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Syncope, Part 2

By DrRich

When you have syncope (loss of consciousness), your doctor’s main concern should be to determine whether you are at high risk for sudden death. Most syncope is benign in nature, but when it is caused by a cardiac problem, sudden death is a real possibility. In Syncope, Part I, we reviewed the cardiac conditions that cause syncope, and discussed your doctor’s first obligation – to rule out these conditions.

Fortunately, most syncope is not cardiac in nature, and thus is not life-threatening. In this article, we will review the non-cardiac causes of syncope, then outline what you should expect from your doctor when you or a loved one have had a syncopal episode.


The non-cardiac causes of syncope

Categories of Non-Cardiac Syncope

Common causes of syncope within categories

Neurologic

Vertebrobasilar TIAs
Subclavian Steal Syndrome
Normal Pressure Hydrocephalus
Seizure Disorder

Metabolic

Hypoxia
Hyperventilation
Hypoglycemia

Vasomotor

Orthostatic Hypotension
Vasovagal Syncope

Neurological causes. For practical purposes there are only four neurological conditions that cause syncope, and none of them are particularly common.

The first two - vertebrobasilar TIAs ( transient ischemic attacks) and subclavian steal syndrome – are actually vascular problems. The vertebrobasilar arteries are located in the back of the neck near the spinal column, and supply blood to the consciousness center of the brainstem. If blood flow to these arteries is interrupted, syncope occurs. Both vertebrobasilar TIAs and subclavian steal are caused by such an interruption in blood flow. (Notably, many doctors immediately worry over the carotid arteries when a patient has syncope. But the carotid arteries – while vitally important – do not supply the consciousness center, and thus interruption in carotid blood flow does not cause syncope.) The doctor should suspect vertebrobasilar TIAs, if that is the cause, after taking a careful medical history. Subclavian steal syndrome reveals itself when the doctor takes the patient’s blood pressure in both arms, and finds the blood pressure in the right arm to be markedly lower than in the left.

Normal pressure hydrocephalus is caused by an accumulation of excess fluid in the brain. It too has a characteristic clinical pattern – it affects elderly patients, who present with a symptom complex of urinary incontinence, dementia, and syncope.

Because of their characteristic presentations, seizure disorders should only rarely be confused with other causes of syncope.

The bottom line is that if your syncope was caused by any of these neurological disorders, your doctor ought to strongly suspect it after doing a careful medical history and physical examination. In the vast majority of patients with syncope, neurological causes can be ruled out before the doctor leaves the bedside.

Metabolic causes of syncope. Similarly, there are only a few metabolic causes of syncope. Hypoxia is reduced oxygen concentration in the blood. Hypoxia severe enough to cause syncope is virtually never seen unless obvious and severe lung or heart disease is present. Thus, the diagnosis of hypoxia is not a problem. Hyperventilation is seen in severe anxiety reactions, and most times the medical history reveals the problem. Hypoglycemia rarely causes syncope, and once again a good medical history – with emphasis on the relationship of syncope to meals or to diabetic medications – should point to this problem.

Vasomotor causes of syncope - where the money is. Vasomotor syncope occurs when the blood vessels in the legs dilate, causing a large proportion of a person’s blood volume to pool in the legs. Since the blood pooling in the legs is not being returned to the heart, the amount of blood pumped by the heart falls dramatically. As a result the blood pressure drops, the brain suddenly is not receiving an adequate amount of oxygen, and syncope occurs.

Once the patient falls to the ground, however, gravity no longer keeps the blood pooling in the legs. Blood returns to the heart, blood flow is restored, and the patient regains consciousness within several seconds. Vasomotor syncope is therefore “self correcting.” (It’s self correcting, that is, unless a helpful soul catches the victim in mid-fall and decides that propping them up is advisable. In this case prolonged unconsciousness, and conceivably permanent brain damage, is possible.)

There are two general kinds of vasomotor syncope.

Normally, when a person stands up, the blood vessels in the legs constrict in order to support the blood pressure in the standing position. Orthostatic hypotension – a fairly common condition – occurs in patients whose blood vessels do not constrict normally when they stand, thus allowing the blood to pool in the legs, and the blood pressure to drop precipitously. This condition is most often caused by prescription drugs, but is also seen in diabetes, Parkinson’s disease, with dehydration, and in several other disorders. A modestly alert physician can easily diagnose orthostatic hypotension simply by taking the blood pressure while the patient is lying down, and again while the patient is standing.

Vasovagal syncope (also known as cardioneurogenic syncope) is the most common cause of syncope, probably accounting for more than 80% of all syncopal episodes. Since vasovagal syncope is simply an exaggeration of a normal neurological reflex, most individuals will experience at least one vasovagal episode in their lifetimes.

