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

The Agony of the Beta Agonists PART 1 of 2 JULY 2015

This was shared from a friend, provider, and colleague. Interesting case. Details changed to protect the innocent, respect privacy laws, comply with all appropriate regulations, and, well.. you get the picture.

SUBJECTIVE
HPI:
94 yo male requests 911 for shortness of breath. HPI  not obtainable due to patient presenting in extremis. The patient is alert, responsive to verbal stimuli, and is in obvious respiratory distress upon arrival. Providers appreciate audible wheezing. Family members relate that the patient is a "DNR" and was last seen acting "a little tired" 12 hours prior.
Meds: Unknown
PMH: COPD, CHF, HTN, HLD, DM

OBJECTIVE
Pt is slightly diaphoretic. BP: 134/92, R: 32, P: 90. ETC02 via NC is 20.
Supraclavicular and intercostal retractions are present as is mild JVD.

12 LEAD ECG:












Case related questions: 
1. What is your prehospital treatment?
2. What are some concerning ECG findings?
3. Is this patient treated as a STEMI alert?

April 2015: Sighting the Subtlety Down Below

CASE: 

A 63 y/o gentleman calls 911 for "chest pressure" and indigestion. The patient is nauseated but denies LOC, SOB, or dizzinesss. The pressure started approximately 1 hour prior to 911 arrival. The patient has a history of hypertension and takes an aspirin daily. He is hemodynamically stable. BP is 110/70, P: 82, R: 16. Sp02: 95% on RA.

12 LEAD ECG:

12 LEAD ECG DISCUSSION:

There is a sinus rhythm. PR depression is present in lead II. There is slight ST segment elevation present in II, III, and aVF. Elevation measures about 1 mm. There is no evidence of recriprocal change. A biphasic T wave is present in lead III and terminal T wave inversion is present in the lateral precordial leads. The QRS axis appears physiologic.

12 LEAD INTERPRETATION: 

Inferior wall STEMI

TREATMENT

The patient was transported to a hospital capable of percutasneous coronary intervention. A right sided ECG was not performed, and NTG was withheld due to the patient's marginal blood pressure or relative hypotension. 325 mg of ASA was administered. The patient's RCA was 75% occluded.

Thanks always to the Baltimore City Fire Department for its endless supply of pathologic 12 lead tracings.

Non Sustained VT: Making a Lasting Impression!

Putting on the Pressure

A 60 yo male presents to EMS with several hours of chest pressure and diaphoresis. A 12 lead ECG is obtained following a 10 beat run of non sustained ventricular tachycardia. Despite the EMT's excitement at "firing up the paddles," the paramedic administers 324 mg of aspirin and prepares for transport to the nearest facility capable of percutaneous coronary intervention. Your partner informs you that the monitor discerns the presence of a paced rhythm. The patient has no previous medical history.


12 LEAD ECG:

12 LEAD ECG Analysis:

A sinus rhythm is present and the rate is regular. Diffuse and concerning ST segment changes appear in this tracing. First, pathologic ST segment elevation occurs in leads V2, V3 and V4. Q waves also appear throughout the tracing. The monitor misinterprets the ischemic Q wave as a pacer spike. The QRS is narrow, so an interventricular conduction delay is less likely responsible for the "false pacer" call. Reciprocal changes appear in lead aVF. There is minimal J point depression in lead III and V6. The baseline is also irregular.


12 Lead ECG Interpretation: 

Sinus rhythm, anterior wall ST segment myocardial infarction.

Comments:

• It is difficult to discern the location of the anatomic lesion based upon this ECG. The large ST segment elevation in the precordial leads suggests involvement of the LAD. The findings of lateral wall ischemia could implicate the circumflex as well. 
• The run of VT was likely due to ventricular irritability. Remember that the most devastating complications of anterior wall ischemia are lethal dysrhythmia and cardiogenuc pulmonary edema 
• Pathologic Q waves generally follow a few rules: (1) larger than a third of the corresponding R wave or (2) measure in excess of 0.03 seconds. Q waves that accompany poor R wave progression are more likely to indicate ischemia. 

Simple STain on the Strain

Sometimes LVH isn't all that simple. The "strain" pattern has been discussed elsewhere on this and other blogs, but this is an example of an atypical, and concerning, ECG:

What's not (so) unusual: 
The ECG reveals a sinus rhythm. The downsloping ST segments and T wave inversions seen in the lateral leads and precordial leads may be expected in the setting of high left ventricular voltage. The pattern of LVH and ST/T wave changes is consistent with, "strain."

