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Mechanical Complications of STEMI

Unfortunately not every patient that suffers a STEMI makes a complete recovery, even if treated with primary PCI. Patients that present late into their infarct have a higher risk of developing a complication.

Here are two cases that illustrate the spectrum of mechanical complications that can occur in the aftermath of an infarct.

Case 1

A 53 year old lady with hypertension and hypercholesterolaemia called an ambulance about 8 hours after the onset of her chest pain.

Vital signs are assessed.

BP: 100/60
HR: 96bpm

The pre-hospital ECG traces obtained by the paramedics are shown:

Both ECGs show clear inferior ST elevation with prominent Q waves. There is reciprocal change anterolaterally but importantly for an inferior MI, heart rate is normal. The ECGs are 50 minutes apart and the changes appear to be slightly worse on her second ECG, but not drastically.

She was still in pain on arrival at the interventional centre and transferred immediately to the cath lab. Her left system showed moderate disease in the circumflex artery. However, as expected, the acute problem was her right coronary artery, which was occluded.

Below you can see the guide catheter engaged with the blocked right coronary artery and no flow is getting past the clot.

A thin angioplasty wire is passed through the thrombus and to the distal vessel. The thrombus was more resistant (i.e. mature) than most acute infarcts, which fit with the 8 hour history of pain.

You can see even passing a 0.014” diameter wire restores some flow. The wire tip is in the posterior descending artery. Reperfusion is often when patients destabilise and indeed the patient’s heart rate dropped to 20bpm and blood pressure to 60mmHg but she responded quickly to atropine and fluid. In the proximal vessel, a filling defect can be seen which is a sizeable thrombus.

A 3.5mm wide and 38mm long drug-eluting stent was placed without complication in her RCA, producing a nice angiographic result. However, the long period of coronary occlusion may well have caused significant myocardial injury. She was kept under close observation.

A satisfying sight for any healthcare professional is seeing a patient’s ST elevation resolve after opening their artery. However, her post procedure ECGs revealed persistent ST elevation.

You can see the evolution of her infarct as the deeply inverted inferolateral T waves revert but her STs remain elevated and develop a more mature ‘rounded’ appearance.

She returned to the ward but deteriorated. Inferior STEMIs carry a more favourable prognosis than anterior (as LV function is normally not as dramatically affected), so clinical instability post procedure should be a concern. On examination she was pain-free but breathless:

RR 24
SO2 92% 2L O2
HR: 80bpm
Chest auscultation: crackles bibasally
Heart sounds: loud pansystolic murmur

A bedside echocardiogram was performed.

A parasternal long axis view reveals the posterior mitral valve leaflet is tethered. The basal posterolateral wall is hypokinetic.

A close up of the valve with colour Doppler demonstrates mitral regurgitation.

An apical 4-chamber (zoomed in) shows the mitral regurgitation is significant.

This parasternal short axis view gives the clearest demonstration of the problem. A regional wall motion abnormality is clearly seen affected the infero-septum and inferior wall. The rest of the left ventricle is contracting well.

Her chest radiograph confirmed the clinical suspicion of pulmonary oedema and she was treated with diuresis. She responded well.

Why did the patient develop pulmonary oedema?

The papillary muscles are very strong muscles connected to the mitral valve to prevent it inverting during ventricular systole. There are two papillary muscles in the left ventricle, each connected to a mitral valve leaflet.

The anterolateral papillary muscle is connected to the anterior mitral valve leaflet and receives a blood supply from both the left anterior descending artery (via a diagonal) and the circumflex artery (via an obtuse marginal). However the posteromedial papillary muscle only has one blood supply, which is the posterior descending artery, a branch of the right coronary artery in 90% of people.

Therefore one can appreciate why mitral valve problems are more common following an inferior STEMI. In this case an almost akinetic segment, which included the posteromedial papillary muscle, caused the posterior mitral valve leaflet to become fixed, causing mitral regurgitation. Even though overall left ventricular function was only mildly impaired on the echocardiogram, the regurgitant pressure into the lungs can precipitate pulmonary oedema.

In more severe cases, the papillary muscle may rupture completely causing a ‘flail leaflet’ and catastrophic mitral regurgitation. It is often fatal. This complication typically occurs 2-7 days following a myocardial infarction, so if a patient suddenly deteriorates in the days after an MI, check for a murmur and organise an urgent echocardiogram. They can develop cardiogenic shock within minutes.

