Syncope Case File

Syncope Case File

Eugene C. Toy, Md, Michael d . Faulx, Md

Case 22

A 21- year-old female college student is seeing you in the outpatient clinic for evaluation of two episodes of “fainting” in the past month. Both episodes were witnessed. The first occurred after she stood up from eating a large dinner while out with friends. She was caught by one friend as she was falling and suffered no significant trauma other than a scraped elbow. She was unconscious for 5–10 seconds, did not have any tonic-clonic muscle movements, did not lose bowel or bladder control, and regained consciousness with some confusion about what happened but otherwise with no significant cognitive impairment. She reported lightheadedness prior to loss of consciousness. The other episode was similar to the first and occurred during a hot day while she was out at a picnic with her family. She was standing for a period of time when she recalled feeling lightheaded and then had a loss of consciousness with loss of postural tone. She has no medical history, and her family history is negative for sudden or unexplained death and is otherwise noncontributory . She denies any fever, chills, sweats, headaches, diarrhea, constipation, palpitations, chest discomfort, shortness of breath, weakness or numbness, change in cognition or memory , or change in motor function. She takes no medications or herbal supplements. She is not on a special diet. She has never smoked an does not use any drugs. She drinks one or two alcoholic beverages per weekend . She is not sexually active. She does not regularly exercise and she drinks four to five cups of coffee daily . On examination she is a healthy, normal-appearing woman in no acute distress. Her temperature is 98°F, heart rate 70 bpm, and blood pressure 110/ 60 mmHg. A comprehensive physical examination is entirely within normal limits. A complete blood count and a basic metabolic panel are within normal limits. ECG shows sinus rhythm 70 bpm, normal axis, normal PR and QT intervals, normal QRS duration, and is generally unremarkable without evidence of preexcitation or ST abnormalities.

• What is the most likely diagnosis?
• What is the best next diagnostic step?
• What is the best next step in therapy ?

Answer to Case 22:

Syncope

Summary: A 21-year-old healthy woman presents to the outpatient clinic with two episodes of loss of consciousness. The first episode occurred when she stood up after eating a large meal. The second episode occurred during a particularly hot day while standing for a period of time. Review of systems was negative, without palpitations, chest pain, or shortness of breath. She has no past medical history, and family history is noncontributory. Her exam is unremarkable. Her CBC and BMP were within normal limits. Her ECG is normal.

• Most likely diagnosis: Reflex (neurally mediated) syncope.
• Next diagnostic step: Orthostatic vital signs and tilt table test.
• Next step in therapy: Adequate fluid hydration and avoidance of triggers.

ANALYSIS

Objectives

1. Know the diagnostic approach to syncope.
2. Understand that syncope can be caused by varying etiologies and mechanisms that have a common result of loss of consciousness.
3. Understand that treatment is dependent on the cause.
4. Be familiar with the different modalities of treatment for reflex syncope, including first-line lifestyle modification and supportive measures.

Considerations

This is a 21-year-old woman who is otherwise healthy. Her history is consistent with reflex (neurally mediated) syncope. Her episodes of loss of consciousness were preceded by lightheadedness. The first episode occurred after a change in posture, and may have been exacerbated by the large meal and resultant shunting of blood to the digestive system. The second episode occurred after standing for a period of time and may have been exacerbated by the heat.

If the patient had a sudden loss of consciousness without preceding symptoms or without precipitating factors, then this would be more suggestive of an arrhythmic cause such as a tachy- or bradyarrhythmia. She denies palpitations or chest discomfort, which would also be worrisome for an arrhythmic cause. Her ECG is normal without findings indicating arrhythmia development (such as a long QT interval or ST elevations consistent with a Brugada pattern). She denies shortness of breath, and her cardiac exam is normal, suggesting that a significant valvular abnormality, such as severe aortic stenosis, or other structural abnormality, such as hypertrophic obstructive cardiomyopathy, is unlikely. Her carotid exam did not reveal any bruit, and the scenario is unlikely to be due to bilateral carotid artery stenosis. Her witnessed episodes were devoid of tonic-clonic movements or loss of bowel or bladder control, which would be suspicious for seizure activity. Her episodes resulted in minor skin abrasions, suggesting that pseudoseizure or factitious behavior is less likely. A normal CBC and BMP point away from metabolic derangements affecting neurocognitive function. Likewise, she denies significant alcohol or drug use.

