Human Exposure To Vacuum: Part 2

In my first post on this topic, I discussed some physics and physiology, in an effort to predict and explain the likely consequences for a person exposed to the vacuum of space.

In this part, I’m going to look at the evidence from animal experiments and human accidents.


The animal decompression experiments were carried out in the 1960s. The original reports used to be available on-line, but they seem now to have vanished. I suspect the organizations involved have concerns about being associated with these experiments, even though they took place half a century ago. They are, however, summarized in the second edition of the Bioastronautics Data Book, and in a 1968 NASA report entitled Rapid (Explosive) Decompression Emergencies in Pressure-Suited Subjects (5.7 MB pdf). The NASA report (NASA CR-1223) provides more physiological detail, and that’s what I’m using for the information below unless otherwise stated.

Boiling and swelling

Dogs were decompressed to ambient pressures of 2 mmHg—effectively a vacuum, and well below the 47 mmHg pressure threshold that marks the Armstrong Limit, the point at which water boils at body temperature. This decompression was accompanied by

… violent evolution of water vapor with swelling of the whole body of dogs.

The Bioastronautics Data Book adds that the body swelled to “perhaps twice as much as its normal volume”.* How fast did that happen? Experiments in which the gaseous composition of the subcutaneous bubbles was monitored showed:

At first there appears to be a rapid conversion of liquid water to the vapor phase which reaches a peak at one minute and continues at a slower rate for several minutes. There is an initial rush of carbon dioxide, nitrogen, and oxygen into the pocket, but carbon dioxide and the nitrogen soon become predominant.

So these whole-body decompression experiments produced different results from the isolated hand experiments I described at the end of Part 1. When the whole body is decompressed there’s a prompt, extensive formation of water vapour bubbles in the subcutaneous tissue—no sign of the delayed onset of swelling (by up to ten minutes) that was found in the hand experiments. Either there’s something unusual about human hands, or something about being connected to an undecompressed body delayed the onset of swelling in the hand experiments.

As soon as the water vapour bubbles form, gases dissolved in the  tissues diffuse into them. These experiments were carried out breathing air, so nitrogen is the major gas to enter the bubbles, with carbon dioxide a more minor component. Oxygen levels in the tissues are falling rapidly, so the oxygen content of the bubble gas will initially rise, and then fall off dramatically.

Did the blood boil? The technical term for this is ebullism (Latin “out-boiling”), and some of the animals were monitored for the formation of bubbles in the circulation. (I don’t have access to the original publication, but I presume this was done fluoroscopically—by continuous X-ray screening—given that this was all happening in the 1960s, before ultrasound became a diagnostic tool.)

Yes, the blood did indeed boil:

Almost immediately after decompression to an ambient atmospheric pressure at which ebullism can occur, vapor bubbles form at the entrance of the great veins into the heart, then rapidly progress in a retrograde fashion through the venous system to the capillary level.

This backward propagation of the bubbles may be because there is a slight pressure gradient along the length of the veins, from the capillaries to the heart, but it might also be because small bubbles are forming at the periphery, washing centrally, and growing or grouping into larger bubbles as they go.

Venous return is blocked by this “vascular vapor lock.” This leads to a precipitous fall in cardiac output, a simultaneous reduction of the systemic arterial pressure, and the development of vapor bubbles in the arterial system and in the heart itself, including the coronary arteries.

As soon as the right side of the heart contains a significant volume of gas, it can’t work as a liquid pump any more—it just compresses and recompresses the gas volume it contains. So flow to the lungs and the left side of the heart is prevented, the left side of the heart has nothing to pump, and the arterial blood pressure begins to fall. As soon as it falls below the critical 47 mmHg, the arterial circulation starts to fill with gas, too.

Systemic arterial and venous pressures then approach equilibrium in dogs at 70 mm Hg. At ebullism altitudes, one can expect vapor lock of the heart to result in complete cardiac standstill after 10-15 seconds, with increasing lethality for exposures lasting over 90 seconds. Vapor pockets have been seen in the heart of animals as soon as 1 second after decompression to 3 mm Hg.

That figure of 70 mmHg for the pressure in the blood vessels at cardiac arrest is interesting. Since it’s higher than the vapour pressure of water at body temperature, it presumably reflects the additional presence of nitrogen in the bubbles.

While the nitrogen in the tissue bubbles isn’t a serious problem, its presence in the circulation is. Recompression quickly causes the big water vapour bubbles to collapse back to the liquid phase. If the heart is still beating, the disappearance of these large bubbles means it can start working as a pump again. But nitrogen takes some time to redissolve, so it persists as small bubbles that are then showered into the circulation:

Upon recompression, the water vapor returns immediately to liquid form but the gas components remain in the bubble form. When circulation is resumed, these bubbles are ejected as emboli to the lungs and periphery. Cardiac arrythmias often occur as do focal lesions in the nervous system. These are probably a result of infarct by inert gas bubbles.

