1. SYNCOPE Suggestions for Lecturer -1-hour lecture
-Use GNRS slides alone or to supplement own teaching materials.
-Refer to GNRS for further content and for strength of evidence (SOE) levels.
-Refer to Geriatrics At Your Fingertips for updated information on patient evaluation and management.
-Supplement lecture with handouts.
-The GNRS Teaching Slides reflect care that can be provided to older adults in all settings. The words patient, resident, and older adult have been used interchangeably, as have the words provider, clinician, and primary care provider. Given the continually ongoing changes in health care today, some of the guidelines around reimbursement may have changed since publication.

2. OBJECTIVES
Know and understand:
Factors that may lead to syncope in older adults
Elements of evaluation (history, physical examination, testing) of older adults with syncope
Treatment options for syncope

3. TOPICS COVERED
Natural History: Diagnosis and Prognosis
Pathophysiology
Evaluation: History, Physical Exam, Diagnostic Testing
Treatment

4. SYNCOPE: INTRODUCTION (1 of 2)
A symptom complex composed of a sudden and transient loss of consciousness resulting from a temporary interruption of global cerebral perfusion
A common reason for evaluation in both outpatient clinics and emergency departments, and for hospital admission
Annually it accounts for approximately 3% of emergency department visits and 2%–6% of hospital admissions

5. SYNCOPE: INTRODUCTION (2 of 2)
Incidence of syncope increases with age
Incidence doubles in those ≥70 years old, and the rate among those ≥80 years old is three to four times that seen among younger people
Approximately 80% of patients hospitalized for syncope are ≥65 years old
Potential causes range from those that are benign and self-limiting to those that are life threatening
In older adults, the cause of syncope can often be multifactorial, adding to the diagnostic difficulty

6. SYNCOPE: NATURAL HISTORY
Decreases in Cardiac Output or Peripheral Vascular Resistance, or both Decreased Systemic Blood Pressure and Reduced Cerebral Perfusion Syncope Causes may be benign or life-threatening Causes may be multifactorial Must consider adverse effects of drugs as a cause

7. COMMON CAUSES OF SYNCOPE
Neurally mediated
Cardiac rhythm disturbances
Decreased intravascular volume due to blood loss or dehydration
Alterations in the peripheral vasculature due to arterial vasodilation or increased venous pooling
Medication related
Localized atherosclerotic diseases, such as vertebral basilar insufficiency and subclavian steal, can result in syncope without alteration in systemic blood pressure. These causes are uncommon.
Epileptic seizure, a common cause of transient loss of consciousness, is no longer categorized as a cause of syncope, because seizure is not mediated by a decrease in cerebral perfusion
It is important to differentiate a seizure from syncope as a cause of transient loss of consciousness

8. DISTINGUISHING CHARACTERISTICS OF SEIZURE AND SYNCOPE
Phase
Sign/Symptom
Seizure
Cardiac Syncope Due to Arrhythmia
Vasovagal Syncope
Before
Position
Any
Upright; aborted by lying flat
Warning/prodrome
None
<5 seconds
Seconds to minutes
Precipitant
Usually absent
Absent
Present
Palpitations
Sometimes
Nausea/diaphoresis
Rare
Common
Visual changes
During
Tone
Rigid
Flaccid
Motionless, relaxed
Pulse
Rapid
Absent or faint
Slow, faint
Color
Pale or normal
Blue, ashen
Pale
Incontinence
Very rare
Eye findings
Tonic eye deviation
Variable pupils
Dilated, reactive pupils
Oral frothing
After
Type of recovery
Slow, incomplete
Rapid, complete
Fatigue common
Mental status
Disorientation
No retrograde amnesia
Focal neurologic findings
Characteristics most distinctive in determining the cause of syncope are highlighted in bold.

9. SYNCOPE: PROGNOSIS (1 of 2)
Depends on the underlying cause
Cardiac causes have the worst prognosis
1-year mortality is 18%–33%, with deaths chiefly due to underlying disease, not syncope
Noncardiac causes
1-year mortality of approximately 6%

10. SYNCOPE: PROGNOSIS (2 of 2)
Neurally mediated or vasovagal syncope
Vasovagal mechanisms as the cause of syncope in approximately 30%–50% of patients >65 years old
Some suggestion that vasovagal syncope in older adults is often associated with comorbid illness that can increase overall mortality
No cause found In approximately 10%–20% of syncopal patients
Prognosis for these patients is no worse or better than that of the general population
Neurally mediated or vasovagal syncope, which has a benign prognosis in the young, was once thought to be an unusual cause of syncope in older adults. However, reports from syncope evaluation centers have found vasovagal mechanisms as the cause of syncope in approximately 30%–50% of patients >65 years old (SOE=A). It has not been established that vasovagal syncope in older adults has the same benign prognosis as it does in younger individuals, because there has been some suggestion that vasovagal syncope in older adults is often associated with comorbid illness that can increase overall mortality (SOE=B).

