David Krason, MD

 

Case

A 38-year-old construction worker without significant medical history presents following witnessed syncope at her job, after standing for at least 2 hours on a particularly warm day. She reported an episode of syncope under similar circumstances 2 months prior. With each episode, she experienced “tunneling” of peripheral vision, then loss of consciousness without palpitations or incontinence. Her physical exam, vital signs (including orthostatic blood pressures), labs, and ECG were unremarkable.

Brief overview

When evaluating a patient admitted for syncope or falls, the hospitalist must address a number of questions: a) Did the patient actually have syncope?; b) What factor(s) precipitated the syncope?; c) How might similar events be prevented or mitigated in the future?; and d) Is the patient at high risk for a serious adverse outcome (for example, ventricular dysrhythmia, cardiac arrest, intracranial bleed, or death) and, therefore, in need of more immediate or intensive work-up?

The American College of Cardiology, American Heart Association, and Heart Rhythm Society guidelines define syncope as “a symptom that presents with an abrupt, transient, complete loss of consciousness, associated with inability to maintain postural tone, with rapid and spontaneous recovery” with cerebral hypoperfusion as the presumed mechanism.¹ Furthermore, “there should not be clinical features of other nonsyncope causes of loss of consciousness, such as seizure, antecedent head trauma, or apparent loss of consciousness (that is, pseudosyncope).”¹

A careful history revolving around the patient’s behavior prior to, during, and following the event, a thorough past medical history, and a review of current medications are essential. Potential obstacles in obtaining details of the event include lack of witnesses, patient’s inability to recall the experience, and inaccurate description of convulsive syncope as a “seizure” by bystanders.²

Certain characteristics may help identify types of syncope based on clinical presentation. Major categories of syncope include neurally mediated syncope (that is, vasovagal, situational, and carotid sinus hypersensitivity), orthostatic hypotension, and cardiac syncope – which may occur in the setting of acute events such as myocardial infarction, cardiac tamponade, aortic dissection, or pulmonary embolism (PE).
 

Overview of data

Obtaining a detailed history is crucial to understanding both the etiology of the syncopal event and determining which patients are at high risk for adverse outcomes. The etiology of syncope can be determined by history alone in 26% of patients younger than 65 years.³ Data on the prevalence of syncope by cause varies widely. As a general rule, in younger patients, especially those under 40 years of age, neurally mediated syncope is most common. As patients age, orthostatic hypotension and cardiac causes (including arrhythmias and structural diseases) occur more frequently, though neurally mediated syncope is still the most common.

Hospitalists should bear in mind that clear categorization of syncope is often challenging in the elderly. Retrograde amnesia can be seen following syncope in the aged, and even patients who can provide a history may not necessarily provide an accurate account of the event. For example, up to one half of patients who undergo tilt-table testing and have an observed episode of syncope deny that loss of consciousness ever occurred.⁴ Repeated falls in an elderly patient may also require an evaluation for syncope. The typical prodromal symptoms and characteristics of cardiac and neurally mediated syncope also tend to overlap in elderly patients. In a study that examined 46 variables in various age groups, only myoclonic movements during syncope and syncope during physical activity or when supine helped differentiate cardiac from neurally mediated syncope in patients over 65 years of age. Polypharmacy may also increase the susceptibility of the elderly to both orthostatic hypotension and vasovagal syncope.⁵ Though rare in younger patients, carotid sinus syncope should be considered in the older population, particularly under certain circumstances.

To aid the clinician in risk stratifying patients as relates to the likelihood of serious outcomes, a number of studies propose risk predictors for syncope (for example, the San Francisco Syncope Rule [SFSR], Evaluation of Guidelines in Syncope Study [EGSYS], Short-Term Prognosis of Syncope, Boston Syncope Rule, and the Risk Stratification of Syncope in the Emergency Department rule, to name a few). Unfortunately, the definition of and the timing of the adverse outcomes related to syncope often vary among studies, with reported risk factors ranging from anemia to hypotension on presentation to positive fecal occult blood testing, elevated brain natriuretic peptide, and various ECG findings. Nevertheless, several consistent predictors of serious adverse outcomes tend to emerge, such as hemodynamic instability, anemia, abnormal ECG, evidence of heart failure or structural heart disease, and acute coronary syndrome or its attendant symptoms.

