Photo credit: Image courtesy of Harvey Connor, AS, NRP, Professor of EMS, Oklahoma City Community Colege, Oklahoma City, OK.
Photo credit: Reproduced with permission by Jason E. Roediger, CCT, CRAT, and Ken Grauer, MD: https///www.kg-ekgpress.com/ecq-wellens syndrome/
Photo credit: Strip courtesy of Stephen W. Smith, MD, Hennepin County Medical Center, Minneapolis, MN, Associate Profesor of Emergency Medicine, University of Minnesota, from Dr. Smith’s ECG Blog.
A wise man once said, “When you hear hoof beats look for horses, not zebras.”
That’s usually pretty good advice…unless you’re in the Serengeti. The same caveat applies when studying the ECG of a patient who just doesn’t seem to fit the usual picture.
Most EMS education programs do a good job getting students to the point where they can spot signs of myocardial infarctions on 12-lead ECGs that show the usual signs of ST segment elevation (STEMI). Time constraints often limit the opportunity to go further into conditions that are not as easy to spot and are relatively rare occurrences, but some of those conditions have significant morbidity and mortality, and knowledge of them can be helpful to the savvy medic. We will discuss two such conditions and demonstrate how they look on a 12-lead ECG.
The first such condition involves Wellens syndrome (or sign), a pattern of T-wave changes associated with left anterior descending (LAD) artery occlusion. This condition has only been described for approximately 30 years, and it is important because it signals a condition that can lead to a disastrous cardiac event.1
The patient may present with chest pain and unstable angina, but with an ECG that lacks Q waves, significant ST-elevation or abnormal R-wave progression in the precordial leads. In other words, it looks pretty normal unless you know what to look for—the characteristic T-wave changes that indicate a degree of coronary artery disease that can progress to a disastrous anterior wall MI. Proximal occlusion of the left coronary artery is often referred to as “the widow-maker” because it affects the circulation of such a large part of the myocardium.2
Wellens appears before infarction begins, and identifying it can make the difference in whether your patient progresses to an infarction. There are a number of causes associated with Wellens: the usual atherosclerosis and coronary artery disease, increased myocardial oxygen demand and other causes of stress on the heart. Cocaine use has also been associated with the syndrome.2
Your patient may complain of chest pain or pressure, tightness or heaviness, which may or may not be induced by activity. The usual associated signs and symptoms such as pain radiating to the jaw, shoulder, arm or neck; sweating; nausea; vomiting; and fatigue are often present.
One may be led astray because the usual treatment for angina—rest, oxygen and nitroglycerin—may stop the pain. Alleviation of the symptoms, however, does not mean you have averted the MI. Your patient is still at significant risk for LAD occlusion.
The ECG in Figure 1 is typical of the T-wave changes in Wellens syndrome. Notice the deeply inverted T waves in leads V3–V5, and the biphasic T waves in V2. This is the most common presentation; however, sometimes there is also a significant biphasic T wave in some of the other chest leads.
Figure 2 shows characteristic T wave inversion and “dip” in V3 and V4, and typical biphasic T waves in V1, V2 and V3.3 These findings may seem subtle at first, but after studying them they become more apparent.
Now, you may ask, “Why is this so important for me to know?” The answer depends on one critical fact: The signs typically show up only when the patient is pain-free.
Let’s say your patient presents with typical anginal pain. You run a 12-lead and see no signs of STEMI, so you give your patient oxygen and nitroglycerin and the pain goes away. Your patient has a history of angina and thanks you for your help, refusing further treatment and transport.
You’re content that you’ve done a great job and your patient is happy, so you return to service. Two days later you’re called to take care of the same patient, who’s now in cardiac arrest and ultimately does not survive. Autopsy shows 99% occlusion of her left coronary artery. You break out into a cold sweat when a friend who just finished an advanced cardiology course points out the obvious Wellens syndrome in the ECG you obtained during your first visit with this patient.
Now you know that if you had spotted the signs of LAD stenosis you would have urged your patient to go to the hospital and she might have lived.
Next we will discuss Brugada syndrome. Brugada syndrome signals a genetic condition that can be identified by characteristic findings on a 12-lead ECG. The significance of Brugada is that it often results in sudden, unexplained death in relatively young patients, typically those younger than 50 years of age. Often these patients die in their sleep. The contributing dysrhythmia is usually polymorphic ventricular tachycardia leading to ventricular fibrillation.3 Interestingly, the syndrome seems to be more prevalent in Southeast Asia, and represents the most common cause of sudden unexpected death (SUDS) in Thailand. This is significant as there are now many people of Southeast Asian descent living in the United States. The condition is more prevalent in men than women.
So, you ask, if Brugada usually presents with sudden death, how does knowing about it help anybody? The answer is not all patients with Brugada die without prior warnings. The typical patient with undiagnosed Brugada will be a male in his 40s who presents with a history of unexplained syncopal episodes and unexplained ventricular dysrhythmias. For the patient who is lucky enough to simply present with a syncopal episode and perhaps some runs of ventricular tachycardia that you deal with appropriately, being able to spot the signs of Brugada can help stave off another episode that might result in sudden death.
In Figure 3, the significant findings are in V1 and V2. V1 shows an elevated ST segment followed by a downslope that looks like an escalator seen from the side. V2 shows ST elevation also, but the final portion of the T wave also shows the characteristic diagonal downslope. This unique, straight downslope of the T wave is the characteristic sign of Brugada syndrome. This may occur in more than one lead but typically is seen in leads V1, V2 and V3.
A search of the Internet for Brugada syndrome images will reveal a number of different examples to look at. Since this condition has so recently been described, it is not uniformly presented in the current EMS texts.
One might think that the strip in Figure 3 shows a septal infarct because of the ST elevation in leads V1 and V2; however, this is not the case. Brugada is often mistaken for a STEMI, and while it can mask an anterior STEMI, that is not the case here.
While rare, this condition can be fatal, and the medic who is lucky enough to spot this pattern in a living patient can make a profound difference in that patient’s life. The condition can be managed with an implanted pacemaker/defibrillator.
Many medics are taught or believe that a 12-lead ECG is unnecessary unless an MI is suspected. Perhaps it has not been stressed enough that any patient with chest pain or any sign of a cardiac event should get a 12-lead ECG immediately.
The consequences of missing out on identifying a patient with one of these conditions can be tragic for the patient, and if a medic happens to “catch” one of these conditions, so much the better. Preventive measures can be taken and a life may be saved.
A wise man once said that all discomfort between the nose and the pelvis is cardiac-related until proven otherwise, and it is also true that “with lead II you have no clue.” In other words, only with a 12-lead ECG can one see the changes that illustrate Wellens and Brugada syndromes.
The savvy medic will investigate every unusual presentation that might suggest a cardiac event or an abnormal cardiac problem with at least a 12-lead ECG and, in appropriate cases, a 15- or 18-lead tracing.
An excellent online resource is The EKG Club, a Yahoo group open to all healthcare professionals who wish to participate in discussions about EKGs.
William E. “Gene” Gandy, JD, NREMT-P, has been a paramedic and EMS educator for over 30 years. He lectures on medical/legal aspects of EMS and lives in Tucson, AZ.
Steven “Kelly” Grayson, NREMT-P, CCEMT-P, is a critical care paramedic for Acadian Ambulance in Louisiana. He is the author of the book En Route: A Paramedic’s Stories of Life, Death, and Everything In Between, and the blog A Day in the Life of An Ambulance Driver.