I. Evaluation and Management of Syncope: What every physician needs to know.
Syncope is a symptom not a diagnosis. Syncope is characterized by transient loss of consciousness (TLOC) due to a spontaneously self-limited (usually at most a minute or two) period of cerebral hypoperfusion.
The term “presyncope” is best used to depict a period of time just prior to syncope in which the patient may report any of a variety of warning or prodromal symptoms or signs (e.g., light-headedness, visual “gray-out,” palpitations, and nausea.). “Near-syncope” is a term that reflects symptoms that seem to be leading to a full syncope event, but the latter does not materialize.
Thus, “near syncope” is best used when the symptomatic episode is limited to the occurrence of only prodromal symptoms without actually subsequent loss of consciousness. Research suggests that the basis for near-syncope in a given individual may not be the same as the cause of true syncope in the same person. Consequently, near-syncope should not be used as a surrogate for syncope when diagnostic testing is undertaken.
The term “syncope” is often used by physicians both in casual conversation, as well as during documentation of the patient’s history when an individual presents after having recovered from an apparent temporary loss of consciousness. However, such usage is both incorrect and the source of much wasted diagnostic effort and expense. TLOC is a more precise initial descriptor and should be employed.
In essence, even though a patient might ultimately be considered to have suffered a true syncopal episode, the initial presentation should not be automatically considered to have been ‘syncope’. The patient usually has come with complaints such as having experienced a ‘blackout’ or ‘collapse’. It is the physician’s responsibility to determine whether the episode was indeed a ‘syncope spell’ or some other cause of real or apparent TLOC. Thus, in every case, the evaluation begins with TLOC, and only later (usually after a careful history has been obtained), if warranted, is it appropriate to shift the focus to syncope.
Once it is concluded that the presenting symptom was syncope, the next steps are:
1. Assessing the likely cause
2. Advising the patient regarding prognosis both in terms of recurrence risk, and mortality, and
3. Initiating a treatment strategy
The last two of these steps is critically dependent on the first being correct, and on whether the patient has any evidence of underlying cardiovascular disease.
Syncope has many causes. However, in the vast majority of cases the basis for cerebral hypoperfusion is a self-limited period of systemic hypotension (acute severe transient hypoxemia, as in airliner decompression, is certainly an alternative possibility but is very rare). Consequently, subsequent investigation of syncope focuses on those etiologies that could trigger a transient drop in blood pressure.
The principal considerations are summarized below. However, in many cases, “syncope-mimics” also enter the diagnostic equation (e.g., psychogenic pseudo-syncope [conversion reactions], narcolepsy, malingering), and these can prove to be challenging for physicians to deal with.
The principal conditions that cause syncope due to transient global cerebral hypoperfusion may be classified as follows:
A. Reflex (Neurally-mediated reflex) syncope
Vasovagal (or “common”) faint in which the triggering of an as yet inadequately understood neural-reflex leads to inappropriate vaso/veno dilation with either severe bradycardia or at least insufficient heart rate compensation (Figure 1); the result is cerebral hypoperfusion and loss of consciousness, often accompanied by premonitory symptoms such as feeling hot or cold, palpitations, and nausea.
The triggers for the initial sympathetic activation, which in turn is responsible for reflex parasympathetic activation, may be emotional distress, medical instrumentation, fear, and in some cases prolonged orthostatic stress.
Situational faints are similar in nature to vasovagal syncope, but the triggers are more readily identifiable. Typical triggers in susceptible individuals include severe cough, defecation, micturition, visceral pain, and postexercise or postprandial situations.
Carotid sinus syncope is usually associated with demonstrable carotid sinus hypersensitivity (i.e., abnormal response to carotid sinus massage). This condition tends to be restricted to older patients and often those with atherosclerotic vascular disease.
It is now considered an important cause of otherwise unexplained falls in older individuals. The diagnosis is best made if the history suggests that the collapse was associated with neck movement, although such an association is uncommon.
The finding of loss of consciousness during carotid sinus massage (CSM) due to marked bradycardia and/or as a result of vasodepressor hypotension (best demonstrated during CSM with the patient studied on a tilt-table in the head-up position) may also be considered diagnostic if no other causes can be identified.
B. Orthostatic hypotension (OH)
Immediate (initial) OH refers to the abrupt drop in blood pressure that may be observed almost immediately after change of posture from supine or seated to standing. The phenomenon is almost universal, and occasionally causes transient ‘gray-out’ in even healthy individuals.
However, fainting may occur in some cases. The drop in blood pressure occurs as gravity displaces almost a liter of blood from the upper parts of the body to the splanchnic bed and legs.
Generally, vasoconstriction and modest tachycardia promptly respond to compensate. However, in some patients (e.g., older, dehydrated, certain neurologic conditions) may not compensate quickly or sufficiently, and syncope occurs. In older patients (who are often amnestic for any prodrome), the collapse may be mistaken for an accidental fall and the real cause is missed.
Delayed (classical) OH tends to occur some minutes after movement to upright posture . When the blood pressure is recorded in such cases, it tends to dwindle over time and the faint occurs when systemic pressure is low enough that cerebrovascular autoregulation is no longer able to compensate. In some instances, the collapse may not occur for 10 to 15 minutes after the change in posture.
Unlike Immediate OH, the delayed form is more troublesome and is more often associated with important predisposing medical conditions, including: volume depletion, primary or secondary autonomic failure, drug effects, and deconditioning. Primary autonomic failure may be indicative of Parkinson’s disease, Lewy body dementia, and multisystem atrophy.
Secondary autonomic failure is observed in patients with diabetes mellitus, alcohol abuse, amyloidosis, uremia, and spinal cord injuries. Drug-induced hypotension is particularly important, and can be the result of treatment with any of a variety of agents including diuretics, antihypertensives, adrenergic blockers, and antidepressants.
C. Cardiovascular causes
The recent European Society of Cardiology syncope practice guidelines now combine cardiac causes of syncope, along with other cardiovascular disorders that may trigger syncope. In many of these cases, hypotension is triggered directly as a consequence of a drop in cardiac output such as may be expected with abrupt onset of either a bradyarrhythmia or tachycardia.
