SYNCOPE

Joseph A. Spinner, MD • Santiago O. Valdes, MD, FAAP

 BASICS

DESCRIPTION

•  Transient loss of consciousness characterized by unresponsiveness, loss of postural tone, and spontaneous recovery; usually caused by cerebral hypoxemia

•  System(s) affected: cardiovascular, nervous

EPIDEMIOLOGY

Incidence

•  Up to 20% of adults will have ≥1 episode by age 75 years; 15% of children <18 years of age

•  Accounts for 1–6% of hospital admissions and ~3% of emergency room visits

Prevalence

•  Annual prevalence of fainting spells resulting in medical evaluation was 9.5/1,000 inhabitants.

•  In institutionalized elderly (>75 years of age) is 6%

ETIOLOGY AND PATHOPHYSIOLOGY

•  In some cases, vagal response leads to decreased heart rate.

•  Systemic hypotension secondary to decreased cardiac output and/or systemic vasodilation leads to a drop in cerebral perfusion and resulting loss of consciousness.

•  Cardiac (obstruction to outflow)

–  Aortic stenosis

–  Hypertrophic cardiomyopathy: most common cause of sudden cardiac death during exercise in young athletes

–  Pulmonary embolus

•  Cardiac arrhythmias

–  Sustained ventricular tachycardia (VT)

–  Supraventricular tachycardia (SVT) (atrial fibrillation, atrial flutter, reentrant SVT)

–  Torsades de pointes (TdP)

–  Bradyarrhythmia

  2nd- and 3rd-degree AV block

  Sick sinus syndrome

•  Noncardiac

–  Reflex-mediated vasovagal (neurally mediated syncope [NMS]/neurocardiogenic): inappropriate vasodilation leading to neurally mediated systemic hypotension and decreased cerebral blood flow, situational (micturition, defecation, cough, pain, emotions, hair combing)

–  Orthostatic hypotension: Consider volume depletion, pregnancy, anemia, medications.

–  Drug induced: prescription or recreational

–  Neurologic: seizures, transient ischemic attack, disrupted cerebrospinal fluid

–  Metabolic: hypoglycemia

–  Carotid sinus hypersensitivity

•  Vast majority of pediatric cases represent benign alterations in vasomotor tone

•  NMS also most common cause in adult cases

Genetics

Specific cardiomyopathies and arrhythmias may be inherited (i.e., long QT syndrome, catecholaminergic polymorphic VT, Brugada syndrome, hypertrophic cardiomyopathy).

RISK FACTORS

•  Heart disease (acquired or structural)

•  Dehydration

•  Drugs

–  Antihypertensives

–  Vasodilators (including calcium channel blockers, ACE inhibitors, and nitrates)

–  Phenothiazines

–  Antidepressants

–  Antiarrhythmics

–  Diuretics

GENERAL PREVENTION

See “Risk Factors.”

COMMONLY ASSOCIATED CONDITIONS

See “Etiology and Pathophysiology.”

 DIAGNOSIS

HISTORY

•  Careful history, physical exam, and an ECG are more important than other investigations in determining the diagnosis (1)[A].

•  Make sure that the patient or witness (if present) is not talking about vertigo (i.e., sense of rotary motion, spinning, and whirling), seizure, or causes of fall without loss of consciousness. Onset of syncope is usually rapid, and recovery is spontaneous, rapid, and complete. Duration of episodes is typically brief (<60 seconds).

•  Number of previous episodes: Benign causes of syncope tend to be associated with a single episode.

•  Presence of prodromal symptoms: Consider NMS.

–  Elderly patients less likely to experience a prodrome

•  Palpitations or during exercise: Consider cardiac.

•  Position (supine: arrhythmia; erect: NMS, supine → erect: orthostatic hypotension)

•  Prolonged syncope: Consider psychiatric, neurologic.

•  Delayed recovery: Consider neurologic (postictal).

•  Ask for family history of long QT syndrome, Implantable Cardioverter-Defibrillator (ICD), hypertrophic cardiomyopathy, or unexplained sudden cardiac death in young family members.

•  Even after careful evaluation, including diagnostic procedures and special tests, the cause will be found in only 50–60% of the patients.

PHYSICAL EXAM

•  BP and pulse, both lying and standing

–  Orthostatic: Drop in systolic BP >20 mm Hg or rise in HR of >30 bpm.

•  Check for cardiac murmur or focal neurologic abnormality.

DIFFERENTIAL DIAGNOSIS

•  Drop attacks

•  Coma

•  Vertigo

•  Seizure disorder

•  Psychiatric (conversion, somatization): lack hemodynamic and/or autonomic changes

DIAGNOSTIC TESTS & INTERPRETATION

•  Goal is to identify life-threatening conditions or those associated with significant risk of injury (2).

•  Comprehensive medical and family history, physical examination, and ECG should guide future testing (2).

•  No one single test defines the cause of syncope (2).