What's concerning: 
The ST segment elevation present in aVL and V1-V2 is NOT concave and almost horizontal. This type of ST segment change is consistent with ischemia. Furthermore, it appears in an anatomic distribution. ST segment changes in aVL and V1-V2 suggest anterior or anterior lateral ischemia. Though LifeNET measures the ST segment elevation at less than 2 mm, it is nevertheless cause for concern especially given a "typical" story or history consistent with an acute coronary syndrome.

Bottom line and interpretation:
Carefully evaluate ST segment deviation in all leads. Look for atypical elevation and an anatomic distribution of the ECG changes.
Sinus rhythm, ST segment depression and T wave inversion consistent with strain pattern. ST segment elevation in the anterior precordial leads and aVL suspicious for STEMI. 

Where is the culprit lesion? ST segment morphology

CASE STUDY:

Medics respond to the report of someone with chest pain and shortness of breath. Vital signs are stable. Given concern for acute coronary syndrome, a 12 lead ECG is obtained.

12 LEAD ECG

12 LEAD ECG Discussion

There is a sinus rhythm. ST segment changes are widespread. The inferior leads reveal some ST segment straightening but no frank elevation. Profound ST segment elevation in present in leads V2, V3, and V4. Reciprocal change in the form of ST segment depression is present in lead aVL. ST segment morphology is linked to adverse outcomes. The ST segments in this particular case display a concerning, "straight" shape especially prominent in lead V3.

12 LEAD ECG Interpretation

Sinus rhythm, anterior wall ST elevation myocardial infarction. 

Resolution

The patient was delivered emergently to the cardiac catheterization lab. A bare metal stent was placed in the proximal left anterior descending artery. The patient was discharged without complication on hospital day 2. 

August 2014: Right behind you with a STEMI!

A 60 yo male patient reports a sudden onset of chest pain and shortness of breath. The patient rates the pain at an 8/10 and is slightly nauseated. The patient has a history of "borderline" diabetes.

VS:
BP: 140/90, P: 62, R: 16, Sp02: 99%

EXAM:
The patient is slightly diaphoretic and appears uncomfortable. A 12 lead ECG is obtained.

ACTIONS:Do you activate the cath lab?
Do you administer NTG?

12 LEAD ECG: 

12 LEAD ECG CASE DISCUSSION:

The ECG shows a first degree heart block. ST segment elevations are apparent in Leads II, III, and aVF. Reciprocal changes are present in Leads I and aVL. ST segment changes are present in the septal leads of V3 to V4. The diagnosis of a posterior wall myocardial infarction is less likely given (1) the absence of tall R waves and (2) The absence of ST depression in leads V1-V3. However, anytime anterior precordial ST depression appears concurrently with an inferior wall MI, you should consider the diagnosis of a posterior wall infarction. Recall that the posterior descending coronary artery comes from the right coronary artery. It is wise to be cautious with nitroglycerin since this infarction may involve portions of the right ventricle. Have IV access established and consider right sided chest leads if there is concern for a right ventricular infarction. This patient went emergently to the cardiac catheterization lab and was found to have a completely (100%) occluded right coronary artery.  Finally, conduction delays and heart blocks are consistent with ischemia of the sinoatrial node and the conduction system.

12 LEAD ECG INTERPRETATION:
Inferior wall ST elevation myocardial infarction.

Abnormal ECG **Unconfirmed** but I'm worried about ***MEETING ST ELEVATION MI CRITERIA!*** PART 1/2

Family members call 911 for an 80 yo male experiencing chest discomfort. The patient has a history of HTN, dementia. The patient reports chest discomfort that began "a few hours" prior to EMS arrival. The patient reports some mild shortness of breath. The patient is otherwise alert and in mild distress.

PHYSICAL ASSESSMENT
BP: 136/78
P: 60
R: 22
Sp02: 95% on RA
Lung sounds are clear.
Heart tones present, no murmur.
No leg edema.

12 LEAD ECG
















12 LEAD ECG INTERPRETATION
It appears that LifeNet has done the job for you. There are three stars on either side of the ***MEETS ST ELEVATION MI CRITERIA***. Guess there's nothing more to say.