Similarly, acute obstruction to blood flow occurring as a result off an atrial myxoma or severe cardiac tamponade may be expected to trigger symptomatic hypotension. On the other hand, the hypotensive event may be secondary to the triggering of a neural reflex rather than as a direct accompaniment of the structural disturbance; thus the triggering of syncope due to reflex bradycardia and/or vasodepressor responses have been associated with acute myocardial infarction, acute aortic dissection or pulmonary embolism.
1. Arrhythmic causes of syncope
Bradyarrhythmias and tachyarrhythmias (both supraventricular and ventricular) are the most frequent causes of syncope in the cardiovascular category. This latter group also includes the growing list of “channelopathies” (long Q–T syndrome, Brugada syndrome, catecholaminergic ventricular tachycardia, idiopathic progressive conduction system disease, etc.).
In patients with sinus node dysfunction (SND), syncope may be caused by abrupt slowing of the heart rate (e.g., sinus pauses, sinus arrest) or due to a long pause after termination of an atrial tachyarrhythmia in the so-called bradycardia-tachycardia syndrome (BTS). Similarly, transient symptomatic hypotension may occur if an atrial tachycardia (most often atrial fibrillation) starts and the resulting heart rate is too fast to maintain the cardiac output, while at the same time vasoconstrictive compensation is too slow or inadequate or both.
Atrioventricular (AV) conduction disease may also cause syncope, if abrupt conduction block, even if short-lived, slows the heart rate excessively and for a long enough period of time (generally estimated to be approximately 10 seconds or more). Generally, these patients have some evidence on an electrocardiogram (ECG) of conduction system involvement (e.g., bundle-branch block, abnormal frontal axis).
They may then progress to complete or high grade AV block (Figure 2) in which multiple atrial impulses (P waves) are blocked and the ventricular rate is unable to sustain an adequate blood pressure. Other less severe forms of AV block, including Mobitz 1 block (i.e., Wenckebach block) in older patients or Mobitz 2 block in any patient, may be a clue indicating that AV block is the cause of the patient’s problems.
As a rule, paroxysmal supraventricular tachycardia in young to middle-aged individuals rarely cause syncope. However, syncopal symptoms may occur in older patients or those with left ventricular dysfunction.
Conversely, ventricular tachycardias (VTs) are an important cause of syncope. However, the reason is not so much the site of origin of the tachycardia, or even the rate (which is often similar to the paroxysmal supraventricular tachycardias), but the fact that VTs tend to occur in the setting of heart disease.
It is the patient’s ability to maintain an adequate stroke volume at fast rates and also invoke compensatory mechanisms to maintain blood pressure that determine whether syncope occurs. Thus, even slow VT in patients with severe left ventricular dysfunction may cause hypotension.
On the other hand, torsades de pointes VT (Figure 3), which tends to be very fast, can result in syncope in a young or middle-aged patient with long Q–T syndrome, the heart being structurally normal from a contractile perspective. In some patients with an established diagnosis of arrhythmogenic cause of syncope and have a pacemaker placed for the same may present with syncope due to pacemaker malfunction (Figure 4). (Table 4)
2. Structural cardiovascular causes of syncope
Among the more important structural conditions that may be associated with syncope are: acute myocardial infarction, valvular aortic stenosis, acute pulmonary embolism cardiac tamponade, and hypertrophic cardiomyopathy. Less frequently encountered conditions that may also cause syncope include acute aortic dissection, intracardiac tumors (e.g., atrial myxoma), and arrhythmogenic dysplasia.
As noted earlier, the cause of syncope in these settings may be due to direct impact of the lesion (e.g., atrial myxoma), or a reflex effect (e.g., acute aortic dissection) or a combination of both (e.g., acute pulmonary embolism, acute myocardial infarction). Additionally, since these structural abnormalities may coexist with left ventricular disease, conduction system abnormalities, or sinoatrial disturbances, the potential exists for the explanation being multifactorial and complex.
D. Syncope mimics
A number of conditions may present with what appears to be TLOC and might be mistaken to be syncope. While these conditions are not “true syncope” and are not considered further in the remainder of the text, they are noted here for completeness sake.
The most important of these conditions is “pseudosyncope” (neurologists call this “pseudoseizures”). The hallmark is the very high frequency of attacks, usually but not always, unassociated with major injury. It is suspected that these patients may have had some true syncope events at some time in the past, and may have been the subject of abuse. In any case the clinical picture evolves into a severe psychiatric disturbance (possibly a conversion reaction) that needs intensive psychiatric and psychological assistance.
Functional autonomic disturbances may include real or pseudosyncope in the clinical picture. Thus, while syncope is not a major feature of postural orthostatic tachycardia syndrome (POTS) in most cases, it is a subset of the panoply of symptoms that these patients may complain of. Narcolepsy and cataplexy may also masquerade as syncope, and require experienced neurologic consultation to assess.
II. Diagnostic Confirmation: Are you sure your patient has Syncope?
Syncope by definition incorporates a self-limited period of loss of consciousness (usually associated with loss of postural tone as would be expected). A careful medical history obtained by an experienced individual is the key to confirming whether a true syncope has occurred (see below). The development of detailed standardized questionnaires may prove to be a useful diagnostic aid, but as yet there is no single well-proven instrument available.
The one other condition that most physicians concern themselves with in this setting is an epileptic seizure. Seizures are far less common than are syncopal events. In any case, careful history taking and eye-witness accounts may help distinguish the two problems.
In seizures, abnormal movements of the face, tongue, and extremities may be observed before collapse. In syncope, any abnormal jerky movements that occur (and they are common) do so after the loss of consciousness.
The quality of the motor activity is also different, but this may not be readily appreciated by nonexperts. Rhythmic tonic clonic activity(which may be absent some times in temporal lobe seizures) are indicative of seizure, while the jerky motions of syncope due to cerebral hypoperfusion are more erratic.
The postictal state also differs. In seizures the patient may experience postictal confusion or headache. The syncope patient tends to regain alertness promptly but may be fatigued. Incontinence can occur with both conditions, but tongue-biting is very rare with syncope.
In general, more patients are mislabeled as “seizure patients” when they are suffering syncope than vice-versa. Most neurologists would agree that it is important to establish the correct diagnosis, even at risk of recurrence, before labeling the patient and embarking on a futile course of action.
If necessary, video-EEG monitoring should be used. Placement of an insertable loop recorder (ILR) has proven valuable and cost-effective when longer term monitoring is needed.