Overall, her history and evaluation in the office thus far does not raise any red flags or overtly dangerous etiologies and are more likely consistent with reflex syncope. The diagnosis can be strengthened by bedside orthostatic vital signs and a formal tilt table test. If a vasovagal response is seen, then supportive measures and lifestyle modification are first-line therapy.

Approach To:

Syncope

DEFINITIONS

SYNCOPE: Abrupt loss of consciousness, due to global cerebral hypoperfusion, with a concomitant loss of postural tone.

VASOVAGAL RESPONSE: Vasovagal response on tilt table test is an abrupt decrease in heart rate and blood pressure with loss of consciousness and loss of postural tone.

ORTHOSTATIC HYPOTENSION: Orthostatic hypotension on tilt test is defined as a decrease in blood pressure of 20 mmHg systolic and/or 10 mmHg diastolic.

TABLE TILT TEST: An examination where the patient’s BP and HR are assessed while lying on a table that is slowly tilted upwards.

CLINICAL APPROACH

Overview

Syncope is a transient loss of consciousness due to global cerebral hypoperfusion, with a concomitant loss of postural tone. It is abrupt in nature, with a short duration and a spontaneous complete recovery. Other causes of transient loss of consciousness not due to cerebral hypoperfusion, such as seizure or trauma, are therefore, by definition, distinct from syncope. Presyncope, also called “near-syncope,” is the prodrome of syncope without total loss of consciousness. Prodromal symptoms include lightheadedness, nausea, and sweating. Syncope can have cardiac or noncardiac causes. The overall prognosis depends on the cause of the syncope.

Burden Syncope

It is estimated that up to 3% of men and 3.5% of women will experience syncope at some point during their lifetime. The prevalence of syncope increases in older age groups (0.7% in patients between 35 and 44 years old vs 4–6% in patients >75 years old). Episodes of transient loss of consciousness or syncope account for up to 3% of ER visits and up to 6% of hospital admissions. The majority of cases of transient loss of consciousness are attributed to syncope or similar mimicking conditions. The financial burden of syncope is difficult to estimate because of the significant indirect costs of syncope such as loss of earnings of patients or family members. The direct costs associated with syncope are due mostly to the high rate of hospitalization after emergency department evaluation.

Classification

The European Society of Cardiology has published a classification scheme for syncope with three main categories: reflex syncope, syncope due to orthostatic hypotension, and cardiac syncope.

Reflex (neurally mediated) syncope: This includes mechanisms such as vasovagal syncope, situational syncope, carotid sinus syncope, and atypical forms. Vasovagal syncope can be mediated by emotional distress such as pain or the sight of blood, or by orthostatic stress (postural challenge). Examples of situational syncope are syncope occurring after coughing (cough syncope), after micturition (postmicturition syncope), or after eating (postprandial syncope). Carotid sinus syncope is due to hypersensitivity of carotid sinus baroreceptors and can be triggered by mechanical stress (such as a tight shirt collar, or physical palpation such as with a carotid massage).

Syncope due to orthostatic hypotension: This includes syncope due to autonomic failure. Autonomic failure can be primary (such as multiple system atrophy or pure autonomic failure) or secondary (such as due to diabetes or spinal cord injuries). Orthostatic hypotension can also result from alcohol use, or from medications such as diuretics and vasodilators. Finally, intravascular volume depletion (such as from vomiting, diarrhea, or hemorrhage) can result in orthostatic hypotension.

Cardiac syncope: This includes syncope due to arrhythmia or structural heart disease. Significant bradycardia (such as from sinus node dysfunction or AV nodal conduction disease) can result in syncope. Conversely, significant tachycardia (from either a supraventricular or ventricular origin) can result in syncope. Structural heart disease can also cause syncope; hypertrophic obstructive cardiomyopathy, cardiac valvular abnormalities, and cardiac tamponade are examples of cardiac syncope.

