Arthur Lee, 60, arrives at the emergency department (ED) by ambulance after an episode of “faintness” at his job. He experienced a brief loss of consciousness associated with nausea and diaphoresis. Fortunately, he sustained no injuries related to the syncopal episode. A coworker who witnessed the episode called the ambulance because he was concerned that Mr. Lee's signs and symptoms indicated a myocardial infarction (MI), although Mr. Lee didn't have chest pain.
Mr. Lee was quickly sent through the triage area and a 12-lead electrocardiogram (ECG) was obtained and reviewed. He was interviewed by the triage nurse, who determined that he wasn't in the direct sun or in an overheated room. He also wasn't in a stressful situation, nor had he been in the bathroom immediately before the episode. Lastly, he hadn't been coughing prior to the faintness. Any of these above etiologies: heat stroke, emotional stress, micturition, defecation, or cough can account for “situational syncope,” which stems from abnormal autonomic control that can cause a syncopal response.1
Mr. Lee was taken to the observation area of the ED where the attending physician resumed further questioning and diagnostic testing, including serum electrolytes, cardiac marker levels, glucose, and complete blood cell (CBC) count. A chest X-ray ruled out pneumonia or other chest abnormalities. Medication reconciliation was performed by the triage nurse, and upon further examination, it was determined that the patient hadn't taken any medications that might have caused the syncope. Potential medications that were considered in particular included: antihypertensive agents, vasodilators, or insulin (which may have promoted hypoglycemia that resulted in syncope).
Mr. Lee was attached to a bedside cardiac monitor, noninvasive automatic blood pressure (BP) machine, and pulse oximeter immediately upon arrival, to assess for hemodynamic stability and cardiac dysrhythmias. Once the staff determined that Mr. Lee's situation wasn't urgent or critical, they were able to take a thorough history and begin to sort out the puzzle that syncope often presents.
Common clinical problem
Syncope is a spontaneous transient loss of consciousness (due to a sudden, temporary decrease in cerebral blood flow) that resolves fully without prolonged confusion. Inhibition of sympathetic nervous system (SNS) activity causes vasodilation and a precipitous drop in BP, resulting in syncope.1 The American Heart Association Scientific Statement on the Evaluation of Syncope describes it as “a common clinical problem whose most common causes are cardiovascular in origin.”2 However, common doesn't necessarily mean benign—there's actually a high rate of mortality in patients who suffer syncope who have underlying heart disease.2 More than 7 million Americans suffer from syncope and about 3% of all ED visits are due to syncope.2
When a patient arrives at the ED complaining of syncope, rapidly determining the cause of syncope is key—unexplained syncope can hint at more serious underlying conditions. Syncope is commonly classified as noncardiac, cardiac, and unknown.3
Noncardiac syncope (such as vasovagal) accounts for more than 30% of all syncope cases.4 Take a detailed, focused patient history. A witness to the syncopal event can provide important information regarding the period immediately before, the length of the unconsciousness, and any details of the episode.
Vasovagal syncope (or a simple faint) is associated with inhibition of SNS activity (vasodilation), resulting in a decrease in BP, and an increase in parasympathetic nervous system (PNS) activity, resulting in bradycardia.1 Common triggers for a simple faint include extreme exhaustion, prolonged standing position (especially in one spot), hunger, prolonged exposure to high temperatures, fright, severe pain or trauma, venipuncture, and overwhelming emotional stress. A prodromal event that lasts seconds to minutes—such as a feeling of weakness, nausea, diaphoresis, or blurred vision—often precedes the fainting episode. Rarely will the patient have been supine at the time of the event.
The duration of the unconsciousness is usually brief—rarely longer than a few minutes, as long as the causes of the event can be interrupted. Initial assessment findings include a weak or perhaps briefly absent pulse with extremely lowered or undetectable BP.1 Signs and symptoms usually resolve once the patient falls or is no longer in an upright position. Patients may also be diaphoretic with dilated pupils. Seizure-like abnormal movements may be seen and may lead to an inaccurate diagnosis of epilepsy.5
Vasodepressor syncope, also a simple faint, is associated with inhibition of sympathetic activity.1 Noncardiac syncope also includes:
* carotid sinus hypersensitivity, mostly occurring in men age 50 or older, and caused by pressure on the baroreceptors located on the carotid sinus. Typically, this is a result of too tight a collar, turning the head to the side abruptly, or even shaving with pressure placed over the area.
