al. described the way to differentiate CM from ischemia:
In short, the combination of:
(1) positive TaVL(as in this case) and
(2) positive or isoelectric T-wave in lead I (as in this case) and
(3) maximal precordial T-wave inversion greater than the T-wave inversion in lead III (as here: maximal precordial T inversion is in lead V2, at 4.5 mm, and T-wave inversion in lead III is only 2.5 mm)was
92% sensitive and 100% specific for CM, discriminating it from ischemic precordial T-Wave Inversion
Thus, the very well informed physician could differentiate these ECGs from those of an LBBB patient with MI:
1) no concordance
2) no excessive discordance
3) LBBB with tachycardia, probably rate related
4) subsequent T wave inversion that, according to Shvilkin et al., is diagnostic of cardiac memory. It is NOT Wellens’ syndrome.