Many of these predictors, however, would raise the clinical suspicion of most hospitalists for adverse outcomes in their hospitalized patients independent of the presence or absence of syncope. In fact, a meta-analysis has concluded that “None of the evaluated prediction tools (SFSR, EGSYS) performed better than clinical judgment in identifying serious outcomes during emergency department stay, and at 10 and 30 days after syncope.”⁶

Once the patient is hospitalized, further evaluation should be based on a careful history and physical examination. Standard evaluation also includes careful review of medications, an ECG to exclude findings suggestive of arrhythmias as well as structural or coronary artery disease, and orthostatic blood pressure measurements.¹ Additional tests should be considered as deemed appropriate. For example, in patients over 40 years of age without history of carotid artery disease or stroke and in whom no carotid artery bruit is appreciated, a carotid sinus massage may be considered. The correct technique is to massage the sinus on the right then left, each for 5 seconds in both supine and standing positions with continuous heart rate and frequent blood pressure monitoring. Reproduction of syncope, especially concurrent with a cardiac pause of greater than 3 seconds and a systolic blood pressure drop of greater than 50 mmHg, is considered a positive test. Tilt-table testing should be considered in those for whom neurally mediated syncope is suspected but not confirmed, or in patients who might benefit from further elucidation of their prodromal symptoms.

If the patient’s history is concerning for arrhythmia but without supportive ECG findings, ECG monitoring should be considered. The type of monitoring will depend on the frequency of the patient’s symptoms, with consideration given to Holter monitors for more frequent events and external patch or implantable loop recorders considered in more sporadic events. An echocardiogram can be useful in those suspected of having structural heart disease. Although the overall yield of echocardiography is elucidating the cause of syncope is low,⁷ it may help further risk stratify those patients with suspected cardiac syncope and, in some cases, help with consideration of implantable cardioverter defibrillator placement. Cardiac stress testing may be considered for exercise-related syncope or patients suspected of having cardiac ischemia. Head imaging, EEG, and carotid ultrasounds are generally considered very low-yield in patients whose history suggests true syncope.

Of note, a study recently published in the New England Journal of Medicine suggests that the prevalence of PE in patients (median age, 80 years) presenting with a first episode of syncope was 17%, a rate that is substantially higher than historically presumed.⁸ Although the prevalence of PE was highest among patients presenting with syncope of unclear origin (25%), nearly 13% of patients with other explanations for syncope also had PE.


 

 

Application of data

Treatment of syncope will depend on its etiology. Patients with neurally mediated syncope should be educated about avoiding or mitigating potential triggers (for example, orthostatic hypotension, emotional stress, severe cough, straining during urination) and recognizing prodromal symptoms. Such patients should also be counseled regarding physical counter-pressure maneuvers (for example, limb/abdominal contraction, leg crossing, hand grip) and increasing fluid and salt intake. Midodrine, an alpha-adrenergic vasoconstricting agent, may also be considered in patients with recurrent situational neutrally mediated syncope, to be taken an hour before situations that may induce syncope. Patients with carotid sinus syncope should be considered for pacemaker placement. For patients with orthostatic hypotension, potential exacerbating drugs should be held if possible and the patients counseled on liberalizing fluid and salt intake, along with rapid cool water ingestion and physical counter-pressure maneuvers. Abdominal binders, compression stockings, and midodrine, fludrocortisone, or pyridostigmine can also be considered. Treatment of syncope due to cardiac causes depends on the specific cause and should be based on established guidelines. Finally, PE should be treated with anticoagulation and, if needed, more aggressive measures (for example, thrombolysis).

Bottom Line

Our patient likely suffered from neurally mediated vasovagal syncope due to warm conditions, supported by a previous syncopal event under similar conditions. She should be counseled regarding potential physical counter-pressure maneuvers and increased fluid and salt intake when working under warm conditions.

Dr. Roberts, Dr. Krason, and Dr. Manian are hospitalists at Massachusetts General Hospital in Boston.

References

1. Shen W-K et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope. J Am Coll Cardiol. 2017 Aug 1;70(5):e39-e110.

2. Sheldon R. How to differentiate syncope from seizure. Cardiol Clin. 2015 Aug;33(3):377-85.

3. Del Rosso A et al. Relation of clinical presentation of syncope to the age of patients. Am J Cardiol. 2005 Nov 15;96(10):1431-5.