Case 2

An 80 year old man suffered a severe episode of chest pain but did not seek medical attention until about 2 weeks later, by which time he’d become progressively more breathless. His primary care doctor heard a loud, previously undocumented murmur and referred him into hospital.

On examination, in addition to the murmur, he had signs of right sided heart failure with an elevated JVP and peripheral oedema. His ECG revealed inferior Q waves.

Parasternal long axis view: The septum is moving in an unusual jerky fashion and something can be seen in the RV. Despite left ventricular function appearing reasonable, the aortic valve is not opening much suggesting cardiac output is low.

Parasternal short axis: There is a large ventriculo-septal defect in the infero-septal LV. The right ventricle is severely impaired.

Apical 4 chamber:

The LV function is hyperdynamic. The infero-basal septum is tethered near the mitral and tricuspid valves but highly mobile, creating a large VSD. The right ventricular free wall appears to bulge out and the RV is almost akinetic.

Apical 4 chamber colour Doppler:

There is free flow between LV and RV.

Apical 2 chamber. This view demonstrates the bulging from the RV also appears to involve the LV. This is a sealed perforation with aneurysm formation.

In this remarkable loop, the echo probe moves and one can clearly appreciate the defect in the septum, along with the thin membranes sealing the perforation.

What happened?

In addition to problems with the mitral valve, ventricular perforation and ventriculoseptal defects (VSDs) are the two other catastrophic mechanical complications of an MI. LV wall rupture typically occurs in the first 5 days, but some can be as late as a fortnight later. In this case, it is unclear when the complication occurred.

Complete free wall rupture rapidly leads to tamponade and death, but a sub-acute perforation refers to one that has been sealed with thrombus or the pericardium. This remains very high risk for subsequent complete rupture. Somewhat paradoxically the risk of developing any mechanical complication is not proportional to the size of the infarct and small infarcts can pose a large risk.

This patient suffered both a large VSD and a sealed perforation of the inferobasal free wall.


These patients may present in cardiogenic shock and should be managed accordingly. Treatment might include diuresis, vasopressors, inotropes, intra-aortic balloon pump or mechanical cardiac support. The only definitive treatment is invasive, but these patients are exceedingly high risk and optimal timing can be very hard to judge. Most patients will be considered for early surgery but percutaneous closure of VSDs is increasing, to avoid the risk of a general anaesthetic.


  • There are three mechanical complications of acute myocardial infarction: acute mitral regurgitation, VSD and LV rupture
  • They typically occur 2-7 days following an MI
  • Have a high index of suspicion if a patient presents following an MI with a sudden deterioration
  • Symptoms and signs include breathlessness, right-sided heart failure and a new harsh pansystolic murmur
  • Urgent echocardiography is indicated and diagnostic in most cases
  • Treatment is supportive and surgical

Mechanical complications of acute myocardial infarction, accessed 26th February 2016. Available at:

Myths and Cognitive Biases in Interpretation of Wide Complex Tachycardias

“Today, the vogue seems to be an irresistible urge to call VT supraventricular with aberration…” Marriott

A middle-aged male with a complex arrhythmia history contacts EMS after several hours of palpitations.

He has an implantable cardioverter defibrillator (ICD) but denies feeling any activations. He also denies any significant symptoms of dyspnea or discomfort.

Medications: Flecainide, Mexilentine

Vital signs are assessed.

  • RR: 18
  • HR: 136
  • NIBP: 136/91
  • SpO2: 99% on room air

The cardiac monitor is attached.

Wide complex tachycardia with a rate of 136.

A 12-lead ECG is obtained.

There is a monophasic R-wave in lead V1, a right axis deviation (negative QRS in lead I and positive QRS in leads II and III), with positive concordance of QRS complexes in the precordial leads.

The treating paramedics believed the rhythm was supraventricular tachycardia (SVT) with aberrancy. The patient was transported to the Emergency Department.

Another 12-lead ECG was obtained on arrival.

Virtually identical to the prehopsital 12-lead ECG.

In the Emergency Department one physician thought the tachycardia might represent atrial fibrillation or SVT with aberrancy. Another wondered if the ECG showed Wolff-Parkinson-White syndrome.

However, a far more likely explanation is ventricular tachycardia (VT).

As Dr. Marriott observed, many clinicians are unable to resist the siren song of aberrant supraventricular tachycardia or atrial fibrillation.