Other conditions that occasionally appear similar to syncope are generally readily identified by experienced clinicians. Thus, for example, intoxications (e.g., alcohol, other agents) are usually accompanied by clear evidence of substance abuse; any suspicion can be confirmed with blood and urine tests for the intoxicating agents.
Psychogenic pseudosyncope is a far more difficult problem (see earlier discussion) and may only become apparent after considerable diagnostic energy and expense has been expended fruitlessly.
A. History Part I: Pattern Recognition
The initial evaluation of a patient presenting with TLOC in whom syncope is suspected consists of a careful and detailed medical history, physical examination (including orthostatic blood pressure measurements), and 12-lead ECG. The initial evaluation often also includes echocardiography.
Other tests may be selected as appropriate. Usually the most important of these is long-term ECG monitoring. Selection of these latter devices is discussed in more detail later.
Neurologic evaluation is rarely needed, and in the absence of any concern regarding an acute head injury from a fall, the use of head imaging and EEG is discouraged. The importance of the initial evaluation goes well beyond its capability to make a diagnosis as it determines the most appropriate subsequent diagnostic pathways and risk assessment.
The history is the most important element in the initial evaluation of a patient with suspected syncope. The goal is to establish a diagnosis with sufficient confidence that the patient can be advised of both his or her prognosis and a proper treatment strategy.
A carefully obtained comprehensive history (incorporating eyewitness accounts) alone may be diagnostic of the cause of syncope or may suggest the strategy of evaluation (Table 1). The clinical features of the presentation are most important, especially the factors that might have predisposed to syncope.
In this regard it is important to inquire in-depth into as many episodes as the patient and eyewitnesses can recall. It is helpful to start with the most recent event as that may be best recollected. Thereafter work backward. If a pattern is defined, then it may be possible to establish a diagnosis. (Table 1)
B. History Part 2: Prevalence
Syncope is a symptom that is common in the general population, but clinical epidemiologic terms, such as incidence and prevalence, are not readily applicable in understanding the epidemiology of syncope. For instance, as has been pointed out by Sheldon and colleagues, syncope prevalence must approach zero at any given point in time as very few people are unconscious.
Further, syncope is a transient symptom and therefore its true incidence is difficult to assess. Cumulative proportion and cumulative incidence are more meaningful indices that can be used to explain the epidemiology of syncope.
Studies of the approximate frequency of individuals reporting onset of syncope suggest that first episodes tend to occur between the ages of 10 and 30 years. The peak age for syncope susceptibility seems to be around 15 years where the occurrence is a high as 47% in females and 31% in males.
In a cohort study, only 5% had their first syncope above the age of 40 years. Nevertheless, there appears to be a second peak in both men and women above the age of 65 years.
Several studies have reported what can be considered as syncope burden and suggest that 40% of people faint at least once in their lives. Gazenboom et al in Netherlands found that the cumulative incidence of syncope is:
General population: 18.1 to 39.7 per 1,000 patient-years
General practice: 9.3 per 1,000 patient-years, and
Emergency departments: 0.7 per 1,000 patient-years
The recurrence rate of syncope is estimated at approximately 20% to 30% per year in some population studies, with important predictors of recurrent syncopal episodes including:
Age <45 years
A long prior history of multiple syncopal episodes
Multiple recent syncope events
The “prevalence” of the causes of syncope depends strongly on the clinical setting. Thus reflex syncope is the most frequent cause of syncope in any setting (about 40% to 60% in most reports). Orthostatic syncope is likely second in frequency if older patients are included in the population, with cardiovascular causes being third.
The mortality rate depends on the underlying cause of syncope. The 1-year mortality is high in patients with cardiac causes of syncope (18% to 33%), as opposed to patients with noncardiac causes of syncope (0 to 12%).
However, in most studies, the cardiac basis of syncope did not seem to confer a higher mortality when compared to matched controls having similar degree of heart disease. On the other hand, Olshansky et al found that in the SCD-Heft cohort (predominantly class 2 and class3 heart disease, with patients of both ischemic and nonischemic origin), the presence of syncope was associated with higher mortality.
Additional studies examining mortality risk in selected syncope patient subsets are needed. In this regard, it is recognized that in certain disease states, syncope does raise the mortality risk substantially.
For instance, syncope at diagnosis is a predictor of increased risk of sudden death in patients with severe aortic stenosis, hypertrophic cardiomyopathy and also to an important extent in patients with channelopathies, such as Brugada syndrome and long Q–T syndrome, and arrhythmogenic right ventricular dysplasia (ARVD).
Patients with syncope due to noncardiac causes in general have an excellent prognosis. This is especially true in healthy young individuals with a normal ECG and without any evidence of structural heart disease.
C. History Part 3: Competing diagnoses that can mimic Syncope.
The competing diagnoses that may cause real or apparent TLOC and need to be considered as part of the overall clinical assessment of the patient with suspected syncope have been discussed in detail earlier. Table 2 lists the key contenders.
D. Physical Examination Findings.
Certain basic physical findings may be useful in diagnosing the cause of syncope and assessing prognosis. Perhaps the most important is determining whether there is evidence of the presence of underlying structural heart disease (in this case also incorporating ECG and often echocardiographic data).
The absence of any abnormality reduces mortality risk as a cardiac cause is diminished. The presence of an abnormality raises concern regarding cardiac syncope, and its associated increased mortality risk. In either case, however, the possibility of recurrence remains an important consideration and patients need to be advised of this possibility.
Recognition of susceptibility to orthostatic hypotension (OH, see earlier) and carotid sinus syndrome (CSS, see earlier) are possible during a careful initial evaluation. However, clinicians must become knowledgeable about how to do the proper maneuvers and interpret the findings. The European Society of Cardiology (ESC) guidelines offer excellent guidance.
Physical examination can suggest the presence of important underlying structural cardiac disease. For example, the presence of an irregular, rapid or slow heartbeat, cardiac murmur, or severe dyspnea may suggest the presence of structural cardiac disease and lead one to seriously consider a cardiac cause of syncope.
On the other hand, while the presence of carotid vascular bruits may necessitate further assessment on their own merit, they do not provide a basis for syncope. As a rule, carotid Doppler assessment is of little value in the evaluation of the syncope patient.
