As soon as her instructor's dissecting knife cuts into the cadaver's skin, a medical student swoons, falling to the floor. Her fellow students pity her, thinking that she is simply too tenderhearted to be a doctor. They are wrong: her problem is not in her head.

Rather than being unable to endure life's occasional unpleasantness, otherwise healthy people who faint when they see a few drops of blood or if they stand in place too long are survivors. They are displaying a lifesaving mechanism bestowed on them by evolution.

For a long time, doctors viewed this behavior as entirely psychogenic--emotionally induced. In such cases, no organic cause presents itself: the electroencephalogram (EEG) looks normal; pulse rate and blood pressure are slightly raised; the electrocardiogram (ECG) shows the heart is working as it should.

But recent research shows that not all such fainting has a psychological basis. Perhaps 10 percent of people have blacked out at least once at the sight of blood, and another 25 percent have suffered the same fate at one time in their lives from standing in place too long. In such cases, the victim's pulse is slow and weak and may be hard to detect at all. Blood pressure is extremely low, sometimes falling below the detection range of a measurement device; only rarely are the readings higher than 60 over 30 millimeters of mercury. (Normal levels are about 120 over 80 mm Hg.) When the patient regains consciousness, blood pressure and heartbeat quickly return to normal. A few minutes later he or she can usually stand again and feels more or less all right. The patient gives all the indications of having had a temporary, albeit severe, circulatory collapse; the medical term for such episodes is syncope. Such losses of consciousness clearly result from physical processes--and they seem to be systems that make sense from an evolutionary perspective.

Anatomy of a Faint
Only in the past few years have doctors learned that the roots of syncope are in the autonomic nervous system, which is devoted to the control of our inner organs. This system, also known as the vegetative nervous system, generally carries out its functions automatically, and we are not conscious of its operation. It regulates our inner organs through two groups of nerves--one originating in the brain stem (the parasympathetic system), the other in the spinal cord (the sympathetic).

The vagus nerve of the parasympathetic, among other activities, slows the heartbeat and relaxes blood vessels, reducing blood delivery through the body. Its counterpart, the sympathetic, makes the heart muscle pump harder and faster, increasing blood pressure and the amount of blood supplied to the organs. In addition, the sympathetic system constricts smaller arteries, raising blood pressure further.

A victim will topple over when the parasympathetic orders a slower heartbeat, reducing blood flow to the organs. Researchers call this form of fainting vasovagal syncope: a loss of consciousness (syncope) in which the blood vessels ("vasa," from the Latin) are widened and in which the vagus nerve inhibits the heart's actions.

The parasympathetic system and the vagus nerve are controlled by the brain stem or, to be more precise, by the circulatory centers [see box above] in the medulla oblongata, the part of the brain that extends from the back of the head into the spine. One of these centers--the caudal midline medulla (CMM)--is believed to be responsible for vasovagal syncope, because it is able to arouse the vagus nerve strongly, inhibiting the sympathetic system to a degree that can decrease circulation to a low ebb. In animal tests, researchers determined that the vagus nerve is strongly activated in such "blood-induced" fainting, which would explain both the slowed pulse and the virtual stopping of the heart. The resulting unconsciousness was very similar to human fainting--the pulse, for example, was barely detectable and blood pressure was extremely low.

The CMM always activates when an animal loses at least 30 to 40 percent of its blood supply (equivalent to about one and a half to two liters in humans) and blood pressure in the chest falls rapidly. How does the circulatory center get this information? To answer this question, it helps to examine the events taking place after such a massive blood loss. First, to ensure that blood continues to nourish the heart and other vital organs, the body redirects blood out of the large veins near the heart and pulmonary vessels. That shift can quickly make up to an extra liter of blood available, which will, at least for a time, keep pressure up in the coronary arteries.

But as the vessels in the chest continue to empty, and the blood pressure falls rapidly, low-pressure baroreceptors--special blood pressure sensors in the coronary and pulmonary arteries--report this drop to the brain stem. When the level dips below a certain critical value, the CMM signals a circulatory collapse.

An Upside to Falling Down
But now for the really interesting question: What good is the resulting blackout? Wouldn't a mechanism that shuts down a circulatory system that is already weakened by massive blood loss cause even more damage? A 2001 study led by Ian Roberts, now at the London School of Hygiene and Tropical Medicine, may provide the answer. Roberts reviewed survival statistics for accident victims who received different treatments. He found that the previously accepted practice of immediately giving people who have suffered serious internal injuries large transfusions for blood replacement often caused more harm than good.

Roberts had an enlightening explanation for this discovery: the transfusions caused the blood pressure in the injured vessels to rise. As a result, more blood flowed out through the wounds. That flow hindered clotting, so that no barriers to ongoing blood loss could form. He concluded that artificially inducing higher blood pressure with an infusion can disturb the body's natural abilities to reduce blood loss.

A general circulatory collapse ordered by the brain may, therefore, be the body's last-ditch effort to recover after a massive blood loss by halting further bleeding. Because of the advantage of having such an emergency survival assist, the feature was conserved over the course of evolution.

But what about fainting at the mere sight of blood? Here, too, an injury is involved--although it is to someone else. When an observer sees the blood, the visual input of the event is thought to go from the brain's visual processors to the emotion evaluating center in the limbic system, and from there it is relayed to the CMM. The unfortunate person keels over.

Perhaps this type of fainting results from the CMM's attempt to invoke the vasovagal mechanism even in instances of minor wounds. After all, one's chances of survival often would be improved if clotting began before serious bleeding could occur. To accomplish that benefit, the body's protective reaction would have to take place when the brain perceives the first visible evidence of injury. The side effect is that the lower the trigger point is set for the vasovagal circulatory collapse mechanism, the higher the chances of a false alarm, such as fainting at the mere sight of blood--even if it is from another person.

And how about people who collapse after standing in a stationary position for too long? Their bodies are reacting to a similar signal of a blood shortfall, but the cause is different: gravity. As a person stands stock-still, about half a liter of blood can be pulled into veins in the legs. Because gravity constantly presses liquid out of the capillaries in the legs and into surrounding tissue, the blood volume can continue to decline. Ultimately, blood pressure in the chest can drop below the trigger point, and the CMM in the brain stem will order a circulatory collapse.

As science has demonstrated, a person who faints when he sees a wound or stands at attention is not displaying physical frailty but rather a successful (if hair-trigger) survival edge. Maybe it is time to alert the dictionary editors.