This ECG was taken from a 60 year old man who was complaining of severe substernal chest pain, radiating to his left arm and a non-productive cough. They also considered a diagnosis of pericarditisbecause the ST segments seem widespread. The baseline artifact makes it difficult to evaluate for PR segment depression or Spodick's Sign.
The patient's age 60 years and troubling symptoms chest pain radiating to the left arm ruled out BEP for the paramedics. There are also "hyperacute" T waves in the leads with STE. There are ST abnormalities ranging from flattening of the shape to depression, but the bottom line is this patient is a year-old man with substernal chest pain radiating down his left arm!
The patient was treated in the ambulance with chest pain protocols, and was transferred to a hospital with an interventional cath lab. The patient was conculusively diagnosed with an acute M. This is a good ECG to demonstrate subtle changes when, combined with patient presentation, can help us diagnose a coronary event. It helps us emphasize that not all STEMIs will have dome-shaped, "tombstone" ST segments, and that patient symptoms, history, and age are important to consider.
This series shows the evolution of ECG changes in anterior wall M. The patient is an year-old woman with chest pain. She was designated a "cardiac alert" from the field by paramedics. Her proximal LAD was opened and stented in the cath lab. We do not have follow-up information on her.
In addition, the T waves are "hyperacute" - tall, broad, and asymmetrical. This can be an early, transient sign of myocardial injury. Slight reciprocal depressions are seen in the inferior leads. Lead V4 has a T wave inversion that is out of place with the progression of the T waves in V3 and V5. Lead placement may be to blame. Hyperacute T waves in a patient with chest pain should be taken very seriously. In addition, Lead aVL is showing some T wave changes.An 80 year old female presents with one hour of sudden-onset, burning chest pain radiating to her back with associated nausea.
She receives aspirin and sublingual nitroglycerine and continues to have pain. A repeat ECG several minutes later:. When a coronary artery becomes occluded, the ECG begins to change over time in a predictable way. The earliest changes are in T-wave shape and size.
ECG Pointers: Hyperacute T-Waves
Within 30 minutes of artery occlusion the T-wave height and width increases. This is followed by ST-segment elevation and subsequent decrease in R-wave amplitude and Q-wave development. This means that early in arterial occlusion, the T-wave becomes disproportionately large when compared to the QRS complex.
There is 1mm ST elevation in V1-V2. In leads V1-V4, the T-waves are broad-based and are very tall relative to the small R-waves. There is also slight reciprocal ST depression in lead II. A single stent was placed to the LAD. Remember: hyperacute T-waves may be the first sign of arterial occlusion and troponin levels may not be elevated yet.
For several examples of hyperacute T-waves in early coronary artery occlusion check out these cases on Dr. Special thanks to Dr. Marci Gambarota for sharing these ECGs and interesting case with me!
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Contact us at editors emdocs. Powered by Gomalthemes. Toggle navigation. Menu All Content. Previous Post. Next Post. Nov 28th, Jamie Santistevan categories: practice updates. The Case: An 80 year old female presents with one hour of sudden-onset, burning chest pain radiating to her back with associated nausea. An old ECG from 6 months prior: She receives aspirin and sublingual nitroglycerine and continues to have pain.The T wave is the positive deflection after each QRS complex.
It represents ventricular repolarisation. Loss of precordial T-wave balance occurs when the upright T wave is larger than that in V6. This is a type of hyperacute T wave. Inverted T waves are seen in the following conditions:. New T-wave inversion compared with prior ECGs is always abnormal. There are two causes for camel hump T waves:. Dynamic T-wave flattening due to anterior ischaemia above. T waves return to normal once the ischaemia resolves below.
Note generalised T-wave flattening in hypokalaemia associated with prominent U waves in the anterior leads V2 and V3. He has a passion for ECG interpretation and medical education. Read more posts ECG Library. This site uses Akismet to reduce spam. Learn how your comment data is processed.
Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia. Prinzmetal angina. Inverted T-waves in the right precordial leads V are a normal finding in children, representing the dominance of right ventricular forces. Inferior T wave inversion due to acute ischaemia. Inferior T wave inversion with Q waves — prior myocardial infarction. T wave inversion in the lateral leads due to acute ischaemia.