11. PATHOPHYSIOLOGY: MECHANISMS THAT PREVENT SYNCOPE
The integrity of a number of control mechanisms is crucial for maintaining adequate perfusion of the brain and cerebral oxygen delivery after sudden changes in blood pressure
Carotid and aortic baroreceptors
Sympathetic renal stimulation of the renin-angiotensin system
Arteriolar autoregulation

12. PATHOPHYSIOLOGY OF SYNCOPE: EFFECTS OF AGING
Reflex mechanisms are less responsive with aging
Decreased ability to increase heart rate in response to sympathetic stimulation
Increased sensitivity to effects of dehydration, diuretics and vasodilator medications
Comorbidities that affect postural responses are common (eg, diabetes mellitus, Parkinson disease)
Medications may further impair postural reflexes (eg, vasodilators, calcium channel blockers, ACE inhibitors, -blockers, -blockers, tricyclic antidepressants)

13. PATHOPHYSIOLOGY: ADDRESSING CAUSES
Age-related decline in adaptive reflexes, comorbid conditions, and medications can all have a role in older adults presenting with syncope
Address these issues by:
Increasing caution with postural change, physical counter-pressure maneuvers (eg, leg crossing) and compression stockings to increase venous return
Adequate hydration
Simplification of the patient’s medication regimen to eliminate excessive medications

14. SYNCOPE EVALUATION: HISTORY (1 of 2)
An accurate recall of the syncopal event is frequently inadequate because of the high prevalence of cognitive dysfunction in the older population. The medical history, if possible, should be obtained from a witness to the event.
Precipitants?
Eating
Urinating
Coughing
Medication
Emotional stress
Physical exertion
Turning head
Prodromal symptoms?
Chest pain
Palpitations
Dyspnea
Diaphoresis
Presyncope
Nausea
Vomiting
Syncope occurring while sitting or supine suggests a profound hemodynamic disturbance and should raise a concern about a significant cardiac arrhythmia. Syncope occurring during physical exertion should raise the possibility of myocardial ischemia or aortic stenosis. A history of syncope after turning motions of the head should raise the possibility of carotid sinus hypersensitivity.
Chest pain, palpitations, or shortness of breath suggests a cardiac or pulmonary cause. Diaphoresis, presyncope, and GI symptoms, such as nausea or vomiting, can be associated with vasovagal syncope.
Sudden onset of syncope with <5 sec of warning is characteristic of syncope due to a cardiac arrhythmia and should be evaluated as such. However, in older adults, vasovagal syncope can present with short or no prodrome because of inability to precisely recall the event. Thus, if the initial evaluation for arrhythmia in an older adult with syncope without a prodrome is unrevealing, a vasovagal mechanism should also be considered.

15. SYNCOPE EVALUATION: HISTORY (2 of 2)
Medications?
How, when taken, what doses
Relationship to meals and activities
Recent changes
Any witnesses?
Duration of event
Appearance of patient during event (flaccid tone and motionless or increased tone and motion?)
Comorbid conditions?
For example, CAD, Diabetes Mellitus
Many antiarrhythmic medications and other commonly used medications can increase the propensity for ventricular arrhythmias by prolonging the QT interval (for a full current list, see

16. PREDICTING CARDIAC SYNCOPE: EGSYS SCORE
Variable
Score
Palpitations preceding syncope 4
Heart disease or abnormal ECG 3
Syncope during effort
Syncope while supine 2
Precipitating or predisposing factors, or both (warm or crowded place, prolonged orthostasis, fear, pain or emotional distress) –1
Autonomic prodromes (nausea/vomiting)
EGSYS = Evaluation of Guidelines in Syncope Study
Scores ≥3 are associated with higher rates of cardiac syncope and higher mortality.
SOURCE: Data from Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart ;94(12):1620–1626.

