Syncope is a transient loss of consciousness and postural tone followed by spontaneous, complete recovery. Lightheadedness and dizziness, on the other hand, are terms that may imply any one of the following four conditions: (i) near-syncope, i.e., the feeling of impending faint;(ii) vertigo, i.e., an illusion of motion, usually from an inner ear disorder; (iii) disequilibrium (ataxia) from peripheral neuropathy or cerebellar disorder; (iv) non-specific lightheadedness from anxiety. There are three major types of syncope: neurally mediated syncope, orthostatic hypotension, and cardiac syncope. Neurally mediated syncope is the most common type of syncope, accounting for two-thirds of the cases.1–3 It results from an inappropriate response of autonomic reflexes, leading to vasodilatation and bradycardia. It is usually preceded by premonitory symptoms (lightheaded- ness, diaphoresis, nausea, malaise, abdominal discomfort, tunnel vision). However, this may not be the case in a third of patients, more so elderly patients who may not recognize or remember the warning. Palpitations are frequently reported with reflex syncope and do not necessarily imply an arrhythmic syncope.4,5 This syncope does not usually occur in a supine position,4,5 but may occur in a seated position.6 Subtypes of neurally mediated syncope are as follows: This syncope is usually triggered by sudden emotional stress, prolonged sitting or standing, dehydration, or a warm environment, but may also occur without any trigger. It is the most common syncope in young patients (female > male) and, contrary to a common misconception, may occur in the elderly as well.7 Usually, it is not only preceded but followed by nausea, malaise, fatigue, or diaphoresis;4,5,8 the patient’s full revival may be slow and malaise may persist for hours. When the syncope is prolonged >30–60 seconds, clonic movements and loss of bladder control are common.9 Mechanism. Vasovagal syncope is initiated by anything that leads to strong myocardial contractions on an “empty” heart. Emotional stress, reduced venous return (from dehydration or prolonged standing), or vasodilatation (hot environment) stimulates the sympathetic system and reduces the LV cavity size, which leads to strong hyperdynamic contractions in a relatively empty heart. This hyperdynamic cavity obliteration activates the myocardial mechanoreceptors C, initiating a paradoxical vagal reflex with vasodilatation and relative bradycardia.10 Vasodilatation is usually the predominant mechanism (vasodepressor response), particularly in older patients. Hypotension usually precedes bradycardia, hence the limited role of bradycardia in this process; but severe and long asystolic pauses may play a more pronounced role (cardioinhibitory response).7 Diuretic and vasodilator therapies increase the predisposition to vasovagal syncope, particularly in the elderly. On tilt table testing, vasovagal syncope is characterized by hypotension and a relative bradycardia, sometimes severe.10 This syncope is caused by a reflex triggered in specific circumstances such as micturition, defecation, coughing, weightlifting, laughing, or deglutition. The reflex may be initiated by a receptor on the visceral wall (e.g., bladder wall) or by the strain that reduces venous return. Carotid sinus hypersensitivity (CSH) is an abnormal response to carotid massage that is predominantly found in patients over 50 years of age. Spontaneous carotid sinus syndrome is a form of CSH where syncope clearly occurs in a situation that stimulates the carotid sinus (head rotation, head extension, shaving, tight collar); this is a rare cause of syncope (~1% of syncope cases). Conversely, induced carotid sinus syndrome is much more common and represents CSH in a patient with unexplained syncope and without obvious triggers; the abnormal response is induced during carotid massage rather than spontaneously. In induced carotid sinus syndrome, carotid sinus hypersensitivity is a marker of a diseased sinus node or AV node that cannot withstand any inhibition; this diseased node is the true cause of syncope rather than CSH per se, and carotid massage is a “stress test” that unveils conduction disease. Thus, carotid sinus massage is indicated in unexplained syncope regardless of circumstantial triggers. It consists of applying firm pressure over each carotid bifurcation (just below the angle of the jaw) consecutively for 10 seconds. It is performed at the bedside, and may be performed in both supine and erect positions during tilt table testing; erect positioning increases the sensitivity of carotid massage. An abnormal response to carotid sinus massage is defined as any of the following: 11–13 Overall, a