T-waves in ischemia: hyperacute, inverted (negative), Wellen’s sign & de Winter’s sign
Anterior T wave inversion with Q waves due to recent MI. T wave inversion in the inferior and right precordial leads. Prominent U waves due to severe hypokalaemia. Hidden P waves in sinus tachycardia.Wellens syndrome is a pattern of deeply inverted or biphasic T waves in Vwhich is highly specific for a critical stenosis of the left anterior descending artery LAD. Patients may be pain free by the time the ECG is taken and have normally or minimally elevated cardiac enzymes; however, they are at extremely high risk for extensive anterior wall MI within the next few days to weeks.
Due to the critical LAD stenosis, these patients usually require invasive therapy; do poorly with medical management; and may suffer MI or cardiac arrest if inappropriately stress tested. They observed that patients admitted for unstable angina with this ECG finding were at high risk for myocardial infarction. Rhinehart et al describe the following diagnostic criteria for Wellens syndrome:.
There are two patterns of T-wave abnormality in Wellens syndrome:. There is confusion in the literature regarding the naming of the T wave patterns, with some authors using Type 1 Type A for biphasic T waves and Type 2 Type B for inverted.
It may be better to just describe the T wave pattern! ECG patterns in precordial leads of the patients reported. Pattern A was found in four patients; pattern Bin 22 patients. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. This sequence of events is not limited to the anterior leads — similar changes may be seen in the inferior or lateral leads, e.
Also, the inciting event does not necessarily have to be thrombus formation: Wellens syndrome may also occur in normal coronary arteries following an episode of vasospasm, as in this case of cocaine-induced vasospasm.
However, it is safer to assume the worst i.
The T-wave: physiology, variants and ECG features
Also check out Example 5, below. This fantastic ECG series submitted by paramedic Andrew Bishop shows a stuttering pattern of LAD occlusion, reperfusion and re-occlusion in a middle aged lady with chest pain. The ECGs are presented in chronological order, over a 45 minute period from the prehospital environment to the cath lab. Shortly after this series of ECGs was taken, this patient suffered a VF arrest that was refractory to defibrillation.
This was stented, she was successfully cardioverted and subsequently made a good neurological recovery! While the morphology of the T wave changes in Wellens syndrome is often quite distinctive, there are numerous other conditions that may produce similar patterns of precordial T-wave inversion, including:. Explore the links above to appreciate the similarities and differences between these ECG patterns. Apologies for the misinformation… As you can see, these two conditions can be difficult to tell apart!
This is an example of Pseudo-Wellens syndrome due to left ventricular hypertrophy. Consolidate your learning with lessons from the masters of ECG interpretation. Follow the links below for expert commentary, video lessons, case-based discussion and detailed explanations to take your learning to the next level. Asynchronous learning FOAMed evangelist.
This site uses Akismet to reduce spam. Learn how your comment data is processed. Wellens Pattern A Type 1. Is most commonly seen in the lateral leads V, I, aVL. Typically occurs in patients with high QRS voltages, e. EKG Library. Dr Mike Cadogan. Leave a Reply Cancel reply. Blog Stats 40, visitors.A thorough discussion regarding the physiology of the T-wave was previously provided. Only aspects relevant to ischemia will be discussed here. The T-wave is notoriously difficult to judge, which is why a rather comprehensive discussion is warranted.
The normal T-wave will be described first. Then, ischemic T-wave changes — i. It is, however, common to have a negative T-wave in lead V1, which also has a net negative QRS complex i. The transition from ST segment to T-wave should be smooth.
T-wave amplitude is on average 3 mm in V2—V3 in females and it rarely exceeds 8 mm. Note that the amplitude of the T-wave is related to the amplitude of the QRS complex large QRS amplitudes yields large T-wave amplitudes, and vice versa.
Last but not least, the normal T-wave is slightly asymmetric; the slope of the descending limb is slightly steeper than the ascending limb. T-wave abnormalities are common and occur in a wide range of conditions. Unfortunately, many clinicians tend to misinterpret the T-wave and some find it difficult to put T-wave changes into clinical context. Therefore, we will now discuss each T-wave abnormality and clarify common misunderstandings.
T-wave inversion means that the T-wave is negative. By definition the T-wave is negative if the terminal portion of the T-wave is below the baseline. T-wave inversions are actually graded according to the amplitude depth.
Myocardial ischemia may present with any degree of T-wave inversion. It is a wide spread misunderstanding that isolated T-wave inversions indicate acute ongoing ischemia. To clarify, isolated T-wave inversions indicate that there has been ischemia. Ischemic T-wave inversions are symmetric the normal T-wave is asymmetric and may be, but rarely are, deeper than 10 mm. Normalization of T-wave inversion after infarction indicates some recovery in the infarct area.