Initial Tests (lab, imaging)

Consider (not all indicated in all individuals) the following:

•  CBC

•  Electrolytes, BUN, creatinine, glucose (rarely helpful if asymptomatic or presenting hours later)

•  BNP level

•  Cardiac enzymes (only if history suggestive of MI)

•  D-dimer (for pulmonary embolism [PE] workup)

•  Urine pregnancy and urine drug screen

•  Initial cardiac or neuroimaging only if indicated

•  Lung scan or helical CT scan of thorax if history and physical exam suggest PE

Follow-Up Tests & Special Considerations

•  Injuries may occur in up to 1/3 of adult patients.

•  If history and physical suggest ischemic, valvular, or congenital heart disease (2)

–  Exercise stress test (if syncope with exertion) (2)[C]

–  Echocardiogram (2)[B]

•  ECG findings suggesting arrhythmia

–  Bifascicular block, AV block, sinus bradycardia <40 bpm or sinus pause >3 seconds, prolong QTc, preexcitation, alternating BBB

•  If CNS disease suspected (2)[C]

–  EEG

–  Head CT scan

–  Head MRI/MRA if vascular cause is suspected

•  ECG monitoring, either in hospital or ambulatory (Holter) (2)[C]

–  Useful in 4–15% of patients

–  Should be done in patients with preexisting heart disease, palpitations, or recurrent syncope

–  Arrhythmias frequently documented but not always causative

•  Electrophysiologic studies (2)[C]

–  Should be done in patients with heart disease and recurrent syncope, although they may not show whether arrhythmia noted or induced during study is cause of syncope.

–  Induction of VT and dysfunction of His-Purkinje system are the two most common abnormalities.

–  Have been positive in 18–75% of patients

•  Carotid hypersensitivity evaluation (3,4)[C]

–  Carotid hypersensitivity should be considered in patients >40 years old or with syncope during head turning, especially while wearing tight collars, and with neck tumors and neck scars.

–  The technique is not standardized; one side at a time is compressed gently for 20 seconds with constant monitoring of pulse and BP/ECG.

–  Atropine should be readily available.

•  Tilt-table testing (2)[B]

–  Provocative test for vasovagal syncope

–  Often results are not reproducible

–  High false-positive rate

•  Psychiatric evaluation (2)[C]: Anxiety, depression, and alcohol and drug abuse can be associated with syncope.

Diagnostic Procedures/Other

External event recorders or implantable loop recorders may be more helpful than short-term ambulatory monitoring. Helpful in selective patients with recurrent syncope, with yield of 32–80% (3,4)[B].

Test Interpretation

Depends on etiology and presence of underlying cardiac or neurologic conditions

 TREATMENT

•  Maintaining good hydration status and normal salt intake are initial therapy. Educate patients of the premonitory signs of syncope (3)[B].

•  Majority of pediatric patients improve with nonpharmacologic measures

GENERAL MEASURES

•  NMS: reassurance, education, behavior modification

•  Elderly patients without previously recognized heart disease should be admitted if the physician thinks that the cause of syncope is likely cardiac.

•  Patients without heart disease, especially young patients (age <60 years) can be worked up safely as outpatients.

•  Prescribe antiarrhythmics for documented arrhythmias occurring simultaneously with syncope or symptoms of presyncope. Asymptomatic arrhythmias do not necessarily require treatment.

•  The decision to treat patients on basis of arrhythmias or conduction abnormalities provoked or detected during EPS is even more problematic: Does the arrhythmia or conduction abnormality have anything to do with the patient’s symptoms?

•  Most would treat patients with provoked sustained VT with an antiarrhythmic drug that suppressed arrhythmia during study.

•  Rationale for such treatment: Recurrent syncope is less frequent in patients with positive EPS who are treated than it is in those who have negative EPS.

MEDICATION

First Line

•  Geared toward specific underlying cardiac or neurologic abnormalities

•  In cases of recurrent NMS (4)[B]

–  Mineralocorticoids (fludrocortisone)

–  α-Adrenergic agonists (midodrine)

Second Line

•  SSRIs (paroxetine, sertraline, fluoxetine)

•  Vagolytics (disopyramide)

ISSUES FOR REFERRAL

When cardiac or neurologic etiologies are suspected, obtain appropriate consultation, as indicated.

ADDITIONAL THERAPIES

For vasovagal/neurocardiogenic/NMS

•  Counterpressure maneuvers, orthostatic training, and exercise have improved vasovagal symptoms and recurrence (3,5)[C].

•  Head-up tilt sleeping (2)[C]

•  Abdominal binders and/or support stockings (2)[C]

SURGERY/OTHER PROCEDURES

•  ICD placement for patients with cardiac conditions with high risk of sudden death and/or recurrent syncope on medications (i.e., long QT syndrome, catecholaminergic polymorphic VT, hypertrophic cardiomyopathy) (2)[B]

•  Many recommend pacemaker implantation in patients with the following:

–  2nd- (Mobitz type II) and 3rd-degree heart block

–  HV intervals >100 ms

–  Pacing-induced infranodal block

–  Sinus node recovery time ≥3 seconds

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

•  Patients with benign etiologies of syncope with negative ED workups are associated with benign outcomes, even in the presence of other risk factors (6)[B].

