What Causes Fainting: Scientists May Have Found an Answer

A novel investigation reveals relationships between your heart and brain and the fainting response.

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At 7 a.m. on an ordinary spring day, it was business as usual for CBS Los Angeles weatherwoman Alissa Schwartz, who was preparing to deliver the daily forecast. However, in contrast to the reliably sunny skies of LA, Ms. Schwartz’s day soon took a turn for the unexpected: Just before she could deliver her first line, she grew pale, wobbled, and fell to the floor as coworkers looked on in surprise.

Ms. Schwartz experienced syncope, the medical term for fainting or passing out, accompanied by a transient drop in blood supply to the brain.

While scientists have known that dysfunction in the nerves that relay information between your brain and heart contributes to fainting, past attempts to disentangle the precise mechanisms in this nerve network have been challenging.

“We now know that there are receptors in the heart that, when made to fire, will shut down the heart,” Dr. Jan Gert van Dijk, a clinical neurologist at Leiden University Medical Centre, told Nature.

Syncope is usually followed by a quick recovery. “Neurons in the brain are very much like extremely spoiled children,” he added. “They need oxygen, and they need sugar, and they need them now. They stop working very quickly if you deprive them of oxygen or glucose.”

Where before, we only knew what parts of the body are involved in fainting, we now more clearly understand the mechanism that causes it and can begin to attempt pointed, restorative action.

Using techniques that afford unprecedented precision, in a recent Nature study, researchers were able to disentangle a tiny smattering of brain cells, each no larger than a speck of dust and with the power to stall blood to the brain and trigger fainting within seconds.

The Fainting Mechanism at a Cellular Level

The researchers’ goal was to determine precisely what facilitates fainting. They identified a group of neurons with characteristics relevant to heart function, deliberately activated those neurons to see their effect on the heart, and then monitored the heart’s effect on the brain and fainting behavior. As a result, we now have a comprehensive picture of the entire fainting mechanism that occurs in the heart and brain at the cellular level.

Several powerful technologies came together to reveal a neural network that regulates syncope. Our DNA contains 20,000 to 25,000 genes, but not all are active unless they express certain function-specific features for different kinds of cells (for instance, different types of organelles—tiny cellular machinery—or, in this case, a specific type of nerve receptor).

While looking at specialized cells in mice’s vagus nerve—a nerve responsible for regulating heart function—researchers identified cells with a particular genetic characteristic. These cells had receptors that allowed the heart and brainstem to communicate.

The neurons in this network have been hard to study thus far because they are like finding needles in a haystack—thin and diffusely spread out in a massive tangle of other neurons (just think of the cables behind your computer and multiply that exponentially). Researchers genetically modified the detected cells in the mice with fluorescent markers, revealing brain–heart connections.

Charting Brain Function

The researchers then stimulated the identified cells and observed that the cells’ signals slowed the heart’s blood output. A sudden drop in blood flow to the brain, in turn, corresponded to reduced neural activity.

Going a step further, the researchers stimulated the identified vagal neurons connecting the ventricle wall of the heart to the brainstem in the mice. This signaled the neurons to slow the heart’s blood output, resulting in a sudden drop in blood flow to the brain and causing the mice to faint.

The brain is a complex system with multiple feedback loops. Not unlike a thermostat, these feedback loops are responsible for triggering, responding, and rebalancing processes to keep our biorhythm within a narrow margin that supports life.

While carefully monitoring the brain during syncope, researchers found that a small portion of the hypothalamus, the periventricular zone (PVZ), remained active. When they inhibited the PVZ, they found that it took much longer for rats to recover from syncope and concluded that PVZ works with the vagus nerve to rebalance when blood flow is reduced during fainting.

This push-pull relationship between the vagal nerves and the PVS, with consequences for cardiovascular function, coincides with what we know broadly about the human autonomic nervous system (ANS), which regulates homeostasis.

We are constantly vacillating between being over- and under-aroused. When functioning correctly, the ANS ensures we don’t pass out or, conversely, burn ourselves out with overarousal. In the case of syncope, individuals are predisposed to under-arousal, meaning the nervous system is primed for fainting when triggered.

Symptoms and Prevalence of Syncope

As many as about 40 percent of people are likely to experience fainting at some point in their lives owing to a variety of triggers, including heat, hunger, standing quickly, dehydration, or emotional stress (e.g., some people are prone to faint at the sight of blood).

People with syncope may experience temperature changes, feel warm or clammy, or suddenly turn pale. They often report changes in vision—such as seeing spots or experiencing “tunnel vision”—and their eyes may roll back in their head. Fainting often comes on quickly. Feeling lightheaded or dizzy is common with syncope and is usually followed by muscle weakness, leading to a collapse.

Most people regain consciousness within a few seconds to a minute. However, the issue is not to be taken lightly, as falling itself can cause serious injury. Moreover, brain cells will begin to die within two to five minutes in the absence of properly oxygenated blood flow. For these reasons, it’s important to learn what triggers someone’s syncope to help safeguard at-risk individuals.

New Directions in Syncope Treatment

From a scientific standpoint, this synthesis of cardiology and neuroscience at such a precise level illustrates the exciting nature of data-driven medicine when applied holistically across multiple organs. The result is the discovery of an incredibly subtle system with profound effects on regulating consciousness.

Current treatments for syncope indirectly tap into this system. Some interventions attempt to mitigate symptoms with lifestyle modifications to avoid triggers and improve risk factors like hydration or temperature. Others involving medications to adjust blood volume and pressure seek to bolster against a tendency to dip below optimal levels. More invasive measures like pacemakers attempt to stimulate the heart broadly.

Cardiologists have long pondered the root cause of fainting. With the aid of neuroscience, we learn more about the specific neural network underlying this issue and what triggers vagal cells.

This lends hope that, as new precision approaches become possible, they may carry fewer downsides and enable a better quality of life.