cardioinhibitory component is present in ~2/3 of CSH cases. CSH is found in 25–50% of patients over 50 years of age with unexplained syncope or fall, and is almost equally seen in men and women.11 One study correlated CSH with the later occurrence of asystolic syncope during prolonged internal loop monitoring; subsequent pacemaker therapy reduced the burden of syncope.12 Another study, in patients >50 years old with unexplained falls, found that 16% of them had cardioinhibitory CSH; pacemaker placement reduced falls and syncope by 70% compared with no pacemaker therapy in these patients.13 On the other hand, CSH is seen in 39% of elderly patients who do not have a history of syncope or fall, and thus it is important to rule out other causes of syncope before attributing it to CSH. While exertional syncope is alarming for a malignant cardiac or arrhythmic cause, post-exertional syncope is usually a form of vasovagal syncope. Upon exercise cessation, venous blood stops getting pumped back to the heart through the peripheral muscular contraction, yet the heart is still exposed to the catecholamine surge and hypercontracts on an empty cavity. This low preload reduces cardiac output and may trigger a vagal reflex. Post-exertional syncope may also be seen in hypertrophic obstructive cardiomyopathy (HOCM) and aortic stenosis (AS), where the small left ventricular cavity is less likely to tolerate the reduced preload after exercise and is more likely to obliterate. Orthostatic hypotension accounts for ~10% of cases of syncope.1–3 Normally, after the first few minutes of standing, ~25–30% of blood pools in the veins of the pelvis and the lower extremities, strikingly reducing venous return and stroke volume. Upon prolonged standing, additional blood volume extravasates in the extravascular space, further reducing venous return. This normally leads to a reflex increase of sympathetic tone, peripheral and splanchnic vasoconstriction, and an increase in heart rate of 5–20 bpm. Overall, cardiac output (CO) is reduced while blood pressure (BP) is maintained (BP = CO × vascular resistance: vascular resistance ↑, CO ↓). Orthostatic hypotension is characterized by autonomic failure, with a lack of compensatory increase in vascular resistance or heart rate upon standing; or by significant hypovolemia that cannot be overcome by sympathetic mechanisms. It is defined as a drop of SBP ≥20 mmHg or DBP ≥10 mmHg after 30 seconds to 3 minutes of orthostasis. BP is checked immediately upon standing and at 3 (+/-5) minutes of orthostasis; this may be done at the bedside or during tilt table testing.2,4 Some patients may have an immediate BP drop of >40 mmHg upon standing, with a quick return to normal within 30 seconds. This “initial orthostatic hypotension” may be common in elderly patients receiving antihypertensive drugs and may elude detection upon standard BP measurement.2 Other patients with milder orthostatic hypotension may develop a more delayed hypotension later than 3 min (10–15 minutes), as more blood pools in the periphery.14 In some ways, vasovagal syncope is a form of orthostatic hypotension, more delayed and abrupt, with additional vagal involvement. Along with the BP drop, a failure to increase heart rate (<15 bpm) identifies autonomic dysfunction. On the other hand, an excessive increase in heart rate >20–30 bpm may signify a hypovolemic state even if BP is maintained, the lack of BP drop being related to the excessive heart rate increase. Orthostatic hypotension is the most common cause of syncope in the elderly and may be due to: (i) autonomic dysfunction=neurogenic orthostatic hypotension (age, diabetes, CKD, TTR amyloidosis, paraneoplastic syndrome, Parkinson disease), (ii) volume depletion, (iii) drugs that block autonomic effects or cause hypovolemia (vasodilators, β-blockers, diuretics, neuropsychiatric medications, alcohol). Since digestion leads to peripheral vasodilatation and splanchnic blood pooling, syncope that occurs within 1 hour postprandially has a similar mechanism to orthostatic syncope. Supine HTN with orthostatic hypotension– Some patients with severe autonomic dysfunction or severely non-compliant arteries are unable to regulate vascular tone. They display severe HTN when supine, as plasma volume rises, and significant hypotension when upright. POTS is another form of orthostatic failure that occurs most frequently in young women (<50 years old, 86% women). POTS is defined as a striking increase in rate of ≥30 bpm within 5 to 10 minutes of standing, often to an absolute heart rate >120 bpm, with no significant drop in BP (<20 mmHg). Unlike in orthostatic hypotension, BP and cardiac output are maintained through this increase in heart rate, yet