What say you? To cath or not to cath? Treatment? Additional questions?

The Eclectic Equivalent

A 64 yo female calls 911 for chest discomfort. The patient reported chest pressure that waxed and waned in intensity. The discomfort was retrosternal and did not radiate. The patient compared the pressure to previous bouts of "indigestion." The patient experienced associated nausea. No LOC, no diaphoresis. Providers obtain a 12 lead ECG. Vital signs remained stable.

12 Lead ECG

12 Lead ECG Interpretation 

The rhythm is sinus and the rate is regular. ST depressions are present in leads II, III, and aVF. There are also ST depressions noted in the precordial leads V3-V6. R wave progression is preserved, and it appears that R waves reach their maximum amplitude in lead V4. There is no obvious ectopy.

ST elevation of > 1 mm is noted in aVR and V1.

Sinus rhythm, diffuse ST segment depression, ST segment elevation in aVR and V1.

Case Discussion

Providers correctly identify the ECG tracing as a potential STEMI equivalent. The STE in aVR and V1 is concerning for its association with acute left main occlusion. The patient was transported to the cardiac cath lab. Cardiologists discovered a near total occlusion of the left main coronary artery.

aVR has long been cast as the "forgotten lead" in electrocardiography. Studies link ST elevation in aVR to left main disease and cardiogenic shock. There is also data to suggest that patients with changes in aVR are more likely to require surgical intervention and progress into cardiogenic shock. Indeed, ST elevation in aVR is often considered a, "STEMI equivalent" due to its association with a poorer prognosis. Always scrutinize all leads of the electrocardiogram for abnormal ST segment morphology. In some studies, STE in aVR that is greater than the STE in V1 distinguishes left main disease from left anterior descending artery disease.

Findings such as STE in aVR are often labeled, "STEMI equivalents." Though not widely recognized as automatic triggers for cath lab activation, these concerning electrocardiographic findings represent time sensitive conditions that benefit from an early interventional approach. Other equivalents include:

• Posterior wall MI (ST depression anteriorly)
• New left bundle in association with chest pain/ACS history 
• Hyperacute T waves
• The deWinter ST/T complex
• Positive Sgarbossa criteria

References
1. Yamaji H, Iwasaki K, Kusachi S, 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 V1. J Am Coll Cardiol. 2001;38(5):1348-54

2. Nough H, Jorat MV, Varasteravan HR, et al. The value of ST segment elevation in lead aVR for predicting left main coronary artery lesion in patients suspected of acute coronary syndrome. Rom J Intern Med. 2012;50(2):159-64

3. Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiol. 2008;41(6):626-9

Where is the Circulatory Road Block?

Case

An 81 y/o female with DM, HTN, and bilateral lower extremity amputations presents to EMS with chest pain and vomiting. VS: BP: 90/40, P: 80, R:16. Sp02: 95%. The patient is alert and oriented and in mild distress. An ECG is obtained. What is your interpretation ?

12 Lead ECG

ECG Interpretation 

A first degree AV block is present. Deep Q waves and ST elevations are present in the inferior leads III, and aVF. Additional ST segment elevations are present in the anterior precordial leads V3, V4, and V5. Reciprocal depression is present in leads I and aVL. A right bundle branch block is suggested by the positively deflected QRS and increased QRS duration seen in V1. This patient is experiencing a large STEMI given the presence of elevation in multiple territories. ST elevations suggest active injury and ischemia in the inferior and anterior leads. The relative hypotension may indciate cardiogenic shock. Cardiogenic shock complicates a significant percentage of anterior wall myocardial infarctions. Multi-territorial ST elevations indicates a poor prognosis.

Treatment Course 

Providers transmit the 12 lead ECG and alert the receiving facility of an ST elevation myocardial infarction. Aspirin is administered. The patient proceeds directly to the cath lab. The patient had severe, multi-vessel, obstructive coronary artery disease and unfortunately expired from decompensated cardiogenic shock

Key Points

• Remain vigilant for the presence of cardiogenic shock in the presence of anterior wall ischemia
• ST elevations in multiple geographic areas (inferior and anterior in this case) indicate severe disease
• Ventricular fibrillation can also accompany large anterior wall MIs
• Relative hypotension is extremely significant in patients who are accustomed to higher blood pressures. In this case, the patient's marginal blood pressure resulted from acutely decreased cardiac output. 