* situational syncope, which can be caused by cough, deglutition (associated with esophageal spasm), defecation, micturition, or Valsalva maneuvers that decrease venous return. In the case of cough and micturition, middle-aged men are the majority of those affected, although syncope with defecation and deglutition syncope occur equally in men and women.
* glossopharyngeal neuralgia, which occurs as a result of pain around the tongue, tonsillar fossa, or oropharynx. Painful stimuli trigger a parasympathetic response, causing syncope.
Cardiac syncope can result from a sudden reduction in cardiac output, a cardiac dysrhythmia (such as bradydysrhythmia and tachydysrhythmia), or valvular heart disease.1 A significantly higher rate of mortality and morbidity is associated with syncope from a cardiac etiology.6
Bradydysrhythmias can be caused by sinoatrial block, sinus arrest, sick sinus syndrome (SSS), or atrioventricular (AV) block. Bradycardias are more common in older adults due to SSS or high-grade AV block.
Tachydysrhythmias result most commonly from atrial flutter, atrial fibrillation associated with Wolff-Parkinson-White (WPW) syndrome, sustained ventricular tachycardia with structural cardiac disease, or reentrant tachycardias involving the AV node or accessory pathways that bypass part or all of the AV conduction system. Ventricular tachycardia may occur in patients with structural heart disease, particularly in those with an MI, aortic stenosis, hypertrophic obstructive cardiomyopathy, and long QT syndrome.1
Other cardiac-related etiologies of syncope are pericardial tamponade, pulmonary embolism, pulmonary hypertension, atrial myxoma, prosthetic valve thrombus, and, rarely, mitral stenosis.
Assessing the patient
When you assess your patient, obtain his:
* History, including cardiac disease or family history of cardiac disease, prior syncope, or sudden death
* Medication reconciliation, including a list of drugs that may have played a role in the episode. In older adults, be alert for use of tricyclic antidepressants or over-the-counter medications.
* Previous episodes of syncope and presyncope, including how many and how often
* Precipitating factors, including body position
* The types and duration of prodromal signs and symptoms, such as nausea, diaphoresis, chest pain, or severe headache, and the type and duration of recovery signs and symptoms, such as postevent confusion.
After the history, physical findings can provide important information for the evaluation. Check the patient's BP in both arms while the patient is supine, sitting, and standing.
To determine if the syncope is a result of carotid sinus stimuli, carotid sinus massage, unless contraindicated, may be performed by the health care provider. This procedure involves massage to the carotid arteries—right then left (never simultaneously)—to elicit asystole of at least a 3-second duration or BP decrease.6
Determining the cause
Mr. Lee's physician determined that his syncope event wasn't a simple one—the history and the information from the eyewitness confirmed that there was no trigger to cause the syncope. The physician examined the initial ECG for acute ischemic changes and life-threatening dysrhythmias. The next step in the diagnostic evaluation is an echocardiogram to detect underlying heart disease, such as valvular disease or hypertrophic cardiomyopathy (a common cause of sudden cardiac death in young persons).2
If the cardiac workup for syncope had been negative, neurological causes would have next been explored in Mr. Lee, although they're a much less common cause of the problem. Vertebrobasilar insufficiency or basilar artery migraine are neurologic causes of syncope. Signs that may mimic seizures, such as myoclonic jerks or upward gaze deviations, can stem from cardiac causes. One key clue in differentiating a neurological from a cardiac disorder is if the event had occurred with the patient supine. If the event is preceded by an aura or followed by confusion or amnesia, neurological disorder may be the cause.2 The period of unconsciousness tends to be longer and the return of consciousness much slower in seizures. A seizure disorder may initially present as syncope, and can be confirmed by an electroencephalogram (EEG), but may require more extensive testing, such as a sleep-deprived EEG or a 24-hour ambulatory EEG.
Patients with ongoing neurological disease also can have syncope caused not by the disorder, but by the medications taken to treat it, such as tricyclic antidepressants and antiparkinsonian medications.
One common diagnostic test for vasovagal and vasodepressor syncope is the tilt table test, which is long considered the gold standard for diagnosis. Tilt table testing evaluates how well the patient's nervous system can adapt to moving from a supine to an upright position.7 About 50% to 60% of patients with unexplained syncope develop symptoms after 20 minutes on the tilt table.
