A 45 year old male with unknown medical history was taken into police custody under concern for trafficking illegal drugs.

While he was in the back of the squad car he told the police he had swallowed a large amount of cocaine and may need to go to the hospital.  Not long afterwards he became unresponsive and paramedics were called to the scene.

Paramedics found the patient minimally arousable.

Vital signs were assessed.

• RR: 12
• HR: 130
• NIBP: 140/69
• SpO2: 95% on room air
• Temp: 36.8 C / 98.2 F
• BGL: 137

The cardiac monitor shows “sinus tachycardia” (the prehospital ECG is unavailable).

During transport paramedics witness tonic-clonic seizure activity and 2 mg of IV lorazepam is given.

On arrival in the Emergency Department the airway is intact, respirations are shallow, and there is no response to painful stimuli.  A nasopharyngeal airway is placed, the patient is ventilated with a bag valve mask, and then intubated via rapid sequence induction.

A 12-lead ECG is acquired.

The QRS is wide at 138 ms. The QTc is prolonged at 596 ms. P waves can be seen in leads aVL and V3. This is most likely sinus tachycardia with toxicologic widening of the QRS.

200 mEq sodium bicarb is given and another 12-lead ECG is obtained.

The QRS is now 130 ms and the QTc is 587ms.

An additional 200 mEq of sodium bicarb is given and the patient is started on a sodium bicarb drip, 150 mEq in 1,000 mL at 150 mL/hr.

30 minutes later the 12-lead ECG is repeated.

The QRS is now 90 msec with QTc 464 msec.

Now the QRS shows a normal duration but there are some troubling ECG findings.

ST-segment elevation is noted in the right precordial leads (V1-V3) and the high lateral leads (I and aVL), with ST-segment depression in the inferior leads (II, III, and aVF). There are Q-waves in leads V1 and V2 with a QR pattern.

This was thought to be secondary to patient’s cocaine use and not from thrombotic disease so the cardiac cath lab was not immediately activated. Cardiac biomarkers remained negative, and the ST-segments normalized during hospitalization.

Discussion

• Cocaine acts like a Class I antiarrhythmic which causes sodium channel blockade and widening of the QRS complex.
• Treatment of toxicologic widening of the QRS consists of sodium bicarbonate (the sodium helps to overcome the blockade caused by the cocaine).
• If QRS does not improve with sodium bicarbonate an alternative diagnosis other than toxicologic widening of the QRS should be considered.
• Cocaine can also cause QT prolongation via blockade of the K+ rectifier channels.
• Other cardiovascular events such as coronary artery spasm, myocardial infarction, hemorrhagic stroke, and aortic dissection related to sympathomimetic properties of cocaine should be considered in the differential diagnosis.

EMS was dispatched to a 48-year-old female having a seizure.

As they walked into the residence the patient was laying on the couch, not responding to commands. Her carotid pulse was palpable but the radial was absent. She was noted to be cyanotic and breath sounds were clear.

Side stream ETCO2 was placed under a non-rebreather (12 mm Hg) and rapid crystalloid infusion was initiated via an 18G IV.

A 12 Lead was obtained as another first responder went to retrieve the stretcher:

The QRS is wide (160ms) with RBBB morphology (QR in V1). Q-waves and ST-segment elevation are noted in the inferior and anterior leads.

Is this patient having a STEMI?

While the patient was being treated and extricated, a history was obtained from the husband. She had previously been on anticoagulation for a deep venous thrombosis that occurred secondary to hormone therapy. Combining the patient’s history with clinical findings, acute pulmonary embolism was suspected.

Clinical Evaluation of Suspected Pulmonary Embolism

The mortality rate for pulmonary embolism is 10% when diagnosed, but less than 50% are diagnosed at presentation. While there are many signs and symptoms of acute PE, 30% will have no perception of pain, but 90% will admit to a sensation of dyspnea.

Stephen Smith, M.D. presented a similar case recently and made these useful observations:

1. Hypoxia with clear lungs is pulmonary embolism until proven otherwise
2. STEMI only causes hypoxia by causing pulmonary edema
3. Massive pulmonary embolism can result in a STEMI ECG, identical to ACS STEMI
4. Low end tidal CO2 is typical of massive PE.  High end tidal CO2 is typical of severe pulmonary edema.