The History of Present (and Past) Illness

EMS responds to the home of a 69 yo male patient. The patient reports retrosternal chest pain x 3 hours. The patient has taken 2 of his own nitroglycerin without relief. The patient reports mild shortness of breath. He denies nausea or loss of consciousness. The  patient is slightly diaphoretic and states, "you know, this feels entirely similar to my previous MI's." The patient has a history of coronary artery disease, HTN, and placement of three metal stents.

Vital signs:
BP: 180/100
P: 90
R: 22

Sp02: 94%

12 Lead ECG:

12 Lead ECG Interpretation and Discussion:

There is a baseline sinus rhythm. The rate is approximately 80 beats per minute. There is ST segment elevation in lead I. In addition, ST segment elevation is present in leads V2-V4. There are no reciprocal changes in the inferior wall leads. There are non specific ST segment changes (flattening) present in leads V5-V6.  The QRS axis is difficult to determine but the slightly positive complex in lead aVF and the positive complex in lead I put the mean vector at about 0 degrees, or within the physiologically "normal" range. (17 degrees according to the all knowing interpretation software..)
Incidentally, the QRS is decreased in amplitude. Low voltage QRS is concerning in the setting of patients who present in extremis or with hypotension. Low voltages can indicate serious underlying conditions such as pericardial effusion and tamponade. The patient is hypertensive and a bit tachypneic (RR>18). Remain vigilant for the development of pulmonary edema.



The distribution of the ST segment elevation suggests an acute infarction of the heart's septal and anterior walls. Lead I STE may indicate some lateral involement as well. Patients with anterior wall STEMI are at risk for the development of dysrhythmia and congestive heart failure. The routine administration of morphine sulfate, contrary to many established protocols, has not been associated with improved patient outcome. Administer aspirin, nitroglycerin, and transport to a facility capable of percutaneous coronary intervention.

As mentioned in previous cases, ST segment elevation in leads aVR or even V1 may be predictive of a left main coronary artery occlusion. The anterior wall injury pattern, as seen in this ECG, may be due to acute occlusion of the left anterior descending artery or one of its branches. It is challenging to reliably identify the culprit lesion; anatomy is always better defined during the cardiac catheterizaton.

Final ECG Interpretation:
Sinus rhythm, rate of 90, anterior wall STEMI. Probable acute lateral wall ischemia  Low voltage QRS.  

A Serial Case

An elderly male patient is transported to the emergency department following a syncopal episode. The patient reported feeling lightheaded, and experienced two witnessed syncopal episodes lasting for several minutes. Symptoms were made worse when standing up. The patient denied chest pain and reported some mild dyspnea. The patient had been in his usual state of health. The patient's medical history is significant for a tibial fracture several months prior.

Vitals:

Afebrile

BP: 72/P

P: 100

R: 24

Sp02: 92%, poor waveform, on NRB

Physical exam:

Pt is diaphoretic and alert.

Lungs are clear bilaterally.

The patient's abdomen is soft and non tender.
No evidence of lower extremity edema.

(Prehospital) 12 lead ECG:

Upon arrival at the hospital, large bore IV access was secured. A FAST (Focused Assessment with Sonography for Trauma) exam revealed no obvious free fluid and no obvious pericardial effusion. The abdominal aorta appeared grossly normal. The patient remained alert and responded to a bolus of IV crystalloid. A repeat ECG was obtained following another pre-syncopal event in the emergency department.

12 Lead ECG Interpretation and Discussion

On the repeat ECG, a sinus rhythm is present. The electrical axis is physiologic. Artifact interferes with the tracing in the inferior limb leads. ST segment elevation is present in aVR, V1, and V2. The ST segments appear horizontal in shape. That particular morphology is concerning for ischemia. While some mild ST segment depression is present in lead I, there are no clear cut reciprocal changes. The evolving changes suggest a septal wall myocardial infarction.

Final Interpretation

Sinus tachycardia, septal ST segment elevation myocardial infarction

(WRONG!)

Case Conclusion

The patient was transported emergently to the cardiac catheterization lab. The patient's coronary arteries were CLEAN and without evidence of disease. An emergent echocardiogram showed a severely dilated right ventricle with concurrent diastolic dysfunction. The clean coronary arteries and echocardiograpghic findings combined point to a massive pulmonary embolism as the cause of the patient's symptoms. Another subtle clue to this diagnosis was the hypoxia that persisted with high flow oxygen administration.

