Q&A With the Cardiac Arrhythmia Associates of Orlando:
SYNCOPE
What is syncope and how common is this problem?
Syncope is a transient loss of consciousness & postural tone, characterized by unresponsiveness, followed by spontaneous recovery without specific resuscitative measures. This is generally caused by a sudden & global drop in cerebral blood flow. This is a common clinical problem whose origin can often be traced to a cardiovascular event.
An analysis of 822 participants with syncope in the Framingham Heart Study reported an age adjusted incidence of 7.2 / 1000 person years.(1) A vasovagal reaction accounted for 21.2% of the syncopal events. Generally triggered be standing or an emotional reaction. Other causes included cardiac in 9.5%, orthostasis in 9.4%, medication in 6.8%, and stroke in 4.1%. No cause was identified in 36.6% of cases. There is a bimodal incidence in the general population with the peaks affecting teenagers & the elderly (i.e. > 70 yrs old).
The estimated prevalence of syncope in:
• children before age 18 yrs old ~ 15%
• young athletes ~ 6.2%
• military population ages 17 - 27 yrs old ~ 25%
• men & women ages 40 - 49 yrs old ~ 19% over 10 yrs
• Elderly ages > 70 yrs old ~ 23% over 10 yrs.
According to the Center of Disease Control & Prevention and the National Center for Health Statistics data collected from 1992 – 2000 among emergency departments (ED) through out the country syncope was responsible for ~ 7.75% of all ED visits. That translates to 740,000 ED visits annually. The overall admission rate for patients presenting with syncope ~ 32 %, for patients with known heart disease the admission rate is even higher ~ 66%. (2)
What Causes Syncope?
In the general population the most common cause of syncope is vasovagal or “the common faint”, followed by primary arrhythmias. Etiologies can differ among different age groups. For example young patients are most likely to have a neurally mediated form of syncope, conversion or psychiatric reactions & primary arrhythmias like Long QT & Wolff Parkinson White syndromes. In the middle age and elderly population neurally mediated forms of syncope may also occur, but triggered by deglutition, micturition, defecation or cough. Orthostatic hypotension due to autonomic dysfunction or medications should be evaluated. Cardiovascular causes include outlet obstructions such as aortic stenosis or pulmonary embolism. Arrhythmic causes are generally related to underlying structural heart disease such as previous myocardial infarction or cardiomyopathy, but may also include supraventricular tachycardias and bradyarrhythmias.
Where do we begin?
The evaluation & treatment of syncope has evolved through the years with advancement in our understanding of the pathophysiology of its many causes. The main reason to evaluate patients with syncope is to determine whether the patient is at increased risk of death, especially in those with underlying heart disease in whom syncope can be a precursor for sudden cardiac death. In most patients the reasons for the syncope can be determined from a meticulous history & physical exam. This process should include assessment of medications especially anti-arrhythmic agents which can cause pro-arrhythmias as well as anti-hypertensives (i.e. diuretics). Observations by eye witnesses can be particularly helpful. Whereas tonic-clonic seizure like activity can be seen both with neurologic and cardiac causes of syncope, neurally mediated forms of syncope are often followed by fatigue, weakness and nausea. The absence of prodromal symptoms is suggestive of a cardiac arrhythmia.
The initial evaluation does not focus on electrical issues. During the physical exam it is important to evaluate for orthostasis, carotid bruits, and signs of LV dysfunction, pulmonary hypertension and valvular heart disease. A good history and physical, echocardiogram, and stress testing help to rapidly subdivide the high risk from the low risk individual. This is a crucial step. The EKG can be a useful adjunct in evaluating ischemic heart disease, structural heart disease, Wolff Parkinson White syndrome, long QT syndrome & Brugada syndrome.
The mortality in those with structural heart disease and syncope is extraordinarily high and approaches 50% at five years in those who are untreated. I call this "Cardiac Cancer". This is both a high risk, and a high profile scenario. This is an example where appropriate intervention can save lives. For these reason very rapidly evaluating patients felt to possibly have ischemia, or myopathy is so important. Those who have known heart disease, risk factors, over forty, or symptoms of angina or congestive heart failure would merit at least an expedited, if not an inpatient workup.
Many studies, the best of which is the Framingham study, have documented the low cardiovascular mortality in those without intrinsic cardiac abnormalities. Syncope in the patient with known heart disease should be an alarming symptom. It merits the physician carefully assess the situation. The consequences of a mistake are quite high. Once determined to be a low risk individual, without cardiac disease, neurocardiogenic syncope becomes the most likely etiology.