the patient still develops symptoms of severe fatigue or near-syncope, because of flow maldistribution and reduced cerebral flow.2 While POTS, per se, does not induce syncope,2 it may be associated with a vasovagal form of syncope that occurs beyond the first 10 minutes of standing in up to 38% of these patients.15 Autonomic dysfunction is prevalent in POTS, but the universal finding is cardiovascular deconditioning (orthostatic deconditioning). In fact, a period of bedrest following either surgery or a viral illness is frequently the trigger of POTS, often in individuals who are normally very active. Cardiovascular deconditioning can occur rapidly, with as little as 20 hours of bedrest in predisposed patients, hence POTS frequently has an acute onset and a vicious circle of further bedrest and cardiac deconditioning. POTS physiology is similar to the orthostatic intolerance of astronauts returning to Earth.16 Cardiac unloading in space or after bedrest leads to: (a) physiological cardiac atrophy (the converse of athletic hypertrophy) with reduced stroke volume, (b) volume dysregulation (reduced renin-angiotensin) which reduces blood volume, and (c) peripheral autonomic denervation which does not affect the heart, but affects the peripheral vascular resistance, preventing its rise with orthostatic stress. To maintain cardiac output, heart rate rises at rest and more so with orthostasis. In a second form of POTS called hyperadrenergic POTS (30–50% of POTSs), the sympathetic system gets overly activated with orthostasis (SBP rises ≥10 mmHg with standing).10,17 Excessive sympathetic tone drives tachycardia and symptoms here, more than volume or autonomic impairment. The dominant symptom here is palpitation, while dizziness predominates in the first form of POTS. POTS is diagnosed at the bedside, via orthostatic assessment of BP/pulse (3, 5, 10 min), and does not require tilt table testing. Hyperadrenergic POTS is specifically diagnosed by measuring norepinephrine levels after 5–10 min of standing (≥600 pg/ml). The supine pulse is normal in POTS, unlike IST, which is characterized by a more persistent sinus tachycardia, including supine nocturnal tachycardia. Accounting for ~10–20% of cases of syncope, a cardiac etiology is the main concern in patients presenting with syncope, and the main predictor of mortality and sudden death.1,2,8,18,19 Syncope often occurs suddenly without any warning signs (sudden syncope is also called malignant syncope). As opposed to neurally mediated syncope, the post-recovery period is not usually marked by lingering malaise. There are three forms of cardiac syncope: MI/CAD causes syncope only when complicated by arrhythmias or by a shock. Occasionally, fast supraventricular tachycardia causes syncope at its onset, before vascular compensation develops, or at its offset (post-conversion sinus pause). This may occur in patients without major heart disease and usually causes near-syncope, not full syncope.2 Acute medical or cardiovascular illnesses may cause syncope and are sought in the appropriate clinical context: (1) severe hypovolemia or gastrointestinal bleed; (2) large pulmonary embolus with hemodynamic compromise; (3) tamponade; (4) aortic dissection; (5) hypoglycemia. Bilateral critical carotid disease or severe vertebrobasilar disease very rarely causes syncope, and, when it does, it is associated with focal neurologic deficits.2 Vertebrobasilar disease may cause “drop attacks,” i.e., a loss of muscular tone with fall but without loss of consciousness.20 Severe proximal subclavian disease leads to reversal of the flow in the ipsilateral vertebral artery as blood is shunted toward the upper extremity. It manifests as dizziness and syncope during the ipsilateral upper extremity activity, usually with focal neurological signs (subclavian steal syndrome).2 Psychogenic pseudosyncope is characterized by a high frequency of attacks that typically last longer than a true syncope and occur multiple times per day or week, sometimes with a loss of motor tone.2 It occurs in patients with anxiety or somatization disorders. Note Reflex syncope is the most frequent etiology of syncope. However, long asystolic pauses due to sinus or AV nodal block are the most frequent mechanism of unexplained syncope and are seen in >50% of syncope cases on prolonged rhythm monitoring.1,21These pauses may be related to intrinsic sinus or AV nodal disease or, more commonly, to extrinsic effects, such as a vasovagal mechanism. Some European experts favor classifying and treating syncope based on the mechanism rather than the etiology, but this is not universally accepted.1,22 Table 26.1 Features that suggest seizure rather than syncope. Table 26.2 Clinical clues to the diagnosis of syncope.2–5,8 Underlying structural heart disease is the most important predictor of ventricular arrhythmias and death. 