Though not all that elevates is a STEMI, field providers should nevertheless focus on identifying worrisome ST segment changes. The patient's initial ECG was somewhat non-specific. Though close inspection can reveal some slight ST segment elevation of less than 1mm in aVR and V1, it certainly did not meet standardized criteria for STEMI. The second ECG, however, represents a clear-cut evolution. ST segments have become more pronounced (elevated) in the septal leads. The increase in elevation combined with the horizontal plateau of the ST segments in leads V1-V2 suggest an evolving myocardial infarction- or an alternative diagnosis.

The patient presented with a syncopal episode and profound hypotension. Any number of emergent medical conditions can present with those complaints. Pulmonary embolism, internal bleeding, and aortic dissection must be considered in the initial assessment of the hypotensive patient. Unfortunately, there are no "classic" electrocardiographic findings associated with a large PE. That said, the following features can be seen in the setting of a pulmonary embolism.

PULMONARY EMBOLISM ECG FINDINGS

• Sinus tachycardia
• Right bundle branch block or incomplete right bundle branch block
• Deep S wave in lead I, Q wave in lead III, and an interveted T wave in lead III (S1, Q3, T3)
• T wave inversions
• Right axis deviation
• ST segment deviation (depression and elevation)

Sinus tachycardia and right bundle branch block may suggest "heart strain." These are electrical manifestations caused by the right ventricle that is pumping against a greatly increased pulmonary resistance.

aVR Rears its Ugly Elevation

A cardiologist's office calls 911 for an elderly patient who suffered a syncopal episode. The patient presented to the physician's office for a few weeks of bilateral arm pain and fatigue. The patient experienced mild dyspnea on exertion and was undergoing a chemical stress test when he experienced a brief syncopal episode. The patient was pain free at the time of EMS arrival. The patient was awake and alert. Vital signs:
BP: 104/70
P: 100
R: 22/non labored
Sp02: 96%

The cardiologist suggested transport to a facility capable of percutaneous coronary intervention. Why was the cardiologist so concerned (aside from the presence of an elderly patient with syncope in his office)? What's going on with this ECG?

12 lead ECG

12 Lead Interpretation and Discussion

The patient's rhythm is a borderline sinus tachycardia. ST segment elevation is present in leads aVR and V1. Diffuse ST segment elevation is present in the inferior and lateral leads. Though ST segment elevation in lead aVR isn't typically considered a "STEMI," there is sufficient evidence in the emergency cardiology literature that it should be considered as a "STEMI equivalent." ST segment elevation of > 1 mm (or > 0.5 mm in some studies) is associated with obstruction of the left main coronary artery. Furthermore, these patients are more likely to require surgical revascularization (CABG) or experience congestive heart failure. The skilled paramedic will easily recognize the widespread and diffuse ST segment abnormalities. This patient requires evaluation at a facility capable of percutaneous coronary intervention.

Final 12 lead ECG Interpretation

Sinus rhythm, ST segment elevation in leads aVR and V1. Probable acute obstruction of the left main coronary artery. Diffuse ST segment depression in the inferior (II, III, aVF), anterior (V4-V6), and lateral (I, aVL) leads.

Suggested Readings

• Rokos IC, French WJ, Mattu A et al. Appropriate cath lab activation: optimizing electrocardiogram interpretation and clinical decision making for acute ST elevation myocardial infarction. Am Heart Journ. Dec 2010;160(6):995-1003

• Barrabes JA, Figueras J, Moure C, et al. Prognostic value of lead aVR in patients with a first non ST segment elevation acute myocardial infarction. Circulation. 2003;108(81):814-819

• Williamson K, Mattu A, Plautz CU. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006;24:864-874

"Abnormal ECG" and Bypass of the Closest Facility

So.. would you call this one and activate the cath lab from the prehospital ECG? The patient is a 72 year old female with severe uncontrolled hypertension. She called 911 for mild shortness of breath. Her blood pressure is over 200 mm Hg systolic. The patient is awake, alert, and oriented. The paramedic is bypassing a local facility in favor of the closest cardiac interventional center.

What's your analysis?

