• Diagnosis: Explanation
• Treatments

Physiology

Vaso-vagal syncope is caused by the triggering of a paradoxical reflex, which causes a fall in blood pressure and loss of consciousness. There are multiple terms to describe vaso-vagal syncope, including vaso-depressor syncope, neurocardiogenic syncope, cardio-inhibitory syncope, and neurally-mediated syncope, all of which refer to the same reflex. This reflex usually occurs while standing upright although it can on occasion occur while sitting, after exercise, or after a meal. Other sections of this website describe the causes of syncope in these situations.

The classic form of vaso-vagal syncope is though to be caused by the following sequence of events: As described in the previous section on the physiology of upright posture, standing results in a pooling of blood in the legs, which leads to an increase in the activation of the sympathetic nervous system, causing an increase in heart rate, an increase in the force of contraction of the heart and an increase in the resistance of the peripheral blood vessels. All three of these compensatory reflex responses are designed to maintain blood pressure and blood flow throughout the body. As the pooling of blood in the legs results in the heart becoming less full, these reflexes become more intense in order to maintain blood pressure and blood flow. These compensatory reflexes increase in intensity until a critical point is reached, which eventually triggers the vaso-vagal response. At this point, there is in intense contraction of the heart, which is detected by sensors in the heart muscle.

The sensors in the heart are designed to protect it from beating too strongly. They are activated in an all-or-nothing response when the heart muscle is contracting intensely. As an analogy, imagine that the heart is like a rubber hot-water bottle filled with fluid. If the water bottle were filled and you had to empty half the fluid it would be easy to squeeze the bottle and force fluid out. However, if their bottle started off only one-third full and you had to empty 90% of that volume, you would have to squeeze the bottle extremely hard and almost wring it to get 90% of the fluid out. The same thing occurs in the heart. When the heart is relatively full, it contracts and ejects approximately 50% of the blood on each given beat. However, when it becomes less full, it is forced to contract more strongly, ejecting a greater percentage of blood, to maintain blood flow. At some critical point, the heart can eject that amount of blood only by using an extremely contorted, wringing contraction on each beat. This type of contraction triggers the sensors.

Once the sensors are activated, they initiate a shutdown reflex. This reflex involves turning on an inhibitory component of the autonomic nervous system called the parasympathetic nervous system. The entire reflex is designed to shut things down. The most important aspect of his reflex is a dilation of the peripheral blood vessels. Remember that when the heart is under-filled one of the normal compensatory responses to this state besides an increase in heart rate and strength of contraction, is the constricting of peripheral blood vessels to maintain blood pressure. When this paradoxical reflex occurs, however, the blood vessels dilate, which causes a marked drop in blood pressure. As the blood pressure falls the brain becomes inadequately perfused and you lose consciousness. Often, when this reflex occurs, not only does blood pressure fall, but heart rate also falls. The drop in heart rate is caused by the activation of the vagus nerve, a part of the parasympathetic nervous system that innervates the heart’s pacemaker.

This reflex is normal and occurs in all people. What distinguishes those who have recurrent episodes of fainting are two factors: 1) an individual susceptibility to the reflex, and 2) situations that make the individual more likely to trigger the reflex.

Little is known about what makes one individual more likely to trigger the reflex than another. It is possible that the actual structures in the heart may be more or less sensitive to the amount of stretch in the heart. In addition, properties of the heart muscle change over time. For example, the heart and large peripheral blood vessels become stiffer with age, which may lead to a change in the sensitivity of these sensors. The function of the compensatory reflexes that counteract a drop in heart filing when you stand up may also decrease with age. These slow changes in cardiovascular reflexes, structure and function may help explain individual susceptibility to the reflex that causes vaso-vagal syncope. They may explain why someone may live for 30 years without ever fainting, then suddenly have a large number of episodes in a short period. Fainting from this mechanism can start at any age and will often go away eventually.

The other issue determining whether or not a person will develop fainting spells from vaso-vagal syncope is his or her exposure to situations and triggers that activate the reflex. In a sense, every individual has some intrinsic susceptibility to vaso-vagal syncope. Depending on their susceptibility, various triggers may be more or less likely to initiate the reflex that causes it. In a person whose intrinsic susceptibility is high, even mild triggers might induce vaso-vagal syncope. However, in individuals who are not particularly susceptible, an increase in the intensity of a trigger may cause them to faint. In one research study in which investigators were able to induce vaso-vagal syncope in nearly every normal subject simply by increasing the intensity of the triggers that are known to cause it.

