Vigilance Is Needed for More Serious Causes of Syncope

LAS VEGAS – Emergency physicians might see many patients with run-of-the-mill vasovagal syncope but doctors must remain vigilant for those occasional patients whose syncope has a more ominous etiology, recommends Dr. Trevor Lewis.

Syncope – the transient loss of consciousness with an inability to maintain postural tone, followed by spontaneous recovery – accounts for 1%-3% of all emergency department visits, he said at the annual meeting of the American College of Emergency Physicians.

“History is probably the most important thing you can do on anybody who has syncope,” he said. The combination of history and physical examination identifies the etiology in about 40% of cases (Arch. Intern. Med. 1999;159:375-80). Physicians should be especially alert for factors suggesting a more serious cause of the syncopal episode, such as preceding chest pain or headache, lack of prodrome, or occurrence during exertion.

An echocardiogram (ECG) identifies the etiology in less than 5% of cases of syncope. “Some people have said, it’s such a low yield, is it even worth doing? Absolutely,” Dr. Lewis said. “It’s a noninvasive test, takes 2 seconds to do, and you could potentially pick up some life-changing or [life-threatening] arrhythmias. It doesn’t matter if they are 20 or 120, you need to get an ECG on these patients.”

Laboratory work-up is of minimal value, according to Dr. Lewis, medical director of the emergency department at Cook County Hospital in Chicago. “No one has a syncope panel that they draw on patients. It’s pretty much driven by … what’s going on with the patient,” he said. Serial cardiac enzyme monitoring is likewise of little benefit, except when factors point to a cardiac etiology.

“Routine computed tomography (CT) scans are not indicated in cases of syncope to elucidate the cause unless it’s driven by a primary neurologic cause,” as suggested by history and physical examination, he said (Ann. Emerg. Med. 2007;49:431-44).

Dr. Lewis shared with attendees a few pointers for identifying and managing some potentially life-threatening conditions that can cause syncope.

Brugada Syndrome

Patients with Brugada syndrome, an inherited condition, have structurally normal hearts but electrophysiologic abnormalities causing episodes of ventricular tachycardia that can lead to syncope and sudden death.

This syndrome produces distinct ECG findings, according to Dr. Lewis, such as a right bundle branch block appearance and coved or saddle-shaped ST segment elevations.

“If you want to burn [a pattern] into your memory, this is one. … It’s the Brugada ECG,” he said. “If you have a syncopal event and you have a Brugada ECG or Brugada criteria, you have a lifetime mortality of about 27%.”

Once patients with Brugada syndrome become symptomatic, they are usually offered implantable cardioverter defibrillator therapy.

Subarachnoid Hemorrhage

Syncope, possibly preceded by headache, can be the presenting sign of subarachnoid hemorrhage, according to Dr. Lewis.

Of note, 27%-100% of all patients with subarachnoid hemorrhage, depending on the series, have ECG abnormalities such as prolonged QT intervals, large T waves, and ST-segment abnormalities.

“[It is] not going to look like an acute ST-segment MI, but it’s going to look like myocardial ischemia. So sometimes you can be a little confused or thrown off by that,” he said. “Obviously, it’s something where you don’t want to step up and start by giving aspirin or Lovenox until you see the CT scan.”

Hypertrophic Cardiomyopathy

Syncope caused by hypertrophic cardiomyopathy results from arrhythmias, outflow obstruction, and a drop in blood pressure in response to exercise.

“A lot of athletes have this and really don’t find out until they exert themselves,” Dr. Lewis observed. “It is the most common cause of sudden death in athletes.”

About 70%-90% of patients with hypertrophic cardiomyopathy have abnormal ECG findings, showing changes consistent with left ventricular hypertrophy.

Of note, the inverted T waves “are asymmetric, as opposed to ischemic inverted T waves, which are symmetric on both sides,” he said. “So that’s a little bit of a tip-off for these patients.”

Additionally, Q waves might be present in leads II, III, AVF, V5, and V6. “These are sometimes early signs or early indicators of hypertrophic cardiomyopathy that will precede echo findings [in teenagers],” he said.

On echocardiogram, required for definitive diagnosis, a ventricular wall thickness exceeding 15 mm is considered abnormal but may also be a result of physical training, which can complicate diagnosis.

“The one thing you want to remember is to avoid these medications in anybody who has hypertrophic cardiomyopathy: nifedipine, nitroglycerin, and ACE inhibitors,” he said. “These can all worsen the outflow obstruction.”