An echocardiogram can provide useful information regarding underlying heart disease including valvular disease, and is the best tool to determine the presence of hypertrophic cardiomyopathy or an anomalous coronary artery.7
The 12-lead ECG is a simple yet important component in the workup of a patient with syncope. Specific findings can be identified for a probable cause of syncope, including QT prolongation (long QT syndrome), the presence of a short PR interval and a delta wave (WPW syndrome), evidence of an acute MI, or high-grade AV block.
Twenty-four-hour ECG monitoring is indicated for patients at increased risk of a dysrhythmic cause for the syncope in whom an ECG hasn't captured the presence of the dysrhythmia. The 24-hour monitoring may document syncope that isn't accompanied by dysrhythmia or instances of dysrhythmia without syncopal symptoms.6
If the health care provider suspects ischemic heart disease, an exercise stress test may be done, especially if the syncopal episode occurred during or after exercise.
Lastly, if prior evaluation is inconclusive, electrophysiology testing can provide important diagnostic and prognostic information. This invasive test assesses sinus node dysfunction and AV conduction, and most importantly, the presence of ventricular tachydysrhythmias. Patients with syncope who have a concurrent history of coronary artery disease and left ventricular systolic dysfunction (ejection fraction less than 35%) are considered at high risk for sudden cardiac death and are appropriate candidates for an implantable defibrillator, even if no ventricular dysrhythmia is induced.2
Helping Mr. Lee
Mr. Lee's cardiologist decided to order an echocardiogram and monitor him overnight in the cardiac evaluation unit. Although the initial ECG had failed to demonstrate any dysrhythmia, the cardiac monitor quickly detected the potential problem. Mr. Lee was having periods of sinus arrest and periodic slowing of his heart rate into the 30s. Once this was documented, including one episode that caused symptoms similar to his admission symptoms, Mr. Lee's cardiologist could move toward treatment therapy for him. See Treating syncope.
Mr. Lee's final diagnosis was SSS—a term applied to a syndrome encompassing a number of sinus node abnormalities. Sick sinus syndrome usually presents as bradycardia with alternating intermittent rapid regular or irregular atrial tachydysrhythmia (tachybrady syndrome). If the degree of dysfunction is minimal, the patient usually is asymptomatic. Clinical manifestations are due to hypoperfusion of the vital organs, specifically the brain and heart, usually as a result of an inadequate ventricular rate.8 Cardiac syncope resulting from SSS, as well as AV block, is associated with up to 30% mortality at 1 year.8 However, SSS can occur in the absence of other cardiac abnormalities.
Mr. Lee's physician discussed with him his findings and informed him that tachycardia-bradycardia syndrome usually needs a treatment plan for both components. The tachycardia typically is treated with medications that control ventricular rate. Unfortunately, these drugs may exacerbate bradycardia by further depressing sinus node function. In these instances, pacemaker insertion is indicated. Consequently, drug therapy combined with a pacemaker is required for the treatment of tachydysrhythmias in patients with this syndrome. Pacemaker placement is the cornerstone of treatment for symptomatic sinus node dysfunction.8 Mr. Lee received a pacemaker the next day and was discharged the following day with instructions for lifelong follow-up for the device. He was also given specific instructions for any further syncopal episodes in the future (see Patient pointers).
The causes of syncope can be varied and range from benign situational factors to life-threatening dysrhythmias. Health care providers should evaluate all episodes thoroughly so that a patient's risk can be accurately stratified and appropriate diagnostic testing and therapy initiated.
Teach patients with benign syncope techniques to minimize the potential recurrence of the event. Tell the patient not to wear tight collars, to elevate the head of his bed to prevent rapid blood pressure fluctuations on arising, and to take extra time when rising from bed or from a chair.
If the patient had previous syncopal episodes without warning symptoms, he should avoid situations in which sudden loss of consciousness could result in injury, such as driving, swimming without supervision, or operating heavy machinery.1 Teach the patient to lower his head as much as possible when symptoms occur, and include significant others in patient education to ensure appropriate response. If syncope doesn't respond to other measures, the patient may need graduated compression stockings to prevent blood pooling in his legs or prescription drug therapy.1
Patients with noncardiac syncope should avoid situations that may induce a syncopal event (such as standing for long periods of time, remaining in prolonged exposure to high temperatures, or dehydration).
As soon as symptoms develop, the patient should either lie down and elevate his legs or squat down and place his head between his legs to rapidly restore blood flow to the brain. To avoid recurring symptoms, the patient should drink extra water to help increase blood pressure and increase salt intake, with his health care provider's permission.