17. CARDIAC SYNCOPE DUE TO ARRHYTHMIA
Prior to event
Occurs in any position, <5 sec warning
No precipitant; palpitations are sometimes present
No nausea, diaphoresis or visual changes
During event
Flaccid tone; pulse faint or absent
Blue, ashen skin
Incontinence (rare)
Variable pupils, no oral frothing
Recovery
Rapid and complete

18. VASOVAGAL SYNCOPE Prior to event Aborted if person lies flat
Seconds to minutes of warning
Precipitant present; nausea/diaphoresis common
Visual changes are common
During event
Motionless; relaxed tone; slow, faint pulse
Pale color; dilated, reactive pupils
Recovery
Fatigue, nausea, and diaphoresis common
No retrograde amnesia

19. SYNCOPE CAUSED BY SEIZURE
Prior to event
Occurs in any position
No warning or prodrome
During event
Rigid tone; rapid pulse
Tonic eye deviation common
Frothing at mouth
Recovery
Slow, incomplete
Disorientation; focal neurologic findings

20. SYNCOPE EVALUATION: PHYSICAL EXAMINATION (1 of 2)
Should focus on elements raised by the history
Pulse in supine and standing positions
Orthostatic vital signs: Measure BP in both arms, 1 min after standing and again after standing for 3 min
Carotid pulse examination
Delayed upstroke and low volume may identify aortic stenosis
Perform carotid massage only with continuous ECG and resuscitation equipment available
Contraindicated with carotid bruit, CVD, recent MI

21. SYNCOPE EVALUATION: PHYSICAL EXAMINATION (2 of 2)
Cardiac examination for murmurs, extra heart sounds
Stool for occult blood
Neurologic examination for focal deficits

22. SYNCOPE EVALUATION: DIAGNOSTIC TESTING (1 of 4 )
The following slides review the various diagnostic tests that are available for the evaluation of syncope
It is important to remember that not every test is required; the history and physical are used to determine appropriate testing
In all patients, an assessment of orthostatic vital signs, gait, laboratory tests, and ECG are reasonable first steps

23. SYNCOPE EVALUATION: DIAGNOSTIC TESTING (2 of 4)
ECG for all syncopal older adults; assess for:
Acute or remote MI
Conduction abnormalities and pre-excitation, such as Wolff-Parkinson-White
Sinus bradycardia
Prolonged QT interval
Ambulatory ECG
Among patients able and willing to operate loop recorders, diagnostic yield is ~25%
Implantable loop recorders
Consider using in patients when an arrhythmic cause of syncope is suspected but not sufficiently proved
Although an ECG establishes a diagnosis in only 5% of those with syncope, approximately 50% have an abnormal ECG. Abnormalities on an ECG can provide clues for further cardiovascular evaluation; a normal ECG is associated with a more favorable prognosis.
An ambulatory ECG recording can establish or exclude many causes of syncope if the patient experiences syncopal or presyncopal symptoms during the recording. Unfortunately, the occurrence of symptoms during ambulatory ECG monitoring is relatively infrequent in most patients with syncope that remains unexplained after a history, physical examination, and ECG.

24. SYNCOPE EVALUATION: DIAGNOSTIC TESTING (3 of 4)
Echocardiography and Exercise Stress Testing
Most useful in confirming a specific diagnosis suspected by other assessment, otherwise it is low yield
Tilt-table testing
Useful for patients suspected of having vasovagal syncope and those with unexplained syncope who are not suspected of having a cardiac cause.
Electrophysiologic studies
Not recommended for patients with a normal ECG or those without a history of heart disease or symptoms of palpitations
Echocardiography: In the absence of features suggestive of heart disease by history, physical examination, or ECG, two-dimensional echocardiography has a low yield. It is most useful in confirming a specific diagnosis suspected by other assessment. Occult coronary artery disease is also relevant among older adults, and stress testing is often used for screening. In some patients, particularly those with the suggestion of structural cardiac abnormalities and ischemia by history, physical examination, or ECG, it is efficient to perform stress echocardiography as a single procedure.
Tilt-Table Testing: Head-up tilt-table testing results in pooling of blood in the legs, and in susceptible individuals it can trigger syncope mediated by neurocardiogenic mechanisms or confirm postural hypotension. Tilt-table testing is useful for patients suspected of having vasovagal syncope and those with unexplained syncope who are not suspected of having a cardiac cause. Responses to tilt testing performed for evaluation of syncope tend to differ by age among adults without significant structural heart disease. Those ≥65 years old tend to have far higher rates of symptoms due to pure vasodilatation without significant change in heart rate than individuals ≤35 years old. In contrast, individuals ≤35 years old tend to have more profound cardioinhibitory responses, characterized by profound bradycardia or asystole induced by tilt testing. The different patterns of responses suggest that different mechanisms for neurocardiogenic syncope predominate at different ages.
Electrophysiologic Study (EPS): The development of effective noninvasive methods, such as prolonged rhythm monitoring, has decreased the importance of EPS as a diagnostic test. Nevertheless, this test is still useful for diagnosis in suspected intermittent bradycardia, tachyarrhythmia, or in patients with bundle-branch block (suggestive of impending high-grade AV block). EPS is not recommended for patients with a normal ECG or those without a history of heart disease or symptoms of palpitations.

