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List the cardiac etiologies of syncope.
Differentiate between the various cardiac etiologies of syncope.
Discuss the treatment of syncope of cardiac etiology.
Syncope—fainting or passing out—is a medical condition that has been appreciated since the beginnings of medicine. The ancient Greek physician Hippocrates provided the earliest written accounts, and the word itself is derived from a Greek term meaning to interrupt or to cut short.
Syncope is characterized by the abrupt and temporary loss of consciousness followed by a complete, and often rapid, spontaneous recovery. It is commonly related to a brief interruption of adequate cerebral blood flow that disturbs the normal functions of the brain. The exact cause of syncope is often not obvious and not determined in the prehospital environment. In fact, the exact etiology of syncope is often difficult to determine even in the emergency department. Studies have shown that clinicians, despite having reviewed patient history, clinical exam findings and ECG, can identify the cause of syncope only about 50% of the time.1,2 Syncope is often benign, though it can also be the result of a number of potentially life-threatening disease processes (see Table 1). As such, it is important to approach every case of syncope as a symptom of a potentially life-threatening event, despite how benign it may appear to you.
Table 1: Etiologies of Syncope
Neurogenic syndrome (vasovagal episode)
Carotid sinus hypersensitivity
Transient ischemic attack (TIA)
Psychiatric syncope (anxiety, panic disorder)
One study found the following distribution of syncope among 341 patients:3
Cardiac (most often bradydysrhythmia or tachydysrhythmia), 23%;
Neurologic or psychiatric disease, 1%.
Worth noting is that two other studies found unexplained syncope in up to 40% of all cases.2,4
Neurocardiogenic syncope, also known as vasovagal, vasodepressor or orthostatic syncope, is syncope that results from widespread vasodilation that leads to a decrease in blood return to the heart and subsequent decrease in preload, stroke volume, cardiac output and blood pressure. Decreased blood pressure leads to decreased cerebral perfusion and therefore syncope. Cardiac syncope results from bradydysrhythmias and tachydysrhythmias, both of which lead to a decreased cardiac output, a decrease in blood pressure and decreased cerebral perfusion.
Assuming syncope is benign is a dangerous trap. While you may not be able to determine the exact cause, a thorough clinical exam and history can often point you in the right direction. A 12-lead ECG and cardiac monitoring can provide valuable information and help identify those patients with syncope of cardiac etiology.
The American Heart Association identifies several ECG findings that should raise the suspicion of a cardiac etiology of syncope.5 A patient presenting with sinus bradycardia, a prolonged PR interval or bundle branch block may be suffering from sick sinus syndrome or intermittent atrioventricular block, both of which can result in bradycardia, hypotension and syncope. Patients with Wolff-Parkinson-White syndrome, characterized by the presence of a delta wave on ECG, can experience life-threatening atrial tachyarrhythmias. Genetic sodium disorders can result in disease processes such as Brugada syndrome, which can result in life-threatening ventricular tachyarrhythmias.
The European Heart Rhythm Association has published a list of diagnostic criteria for arrhythmia-related syncope diagnosed by ECG.6 The criteria are:
Persistent sinus bradycardia less than 40 bpm or repetitive sinoatrial block or sinus pauses;
Mobitz II second- or third-degree atrioventricular block;
Alternating left and right bundle branch block;
Ventricular tachycardia or rapid paroxysmal supraventricular tachycardia;
Nonsustained episodes of polymorphic VT and long or short QT interval;
Pacemaker or implantable cardiac defibrillator malfunction with cardiac pauses.
A complete review of all of the possible causes of syncope is beyond the scope of this article. This month’s article focuses instead on the cardiac etiologies of syncope through three case studies.
Table 2: Cardiac Etiologies of Syncope
Cardiac valvular disease
Acute myocardial infarction (AMI)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C)
Case #1: Brugada Syndrome
A 38-year-old Vietnamese male presents conscious, alert and oriented to person, place, time and event as he sits in a chair in his living room in no apparent distress. His wife says she called 9-1-1 after he passed out while sitting down and watching television. She says he was out for about 20–30 seconds and acted normal after waking up.
The patient describes an acute onset of “fluttering in my chest” and dizziness, then remembers his wife “shaking me awake.” He says he’d stayed home from work today with a fever and sore throat and denies any chest pain, pressure or discomfort; neck, back or abdominal pain; difficulty breathing; weakness or headache. Following recent diagnoses of hyperlipidemia and hypertension, he was prescribed both Lipitor and hydrochlorothiazide. He has no known drug allergies.