Figure 2 must be studied carefully. It presents characteristics and significance of virtually all clinically relevant T-wave inversions. ECG criteria for acute myocardial infarction:. These leads must have evident R-waves, or R-waves larger than S-waves.If you do not yet have a Google account — it should not take long to register. Comments give US feedback on how well Dr. Saturday, August 11, "Are these hyperacute T-waves?
Written by Pendell Meyers, edits by Steve Smith. My response: "I do not think there are hyperacute T-waves. I see no evidence of occlusion, but remember the ECG is not the only reason to activate.
Would get serial ECGs and observe for evolution, assuming nothing else is concerning. Possible mild hyperK changes, would need baseline. They immediately texted me back, saying "Does his troponin T of 1. Generally, this troponin alone in the context of crushing chest pain is indeed an indication for the cath lab, no matter what the ECG shows. My response: "Not about the ECG. But it should factor into the case as a whole.
Where's the baseline? What's the story? Like the last case, it is not fat or broad.
By itself, it would be concerning but not diagnostic for a hyperacute T-wave. So look next door: V2 has very high voltage followed by expected small STE and positive T-wave which is actually very small for such a large QRS complex. If V3 represented a hyperacute T-wave, V2 should at least hint that its T-wave is at least marginally concerning.
Subtle ECG findings in ACS: Part II Hyperacute T-Waves
But instead V2 is perfectly normal for its QRS. V2 does not corroborate V3. Neither does V4. Additionally, I think this represents a common mistake which happens most often in the transition lead. The "transition lead" is the precordial lead in which the QRS transitions from mostly negative QRS components to mostly positive.
In this case, V2 is predominantly negative, and V4 is predominantly positive. Therefore V3 is the transition lead, and is almost isoelectric. Both V2 and V4 have considerable voltage. You may ask "so where does all this voltage go between V2 and V4? This is sometimes the case in the transition lead, as the QRS is often isoelectric and has multiple conflicting component vectors.
Most often, the transition lead simply has the same overall QRS voltage but with equal R and S components. Sometimes, however, the transition lead produces what appears to be a small QRS complex between two large high voltage QRS complexes.
I think of this as the voltage being "folded up" into the transition lead QRS complex. This helps me understand why the T-wave appears so large in this lead. However, I am unable to find any literature that supports or denies this assertion.What if you could identify a patient with complete coronary vessel occlusion almost immediately after it occurs, before the ST segments begin to elevate?
What if you could pick up the very subtle, early MI? We know that early recognition and intervention improves outcomes in patients with coronary artery occlusion. Sometimes patients presenting with ACS are obvious. Sometimes it seems that the patient has read the textbook. However, more often than not, patients are not obvious, especially in the early stages of ACS. That is why we are concerning ourselves with subtlety. Last time we reviewed the ECG findings associated with left main coronary artery disease, where we discussed the meaning of ST elevation in lead aVR.
Now we are going to turn our attention to the T-waves. The T-wave represents the period of ventricular repolarization on the ECG. The normal T-wave appearance varies based on lead placement, age, and sex. In general, T-waves are tallest in leads II and V4 and will decrease in size with age. A normal T-wave usually has amplitude of less than 5mm in the precordial leads and less than 10mm in the limb leads .
The normal shape of a T-wave is asymmetric, with a slow upstroke and a rapid down stroke. Additionally, the R-wave amplitude should progress normally across the precordial leads. Immediately after coronary artery occlusion, the ECG undergoes predictable temporal changes.
However, the earliest findings on an ECG are subtle changes in the T-wave shape and size. When a coronary artery is occluded, within the first 30 minutes, the T-wave amplitude increases . The next changes are ST-segment elevation and loss of the R-wave amplitude. If the vessel remains occluded, Q-waves develop. Without intervention, the ECG will then begin to exhibit T-wave inversions and eventually, the ST-segments will normalize .
Persistent ST-segment elevation suggests aneurysm formation.
Early in the course of AMI, biochemical markers may not be elevated, although this may be changing in the era of highly sensitive troponin assays. In the early stages of MI, prior to the development of necrosis, the myocardium is suffering from ischemia. Timely revascularization may actually prevent complete infarction and death of the affected portion of the myocardium.
Therefore, recognizing ACS early is beneficial because patients have improved outcome the timelier revascularization occurs , and delay to reperfusion causes larger infarction size and worse functional outcomes . It is well known that new ST-segment elevation represents complete vessel occlusion and transmural infarct. However, the STEMI criteria have limited sensitivity in diagnosing coronary artery occlusion [5, 6, 7].