Let’s look at some of the myths and cognitive biases we frequently encounter in the interpretation of wide complex tachycardias.

“I didn’t see an extreme right axis deviation.”

It is true that an extreme right axis deviation (right superior axis) in the frontal plane — “no man’s land” — is strongly supportive of VT. However, the absence of such an axis does not support a supraventricular origin.

If the focus of the VT is in the basal portion of the LV, or the RVOT, an inferior axis (as seen in our patient) will be found.

“The heart rate was too slow to be VT.”

Ventricular rhythms can present with any rate! When the rate exceeds 110-120 bpm we call it VT, while a rate of 50-110 bpm is called accelerated idioventricular rhythm.

Is VT with a rate of 130 unusual? Hardly! One study examined patients who had episodes of VT after ICD placement. Over 30% of the patients had episodes of VT at rates between 101 and 148 bpm. A more recent study found a similar rate of VT episodes at rates between 130 and 186 bpm.

“The rate seemed a little irregular so I thought maybe AF.”

Certainly, gross irregularity should prompt the clinician to consider AF with aberrant conduction! But the rhythm strip and the 12-lead look quite regular here. Having said that, VT can be irregular for brief periods, usually during the initiation or “wind up” phase.

“The patient didn’t have any symptoms even though it had been going on for hours.”

Ventricular tachycardia can be remarkably well tolerated. This patient, in particular, had a normal ejection fraction, no history of MI, and did not have any concurrent illness or intoxication during the episode.

“The ICD didn’t go off, so it probably wasn’t VT.”

Most ICDs are programmed to shock at a particular rate limit — not based on QRS morphology. Modern devices are also capable of anti-tachycardia pacing (ATP) which is not felt by the patient. It turned out that this patient had a “trigger” rate of 182 bpm.


The most important criterion for ventricular tachycardia is “wide and fast”.

In some circumstances it may be possible to distinguish between VT and SVT with aberrancy.

However, the reasons listed above are not sufficient to do so.

55 year old male with altered mental status, hypothermia, and Osborn waves

A 55 year old man is brought in by EMS for altered mental status.

It is the middle of February and he was found sleeping outside. He smells of alcohol, is moaning on the gurney, and responds to painful stimuli.

Vital signs are assessed.

  • RR: 13
  • HR: 38
  • BP: 110/90
  • Temp: Cold to touch
  • SpO2: Unable to obtain reading

A 12-lead ECG is obtained due to bradycardia and altered mental status.

Sinus bradycardia with a rate of 38. The QRS appears to be wide and there is a large notch or J-wave at the end of the QRS complex. These are classic “Osborn waves” of hypothermia. There is motion artifact due to slight shivering.

At this point the patient’s temperature was found to be 24°C / 75°F by bladder temperature monitoring.

Osborn waves typically have a positive deflection in all leads except aVR and V1. They are known by a number of other names such as the camel-hump sign, late delta waves, hypothermic waves, or prominent J-waves.

In a patient who was found outside in February, they can safely be presumed to represent hypothermia.

The physiologic cause of Osborn waves is not well understood. Since the 1920s many hypothesis have been proposed including anoxia, injury current, acidosis, delayed ventricular depolarization and early ventricular repolarization.

While the treatment of the patient with prominent Osborn waves is based on the precipitating cause, the presence of Osborn waves is related to an increased incidence of ventricular fibrillation.

The patient was aggressively resuscitated with both internal and external warming with warm intravenous fluids and forced heated air blankets.

A repeat 12-lead ECG was performed 2 hours later.

Sinus rhythm with a rate of 60. Osborn waves are still present but they are much smaller.

The patient’s temperature is now 32°C / 89°F.

As the internal temperature improved the patient’s heart rate began to rise and the Osborn waves became less prominent. However, the artifact is worse due to increased shivering.

Rewarming was continued and a third ECG was performed, 3 hours after initial presentation.

Sinus rhythm with a rate of 60. The Osborn waves have resolved. The patient is no longer shivering.

Core temperature at this point was 33°C / 91°F.


Osborn waves consist of a positive deflection at the J-point in all leads except for aVR and V1 where the deflection is negative.

Prominent J-waves can be seen in hypothermia, hypercalcemia, neurovascular accident, vasospastic angina, and Le syndrome d’Haïssaguerre (idiopathic ventricular fibrillation or as a normal variant).