•  Overwhelming majority of children who have completely recovered and without red flags for cardiac or neurologic syncope can be followed as outpatients.

•  Patients with suspected cardiac or neurologic cause for syncope or comorbidities (such as anemia or electrolyte abnormalities) should be admitted for evaluation.

•  In adults: ROSE rule recommends hospital admission if any of the following is present: BNP level ≥300 pg/mL, bradycardia ≤50, + fecal occult blood, anemia with hemoglobin ≤9 g/dL, chest pain associated with syncope, ECG showing Q wave (not in lead III) or oxygen saturation ≤94% on room air (5)

•  Close monitoring of BP and heart rate during initial presentation

•  Discharge criteria

–  Attainment of hemodynamic stability

–  Satisfactory completion of workup for etiology

–  Adequate control of specific arrhythmia or seizure, if present

 ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

•  Frequent follow-up visits for patients with cardiac causes of syncope, especially patients on antiarrhythmics

•  Patients with an unknown cause of syncope rarely (5%) are diagnosed during the follow-up.

DIET

•  No specific diet unless the patient has heart disease

•  Increased fluid and salt intake to maintain intravascular volume in cases of recurrent NMS

PATIENT EDUCATION

•  Reassure the patient that most cardiac causes of syncope can be treated, and patients with noncardiac causes do well, even if the cause of syncope is never discovered.

•  Physical counterpressure maneuvers can prevent recurrences of vasovagal syncope.

•  Physician and patient should carefully consider whether the patient should continue to drive while syncope is being evaluated. Physicians should be aware of pertinent laws in their own states.

PROGNOSIS

•  Cumulative mortality at 2 years

–  Low: young patients (<60 years of age) with noncardiac or unknown cause of syncope

–  Intermediate: older patients (>60 years of age) with noncardiac or unknown cause of syncope

–  High: patients with cardiac cause of syncope

•  Independent predictors of poor short-term outcomes (5,6)[B]

–  Abnormal ECG

–  Shortness of breath

–  Systolic BP <90 mm Hg

–  Hematocrit <30%

–  Congestive heart failure

COMPLICATIONS

•  Trauma from falling

•  Death (see “Prognosis”)

REFERENCES

1.  Kessler C, Tristano JM, De Lorenzo R. The emergency department approach to syncope: evidence-based guidelines and prediction rules. Emerg Med Clin North Am. 2010;28(3):487–500.

2.  Moya A, Sutton R, Ammirati F, et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631–2671.

3.  Romme JJ, Reitsma JB, Go-Schön IK, et al. Prospective evaluation of non-pharmacological treatment in vasovagal syncope. Europace. 2010;12(4):567–573.

4.  Kuriachan V, Sheldon RS, Platonov M. Evidence-based treatment for vasovagal syncope. Heart Rhythm. 2008;5(11):1609–1614.

5.  Reed, MJ, Newby DE, Coull AJ, et al. The ROSE (Risk Stratification of Syncope in the Emergency Department) study. J Am Coll Cardiol. 2010;55(8):713–721.

6.  Saccilotto RT, Nickel CH, Bucher HC, et al. San Francisco Syncope Rule to predict short-term serious outcomes: a systematic review. CMAJ. 2011;183(15):E1116–E1126.

ADDITIONAL READING

•  Anderson JB, Willis M, Lancaster H, et al. The evaluation and management of pediatric syncope. Pediatr Neurol. 2016;55:6–13.

•  Puppala VK, Dickinson O, Benditt DG. Syncope: classification and risk stratification. J Cardiol. 2014;63(3):171–177.

•  Sheldon RS, Grubb BP II, Olshansky B, et al. 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12(6):e41–e63.

•  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. J Am Coll Cardiol. 2006;47(2):473–484.

 SEE ALSO

•  Aortic Valvular Stenosis; Atrial Septal Defect; Carotid Sinus Hypersensitivity; Patent Ductus Arteriosus; Pulmonary Arterial Hypertension; Pulmonary Embolism; Seizure Disorders; Stokes-Adams Attacks

•  Algorithms: Syncope; Transient Ischemic Attack and Transient Neurologic Defects

 CODES

ICD10

R55 Syncope and collapse

CLINICAL PEARLS

•  Careful history and physical exam is key to a diagnosis.

•  Use the ECG/event-recorder to evaluate for arrhythmia.

•  NMS is most common cause in children and adults.

•  Injuries due to syncope are common.

•  True neurologic causes of syncope are very rare.

•  <2% of cases are caused by hyponatremia, hypocalcemia, hypoglycemia, or renal failure.