In effect, these animals suffered a case of the bends (nitrogen bubble emboli) as they recovered from cardiac arrest.


Cardiac arrest evidently occurs in two stages. At first, the heart is still beating, but full of gas and therefore ineffective as a pump. This is called Pulseless Electrical Activity. Recompression at this stage will get rid of most of the bubbles in the circulation, and allow the heart to start working properly again. But in the absence of recompression, rapidly falling oxygen levels and bubbles in the coronary arteries will soon cause the heart to stop beating. The Bioastronautics Data Book reports: “Once heart action ceased, death was inevitable, despite attempts at resuscitation.”

In the dog experiments, after 90 seconds of exposure to near-vacuum the animal’s hearts were still beating, but extremely slowly—about 10 beats per minute. If recompressed at this stage, all the animals survived, but often with transient neurological deficits, presumably from a shower of nitrogen-bubble emboli as the heart started pumping again. Beyond 120 seconds of vacuum exposure, deaths occurred frequently. Squirrel monkeys showed a similar pattern of survival but, interestingly, chimpanzees survived longer, with some making a delayed return to “baseline function” after 3.5 minutes of vacuum exposure.

Consciousness and brain damage

It’s difficult to judge “useful consciousness” from animal experiments. One chimpanzee with EEG monitoring is reported as having useful consciousness of 11 seconds, which I presume means that EEG activity looked normal for that period. The cortex had shut down by 45 seconds, and the whole brain was electrically silent by 75 seconds.

Both squirrel monkeys and chimpanzees showed a range of deficits afterwards, in the form of changes in their behaviour and performance. This sort of thing clearly isn’t good for your brain.

Lung injury

After an episode of decompression, the lungs are affected by bruising and areas of overdistension, presumably caused by gas trapping. The longer the decompression, and the faster its onset, the greater the lung injury. Another problem is atelectasis—regions in which the lung is completely collapsed. During a decompression episode, the airways fill with water vapour. When recompressed, this water vapour collapses back to the liquid phase, and the lung tissue tends to collapse with it.


Someone’s got to have an accident for us to obtain the sort of data we’re interested in here—even in the high days of test-pilot derring-do, no-one was volunteering to be decompressed to vacuum.

We’ve seen from the animals studies that chimpanzees seem to survive vacuum exposure better than dogs. So are humans more like chimps or dogs? We’ve got some survival data that help answer that question.


In 1966, Jim LeBlanc was the victim of a depressurization accident in a vacuum chamber while carrying out spacesuit tests. A hose disconnection caused his suit to rapidly (but not explosively) depressurize. He lost conscious after about 15 seconds. The last thing he remembers is the saliva on his tongue starting to boil. The chamber was completely repressurized within a minute, he recovered consciousness during the repressurization, and was able to stand up almost immediately. Apart from sore ears, he suffered no ill-effects. There is video of the incident:

In 1971, the Soyuz 11 capsule returned to Earth with all three crewmen dead inside: Georgi Dobrovolski, Vladislav Volkov and Viktor Patsayev. A damaged air vent had opened shortly after the separation of the orbital and descent modules. The crew had been exposed to vacuum for 11 minutes, and could not be resuscitated.

From a 2013 article in Space Safety Magazine, we know that the dead men appeared normal apart from facial bruising and evidence of bleeding from the nose and ears. Dobrovolski and Patsayev had apparently tried to unstrap in order to deal with the emergency. Telemetry recorded the subsequent course of events:


In 1982, Kolesari & Kindwall reported a case in which a technician was accidentally decompressed over several minutes to a pressure less than 30 mmHg, and held there for a minute before recompressing. Total time at pressures less than the Armstrong Limit was estimated at between one and three minutes. His heart did not stop, but on removal from the chamber he was bleeding from his lungs, unconscious and showing a type of abnormal posturing associated with brain injury. He remained unconscious for five and a half hours, at which point he was treated in a hyperbaric chamber. He woke up within twenty-four hours and eventually made a complete recovery without neurological problems. In the first two days he showed a spike in a biochemical marker called creatine phosphokinase, which is an indicator of tissue damage—presumably due to a combination of the initial hypoxia and bubble emboli.

From these very sparse data it appears that humans may perform closer to dogs than to chimpanzees, with cardiac arrest intervening somewhere around or just after the two-minute mark. The technician in the 1982 accident made a full neurological recover, but probably only with the aid of a hyperbaric chamber to improve his tissue oxygenation in the aftermath of the accident.