DIAGNOSIS

History

A thorough history should be taken for each patient presenting with loss of consciousness. The diagnosis of syncope as the cause can sometimes be difficult. Complete loss of consciousness, rapid onset, short duration, complete and spontaneous recovery, and loss of postural tone all point to syncope as the cause of loss of consciousness. The prodromal symptoms of syncope can further help elucidate the etiology. Symptoms of postural intolerance are related to cerebral hypoxia resulting from decreased cerebral perfusion. Symptoms related to cerebral hypoxia include lightheadedness, dizziness, imbalance, tunnel vision, blurriness, spotted visual field, and headache. Of note, patients may find that it is possible to abort these symptoms by assuming a sitting or supine posture. The occurrence and severity of symptoms are influenced not only by the quantitative drop of blood pressure but also by the rapidity of blood pressure decline. However, it is noteworthy that elderly patients with chronic orthostatic hypotension may have adaptive mechanisms of cerebral autoregulation such that symptoms may not occur even with extensive fall in blood pressure. Conversely, symptoms such as palpitations or chest pain may point toward a cardiac cause of syncope. Alarming features indicating a high-risk scenario include syncope during exertion, syncope while lying down, family history of sudden cardiac death, or slow recovery from syncope. Appropriate and timely consultation should be obtained if clinical suspicion of high-risk scenarios is present.

Physical Examination

A careful, comprehensive physical examination is essential. Blood pressure should be checked in both arms, and in the supine and standing positions (orthostatic vital signs). Helpful exam findings include signs of dehydration, and presence of carotid bruits, cardiac murmurs, or varicose veins.

Additional Testing

Depending on the history and physical exam findings, further testing can be done. These include 12-lead ECG and cardiac telemetry monitoring (inpatient or ambulatory) when there is concern for arrhythmia or ischemia, carotid sinus massage for a concern of hypersensitivity, echocardiogram to look for structural cardiac abnormalities, or tilt table testing for further evaluation of possible reflex syncope or orthostatic hypotension. Advanced, specialized testing such as circulatory hemodynamics or blood volume measurement can also be useful in some cases.

The tilt table test is a provocative test that moves a patient from a supine position to an upright position (70° tilt) while strapped to a table, for up to 45 minutes. Blood pressure and heart rate are intermittently or continuously measured, and continuous or intermittent ECG monitoring is done. The tilt table test is used to examine autonomic neural regulation of cardiovascular orthostatic responses. Blood pressure and heart rate responses can be helpful in diagnosing the mechanism of syncope such as reflex syncope or orthostatic hypotension. Examples of tilt table results are shown in Figures 22-1 and 22-2. Evaluation of the tilt table test performance showed a sensitivity of 32–85%, specificity of 75–93%, reproducibility of 62–85%, and a false-negative rate of 14%.

Risk stratification scores have been published in order to identify high-risk patients needing urgent evaluation and treatment. For example, the use of the San Francisco Syncope Rule showed that patients with one or more risk factors were at higher risk of serious events at 7 days, with a sensitivity of 98% and specificity of 56%. Risk factors included were abnormal ECG, congestive heart failure, shortness of breath, hematocrit <30%, or systolic blood pressure <90 mmHg. The use of scoring systems such as this can help identify those patients needing inpatient admission and further workup for syncope.

TREATMENT

Treatment for syncope varies according to the cause. If the workup points toward a cardiac cause of syncope (such as severe aortic stenosis), then treatment should be aimed at that particular etiology (such as aortic valve replacement).

If the workup indicates a likely reflex syncope or syncope from orthostatic hypotension, then lifestyle modification can be an effective first-line measure.

Figure 22-1. Vasovagal syncope demonstrated by tilt table testing. Systolic blood pressure (SysBP) and diastolic blood pressure (d iasBP) as well as heart rate (HR) at each stage of tilt (X degrees of tilt – y minutes into each stage) (Rec = supine recovery stage). A vasovagal response is demonstrated here by a rapid decrease in BP and HR during tilt. BP and HR quickly normalize once the patient is brought back to the supine position in the recovery stage.

