Thermal Physiology: Clinical Outcomes of Heat Stroke
This article is for those who work or play in extreme temperatures and are curious about why bad things happen when our bodies overheat. We start with a short introduction of heat stroke before describing many of the scientific and medical reasons why heat stroke is so dangerous.
What is heat stroke?
‘Hyperthermia’ describes the state when a person’s internal body core temperature is abnormally high. If high enough, hyperthermia leads to heat stroke. Heat stroke is clinically diagnosed when a person’s core temperature is at least 104oF and they experience central nervous system dysfunction (for example, confusion, dizziness, seizures, or coma).
Heat stroke comes in two distinct categories – exertional heat stroke and classical heat stroke. Both occur because core temperature increases beyond a safe threshold due to an inability to maintain stable internal temperature, but for different reasons.
Classical Heat Stroke
Classical heat stroke, or CHS, is often passive. Even resting, when metabolic heat production is minimized, classical heat stroke occurs if the body cannot keep cool due to environmental heat exposure. It generally requires a relatively hot ambient temperature.
Classical heat stroke most often affects the very young and very old, since these populations have underdeveloped (infants and children) or compromised (elderly, the chronically ill) thermoregulatory systems. CHS often occurs after several hours or days of high heat exposure, such as during heat waves, as the hot environment slowly increases the body’s core temperature.
Two unfortunate episodes of mass classical heat stroke occurred during the Chicago heat wave of 1995 and a widespread heat wave in France during 2003. The week of and following the Chicago heat wave, 465 deaths were certified as heat-related (a likely undercount), while no such deaths occurred the week prior. Over 51% of those who died were at least 75 years old.
The French heat wave was orders of magnitude worse, with 14,800 excess deaths associated with extreme heat between August 1st and 20th. In Paris hospitals alone, deaths spike 138%. These astronomical numbers are partly due to a widespread lack of air conditioning in retirement homes and hospitals in France, a country with a historically temperate climate.
Exertional Heat Stroke
It’s a safe assumption that, by your interest in Qore Performance, you are less susceptible to classical heat stroke. Instead, exertional heat stroke – or EHS – is the heat stroke type you are likely to experience. It is no less dangerous. Exertional heat stroke is most common in young and middle age, healthy adults.
EHS occurs even in relatively cooler environmental conditions. EHS cases have occurred during temperatures below 70oF, especially during periods of intense exertion. The classic example is the Falmouth road race in Massachusetts, famous for the number of heat stroke cases experienced every year. In recent years, an average of 22 runners– fit, competitive contestants who train for this event – are medically treated for heat illness each race.
This is because exertional heat stroke is driven primarily by – as the name suggests - heavy levels of exertion. During exertion, metabolic waste heat is produced that must be dissipated from the working individual (see this Qore Performance article for more). When the rate of metabolic waste heat production exceeds our ability to dump this heat into the surrounding environment, core temperature rises. Unless the working individual takes a break to cool down, this excess heat builds until it triggers heat exhaustion or heat stroke. Because EHS depends so much on the working effort of an individual and factors impacting heat release like occupational or protective clothing, it can occur much more quickly than classical heat stroke – even within the span of a single run race.
Cooked at 104 degrees
The defining symptoms of heat stroke are a body core temperature above 104oF and central nervous system dysfunction, i.e., problems with the brain. This is often characterized by neurological symptoms like confusion, seizures, or coma, and (potentially irreversible) organ damage to the liver, kidneys, intestines, and cardiovascular system.
Brain Damage
According to some researchers, the absolute hottest internal temperature a human body can withstand for at least 45 minutes is somewhere around 107oF, but internal temperature as low as 104oF appear sufficient to trigger irreversible changes to cell protein structures. In other words, above 104oF, some proteins that hold cells together start to denature, i.e., come apart, ultimately leading to cell death. The higher the body temperature, the faster this “melting” happens.
Moreover, the number and rate of cell death increase exponentially the longer core temperature remains elevated. Cellular damage incurred from heat stroke may continue to manifest after a return to normal body temperature as cells continue to die for several days.
At the cell level, the sequence from extreme heat to brain damage is multi-faceted and yet to be fully understood. What is known is the brain is uniquely vulnerable to injury from heat (one doctor goes as far as stating brain cells are “exquisitely sensitive” to high core temperature).
Reasons why the brain is so vulnerable to heat stroke damage extend beyond the direct effects of heat on cellular proteins. During heat stroke, our bodies react with an inflammatory response similar to what we experience during infection. This reaction can damage the blood-brain barrier. Our bloodstream transports waste products to places like our kidneys, so it contains many substances we want to keep away from brain cells. A damaged blood-brain barrier allows leakage from the blood stream, introducing potentially toxic products into the brain and causing swelling.
Gut Reactions
The blood-brain barrier isn’t the only part of the body to “leak” during heat stress. During periods of high core temperature, we maximize blood flow and blood vessel volume at the skin surface to promote cooling. In prioritizing blood flow to the skin, less immediately critical organs in the body receive less blood; among these organs are the intestines.