While the true physiologic cause of Osborn waves is not known their presence can indicate a progression to ventricular fibrillation.

Osborn waves that are secondary to hypothermia should improve with patient warming.

Hypothermia also causes bradycardia, prolonged PR, QRS and QTc intervals, ventricular ectopy and atrial fibrillation.

Shivering may contribute to poor 12-lead ECG data quality but usually disappears below a threshold temperature.


Prehospital Use of 10% Dextrose for Management of Severe Hypoglycemia


Diabetic emergencies constitute a substantial percentage of ‘9-1-1’ calls and emergency department visits, with occurrences expected to rise as the percentage of the population diagnosed with diabetes mellitus (DM) increases.1 Severe hypoglycemia, or “diabetic shock”, is generally thought to be a true medical emergency, and treatment has been made widely available for prehospital professionals to provide to patients who are  suffering from dangerously low blood glucose levels (BGL).

Traditionally, hypoglycemia which produces unconsciousness warrants obtaining vascular access and administering highly concentrated dextrose-containing solutions intravenously in order to swiftly restore patients to a euglycemic state, but there’s a lack of consensus about just how fast those solutions should be given, or how concentrated that solution should be. A preliminary search of the various treatment algorithms used around North America, the UK, and Australia will turn up two primary methods of dextrose administration (or variations of them). They include:

  • Give highly concentrated Dextrose-containing solutions (50% Dextrose in water, or D50W) in an IVP bolus, titrated to effect, with doses ranging from 0.25g/kg to 0.5g/kg (up to 50g) and given over a short period of time.2
  • Or, give a diluted dextrose-containing solution (typically 10% Dextrose in water, or D10W), titrated to effect and infused over a longer period of time (typically 5 to 15 minutes).3

The former appears to be more prevalent amongst North American providers, while the latter is more commonly utilized in the UK and Australia.

Does one method work faster than the other?

It’s fair to think that the administration of push-dose 50% Dextrose should result in a quicker resolution of hypoglycemia when we’re comparing to an infusion of D10W, but a study published in the Emergency Medicine Journal in 2005 suggests otherwise.4 The authors compared the time from administration of treatment to the return of normal consciousness (as defined by a Glascow Coma Score of 15) following the administration of incremental doses of 50 ml of D10W (5 grams) vs 10ml aliquots of D50W (5 grams), repeated as necessary. Both groups had almost the exact same time to recovery, averaging about eight minutes each,  despite the fact that the D10W group only required a median dose of 10 grams, while the D50W group received a median dose of 25 grams.

Will administering less dextrose result in rebound hypoglycemia?

An article submitted by Kiefer et al, published in Prehospital and Disaster Medicine in 2014, looked at the feasibility, safety, and efficacy of 10% Dextrose for prehospital treatment of hypoglycemia.5 They utilized 100 ml infusions of D10W (10 grams), and over an 18-week period they treated 164 patients, and only 29 of them (18%) required a second dose, and only one required a third dose. They found no reports of adverse events related to the use of D10W, and their analysis of the data suggested that there was “little or no short-term decay in blood glucose values after D10 administration.” Additionally, an article published in 2015 by Arnold et al in the Journal of Intensive Care Medicine demonstrated that the implementation of a careful, titratable approach to the management of hypoglycemia for critically ill patients resulted in less glycemic variability following treatment.6

What are the risks of over-correcting hypoglycemia?

While the data suggests that D10W use is unlikely to result in undertreatment, there’s significant data which shows that the routine use of 50% Dextrose results in an unpredictable over-correction of blood glucose levels. This isn’t new information, as a study published in 1986 looked at the rise in blood glucose levels in both diabetic and non-diabetic patients patients who received a standard bolus of 25 g D50W.7 They found that blood glucose levels rose anywhere between 2.06 mmol/L to 20.56 mmol/L, which equates to a range of 37 to 370 mg/dl.  A massive and sudden jump in glucose levels can have many deleterious side effects, including hyperglycemia, glycosuria, hyperosmolar syndrome, and increased morbidity/mortality for patients with concomitant sepsis, MI, or CVA.

