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. 

Casting a Wide Net for Wide Complex Tachycardia 1/2

A 40 yo female is brought into the emergency department. The patient is unresponsive, hypotensive, and tachycardic. EMS providers are assisting ventilations with a bag valve masked and have attempted defibrillation without success. Paramedics state that the patient was somnolent prior to the arrest and has no cardiac history. A 12 lead ECG is obtained upon arrival at the emergency department.

BP:    80/50
P:      150
R:      12/assisted
Spo2: 100% via BVM


What are your thoughts on the 12 lead?

What is your next course of action?

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.

Purple Pacer People: Does the 12 Lead ECG Show the Whole Story? 1/2

CASE PRESENTATION 

CC:          SOB
HPI:         80 yo male with sudden onset SOB during walk. Pt recalls feeling sick and then experienced syncopal eposide. Pt denies CP. Denies recent illness.
EXAM:    Pale, anxious, diaphoretic. VS: BP: 107/70, P: 107, R: 20. Sp02: 89%. Pt retracting; clear lung sounds.
ASESS:  Severe respiratory distress
PLAN:     Vitals, 12 lead, high flow oxygen, fluid bolus, 324 mg ASA


12 LEAD ECG

12 LEAD ECG RHYTHM STRIP

EMS and ED COURSE

The providers package the patient for transport. The patient becomes progressively more short of breath. Truncal cyanosis appears and is refractory to high flow oxygen. The patient has seizure-like activity upon arrival to the ED. Compressions are started and the patient expires following thirty minutes of failed reususcitation. 

What clues are provided by the patient's history or 12 lead ECG? 

Deadly 12 Lead ECG Diagnosis: Pulmonary Embolism

Its well known that there are things other than STEMI that stand ready to confound, perturb, and otherwise confuse your clinical impression. Pulmonary embolism (PE)  is one of those things. Massive PE has been linked to all sorts of ECG changes. A recent article printed in the American Journal of Emergency Medicine highlighted some of the ECG features associated with cardiogenic shock:

• The S1 Q3 T3 sign
• qR in lead V1
• T wave inversions in V2-V4
• STE in lead V1
• STE in lead aVR

These problematic ECG signs come as no surprise to fellow ECG enthusiasts. The incomplete right bundle branch pattern + T wave inversion indicate "heart strain" that accompanies large pulmonary emboli, 

Here's a recent prehospital 12 lead concerning for pulmonary embolism: 

Bottom line:

The ECG represents a valuable screening tool. Though its not particularly sensitive or specific for pulmonary embolism, there are definitely patterns that should alert the clinician to an adverse outcomes. In the setting of suspected pulmonary embolism, for example, watch out for:

• Right bundle branch block
• Anterior T wave inversions
• STE in aVR or V1

Pointy ST Segments and Abnormal Labs

Your crew responds to a local skilled nursing facility for a patient with "abnormal labs." The nurse tells you that the patient's "K was elevated." The patient reports a near syncopal episode approximately 40 minutes prior to arrival. The patient feels weak and dizzy. No chest pain, shortness of breath, or vomiting is endorsed. The patient is ill appearing but awake, alert, and oriented.

Vital signs:
BP: 82/40
P: 49
R: 16
Sp02: 86% on room air

A 12 lead ECG is obtained:

12 Lead ECG Discussion

The rhythm is sinus bradycardia. Unless this 80 year old is a marathon runner, the rate is abnormal. Furthermore, the bradycardia occurs in association with (1) near syncope and (2) abnormal vital signs. ST segment elevation is seen in leads II, III, and aVF. Reciprocal change in the form of ST segment depression is seen in lead aVL. STE is also observed in the lateral precordial leads. The R waves are tall in V2 and V3 but there is no concurrent ST segment depression to suggest involvement of the heart's posterior wall. Q waves, though not pathologic, appear in leads II, III, and aVF, and favor the diagnosis of ischemia.

12 Lead ECG Interpretation 

Sinus bradycardia, Inferior-lateral ST segment myocardial infarction. 

Case Discussion

This case presents more than a few dilemmas and teaching points. First, it emphasizes the association between dizziness, weakness, and acute coronary syndromes. Elderly patients may not present with the classic "chest pain" or "chest pressure." Dyspnea, dizziness, and weakness are well known anginal equivalents and should be aggressively investigated, especially in the setting of abnormal vital signs. The presence of peaked T waves might suggest underlying hyperkalemia. The changes associated with hyperkalemia are usually diffuse. The STE in this ECG follows an anatomic (inferior-lateral) pattern. If there is concern for "abormal labs," then the administration of calcium is probably warranted. Calcium should always be considered first line in the management of hyperkalemic emergencies.