E. What diagnostic tests should be performed?
In terms of deciding upon a diagnostic testing strategy, it is mandatory that careful consideration be first given to the likely contending etiologic diagnoses. A shotgun approach is costly and often ineffective.
The choice of tests is best determined after the medical history is carefully obtained and the risk of underlying structural heart disease (including familial conditions) has been assessed. The latter is termed the “initial evaluation,” and it is the cornerstone upon which a diagnostic strategy is established.
Before ordering any diagnostic tests, the clinician should be reasonably certain that the presenting symptom is indeed syncope and not other TLOC conditions, such as a seizure, intoxication, or head trauma. In essence, the initial evaluation should answer three important questions:
Has the patient indeed experienced syncope?
Are there any apparent clues from the history, ECG, and physical examination regarding what could have caused the syncope episode(s)?
Is there any indication that the patient has underlying cardiac disease and suggesting that syncope could be related to a high-risk cardiovascular condition?
The initial evaluation is able to define the most likely cause of syncope in 23% to 50% of cases. In this regard, a 12-lead ECG is generally considered to be part of the initial evaluation, although it may not be absolutely essential in all cases (e.g., a young otherwise healthy patient with classic symptoms indicating vasovagal syncope).
If the initial evaluation suggests a likely cause of syncope, then any subsequent testing may not be needed. However, should the physician wish to confirm the suspected diagnosis, the choice of testing should be focused on the specific condition under consideration.
Thus a tilt-table test or active standing test may be used to support a diagnosis of vasovagal syncope or orthostatic syncope. An electrophysiologic study (EPS) may help to confirm the presence of severe conduction system disease, inducible tachyarrhythmias, or (with less certainty) sinus node dysfunction (Table 3).
If the initial evaluation does not define the cause, then the next step is to risk-stratify patients and make the determination whether to admit the patient for evaluation or to discharge the patient and recommend out-patient work up. The latter is best conducted promptly (i.e., within 3 to 4 days) in a setting that specializes in the care of such patients (i.e., so-called “syncope clinic”). In either case, the choice of diagnostic tests should be based on probable causes derived from the history. In many cases, if there is no clear direction evident, specialty consultation from a syncope clinic practitioner may be helpful. (Table 3)
There are many tests that can be employed in defining the cause of syncope. However, the specific indications, utility, and limitations for each test must be understood to ensure that they are selected in a cost-effective manner. The most important of these tests and their primary utility are outlined here:
Carotid sinus massage (CSM)
Indications: In patients >40 years of age presenting with syncope of unclear etiology.
When is the test diagnostic?
Ideally, this test should be with the patient in a head-up position on a tilt table. If CSM reproduces syncope under these conditions with documentation of hypotension due to asystole or a ventricular pause of >3 seconds and /or fall in systolic blood pressure >50 mm Hg then the diagnosis is supported. Similar findings without reproduction of syncope are less convincing but often are relied upon if no competitive explanation is apparent.
CSM should be avoided in patients with a history of cerebrovascular accident (CVA) or stroke within 3 months of the test, or patients with carotid bruits unless significant carotid stenosis is excluded with a Doppler ultrasound.
Older patients in whom there is a clinical suspicion of orthostatic hypotension of any etiology.
When is this test diagnostic?
The test may be done in two ways, but in either case it is best to use beat-to-beat noninvasive blood pressure monitoring (e.g., Finometer). Active standing is likely the better of the two methods.
The patient is seated or supine and then physically moves to the standing position. The second method employs passive movement to head-up posture on a tilt-table. OH is defined as a decrease in systolic blood pressure (SBP) >20 mm of Hg and >10 mm of Hg, usually within 3 to 5 minutes of changing position from supine to an upright position.
Delayed responses may also be observed as discussed earlier. For patients who are initially hypertensive, the recent consensus document calls for >30 mm Hg drop of systolic pressure for a positive test. In any case, the medical history must be consistent with the laboratory findings before a reliable clinical diagnosis can be established.
Tilt-table testing was derived from early physiological studies examining human responses to extended upright posture. The test was introduced in the mid-1980s as a means of assessing susceptibility to vasovagal syncope.
It is usually done in a quiet room with continuous ECG and beat-to-beat blood pressure recording. The protocol calls for a 70- degree head-up tilt in a drug free state. Thereafter, if the test is not diagnostic, provocative pharmacologic agents (isoproterenol, nitroglycerin) may be used. These agents improve test sensitivity, but degrade specificity.
Main indication—Assess susceptibility to vasovagal syncope in patients in whom reflex syncope is suspected clinically but could not be confirmed by history and physical findings. It should be noted that the test should not be used to assess efficacy of therapeutic interventions.
-If patient had associated jerking movements but the episode is not definitive for seizure. Tilt-table testing can be helpful in distinguishing syncope from seizure.
-In elderly patients with dementia where good clinical history is difficult to obtain and a fall due to loss of balance needs to be distinguished from a true syncope.
-Distinguish syncope due to pure orthostatic hypotension from other causes of symptomatic hypotension (reflex syncope, some cases of postural orthostatic tachycardia syndrome [POTS]).
When is the test diagnostic?
The diagnosis of reflex syncope can be established when there is reproduction of symptoms with upright tilt and the recordings document sufficient hypotension (either due to marked bradycardia or due to a vasodepressor response with or without bradycardia).
Contraindications: Usually safe. The contraindications are mainly relative and restricted to those conditions in which the practitioner wishes to avoid use of isoproterenol (ischemic heart disease, uncontrolled hypertension [HTN], left ventricular [LV] outflow obstruction). Nitroglycerin is a potential alternative provocative agent and has proved to be very safe.
ECG monitoring is indicated for diagnosing intermittent bradyarrhythmias and tachyarrhythmias that could cause a syncopal or a near syncopal episode. It is very important to remember that ECG monitoring is indicated only when there is a high pretest probability of identifying an arrhythmia associated with syncope. ECG monitoring is done in two settings:
1. Inpatient: Inpatient monitoring is rarely useful unless the patient is having very frequent events. Given the cost of in-hospital monitoring, it is indicated only when the patient is deemed to have a high risk of life threatening arrhythmias. Such patients include those with:
Acute congestive heart failure or acute myocardial infarction (present or very recent)
Syncope episode associated with exertion or palpitations
Family history of sudden cardiac death (SCD)
Nonsustained VT on presentation
Prolonged or shortened QT interval
Brugada pattern on admission EKG
New bifascicular block on ECG
Severe sinus bradycardia on admission (HR <40 bpm)
2. Outpatient: Outpatient ECG monitoring as a rule should still be considered for patients with a high probable risk of arrhythmogenic syncope. The following types of monitoring may be considered:
Holter monitoring usually for 24- to 48-hour period and sometimes for a 7-day period. This of more valuable in patients with very frequent (e.g., daily or more than once daily episodes) loss of consciousness, where there is higher chance of symptom ECG correlation.