Your clinical exam reveals skin that is warm and dry to the touch with normal color. The rest of the physical exam is normal. His vital signs are: HR, 82/min., strong and regular; BP, 126/78 mmHg; RR, 14/min. with good tidal volume; SpO2, 95% on room air. His blood glucose is 111 mg/dL, and his lead II ECG shows normal sinus rhythm (NSR). His 12-lead ECG (Figure 1) shows NSR with 1–1.5 mm of ST-segment elevation in leads V1 and V2. You note the ST segments have a “coved” appearance.
Working Through the Cardiac Causes of Syncope
Approaching this case from the cardiac perspective, we can narrow the possible etiologies of this patient’s syncope fairly effectively. Clinically, he has no signs or symptoms that would suggest pericarditis or pericardial tamponade as the etiology, nor does he have the ECG findings characteristic of these entities. Likewise, he has neither a history of arrhythmogenic right ventricular dysplasia/cardiomyopathy nor the clinical signs, symptoms or ECG findings associated with it. He is not currently experiencing bradycardia or tachycardia, but that doesn’t mean he didn’t have an episode of such. ST-segment elevation in leads V1 and V2 of the 12-lead ECG could suggest acute myocardial infarction. However, these ECG findings, as well as some of the clinical exam and history findings, are also consistent with Brugada syndrome, which can result in paroxysmal episodes of ventricular tachycardia or atrial fibrillation. This would explain the patient’s acute onset of palpitations and syncope. The patient does not have a pacemaker or ICD implanted, ruling both of those out as possible causes.
Brugada syndrome is a genetic disorder characterized by abnormal ECG findings, tachyarrhythmias and an increased risk of sudden cardiac death. The genetic disorder results in defective myocardial sodium channels that shorten the action potential (a type of sodium channelopathy) and increase the risk of cardiac arrhythmia, including ventricular tachycardia (with or without a pulse) and ventricular fibrillation.
The ECG characteristics of Brugada pattern and syndrome are not always present, but can be exacerbated by a number of factors, including fever, hypothermia, drugs (alpha agonists, beta blockers, calcium channel blockers, cocaine, alcohol, tricyclic antidepressants), electrolyte abnormalities (hyper- and hypokalemia, hypercalcemia), myocardial ischemia and electrical cardiac interventions such as pacing and cardioversion. During a period of stress brought about by one of these factors, the patient experiences myocardial irritability, the characteristic ECG pattern emerges, and the risk of cardiac dysrhythmia increases. The patient in this case had an obvious stressor, an illness with a fever.
The prevalence of the ECG changes typical of Brugada pattern are particularly high in males of Asian descent.7 The first onset of symptoms (VT, VF, syncope, sudden death), and therefore diagnosis, is around 40 years of age, though Brugada syndrome can be diagnosed at any age. This is what makes it so dangerous: It is subclinical until it is life-threatening.
To be diagnosed with Brugada syndrome, a patient must have the typical ECG features as well as one of the following clinical criteria:
History of VF/VT;
Family history of sudden cardiac death;
Family history of coved-type ECG pattern;
Agonal respirations during sleep;
Inducibility of VT/VF during electrophysiology study.
The ST-segment elevations characteristic of Brugada syndrome are not always present on ECG but are frequently “unmasked” by one of the factors previously listed. The specific ECG changes characteristic of Brugada syndrome are:
Typically found in V1–V2;
RBBB or incomplete RBBB pattern;
“Coved” type (Figure 2);
“Saddle” type (Figure 3).
Moving the V1 and V2 ECG leads up one intercostal space may increase the sensitivity of the ST-segment changes, making identification of the ECG pattern of Brugada syndrome easier.8 The coved ST-segment pattern is the most concerning, as it seems to be more associated with adverse outcomes than the saddle pattern.
There are no clinical exam findings specific to Brugada pattern or syndrome itself. A patient experiencing a cardiac dysrhythmia secondary to Brugada syndrome may experience syncope during a tachydysrhythmic event or cardiac arrest during episodes of VF/VT.
As discussed in the previous section, there are multiple factors that can result in unmasking of the ECG patterns characteristic of Brugada syndrome. As such, the clinical exam and HPI findings associated with such factors may be present. For example, the patient in this case had a fever, which may have contributed to the unmasking of his previously undiagnosed Brugada syndrome. His fever was not the result of Brugada syndrome but may have been associated with it.