Which patients require EP studies?
An EP Study is a direct assessment of the patient’s conduction system and screens for inducible arrhythmias. It is an outpatient hospital procedure which is done with mild sedation and takes approximately an hour. It is especially helpful in those in whom a vagal etiology is felt to be a less likely cause of syncope. It can pinpoint numerous abnormalities which can be treated which cause loss of consciousness. These range from abnormalities of impulse formation or conduction which would cause bradycardia, to inducible ventricular arrhythmias. EP testing, though invasive, is done via venous access, uses no dye, and is very low risk even in very high risk patients. After an evaluation of LV function, and screen for ischemia, it is an early tool in the evaluation of syncope for those with cardiac disease. Again, the entities which we are looking for are very high risk, and treatable so that patient lives can be protected from sudden death secondary to ventricular tachycardia. The mortality from outpatient cardiac arrest is in the 95% range. Identification of these individuals before this happens is critical.
What is the role of Tilt Table testing in the evaluation of syncope?
A tilt table test is a helpful aid in the evaluation of recurrent neurocardiogenic (formerly termed vasovagal) syncope. It employs a bed able to lift the patient from a supine position to an 80 degree upright position. The patient is secured to the bed with the help of several wide straps and a foot board provides additional support. An intravenous line is the most invasive aspect of this test. Protocols are varied but most employ upright posture for 10-20 minutes at baseline and a similar amount of time after drug stimulation. The purpose of this is to accumulate the majority of the blood volume in the leg veins, therefore mimicking a hypovolemic state. The decrease in venous return activates the sympathetic nervous system in an effort to maintain an adequate cardiac output. Drug stimulation consists of increased sympathetic stimulation with isoproterenol or further increase in venous pooling by using sublingual nitroglycerin, a potent venodilator. The final objective is to trigger a parasympathetic reflex which results in bradycardia and/or hypotension which in this extreme situation results in syncope or near-syncope from decreased cerebral perfusion. Once the patient's clinical scenario is replicated, the table is immediately lowered, resulting in restoration of cerebral blood flow by gravity. The test is exceedingly safe and is usually performed in an outpatient or office setting.
The test's usefulness depends on the replication of the patient's symptoms surrounding recurrent syncopal events. It is less important to achieve actual syncope than to recreate the typical symptoms that accompany syncope. Very often patients will report diaphoresis, nausea, dyspnea, flushing, clamminess and other typical symptoms. These vary widely from patient to patient but are recognizable to the patient if they have happened to him/her before, even before bradycardia and hypotension can be detected. Syncope can be induced in many patients that have never before had it, therefore a test is only "positive" if it also replicates the patient's symptoms. The main utility of the test is verifying that symptoms can be replicated and correspond to this relatively benign condition. A "negative" test is of little value as it does not exclude the presence of syncope, it just tells you that on that given instance you were unable to produce the clinical syndrome. It is for this reason that the test cannot be used to "clear" a patient following a syncopal event. Only clinical observation on therapy, showing a prolonged absence of syncopal events, is of significance.
When should driving restrictions be lifted?
The recommendation of restricting a patient’s driving privileges because the patient may be a danger to himself or to others on the roadway is reasonable but can be a very sensitive subject. Many times it affects our patients’ livelihood and quality of life. Restriction times vary from state to state, but generally range from 3 – 6 months of being syncope - free after therapy has been instituted. Data gathered to formulate the latest European Guidelines would suggest that the risk for a motor vehicle accident due to syncope is low and there is no evidence that waiting for three asymptomatic months will guarantee no further attacks. However, this is the latest consensus. Restrictions will also differ based on the vehicle and the type of driving (i.e. commercial versus private).
Written by Aurelio Duran, M.D., Luis G. Alvarez, M.D., Roland A. Filart, M.D. and Pavel A. Guguchev, M.D. are Board Certified in Cardiology and Clinical Electrophysiology. Together they make up the Cardiac Arrhythmia Associates of Orlando, affiliated with Orlando Heart Center.
Partners of Dr. Mark Steiner, Cardiologist in Orlando
References:
(1) Soteriades ES, Evans JC, Larson MG et. al., Incidence and prognosis of syncope NEJM 2002: 347:878-885.
(2) Sun BC, Emanuel JA, Camargo CA Jr., Acad Emergency Med 2004;11:1029-1034
(3) Sorajja, D, Cardiosource Review Journal 2006;15: 12-15.
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