The NASA CR-1223 report lists a number of episodes of explosive or rapid decompression (one fatal). In particular, there are notes on three men who were decompressed by about 250 mmHg (from the equivalent of 8,000 ft to 22,000 ft) over two seconds—a relatively mild change by the standards we’re discussing here, which would probably have been relatively uneventful without the attempt at breath-holding.

The first subject was a 42-year-old pilot who inadvertently held his breath at the instant of decompression. He immediately experienced an upper abdominal pain of moderate severity and then lost consciousness. His respirations were noted to be irregular and in the nature of short gasps. Consciousness was regained on reaching ground level about one-half minute after the decompression.

This looks like a fainting episode induced by trying to hold pressure in the lungs that was higher than the pressures in his heart.

A twenty-three-year-old altitude chamber technician is believed to have held his breath at the time of decompression. Almost immediately he noted generalized chest pain and collapsed about twenty seconds later. There were no voluntary respiratory movements. Artificial respiration was begun at once. His skin was cyanotic, cold and clammy. Blood pressure was 126/80 and the pulse was regular at 90 per minute. Voluntary respiration began about two minutes after the rapid decompression but he remained unconscious for about five minutes. On recovering consciousness, he noted weakness of the right arm, numbness of the face, headache and blurred vision. He was nauseated and vomited. The paresis and numbness disappeared rapidly but the clinical picture of shock, an ashen pallor with cold wet skin, persisted for a half hour. His blurred vision cleared about five hours post decompression, the nausea and vomiting lasted six hours and the headache subsided in about eight hours. An x-ray of the chest was normal.

That looks like a near-fatal shower of air emboli that were squeezed into the lung blood vessels by the high pressure in the lungs.

In the third case , a thirty-three-year-old pilot was near the
peak of inspiration when decompression started. Initially, he noted the expulsion of air from his nose and mouth. This was followed by a severe left parasternal pain. Within a few seconds he felt weak and giddy and shortly thereafter became unresponsive. His respirations were irregular, shallow and associated with a hacking cough. During the descent to ground level he exhibited several uncoordinated twitching movements of the upper extremities. The pulse was 45 per minute about two minutes after the decompression. He was in shock and had an ashen pallor and cold, clammy skin. The patient was unconscious for about ten minutes. In the meantime the blood pressure and pulse stabilized at 130/76 and 80 per minute, respectively. The patient had a complete quadriplegia, as well as the loss of tactile sensation for the initial twenty minutes following the decompression.[…]
Chest x-rays taken about one hour after the incident showed a
pneumomediastinum, a small pneumothorax of the left apex and air in the soft tissues of the neck.

There seems to have been temporary damage from emboli, as in the previous case, but accompanied by air squeezing into the chest cavity, into the tissues around the heart, and then up into the neck.

All of the above is a pretty powerful argument for not attempting to hold your breath when decompressing.

And finally … Joseph Kittinger’s hand

Project Excelsior was a series of three simulated high-altitude bailouts that took place during 1959 and 1960. Captain Joseph Kittinger ascended in an open gondola suspended from a helium balloon, and then returned to the ground by parachute.  All his jumps were from altitudes well above the Armstrong Limit, so he wore a pressure suit. He described the three jumps in an article for the December 1960 edition of National Geographic.

On his third ascent, Kittinger noted at an altitude of about 43,000 ft that his right hand didn’t feel normal, and realized that his suit glove had failed to pressurize. As he wrote later:


He and his depressurized hand then rode up to 102,800 ft and spent 12 minutes at altitude, after which he bailed out of his gondola and took 14 minutes to descend to the ground.

[Dr. Dick Chubb] looks at the swollen hand with concern. Three hours later the swelling will have disappeared with no ill effect.

Since the ascent took an hour and a half, it’s likely that Kittinger’s hand spent more than an hour above the Armstrong Limit of 63,000 ft. And the idea that Kittinger’s hand spent an hour in near-vacuum without suffering lasting damage or causing his death seems to be a powerful internet meme, brought up whenever the topic of human vacuum exposure is discussed.

But what happened to Kittinger’s hand is quite complicated, and probably not very informative about vacuum exposure generally.

It’s difficult to say exactly what pressure Kittinger’s body was at. He was wearing an MC-3A partial pressure suit—an outfit that relied on tight lacing and multiple inflating bladders to apply approximately uniform pressure to the body at altitude. Its main function was to allow pressure breathing—the wearer could breathe oxygen from a source at higher-than-ambient pressure, and the suit would compress his body to prevent dangerous pressure gradients being created within his lungs and circulatory system. Some residual pressure gradient commonly occurred—breathing from a source with a pressure 30 mmHg above the suit pressure was not dangerous, and could be performed for some time. But even breathing oxygen, Kittinger’s suit would need to compress his body by at least 100 mmHg to allow him to breathe at his maximum altitude.