Long QT Syndrome

Patients with long QT syndrome have a genetic defect causing lengthening of ventricular repolarization, according to Dr. Lewis. Syncope occurs during episodes of polymorphic ventricular tachycardia that appear to be precipitated by stress and usually resolve spontaneously.

The ECG shows a prolonged rate-corrected QT interval (QTc). Patients’ lifetime risk of syncope and sudden death rises with this interval, from 5% at an interval of less than 440 milliseconds to 50% at an interval of greater than 500 milliseconds.

“First of all, when somebody comes in with a prolonged QTc, you want to rule out treatable causes,” he said. These include myocardial ischemia; electrolyte perturbations; certain psychiatric, cardiovascular, and antiemetic medications; and methadone.

Arrhythmogenic Right Ventricular Dysplasia

Another inherited condition, arrhythmogenic right ventricular dysplasia (ARVD) is the second most common cause of structural heart disease–related sudden cardiac death in adolescents.

The findings on an ECG can be subtle, according to Dr. Lewis. Patients have inverted T waves in the precordium, a QRS width greater than 110 milliseconds, and if ventricular tachycardia is captured, a left bundle branch block morphology. “But the tip-off is these little waves called epsilon waves,” which occur at the end of QRS complexes and look much like P waves.

ARVD is “very tough to diagnose [from the ECG]. I am sure people miss this stuff all the time,” he commented.

“From your standpoint, if a kid comes in and had a sudden syncopal event, there was no prodrome, this kid at least needs an echo,” he said. “So you might not pick it up on ECG, but you probably will pick it up on echo and see that there is something obviously wrong with his right ventricle.”

Pulmonary Embolism

Syncope in patients with pulmonary embolism occurs when right heart failure begins to cause left heart failure. They develop systemic hypotension and hypoperfusion, and lose consciousness, Dr. Lewis said.

“If someone comes in in the setting of a syncopal event and they have a pulmonary embolism, you should be concerned about it,” he noted. “There is very high association between syncope and having proximal pulmonary embolisms.”

Hence, such patients should be especially closely monitored because their condition can deteriorate rapidly, he cautioned.

Aortic Dissection

Approximately 13% of patients with aortic dissection experience syncope (Am. J. Med. 2002;113:468-71).

“It can indicate dangerous complications,” Dr. Lewis said. “If a patient ‘syncopizes’ from a dissection, you have to be concerned about two things: One, you want to make sure that they don’t have tamponade and two, that they don’t have a stroke.”

The former occurs if the dissection extends proximally and reaches the pericardium, decreasing stroke volume; the latter occurs when the dissection causes cerebral hypoperfusion.

“Syncope is also a frequent presenting sign in patients who have painless aortic dissections,” he said (Mayo Clin. Proc. 2004;79:1252-7). “Probably the scariest thing you could ever think of is having a patient with a painless aortic dissection. … It is going to be kind of tough to pick up on these patients, but always keep that in your differential when someone comes in with a syncopal event.”

Dr. Lewis had no significant financial relationships to disclose.

LAS VEGAS – Emergency physicians might see many patients with run-of-the-mill vasovagal syncope but doctors must remain vigilant for those occasional patients whose syncope has a more ominous etiology, recommends Dr. Trevor Lewis.

Syncope – the transient loss of consciousness with an inability to maintain postural tone, followed by spontaneous recovery – accounts for 1%-3% of all emergency department visits, he said at the annual meeting of the American College of Emergency Physicians.

“History is probably the most important thing you can do on anybody who has syncope,” he said. The combination of history and physical examination identifies the etiology in about 40% of cases (Arch. Intern. Med. 1999;159:375-80). Physicians should be especially alert for factors suggesting a more serious cause of the syncopal episode, such as preceding chest pain or headache, lack of prodrome, or occurrence during exertion.

An echocardiogram (ECG) identifies the etiology in less than 5% of cases of syncope. “Some people have said, it’s such a low yield, is it even worth doing? Absolutely,” Dr. Lewis said. “It’s a noninvasive test, takes 2 seconds to do, and you could potentially pick up some life-changing or [life-threatening] arrhythmias. It doesn’t matter if they are 20 or 120, you need to get an ECG on these patients.”

Laboratory work-up is of minimal value, according to Dr. Lewis, medical director of the emergency department at Cook County Hospital in Chicago. “No one has a syncope panel that they draw on patients. It’s pretty much driven by … what’s going on with the patient,” he said. Serial cardiac enzyme monitoring is likewise of little benefit, except when factors point to a cardiac etiology.

