SYNCOPE, REFLEX (VASOVAGAL SYNCOPE)

Melinda Y. Kwan, DO, MPH • Norton Winer, MD

 BASICS

Syncope is a reversible loss of consciousness and postural tone secondary to systemic hypotension and cerebral hypoperfusion due to vasodilation and/or bradycardia (rarely, tachycardia) with spontaneous recovery and no neurologic sequelae. The term syncope excludes seizures, coma, shock, or other states of altered consciousness.

DESCRIPTION

•  Derived from the Greek term syncopa, meaning “to cut short”

•  Sudden, transient loss of consciousness characterized by unresponsiveness, falling, and spontaneous recovery

•  Common cause of syncope in all age groups, especially in patients with no evidence of neurologic or cardiac disease

•  Four main types: vasovagal or neurocardiogenic syncope, situational syncope, orthostatic hypotension, carotid sinus hypersensitivity, and glossopharyngeal/trigeminal neuralgia syncope (uncommon) (1)

EPIDEMIOLOGY

•  Mortality: cardiac-related syncope 20–30% and 5% in idiopathic syncope

•  Age: any age

Incidence

•  Ranges from 7.5% in children aged <18 years and 15% in adults aged >70 years

•  36–62% of all syncopal episodes

•  30% recurrence rate

Prevalence

22% in the general population

ETIOLOGY AND PATHOPHYSIOLOGY

Cause: an abnormal interaction of the normal mechanisms for maintaining BP and upright posture

•  In normal individuals, upright posture results in venous pooling and transient decrease in BP.

•  Neurally induced syncope may result from a cardioinhibitory response, a vasodepressor response, or a combination of the two.

•  Increased cardiovagal tone leads to bradycardia or asystole and decreased peripheral sympathetic activity leads to venodilation and hypotension (2).

•  Vasovagal syncope usually has a precipitating event, often related to fright, pain, panic, exercise, noxious stimuli, or heat exposure (2).

•  Carotid sinus syncope is precipitated by position change, turning head, or wearing a tight collar (possible neck tumors or surgical scarring).

•  Situational syncope is related to micturition, defecation, postexercise, cough, or swallow (3).

•  Glossopharyngeal syncope is related to throat or facial pain (4).

Genetics

Vasovagal syncope: strong heritable component to the etiology of >20% of cases

RISK FACTORS

•  Low-resting BP

•  Age: older age

•  Prolonged supine position with resulting deconditioning of autonomic control

GENERAL PREVENTION

Avoidance of precipitating events or situations. Optimization of diabetes mellitus (DM) control, elastic stockings, adequate hydration. Limited evidence suggests that polydipsia may reduce recurrences.

COMMONLY ASSOCIATED CONDITIONS

•  Cardiopulmonary disorders: CHF, MI, arrhythmias, hypertrophic obstructive cardiomyopathy, HTN, PE pulmonary embolism

•  Neurologic disorders: autonomic dysfunction, Shy-Drager, Parkinson disease, multiple system atrophy, transient ischemic attack, vertebrobasilar insufficiency, peripheral neuropathy

•  Psychiatric disorders:

–  Generalized anxiety disorder

–  Panic disorder

–  Major depression

–  Alcohol dependence

 DIAGNOSIS

HISTORY

•  Evaluation of syncope and presyncope are the same.

•  Important first to rule out cardiac syncope

•  Neurally mediated syncope is preceded by blurred vision, palpitations, nausea, warmth, diaphoresis, or light-headedness, or there may be history of nausea, warmth, diaphoresis, or fatigue after syncope (5)[C].

•  Vasovagal syncope

–  Three phases: prodrome, loss of consciousness, and postsyncope

–  Precipitating event or stimulus is usually identified, such as panic, fright, pain, or exercise.

–  Athletes may have after exertion (diagnosis of exclusion).

–  Position: can be preceded by prolonged standing but can occur from any position; generally resolves when the patient becomes supine

  Preceding events: as discussed above

  Prodrome: as listed above for neurally mediated syncope

–  Duration: generally brief (seconds to minutes)

–  Recovery: may be prolonged with persistent nausea, pallor, and diaphoresis but without neurologic change or confusion

•  Carotid sinus syncope is precipitated by position change, after turning head, or wearing a tight collar.

•  Situational syncope is related to micturition, defecation, or coughing.

•  Glossopharyngeal syncope (less common) is related to throat or facial pain (4)[C]

–  Precipitating events or situations may include panic, pain, exercise, micturition, defecation, coughing, or swallowing.