4. Blanc JJ. Syncope: Definition, epidemiology, and classification. Cardiol Clin. 2015 Aug;33(3):341-5.

5. Matthews IG et al. Syncope in the older person. Cardiol Clin. 2015 Aug;33(3):411-21.

6. Costantino G et al. Syncope risk stratification tools vs clinical judgment: An individual patient data meta-analysis. Am J Med. 2014 Nov;127(11):1126.e13-25.

7. Chiu DT et al. Are echocardiography, telemetry, ambulatory electrocardiography monitoring, and cardiac enzymes in emergency department patients presenting with syncope useful tests? A preliminary investigation. J Emerg Med. 2014;47:113-8.

8. Prandoni P et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med. 2016 Oct;375(20):1524-31.

9. Sheldon RS et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol. 2011 Mar-Apr;27(2):246-253.

10. Moya A et al. Guidelines for the diagnosis and management of syncope (version 2009): the Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Eur Heart J. 2009 Nov;30(21):2631-71.

Additional reading

1. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol. 2012 May; 59(18):1583-91.

2. Rosanio S et al. Syncope in adults: systematic review and proposal of a diagnostic and therapeutic algorithm. Int J Cardiol. 2013 Jan;162(3):149-57.

 

Case

A 38-year-old construction worker without significant medical history presents following witnessed syncope at her job, after standing for at least 2 hours on a particularly warm day. She reported an episode of syncope under similar circumstances 2 months prior. With each episode, she experienced “tunneling” of peripheral vision, then loss of consciousness without palpitations or incontinence. Her physical exam, vital signs (including orthostatic blood pressures), labs, and ECG were unremarkable.

Brief overview

When evaluating a patient admitted for syncope or falls, the hospitalist must address a number of questions: a) Did the patient actually have syncope?; b) What factor(s) precipitated the syncope?; c) How might similar events be prevented or mitigated in the future?; and d) Is the patient at high risk for a serious adverse outcome (for example, ventricular dysrhythmia, cardiac arrest, intracranial bleed, or death) and, therefore, in need of more immediate or intensive work-up?

The American College of Cardiology, American Heart Association, and Heart Rhythm Society guidelines define syncope as “a symptom that presents with an abrupt, transient, complete loss of consciousness, associated with inability to maintain postural tone, with rapid and spontaneous recovery” with cerebral hypoperfusion as the presumed mechanism.¹ Furthermore, “there should not be clinical features of other nonsyncope causes of loss of consciousness, such as seizure, antecedent head trauma, or apparent loss of consciousness (that is, pseudosyncope).”¹

A careful history revolving around the patient’s behavior prior to, during, and following the event, a thorough past medical history, and a review of current medications are essential. Potential obstacles in obtaining details of the event include lack of witnesses, patient’s inability to recall the experience, and inaccurate description of convulsive syncope as a “seizure” by bystanders.²

Certain characteristics may help identify types of syncope based on clinical presentation. Major categories of syncope include neurally mediated syncope (that is, vasovagal, situational, and carotid sinus hypersensitivity), orthostatic hypotension, and cardiac syncope – which may occur in the setting of acute events such as myocardial infarction, cardiac tamponade, aortic dissection, or pulmonary embolism (PE).
 

Overview of data

Obtaining a detailed history is crucial to understanding both the etiology of the syncopal event and determining which patients are at high risk for adverse outcomes. The etiology of syncope can be determined by history alone in 26% of patients younger than 65 years.³ Data on the prevalence of syncope by cause varies widely. As a general rule, in younger patients, especially those under 40 years of age, neurally mediated syncope is most common. As patients age, orthostatic hypotension and cardiac causes (including arrhythmias and structural diseases) occur more frequently, though neurally mediated syncope is still the most common.