External loop recorders: These devices have loop memory and typically store 5 to 15 minutes of pre-activation ECG. The most effective of these are the mobile cardiac outpatient telemetry (MCOT) systems such as Cardionet. Patient compliance is a limitation, as some patients may not like wearing them for more than a few weeks.
Implantable loop recorders: These are the ideal devices for detecting infrequent symptomatic events. They are implanted under the skin using local anesthetic in much the same way that a pacemaker is implanted, but there are no intravascular wires and the incision is only about 1.5 cm in length.
The initial cost is higher than a wearable recorder, but several studies have shown that the cost per correct diagnosis is substantially less. Early use of ILRs in the evaluation of syncope is justified.
Cardiac electrophysiologic study (EPS)
For the evaluation of syncope, EPS has proven useful mainly in patients with underlying structural heart disease or suspected paroxysmal supraventricular tachycardia (PSVT). EPS should be considered in the following settings:
In syncope in a patient with known structural heart disease in whom ventricular tachyarrhythmias are thought to be a probable cause. EPS is useful in identifying susceptibility to these arrhythmias.
In syncope in patients with premonitory symptoms of palpitations (PSVT or VT are possibilities), but in whom monitoring has been ineffective.
In syncope with bundle branch block to assess risk of high degree AV block playing a role.
In Brugada syndrome to assess arrhythmia inducibility (a controversial indication).
In asymptomatic bradyarrhythmias of sinus node origin. EPS may be useful in establishing the severity of the condition and the likelihood of sinus node disease being a contributor to symptoms (a controversial indication).
Adenosine triphosphate (ATP) testing
This test is controversial. It may have value in identifying a subgroup of syncope patients in whom pacing therapy might be helpful. These are usually middle-aged to older women without substantial cardiac disease. The test remains under evaluation.
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Routine biochemical or hematologic laboratory studies are rarely of value in the syncope evaluation of a syncopal episode. However, in certain cases, when the initial evaluation is appropriately supportive, certain tests may have utility; these tests should be used judiciously, and their results must be consistent with the patient’s history and presentation before they can be considered to be of diagnostic utility.
A basic metabolic panel can be useful in identifying prerenal azotemia, hypernatremia or hyponatremia, or hyperkalemia or hypokalemia. The first of these findings may help the clinician support a syncope diagnosis based on orthostatic hypotension due to hypovolemia/dehydration. The remaining findings could favor a conduction disturbance (i.e., inexcitable tissues in hyperkalemia) or tachyarrhythmias (e.g., torsade de pointes in hypokalemia).
A complete blood count (CBC) may be helpful if the medical history supports a concern that blood loss or anemia may be provoking syncope, or increasing susceptibility to syncope, in a previously stable patient.
In patients with syncope due to severe bradycardia or asystole, a thyroid function testing may be used to rule out any underlying thyroid disease.
If the patient has prominent respiratory symptoms, then checking oxygen saturations and/or arterial blood gases may be useful. Although uncommon, chronic hypoxia or acute upon chronic hypoxia may predispose to symptomatic bradycardia or tachycardia.
Serial cardiac enzymes can be helpful if acute myocardial ischemia is suspected to have triggered the syncope.
Specific drug levels have a role to play in assessment of those infrequent syncope cases in which drug toxicity is suspected. In the past, digitalis toxicity was a relatively frequent concern, but that is far less common today. On the other hand, many drugs may be associated with syncope (Table 4) and physicians may at times need to ascertain whether one or the other agent is a contender in the differential diagnosis.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Echocardiography is often of value in the syncope evaluation when there is suspicion of structural heart disease being present. The goal is to ascertain both the nature and severity of underlying structural heart disease.
The presence of cardiac disease increases the risk of a cardiac cause of syncope, and impacts prognosis as syncope of cardiac cause is associated with a worrisome mortality risk. Thus the echocardiogram has utility for both diagnosis and risk stratification.
Certain conditions that may present as syncope are particularly amenable to assessment by echo; these include: valvular aortic stenosis, obstructive cardiac tumors, hypertrophic cardiomyopathy, cardiac tamponade, acute aortic dissection, and congenital anomalies of coronary arteries.
CT scan of the chest is appropriate when acute pulmonary embolism is suspected as a basis for syncope.
Nuclear cardiac imaging or computed tomography (CT) angiography are rarely of value in syncope patients. If acute coronary syndrome enters the differential diagnosis of a syncope patient, then coronary arteriography is a better choice.
CT or magnetic resonance (MR) scans of the head have no utility in the diagnostic evaluation of syncope. In some cases they may be warranted if the patient’s collapse resulted in head injury. However, in such cases the imaging is to exclude a possible consequence of syncope, not its cause.
For the most part, physicians only see syncope patients after the victim has recovered from the acute event. Consequently, it is rare that the practitioner actually witnesses the episode. However, should that occur, basic assessment of the patient entails determining if a pulse and respirations are present.
If so, the victim should be maintained on his or her side in a gravitationally neutral position until full recovery of consciousness has occurred. Thereafter, documentation of the observed events is wise, as eyewitness accounts can substantially facilitate subsequent diagnostic evaluation.
A. Immediate management.
Inasmuch as the physician is rarely involved with care of the patient during an acute event, immediate management when the patient comes for evaluation depends primarily on the practitioner’s initial assessment as described earlier. During this step, the need for in-patient assessment versus out-patient evaluation is made.
The patients who need to be considered for inpatient monitoring are mainly those with cardiac causes of syncope, in particular:
Patients with suspected acute myocardial ischemia
Severe ischemic or nonischemic cardiomyopathy
Suspected to be high risk for life-threatening arrhythmias (e.g., long Q–T syndrome, Brugada syndrome, etc.)