25. SYNCOPE EVALUATION: DIAGNOSTIC TESTING (4 of 4)
Neurologic testing (CT or MRI, and/or EEG)
Not generally required
Appropriate in situations when focal neurologic signs or symptoms are present or when the history suggests seizure or trauma
Consider autonomic evaluation if signs and symptoms of autonomic dysfunction are present

26. SYNCOPE: IS HOSPITAL ADMISSION REQUIRED?
Older patients are frequently hospitalized for evaluation because they are presumed to be higher risk
However, patients with no risk factors for adverse events were found to have no significant increase in adverse events regardless of age
A specialized syncope observational unit in the hospital setting has been shown to reduce hospital admission and expedite the diagnosis of potential causes of syncope

27. RISK FACTORS FOR ADVERSE PROGNOSIS IN SYNCOPE
Symptoms
Chest pain
Shortness of breath
Palpitations or rapid heart beat
GI bleeding
Cardiac history
Coronary artery disease
Heart failure
Hypertrophic cardiomyopathy
Pacemaker or defibrillator
Antiarrhythmic medications
Ventricular tachycardia or ventricular fibrillation
Syncope characteristics
Syncope during exercise
>1 episode within 6 months
Family history
First-degree relative with sudden death, hypertrophic cardiomyopathy, Brugada syndrome, or long QT syndrome
Physical examination
Tachypnea
Hypoxia (O2 saturation <90%)
Sinus heart rate <50 beats/min or >100 beats/min
Systolic blood pressure <90 mmHg
Heart murmur
Volume depletion
Neurologic deficits
ECG abnormalities
Q waves
Ischemic ST segment or T wave changes
Ventricular or supraventricular arrhythmias, including rapid atrial fibrillation
Second- or third-degree AV block
Corrected QT interval >500 ms
Laboratory abnormalities
Hematocrit <30%
Occult blood in feces
SOURCE: Data from Grossman SA, Chiu D, Lipsitz L, et al. Can elderly patients without risk factors be discharged home when presenting to the emergency department with syncope? Arch Gerontol Geriatr. 2014;58:110–114.
Note: Patients with no risk factors for adverse prognosis can likely be safely dismissed from the emergency department without hospitalization.

28. TREATMENT OF SYNCOPE (1 of 5)
Goals of treatment: Improve quality of life and prevent physical injuries
Focus on treating the underlying disorder
In older patients, treatment of multiple possible causes is often necessary
Discontinuation of medications that increase the risk of syncope is always an early step
Polypharmacy is increasingly identified as a risk of syncope because of the actual number of medications and risk of interaction and adverse effects, and potentially because of the number of comorbid conditions requiring complex pharmacotherapy. Before any new medication is added, the medication list must be reviewed for potential culprits (in particular, α-antagonists, clonidine, vasodilators, and excessive diuretics). Timing of medication administration should also be reviewed, and shifting antihypertensive medications to evening administration may reduce daytime orthostatic symptoms.

29. TREATMENT OF SYNCOPE (2 of 5)
Reflex Syncope and Postural Hypotension
Nonpharmacologic measures with physical counter-pressure maneuvers
Leg crossing, arm tensing, hand grip, and buttock clenching are able to induce a significant blood pressure increase during the phase of impending reflex syncope so that the patient can avoid or delay losing consciousness
Compression stockings and abdominal binders
Smaller and frequent meals can be effective in patients with postprandial hypotension

30. TREATMENT OF SYNCOPE (3 of 5 )
Medical Management
Midodrine
Increases vasoconstriction, may help with persistent postural hypotension
Use with caution: May cause supine hypertension in those with decreased vascular compliance
Monitor blood pressure response and symptoms
Pyridostigmine
Increases both standing blood pressure and peripheral resistance, attenuating orthostatic blood pressure
Adverse effects: Abdominal cramps, diarrhea, urinary urgency
Use with close supervision, older adults may not tolerate adverse effects

31. TREATMENT OF SYNCOPE (4 of 5 )
Medical Management
Volume expansion with added salt
Fludrocortisone
Both increase renal sodium retention and intravascular volume
May be effective in patients with persistent postural hypotension