“Routine computed tomography (CT) scans are not indicated in cases of syncope to elucidate the cause unless it’s driven by a primary neurologic cause,” as suggested by history and physical examination, he said (Ann. Emerg. Med. 2007;49:431-44).

Dr. Lewis shared with attendees a few pointers for identifying and managing some potentially life-threatening conditions that can cause syncope.

Brugada Syndrome

Patients with Brugada syndrome, an inherited condition, have structurally normal hearts but electrophysiologic abnormalities causing episodes of ventricular tachycardia that can lead to syncope and sudden death.

This syndrome produces distinct ECG findings, according to Dr. Lewis, such as a right bundle branch block appearance and coved or saddle-shaped ST segment elevations.

“If you want to burn [a pattern] into your memory, this is one. … It’s the Brugada ECG,” he said. “If you have a syncopal event and you have a Brugada ECG or Brugada criteria, you have a lifetime mortality of about 27%.”

Once patients with Brugada syndrome become symptomatic, they are usually offered implantable cardioverter defibrillator therapy.

Subarachnoid Hemorrhage

Syncope, possibly preceded by headache, can be the presenting sign of subarachnoid hemorrhage, according to Dr. Lewis.

Of note, 27%-100% of all patients with subarachnoid hemorrhage, depending on the series, have ECG abnormalities such as prolonged QT intervals, large T waves, and ST-segment abnormalities.

“[It is] not going to look like an acute ST-segment MI, but it’s going to look like myocardial ischemia. So sometimes you can be a little confused or thrown off by that,” he said. “Obviously, it’s something where you don’t want to step up and start by giving aspirin or Lovenox until you see the CT scan.”

Hypertrophic Cardiomyopathy

Syncope caused by hypertrophic cardiomyopathy results from arrhythmias, outflow obstruction, and a drop in blood pressure in response to exercise.

“A lot of athletes have this and really don’t find out until they exert themselves,” Dr. Lewis observed. “It is the most common cause of sudden death in athletes.”

About 70%-90% of patients with hypertrophic cardiomyopathy have abnormal ECG findings, showing changes consistent with left ventricular hypertrophy.

Of note, the inverted T waves “are asymmetric, as opposed to ischemic inverted T waves, which are symmetric on both sides,” he said. “So that’s a little bit of a tip-off for these patients.”

Additionally, Q waves might be present in leads II, III, AVF, V5, and V6. “These are sometimes early signs or early indicators of hypertrophic cardiomyopathy that will precede echo findings [in teenagers],” he said.

On echocardiogram, required for definitive diagnosis, a ventricular wall thickness exceeding 15 mm is considered abnormal but may also be a result of physical training, which can complicate diagnosis.

“The one thing you want to remember is to avoid these medications in anybody who has hypertrophic cardiomyopathy: nifedipine, nitroglycerin, and ACE inhibitors,” he said. “These can all worsen the outflow obstruction.”

Long QT Syndrome

Patients with long QT syndrome have a genetic defect causing lengthening of ventricular repolarization, according to Dr. Lewis. Syncope occurs during episodes of polymorphic ventricular tachycardia that appear to be precipitated by stress and usually resolve spontaneously.

The ECG shows a prolonged rate-corrected QT interval (QTc). Patients’ lifetime risk of syncope and sudden death rises with this interval, from 5% at an interval of less than 440 milliseconds to 50% at an interval of greater than 500 milliseconds.

“First of all, when somebody comes in with a prolonged QTc, you want to rule out treatable causes,” he said. These include myocardial ischemia; electrolyte perturbations; certain psychiatric, cardiovascular, and antiemetic medications; and methadone.

Arrhythmogenic Right Ventricular Dysplasia

Another inherited condition, arrhythmogenic right ventricular dysplasia (ARVD) is the second most common cause of structural heart disease–related sudden cardiac death in adolescents.

The findings on an ECG can be subtle, according to Dr. Lewis. Patients have inverted T waves in the precordium, a QRS width greater than 110 milliseconds, and if ventricular tachycardia is captured, a left bundle branch block morphology. “But the tip-off is these little waves called epsilon waves,” which occur at the end of QRS complexes and look much like P waves.

ARVD is “very tough to diagnose [from the ECG]. I am sure people miss this stuff all the time,” he commented.

“From your standpoint, if a kid comes in and had a sudden syncopal event, there was no prodrome, this kid at least needs an echo,” he said. “So you might not pick it up on ECG, but you probably will pick it up on echo and see that there is something obviously wrong with his right ventricle.”

