A Momentary Pause in the Act Of Dying

Low blood volume in Myalgic Encephalomyelitis. It's shocking. An interview with David Bell, M.D.

Copyright 2025 Hillary Johnson. All Rights Reserved.

In 1980 while on staff at Life magazine I reported on the nation’s first emergency room dedicated to treating trauma victims who were in danger of circulatory shock. Also called “hypovolemic shock” and “hemorrhagic shock,” it’s a potentially deadly condition caused by significant blood loss. In trauma victims, blood loss is usually caused by either external wounds or internal bleeding.

‍The Shock Trauma Center, as it was called, was housed in the University of Maryland hospital in Baltimore. Nurses and surgeons at this one-of-a-kind emergency center were trained to follow a multi-step protocol developed by the late R. Adams Cowley, a heart surgeon. "Shock," Cowley wrote, "is a momentary pause in the act of dying." The point was to stop the dying by stopping the shock. Cowley believed trauma doctors had a “golden hour” before a patient in shock lost so much blood they would die of their trauma—not necessarily immediately, but nearly always within a few days or weeks—if they were not treated according to this protocol. Today, as then, Cowley’s “golden hour” is considered a guidepost, not a hard rule. Cowley’s basic shock protocol is followed at most ER trauma centers today.

Blood carries oxygen-rich red cells to all the tissues of the body. A lack of oxygenation by way of slowed blood circulation results in cell death. Depending on degree, blood loss can lead to a cascade of lethal effects, including a shutting down of major organs: kidneys, liver, lungs, heart and brain. When shock results in inadequate blood flow to the brain, it’s called "ischemic hypoxia."

Patients suffering from traumatic shock are always in serious jeopardy, even when they receive treatment at trauma units in emergency rooms. Epidemiological research papers published in 1995 and 2003 found that death rates from hemorrhagic shock in civilian trauma units ranged from 21 to 39 percent of all trauma deaths. The seriousness of the problem has hardly waned. A 2016 study Danish study calculated that in emergency rooms a shock diagnosis had a “7-day and a 90-day mortality of 23.1% and 40.7 %.”

The Baltimore hospital experts rushed to stabilize patients by supplying fluids and assessing their injuries. Everyone seemed to know their role in the grizzly ballet. Blood loss didn’t necessarily mean the blood was flowing out of the body. Invisible internal injuries resulting from blunt force trauma, particularly common in vehicular accidents, were of particular concern. Blood might be cascading into the interior of the body due to an injury directly to an organ or the body’s vasculature system—the blood vessels carrying blood throughout body—or both. If the source of the internal bleed went undetected, patients could bleed to death internally in short order.

By ten o’clock in the evening, a helipad on the hospital’s roof was in near-continual use as people with gunshot and stab wounds, victims of car accidents and—with gruesome regularity—motorcycle accident victims, arrived. Teams of doctors and nurses rushed up the stairs to await shock trauma patients on the roof, their scrubs flapping violently in the downdraft created by whirring helicopter blades.

One evening I witnessed a teenager arrive on a stretcher with a portion of his brains lying next to his head. He had collided with a car while traveling at 60 mph on his motorcycle and landed fifty feet from the point of impact. With weary resignation, lacking irony, ER staff called motorcycles “murdercycles." ‍

At the center of my story was a man without any visible injuries who had been in a freeway accident. A boat slid off a trailer onto the road ahead of him and his car skidded into it with tremendous velocity. When he arrived at the shock trauma unit, he was alert and talking. Within the hour, he was floating in and out of consciousness, ashen-faced and clammy. A senior surgeon, arms folded, paced nearby awaiting the results of imaging and blood tests. Upon evaluating the tests, the surgeon ordered staff to move the accident victim into surgery immediately. There, the doctor removed the man’s spleen, the source of internal hemorrhaging. Two hours later, however, blood continued to drain from the man's body through a clear plastic tube. The surgeon reopened the man's abdomen and removed part of his pancreas. Finally, the blood stopped, but he remained "critical," with a 50-50 chance of survival, according to the surgeon.

Essentially a triage center akin to a field hospital in a war zone, the shock trauma unit made for riveting life and death drama, even if covering the story left me with several months of PTSD. Soon after, a documentary, then a feature movie and more recently, a mini-series, were made about the Baltimore center.

I felt an affinity with the man whose ordeal I had written about and I stayed in touch with him long after the story was published. Months passed before his full recovery and even then, although he was able to return to this job, he admitted to me that he felt something was “off.” By all outward signs, he was well, but he continued to believe the accident had changed his ability to think—his perceptions—in ways that were hard to describe. He felt he was not the same. His life had been saved, but I wondered if he had experienced some degree of ischemic hypoxia, brain damage resulting from a lack of oxygenated blood, in the ordeal.

