STEMI 2.0

Though coronary artery disease (CAD) has experienced a reduction in mortality over the last four decades, it remains one of the leading causes of death in people over age 35. The prevalence of CAD is rising worldwide, in part due to an increasing westernization of diet in developing countries.¹

The more concerning manifestation of CAD is acute coronary syndrome (ACS), representing any patient with clinical signs and/or symptoms of acute myocardial ischemia or infarction. ACS may present as any of three subtypes: ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina (UA).

In the prehospital arena, a majority of the focus is paid to patients with STEMI, given its associated high mortality and morbidity, especially if left untreated.² More recently newly developed systems of care, aimed at increasing the recognition and timely and appropriate treatment of STEMI patients, frequently rely on EMS for the initial recognition of these dangerously ill patients.

STEMI Definition 

EKGs with concern for STEMI are further described based on anatomic location, based on the finding of at least 1 mm of ST-segment elevation in two or more anatomically contiguous leads (see Table 1).

The inferior leads of the EKG correlate with the inferior aspect of the heart, therefore (in that 80% of right-dominant patients) STEMIs in this area commonly will be due to an occlusion of the RCA. Septal lead elevation frequently represents infarction from the LAD or early branches of the LCx. Anterior MIs are usually a result of LAD or, more concerningly, left main coronary artery occlusions. Isolation lateral elevation, though rare, can be the result of either distal LCx or RCA lesions. More commonly the lateral leads are in addition to anterior or inferior elevation, representing more proximal occlusion of the same coronary arteries (LCx/LAD or RCA).

While the above patterns are “textbook,” anatomic variations result in aberrations from the typical pattern and clinical presentations. Still, the ability to identify the likely culprit vessel may be of paramount importance in providing patient care.

STEMI Syndromes

Inferior + Right Ventricle—As the RCA travels its path, it not only supplies the inferior wall of the left ventricle but also the near-entirety of the right ventricle. Depending on the location of the infarction, there may be involvement of the right ventricle as well. As this is the receptacle for all the body’s venous return, any decrease in contractility can cause significant hypotension, as blood cannot move from the right side to the left.

To combat this treatment may pivot to prioritize fluid resuscitation rather than venodilation. Recognition of right-ventricular infarctions begins with the identification of an inferior MI; however, this only evaluates the inferior aspect of the left ventricle. To determine whether the right ventricle is involved requires a right-sided EKG. Most commonly this is accomplished by moving a single lead (V4) to the same intercostal space but on the contralateral side of the chest; thus it becomes an anterior lead of the right ventricle (V4R). Alternatively, all six of the precordial leads may be transposed, allowing for V1R-V6R to be evaluated. ST-segment elevation in any right-sided lead is indicative of right-ventricular involvement, and these patients must be considered “preload dependent.” Whereas traditional education has taught the absolute avoidance of agents such as nitroglycerin, a more appropriate approach would be to ensure that the patient is appropriately volume resuscitated before the cautious use of nitrates. Given these considerations, at minimum, evaluation of V4R should routinely be performed for all patients suffering from an inferior STEMI.

Anterior + left heart failure—The major function of the LAD, LCx, and their branches is to supply blood to the left ventricle, the workhorse chamber of the heart. When these vessels become occluded, resulting in an anterior MI, dysfunction of the left ventricle is a common outcome. Consequences are twofold: First, systemic hypotension may develop due to decreased left-ventricular cardiac output. Then, as pressure builds backward, pulmonary edema begins, resulting in dyspnea and hypoxia. 

When encountered with an anterior MI, there should be a high index of suspicion for development of hypotension. Since patients with CAD often live with baseline hypertension, normal readings may be representative of relative hypotension and should be considered accordingly.

Pulmonary edema, which accompanies left ventricular failure, can be insidious at first but may progress rapidly, depending on factors such as a more proximal coronary artery lesion. Some early, more benign findings, such as tachypnea and dry cough, typically precede the more severe symptoms of hypoxia, respiratory distress, and the classic pink, frothy sputum, which often immediately precedes a respiratory arrest.

Noninvasive positive-pressure ventilation (NIPPV) using a continuous positive airway pressure (CPAP) device is a great first-line treatment in awake patients who can tolerate it, while more obtunded patients or those who will not tolerate the device may require endotracheal intubation or other advanced airway management.

NIPPV works by stenting open the fluid-filled alveoli, allowing for adequate oxygenation to occur. Further, it may help decrease preload and redistribute blood flow, improving cardiac output. Ultimately, these patients may require vasopressors (e.g. norepinephrine) and/or inotropes (e.g. dobutamine) to ensure adequate cardiac output, especially in decompensated cardiogenic shock secondary to a large anterior MI. Thus, systems not including vasoactive medications  may add them to their clinical armamentarium, either in pre-made or paramedic-mixed infusions, or the increasingly popular “push-dose” formulations. 

Septal + ventricular aneurysm—Septal MIs, while not prone to any specific acute complications, may develop in the subsequent weeks of a life-threatening septal aneurysm. These are the result of necrotic myocardium, which balloon out the left ventricle, forming a relatively thin-walled portion prone to rupture. In addition to significant mortality, they may lead to left-to-right ventricular shunts and subsequent acute right heart failure, or cor pulmonale. Blood that pools in these aneurysms may clot, with the potential for arterial embolization resulting in acute strokes, ischemic limbs, or ischemic bowel. The potential for these sequelae, especially given their non-cardiac nature, stress the importance of thorough history taking, medical inquiry, and physical exam.