Hospitalists should bear in mind that clear categorization of syncope is often challenging in the elderly. Retrograde amnesia can be seen following syncope in the aged, and even patients who can provide a history may not necessarily provide an accurate account of the event. For example, up to one half of patients who undergo tilt-table testing and have an observed episode of syncope deny that loss of consciousness ever occurred.⁴ Repeated falls in an elderly patient may also require an evaluation for syncope. The typical prodromal symptoms and characteristics of cardiac and neurally mediated syncope also tend to overlap in elderly patients. In a study that examined 46 variables in various age groups, only myoclonic movements during syncope and syncope during physical activity or when supine helped differentiate cardiac from neurally mediated syncope in patients over 65 years of age. Polypharmacy may also increase the susceptibility of the elderly to both orthostatic hypotension and vasovagal syncope.⁵ Though rare in younger patients, carotid sinus syncope should be considered in the older population, particularly under certain circumstances.

To aid the clinician in risk stratifying patients as relates to the likelihood of serious outcomes, a number of studies propose risk predictors for syncope (for example, the San Francisco Syncope Rule [SFSR], Evaluation of Guidelines in Syncope Study [EGSYS], Short-Term Prognosis of Syncope, Boston Syncope Rule, and the Risk Stratification of Syncope in the Emergency Department rule, to name a few). Unfortunately, the definition of and the timing of the adverse outcomes related to syncope often vary among studies, with reported risk factors ranging from anemia to hypotension on presentation to positive fecal occult blood testing, elevated brain natriuretic peptide, and various ECG findings. Nevertheless, several consistent predictors of serious adverse outcomes tend to emerge, such as hemodynamic instability, anemia, abnormal ECG, evidence of heart failure or structural heart disease, and acute coronary syndrome or its attendant symptoms.

Many of these predictors, however, would raise the clinical suspicion of most hospitalists for adverse outcomes in their hospitalized patients independent of the presence or absence of syncope. In fact, a meta-analysis has concluded that “None of the evaluated prediction tools (SFSR, EGSYS) performed better than clinical judgment in identifying serious outcomes during emergency department stay, and at 10 and 30 days after syncope.”⁶

Once the patient is hospitalized, further evaluation should be based on a careful history and physical examination. Standard evaluation also includes careful review of medications, an ECG to exclude findings suggestive of arrhythmias as well as structural or coronary artery disease, and orthostatic blood pressure measurements.¹ Additional tests should be considered as deemed appropriate. For example, in patients over 40 years of age without history of carotid artery disease or stroke and in whom no carotid artery bruit is appreciated, a carotid sinus massage may be considered. The correct technique is to massage the sinus on the right then left, each for 5 seconds in both supine and standing positions with continuous heart rate and frequent blood pressure monitoring. Reproduction of syncope, especially concurrent with a cardiac pause of greater than 3 seconds and a systolic blood pressure drop of greater than 50 mmHg, is considered a positive test. Tilt-table testing should be considered in those for whom neurally mediated syncope is suspected but not confirmed, or in patients who might benefit from further elucidation of their prodromal symptoms.

If the patient’s history is concerning for arrhythmia but without supportive ECG findings, ECG monitoring should be considered. The type of monitoring will depend on the frequency of the patient’s symptoms, with consideration given to Holter monitors for more frequent events and external patch or implantable loop recorders considered in more sporadic events. An echocardiogram can be useful in those suspected of having structural heart disease. Although the overall yield of echocardiography is elucidating the cause of syncope is low,⁷ it may help further risk stratify those patients with suspected cardiac syncope and, in some cases, help with consideration of implantable cardioverter defibrillator placement. Cardiac stress testing may be considered for exercise-related syncope or patients suspected of having cardiac ischemia. Head imaging, EEG, and carotid ultrasounds are generally considered very low-yield in patients whose history suggests true syncope.

Of note, a study recently published in the New England Journal of Medicine suggests that the prevalence of PE in patients (median age, 80 years) presenting with a first episode of syncope was 17%, a rate that is substantially higher than historically presumed.⁸ Although the prevalence of PE was highest among patients presenting with syncope of unclear origin (25%), nearly 13% of patients with other explanations for syncope also had PE.