What About the Rate? 

This patient also presents with symptomatic bradycardia. A well accepted axiom in EMS and emergency medicine is, "fix the rate FIRST." EMS protocols would probably advocate for a healthy dose of atropine. Ischemia of the SA node (caused by RCA occlusion) can certainly result in a symptomatic bradycardia, heart blocks, and other types of badness. However, be cautious when administering atropine to a patient suffering from an active MI. Atropine will increase myocardial demand and have the potential to exacerbate ischemic symptoms. A gentle fluid bolus may suffice to mitigate hypotension, and opening of an occluded RCA will make everything right as rain...

KEY POINTS:

• Fix the rate first (WITH CAUTION in cases of active ischemia!) 
• Calcium is first line in the treatment of suspected hyperkalemia and ECG changes
• Weakness, dizziness, and syncope should be regarded as anginal equivalents- especially in the elderly 
• Inferior wall myocardial infarction can produce bradycardia, heart blocks, and syncope

Special thanks to JoElyn for providing these ridiculously complex ECGs! (And best wishes as a newly minted registry medic...) 

STill a STEMI? PART 2/2

The 80 year old male patient feels better following the administration of aspirin and NTG. The ECG is unchanged (since you're one of those providers with an incredible attention to detail, you've already recorded 2 or 3 ECGs).  Chest pain is currently 2/10, and the shortness of breath is resolved.The patient is stable and loaded into the back of your ambulance for transport to:

1) The closest facility?
2) The closest cath capable facility?

You pour over the ECG and make the call.

LEAD V1

• Lead V1 shows approximately 1 mm of elevation at the J point. The baseline is a bit wavy, however the elevation is measured at one small box.

LEAD V2

• Again, there is a slight amount of ST elevation present in leads V2-V3. Elevation is approximately 1.5mm-2mm. 

LEADS aVL and aVF

• You screen the ECG for evidence of reciprocal change, but there is no evidence of ST segment depression in the (1) inferior leads or (2) lateral leads. Again, the wavy baseline interferes with the finer details. Reciprocal change, if present, can solidify your impression of STEMI. 

The Final (non satisfying) Answer

The ECG reveals a sinus rhythm. There is a slight amount of ST segment elevation present in the precordial leads. The ECG does not meet the strict definition of STEMI. In male patients, recall that STE of greater than 2 mm / 2 small boxes must be present in the precordial leads. Specifically, AHA/ACC guidelines state that STEMI is diagnosed if > 2 mm of elevation is present in leads V2 or V3. Elevation of one small box in 2 contiguous limb leads also satisfies diagnostic criteria. There is also the absence of dynamic change when serial ECGs are examined. There is also no evidence of reciprocal change. The ST segment elevation appears physiologic and accentuated by a wavy baseline. That said, I'd probably transport the patient to a cath capable facility. When ECG findings are equivocal, it is important to look at the PATIENT. In an 80 yo male with a significant past medical history and concerning presentation, it is best to err on the side of caution. Myocardial infarction should probably be at the top of everyone's list, and a certain amount of overtriage to regional STEMI centers is acceptable. Though this ECG does not meet strict criteria for the diagnosis of STEMI, the patient's (1) advanced age and (2) concerning presentation probably warrant a trip to a cath capable facility. Sometimes, it is impossible to achieve diagnostic certainty. If patient stability and local protocols permit, a trip to a cath-capable facility is probably a good idea. Optimizing the quality of your tracing is a wonderful strategy; patient movement should be kept to a minimum when obtaining the tracing. Tachypnea, diaphoresis, and cellular phones have all been implicated as causes of interference with the ECG tracing. Finally, the presence of absence of relief following administration of NTG is unreliable for the diagnosis of acute myocardial ischemia. 

INTERPRETATION

Sinus rhythm with ST segment elevation in the septal precordial leads. Agree with LifeNET.  :-/  Acute septal MI was indeed considered. 

PREHOSPITAL TREATMENT

Serial 12 lead ECGs. Aspirin and nitroglycerin as needed for pain. Transport to a cardiac interventional center. Oxygen only if hypoxic or severe respiratory distress.

CASE RESOLUTION

The patient was admitted to the medicine floor for further observation. Serial ECGs were unchanged, and troponin measurements were normal. The patient had a bedside echocardiogram which did not show any acute wall motion abnormalities suggestive of acute infarction. The patient was scheduled for an inpatient nuclear medicine stress test.  

RESOURCES

There's a great discussion, complete with visual examples, of septal STE patterns at the Life in the Fastlane blog.  Check it out!