The glove that had failed was made of leather and nylon, with lacing at the back to ensure a snug fit, and an internal bladder across the back of the hand, which should have inflated to generate the necessary counterpressure to balance that in the rest of the suit. It was similar in construction to the pair below:

David Clark Company S612 partial pressure gloves
From Dressing For Altitude (17.8 MB pdf), page 160

So as Kittinger’s altitude increased and his suit inflated, his body pressure (and in particular, the pressure in his blood vessels) would ramp steadily higher relative to the tissues in his hand. Critically, the venous pressure in his arm would rise until it was ∼100 mmHg higher than normal venous pressure in his hand. Valves in the veins would prevent blood squeezing backwards down this pressure gradient, but arterial blood was still entering his hand, at an abnormally high relative pressure. The only thing that could happen was for the veins and capillaries to fill with blood until their pressure rose to match the suit pressure in Kittinger’s arm, at which point a trickle of blood flow out of his hand would resume.

So intravascular pressures everywhere in his hand would have very quickly risen to exceed 47 mmHg—there would be no gas formation in the blood vessels of his hand.

And, at those grossly abnormal pressures, his capillaries would have started to leak fluid into the surrounding tissues—he would develop oedema in his hand. The combination of oedema and (above the Armstrong Limit) water vapour bubbles would quickly expand the tissues of his hand until it completely filled the snugly fitted glove. Tissue pressure would then rise further as more oedema squeezed out of the capillaries, and eventually the water vapour bubbles would collapse back into the liquid phase as his tissues pressures exceeded 47 mmHg.

To what extent that process completed during Kittinger’s time above the Armstrong Limit we don’t know—but the fact that his hand was still swollen for a couple of hours after he returned to the ground implies that something other than water vapour was present in the tissues. Although in his National Geographic article Kittinger says he was “breathing oxygen”, Dennis R. Jenkins, in Dressing For Altitude (17.8 MB pdf) writes that the breathing-gas mix for Project Manhigh, the precursor to Project Excelsior, was 60% oxygen, 20% nitrogen and 20% helium, because of concerns about fire hazard. So it may be that Kittinger had a mixture of residual inert gas bubbles and oedema in the swollen hand Dr Chubb examined with concern.


Tissues do swell with gas, promptly, and up to approximately double their normal size. Evidence of blood boiling can appear as early as one second after depressurization, and gas bubbles will get big enough within 10-15 seconds to prevent the heart pumping blood. Prompt repressurization will immediately fix this pump problem but, if you’ve been breathing nitrogen, you may then endure a shower of residual nitrogen emboli into your circulation, causing transient neurological problems. After a couple of minutes depressurized your heart will stop, and it will then become much more difficult to resuscitate you. At about the same time, the neurological insult and tissue damage from hypoxia become so severe that it’s likely you’ll need advanced medical facilities and access to hyperbaric medicine to recover unimpaired. Transient attempts at breathholding (or even being caught at the top of a deep breath in) are likely to have nasty consequences due to lung injury and air leaks into the blood vessels and tissues.
It seems likely that the actual Time of Useful Consciousness will be established by a race between falling oxygen concentrations in the blood and the onset of cardiac arrest because of gas bubbles filling the heart—there’s not much hope of anything longer than ten seconds, and (as I described in Part 1) reason to believe it might be significantly shorter than that.

For me, it’s interesting that there are two opposing schools of speculation about vacuum exposure out there, neither of which is accurate. In one, people are imagined to explode or freeze within seconds of exposure to space—certainly untrue. In the other, which seems to be almost a reaction to the excesses of the first, there’s the idea that the skin and blood vessels are somehow tight enough to stop widespread and immediate gas formation in the blood and tissues—again, as demonstrated by experiment, also untrue.

The truth, as ever, lies somewhere in the middle.

* This prompts the question of whether all that internal evaporation of water might not cause a significant fall in body temperature.
If we take a doubling of body volume as a ball-park figure for the volume of water vapour evolved, we could put it at about 80 litres. Steam tables tell us that, at an absolute pressure of 47 mmHg (that’s -713 mmHg on the “gauge” scale used in steam tables), a gram of water generates about 22.8 litres of vapour—so doubling an adult human’s size under these conditions requires the evaporation of only about 3.5 g of water. Our trusty steam table also tells us that, at 37ºC, this will require about 8.5 kJ of energy. But the specific heat capacity of water is 4.2 kJ/kg/ºC, making the heat capacity of an 80-kg person about 336 kJ/ºC. So all that internal evaporation is only enough to cool a person by a fortieth of a degree Celsius.

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