 

 

Application of data

Treatment of syncope will depend on its etiology. Patients with neurally mediated syncope should be educated about avoiding or mitigating potential triggers (for example, orthostatic hypotension, emotional stress, severe cough, straining during urination) and recognizing prodromal symptoms. Such patients should also be counseled regarding physical counter-pressure maneuvers (for example, limb/abdominal contraction, leg crossing, hand grip) and increasing fluid and salt intake. Midodrine, an alpha-adrenergic vasoconstricting agent, may also be considered in patients with recurrent situational neutrally mediated syncope, to be taken an hour before situations that may induce syncope. Patients with carotid sinus syncope should be considered for pacemaker placement. For patients with orthostatic hypotension, potential exacerbating drugs should be held if possible and the patients counseled on liberalizing fluid and salt intake, along with rapid cool water ingestion and physical counter-pressure maneuvers. Abdominal binders, compression stockings, and midodrine, fludrocortisone, or pyridostigmine can also be considered. Treatment of syncope due to cardiac causes depends on the specific cause and should be based on established guidelines. Finally, PE should be treated with anticoagulation and, if needed, more aggressive measures (for example, thrombolysis).

Bottom Line

Our patient likely suffered from neurally mediated vasovagal syncope due to warm conditions, supported by a previous syncopal event under similar conditions. She should be counseled regarding potential physical counter-pressure maneuvers and increased fluid and salt intake when working under warm conditions.

Dr. Roberts, Dr. Krason, and Dr. Manian are hospitalists at Massachusetts General Hospital in Boston.

References

1. Shen W-K et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope. J Am Coll Cardiol. 2017 Aug 1;70(5):e39-e110.

2. Sheldon R. How to differentiate syncope from seizure. Cardiol Clin. 2015 Aug;33(3):377-85.

3. Del Rosso A et al. Relation of clinical presentation of syncope to the age of patients. Am J Cardiol. 2005 Nov 15;96(10):1431-5.

4. Blanc JJ. Syncope: Definition, epidemiology, and classification. Cardiol Clin. 2015 Aug;33(3):341-5.

5. Matthews IG et al. Syncope in the older person. Cardiol Clin. 2015 Aug;33(3):411-21.

6. Costantino G et al. Syncope risk stratification tools vs clinical judgment: An individual patient data meta-analysis. Am J Med. 2014 Nov;127(11):1126.e13-25.

7. Chiu DT et al. Are echocardiography, telemetry, ambulatory electrocardiography monitoring, and cardiac enzymes in emergency department patients presenting with syncope useful tests? A preliminary investigation. J Emerg Med. 2014;47:113-8.

8. Prandoni P et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med. 2016 Oct;375(20):1524-31.

9. Sheldon RS et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol. 2011 Mar-Apr;27(2):246-253.

10. Moya A et al. Guidelines for the diagnosis and management of syncope (version 2009): the Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Eur Heart J. 2009 Nov;30(21):2631-71.

Additional reading

1. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol. 2012 May; 59(18):1583-91.

2. Rosanio S et al. Syncope in adults: systematic review and proposal of a diagnostic and therapeutic algorithm. Int J Cardiol. 2013 Jan;162(3):149-57.

 

Case

A 38-year-old construction worker without significant medical history presents following witnessed syncope at her job, after standing for at least 2 hours on a particularly warm day. She reported an episode of syncope under similar circumstances 2 months prior. With each episode, she experienced “tunneling” of peripheral vision, then loss of consciousness without palpitations or incontinence. Her physical exam, vital signs (including orthostatic blood pressures), labs, and ECG were unremarkable.

Brief overview

When evaluating a patient admitted for syncope or falls, the hospitalist must address a number of questions: a) Did the patient actually have syncope?; b) What factor(s) precipitated the syncope?; c) How might similar events be prevented or mitigated in the future?; and d) Is the patient at high risk for a serious adverse outcome (for example, ventricular dysrhythmia, cardiac arrest, intracranial bleed, or death) and, therefore, in need of more immediate or intensive work-up?

The American College of Cardiology, American Heart Association, and Heart Rhythm Society guidelines define syncope as “a symptom that presents with an abrupt, transient, complete loss of consciousness, associated with inability to maintain postural tone, with rapid and spontaneous recovery” with cerebral hypoperfusion as the presumed mechanism.¹ Furthermore, “there should not be clinical features of other nonsyncope causes of loss of consciousness, such as seizure, antecedent head trauma, or apparent loss of consciousness (that is, pseudosyncope).”¹

A careful history revolving around the patient’s behavior prior to, during, and following the event, a thorough past medical history, and a review of current medications are essential. Potential obstacles in obtaining details of the event include lack of witnesses, patient’s inability to recall the experience, and inaccurate description of convulsive syncope as a “seizure” by bystanders.²

Certain characteristics may help identify types of syncope based on clinical presentation. Major categories of syncope include neurally mediated syncope (that is, vasovagal, situational, and carotid sinus hypersensitivity), orthostatic hypotension, and cardiac syncope – which may occur in the setting of acute events such as myocardial infarction, cardiac tamponade, aortic dissection, or pulmonary embolism (PE).
 

