Syncope

Mechanisms

Syncope by whatever mechanism is caused by a lack of adequate cerebral blood flow with loss of consciousness and inability to remain upright.

Primary cardiac causes of syncope ( Table 87.4 ) include arrhythmias such as long QT syndrome (LQTS), Wolff-Parkinson-White syndrome (particularly with atrial fibrillation), ventricular tachycardia (VT), and occasionally supraventricular tachycardia (see Chapter 462 ). VT may be associated with hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy, repaired congenital heart disease, or a genetic cause such as catecholaminergic polymorphous ventricular tachycardia (CPVT). Other arrhythmias that may lead to syncope are bradyarrhythmias such as sinus node dysfunction and high-grade second- or third-degree atrioventricular (AV) block. Patients with congenital complete AV block may present with syncope. Syncope may also be caused by cardiac obstructive lesions, such as critical aortic stenosis, or coronary artery anomalies, such as an aberrant left coronary artery arising from the right sinus of Valsalva. Patients with primary pulmonary hypertension or Eisenmenger syndrome may experience syncope. In all the obstructive forms of syncope, exercise increases the likelihood of an episode because the obstruction interferes with the ability of the heart to increased cardiac output in response to exercise.

Noncardiac causes of loss of consciousness include epilepsy, as well as basilar artery migraine, hysterical syncope, and pseudoseizures (see Table 87.1 ). Occasionally, patients with narcolepsy may present with syncope. Hypoglycemia and hyperventilation may also present as syncope.

Evaluation

The most important goal in the evaluation of the new patient with syncope is to diagnose life-threatening causes of syncope so that these causes can be managed. Many patients presenting with sudden cardiac arrest caused by conditions such as LQTS will have previously experienced an episode of syncope, so the presentation with syncope is an opportunity to prevent sudden death.

The most important tool in evaluation is a careful history . The characteristics of cardiac syncope differ significantly from the prodrome seen in neurocardiogenic syncope ( Table 87.5 ). Several red flags can be identified that should lead the clinician to suspect that the mechanism is a life-threatening cardiac cause rather than simple fainting ( Table 87.6 ). The occurrence during exercise suggests an arrhythmia or coronary obstruction. Injury because of an episode of syncope indicates sudden occurrence with a lack of adequate prodromal symptoms and suggests an arrhythmia. The occurrence of syncope while recumbent would be quite unusual in a patient with neurocardiogenic syncope and therefore suggests a cardiac or neurologic cause. Occasionally, a patient with syncope caused by a tachyarrhythmia will report the sensation of a racing heart before the event, but this is unusual.

A careful family history is essential in evaluation of syncope. Specifically, if there are first-degree relatives with inherited syndromes, such as a LQTS or HCM, this should lead to more specific evaluation of the patient. Also, if relatives died suddenly at a young age without a clear and convincing cause, inherited cardiac arrhythmias or cardiomyopathies should also be suspected.

Patients with a history of heart disease, especially cardiac repair, may have causes that are specific to their repair. Sinus node dysfunction is common after the Senning or Mustard procedure for transposition of the great vessels. VT may be seen after repair of tetralogy of Fallot. A patient with a history of septal defect repair should be evaluated for the late occurrence of AV block, and patients with an implanted pacemaker should be evaluated for pacemaker lead failure.

The physical examination may also offer clues ( Table 87.6 ). Patients with HCM may have a prominent cardiac impulse and/or an ejection murmur, as will patients with aortic stenosis. The patient with primary pulmonary hypertension will have a loud and single second heart sound and may also have an ejection click and the murmur of pulmonary insufficiency. Scars from prior cardiac surgery and pacemaker implantation would be evident.

All patients presenting with a first episode of syncope must have an electrocardiogram obtained, looking primarily for QT interval prolongation, preexcitation, ventricular hypertrophy, T-wave abnormalities, and conduction abnormalities. Other tests that may be needed depending on the results of the initial evaluation may include echocardiography, exercise testing, cardiac MRI, or 24 hr Holter monitoring. In patients for whom there is a strong suspicion of a paroxysmal arrhythmia, an implantable loop recorder may be the most effective means of diagnosis. Additional tests to look for anemia, hypoglycemia, drugs of abuse, and other etiologies noted in Table 87.1 will be determined by the history and physical examination.

Treatment

Therapy for vasovagal syncope includes avoiding triggering events (if possible), fluid and salt supplementation, and if needed, midodrine (see Chapter 87.1 , Table 87.7 ). Immediately after the event, the patient should remain supine until symptoms abate to avoid recurrence.

Treatment for cardiac causes of syncope will be determined by the diagnosis. If a reentrant tachycardia (AVNRT, AVRT) is found, then a catheter ablation is indicated. If bradycardia from AV block was the cause of the syncope, a pacemaker may be warranted. Patients with syncope from medically refractory malignant arrhythmias, as may be seen in HCM, LQTS, arrhythmogenic cardiomyopathy, or CPVT, require an implantable cardioverter-defibrillator. Patients with structural heart disease (valvular disease or coronary artery anomalies) should be referred for surgery.