Other structural heart disease (e.g., hypertrophic cardiomyopathy, severe valvular disease)
In patients with noncardiac causes of syncope, the need for admission may depend on the suspected cause of the fainting or social issues. Thus, while orthostatic syncope does not typically warrant admission, hospitalization may be needed if the faint was triggered by severe dehydration or acute blood loss anemia. Similarly, in-patient care may be warranted in elderly and/or frail patients who are deemed to be at high risk of physical injuries if syncope should recur.
B. Physical Examination Tips to Guide Management.
In most cases, the fainter is fully recovered when seen by the clinician for diagnostic evaluation. Consequently, there is rarely any opportunity to record physical findings during spontaneous events. However, eyewitness accounts can be of value, even when derived from individuals who have no specific medical training.
Eyewitness reports of physical findings at the time of collapse may help distinguish true syncope from other forms of TLOC and may even help to determine the specific cause of syncope. Often, especially in older fainters, these details are not reported by the patient as they became amnestic or were unconscious. Consequently, eyewitness accounts should be sought out during the initial evaluation of the patient.
Pertinent, potentially useful physical findings at the time of the collapse might include one or more of the following:
The presence of seemingly inexplicable facial, tongue, or limb movements beginning before collapse favors the diagnosis of a seizure disorder, whereas jerky muscular movements that start after onset of the loss of consciousness favors a syncope diagnosis. It should be noted that “jerking” movements occur commonly in syncope patients, but the movements differ from those seen in epilepsy.
In syncope, the movements tend to be smaller, of briefer duration, and not synchronous over the body. The difference from the much more massive and synchronous clonic movements can be helpful in diagnosis, but making such a distinction is beyond the experience of most bystanders including medically trained individuals.
Details of the nature of the collapse may be valuable. Most syncope patients fall limply, whereas epilepsy patients tend to collapse rather more stiffly.
An apparent faint in the midst of vigorous exercise suggests a cardiac cause, while faints early after completion of such exercise is more likely neural-reflex in origin (possibly triggered by relative volume depletion).
Collapse associated with a rapid pulse may provide a clue to a tachyarrhythmia cause. Conversely, recognition of a slow weak pulse may lead to a greater likelihood of a bradycardia cause or neural-reflex mediated etiology. Unfortunately, not many eyewitnesses have the skill or presence of mind to make such observations.
Marked pallor in conjunction with cold clammy skin favors neural-reflex syncope (vasovagal or situational syncope).
Syncope associated with abrupt neck movement in older individuals (usually >50 years) suggests the possibility of carotid sinus syndrome.
Collapse shortly after changing posture (e.g., arising from seated position) favors orthostatic syncope, but may not be remembered by fainters (especially older fainters).
Multiple “faints” in a brief period of time, or faints with eye lids tightly closed, or faints that favor pseudosyncope rather than a true faint.
Collapse associated with seeming difficulty breathing suggests a cardiac origin or pulmonary embolism. On the other hand, faints in younger individuals associated with apparent emotional upset and/or tachypnea favor reflex syncope or possibly an acute anxiety spell (pseudosyncope).
Observations by the clinician in the emergency department or clinic
Most often the physician is restricted to recording physical findings that remain to be observed after the victim has fully recovered. Nevertheless, certain findings may be helpful in defining potential causes for the collapse and providing a strategic direction for subsequent evaluation (i.e., specific direction for selecting imaging or other tests).
Evidence of trauma resulting from the collapse should be documented. In this regard, tongue biting is more typical of seizure than of syncope.
Postevent confusion is more typical of seizure, but fatigue is common after vasovagal faints.
Susceptibility to orthostatic hypotension (see earlier discussion diagnostic criteria) should be obtained in all TLOC patients if circumstances permit. A positive finding, if consistent with the medical history of the event (and eyewitness accounts when available), may clinch the diagnosis without need for further testing.
Physical findings during carotid sinus massage (CSM) may be considered to be part of the physical examination as it is a generally recommended diagnostic step in all older (>55 years) syncope patients. However, the results of CSM should be interpreted with care.
For many years, a CSM-induced ventricular pause >3 seconds duration was been considered a positive response. However, such a finding only suggests the presence of a hypersensitive carotid sinus, but is insufficient to support a diagnosis of carotid sinus syndrome (CSS).
The ESC syncope guidelines recommend that CSS be diagnosed only if there is CSM-induced reproduction of symptoms (usually only achieved if CSM is done with the patient in an upright posture), or if the clinical history supports the diagnosis (e.g., syncope associated with neck movement). In the absence of either of these findings, a CSM-induced pause >5 seconds in duration may be accepted as diagnostic if other contending diagnoses have been excluded.
Pathologic cardiac and vascular murmurs, and peripheral pulse findings may be suggestive of severe aortic stenosis or idiopathic hypertrophic cardiomyopathy; if present, the significance of such murmurs may reasonably evaluated by echocardiographic study.
Differences in blood pressure/pulse in each arm, when identified, may indicate subclavian steal or aortic dissection. Confirmatory imaging is then the next step.
Signs of focal neurologic lesions, such as hemiparesis, dysarthria, or diplopia and vertigo, or signs of parkinsonism suggest but are not diagnostic of a neurologic cause. Thus evidence of a stroke may suggest that the collapse was not syncope, but due to loss of stability. A patient with signs of parkinsonism may raise concerns of orthostatic syncope or an accidental fall. Such patients warrant a neurologic evaluation.
C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.
The majority of faints are neural-reflex in nature, particularly vasovagal syncope. To date, there is no evidence that tilt-table testing has any value in regard to assessing therapy of vasovagal syncope or related situational faints. Therefore, while of value as an initial diagnostic tool in selected cases of vasovagal syncope, its use in assessment of subsequent treatment is not recommended.
In patients with orthostatic syncope, many current therapies have the potential to aggravate supine hypertension. This problem requires clinical monitoring and treatment adjustments. However, such monitoring is usually readily achieved in the clinic without special tests.
Orthostatic testing (i.e., active standing, tilt-table testing) during follow-up might have merit in orthostatic syncope in those cases in which the medical history alone is not reliable (e.g., forgetful and/or demented patients). Similarly, periodic ECG monitoring and/or ILR use may have a role in similar cases in whom paroxysmal arrhythmias were found to be the cause of fainting. However, in most cases, a careful history is likely to be just as helpful if the patient is a reliable reporter.