32. TREATMENT OF SYNCOPE (5 of 5)
Role of Pacemakers
Mainstay of treatment for sinus node dysfunction or high grade AV block
Permanent pacing is indicated when syncope or near syncope is correlated with bradycardia after ensuring that medications that may be causing bradycardia have been discontinued, if indicated after a risk vs benefit analysis
Not recommended in patients with unexplained syncope or falls without documentation of bradycardia
Although the recommendation to avoid pacemaker placement but rather discontinue medications causing bradycardia in patients taking them makes sense, often these medications are treatment for a significant cardiac condition (ie, β- blockers) or dementia (acetylcholinesterase inhibitors). Acetylcholinesterase inhibitors are associated with a significant risk of bradycardia, and bradycardic patients have a significant risk of syncope. Although recommendations for when it is appropriate or necessary to discontinue acetylcholinesterase inhibitors are needed, the risk of these medications in patients with bradycardia may outweigh the benefits.

33. SUMMARY (1 of 2)
In older adults the cause of syncope is often multifactorial
Important to review the medication list of each patient, as medications are commonly implicated as a source of syncope
Most diagnostic procedures for syncope are expensive and have a low yield unless findings from the history and physical suggest a particular cause

34. SUMMARY (2 of 2)
Important to rule out cardiac conditions as a cause of syncope as they are associated with worse prognosis
Treatment of syncope focuses on treating the underlying disorder

35. CHOOSING WISELY
Recommendations for Syncope, based on the American Board of Internal Medicine Foundation’s Choosing Wisely® Campaign:
Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms.
In the evaluation of simple syncope and a normal neurologic examination, do not obtain brain imaging studies (CT or MRI).

36. CASE (1 of 3)
A 68-year-old man lost consciousness twice in the last several months. His daughter witnessed the second event.
Patient was washing dishes when he suddenly felt lightheaded, looked pale and sweaty, and collapsed to the floor.
He felt lightheaded for about 30 sec before losing consciousness.
He awoke within 30 sec and was back to baseline within 1 minute of the event.
History: hyperlipidemia, stroke, Parkinson disease, diabetes mellitus
Examination
Blood pressure 129/78 mmHg
Normal cardiopulmonary and neurologic findings
ECG: no significant abnormalities

37. CASE (2 of 3)
Which one of the following would most likely establish the diagnosis?
Electroencephalography
Tilt table test
Magnetic resonance imaging of the brain
Doppler ultrasonography of the carotid artery
24-Hour Holter monitoring

38. CASE (3 of 3)
Which one of the following would most likely establish the diagnosis?
Electroencephalography
Tilt table test
Magnetic resonance imaging of the brain
Doppler ultrasonography of the carotid artery
24-Hour Holter monitoring
ANSWER: B
A head-up tilt table test is used to identify autonomic dysfunction that can contribute to a syncopal event. This patient had a syncopal event associated with prolonged standing, suggesting autonomic dysfunction. Further, his history of Parkinson disease and diabetes puts him at increased risk of autonomic dysfunction. Orthostatic vital signs should be obtained before testing to evaluate for orthostatic hypotension.
Electroencephalography is appropriate if seizure is suspected to evaluate for epileptiform activity. However, this patient had a short syncopal episode preceded by lightheadedness, and with rapid return to baseline. Because there is no evidence of seizure activity, the test would not likely yield a diagnosis.
Magnetic resonance imaging of the brain should be obtained if there is suspicion of structural abnormalities, but it has no role in routine evaluation of syncope if there are no focal neurologic signs or symptoms. This patient has normal findings on neurologic examination.
Doppler ultrasonography of the carotid artery is not indicated in the routine evaluation of syncope. It can be used to measure blood flow velocities within the cervical carotid arteries, which supply blood to the anterior circulation of the brain. A syncopal episode can in rare cases be caused by decreased perfusion to the posterior circulation (not the anterior circulation) of the brain, specifically to the reticular activating system in the brainstem. In order for carotid disease to lead to syncope, simultaneous compromise of blood flow in both carotid arteries would be required, which is extremely unlikely.
Ambulatory external Holter monitoring devices are often used for 1–2 days. Because in most cases symptoms do not recur during the monitoring period, the positive diagnostic yield of Holter monitoring for syncope evaluation is low. However, a Holter monitor or an ambulatory loop recorder might be considered for this patient if evaluation with tilt table test is unrevealing.

39. GNRS5 Teaching Slides Editor: Barbara Resnick, PhD, CRNP, FAAN, FAANP, AGSF GNRS5 Teaching Slides modified from GRS9 Teaching Slides based on chapter by J. William Schleifer, MD and Win-Kuang Shen, MD and questions by Stephen Krieger, MD and Asaff Harel, MD Managing Editor: Andrea N. Sherman, MS Copyright © 2016 American Geriatrics Society