‍What does this have to do with ME?

People who suffer from ME are not admitted to shock trauma units for blood loss and impending shock. There is evidence, however, that many are suffering from mild to severe blood loss, in some cases blood loss that is equivalent to trauma victims who are bleeding externally or internally.

The issue of blood loss in ME became more real to me when, in 2018, I reached out to retired doctor David Bell for an interview. Bell agreed to the interview, adding, “I know what I want to talk about—low blood volume.”

Our interview took place in that year, although I spoke with Bell again recently. He is retired and living in his Victorian farmhouse next to Lake Ontario in Lyndonville, a small town at the northern border of New York state mid-way between Rochester and Buffalo. Bell purchased the house decades ago after graduating from Tufts University medical school and began practicing pediatric medicine in the rural area. His peaceful practice was upended in 1984 by an outbreak of ME among schoolchildren who were his patients.

It wasn’t until Bell and I began to discuss his preferred topic in some detail that I remembered the Life story. I had once understood shock very well, but only as it applied to victims of acute trauma. Nearly forty years later, as I listened to Bell’s observations, I realized that the same physiological principles and indexes of harm may apply to ME sufferers because they, too, may be in shock.

Bell’s interest in this aspect of ME was longstanding. Orthostatic intolerance, or hypotension, is common if not universal in ME and the symptom opened the door to Bell’s blood volume discoveries. It’s characterized by a sudden drop in blood pressure when the patient sits up or stands up after sitting or lying prone. Symptoms like fainting, dizziness, cognitive difficulties and weakness may occur. Also called "postural orthostatic hypotension," it's an autonomic disorder, an involuntary, neurally mediated symptom. In extreme cases, falling blood pressure will cause the ME patient to pass out upon standing. According to Bell, fainting is a more common consequence in children and in fact is rare in adults, who Bell says are better able to compensate. Nevertheless, depending on how adults with ME are manipulated on tilt tables, they can almost always be made to faint.

In the mid-1990s, deeply curious about low blood volume in his ME patients, Bell called a specialist named David H. P. Streeten. The latter was a professor at nearby Syracuse University and considered an expert in orthostatic hypotension.

Somehow, Bell was able to garner Streeten’s interest in hypovolemia in ME patients. Bell remembers that when Streeten began to evaluate sufferers, his unfamiliarity with the disease turned to fascination.

“He had never heard of chronic fatigue syndrome,” Bell remembers. “but he was really impressed.”

Bell and Streeten conducted investigations in the late 1990s that demonstrated severe hypovolemia in the disease. In some cases, the blood loss was greater than 50 percent, well past the level the medical establishment considered the most severe, known as "Class IV" shock.

Indeed, the loss of blood was akin to that of the patients I saw in the shock trauma unit in Baltimore. Yet, as Bell noted, for some unknown reason ME patients weren't dying in a matter of hours from organ failure—even if their blood loss was as severe.

‍"We don't see that in ME," Bell told me. "Low blood volume happens very subtly. Somehow, there must be a compensation, because it's not recognized as shock. But it is shock."

‍Whatever the compensatory mechanism, it's powerful. Bell noted that a trauma victim with a blood volume shortage of two liters would die, but ME patients with the same shortage do not die, at least not immediately, though their physical suffering is profound.

‍"In shock patients," Bell continued, "one sees all those things that we associate with ME. Cognitive difficulty, extreme fatigue, confusion, ashen complexion and their pulse leaping upward if they try to stand--the whole clinical picture. This also goes hand in hand with orthostatic hypotension."

Bell likes to cite an anecdote about an astronaut who lost about 15 percent of her blood volume on a space flight. Whisked to a podium to speak after landing, the astronaut collapsed, unable to stand upright as gravity pulled even more blood away from her brain to her legs.

When Bell sought him out, David Streeten was an emeritus professor of medicine at the State University of New York Upstate Medical University in Syracuse. Streeten’s authoritative monograph, Orthostatic Disorders of the Circulation: Mechanisms, Manifestations and Treatment (Plenum Medical, 1986) continues to be considered a classic work on the topic. Bell came to admire Streeten enormously. Unfortunately, Streeten died in 2000, just two years after the collaborators’ first paper on low blood volume in ME was published. He was seventy-nine. In an obituary about Streeten, published in the Journal of Clinical Endocrinology & Metabolism on February 1, 2001, the authors wrote, “(Streeten was) a world authority on abnormal postural effects on blood pressure.”