Patients with situational syncope can learn to avoid triggering events, such as eating smaller meals or sitting down (for men) to urinate. Patients with syncope from orthostatic hypotension can learn to avoid exacerbating conditions such as volume depletion (eg, from dehydration) or vasodilation (eg, from alcohol use). Physical countermaneuvers and simple postural maneuvers such as leg crossing, isotonic thigh muscle contractions, or squatting can be effective in aborting syncopal episodes if performed at the onset of symptoms. Leg compression support stockings are effective in patients with orthostatic hypotension or postural venous pooling. An abdominal binder and small frequent meals can be useful in patients with postprandial reflex syncope. For those with supine hypertension and postural hypotension,

Figure 22-2. Orthostatic hypotension demonstrate by tilt table testing. Systolic blood pressure (SysBP) and diastolic blood pressure (d iasBP) as well as heart rate (HR) at each stage of tilt (Xdegrees of tilt – y minutes into each stage; Rec = supine recovery stage). Systolic and diastolic orthostatic hypotension is demonstrated here. Blood pressure normalizes during the supine recovery stage.

elevation of the head off the bed by 6–8 in may be useful. Normalized or increased salt intake (2–4 g/day) and fluid hydration using electrolyte-balanced fluids can be attempted. Finally, orthostatic exercise training and a supervised cardiac rehabilitation program may be of benefit.

Pharmacologic treatment of reflex syncope (such as beta-blockers, midodrine, or serotonin reuptake inhibitors) has for the most part been disappointing in terms of efficacy. On the other hand, midodrine, an alpha agonist resulting in increased blood pressure, may have some benefit in patients with chronic autonomic failure. Fludricortisone, a mineralocorticoid resulting in volume expansion, has been shown to be effective in some patients with syncope from orthostatic hypotension. Cardiac pacemaker implantation for reflex syncope with bradycardia has not shown a consistent benefit and may be of limited use, such as in patients with severe spontaneous bradycardia.

CASE CORRELATION

• See also Case 1 (acute coronary syndrome/STEMI), Case 2 (acute coronary syndrome/NSTEMI), Case 3 (cardiogenic shock), Case 6 (acute valvular regurgitation), Case 8 (hypertrophic obstructive cardiomyopathy), Case 10 (valvular stenosis), Case 11 (atrial fibrillation and flutter), and Case 12 (bradycardias).

COMPREHENSION QUESTIONS

Match the following mechanisms (A–F) as being the most likely cause of loss of consciousness in the following scenarios (22.1–22.4):

A. Reflex syncope

B. Severe aortic stenosis

C. Seizure

D. Pseudoseizure or factitious disorder

E. Tachyarrhythmia

F. Bradyarrhythmia

22.1 A 65-year-old man with a history of coronary artery disease and prior myocardial infarction has had a feeling of intermittent rapid heartbeats for the past month. One week ago he was sitting watching television when he had a sudden loss of consciousness.

22.2 A healthy, 16-year-old girl with no medical history had an episode of loss of consciousness while having her blood drawn for routine lab testing.

22.3 A 40-year-old man with a history of a “heart murmur” had an episode of loss of consciousness while playing soccer.

22.4 A 25-year-old man had an episode of unresponsiveness for 1–2 minutes associated with jerking motions of his limbs and tongue biting with loss of bowel and bladder control.

ANSWERS

22.1 E. This episode is concerning for ventricular tachycardia. Prior myocardial infarction can predispose a patient to develop scar-related ventricular tachycardia.

22.2 A. This episode is consistent with vasovagal syncope, a form of reflex syncope.

22.3 B. Severe aortic stenosis can be a cause of exertional syncope due to obstruction of cardiac outflow.

22.4 C. Unresponsiveness with tonic-clonic movements and loss of bowel and bladder control is consistent with generalized seizure activity.

References

Brignole M, Benditt D. Syncope: An Evidence-Based Approach. New York, NY: Springer; 2011. 

Fouad-Tarazi F, Mayuga KA, Wang H. Syncope. In: Garcia MJ, ed. NonInvasive Cardiovascular Imaging: A Multimodality Approach, Philadelphia, PA: Lippincott Williams & Wilkins; 2009. 

Fouad-Tarazi F, Shoemaker L, Mayuga K, Jaeger F. Syncope. In: Carey WD, ed. Current Clinical Medicine. 2nd ed. New York, NY: Elsevier; 2010. 

Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006;47:448–454. 

Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631–2671.

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