12 Lead ECG

 

12 Lead ECG Interpretation and Discussion

A baseline sinus rhythm is present. There is a significant amount of artifact that interferes with interpretation in the limb leads. A fusion beat is seen in the limb lead tracings. However, there is > 1mm of ST segment elevation in lead III. Lead aVF also has minimal ST segment elevation. Pathologic Q waves are present in contiguous leads (III and aVF). Though an isolated Q wave is common in limb lead III, the presence of Q waves in contiguous inferior leads (III and aVF) suggests ischemia. In addition, ST segment depression is present in the reciprocal leads of I and aVL. This finding further supports the presence of acute injury. ST segment elevations are also seen in leads aVR and V1. As discussed in a previous case, the presence of STE in leads aVR and V1 may predict obstruction of the left main coronary artery. Poor R wave progression is present across the precordial leads V2-V6. This finding  (the loss of R wave amplitude) is consistent with the machine generated diagnosis of "anterior infarct, age undetermined." These findings, when put together, reveal an inferior wall STEMI. This patient is best cared for at a facility capable of percutaneous cardiac intervention.

Final interpretation

Sinus rhythm, inferior wall STEMI. Anterior wall ischemia. Reciprocal changes in the form of ST depression present in the anterior-lateral limb leads.

Ante up!

CASE PRESENTATION

The patient is a 40 yo male reporting a 9/10 pressure in the center of his chest. The patient appears pale and diaphoretic.

Family history is significant for early coronary artery disease. The patient felt well prior to experiencing the "pressure in his chest."

What does the 12 lead ECG show ?
Where is this patient's occlusion ?

12 LEAD ECG INTERPRETATION

Sinus rhtyhm, rate of 60, anterior lateral STEMI

A baseline sinus rhythm is present. ST segment elevation is seen in leads V1-V5. Leads I and aVL also reveal significant > 1 mm elevation of the ST segment. Reciprocal changes in the form of ST segment depression are best visualized in the inferior limb leads III and aVF.

The distribution of ST elevation across most of the precordium suggests obstruction of the left main or left anterior descending artery. The LAD supplies blood to the left ventricule. Diagnonal branches of the left coronary artery supply the lateral wall of the left ventricle. Occlusion of a diagnoal branch corresponds to ST elevation in leads I and aVL.

EMS PEARLS
Complications related to a massive anterior myocardial infarction include:
1. Dysrhythmia (VT/VF)
2. Congestive heart failure

Congestive heart failure may occur when approximately 40% of the LV muscle mass is lost to infarction.

You make the call!

This patient presented to an outside hospital for palpitations following the use of a routine anti-asthma medication. The patient reported chest discomfort and some associated shortness of breath shortly after medication administration. The patient's vital signs remain stable, and her lung sounds were clear. The remainder of the physical examination was unremarkable. An emergency physician obtained a routine ECG. The patient's vital signs were stable and the physical examination was unremarkable.  

The patient was transferred to a tertiary care facility for cardiac catheterization.

1. What's your interpretation of the 12 lead?
2. What are some diagnostic considerations?

12 lead ECG Interpretation
Sinus rhythm, rate approximately 70, diffuse ST segment elevation
There is a baseline sinus rhythm. Widespread ST segment elevation is present in leads I, aVL, II, III, aVF, and in the anterior-lateral precordial leads. The R waves and ST segment depression in leads V1 and V2 are consistent with posterior wall ischemia. The ST segments themselves are mostly convex. The convexity of the ST segment is also suggestive of ischemia. Infarction of the heart's anterior, inferior, lateral, and posterior walls could conceivably produce the diffuse ST segment changes seen in this ECG.

12 lead ECG Discussion and Case Resolution
There are several considerations to bear in mind when looking at diffuse ST segment elevations:
1. Massive myocardial infarction
2. Pericarditis
3. Ventricular wall aneurysm 
4. Coronary vasospasm

The patient's clinical picture (and overall well appearance) is not consistent with the diagnosis of a massive myocardial infarction.

The ST elevations in pericarditis are usually more CONCAVE in appearance. Reciprocal changes are never associated with pericarditis. PR segment depression is also present in pericarditis.

Ventricular wall aneurysm usually presents electrocardiographically with Q waves and diffuse ST segment elevations. There may be a loss of R wave progression across the precordial leads.

There was no lesion amenable to intervention at the time of angiography. The patient's echocardiogram revealed a preserved ejection fraction with some mild, but diffuse, hypokinesis. The patient was diagnosed with coronary artery vasospasm.

