Image of the Day 40: Anteroseptal STEMI (Hyperacute T Wave)

41 years old gentleman, ex smoker with family history of Ischemic heart disease presented with central sharp chest pain one and half hour prior to presentation to casualty. Pain is non radiating, persistent with score of 9-10/10 and associated with shortness of breath, palpitation, nausea and vomiting. BP on arrival 184/128, Pulse rate 62/min.

ECG shows sinus rhythm with Left Axis deviation,  rate of 80 b.p.m with presence of hyper acute T wave with ST elevation of lead V1-V4 and reciprocal ST depression in lead II,III, aVF.

Patient was load with T.Aspirin 300mg stat, T. Clopidogrel 300mg stat, S/L GTN 0.5 Mg X1, IV Morphine 3mg and IV Metoclopromide 10 mg. IV streptokinase 1.5 Megaunit in 100cc D5% was commerced after BP stabilization with IV GTN Infusion.

ECG upon patient presentation

 

Subsequent ECG 5 minute before presentation shows progressively increase in T wave and ST height

 

Immediately Post Streptokinase shows poor R wave progression in V1-V3, upsloping of ST segment in V4-V5 and slightly reduce in ST segment height in V1-V3

30 minute post streptokinase. Not much changes seen

1 Hour post streptokinase shows reperfusion ischemia and variable block

24 hour post streptokinase shows formation of Q wave in V1-V4 and normalization of ST segment elevation as well as T inversion in lead V1-V3.

Well i definetely learns something from this case. Most of the time, i will get straight forward ST elevation and not hyper acute T wave. The tips to recognize pure ST Elevation MI of anteroseptal infarct is large T wave and reciprocal changes in inferior lead. Present of risk factor like in this gentleman; age, hypertensive emergency, smoker and age and together with history of chest pain will give stronger points pointed to cardiac event.

Another differential diagnosis should also be think of especially ventricular aneurysm and also other cause ST elevation (refer to my post ABCD Help in ST Elevation ECG)

Another tips if you see this ECG especially in younger age patient is possibility of Coccaine induce Myocardial Infarction.

Let us revise the ST and T wave changes in Acute Myocardial Infarction

Disclaimer: Image taken from ECG pedia and not belong to blog author

 A very good reading material for Anterior ST elevation is from this website Life In The Fast Lane: Anterior Myocardial Infarction [link]

 This ECG taken from the Life in the Fast Lane website is almost identical to the ECG of the patient that has been discussed earlier on.

• ST elevation is maximal in the anteroseptal leads (V1-4).
• Q waves are present in the septal leads (V1-2).
• There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.
• There are hyperacute (peaked ) T waves in V2-4.
• These features indicate a hyperacute anteroseptal STEMI 

* Source: Life in the Fast Lane website by Edward Burns

Ok, this interesting clinical PEARL tips is taken from Edward Burns article and not written by myself. I just found it interesting and share it here just in case you are not in the mood to click on the above link.

Clinical Relevance

        Anterior STEMI results from occlusion of the left anterior descending artery (LAD).

        Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.

        A study comparing outcomes from anterior and inferior infarctions (STEMI + NSTEMI) found that on average, patients with anterior MI had higher incidences of in-hospital mortality (11.9 vs 2.8%), total mortality (27 vs 11%), heart failure (41 vs 15%) and significant ventricular ectopic activity (70 vs 59%) and a lower ejection fraction on admission (38 vs 55%) compared to patients with inferior MI.

        In addition to anterior STEMI, other high-risk presentations of anterior ischaemia include left main coronary artery (LMCA) occlusion, Wellens’ syndrome and De Winter’s T waves.

How to Recognise Anterior STEMI

        ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL).

        Reciprocal ST depression in the inferior leads (mainly III and aVF).

NB. The magnitude of the reciprocal change in the inferior leads is determined by the magnitude of the ST elevation in I and aVL (as these leads are electrically opposite to III and aVF), hence may be minimal or absent in anterior STEMIs that do not involve the high lateral leads.

Patterns of Anterior Infarction

The nomenclature of anterior infarction can be confusing, with multiple different terms used for the various infarction patterns. The following is a simplified approach to naming the different types of anterior MI.

The precordial leads can be classified as follows:

        Septal leads = V1-2

        Anterior leads = V3-4

        Lateral leads = V5-6

The different infarct patterns are named according to the leads with maximal ST elevation:

        Septal = V1-2

        Anterior = V2-5

        Anteroseptal = V1-4

        Anterolateral = V3-6, I + aVL

        Extensive anterior  / anterolateral = V1-6, I + aVL

(NB. While these definitions are intuitive, there is often a poor correlation between ECG features and precise infarct location as determined by imaging or autopsy. For an alternative approach to the naming of myocardial infarctions, take a look at this 2006 article from Circulation)

Three other important ECG patterns to be aware of:

        Anterior-inferior STEMI due to occlusion of a “wraparound” LAD: simultaneous ST elevation in the precordial and inferior leads due to occlusion of a variant (“type III”) LAD that wraps around the cardiac apex to supply both the anterior and inferior walls of the left ventricle.

        Left main coronary artery occlusion: widespread ST depression with ST elevation in aVR ≥ V1

        Wellens’ syndrome: deep precordial T wave inversions or biphasic T waves in V2-3, indicating critical proximal LAD stenosis (a warning sign of imminent anterior infarction)

        De Winter’s T waves: upsloping ST depression with symmetrically peaked T waves in the precordial leads; a “STEMI equivalent” indicating acute LAD occlusion.

Credit to Dr Aslannif Roslan, Dr Azlan Kamalludin and Dr Azlean for sharing knowledge and tips...

Image of the Day 38: Approach to Ear Trauma

A 20 year old Indonesian worker was using a bamboo pole during working at palm oil plantation when the pole break and piece of the bamboo penetrate his right ear. The bamboo was removed under procedural sedation and analgesia. The defect was then sutured and he was discharged with antibiotic and pain medication

This 5 year old kid was playing with fish hook and accidentally hit his left ear. The tip of the fish hook was cut using the wire cutter and the hook was then pulled out.

This 50 year old gentleman accidentally cut his with the sickle during farming. noted that the ear already avulsed and anatomically disfigured. The external meatus of the ear also came out from it's place. Patient was posted for ear repair under general anesthesia. 

 Discussion

After lips injury, ear trauma come seconds in term of difficulty in repairing the facial injury. In managing ear trauma, it is important to treat the current presenting complaint as well as preventing the complication.

The aim of managing ear trauma are as follow; 1) Maintaining the cosmesis by repairing the injury as symmetrical to the counter ear. 2) Avoidance of hematoma, and 3) Prevention of infection.

Whenever patient come with ear trauma, it is very important to rule out presence of other injury especially basal skull fracture and tympanic membrane perforation.

Superficial laceration wound can be sutured using 6-0 non absorb-able suture material for five to six days. It is very important to maintain the homeostasis in order to prevent hematoma formation.

Untreated hematoma formation may lead to abnormal cartilage production that will calcify and producing deformed ear known as cauliflower ear.

Whenever present, exposed cartilage must be covered to reduce infection, erosive chondritis and subsequent necrosis.

It is best to refer ear injury with avulsed tissue, crushed cartilage and auricular hematoma to plastic surgeon or ENT specialist.