SVT or VT or SVT ***Abnormal ECG Unfonfirmed***

CASE PRESENTATION

A 50 yo male calls EMS for palpitations and chest discomfort. A 12 lead ECG (of course!) is obtained. The patient is short of breath and symptomatic. He remains awake, alert, oriented, and slightly diaphoretic. No obvious history.

12 LEAD ECG

12 LEAD ECG

ECG ANALYSIS AND INTERPRETATION

This ECG is particularly challenging, especially when the patient is symptomatic. Lifenet is raising all of the appropriate alerts, and you're faced with a couple of immediate treatment decisions. First, let's tackle therapy. 

1. In general, FIX THE RATE FIRST! Not only will fixing the rate provide relief from demand ischemia, but it may provide you with a diagnosis. This ECG is rapidly marching a long, and its very difficult in the heat of the moment to sort out p waves from QRS complexes from flutter waves. Demand ischemia occurs when the heart is unable to fill.

2. Unstable patient=SHOCK

3. Stable patient=consider drug therapy. In this case, adenosine **MAY** be an appropriate first line drug because the tachycardia is either some type of aberrant SVT or monomorphic VT

4. There are WIDESPREAD repolarization changes which I suspect are complicated by some lead placement issues. The narrow-looking complex in V2 doesn't fit with the rest of the ECG

5. The ECG is regular and FAST. VT usually occurs at a rate of 150; other differentials to consider in the setting of narrow complex tachycardia that is regular include SVT and A flutter. Intermittent and regularly occurring (small) positive deflections appear in this ECG to suggest an underlying atrial flutter rhythm

6. Examining lead one, the RIGHT rabbit ear is "taller." This favors SVT. Interestingly enough, RSR' complexes with a taller LEFT rabbit ear favor ventricular tachycardia. 

7. Other features that favor VT are absent, such as:
-AV dissociation
-Fusion beats
-Entirely positive or negative concordance in the chest (precordial) leads. This finding is best described as when the QRS complexes all point in the same (positive or negative) direction

8. With regard to the widespread ST segment elevation, it is never a bad idea to transport to a center capable of percutaneous coronary intervention. In this case, I suspect the widespread ECG changes (lots of ST segment depression) are due to repolarization  abnormalities or rate related ischemia. There doesn't appear to be a clear-cut anatomic distribution of the elevation. 

I shall offer my humble interpretation reminiscent of several recent radiology reads:
Regular, wide complex tachycardia suggesting either VT or an aberrantly conducted supraventricular rhythm. 2:1 atrial flutter is also in the differential. Correlate clinically. 

So the bottom line remains that I don't have a definitive interpretation here. Perhaps some of the other online ECG gurus could weigh in and provide some direction. What is clear, however, is that providers should keep some core principles in mind when confronted with a concerning and potentially confounding ECG:
1. Fix the rate first

2. Treat wide complex tachycardia as VT 

3. Always consider ischemia in your differential diagnosis

***Abnormal EKG Unconfirmed*** CONSIDER BRUGADA SYNDROME, Consider Ischemia

EMS crews respond to the report of a sick 70 year old male. An ECG is obtained. As your crew performs patient assessment and works on obtaining IV access, your astute EMT obtains a 12 lead ECG.

1) What's your interpretation ?
2) What is an emergency-focused differential that is consistent with this ECG?
3) Why NOT Brugada ?

12 LEAD ELECTROCARDIOGRAM

First, there is a wavy baseline that interferes with rhythm interpretation. The rhythm is obviously bradycardic and the rate is consistent with a ventricular etiology. The complexes are wide, bizarre, and irregular. There is evidence of ST segment elevation in (possibly) V1 and V2. ST elevation may also be present in Lead II. Diffuse ST segment depression is present in leads I, III, aVF, V5-V6. 

Interpretation

Ventricular rhythm, diffuse ST-T segment depression

Differential diagnosis

Ischemia
Hyperkalemia
Myocardial infarction

Therapy
As this ECG arrived in my inbox without any clinical context, it seems reasonable to consider calcium. In the late stages of hyperkalemia, the QRS can widen considerably and the p waves simply disappear. If the patient presented with a story concerning for ischemia, transport to a cath capable hospital would comprise an excellent treatment plan!