PHYSICAL EXAM

•  Vital signs, including orthostatics and bilateral BP

•  Cardiac exam: volume status, murmurs, rhythm, carotid bruits

•  Neurologic exam: signs of focal deficit

•  Assess for occult blood loss, including guaiac.

•  Dix-Hallpike to rule out benign paroxysmal vertigo

DIFFERENTIAL DIAGNOSIS

•  Seizure

•  Arrhythmia

•  Hypoglycemia

•  Cardiac syncope

•  Cerebrovascular syncope

•  Orthostatic hypotension

•  Drop attacks

•  Psychiatric illness

DIAGNOSTIC TESTS & INTERPRETATION

As indicated by history and physical, includes basic tests to rule out the three main reasons for syncope: hypoglycemia, arrhythmia, and anemia

Initial Tests (lab, imaging)

•  Blood sugar

•  ECG should be ordered for all patients. Abnormal ECG findings are common in patients with cardiac syncope.

•  CBC to rule out anemia

•  Head CT, MRI/MRA, carotid ultrasound only in patients whose history or physical exam suggests a neurologic cause of syncope

–  The 2007 American College of Emergency Physicians (ACEP) Guidelines for diagnostic testing for syncope are as follows (6):

  Level A recommendations: standard 12-lead ECG

  Level B recommendations: none specified

  Level C recommendations: laboratory testing and investigations, including echocardiography or head CT, to be performed only if indicated by specific findings in the history or physical examination

Follow-Up Tests & Special Considerations

•  24-hour Holter monitoring only in patients with a high probability of cardiac cause of syncope and/or abnormal ECG findings

•  A low hemoglobin without obvious cause of bleed would warrant a guaiac, CT head to rule out subarachnoid hemorrhage (SAH), CT abdomen to rule out retroperitoneal bleed.

•  Negative imaging will prompt workup for alternative causes.

•  Stroke, bleed, or carotid stenosis will require appropriate disease-oriented management.

•  EEG only when history or physical exam is very suggestive of seizure activity

•  Implantable loop recorder

Diagnostic Procedures/Other

•  Head-up tilt table testing:

–  Contraindicated in patients with known cardiac or neurovascular disease or in pregnancy

–  Indicated for recurrent syncope or single episode accompanied by injury or risk to others (e.g., pilots, surgeons)

–  Uses positional changes to reproduce symptoms

–  Positive tests are diagnostic for vasovagal syncope.

•  Carotid sinus massage, only in a monitored setting (i.e., BP and HR monitoring, IV access):

–  Contraindicated in patients with carotid disease (careful auscultation prior to massage is essential)

–  Pressure at the angle of the jaw for 5 seconds with simultaneous ECG monitoring

–  Positive tests (causing syncope or cardiac pause >3 seconds) are diagnostic of carotid sinus syncope.

•  Psychiatric evaluation: to rule out anxiety, depression, and alcohol abuse

 TREATMENT

Therapy is primarily for recurrent syncope. Situational syncope will not warrant any treatment.

GENERAL MEASURES

Recognition and avoidance of precipitating events or situations; medical management is based on small, nonrandomized clinical trials.

First Line

•  Nonpharmacologic treatment

–  Includes patient counseling

  Development of coping skills

  Increased salt and fluid intake

–  Moderate exercise training

  Isometric muscle contractions

  Leg crossing and buttocks clenching

  Intense gripping of the hands and tensing of the arms

  These maneuvers increase cardiac output and arterial blood pressure (7).

–  Tilt-table training

  Progressively prolonged periods of enforced upright posture

Second Line

•  α-Agonists are mainly used for orthostatic hypotension.

–  Midodrine is commonly used. It increases peripheral vascular resistance and venous return. Side effects include HTN, paresthesia, urinary retention, “goose bumps,” hyperactivity, dizziness, tremor, and nervousness.

•  SSRIs: Paroxetine and fluoxetine are SSRIs useful in treating neurocardiogenic/vasovagal syncope.

–  Serotonin affects BP and HR via the central nervous system. Serotonin decreases a sympathetic withdrawal response to rapid increases in serotonin levels.

–  Side effects include weight gain, nausea, anxiety, sexual dysfunction, and insomnia.

•  Mineralocorticoids: Fludrocortisone has been found helpful mainly in orthostatic hypotension.

–  Helpful in renal sodium absorption and increasing the vasoconstrictive peripheral vascular response

–  Adverse reactions include fluid retention, HTN, CHF, peripheral edema, and hypokalemia.

•  β-Blockers: Metoprolol, atenolol, or pindolol are mainly used for postural tachycardia syndrome (POTS).

