Why Does Your Vision Go Black When You Stand Up Too Fast?

You’ve been sitting for a while. You stand up fast. And for a second — maybe two — the world goes grey. Your vision tunnels. You might feel lightheaded. You might have to grab the back of the chair.

Then it passes.

This happens to almost everyone at some point. Most people file it under “weird body thing” and forget it. But there’s a precise sequence of events happening in your circulatory system, and once you know what it is, you’ll recognize it for what it actually is: your body racing to catch up with a decision you made too quickly.

Gravity Is Relentless

Your cardiovascular system is constantly fighting gravity. When you’re upright, your heart has to push blood upward against a 5-foot column of hydrostatic pressure to reach your brain. It manages this through tone — the walls of your blood vessels maintain a baseline constriction that keeps pressure up even when you’re not moving.

When you sit or lie down, blood redistributes. A significant portion — roughly 500 to 1,000 milliliters — pools in the veins of your legs and abdomen. Your cardiovascular system adjusts to this. It relaxes a little. Heart rate drops slightly. The whole system calibrates to the new configuration.

Then you stand up.

Gravity immediately pulls blood toward your lower body. Your venous return — the blood coming back to the heart — drops suddenly. The heart gets less to pump. Cardiac output falls. And for a brief moment, the pressure feeding blood to your brain decreases.

The Lag That Causes the Problem

Your body knows exactly how to fix this. You have baroreceptors — pressure-sensitive nerve endings — in the walls of your carotid arteries (in your neck) and in the aortic arch (above your heart). They monitor blood pressure continuously, thousands of times per minute.

When they detect a pressure drop, they fire. The signal goes to the cardiovascular control centers in the brainstem. The response: the sympathetic nervous system activates. Heart rate increases. The heart contracts harder. Blood vessels throughout the body constrict, pushing more blood upward.

The system works. Within about 15 to 30 seconds of standing, blood pressure is usually fully restored.

But there’s a lag.

From the moment you stand to the moment your sympathetic system has fully compensated: somewhere between 0.5 and 2 seconds. Usually less than a second. Usually invisible.

Except in your vision.

Why Vision Goes First

Your brain consumes about 20% of the body’s oxygen despite being only 2% of its mass. It tolerates deprivation poorly — neurons start struggling within seconds of inadequate blood flow.

The occipital cortex — your visual processing center — sits at the back of your head. It’s supplied largely by the posterior circulation, which runs through the vertebral arteries up the back of the skull. This circulation is slightly more vulnerable to pressure drops than the anterior circulation feeding the frontal lobes.

When pressure drops briefly during standing, the posterior circulation feels it first. Visual cortex activity dims. The edges of your vision darken — greying out, sometimes full blackout — before anything else.

Your frontal lobes tend to stay online. Your thinking is clear. It’s specifically vision that goes. That’s why the experience is so strange: you’re completely aware of what’s happening, you just can’t see well for a second.

The technical name is orthostatic hypotension — ortho (upright) static (standing), hypotension (low pressure). A transient version happens to most people occasionally. A persistent version — defined as a drop of at least 20 mmHg in systolic pressure within 3 minutes of standing — affects roughly 5% to 30% of the population depending on age, and is more common in people who are dehydrated, on certain medications, or who haven’t eaten.

When the System Fails More Persistently

For some people, the compensation mechanism doesn’t kick in reliably. This is POTS — Postural Orthostatic Tachycardia Syndrome. When someone with POTS stands up, their heart rate jumps by more than 30 beats per minute (often 40 or 50) in an attempt to compensate for inadequate vascular constriction. The heart races trying to solve a problem the blood vessels should have handled.

The result: dizziness, heart pounding, sometimes nausea or fainting. Not just when standing up quickly — but routinely, whenever they move from horizontal to vertical.

POTS affects an estimated 1 to 3 million Americans, predominantly women, and was frequently dismissed for years as anxiety. The mechanism is now well understood: a failure of the autonomic nervous system to adequately constrict peripheral vessels when upright. It’s a dysautonomia, not a psychological complaint.

Long COVID has significantly expanded the number of people with POTS-like symptoms — the current best hypothesis is that COVID-related autonomic nerve damage disrupts the same baroreflex pathways.

The Fix Is Simple (Usually)

For the occasional head rush, the fix is preemptive: stand more slowly. Give your baroreceptors time to signal before you’re fully upright. Clench your leg muscles before standing — this mechanically pushes venous blood back toward the heart, reducing the initial drop. Drink water.

For persistent orthostatic hypotension: more water, more salt (counterintuitive, but sodium helps retain fluid volume), compression socks (mechanical venous return assist), and in some cases medications.

The underlying truth is that your cardiovascular system isn’t magic. It’s a feedback loop with a response time. You move faster than it can keep up, briefly. Usually it catches you within a second.

That grey-out moment isn’t your brain failing. It’s your brain momentarily underfunded while your body rushes to restore pressure. It lasts as long as the lag between the problem and the correction.

Most of the time: less than a second.

Long enough to notice. Fast enough not to matter.

The body is always catching up. You just usually don’t feel it.