You should think Brugada syndrome anytime you’re presented with a healthy male of Asian descent who has experienced a syncopal episode. The presence of any of the exacerbating factors listed above, along with syncope and ST-segment elevation in V1 and V2, should also increase your suspicion. The patient in Case #1 had two identifiable exacerbating factors for Brugada syndrome.
In the presence of witnessed ventricular dysrhythmia with other cardiac symptoms, the differentiation between STEMI and the ST-segment elevation in V1 and V2 characteristic of Brugada syndrome is much more difficult. In such cases prehospital providers should treat for STEMI rather than risk missing the diagnosis in any patient with Brugada syndrome and witnessed ventricular dysrhythmia.
There is no treatment for Brugada syndrome. The patient in Case #1 does not require oxygen, as his pulse oximetry is greater than 94% and he has no shortness of breath. He does require intravenous access and cardiac monitoring with serial 12-lead ECGs performed en route to the emergency department. Having EMS EKGs for comparison in the hospital can be lifesaving, as there may be a transient morphology that is not seen later after antipyresis and fluids.
If a patient presents with Brugada syndrome and a brady- or tachydysrhythmia, treat the dysrhythmia per your local protocols with medication or the appropriate electrical intervention. Amiodarone is the most effective antidysrhythmic for the treatment and prevention of ventricular dysrhythmias associated with Brugada syndrome.9 If you have questions or concerns regarding the proper treatment of your patient, consult with medical control and determine a plan together. Remember, these patients and their ECGs can be difficult to interpret, which makes deciding upon a treatment plan difficult.
In-hospital treatment of patients with Brugada syndrome is focused on the implantation of an implantable cardioverter-defibrillator (ICD), and patients will usually be referred for genetic testing.
Case #2: Long QT Syndrome
A 42-year-old female presents conscious, alert and oriented to person, place, time and event, sitting in a chair in the lobby of a women’s shelter after a syncopal episode. A counselor from the shelter says the woman was sitting in a chair, in no distress, when she suddenly complained of being dizzy and passed out. The counselor and a colleague laid the patient on the floor and called 9-1-1. She says there was no seizure activity, and the patient was out for 15–20 seconds, after which she “woke up and acted normal—she knew her name, recognized me and knew where she was.”
The patient reports she awoke at 6 this morning from a good night’s sleep without any complaint, then had her typical breakfast of eggs, toast and grapefruit juice. It is now 11:54 a.m. She has experienced several episodes of dizziness, weakness and palpitations over the past three hours, each lasting about 10 seconds, but that this one “lasted longer, and I passed out.” At no time did she experience chest pain, pressure or discomfort; difficulty breathing; neck, back or abdominal pain; or headache.
The patient describes a history of prescription opiate abuse for which she is currently in rehab and taking methadone. Her counselor reports the patient is current with her treatment and has not had any relapses since starting the program three months ago. In addition, she has a history of depression, for which she’s been prescribed Prozac, and is on an unknown oral contraceptive.
The patient also describes a recent episode of vomiting and diarrhea for which she sought treatment at a local emergency department. She was diagnosed with gastroenteritis and prescribed ondansetron (Zofran), which she is currently taking and has been compliant with. She has no other significant medical history or medications and no allergies. Your clinical exam reveals her skin to be warm and dry to the touch with normal color. The rest of the clinical exam is normal. Her vital signs are: HR, 76/min., strong and regular; BP, 116/60 mmHg; RR, 16/min. with good tidal volume; SpO2, 96% on room air. Her blood glucose is 109 mg/dL via glucometer, and her temperature via tympanic thermometer is 98.8ºF (37.1ºC). Her lead II ECG shows normal sinus rhythm. Her 12-lead ECG (Figure 4) shows NSR with no acute ST-segment changes.
Working Through the Cardiac Causes of Syncope
As with Case #1, we can narrow the possible etiologies of this patient’s syncope fairly effectively. She is not currently experiencing bradycardia or tachycardia, and her 12-lead ECG at first appears normal, without changes consistent with an ST-segment elevation myocardial infarction (STEMI). However, she did complain of palpitations, a symptom typically associated with tachydysrhythmia, and a close examination reveals she has a prolonged QT interval. This is most likely the result of her taking multiple medications (methadone, Prozac and an oral contraceptive), all of which prolong the QT interval and increase the risk of paroxysmal ventricular dysrhythmia, specifically torsades de pointes (TdP). Zofran may have been the medication that made her QT interval dangerously prolonged.