A number of situations can make someone more likely to develop vaso-vagal syncope. The most common example is dehydration, When a person is dehydrated, his overall blood volume is educed below normal. This results, on average, in a heart chamber that is under-filled. When the individual stands up, a certain amount of blood will pool in the lower extremities. Because the heart chamber is starting with a lower volume of blood in it, this drop in filling of the heart chambers triggers the first set of compensatory reflex responses. The heart is then extremely under-filled. It beats faster and more strongly. This activates the sensors that cause vaso-vagal syncope.

At other times, even when the person is not dehydrated, the heart may become markedly under-filled in response to upright posture. This could when either there is clearly greater than normal pooling of the blood in the legs, or when the body is unable to properly compensate for normal pooling. For example, alcohol causes a dilation of both the peripheral blood vessels and the veins in the legs, resulting in both a greater pooling of blood and diminished constriction of blood vessels when upright. Alcohol not only produces a greater stimulus by causing a greater drop in filing of the heart, but also blocks the compensatory reflexes that are designed to maintain blood pressure. In people who are susceptible to vaso-vagal syncope, drinking alcohol may be just enough of a trigger to induce syncope even when they are not dehydrated.

Patients taking drugs that either cause an increase in blood pooling in the legs, or which prevent constriction of blood vessels in the legs, experience similar problems. Vasodilators are often used to treat high blood pressure. Although these drugs may be therapeutic in lowering blood pressure in patients who have hypertension, they may at times cause excessive drops in blood pressure and vaso-vagal syncope.

Another situation that may make vaso-vagal syncope more likely is the consumption of a large meal. Approximately 30 minutes to one hour after a large meal the blood vessels in the gut dilate, sending blood towards the intestines to allow digestion to occur properly. Blood pools in the abdomen, lowering the amount that returns to fill the heart chambers. If the person then stands, additional blood will pool in the legs, causing further stress on the circulatory system. This is called post-prandial hypotension, and may be a cause of syncope in some patients.

There is increasing evidence that sleep deprivation blunts the reflexes that maintain blood pressure when upright. This is a new area of research although I have commonly heard from patients that on days when they are not well-rested or are sleep-deprived, they are more likely to feel lightheaded when standing or develop vaso-vagal syncope.

Finally, there are patients who appear to have an exaggerated compensatory response to decreases in filling pressure in the heart. At stressful times, when upright, these patients develop an excessive increase in heart rate and contraction in response to normal standing. Although these individuals show normal amounts of blood pooling in the extremities, this excessive compensatory response may suffice to trigger the reflex.

Neurocardiogenic (Vaso-vagal) Syncope: Treatment

The treatment of vaso-vagal syncope depends in part on the mechanism causing the triggering of the reflex. The only way to treat vaso-vagal syncope is to prevent the reflex from occurring. Treatments are designed either to prevent the occurrence of a stimulus that may trigger the reflex or to attempt to alter an individual susceptibility to its activation. There are multiple types of treatments including changes in diet, medications, exercise, and even pacemaker therapy for some patients with this disorder. Not everybody with vaso-vagal syncope needs to be treated; the decision to treat a patient with vaso-vagal syncope is based, in part, on the frequency and severity of an individual’s symptoms and the likelihood that a recurrent event might produce trauma from falling.

One of the classes of drugs most commonly used to treat vaso-vagal syncope is beta blockers. Beta blockers block the effects of stress on the heart. This refers no only to the effects of psychological stress of the heart, but more important, to physiologic stress on the heart. If you review the mechanism of vaso-vagal syncope described in the prior section, you will remember that the reflex that causes vaso-vagal syncope is triggered from an intense contraction of the heart muscle around the relatively empty chamber. Beta blockers blunt the ability of the heart to reach such an intense contraction. In its absence the reflex does not get triggered. For many patients, beta blockers are effective treatments for vaso-vagal syncope.

There is one paradoxical aspect of this approach to treatment of which you might be aware. Beta blockers are known to lower blood pressure slightly (they are often used as medicines to treat high blood pressure) and they also cause a drop in heart rate. Vaso-vagal syncope, when it occurs, may in fact cause a sudden drop in blood pressure as well as a drop in heart rate. This may seem paradoxical because the drug you are using to treat vaso-vagal syncope can also induce a drop in blood pressure and heart rate. However, in vaso-vagal syncope, the drop in blood pressure and heart rate is a sudden and transient response to the activation of the reflex. If the reflex is unable to be triggered, as is the case while on beta blockers, patients will never develop the drop in blood pressure and drop in heart rate that causes vaso-vagal syncope. There are numerous research studies documenting the efficacy of beta blockers in patients with vaso-vagal syncope. However, there are patients who did not respond well to this line of therapy, and other therapies may be more appropriate.