Pulmonary Embolism

Syncope in patients with pulmonary embolism occurs when right heart failure begins to cause left heart failure. They develop systemic hypotension and hypoperfusion, and lose consciousness, Dr. Lewis said.

“If someone comes in in the setting of a syncopal event and they have a pulmonary embolism, you should be concerned about it,” he noted. “There is very high association between syncope and having proximal pulmonary embolisms.”

Hence, such patients should be especially closely monitored because their condition can deteriorate rapidly, he cautioned.

Aortic Dissection

Approximately 13% of patients with aortic dissection experience syncope (Am. J. Med. 2002;113:468-71).

“It can indicate dangerous complications,” Dr. Lewis said. “If a patient ‘syncopizes’ from a dissection, you have to be concerned about two things: One, you want to make sure that they don’t have tamponade and two, that they don’t have a stroke.”

The former occurs if the dissection extends proximally and reaches the pericardium, decreasing stroke volume; the latter occurs when the dissection causes cerebral hypoperfusion.

“Syncope is also a frequent presenting sign in patients who have painless aortic dissections,” he said (Mayo Clin. Proc. 2004;79:1252-7). “Probably the scariest thing you could ever think of is having a patient with a painless aortic dissection. … It is going to be kind of tough to pick up on these patients, but always keep that in your differential when someone comes in with a syncopal event.”

Dr. Lewis had no significant financial relationships to disclose.

LAS VEGAS – Emergency physicians might see many patients with run-of-the-mill vasovagal syncope but doctors must remain vigilant for those occasional patients whose syncope has a more ominous etiology, recommends Dr. Trevor Lewis.

Syncope – the transient loss of consciousness with an inability to maintain postural tone, followed by spontaneous recovery – accounts for 1%-3% of all emergency department visits, he said at the annual meeting of the American College of Emergency Physicians.

“History is probably the most important thing you can do on anybody who has syncope,” he said. The combination of history and physical examination identifies the etiology in about 40% of cases (Arch. Intern. Med. 1999;159:375-80). Physicians should be especially alert for factors suggesting a more serious cause of the syncopal episode, such as preceding chest pain or headache, lack of prodrome, or occurrence during exertion.

An echocardiogram (ECG) identifies the etiology in less than 5% of cases of syncope. “Some people have said, it’s such a low yield, is it even worth doing? Absolutely,” Dr. Lewis said. “It’s a noninvasive test, takes 2 seconds to do, and you could potentially pick up some life-changing or [life-threatening] arrhythmias. It doesn’t matter if they are 20 or 120, you need to get an ECG on these patients.”

Laboratory work-up is of minimal value, according to Dr. Lewis, medical director of the emergency department at Cook County Hospital in Chicago. “No one has a syncope panel that they draw on patients. It’s pretty much driven by … what’s going on with the patient,” he said. Serial cardiac enzyme monitoring is likewise of little benefit, except when factors point to a cardiac etiology.

“Routine computed tomography (CT) scans are not indicated in cases of syncope to elucidate the cause unless it’s driven by a primary neurologic cause,” as suggested by history and physical examination, he said (Ann. Emerg. Med. 2007;49:431-44).

Dr. Lewis shared with attendees a few pointers for identifying and managing some potentially life-threatening conditions that can cause syncope.

Brugada Syndrome

Patients with Brugada syndrome, an inherited condition, have structurally normal hearts but electrophysiologic abnormalities causing episodes of ventricular tachycardia that can lead to syncope and sudden death.

This syndrome produces distinct ECG findings, according to Dr. Lewis, such as a right bundle branch block appearance and coved or saddle-shaped ST segment elevations.

“If you want to burn [a pattern] into your memory, this is one. … It’s the Brugada ECG,” he said. “If you have a syncopal event and you have a Brugada ECG or Brugada criteria, you have a lifetime mortality of about 27%.”

Once patients with Brugada syndrome become symptomatic, they are usually offered implantable cardioverter defibrillator therapy.

Subarachnoid Hemorrhage

Syncope, possibly preceded by headache, can be the presenting sign of subarachnoid hemorrhage, according to Dr. Lewis.

Of note, 27%-100% of all patients with subarachnoid hemorrhage, depending on the series, have ECG abnormalities such as prolonged QT intervals, large T waves, and ST-segment abnormalities.