Posterior—A lesser-known accompaniment of inferior and lateral MIs is the posterior STEMI, which can also present (though rarely) in isolation. When involved, posterior STEMIs represent a significantly larger area of left-ventricular involvement, increasing the likelihood of left-ventricular failure or death. Posterior ischemia can initially be recognized on a 12-lead EKG as tall, upright R-waves in leads V1–3 with ST-segment depression and upright T-waves. These can be confirmed by performing a posterior EKG, with leads V4–6 moved to their corresponding posterior positions to create leads V7–V9, which should be evaluated for ST-segment elevation. Any of the above findings, even if isolated to posterior changes, should be treated in a similar fashion to any other STEMI, including early activation of a receiving cardiac catheterization team.

Electrophysiologic considerations—As well as the myocardium, the coronary arteries are responsible for supplying blood to the nerves and nodes of the heart’s electrical conduction system. The sinoatrial (SA) node, responsible for the normal pace-setting of the heart, rests in the right atrium and is thus supplied by the RCA. Therefore, inferior MIs may result in atrial dysrhythmias such as sinus bradycardia. When combined with right-ventricular ischemia and dysfunction, acute cor pulmonale (right heart failure) may develop. In contrast, the atrioventricular (AV) node, responsible for slowing and transmitting electrical conduction from the atria to the ventricle, rests just to the right of the interatrial septum and is supplied by both the LAD and RCA. Though this potential for collateral circulation may be beneficial, large infarctions of either artery (anterior, septal, or inferior) may result in significant atrioventricular conduction delays, heart blocks, and bradycardia. Therefore, prophylactic placement of pacemaker pads may allow for more immediate treatment if these patients’ clinical course were to suddenly decline.

STEMI extension—While not necessarily a STEMI syndrome, the concept of STEMI extension warrants some attention. An MI by nature is a dynamic process, with infarct size increasing as the ischemia is left untreated and the STEMI progresses. Very similar to strokes, there are two zones of infarction—the umbra and penumbra. The umbra is the area that has already infarcted, while the penumbra is an ischemic, at-risk area which, when coupled with factors such as poor collateral blood flow, a high degree of occlusion, and lack of acute medical care, may also necrotize. Both areas are ultimately due to cellular hypoperfusion and may be due to either a worsening of the initial occlusion of the culprit vessel or an increased demand on adjacent myocardium, causing further ischemia.

From a clinical standpoint STEMI extension should promote two thoughts: First, that all patients with STEMI are ever-evolving and require constant reassessments of vitals and symptoms to determine whether the patient’s clinical presentation is worsening. Further, serial EKGs should be performed to monitor for new or worsening lead changes, raising concern that a larger area of the heart is infarcting. Second, it should encourage the use of early, appropriate, and aggressive application of ACS care, including aspirin, nitroglycerin, oxygen when indicated, and pain control. This may have a large impact on reducing the amount of penumbra that infarcts, potentially preventing worsened morbidity and mortality. 

STEMI Equivalents

A number of EKG findings should raise clinical suspicion to the same level as that of a patient with an acute STEMI. These STEMI equivalents, while often erroneously not included in cardiac catheterization lab activation criteria, carry similar risk to their traditional STEMI counterparts. Early recognition, treatment, and hospital notification may improve outcomes.

Wellens’ sign—Wellen’s sign, characterized as deep, symmetric, and inverted T-waves in the precordial leads, is concerning for a proximal LAD occlusion. There are two types of Wellens’ sign, thought to represent different ends of the same spectrum of ischemia. First Type A Wellens occurs and can be seen with a normal initial upstroke followed by an inverted terminal portion of the T-wave. As the ischemia progresses, the T-wave will completely invert, forming the more classic Type B pattern. When Wellens’ sign is present, urgent coronary catheterization should be considered.

De Winter’s T-waves—De Winter’s T-waves, also seen in proximal LAD lesions, are reported to occur in approximately 2% of anterior STEMIs. They are seen as peaked T-waves in the anterior leads preceded by small ST-segment depression. Given the similarity to standard ischemic EKG patterns, De Winter’s T-waves often remain unrecognized. Given the significant proximal occlusion of the anterior coronary arteries, patients with this EKG finding may develop significant hypotension and pulmonary edema.

Transient STEMI—In some cases STEMI changes and symptoms can significantly improve or resolve after appropriate ACS therapies are begun, especially in the case of coronary artery vasodilators such as nitroglycerin. This poses a dilemma for the care team. This is compounded in instances in which the prehospital EKG shows concerning findings but the initial ED one does not. These patients, despite their transient STEMI (TSTEMI) findings, should still undergo emergent cardiac catheterization and, if indicated, percutaneous coronary intervention.³ Even if transient changes are recognized en route to a hospital, notification and activation of a cardiac catherization team should be performed to best advocate for the patient and to optimize their outcome.

Conclusion

The basics of ACS and STEMI care may be considered routine knowledge for many providers. However, incorporating next-level evaluation such as identification of the suspected occluded vessel, anticipating associated findings based on anatomic location, and searching for equivalent findings will help ensure best possible care.  

References

1. Sanchis-Gomar F, Perez-Quilis C, Leischik R, Lucia A. Epidemiology of coronary heart disease and acute coronary syndrome. Ann Transl Med, 2016; 4(13): 256. 

2. Washington University School of Medicine Department of Medicine. “ST-Segment Elevation Myocardial Infarction.” In: Washington Manual of Medical Therapeutics, Vol. 53.

3. Meisel SR, Dagan Y, Blondheim DS, et al. Transient ST-elevation myocardial infarction: Clinical course with intense medical therapy and early invasive approach, and comparison with persistent ST-elevation myocardial infarction. Am Heart J, 2008; 155(5): 848–54. 

Caleb Rees, MD, is a former paramedic and emergency medicine resident at JPS Health Network, Fort Worth, Tex.

Veer Vithalani, MD, FACEP, is associate medical director for MedStar Mobile Healthcare in Fort Worth, Tex., and EMS director for JPS Health Network.