Using the ECG to Diagnose a Pulmonary Embolism

The ECG cannot “make the diagnosis” of PE, but can certainly be used to bolster the diagnosis and prompt further evaluation. Changes in the ST/T waves are normally seen in massive PE, and when present can help identify patients that are likely to deteriorate if immediate intervention is not performed. Had an appropriate history not been obtained in the case above, the ST-segment elevation could have been considered a coronary occlusion.

While many are familiar with the ECG finding known as “S1Q3T3” (S-wave in lead 1, Q-wave in lead III, and inverted T-wave in lead III), in a study comparing the incidence of various ECG findings in PE, Chan TC (2001) found that this finding is present only 11-50% of the time.

Sinus tachycardia is the most common ECG finding and is present 8-69% of the time, T-wave inversions in leads III and aVF are present 17-35% of the time, and T-wave inversions in leads V1 and V2 are present 27-68% of the time. Any time you see inferior or anterior T-wave inversions you should consider acute pulmonary embolism in your differential diagnosis.

This ECG is not a representative case of these changes but for a detailed explanation of ECG changes associated with PE you can review Dr. Ken Grauer’s ECG Blog #119.

Ischemia in Acute Pulmonary Embolism

Under normal physiological conditions, the right ventricle has very little resistance relative to the left ventricle. During acute, massive PE, there is increased right ventricular afterload that causes right ventricular dilation and an increasing workload that leads to severe demand ischemia of the right ventricle, which is already prone to ischemia because of the non-dominant blood supply.

It can be extremely difficult at times to distinguish between acute coronary occlusion and PE, which is why prehospital history can be invaluable. Flight Surgeon Dr. Samuel M Galvagno said:

“Indeed, in the management of PE, the prehospital provider’s history may provide the most important clue to the underlying disease process for patients who deteriorate before interrogation by emergency department staff”.

ETCO2 in Acute Pulmonary Embolism

When a blood clot occludes a pulmonary artery the lack of blood flow to the alveoli causes an increase in dead space ventilation. Areas of the lungs that once participated in gas exchange can no longer do so. Clinically, the SpO2 will remain low or not reflective of the amount of oxygenation. As dead space increases, ETCO2 decreases.

Case Conclusion

Immediately before transport the patient became extremely bradycardic and with agonal respirations. She was promptly intubated and given 1 mg of Atropine. The heart rate significantly improved but she remained in profound shock and cyanotic despite maximal oxygen therapy.

During transport she lost a pulse and had an asystolic arrest. Transport time to the ER was approximately 1.5-2 minutes, so chest compressions were started and the receiving facility was notified of the probable massive pulmonary embolism and cardiac arrest.

The receiving physician agreed that PE was the likely diagnosis. It just so happened that an interventionalist was in the ER and was pulled over to assist in the resuscitation. ROSC was achieved and an echo was performed showing acute right heart strain.

The patient was transported to the operating theater. Direct intra-arterial tPA was administered and clot extraction was attempted. The patient rearrested and further attempts at resuscitation was unsuccessful.

References
1.) Brady, William, and Jonathon Dean Truwit. Critical Decisions In Emergency And Acute Care Electrocardiography. Chichester, West Sussex: Wiley-Blackwell, 2009. Print.
2.) EMCrit, About, Josh Farkas, and the Crew. “Two EKG Patterns Of Pulmonary Embolism Which Mimic MI”. EMCrit. N.p., 2014. Web. 31 Dec. 2015.
3.) Galvagno, Samuel M. Emergency Pathophysiology. Jackson, Wyo.: Teton NewMedia, 2003. Print.
4.) Hqmeded-ecg.blogspot.com,. “Dr. Smith’s ECG Blog: Sudden Severe SOB And ST Segment Elevation: What Is The Diagnosis And Treatment?”. N.p., 2015. Web. 31 Dec. 2015.
5.) Marx, John A et al. Rosen’s Emergency Medicine. Philadelphia: Mosby/Elsevier, 2010. Print.

EMS (with physician on board) is dispatched to a 42-year-old male with a chief complaint of chest pain and “possible heart attack.”

The patient is found lying on the couch. He appears to be reasonably comfortable and indicates that “the pain has eased a bit” since EMS was contacted.

While the patient is being undressed and the monitoring leads are attached a quick and focused history is obtained using the “SOCRATES” mnemonic.

