Cardiac syncope occurs most frequently in patients with complete atrioventricular block and a heart rate of 40 beats or less per minute (Stokes-Adams attacks, or Adams-Stokes-Morgagni syndrome). The block may be persistent or intermittent; it is often preceded by fascicular or second-degree heart block. Ventricular arrest of 4 to 8 s, if the patient is upright, is enough to cause syncope; if the patient is supine, the asystole must last 12 to 15 s. After asystole of 12 s, according to Engel, the patient turns pale and becomes momentarily weak or may lose consciousness without warning; this may occur regardless of the position of the body. If the duration of cerebral ischemia exceeds 15 to 20 s, there are a few clonic jerks. With still longer asystole, the clonic jerks merge with tonic spasms and stertorous respirations and the ashen-gray pallor gives way to cyanosis, incontinence, fixed pupils, and bilateral Babinski signs. As heart action resumes, the face and neck become flushed. The report of this sequence of signs by a dependable observer helps to distinguish syncope from epilepsy. In cases of even more prolonged asystole (4 to 5 min), or if the patient is trapped in an upright or seated position for briefer periods, there may be cerebral injury caused by a combination of hypoxia and ischemia. Coma may persist or may be replaced by confusion and other neurologic signs. Focal ischemic changes, often irreversible, may then be traced to the fields of occluded atherosclerotic cerebral arteries or the border zones between the areas of supply of major arteries. Cardiac faints of the Stokes-Adams type may recur several times a day. The heart block is usually intermittent at first, and between attacks the electrocardiogram (ECG) may show no evidence of heart disease. A continuous ECG using a Holter monitor or telemetry is then needed to demonstrate the arrhythmia (see further on).
Less easily recognized are faintness and syncope caused by dysfunction of the sinus node, and manifested by marked sinus bradycardia, sinoatrial block, or sinus arrest (“sick sinus syndrome”). The nodal block results in prolonged atrial asystole. Supraventricular tachycardia or atrial fibrillation may occur, alternating with sinus bradycardia (bradycardia–tachycardia syndrome).
Tachyarrhythmias alone are less likely to produce syncope. Certainly, intermittent ventricular fibrillation can cause fainting, and supraventricular tachycardias with rapid ventricular responses (usually over 180 beats per minute) cause syncope when sustained, predominantly in patients who are upright at the time. The long QT syndrome is a rare familial condition in which syncope and ventricular arrhythmias are prone to occur. Mutations in at least six different genes encoding cardiac sodium and potassium channels cause this syndrome. Another inherited syndrome with right bundle branch block and ST-segment elevation in the right precordial leads is known to cause syncope and even sudden death (Brugada syndrome). Some patients with mitral valve prolapse seem disposed to syncope and presyncope and an inordinate number are also said to have panic attacks but these associations, like others with mitral valve prolapse, have never been adequately settled.