Long QT Syndrome
Long QT syndrome (LQTS) is a disorder of myocardial repolarization characterized by a long QT interval on the ECG. A long QT interval increases the risk of “R-on-T” phenomenon and ventricular tachydysrhythmias. It is associated with an increased risk of torsades de pointes and can be life-threatening.10 Other cardiac dysrhythmias associated with LQTS include atrial tachydysrhythmias and bradycardias, and atrioventricular blocks are possible.11 LQTS can be genetic or acquired. Congenital long QT syndrome results from a mutation of a gene that codes for cardiac ion channels and is often not clinically apparent until the patient is exposed to a drug or other risk factor.10 Acquired LQTS often results from drugs, hypokalemia, hypomagnesemia and hypocalcemia.
The list of QT-prolonging drugs is ever-evolving and too extensive to list here but is available on the Web from numerous sources, including www.crediblemeds.org. Some major classes of drugs that prolong the QT interval include:10,12
Certain gastric motility medications (metoclopramide, droperidol, ondansetron).
Most of the drugs that can produce LQTS do so by interfering with ion movement across the cardiac cell membrane through potassium channels.
Risk factors for drug-induced TdP include taking high doses of a QT-prolonging drug and concurrent use of more than one QT-prolonging drug, both of which were present in this patient. Recall that she was taking methadone as part of her prescription drug rehabilitation and ondansetron for her nausea and vomiting. Both of these drugs prolong the QT interval.
The QT interval is typically measured in lead II of a 12-lead ECG from the beginning of the QRS complex to the point at which the T wave ends. The QT interval varies inversely with the heart rate: As the heart rate increases, the QT interval decreases, and as the heart rate decreases, the QT interval increases. Therefore, a correction for heart rate is required to determine if a QT interval is within normal limits. The corrected QT interval, or QTc, is derived using Bazett’s formula: QTc = QT interval/square root of the RR interval in seconds.
The 2010 AHA/ACC scientific statement on prevention of TdP in hospital settings recommended that a QTc over the 99th percentile should be considered abnormally prolonged.13 In men this corresponds to a QTc of more than 470 ms. In women a QTc of more than 480 ms is considered prolonged. A QTc over 500 ms is considered highly abnormal for both men and women.
Remember that a prolonged QT by itself is not necessarily the issue—the increased risk of lethal cardiac dysrhythmia, especially TdP, is!
TdP, the most common cardiac dysrhythmia associated with LQTS, is a term first used by French physician Francois Dessertenne in 1966 as a polymorphic ventricular tachycardia characterized by a pattern of twisting points (Figure 5).14 There are several ECG findings characteristic for TdP:15
Frequent changes in the amplitude and morphology of the QRS complexes around the isoelectric line, resulting in a “twisting” appearance;
Episodes of drug-induced TdP frequently start with a premature ventricular complex, followed by a compensatory pause and then another PVC that typically falls close to the peak of the T wave. This can result in R-on-T phenomenon;
The first beats of TdP are typically slow and build up in rate, resulting in a “warm-up” phase, with the heart rate typically reaching 160–240 bpm;
TdP will typically terminate spontaneously, with the last beats slowing down in rate.
There are no clinical exam findings specific to LQTS itself. A patient experiencing a cardiac dysrhythmia secondary to LQTS may experience weakness and dizziness at exertion or rest, shortness of breath, chest pain or pressure or discomfort, palpitations, syncope and cardiac arrest. Arguably, the presence of a cardiac dysrhythmia makes it easier to identify the cardiac etiology of a patient’s syncope. However, patients will often experience paroxysmal cardiac dysrhythmias and may have returned to a sinus rhythm by the time EMS arrives and evaluates them.
Careful evaluation of the ECG is required to identify a long QT segment. In addition, thorough and deliberate consideration of the patient’s past medical history and medication usage can play an important role in the identification of LQTS and the possibility of paroxysmal cardiac dysrhythmias.
If a patient presents with LQTS and cardiac dysrhythmia, treat the dysrhythmia per your local protocols with medication or the appropriate electrical intervention. The AHA guidelines for treatment of patients taking QT-prolonging drugs with LQTS and paroxysmal episodes of TdP recommend the use of magnesium sulfate.15 The recommended dose is 2 grams via IV infusion. Repeat infusions of that amount can be given if TdP persists. If TdP does not terminate spontaneously or respond to magnesium sulfate, or if the patient is unstable, perform cardioversion or defibrillation immediately. The exact mechanism responsible for the effects of magnesium sulfate in TdP is unknown.