Reduced blood flow to the gastrointestinal organs increases the permeability of the intestinal lining. This is as bad as it sounds. Things in our intestines, like semi-digested food or the host of various bacteria living in the tract between stomach and colon, do not belong in our bloodstream. Quoting medical Drs. Walter and Carrarettlo on the topic, this “loss of gastrointestinal barrier integrity” allows “gut bacterial translocation” in the body. The result is whole-body inflammation and the introduction of endotoxins creating a sepsis-like reaction leading to a host of physiological challenges and injury.
Kidney & Liver
The kidney and liver organs don’t fare much better during hyperthermia. Oxidative stress is one pathway affecting kidney and liver (among other organs) function. Sparing you most of the medical jargon, heat stroke increases oxidative stress by causing an imbalance in the production of Reactive Oxygen Species, or ROS. This class of molecules, though important, damages cells when not tightly regulated. ROS generated during hyperthermia can “trigger apoptosis pathways”, medical speak for programmed cell death. Essentially, our cells recognize they can’t properly function after heat damage and initiate self-destruction.
The liver, which has a relatively high iron content and a role in oxidative metabolism (using oxygen to generate energy), is especially susceptible to damage from excess ROS. This leads to a cell death pathway known as “ferroptosis” in the liver, increasingly recognized as a marker of heat stroke.
Like the gut, the liver and kidney also contend with a reduced blood flow during hyperthermic conditions. The kidney, which has the leading role in filtering toxins from our blood, gets especially stressed. As discussed above, a hyperthermic person during heat stroke will have a kidney likely confronting excessive amounts of toxins leaking into the blood stream.
During heat stress the kidney has a reduced volume of blood to filter, since the body has prioritized blood flow to the skin for cooling. In many cases, a person experiencing heat stroke is also dehydrated, further reducing blood plasma volume the kidney has to work with. It’s a bit like using a kitchen water filter to suddenly start filtering industrial waste – it’s not likely up to the task!
Heart
The cardiovascular system sits at the center of the body’s attempt to thermoregulate, placing it under extraordinary strain during exertional heat stroke. To meet the simultaneous demands of supplying blood to muscles and brain while also sending as much blood as possible to the skin to dissipate heat, the heart is forced to pump fast and hard, often reaching near-maximal output.
Like other organs, cells in heart tissue can be directly damaged by heat. Complicating the heart’s job, blood pressure often drops, the result of dehydration and blood vessel expansion to accommodate increased flow. The already overworked heart is forced to pump harder to maintain the same flow rate with a reduced supply of blood. Complications of a hot, overworked heart manifest as abnormal heart rhythms, reduced cardiac output, or circulatory collapse – not symptoms conducive to long term health or survival! One of the most common causes of death during heat waves, especially among the elderly, is cardiac arrest – heat stroke generated heart failure.
Heat Stroke Outcomes
The single greatest factor determining a person’s prognosis following heat stroke is the length of time spent with at elevated core temperature. In one of the largest studies of its type, 521 documented cases of exertional heat stroke (primarily in military and athlete cohorts) analyzed by researchers at the Korey Stringer institute determined why some survived, some died, and some had lasting complications.
Of the 521 heat stroke cases considered, 23 were fatal – a 4.41% death rate. In all fatal cases, the heat stroke victim did not receive treatment capable of cooling body core temperature by at least 0.27oF per minute.
A further 117 heat stroke victims, or 22.5% of the cases, survived but experienced medical complications following heat stroke. Rapid cooling intervention was found to be strongly protective, preventing complications and organ damage. Only four cases where rapid cooling was applied resulted in long term damage despite the cooling intervention, while the remaining 113 cases received inadequate or no cooling intervention.
Other studies on exertional heat stroke fatalities are less optimistic. Fatality rates around 27% are sometimes cited. The different fatality rates likely results from the population considered – young, healthy athletes and military members are more likely to survive heat stroke and less likely to have long term complications than an average person.
A large minority of exertional heat stroke victims experience long term complications. A study following the progress of 57 athletes and military members found 19% self-reported some level of central nervous system dysfunction, such as slower thought process and impaired memory, six months following their heat stroke. A year later, these dysfunctions had still not resolved for some.
Post-heat stroke results are usually more encouraging in a military-specific study population. According to a study of military heat stroke cases published in Military Medicine, only 2% of heat strokes resulted in death. This “strikingly low” mortality rate was attributed to military medical practices that aggressively identifies and treats exertional heat stroke.
In the end, the best way to ensure a favorable heat stroke outcome is to not get heat stroke in the first place!
---
About the author: Dr. Erik Patton holds a PhD from Duke University where he conducted research on the challenges rising temperatures pose for military training. An Army veteran, Erik has served in a variety of extreme climates ranging from deserts in the U.S. Southwest and Middle East (120oF) to Arctic conditions in central Alaska (-42oF).