“[Streeten] called the symptom ‘delayed orthostatic hypotension’ in (ME) patients,” Bell remembers. “He [did so] because in ME patients, it wasn’t a sudden thing—as if you stood up and immediately fell down. For Streeten, it was the chronicity of the symptom and the fact that it didn’t happen all at once.”

Together, Bell and Streeten published a paper called “Circulating Blood Volume in Chronic Fatigue Syndrome” in the Journal of Chronic Fatigue Syndrome in 1998.* By any standard, it’s fair to say the majority of patients in this study were suffering from blood loss that put them in the category of shock—or, to borrow Bell’s phrase, “persistent shock.”

Medicine has long staged hypovolemia into four classes. Class IV, “severe,” is reserved for a blood loss greater than 40 percent. One patient in Bell and Streeten’s study had a red cell mass that was just 46 percent of her predicted normal, less than half of normal. The majority of patients, sixteen of nineteen, had significantly reduced red blood cell volumes that were "quite striking," Bell and Streeten wrote.

‍They evaluated blood volume by measuring red blood cells, which typically comprise fifty-five percent of blood volume. They also measured plasma, the liquid portion of the blood that remains when cells are removed.

Given the financial limitations that perennially beset ME research, theirs was a pilot study, although one with profound implications. Sixteen of the nineteen patients had a reduced red blood cell mass. Eleven of the nineteen had abnormally low plasma volumes. Twelve patients were found to have subnormal “total circulating blood volume,” which includes red blood cells, white blood cells, and plasma.

They concluded, “The high prevalence and frequent severity of the low RBC (red blood cell) mass suggest that this abnormality might contribute to the symptoms of CFS by reducing the oxygen-carrying power of the blood reaching the brain in many of these patients.” (Italics added)

In another experiment, Bell and Streeten encased ME sufferers in military anti-shock trousers (MAST), inflatable pants that work by compressing the lower limbs and pushing blood toward the upper body and brain in an effort to prevent shock. MAST pants were invented during the Vietnam War and initially used to help wounded soldiers survive what could have been fatal shock from blood loss during transport to surgical units. Bell and Streeten’s hypothesis was that if blood could be pushed to the brain in ME sufferers by using MAST pants just as in a wartime rescue, the symptoms of orthostatic hypotension--tumbling blood pressure, dizziness, extreme fatigue--might be reversed.

The doctors reported that improvement in all ME symptoms, including sudden-onset mental clarity, was immediate when patients donned MAST trousers. Nevertheless, the MAST study was a proof-of-concept exercise. Wearing inflatable pants, which feel like a lower body blood-pressure cuff, for any reason other than transport to a trauma unit is hardly practical, of course. Let it not go unreported, however, that one of Bell's patients bought a pair so she could stand at her sink and wash dishes.

‍Intriguingly, although Bell and Streeten discovered that a majority of patients they studied had blood volumes as low or lower than fifty percent of normal, there existed a dramatic demarcation between genders that has never been published. Blood loss in women greatly exceeded blood loss in men.

‍"Women's blood loss was twice as severe as men's," Bell said. "All patients had a loss of blood, but women were twice as bad. I have no idea why, but it's a very important point--that women have the blood loss much more than men."

‍Certainly, some clinicians have observed--including Bell and another longtime ME expert, Paul Cheney (d. 2021), who evaluated thousands of patients--that women with ME tend to be more ill than men with the disease. According to Cheney, women were also significantly less likely to recover. Better known is the fact that the ratio of women to men with ME appears to be somewhere between four or possibly five to one.

‍Another point of demarcation between genders and severity of illness is the fact that in those men Bell tested, the most severely ill did not appear to suffer from low blood volume at all. The finding remains anecdotal but obviously worth exploring.

‍"The correlation between low blood volume and degree of illness is not clear, it's not linear," Bell said. "A perfect low blood volume study would compare men and women of varying severities of illness and would have a number of participants. You would need controls to see whether the length of illness was a factor. Let's say you had one hundred patients and ten were almost recovered, would their blood volume be back to normal or still really bad? Does the blood volume vary with the severity of the illness? And is it a predictor of normality? Does blood volume predict recovery? If it went back to normal at some point in the disease, does the patient recover?"

‍A large study like the one Bell described, he added, might turn heads in the scientific community.

‍"If there were a correlation between blood volume and recovery," Bell said, "That would really jump-start the research on blood volume."

‍Unfortunately, Bell continued, people hear about low blood volume in ME and are nonplused.