• Site: Retrosternal
• Onset: The pain started about 1 hour ago while folk dancing at a party and become progressively worse over about 10 minutes
• Character: Poorly localized “tightness” or “discomfort”
• Radiation: Both arms and back
• Alleviating factors: Nothing makes the pain feel better
• Timing: The pain is persistent and follows no pattern
• Exacerbating: The pain seemed worse while walking to his car
• Severity: 8/10

The patient is diaphoretic but it is not clear whether it is from dancing or related specifically to the chest discomfort. He denies nausea, vomiting, palpitations, or shortness of breath, and states that he has not collapsed.

Social history: Smoking (40 pack years) and liberal alcohol use
Medical history: Hypertension
Medications: Unknown antihypertensive
Allergies: NKDA

Vital signs:

• RR: 16
• HR: 84
• NIBP: 125/82
• Temp:
• SpO2: 98% on room air

Physical exam:

The patient is a slightly overweight, stocky male, in no apparent distress. Mentation and speech are normal. Respirations appear normal. Breath sounds are clear bilaterally. Abdomen is soft and non-tender. No JVD or pitting edema. Strong radial pulses are noted bilaterally.

With this focused history and physical, acute coronary syndrome (ACS) is highest on list of differential diagnosis, with pulmonary embolism (PE) and aortic dissection possible, but much lower on the list.

A 12-lead ECG is obtained.

ST-segment elevation is noted in leads II, III, and aVF with reciprocal changes in leads I and aVL. STE III > STE II suggests occlusion of the right coronary artery (RCA) which suggests the possibility of RV infarction. Of note, there is a small amount of ST-segment elevation in lead V1 (also suggestive of RV infarction).

A right-sided 12-lead ECG is obtained. To accomplish this, the EMS crew places the precordial leads in the mirror-image position on the right side of the patient’s chest.

Editor’s note: Sometimes leads V1 and V2 are left in place and only leads V3-V6 are moved over to mirror image position on the patient’s right side.

ST-segment elevation is noted in leads V2R, V3R, V4R, V5R, and V6R suggesting proximal occlusion of the RCA and right ventricular infarction.

Prehospital treatment:

• Aspirin 250mg PO
• Ringers lactate 500 ml
• 50 mcg of Fentanyl
• Oxygen was not given as the patient reported and presented no signs of dyspnea
• A trial dose (0.4 mg) NTG SL was given as RV infarction is a (relative) contraindication

The local receiving hospital and PCI unit are contacted by cell phone and the cardiac cath lab is activated.

Additional anticoagulant and antiplatelet therapy is given in the field.

• Heparin 5000 units IV
• Prasugrel 60 mg PO

The 15-minute ride to the PCI center is uneventful and patient’s symptoms improve.

The local ED team is notified of patient’s arrival and the transfer goes smoothly. The ED physician even exchanges a “high five” with the EMS crew.

As the prehospital physician is finishing his paperwork and discussing details of the case with the receiving physician, the nurses call for help. The team rushes into the resuscitation room to find the patient unresponsive with VF on the monitor.

CPR is initiated and the patient is defibrillated a total of 3 times. After the 3^rd shock the patient erupts into wild seizure-like activity and lets out a scream followed by wild, deep inspirations.

The monitor shows a perfusing rhythm with a strong carotid pulse. The patient wakes up and asks, “What just happened?”

The patient is whisked away to the cardiac cath lab where a 95% occlusion to the RCA is successfully opened and stented. The patient is discharged a few days later.

Take-away points:

• Know your differentials and obtain a swift, focused history (SOCRATES is a useful checklist)
• All patients with chest pain should receive a 12-lead ECG early in the patient encounter
• When the patient is suffering acute inferior STEMI a right-sided 12-lead ECG can help to identify right ventricular infarction
• Be careful with nitroglycerin in the setting of right ventricular infarction
• STEMI patients should be monitored continuously with defibrillation pads in place.
• Don’t let your guard down! As Napoleon warned centuries ago, “The moment of greatest vulnerability is the instant immediately after victory.”

References:
1. https://en.wikipedia.org/wiki/SOCRATES_(pain_assessment)
2. Akbar A et al: Does this patient have an AMI? JAMA 1998;280(14):1256-63
3. Morris F, Brady WJ. ABC of clinical electrocardiography: Acute myocardial infarction-Part I. BMJ. 2002; 324: 831-4
4. http://emcrit.org/podcasts/emcrit-book-club-on-combat-by-grossman