The reflex responsible for vasovagal syncope works like this: A person is exposed to some stimulus (such as a needle stick) that initiates the reflex. The “stimulated” nerves (the nerves of the stuck finger, for instance) send an electrical signal to the vasomotor center in the brainstem. (The vasomotor center determines the body’s vascular “tone.”) The vasomotor center, in turn, signals the blood vessels in the legs to dilate, causing the blood to pool in the legs, and producing syncope. This same reflex also causes a drop in the heart rate, but usually it is the pooling of blood in the legs – and not the slow heart rate – that produces loss of consciousness.

The “stimulus” that triggers a vasovagal episode can be any one of hundreds of things. As already noted, pain is a common cause of fainting. Other common triggering events include the sight of blood, receiving upsetting news, or standing motionless for long periods (such as with soldiers standing at parade rest).

Anyone can have vasovagal syncope given an adequate triggering event, but many people are particularly prone to these episodes, and often with relatively mild triggers. These individuals tend to relate histories of syncope dating back to adolescence, and frequently will describe several different of triggering events. While, as noted, there are scores of possible triggering events for vasovagal syncope, some are quite characteristic and almost always point to vasovagal syncope. Syncope occurring after urinating, defecating, coughing or swallowing, or syncope associated with pain, fright, the sight of blood, or other noxious stimuli, is almost always vasovagal.

In these and other ways, vasovagal syncope tends to be highly situational. It is more likely to occur after a viral illness, after exercise, after a warm shower, or early in the morning – any time that relative dehydration is present, and dilation of the blood vessels in the legs would be more likely to produce a significant drop in blood pressure. Furthermore, vasovagal syncope is often preceded by a few seconds or a few minutes of warning symptoms. Often, these symptoms include lightheadedness, ringing in the ears, visual disturbances, sweating and/or nausea. Because of such “warning symptoms,” people who have had one or two episodes of syncope are frequently able to tell when an event is about to occur. And importantly, if they recognize the warning symptoms, they are able to abort the blackout simply by lying down and elevating the legs. (“Aborting” syncope is not possible with most other forms of syncope.)

Given these characteristic features and the situational nature of this condition, doctors can make the correct diagnosis in the vast majority of patients with vasovagal syncope simply by asking right questions and listening carefully to the answers.

How syncope should be evaluated

Having reviewed the causes of syncope, we now turn to the issue of how your doctor should go about sorting through these possibilities. The appropriate workup of syncope can be reduced to three steps:

Step 1: A thorough history and physical examination.

We have seen why this is important – the history and physical examination give vital clues in diagnosing nearly all causes of syncope.

A careful history consists of asking details about each and every syncopal episode the patient has had, including a detailed history of when it occurred, what the patient was doing, whether there was any warning, how long it lasted, whether consciousness was regained as soon as the patient fell down, and whether the patient has found a way to abort the episodes. The physical examination should include thorough neurological and cardiac exams, and taking the blood pressure in each arm and while the patient is lying (or sitting) and standing.

By the end of the history and physical, your doctor, at the least, ought to have an excellent idea as to what is causing your syncope. When she is finished with this preliminary assessment, your doctor should be ordering no more than one or two directed tests to confirm her suspicions. She should be able to tell you what she thinks is the problem, and should even be giving you some idea of what the treatment will entail.

If your doctor has finished up with you and is standing there, shaking her head, ordering a shotgun-load full of tests and procedures, you’re both in for a very hard time.

Step 2: Directed tests or studies

After the history and physical:

- If your doctor suspects a neurological cause, then she will probably order a brain scan or EEG, or in some cases, angiography (a dye study to visualize the arteries to the brain) to confirm the diagnosis.

- If your doctor has diagnosed or strongly suspects vasodepressor syncope, therapy should be initiated. In some cases, a tilt table study may be useful in confirming the diagnosis.

- If your doctor suspects a cardiac cause, or if she has no good idea as to what is causing your syncope, a non-invasive cardiac workup should be done immediately. In most cases, this work-up will consist of an echocardiogram, and in some cases a stress test.

Step 3: If the cause of syncope remains unknown after Step 2

- If underlying heart disease was discovered in Step 2, you should be referred for a full cardiac evaluation. In general, this evaluation would consist of not only a standard heart catheterization (in which the coronary arteries are visualized), but also an electrophysiology study (a catheterization evaluating the propensity of the heart to develop life-threatening arrhythmias).

- If no underlying heart disease is apparent after Step 2, your doctor might consider ambulatory monitoring (where you wear a cardiac monitor at home for some length of time), tilt table testing, and possibly stress testing if not performed during Step 2. If syncope remains undiagnosed after these studies, an electrophysiology test should be considered.

Using this general approach, your doctor should be able to diagnose the cause of your syncope quickly and accurately, and initiate appropriate therapy before too much time has passed.

Click here for  Syncope - Part 3 - Treatment.

 

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