–  Block peripheral vasodilators and ventricular mechanoreceptor stimulation.

–  Stabilization of HR and BP

–  Side effects: hypotension and bradycardia (with worsening of syncope), fatigue, depression, and sexual dysfunction

–  Contraindicated in asthma

ISSUES FOR REFERRAL

Neurology or cardiology, as needed

ADDITIONAL THERAPIES

Use of support/pressure stockings

COMPLEMENTARY & ALTERNATIVE MEDICINE

These include treatments for underlying heart disease or precipitating factors like anxiety. None of these are proven therapies.

•  Nutrition and supplements: omega-3 fatty acids, multivitamin, CoQ10, acetyl-L-carnitine, α-lipoic acid, and L-arginine

•  Herbs: Green tea (Camellia sinensis), bilberry (Vaccinium myrtillus), ginkgo (Ginkgo biloba)

•  Homeopathy: Carbo vegetabilis, opium, sepia

•  Acupuncture: It may precipitate fainting.

SURGERY/OTHER PROCEDURES

Pacemaker placement may be of use in patients with frequent neurocardiogenic/vasovagal syncope that is refractory to other therapies (3)[C].

•  Prevents prolonged bradycardia or asystole during syncopal episodes

•  Long-term effect

•  Invasive placement procedure

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

2007 ACEP guidelines mandate that the patient be admitted if (6):

•  Level B recommendations

–  Admit patients with syncope and evidence of heart failure or structural heart disease.

–  Admit patients with syncope and high-risk factors.

•  High-risk stratification is based on the following factors:

–  Older age and associated comorbidities

–  Abnormal ECG, hematocrit (Hct) 30 (if obtained)

–  History or presence of heart failure, coronary artery disease, or structural heart disease

•  Additional causes to admit

–  Syncope occurring during exercise

–  Syncope causing severe injury

–  Family history of sudden death

•  IV fluids to stabilize HR and BP

•  Isotonic crystalloids, as needed

•  Vital sign monitoring

•  Discharge when hemodynamically stable and workup satisfactory

 ONGOING CARE

DIET

•  Increased salt intake may be helpful if not contraindicated (2)[C].

•  Maintain fluid intake.

PATIENT EDUCATION

•  To identify and avoid precipitating events or situations

•  Avoid dehydration, alcohol consumption, warm environments, tight clothing, and long periods of standing motionless.

•  Recognize presyncopal symptoms.

•  Use behaviors, such as lying down, to avoid syncope.

PROGNOSIS

May be recurrent but not life-threatening

COMPLICATIONS

May result in injury from fall

REFERENCES

1.  Angaran P, Klein GJ, Yee R, et al. Syncope. Neurol Clin. 2011;29(4):903–925.

2.  Raj SR, Coffin ST. Medical therapy and physical maneuvers in the treatment of the vasovagal syncope and orthostatic hypotension. Prog Cardiovasc Dis. 2013;55(4):425–433.

3.  Walsh K, Hoffmayer K, Hamdan M. Syncope: diagnosis and management. Curr Probl Cardiol. 2015;40(2):51–86.

4.  Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. 2004;329(7461):336–341.

5.  Chen LY, Benditt DG, Shen WK. Management of syncope in adults: an update. Mayo Clin Proc. 2008;83(11):1280–1293.

6.  Huff JS, Decker WW, Quinn JV, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg Med. 2007;49(4):431–444.

7.  Coffin ST, Raj SR. Non-invasive management of vasovagal syncope. Auton Neurosci. 2014;184:27–32.

ADDITIONAL READING

•  Lelonek M. Genetics in neurocardiogenic syncope. Przegl Lek. 2006;63(12):1310–1312.

•  Márquez MF, Urias-Medina K, Gómez-Flores J, et al. Comparison of metoprolol vs clonazepam as a first treatment choice among patients with neurocardiogenic syncope. Gac Med Mex. 2008;144(6):503–507.

 SEE ALSO

Algorithms: Syncope; Transient Ischemic Attack and Transient Neurologic Defects

 CODES

ICD10

R55 Syncope and collapse

CLINICAL PEARLS

•  History should include a careful analysis of the events preceding the attack.

•  It is important to rule out cardiologic or neurologic pathology.

•  Prodrome is often present.

•  Recovery may be prolonged, with persistent symptoms but no neurologic deficit or confusion.

•  Patient counseling to avoid precipitating situations or events is the first-line treatment.

•  Pregnant females can have reflex syncope when moving from supine to lateral decubitus or upright positions.