103 Loss of Consciousness Without Syncope Pathophysiological Classification of Syncope Syncope and the Causes of Consciousness Syncope Due to Orthostatic Hypotension History and Physical Examination Holter Monitor, Mobile Telemetry, and Implantable Loop Recorders Prognosis and Risk Stratification and Hospitalization Syncope is a common clinical problem accounting for 1% to 3% of all emergency department visits and 6% of hospital admissions in the United States and Europe.1,2 Individuals have a cumulative lifetime incidence of syncope of 30% to 40%.3,4 It is estimated that $2.4 billion are spent on syncope-related hospitalizations annually.5 Reflex syncope is most commonly diagnosed. First vasovagal fainting episodes typically occur in characteristic age ranges, peaking in early adolescence and again in elderly men and women older than 70 years.6 Women are more likely to faint than men.7,8 The workup and prognosis associated with syncope is dictated by the history, physical examination, and ultimately the condition that resulted in syncope. Syncope prevalence varies significantly according to patient age and study setting. Despite the fact that referral bias is present when comparing populations of individuals in an emergency department compared with those in the general population, several generalizations can be made. Reflex syncope is most commonly diagnosed and found to have an excellent prognosis in most studies. Depending on the patient population and study setting, either orthostasis or cardiac syncope are the second most common etiologies. Studies enrolling patients admitted to the hospital for syncope consistently report a 20% prevalence of cardiac syncope.9 Although population-based studies tend to report higher rates of orthostatic hypotension and lower rates of cardiac syncope.10 Epidemiologic data obtained with a survey is often dependent on patient recall. Given the fact that almost half of individuals with syncope do not seek medical attention, data sets taken from general population surveys are often skewed.6 To complicate matters further, one must be vigilant for conditions masquerading as syncope. If syncope involves a transient loss of consciousness, then what causes consciousness? This discussion is often cast in philosophical or ethical terms, but this chapter is intended to focus on the physical or biochemical. There are common denominators for the many causes of syncope described elsewhere in this chapter. Loss of consciousness is caused by active suppression of neuro–central nervous system processes needed for wakefulness or obtundation of such processes by lack of blood flow that occurs with most forms of syncope. The broad spectrum of relevant neurologic sites and neurotransmitters are summarized in Table 101-1. A complete review is available in an on-line article from the Canadian Institute or Neurosciences, Mental Health, and Addiction (www.cihr-irsc.gc.ca).11 Another parallel mechanism that helps to maintain wakefulness is the inhibition of sleep. The idea of some form of common denominator is suggested by electroencephalograph findings during syncope. These tend to be the same for all forms of syncope, but distinct from changes seen in epilepsy.12 On a more basic level, changes in protein conformation governed by quantum mechanical forces can play a role in consciousness and life itself.13,14 There might be a distinction between loss of consciousness and loss of any memory of events during a specific time. This distinction has been studied extensively regarding the mechanism of anesthetic agents.15 Nevertheless, a 24-page review article ultimately concludes that “a comprehensive explanation of the mechanism by which anesthetics cause loss of consciousness (LOC) has not yet been developed.”15 Several terms in the literature have been used to describe reflex or neurally mediated syncope. The 2006 American Heart Association guidelines used the term neurocardiogenic syncope to encompass neurally mediated, vasodepressor, and vasovagal syncope.16 These entities are characterized by the same pathophysiological triggers evoking syncope via an efferent signal resulting in vasodepressor, cardioinhibitory, or mixed responses Vasovagal syncope is defined as the common fainting spell, typically provoked by emotion or orthostatic stress. Patients often report prodromal symptoms such as nausea and diaphoresis before syncope. Situational syncope occurs when a specific physical activity elicits reflexes causing a transient loss of consciousness. Commonly reported triggers include exercise, cough, swallowing, urination, and defecation. Situational syncope is closely related to vasovagal syncope, and often the distinction between the two is blurred. Carotid sinus syncope is a rare form of reflex syncope typically present in adults older than 40 years. Carotid sinus hypersensitivity can be elicited by performing sequential carotid sinus massage for 10 seconds in both supine and erect positions. A sinus pause for more than 3 seconds or a fall in blood pressure greater than 50 mm Hg defines carotid sinus hypersensitivity.17 Classical OH is defined as an abnormal decrease in systolic BP by 20 mm Hg or more or a decrease in diastolic BP by 10 mm Hg or more within 3 minutes of standing.18,19 The orthostatic intolerance syndromes include OH that differs from classical OH in the onset and severity of symptoms. Included in this group is the postural orthostatic tachycardia syndrome (POTS), typically noted in young women with severe orthostatic symptoms usually accompanied by a marked rise in heart rate after standing. Etiologies of OH include primary and secondary autonomic failure, drug induced OH, and volume depletion. Primary autonomic failure includes Parkinson’s disease, multiple system atrophy (Shy-Drager syndrome) and pure autonomic failure. Secondary autonomic failure is more commonly observed in patients with diabetes, amyloidosis, uremia and spinal cord injuries. An uncommon variant that is very difficult to treat is paroxysmal withdrawal of sympathetic tone. 20 A complete review of OH and autonomic failure is not within the scope of this chapter and may be found elsewhere. 21 Cardiac syncope is syncope due to tachyarrhythmia, bradyarrhythmia or structural heart disease. It is the most common cause of syncope after neural reflex syncope and OH. According to the Framingham Heart Study, 10% of individuals presenting with a syncopal episode had a cardiac etiology. Those with cardiac disease had a greater prevalence of cardiac syncope when compared to those without cardiac disease, 20% and 5% respectively. The risk of death associated with cardiac syncope was doubled when compared to subjects without syncope. 6 Other studies, performed in emergency department or special syncope unit settings, report a prevalence of cardiac syncope ranging from 5% to 37%.9,10,22,23 The differential diagnosis of cardiac syncope can be found in Box 103-1. Arrhythmia related syncope occurs as a result of the inability of the heart and vascular system to rapidly compensate for a change in cardiac output. There is a continuum between syncope and coma. When patients do not regain consciousness following syncope, as a result of prolonged hypotension and cerebral hypoperfusion, the diagnosis of cardiac arrest must be invoked. 17 Disorders limiting cardiac outflow must be considered in the differential diagnosis of cardiac mediated syncope. Syncope is often due to a combination of vasoregulatory failure in combination with an obstruction to cardiac output. Myocardial ischemia or infarction, aortic stenosis, hypertrophic obstructive cardiomyopathy and mitral stenosis are just a few examples of these entities. Box 103-2 lists the causes of cardiac syncope. The reader is referred to chapters in this text dedicated to the natural history and treatment of tachyarrhythmia and bradyarrhythmia for a more detailed account of incidence, prevalence, diagnosis and treatment of disorders responsible for cardiac syncope. Box 103-2 Neurologic Sites and Neurotransmitters Responsible for Consciousness*
Syncope
Epidemiology
Prevalence of Syncope
Syncope and the Causes of Consciousness
Reflex Syncope
Syncope Due to Orthostatic Hypotension
Cardiac Syncope
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