Looking beyond some of the more obvious adverse effects of over-correcting hypoglycemia, “The Rollercoaster Effect” is a commonly described short-term side effect brought about following the prehospital administration of D50W, especially in brittle diabetics, or those who have difficulty in controlling their own blood sugars. The wide range of blood glucose levels experienced over a short span of time can precede weeks of glycemic variability, which can make insulin management remarkably more difficult, and often leads to repeated periods of hypo/hyperglycemia. This leads to increased EMS activation and emergency room visits over the coming days, and exposes the patient to more risk of short-term and long-term complications. Perhaps not surprisingly, some samples of patients report having much less incidence of this roller coaster effect after they’ve been treated by EMS personnel who utilized 10% Dextrose infusions, compared to times that they’ve been treated with push-dose D50W for management of their hypoglycemia.


Emergency medicine has come a long ways since the days of blindly giving every unconscious patient D50W (see: “the coma cocktail”). Use of 10% Dextrose appears to be safe, effective, and efficient for the emergent management of clinically significant hypoglycemia. Protocols and guidelines which recommend the use of D10W instead of D50W are becoming common practice worldwide, and expert opinion supports the implementation of this practice for prehospital providers. Benefits include cost efficiency, reduced glycemic variability, and a decreased risk of side effects including nausea, vomiting, and venous irritation or phlebitis.

For more on this topic, here are a few posts from various sources:


  1. American Diabetes Association. (2014). National diabetes statistic report. Retrieved from
  2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2013). Hypoglycemia: Clinical practise guidelines. Canadian Journal of Diabetes, 37(1), S69-S71. Retrieved from
  3. Walden, E., stanisstreet, D., Jones, C., & Graveling, A. (2013). The hospital management of hypoglycaemia in adults with diabetes mellitus. Joint British Diabetes Society Guidelines. 1-31. Retrieved from
  4. Moore, C., & Woollard, M. (2005). Dextrose 10% or 50% in the treatment of hypoglycaemia out of hospital? A randomised controlled trial. Emergency Medical Journal, 22, 512-515. doi:10.1136/emj.2004.020693
  5. Kiefer, M. V., Hern, H. G., Alter, H. J., & Barger, J. B. (2014). Dextrose 10% in the treatment of out-of-hospital hypoglycemia. Prehospital and Disaster Medicine, 29, 190-194. doi:10.1017/S1049023X14000284
  6. Arnold, P., Paxton, R. A., McNorton, K., Szpunar, S., & Edwin, S. B. (2015). The effect of a hypoglycemia treatment protocol on glycemic variability in critically ill patients. Journal of Intensive Care Medicine, 30(3), 156-60. doi: 10.1177/0885066613511048
  7. Adler, P. M. (1986). Serum glucose changes after administration of 50% dextrose solution: Pre- and in-hospital calculations. American Journal of Emergency Medicine, 4(6), 504–506.

Cardiac Cath Lab Activation for Subtle Acute Inferior STEMI

EMS responds to a 78 year old male complaining of chest pain. On initial observation the patient is pale, cool, and diaphoretic. He says to the treating paramedic, “I think I’m having a heart attack.” He states that he was watching TV when he felt a crushing pain that radiated to his arm and jaw.

Pertinent Medical History

  • CABG X 2
  • Stents
  • CVA
  • Hernia Repair

Vital Signs

  • RR: 17
  • HR: 75
  • NIBP: 146/80
  • SpO2: 98% on room air

The following 12 Lead was acquired.

Sinus rhythm with ST depression in leads I, aVL, V2-V4, and 1mm of elevation in lead III.

Is this ECG diagnostic for an acute STEMI?

The Guidelines require new ST-segment elevation, measured at the J-point in at least 2 contiguous leads of ≥ 2 mm (men) or ≥ 1.5 mm (women) in leads V2-V3 and/or ≥ 1 mm in other contiguous leads or the limb leads.

Using this criteria, the EKG is only about 45% sensitive for an acute MI. That means that if we strictly went by mm criteria only 45 out of every 100 patients experiencing acute STEMI would be picked up on the 12-lead ECG. That’s a lot of missed occlusions.

Conversely, many patients have ST-segment elevation at baseline that is not the result of acute coronary occlusion.

In this case lead III is the only lead that if blown up may have about 1 mm of ST-segment elevation.

According to the treating paramedic, the patient presented with classic signs and symptoms. It may be important to note that this was an experienced paramedic and his gut told him the patient was experiencing a heart attack, so he activated the cardiac cath lab.

There were no observable changes on serial prehospital 12-lead ECGs. However, there was a difference noted on the 12-lead ECG obtained on arrival in the Emergency Department.