1823–25 Thus, the primary goal of syncope evaluation is to rule out structural heart disease by history, examination, ECG, and echocardiography. The etiology of syncope is determined by history and physical examination alone in up to 50% of cases, mainly vasovagal syncope, ortho- static syncope, or seizure.2,3,17 Always check blood pressure both lying and standing and in both arms, and obtain an ECG. Perform carotid massage in all patients older than 50 years if syncope is not clearly vasovagal or orthostatic and if cardiac syncope is not likely. Carotid massage is contraindicated if the patient has a carotid bruit or any history of stroke. ECG establishes or suggests a diagnosis in 10% of patients (Table 26.3).2,8,18,26 A normal ECG, or mild non-specific ST–T abnormality, suggests a low likelihood of cardiac syncope and is associated with an excellent prognosis. The ECG is abnormal in 90% of cases of cardiac syncope and only 6% of cases of neurally mediated syncope.27 In one study of syncope patients with a normal ECG and a negative cardiac history, none had an abnormal echocardiogram.28 If the history suggests neurally mediated syncope or orthostatic hypotension, and the history, examination, and ECG are not suggestive of CAD or any other cardiac disease, the workup is stopped. Figure 26.1 Management of syncope. Also, consider severe hypovolemia, bleeding, pulmonary embolism, and tamponade and rule them out clinically. Carotid Doppler and head CT scan are not indicated, especially given that carotid stenoses, per se, very rarely lead to syncope. †EP study may have missed bradyarrhythmias and some forms of VT. CAD, coronary arterial disease; EF, ejection fraction; EP, electrophysiological; LVH, left ventricular hypertrophy; HCM, hypertrophic cardiomyopathy; ICD, implantable cardioverter defibrillator; PM, pacemaker. Table 26.3 ECG or rhythm monitor findings suggestive of cardiac syncope. If the patient has signs or symptoms of heart disease (angina, dyspnea, clinical signs of HF, murmur), a history of heart disease, or exertional or malignant features, heart disease should be sought, and the following performed: Often, the workup may be stopped, and syncope considered neurally mediated. The likelihood of cardiac syncope is very low in patients with normal ECG and echocardiography, and several studies have shown that patients with syncope who have no structural heart disease have a normal long-term survival.19,25,30 Yet, SVT or fast AF may be seen in patients with no clear underlying heart disease and may cause near syncope, or rarely, full syncope (particularly when a pause occurs at the conversion of AF into sinus rhythm). The following workup may be ordered if syncope has no clear trigger or prodrome and is associated with physical injury (especially if recurrent):2,3,18 Beware that pauses and high-grade AV block may be due to a vasovagal mechanism (Figure 26.3). The finding of non-sustained VT on monitoring increases the suspicion of VT as a cause of syncope, but does not prove it or dictate an ICD, per se.
26
Syncope
I. Neurally mediated syncope (reflex syncope)
A. Vasovagal syncope (neurocardiogenic syncope)
B. Situational syncope
C. Carotid sinus hypersensitivity
D. Post-exertional syncope
II. Orthostatic hypotension and postural orthostatic tachycardia syndrome
A. Orthostatic hypotension
B. Postural orthostatic tachycardia syndrome (POTS)
III. Cardiac syncope
IV. Other causes of syncope
V. Syncope mimic: seizure (see Table 26.1)
Urinary incontinence is not helpful, as it frequently occurs with syncope as well as seizure
VI. Clinical clues (see Table 26.2)
Position during syncope
Situation during syncope
Prodromes (abdominal discomfort, malaise, palpitations, nausea, blurry vision)
How consciousness is regained after syncope
Color during syncope
Duration
Underlying heart disease, chest pain → cardiac syncope
Multiple neuropsychiatric or blood pressure medications → reflex or orthostatic syncope
The presence or the lack of injury does not help differentiate cardiac from reflex syncope
Multiple syncopal recurrences (≥3) suggest a reflex or orthostatic syncope (one is less likely to survive three spells of cardiac syncope). This is particularly true if the interval between spells is >4 years8
VII. Diagnostic evaluation of syncope (Figure 26.1)
A. Basic initial strategy
B. If the heart is normal clinically and by ECG
C. If the patient has signs or symptoms of heart disease
D. If no heart disease is suggested by ECG and echocardiography
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