“[It is] not going to look like an acute ST-segment MI, but it’s going to look like myocardial ischemia. So sometimes you can be a little confused or thrown off by that,” he said. “Obviously, it’s something where you don’t want to step up and start by giving aspirin or Lovenox until you see the CT scan.”

Hypertrophic Cardiomyopathy

Syncope caused by hypertrophic cardiomyopathy results from arrhythmias, outflow obstruction, and a drop in blood pressure in response to exercise.

“A lot of athletes have this and really don’t find out until they exert themselves,” Dr. Lewis observed. “It is the most common cause of sudden death in athletes.”

About 70%-90% of patients with hypertrophic cardiomyopathy have abnormal ECG findings, showing changes consistent with left ventricular hypertrophy.

Of note, the inverted T waves “are asymmetric, as opposed to ischemic inverted T waves, which are symmetric on both sides,” he said. “So that’s a little bit of a tip-off for these patients.”

Additionally, Q waves might be present in leads II, III, AVF, V5, and V6. “These are sometimes early signs or early indicators of hypertrophic cardiomyopathy that will precede echo findings [in teenagers],” he said.

On echocardiogram, required for definitive diagnosis, a ventricular wall thickness exceeding 15 mm is considered abnormal but may also be a result of physical training, which can complicate diagnosis.

“The one thing you want to remember is to avoid these medications in anybody who has hypertrophic cardiomyopathy: nifedipine, nitroglycerin, and ACE inhibitors,” he said. “These can all worsen the outflow obstruction.”

Long QT Syndrome

Patients with long QT syndrome have a genetic defect causing lengthening of ventricular repolarization, according to Dr. Lewis. Syncope occurs during episodes of polymorphic ventricular tachycardia that appear to be precipitated by stress and usually resolve spontaneously.

The ECG shows a prolonged rate-corrected QT interval (QTc). Patients’ lifetime risk of syncope and sudden death rises with this interval, from 5% at an interval of less than 440 milliseconds to 50% at an interval of greater than 500 milliseconds.

“First of all, when somebody comes in with a prolonged QTc, you want to rule out treatable causes,” he said. These include myocardial ischemia; electrolyte perturbations; certain psychiatric, cardiovascular, and antiemetic medications; and methadone.

Arrhythmogenic Right Ventricular Dysplasia

Another inherited condition, arrhythmogenic right ventricular dysplasia (ARVD) is the second most common cause of structural heart disease–related sudden cardiac death in adolescents.

The findings on an ECG can be subtle, according to Dr. Lewis. Patients have inverted T waves in the precordium, a QRS width greater than 110 milliseconds, and if ventricular tachycardia is captured, a left bundle branch block morphology. “But the tip-off is these little waves called epsilon waves,” which occur at the end of QRS complexes and look much like P waves.

ARVD is “very tough to diagnose [from the ECG]. I am sure people miss this stuff all the time,” he commented.

“From your standpoint, if a kid comes in and had a sudden syncopal event, there was no prodrome, this kid at least needs an echo,” he said. “So you might not pick it up on ECG, but you probably will pick it up on echo and see that there is something obviously wrong with his right ventricle.”

Pulmonary Embolism

Syncope in patients with pulmonary embolism occurs when right heart failure begins to cause left heart failure. They develop systemic hypotension and hypoperfusion, and lose consciousness, Dr. Lewis said.

“If someone comes in in the setting of a syncopal event and they have a pulmonary embolism, you should be concerned about it,” he noted. “There is very high association between syncope and having proximal pulmonary embolisms.”

Hence, such patients should be especially closely monitored because their condition can deteriorate rapidly, he cautioned.

Aortic Dissection

Approximately 13% of patients with aortic dissection experience syncope (Am. J. Med. 2002;113:468-71).

“It can indicate dangerous complications,” Dr. Lewis said. “If a patient ‘syncopizes’ from a dissection, you have to be concerned about two things: One, you want to make sure that they don’t have tamponade and two, that they don’t have a stroke.”

The former occurs if the dissection extends proximally and reaches the pericardium, decreasing stroke volume; the latter occurs when the dissection causes cerebral hypoperfusion.

“Syncope is also a frequent presenting sign in patients who have painless aortic dissections,” he said (Mayo Clin. Proc. 2004;79:1252-7). “Probably the scariest thing you could ever think of is having a patient with a painless aortic dissection. … It is going to be kind of tough to pick up on these patients, but always keep that in your differential when someone comes in with a syncopal event.”

Dr. Lewis had no significant financial relationships to disclose.