There is worsening of ST-segment elevation in the inferior leads, new ST-segment elevation in lead V6, and the reciprocal ST-segment depression in leads V1-V3 now looks diagnostic for posterior extension.

When I showed the initial ECG to other providers, most were quick to point out that the ECG was “not diagnostic” because of the absence of ST-segment elevation in 2 contiguous leads.

This is not surprising. Most ECG courses spend a lot of time going over “slam dunk” ECGs with significant ST-segment elevation so that students don’t learn to appreciate subtle signs of acute STEMI.

Looking at the first ECG we can be almost certain that the patient is experiencing acute inferior STEMI even though it does not meet millimeter criteria.

The ST-segment depression must be explained. One of the most salient points that impacted my understanding of subtle occlusions is that ischemia does not localize.

We have all been taught that subendocardial ischemia presents as ST-segment depression whereas transmural (epicardial) ischemia from coronary occlusion typically manifests as ST-segment elevation.

Subendocardial ischemia typically presents with ST-segment elevation in lead aVR with widespread ST-segment depression that does not “localize” to a particular set of leads.

In this case there is isolated ST-segment depression in the high lateral leads (I and aVL) and in the anterior leads (V1-V4).

This means that the most probable explanation for the ST-segment depression is not ischemia, but reciprocal changes from an inferior-posterior STEMI!

Always consider the possibility that a subtle STEMI is present when there is isolated ST-segment depression on the 12-lead ECG.

ST-segment depression in lead aVL is highly sensitive for acute inferior STEMI. If there is ST-segment depression in lead aVL you should consider the possibility of acute inferior STEMI, especially if there is ST-segment elevation in lead III.

ST-segment depression in lead aVL can precede ST-segment elevation in the inferior leads!

However, ST-segment depression in lead aVL can also be caused by so-called “secondary” ST/T-wave abnormalities. However, we can easily rule those out in this case because:

  • The QRS is not wide – There’s no bundle branch block or WPW pattern
  • There’s no high voltage – Left ventricular hypertrophy is not present
  • The QRS/T angle is not “wide” – Normally in the presence of a secondary ST/T-wave abnormality there is a general pattern of T-wave discordance. That means that when the majority of the QRS complex is positive the T-wave should be negative. When the majority of the QRS complex is negative, the T-wave should be positive.

Therefore the ST-segment changes in the initial ECG should be considered primary — due to acute STEMI.

Left ventricular hypertrophy is the most common of STEMI mimics, so it may be worthwhile to review the criteria here.

What about activating the cardiac cath lab for subtle STEMIs?

Cardiac cath lab activation should be reserved for clear-cut STEMI.

Most prehospital protocols require some combination of millimeter criteria, reciprocal changes, computerized interpretation, or ECG transmission.

With appropriate education, training, and feedback, decision rules can be created to catch more subtle STEMIs but it requires buy-in from Emergency Medicine and Cardiology.

Whether there is prehospital cardiac cath lab activation or not it makes sense to transport these patients to PCI-capable hospital if possible.

STEMI is a dynamic process. If subtle changes are present, serial ECGs often reveal dynamic changes that will then prompt cardiac cath lab activation.

Case Conclusion

After the ECG was obtained in the Emergency Department the patient was taken to the cardiac cath lab. The patient suffered ventricular fibrillation and required defibrillation. He was found to have an occluded vein graft from previous bypass. The patient was re-perfused and is now doing fine.


Smith, Stephen. “ST-depression limited to inferior leads is reciprocal to high lateral wall and represents STEMI” Dr. Smith’s ECG Blog. Web. 14 Jan 2009

Bouthillet, Tom. “Ischemia Does Not Localize! What Does It Mean? – ECG Medical Training.” ECG Medical Training. N.p., 18 Jan. 2016. Web. 03 Feb. 2016.

Mckenna, Kim D., Elliot Carhart, Daniel Bercher, Andrew Spain, John Todaro, and Joann Freel. “Simulation Use in Paramedic Education Research (SUPER): A Descriptive Study.” Prehospital Emergency Care 19.3 (2015): 432-40. Web.

“What’s the Point of ST Elevation?” — Carley Et Al. 19 (2): 126. N.p., n.d. Web. 03 Feb. 2016. “Which Patient Should Get Acute Cath Lab Activation in MI?” EMCrit. N.p., 29 Mar. 2015. Web. 03 Feb. 2016.