Case #3: Third-Degree Heart Block
A 68-year-old male presents conscious, alert and oriented to person, place, time and event. He lies on his couch without any complaint. The patient’s wife and another couple are present. His wife says she witnessed the patient have a syncopal episode while they were playing cards. She and the others describe a 40-second episode of loss of consciousness during which he was unarousable with loud verbal or painful stimuli. They placed the patient on the couch, and he regained consciousness soon after. He was noted to be alert to person, place and time immediately after, and in fact said, “Oh, I think I passed out.”
The patient says he experienced an acute onset of dizziness, and “everything went black real fast.” He denies any chest pain, pressure or discomfort; difficulty breathing; weakness; or headache, back or abdominal pain during this event, and says he is complaint-free and feels fine now. He has a history of “heart problems,” including one AMI in the past. He also has a history of hypertension. His medications include diltiazem and nitroglycerin, and he has no allergies. His vital signs are: HR, 50/min., strong and regular; BP, 132/78 mmHg; RR, 16/min. with good tidal volume; SpO2, 95% on room air. His blood glucose is 119 mg/dL. His lead II ECG shows a paced rhythm. The 12-lead ECG is shown in Figure 6. As you evaluate the patient’s 12-lead ECG, he suddenly loses consciousness, and you note the cardiac rhythm on Figure 7.
Working Through the Cardiac Causes of Syncope
The cause of this patient’s syncope should be very evident. He initially presented with elevated ST segments in leads II, III and aVF, indicating a possible right coronary artery (RCA) occlusion myocardial infarction. Then the patient entered a third-degree heart block—a likely cause of his syncope, as his cardiac output dropped significantly.
Atrioventricular (AV) block results from an anatomical or functional impairment of the cardiac conduction system that results in a delay or cessation in the transmission of an electrical impulse from the atria into the ventricles. The different types of AV block include:
First-degree AV block;
Second-degree AV block;
Mobitz type I;
Mobitz type II;
Third-degree AV block.
There are numerous etiologies of AV block.16 Increased vagal tone secondary to mechanisms such as carotid sinus massage, hypersensitive carotid sinus syndrome, pain, bearing down and sleeping can all result in AV block. Disease of the cardiac conduction system can result in fibrosis and sclerosis of the conduction system that interferes with electrical impulse conduction. Congenital heart disease, cardiomyopathies, myocarditis and electrolyte disturbances such as hyperkalemia can all contribute to AV block as well. Numerous medications, including digitalis, beta blockers, calcium channel blockers, amiodarone and adenosine can precipitate an AV block. The patient in Case #3 had an AV block that was most likely the result of RCA occlusion and AMI. Approximately 20% of individuals who have an AMI will develop an AV block: Eight percent percent will develop a first-degree block, 5% a second-degree block, and about 6% a third-degree block.16
The patient in Case #3 presented with an intermittent third-degree, or complete, heart block. In third-degree heart block, there is a complete interruption of all impulses traveling through the AV node from the atria to the ventricles, resulting in none of the atrial impulses being conducted to the ventricles. Without any impulses coming from the atria, a foci in the AV junction or ventricular myocardium will take over as the pacemaker and generate an escape rhythm, allowing maintenance of a perfusing rhythm.
The specific ECG characteristics of third-degree heart block include:
A regular atrial rate characterized by normal P waves;
A regular ventricular rate characterized by a slow, wide QRS if the origin is ventricular, and possibly a slow, narrow QRS if the origin is junctional;
Complete disassociation of the atrial and ventricular rhythms.
Patients with third-degree heart block can vary widely in their presentation depending on their cardiac output. Patients who maintain an adequate cardiac output despite the presence of a third-degree heart block may have minimal, if any, complaints. Patients with decreased cardiac output may experience varying degrees of weakness with or without exertion, dizziness, chest pain or pressure or discomfort, difficulty breathing and syncope. Third-degree heart block can also exacerbate preexisting diseases such as heart failure and angina, resulting in acute worsening of their signs and symptoms.
The treatment of third-degree heart block is driven by the patient’s clinical condition. All patients should have oxygen administered via the appropriate device to maintain a saturation of at least 94%, have an IV established and be placed on a cardiac monitor. Perform a 12-lead ECG to best determine the cardiac rhythm. For patients who are hemodynamically unstable, immediate transcutaneous pacing (TCP) is indicated. The AHA defines patients as unstable if any of the following are present:17
New-onset altered mental status;
Signs of shock;
Ischemic chest discomfort;
Acute heart failure.