Follow-up hematologic or biochemical laboratory testing are rarely needed. Perhaps they can be justified if syncope was deemed due to acute blood loss, anemia, or major electrolyte disturbances (e.g., conduction system disturbances associated with severe hyperkalemia or hypokalemia, or hypovolemia). Similarly, in elderly or demented patients with syncope due to repeated but subtle infections (e.g., urinary tract infections), such testing may be warranted. Echocardiographic reassessment is also reasonable in the case of suspected outflow tract obstruction being treated medically.
D. Long-term management.
The principal goals of treatment in syncope patients is to avert recurrences and diminish the adverse impact of syncope recurrences on quality-of-life, including risks of injury from falls. Preventing premature mortality is also an important priority, but for the most part the risk of death is primarily determined by the severity of underlying cardiac and vascular disease rather than the syncope itself. Thus, aggressive management of structural cardiovascular disease is mandatory, but alone may not be sufficient to prevent syncope recurrences.
Recommended long-term treatment strategies for the various causes of syncope may be summarized as follows:
For the most part, reflex fainting has a low immediate mortality risk, and therefore the goals of long-term treatment are to prevent recurrence and limit injuries.
In the case of vasovagal and situational syncope, the first step is education and assurance regarding the benign (from a mortality perspective) nature of the condition. Education consists of recognition of warning symptoms, and appropriate physical counter-maneuvers (PCMs) (e.g., sitting, squatting, leg crossing) when appropriate.
The patient must also be made aware of circumstances that increase risk of an event (overcrowded places, fearful situations, prolonged cough, micturition), early recognition of prodrome symptoms. In the case of situational faints (e.g., cough syncope, post-micturition syncope, etc.) avoidance of the trigger may be difficult but can be addressed (e.g., cough suppression, sitting while voiding, etc.)
In the case of CSS, education is similarly recommended. However, most CSS patients are best treated by cardiac pacemakers.
PCM should be probably the first line of management for vasovagal syncope. PCMs include maneuvers that will increase the blood pressure (e.g., crossing legs, hand grip, and arm tensing) that can abort or delay attacks if performed on recognizing prodromal symptoms. In the longer-term, physical exercise (lower body isometrics, rowing), and standing training may diminish susceptibility.
The pharmacologic management of reflex syncope (and especially vasovagal syncope) is at best restricted to those patients in whom hydration and physical maneuvers have not been completely successful. Only two agents appear to be helpful; specifically, midodrine and the salt retaining mineralocorticoid, fludrocortisone.
Some pharmacologic treatments for vasovagal syncope are still used in clinical practice despite the fact that there is little evidence of benefit, and some have been shown to be ineffective in clinical trials. These include:
Beta-adrenergic blockers (except possibly in “older” fainters (>40 years of age)
The alpha-adrenergic agonist midodrine (actually a pro-drug with an active metabolite) may be effective in some patients, but is only rarely the complete answer. Attention to increased hydration, enhanced salt intake, and physical exercise remain crucial treatment components.
Fludrocortisone is currently the subject of a multicenter randomized trial in vasovagal syncope where it has shown some benefit (Prevention of Syncope Trial [POST 2]). The complete article should be reported in 2012.
Based on findings from several randomized clinical trials, it is clear that cardiac pacing has only a small role to play in prevention of vasovagal syncope recurrences. However, the International Study on Syncope of Uncertain Etiology (ISSUE 2) study suggests potential value in patients in whom severe spontaneous bradycardia has been demonstrated by ECG monitoring during spontaneous faints. Pacing is also useful in carotid sinus syndrome.
2. Orthostatic syncope
Orthostatic syncope is an extremely common problem, especially in the elderly or frail. However, it can occur in even very fit persons who become deconditioned (e.g., astronauts returning from a low gravity environment, patients hospitalized for an extended time).
The basic problem is either volume depletion or failure of the appropriate compensatory cardiac and vascular mechanisms with change from a gravitationally neutral position (i.e., seated, supine) to a standing position. In many instances, prescribed drugs undermine these compensatory responses while in others there is evidence of autonomic failure.
As in the case of reflex syncope, treatment should start with education regarding the underlying condition. In many cases, removal or reduction of dosage of certain drugs that the patient is currently being treated with (e.g., diuretics, vasodilators) may be the first appropriate step.
As with reflex syncope, PCMs may prove helpful acutely. Longer-term, physical exercise (lower body isometrics, rowing), and standing training may offer benefit. Unfortunately, there is a paucity of evidence favoring any of these modalities.
As noted above, many prescribed drugs are in fact the cause of the problem. This aspect of “pharmacologic” therapy should be addressed first.
Thereafter, drug therapy is very similar to that employed for the reflex faints. However, treatment in these often older patients is complicated by the tendency for drugs to aggravate supine hypertension.
Typically, it is necessary to accept higher baseline blood pressure in this population than is normally recommended. Frequently, sustained systolic pressure in the 150 to 260 mm Hg range must be tolerated; the balance (which must be carefully discussed with patients and family members) is stroke/myocardial infarction risk versus falls and physical injury risk.
With the above caveats in mind, increased salt and volume in the diet and judicious use of drugs such as midodrine and fludrocortisone may be useful. However, aggravation of supine hypertension must be monitored as noted earlier, and excessive hypertension should be dealt with in the context of the patient’s overall picture. Table 5 summarizes certain therapeutic approaches to orthostatic syncope.
3. Syncope due to cardiac arrhythmia
The goals of treatment are to prolong survival, prevent recurrence, and improve quality-of-life. The specific treatment approach depends on the type of arrhythmia, and whether the problem is due to a primary conduction system disease (i.e., intrinsic abnormality) secondary to extrinsic agents (e.g., drugs, autonomic disturbances).
The following provides key points to consider in treatment:
In patients with syncope due to bradyarrhythmias of any cause, the first step is elimination of any drugs that may be causing or aggravating bradycardia.
In symptomatic patients (i.e., syncope, near-syncope) with sinus node dysfunction (SND) and demonstrable bradyarrhythmias (i.e., sinus pauses, sinus arrest, asystole after termination of paroxysmal atrial tachyarrhythmias), cardiac pacemaker therapy is indicated and is highly effective. However, in SND patients, permanent pacing relieves symptoms but may not prolong survival.