WHY NOT BRUGADA?
The ECG software seems a bit confused by the wandering baseline and the presence of atypical ST segment elevation. Brugada, however, is a curious interpretation because it is a clinically distinct entity that involves specific clinical and electrocardiographic findings. Brugada syndrome was first described in the 1990's. It is the result of an abnormality in the cardiac sodium channel gene. It iis associated with sudden cardiac death in certain patients. The Life in the Fast Lane blog has an excellent (and succint) review of this syndrome.

Brugada syndrome presents commonly following a syncopal episode. The patient may not complain of any chest pain or shortness of breath. The syncope is usually caused by a transient ventricular dysrhythmia. It is most commonly diagnosed in younger aged Asian males.

EKG Findings in The Brugada Syndrome
Atypical ST segment elevation is the hallmark of Brugada syndrome. Typically, there is a "coved" type of ST segment elevation present in leads V1-V3 .Another type of ST segment abnormality seen in the syndrome include a "saddle-back" deformity:

Treatment
Treatment is directed at correction of the underlying defect. Because these patients are at increased risk for death, they will usually benefit from a cardiology referral and consideration of AICD insertion.

Key Brugada points for the EMS provider:

• Brugada syndrome is a clinical entity consisting of distinct ECG and clinical characteristics
• Perform an ECG in ALL patients following a syncopal episode
• Scrutinize the ECG for atypical, "coved" or "saddle back" ST segment abnormalities, especially in the precordial leads

Way Too Overdue: Subtle STEMIs, Stubborn Platelets. Part 2/2

EMS is attending to a patient with chest discomfort. A 48 yo female presents to EMS with hypertension, right sided chest pain, and the following EKG.

12 lead EKG interpretation:

There is a baseline sinus rhythm. There is minimal, but significant, ST segment elevation in leads III and aVF. Reciprocal change in the form of ST segment depression is seen in the anterior/high lateral leads. The precordial leads do not exhibit ST segment depression which makes the diagnosis of posterior wall extension less likely. This ECG is consistent with a (subtle) inferior wall ST elevation myocardial infarction.

Case discussion:

Female patients, diabetic patients, elderly patients, and patients with a history of cocaine use are at increased risk for atypical presentations of acute coronary syndromes. Cocaine causes platelet aggregation and accelerates the development of coronary plaque. Cocaine is directly toxic to myocytes and can also induce vasospasm. Providers should remain vigilant for atypical presentations and treat accordingly.

EMS transports this patient to a STEMI center and administers NTG and ASA in accordance with established protocol. The patient does not experience any hypotension and remains hemodynamically stable. Chest pain resolves upon arrival to the ED. The patient undergoes emergent coronary angiography and has a 100% occlusion of the RCA. The lesion is ballooned. Initial troponins are positive. The patient is rapidly transitioned to a cardiac step down unit and has an uneventful recovery.

Way Too Overdue: Subtle STEMIs and Stubborn Platelets March 2016 PART 1/2

SUBJECTIVE:
EMS responds to the report of a 48 yo female with chest pain. Upon arrival, the patient is in mild distress and reports sharp, intermittent, right sided chest discomfort lasting for approximately 30 minutes. The patient reports nausea, some slight diaphoresis, and denies vomiting. The patient reports recent intake of cocaine and has a history of substance abuse. The patient has no allergies.

PMHX:
HIV
HTN

OBJECTIVE: 
The patient is awake, alert, oriented, and seated in a chair. BP: 160/100, P: 80, R: 72. Sp02: 97% on RA. Lungs are clear to auscultation bilaterally. Heart sounds are regular. The abdomen is soft and the remainder of the physical assessment is unremarkable. Peripheral pulses are strong and equal.

A 12 lead ECG is obtained:

What's your interpretation and treatment plan? 
An intravenous line is started.