Overview of data

Obtaining a detailed history is crucial to understanding both the etiology of the syncopal event and determining which patients are at high risk for adverse outcomes. The etiology of syncope can be determined by history alone in 26% of patients younger than 65 years.³ Data on the prevalence of syncope by cause varies widely. As a general rule, in younger patients, especially those under 40 years of age, neurally mediated syncope is most common. As patients age, orthostatic hypotension and cardiac causes (including arrhythmias and structural diseases) occur more frequently, though neurally mediated syncope is still the most common.

Hospitalists should bear in mind that clear categorization of syncope is often challenging in the elderly. Retrograde amnesia can be seen following syncope in the aged, and even patients who can provide a history may not necessarily provide an accurate account of the event. For example, up to one half of patients who undergo tilt-table testing and have an observed episode of syncope deny that loss of consciousness ever occurred.⁴ Repeated falls in an elderly patient may also require an evaluation for syncope. The typical prodromal symptoms and characteristics of cardiac and neurally mediated syncope also tend to overlap in elderly patients. In a study that examined 46 variables in various age groups, only myoclonic movements during syncope and syncope during physical activity or when supine helped differentiate cardiac from neurally mediated syncope in patients over 65 years of age. Polypharmacy may also increase the susceptibility of the elderly to both orthostatic hypotension and vasovagal syncope.⁵ Though rare in younger patients, carotid sinus syncope should be considered in the older population, particularly under certain circumstances.

To aid the clinician in risk stratifying patients as relates to the likelihood of serious outcomes, a number of studies propose risk predictors for syncope (for example, the San Francisco Syncope Rule [SFSR], Evaluation of Guidelines in Syncope Study [EGSYS], Short-Term Prognosis of Syncope, Boston Syncope Rule, and the Risk Stratification of Syncope in the Emergency Department rule, to name a few). Unfortunately, the definition of and the timing of the adverse outcomes related to syncope often vary among studies, with reported risk factors ranging from anemia to hypotension on presentation to positive fecal occult blood testing, elevated brain natriuretic peptide, and various ECG findings. Nevertheless, several consistent predictors of serious adverse outcomes tend to emerge, such as hemodynamic instability, anemia, abnormal ECG, evidence of heart failure or structural heart disease, and acute coronary syndrome or its attendant symptoms.

Many of these predictors, however, would raise the clinical suspicion of most hospitalists for adverse outcomes in their hospitalized patients independent of the presence or absence of syncope. In fact, a meta-analysis has concluded that “None of the evaluated prediction tools (SFSR, EGSYS) performed better than clinical judgment in identifying serious outcomes during emergency department stay, and at 10 and 30 days after syncope.”⁶

Once the patient is hospitalized, further evaluation should be based on a careful history and physical examination. Standard evaluation also includes careful review of medications, an ECG to exclude findings suggestive of arrhythmias as well as structural or coronary artery disease, and orthostatic blood pressure measurements.¹ Additional tests should be considered as deemed appropriate. For example, in patients over 40 years of age without history of carotid artery disease or stroke and in whom no carotid artery bruit is appreciated, a carotid sinus massage may be considered. The correct technique is to massage the sinus on the right then left, each for 5 seconds in both supine and standing positions with continuous heart rate and frequent blood pressure monitoring. Reproduction of syncope, especially concurrent with a cardiac pause of greater than 3 seconds and a systolic blood pressure drop of greater than 50 mmHg, is considered a positive test. Tilt-table testing should be considered in those for whom neurally mediated syncope is suspected but not confirmed, or in patients who might benefit from further elucidation of their prodromal symptoms.