In syncope patients in whom AV conduction system disease is documented and sufficiently severe to account for symptoms, cardiac pacing should be considered. The ESC syncope guidelines provide specific pacing indications.
In patients with syncope due to supraventricular tachycardias or atrial flutter, transcatheter ablation should be considered. This procedure has a very high success rate (>95%) and very few complications.
In patients with acquired prolonged Q–T and syncope due to torsades de pointes, elimination of drugs that prolong Q–T interval is the essential step. In the case of congenital long Q–T syndrome, Brugada syndrome, and other channelopathies, management may entail beta-blockers in some cases and ICD therapy in others, or both. The management of these patients is in evolution and readers are advised to monitor the latest guidelines and expert consensus statements.
Symptomatic ventricular tachycardias (VT) that occur in the absence of structural heart disease may in some cases be amenable to ablation (e.g., outflow tract VTs, idiopathic fascicular VTs), but often require ICD treatment (e.g., channelopathies). In patients with ischemic or nonischemic cardiomyopathies, symptomatic VT generally is treated with an ICD, although ablation may also be recommended in select cases.
In these patients it is important to explain carefully to the patient and family that ICD therapy may not prevent recurrence of syncope (since it takes time to recognize and treat the arrhythmia), but does reduce risk of sudden cardiac death. Finally, while antiarrhythmic drugs no longer are the most prominent treatment strategy for VT, drugs such as beta-adrenergic blockers, amiodarone, sotalol and dofetilide often have an important ancillary role for arrhythmia prevention.
4. Syncope due to structural heart disease
The goal of treatment is to prevent recurrence and reduce risk of sudden cardiac death by correcting/ameliorating the underlying structural problem.
In this setting the appropriate treatment depends on establishing a correct diagnosis. For the most part, the presence of a severe structural abnormality defines the course of treatment. However, these patients also have increased risk of arrhythmic syncope, and this additional complexity must be considered in the diagnostic assessment.
Severe aortic or mitral valvular stenosis, intracardiac tumors atrial myxoma, and congenital coronary artery anomalies are best treated surgically. On the other hand, conditions such as hypertrophic cardiomyopathy (HCM) are more complex.
The role of drug therapy versus surgical myectomy needs individualized consideration. Nevertheless, ICD therapy is often also recommended in HCM patients presenting with syncope.
E. Common Pitfalls and Side-Effects of Management
Syncope is a symptom and the underlying cause needs to be correctly identified as effective treatment strategies are very specific to the underlying etiology (e.g., orthostatic syncope could be due to drug effects, autonomic failure, volume depletion, or a combination of factors. The appropriate treatment strategies differ depending on these specifics).
Syncope should be clearly distinguished from other causes of TLOC, such as seizure disorders, concussion, intoxication, and syncope mimics. Failure to distinguish true syncope from other forms of TLOC may lead to incorrect therapy and inappropriate “labeling” of patients (e.g., many syncope patients have been mistakenly labeled as having drug-resistant epilepsy until the correct diagnosis was established, often years later).
IV. Management with Co-Morbidities
The cornerstone of syncope treatment is to identify the underlying cause and adopt a cause-specific treatment strategy. Not infrequently, comorbidities contribute to syncope susceptibility (Table 6).
V. Patient Safety and Quality Measures
A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.
The principal safety concern in patients with syncope is the risk of physical injuries due to loss of consciousness. Less frequent, but of public health importance are the risks associated with driving, flying, and operating heavy machinery. Treatment should also focus on educating the patient regarding the importance of avoiding potentially hazardous situations, and being alert for and promptly responding to warning symptoms to reduce injury risks, which include:
Home and work place safety assessment may be important in some patients, particularly for elderly individuals or persons with high-risk occupations or avocations.
Identification of underlying cause and distinguishing syncope from other causes of transient loss of consciousness again is the key.
Accurate “risk stratification” when undergoing initial evaluation to ascertain whether a patient is suitable for outpatient assessment.
Education and reassurance in patients with reflex syncope so that they do not come to the emergency room every time there is a syncopal episode.
Education regarding safety precautions can help prevent dangerous injuries that trigger preventable hospital admission.
B. What's the Evidence for specific management and treatment recommendations?
The European Society of Cardiology Practice Guidelines (2009) provide recommendations and evidence grades in detail.
Moya, A, Sutton, R, Ammirati, F. “Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS). Guidelines for the diagnosis and management of syncope (version 2009)”. Eur Heart J. vol. 30. 2009. pp. 2631-71.
Strickberger, SA, Benson, DW, Biaggioni, I. “American Heart Association Councils on Clinical Cardiology; Cardiovascular Nursing, Cardiovascular Disease in the Young; Stroke; Quality of Care and Outcomes Research Interdisciplinary Working Group; American College of Cardiology Foundation; Heart Rhythm Society; American Autonomic Society. AHA/ACCF scientific statement on the evaluation of syncope”. Circulation. vol. 113. 2006. pp. 316-27.
C. DRG Codes and Expected Length of Stay.
ICD 10 Code—R55
Syncope is a symptom code. Do not list symptom codes as principal diagnosis when a related definitive diagnosis has been determined.
Expected length of stay is variable as it depends on the underlying cause. If diagnosed as reflex syncope on initial evaluation, the patient may not need inpatient admission. There are exceptions, however, such as the older or frail individual who may not have an appropriately protective home environment.
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- I. Evaluation and Management of Syncope: What every physician needs to know.
- II. Diagnostic Confirmation: Are you sure your patient has Syncope?
- A. History Part I: Pattern Recognition
- B. History Part 2: Prevalence
- C. History Part 3: Competing diagnoses that can mimic Syncope.
- D. Physical Examination Findings.
- E. What diagnostic tests should be performed?
- 1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- 2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- III. Management.
- A. Immediate management.
- B. Physical Examination Tips to Guide Management.
- C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.
- D. Long-term management.
- E. Common Pitfalls and Side-Effects of Management
- IV. Management with Co-Morbidities
- V. Patient Safety and Quality Measures
- A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.
- B. What's the Evidence for specific management and treatment recommendations?
- C. DRG Codes and Expected Length of Stay.