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Syncope
Santiago O. Valdes, MD, FAAP
image 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
  • Annually prevalence of fainting spells resulting in medical evaluation was 9.5/1,000 inhabitants (1).
Prevalence
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
    • Pulmonary embolus
  • Cardiac arrhythmias
    • Sustained ventricular tachycardia (VT)
    • Supraventricular tachycardia (SVT) (atrial fibrillation, atrial flutter, reentrant SVT)
    • 2nd- and 3rd-degree AV block
    • Sick sinus syndrome
  • Noncardiac
    • Reflex-mediated vasovagal (neurocardiogenic/neurally mediated), situational (micturition, defecation, cough, hair combing)
    • Orthostatic hypotension
    • Drug induced
    • Neurologic: seizures; transient ischemic attack (can in theory cause syncope but presentation usually markedly clinically different from pure syncope)
    • Carotid sinus hypersensitivity
    • Psychogenic
Genetics
Specific cardiomyopathies and arrhythmias may be familial (i.e., long QT syndrome, catecholaminergic polymorphic VT, Brugada syndrome, hypertrophic cardiomyopathy).
RISK FACTORS
  • Heart disease
  • 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.”
image DIAGNOSIS
PHYSICAL EXAM
  • BP and pulse, both lying and standing
  • Check for cardiac murmur or focal neurologic abnormality.
DIFFERENTIAL DIAGNOSIS
  • Drop attacks
  • Coma
  • Vertigo
  • Seizure disorder
DIAGNOSTIC TESTS & INTERPRETATION
History and physical examination should guide laboratory testing.
Initial Tests (lab, imaging)
Consider (not all indicated in all individuals) the following:
  • CBC
  • Electrolytes, BUN, creatinine, glucose (rarely helpful: <2% have hyponatremia, hypocalcemia, hypoglycemia, or renal failure causing seizures)
  • Cardiac enzymes (only if history suggestive of cardiac ischemia)
  • D-dimer (for pulmonary embolism workup)
  • hCG
  • Lung scan or helical CT scan of thorax if history and physical exam suggest pulmonary embolism (PE)
Follow-Up Tests & Special Considerations
  • If history and physical suggest ischemic, valvular, or congenital heart disease (3)
    • ECG (3)[A]
    • Exercise stress test (if syncope with exertion) (3)[C]
    • Echocardiogram (3)[B]
    • Cardiac catheterization
  • If CNS disease suspected (3)[C]
    • EEG
    • Head CT scan
    • Head MRI/MRA when vascular cause is suspected
    • Do not order these tests without hints of CNS disease on history or physical exam.
  • ECG monitoring, either in hospital or ambulatory (Holter) (3)[C]
    • Useful in 4-15% of patients
    • Should be done in patients with heart disease or recurrent syncope
    • Arrhythmias frequently documented but not always associated with syncope
  • Electrophysiologic studies (3,4)[C]
    • Have been positive in 18-75% of patients
    • Induction of VT and dysfunction of His-Purkinje system are the two most common abnormalities.
    • 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
  • Carotid hypersensitivity evaluation (3,4)[C]
    • Carotid hypersensitivity should be considered in patients 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 ± isoproterenol infusion (3)[B],(4)[C]
    • Provocative test for vasovagal syncope
    • Perform if cardiac causes have been excluded; role in workup of patients with syncope of unknown origin
    • Protocol is not standardized but has been reported positive (symptomatic hypotension and bradycardia) in 26-87% of patients; also positive in up to 45% of control subjects.
  • Psychiatric evaluation (3)[C]: Anxiety, depression, and alcohol and drug abuse can be associated with syncope.
Diagnostic Procedures/Other
Patient-activated implantable loop recorders can record 4 to 5 minutes of retrograde ECG rhythm. 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
image TREATMENT
Maintaining good hydration status and normal salt intake are initial therapy. Educate patients of the premonitory signs of syncope (5)[B].
GENERAL MEASURES
  • 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.
  • P.1005

  • 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 vasovagal/neurocardiogenic/neurally mediated syncope (6)[B]
    • &agr;-Adrenergic agonists (midodrine)
    • Mineralocorticoids (fludrocortisone)
    • &bgr;-Adrenergic blockers
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/neurally mediated syncope
  • Counterpressure maneuvers, orthostatic training, and exercise have improved vasovagal symptoms and recurrence (3,5)[C].
  • Head-up tilt sleeping (3)[C]
  • Abdominal binders and/or support stockings (3)[C]
SURGERY/OTHER PROCEDURES
  • Implantable cardioverter-defibrillator (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) (3)[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
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
Patients with benign etiologies of syncope with negative ED workups are associated with benign outcomes, even in the presence of other risk factors (7)[B].
Patients with suspected cardiac or neurologic cause for syncope should be admitted to the hospital for evaluation.
  • Support ABCs.
  • Stabilize heart rate and BP, typically with IV fluids.
IV Fluids
Use isotonic crystalloid fluids for fluid resuscitation, if needed.
Nursing
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
image 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 vasovagal syncope
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 (8,9)[B]
    • Abnormal ECG
    • Shortness of breath
    • Systolic BP <90 mm Hg
    • Hematocrit <30%
    • Congestive heart failure
REFERENCES
1. Malasana G, Brignole M, Daccarett M, et al. The prevalence and cost of the faint and fall problem in the state of Utah. Pacing Clin Electrophysiol. 2011;34(3):278-283.
2. Kessler C, Tristano JM, De Lorenzo R. The emergency department approach to syncope: evidencebased guidelines and prediction rules. Emerg Med Clin North Am. 2010;28(3):487-500.
3. 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.
4. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol. 2012;59(18):1583-1591.
5. Romme JJ, Reitsma JB, Go-Schön IK, et al. Prospective evaluation of non-pharmacological treatment in vasovagal syncope. Europace. 2010;12(4):567-573.
6. Kuriachan V, Sheldon RS, Platonov M. Evidencebased treatment for vasovagal syncope. Heart Rhythm. 2008;5(11):1609-1614.
7. Grossman SA, Fischer C, Kancharla A, et al. Can benign etiologies predict benign outcomes in high-risk syncope patients? J Emerg Med. 2011;40(5):592-597.
8. Quinn JV, Stiell IG, McDermott DA, et al. Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes. Ann Emerg Med. 2004;43(2):224-232.
9. 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
&NA;
  • Parry SW, Tan MP. An approach to the evaluation and management of syncope in adults. BMJ. 2010;340:c880.
  • 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.
  • 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.
  • 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.
See Also
&NA;
  • Aortic Valvular Stenosis; Atrial Septal Defect (ASD); 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
&NA;
ICD10
R55 Syncope and collapse
Clinical Pearls
&NA;
  • A careful history and physical exam are key to a diagnosis.
  • Use the ECG/event-recorder to evaluate for cardiac conditions.
  • True neurologic causes of syncope are very rare; by far, cardiac causes are more common.
  • <2% of cases are caused by hyponatremia, hypocalcemia, hypoglycemia, or renal failure causing seizures.