‍"They think, what's the big deal? But at a certain point of low blood volume, you're having a form of shock."

‍Severe hypovolemia, or shock, in ME provides compelling hypotheses not only about numerous pathological symptoms but about possible mechanisms of death. We have heard about patients relying on gastric feeding tubes or PIIC lines to sustain their lives or, when these routes of sustenance fail, starving to death, all because they have lost the ability to swallow. Inability to swallow is an autonomic or neurologic sign, an involuntary response to brain damage. Could the source of that damage be ischemic hypovolemia?

“If you look at hypovolemia, death is considered as low blood flow to the brain,” Bell says, “If you have a diminished blood supply to the brain, I think it may have an effect on the ability to swallow.”

Blood volume may be an important measurement in cases where patients are having autonomic symptoms such as an inability to chew or swallow. Perhaps all ME deaths in which starvation is the endpoint should be investigated for brain damage due to shock.

Low blood volume also makes blood thicker, or more viscous, than normal. Instances of cardiac and thrombotic or stroke-related maladies experienced by ME patients may be hypothesized as resulting from unusually thick blood due to hypovolemia.

Bell noted that infectious agents, too, can cause “infective shock,” which may follow on the heels of sepsis. In sepsis an infection spirals out of control, resulting in a massive inflammatory response. Infective shock is also known as “septic shock.”

“Any severe infection can cause septic shock,” Bell said. “You get an overwhelming infection, and the body shuts down and you go into septic shock.”

In such cases blood pressure plunges and vital organs may be damaged—most seriously, the brain. Organs are deprived of oxygenated blood just as they are in hemorrhagic shock.

In septic shock, the mechanism of blood loss is primarily due to a high rate of capillary leak, called a “tell-tale signal” of septic shock by one expert. During capillary leak, a syndrome in its own right, proteins in the blood seep through weakened capillaries from the intravascular system into the “interstitial spaces” in the body. The latter are defined as the “small, narrow spaces between tissues or parts of an organ.”

In ME, as in septic shock, is the blood leaking into the interstitial spaces in the body? Bell believes it’s a possibility.

“The capillaries may be infected,” Bell postulated.

“[A causative pathogen] has never been shown in [ME], but it’s probable,” Bell added. “If [ME] is an infection, then it could be a form of septic shock. And if a person has low blood volume and fifty percent of their blood is not getting to their brain, they will have septic shock persistently—because the blood is not getting where it’s needed.”

“This disease could be a form of persistent septic shock—if it’s an infection.”

A notion that ME patients might be in a persistent, if unrecognized, state of shock—meaning they do not have enough blood circulating to their tissues and vital organs because it is leaking through their capillaries into the interstitial space between cells—seems plausible. Certainly, Bell’s research in the late 1990's on low blood volume will resonate with any ME patient who has ever read the following on their radiology reports: “significant hypoperfusion in both hemispheres,” (reduced blood flow to the brain) and/or “diminished gray” and/or “diminished white matter.”

‍"Loss of brain tissue could be a result of cell death due to hypoxia (lack of oxygen)," Bell said. "Potentially, all the neurological symptoms of ME are all due to hypoxia."

Abstract from Bell's and Streeten's 1998 "Circulating Blood Volume in Chronic Fatigue Syndrome:” Chronic fatigue syndrome (CFS) is an illness associated with severe activity limitation and a characteristic pattern of symptoms despite a relatively normal physical examination and routine laboratory evaluation. The recent description of delayed orthostatic hypotension in patients with CFS, and previous findings of reduced red blood cell (RBC) mass in other patients with orthostatic hypotension not known to have CFS, led us to measure RBC mass and plasma volume in 19 individuals (15 female, four male) with well characterized, severe CFS. RBC mass was found to be significantly reduced (p < 0.001) below the published normal range in the 16 women, being subnormal in 15 (93.8%) of them as well as in two of the four men. Plasma volume was subnormal in 10 (52.6%) patients and total blood volume was below normal in 12 (63.2%), The high prevalence and frequent severity of the low RBC mass suggest that this abnormality might contribute to the symptoms of CFS by reducing the oxygen-carrying power of the blood reaching the brain in many of these patients.

‍*The Journal of Chronic Fatigue Syndrome was published by Taylor & Francis from 1995 to 2007.

Next up: An important 1987 discovery may explain low blood volume in ME. Plus, the fate of a commercial test that measures blood volume.

If you find my posts helpful to you, please consider helping to support me with your paid subscription. Just $5 a month helps to support me and allows me to keep reporting on ME exclusively.