If the patient’s history is concerning for arrhythmia but without supportive ECG findings, ECG monitoring should be considered. The type of monitoring will depend on the frequency of the patient’s symptoms, with consideration given to Holter monitors for more frequent events and external patch or implantable loop recorders considered in more sporadic events. An echocardiogram can be useful in those suspected of having structural heart disease. Although the overall yield of echocardiography is elucidating the cause of syncope is low,⁷ it may help further risk stratify those patients with suspected cardiac syncope and, in some cases, help with consideration of implantable cardioverter defibrillator placement. Cardiac stress testing may be considered for exercise-related syncope or patients suspected of having cardiac ischemia. Head imaging, EEG, and carotid ultrasounds are generally considered very low-yield in patients whose history suggests true syncope.

Of note, a study recently published in the New England Journal of Medicine suggests that the prevalence of PE in patients (median age, 80 years) presenting with a first episode of syncope was 17%, a rate that is substantially higher than historically presumed.⁸ Although the prevalence of PE was highest among patients presenting with syncope of unclear origin (25%), nearly 13% of patients with other explanations for syncope also had PE.


 

 

Application of data

Treatment of syncope will depend on its etiology. Patients with neurally mediated syncope should be educated about avoiding or mitigating potential triggers (for example, orthostatic hypotension, emotional stress, severe cough, straining during urination) and recognizing prodromal symptoms. Such patients should also be counseled regarding physical counter-pressure maneuvers (for example, limb/abdominal contraction, leg crossing, hand grip) and increasing fluid and salt intake. Midodrine, an alpha-adrenergic vasoconstricting agent, may also be considered in patients with recurrent situational neutrally mediated syncope, to be taken an hour before situations that may induce syncope. Patients with carotid sinus syncope should be considered for pacemaker placement. For patients with orthostatic hypotension, potential exacerbating drugs should be held if possible and the patients counseled on liberalizing fluid and salt intake, along with rapid cool water ingestion and physical counter-pressure maneuvers. Abdominal binders, compression stockings, and midodrine, fludrocortisone, or pyridostigmine can also be considered. Treatment of syncope due to cardiac causes depends on the specific cause and should be based on established guidelines. Finally, PE should be treated with anticoagulation and, if needed, more aggressive measures (for example, thrombolysis).

Bottom Line

Our patient likely suffered from neurally mediated vasovagal syncope due to warm conditions, supported by a previous syncopal event under similar conditions. She should be counseled regarding potential physical counter-pressure maneuvers and increased fluid and salt intake when working under warm conditions.

Dr. Roberts, Dr. Krason, and Dr. Manian are hospitalists at Massachusetts General Hospital in Boston.

References

1. Shen W-K et al. 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope. J Am Coll Cardiol. 2017 Aug 1;70(5):e39-e110.

2. Sheldon R. How to differentiate syncope from seizure. Cardiol Clin. 2015 Aug;33(3):377-85.

3. Del Rosso A et al. Relation of clinical presentation of syncope to the age of patients. Am J Cardiol. 2005 Nov 15;96(10):1431-5.

4. Blanc JJ. Syncope: Definition, epidemiology, and classification. Cardiol Clin. 2015 Aug;33(3):341-5.

5. Matthews IG et al. Syncope in the older person. Cardiol Clin. 2015 Aug;33(3):411-21.

6. Costantino G et al. Syncope risk stratification tools vs clinical judgment: An individual patient data meta-analysis. Am J Med. 2014 Nov;127(11):1126.e13-25.

7. Chiu DT et al. Are echocardiography, telemetry, ambulatory electrocardiography monitoring, and cardiac enzymes in emergency department patients presenting with syncope useful tests? A preliminary investigation. J Emerg Med. 2014;47:113-8.

8. Prandoni P et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med. 2016 Oct;375(20):1524-31.

9. Sheldon RS et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J Cardiol. 2011 Mar-Apr;27(2):246-253.

10. Moya A et al. Guidelines for the diagnosis and management of syncope (version 2009): the Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Eur Heart J. 2009 Nov;30(21):2631-71.

Additional reading

1. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol. 2012 May; 59(18):1583-91.

2. Rosanio S et al. Syncope in adults: systematic review and proposal of a diagnostic and therapeutic algorithm. Int J Cardiol. 2013 Jan;162(3):149-57.