The Subtlety of STE and its Anatomy

This tracing was discussed at a recent STEMI committee meeting. Its much easier to spot the ischemic changes once the diagnosis is known.....

Subtle STE or artifactual nonsense ?

12 LEAD ECG INTERPRETATION

Baseline sinus rhythm, occasional fusion beats and premature atrial contractions in a bigeminal pattern, ST segment elevation in septal leads

This ECG interpretation is far from obvious. Typical criteria for activation of the cardiac catheterization lab includes at least 2 mm or greater of STE in contiguous precordial leads. Close inspection reveals minimal ST elevation in leads V2 and V3. Clear cut reciprocal changes are not present. The ST segment's shape is far from reassuring: it has a horizonal and ischemic-type appearance in lead V2.

This ECG requires you to bust out the calipers because there is a constant PR interval buried within the premature and fusion beats. At first glance, the irregular rhythm suggests atrial fibrillation. The presence of consistent PR intervals, however, rules out that diagnosis. On most tracings, P waves are best visualized in leads II and V1.

The patient went to the cardiac cath lab; the diagnosis of an acute occlusion of the "ramus." The ramus is simply an intermediate branch of the left coronary artery (LCA)  that arises in between the left anterior descending (LAD) artery and the left circumflex coronary artery. The "ramus" is abbreviated as "Int" in the illustration below.


For those of use who are more visual learners, this picture is furnished courtesy of:
http://www.cardiologysite.com/html/lad.html

The Bottom Line: NTG and ECG

A patient walked into the triage area and reported chest pain, nausea, and "indigestion" for several hours. Initial vitals were stable. After a dose of nitroglycerin, the patient's "stable" vital signs had left the building. Though conscious, a repeat set of vitals (following the NTG dose) was as follows:
BP: 76/40
(Taken mutiple times on multiple extremities)
P: 72
Sp02: 89%
The hypotension resolved after a fluid bolus. An ECG finding (conveniently circled by an alert resident) reveals the answer to the hypotension story..

Right Sided 12 LEAD ECG

12 LEAD ECG INTERPREATION AND DISCUSSION

A baseline sinus rhythm is present. ST segment elevations are seen in the inferior wall leads II, III, and aVF. Expected reciprocal changes in the form of ST segment depressions are seen in leads I and aVL. The right sided chest lead V4 (V4R)  shows ST elevation. STE in V4R indicates right ventricular infarction. These patients are preload dependent. Nitroglycerin is a potent vasodilator. When this drug is administered in the setting of a right ventricular infarction, it can cause significant hypotension. The precipitous drop in blood pressure usually resolved after a fluid bolus.

PEARLS

• Initiate IV access prior to nitroglycerin administration in patients with inferior wall changes
• Look for right ventricular myocardial infarction by obtaining right sided chest leads
• Right ventricuar infarction usually co-exists with inferior wall ischemia
• STE in II, III, aVF ? Start an IV and reassess folliwing NTG administration!

The Forgotten 12th Lead

A 70 yo patient presented to the ED with chest discomfort, diaphoresis, and nausea. The patient had a history of coronary artery disease and was hemodynamically stable. The patient stated that his retrosternal discomfort was similar his previous "heart attacks." The patient was pain free by the time he was moved into a monitored bed. An initial troponin level sent from triage was negative. Here's the triage EKG:

12 lead EKG interpretation
Sinus rhythm, diffuse ST segment depression, ST segment elevation in lead aVR

Discussion
The ECG, coupled with the patients presentation, is concerning for ischemia. At first glance, this ECG does not meet criteria for activation of the cath lab. A closer look at this ECG reveals cause for concern. There is ST segment elevation present in lead aVR. Often forgotten, overlooked, and otherwise thrown away, lead aVR provides important cluses to underlying cardiovascular disease. ST segment elevation in lead aVR may actually predict acute occlusion of the left main coronary artery. Specifically, STE in aVR that is LESS than STE present in lead V1 is associated with left main occlusion.

References
Gorgels APM, Engelen DJM, Wellens HJJ. Lead aVR a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol. 2001;38:1355-1356
http://content.onlinejacc.org/cgi/content/full/38/5/1355
Mattu A. Lead aVR: importance of the "forgotten 12th lead" in patients with ACS. Medscape Emergency Medicine. 2009. Available at: http://www.medscape.com/viewarticle/589781. Accessed February 2012