Provide sedation when administering TCP, and consider it after the correction of hypotension in unstable patients. The patient in Case #3, after being rendered unconscious, was an obvious candidate for TCP, as he was indeed unstable and the 12-lead ECG seemed to indicate the cause of his heart block was pacemaker malfunction.
If a patient presents hemodynamically stable in third-degree heart block, try to identify the possible cause and correct any that are reversible. For example, AMI should be treated per protocol in an effort to reduce myocardial ischemia, and drug overdoses (such as by calcium channel blocker) should be identified and treated appropriately.
Atropine is not recommended for use in cases of third-degree heart block or second-degree Mobitz type II heart block, as the location of the block is most likely to be in non-AV nodal tissue and therefore not responsive to atropine. Consequently, increasing the atrial rate will not result in an increase in ventricular rate. For first- and second-degree Mobitz type I heart blocks, you can administer atropine 0.5 mg every 3–5 minutes to a maximum dose of 3 mg.17
For patients in heart block who are unresponsive or not candidates for atropine and for whom TCP is not immediately available, consider dopamine or epinephrine infusion.17 Dopamine is a catecholamine with both alpha- and beta-adrenergic properties. Dopamine infusion in patients with bradycardia and hypotension can be initiated at 5–20 mcg/kg/min. and titrated to a desired and adequate blood pressure. Epinephrine is also a catecholamine with both alpha- and beta-adrenergic properties. Like dopamine, it can be titrated to a desired blood pressure after an initial starting infusion dose of 2–10 mcg/min.
After correction of the patient’s bradycardia and an improvement of his hypotension, his AMI should be treated. He is showing 12-lead ECG findings consistent with an inferior wall AMI, so right-sided involvement should be suspected and a right-sided ECG acquired. If the right-sided ECG shows the right ventricle is involved, support the patient’s preload with the administration of fluid volume, as he will be preload dependent. Also administer aspirin, providing the patient does not have an allergy. The use of nitrates in right-sided AMI is controversial and not without the potential danger of profound hypotension. Paramedics should follow their local protocol and consult with online medical direction prior to giving nitrates in such cases. In the absence of right-sided AMI, administer nitrates per protocol, maintaining a systolic blood pressure of at least 90–100 mmHg.
1. Brignole M, Menozzi C, Bartoletti A, et al. A new management of syncope: prospective systematic guideline-based evaluation of patients referred urgently to general hospitals. Eur Heart J, 2006 Jan; 27(1): 76–82.
2. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med, 1997 Jun 15; 126(12): 989–96.
3. Alboni P, Brignole M, Menozzi C, et al. Diagnostic value of history in patients with syncope with or without heart disease. J Am Coll Cardiol, 2001 Jun 1; 37(7): 1,921–8.
4. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine (Baltimore), 1990 May; 69(3): 160–75.
5. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF Scientific Statement on the evaluation of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in collaboration with the Heart Rhythm Society: endorsed by the American Autonomic Society. Circulation, 2006 Jan 17; 113(2): 316–27.
6. Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J, 2009 Nov; 30(21): 2,631–71.
7. Alings M, Wilde A. “Brugada” syndrome: clinical data and suggested pathophysiological mechanism. Circulation, 1999 Feb 9; 99(5): 666–73.
8. Sangwatanaroj S, Prechawat S, Sunsaneewitayakul B, et al. New electrocardiographic leads and the procainamide test for the detection of the Brugada sign in sudden unexplained death syndrome survivors and their relatives. Eur Heart J, 2001 Dec; 22(24): 2,290–6.
13. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation, 2010 Mar 2; 121(8): 1,047–60.
14. Dessertenne F. La tachycardie ventriculaire á deux foyers opposes variables. Arch Mal Coeur Vaiss, 1966; 59: 263–272.
17. Neumar RW, Otto CW, et al. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Part 8: Adult Advanced Cardiovascular Life Support. Circulation, 2010; 122: S729–S767.
Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. He is also a paramedic with AMR: Sonoma Life Support in Santa Rosa, CA. E-mail firstname.lastname@example.org.
Sean M. Kivlehan, MD, MPH, NREMT-P, is an international emergency medicine fellow at Brigham & Women’s Hospital, Harvard Medical School. Contact him at email@example.com.
Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is an educator, e-learning content developer and author of numerous articles and textbook chapters. He is also the clinical education coordinator for AirLink/VitaLink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. Contact him at firstname.lastname@example.org.