Hypothermic Cardiac Arrest Pt1
In this first episode we're going to look at the Physiology involved in hypothermic cardiac arrest, how patients will likely present and what we can do to assess the degree of hypothermia. In the second half We’ll look at management of hypothermic OOHCA, the modifications to guidance, why these occur and what steps we can take and drill to ensure a slickly run arrest.
Causes:
We first need to look at the cause of hypothermia. The most obvious and dramatic is primary hypothermia. This is external exposure and environmental factors that have contributed to a decrease in body temperature. Increasingly this is being seen in the elderly who have notoriously poor thermoregulation anyway, but who are being required to ration their central heating and electricity usage because of rising energy prices.[1]
In addition to this, primary hypothermia deaths are likely in rough sleepers and those who have been exposed to cold water.
Sea temperatures average 6 – 10°C in the winter time, cold water emersion means the body loses heat 2- 5 times faster than it would in air as water is 25 times more conductive of thermal energy [2]. This can cause severe hypothermia and unconsciousness in as little as 30 minutes. [3]
Secondary hypothermia is decreased body temp cause by an internal organic factor. Most common for us to encounter is “cold sepsis” or hypothyroidism, but there are a variety of conditions that can cause impaired thermo regulation.
Recognition:
Recognition of hypothermia is pretty simple, out of a group of people you look for the one that looks like a highly caffeinated smurff. (blue and shaking.)
However what can be tricky is judging how hypothermic someone is. Obviously numerical values are simple to categorise patients and many of us will have been taught under 35°C is mild hypothemia, under 32 is moderate and so on. How ever the challenge pre-hospitally can lie in accurately measuring this temperature.
The standard method of temperature management in the UK ambulance service is tympanic measurement. Whilst most of the research out there is fairly accepting that they accurately report core temperature (or with in a reasonable degree of accuracy) in warm and pyrexic patients, in hypothermia their accuracy is someone dubious.
There Is no clear cut research detailing their accuracy in profoundly cold patients compared to an internal measuring device and manufacturers openly detail that the devices will not measure below 32°C [4]. They are also profoundly inaccurate in wet ears. Not the end of the world, as a good deal of common sense will tell you if you patient is cold, however as we will cover in the second episode a good deal of modifications in cardiac arrest are affected by numerical temperature values.
How then can we categorise hypothermic patients when our thermometer is not entirely reliable. The Swiss staging system is something that can assist us. This is a set of clinical criteria that are suggestive of a correlating internal body temperature
Its worth noting however that the accuracy of the system is poorly evidenced with one recent study stating that up to 50% of patients could be incorrectly categorised based on presenting symptoms. [5] the system is still widely accepted however as hypothermia is a section of medicine that appears to be heavy in expert opinion and light in evidence to support it. I shall discuss this system and its possible applications further in the second part
Presentation and Physiology: The road to Hypothermic cardiac arrest
Typically the cause of a hypothermic cardiac arrest is going to be primary hypothermia. In these cases the body will go through a predictable set of stages before reaching cardiac arrest.
Initially the body does a pretty good job of trying to maintain homeostasis. This is primarily through vasoconstriction to limit the heat lost through skin surface area. Vasoconstriction occurs when peripheral skin temperature reaches
35°C and is maximal on skin temperature reaching 31°C [2]. This can be negatively affected in certain circumstances. Ingestion of alcohol for example which is vasodilator will impede the ability of the body to vasoconstrict, and increase the amount of heat lost initially.
Older patients (over 60) also have this homeostatic factor reduced due to a poor ability to vasoconstrict and poor production and synthesis of the neurotransmitters involved in this response.[2]
This vasoconstrictive response is thought to be responsible for the occurance of cold diauresis. The movement of blood from the peripheries to the central vasculature and the resultant increase of arterial pressure, stimulates the kidneys to process more fluid. This is why the keen skiiers among you might find the Austrian mountains makes you pee a lot (that and the gluwein).
This is important to bare in mind when we come to discuss fluid resuscitation in the 2nd half of this podcast, as theres the potential that these patients may be hypovolaemic and have electrolyte abnormalities. [6]
Once core temperature falls below 35°C the body begins thermogenesis, increasing cellular metabolism to create heat and begins unconscious behavioural movements (fidgeting) and involuntary movements (shivering). This grows more intense as core temperature drops until around 31°C where shivering stops.[2]
During this time as core body temperature falls the patient will experience a significant reduction in motor function. A combination of numbed sensation and distal tissue hypoxia means that fine motor function becomes nearly impossible. Mental function will also begin to deteriorate, initially with mild confusion and slurred speech but eventually progressing to reduced GCS and eventually unconsciousness.
As core body temperature falls below 32°C cardiac instability becomes a risk. Initially Hypothermic patients are likely to present with a sinus bradycardia. This is due to decreased depolarisation of the SA node. Its worth baring in mind that is this is not a vagally induced bradycardia, atropine will bare no benefit. [7] As we will discuss in the 2nd half rewarming is the best anti-arythmic in this case.
In addition to this the patient may present with Osbourne or J-Waves on their ECG. This is due to a difference in electrophysiology of the Peri and Epicardium affecting repolarisation. (Note, there are a multitude of causes for J-Waves on the ECG, hypothermia is just one of these). [8]
Classically Osbourne waves were regarded as a warning sign for impending VF. However there is poor evidence to support this claim and indeed evidence to suggest no correlation in the cases of hypothermia.[8]
Further drops in core temperature will worsen cardiac conduction and it is quite common for patients to develop either AF and / or junctional escape rhythms when core temperature falls under 32°C. [9]
Just prior to unconsciousness certain survival instincts can begin to present. In between 25 – 50% of terminal hypothermic cases “paradoxical undressing” has occurred. This is as it sounds where just prior to death patients have removed some or all of their clothes. It’s thought this is due to a massive vasodilatory event. As the Myothelium and other muscles constricting blood vessels fatigue they “give in” and as blood returns to the peripheries this makes patients feel as though they are burning.[11] [12] (isn’t that just cruel poetry, you freeze to death but feel as though you’re on fire… best of both worlds).
I mention this not only because it is a fascinating phenomenon, but because it is worth bearing in mind as rescuers have been sent down the wrong track in the past thinking patients have been sexually assaulted or murdered.
Another behaviour which can occur in the pre-terminal stages of hypothermia is “burrowing phenomenon”. A Swedish review of police reports noted how in many deaths due to hypothermia, the deceased were found in small spaces, under beds and in closets.
It’s thought that as the brain suffers from hypoperfusion and begins shutting down an evolutionary survival instinct is triggered in these preterminal hypothermic patients; leading them to seek small spaces much like hibernating animals.[10]
A Hypothermic cardiac arrest patient is likely to present in an initial rhythm of either VF or a Low flow PEA. VF occurs due to an R on T phenomena (or Phase 2 re-entry). Due to the slow conductivity of the heart, a depolarisation wave can occur at the same time the ventricles are in a repolarisation phase [13]. This causes the cells to fibrillate.
Hopefully that has been a useful if not interesting summary of hypothermia. In the next episode we will discuss management of hypothermic OOHCA and the modifications we should be making.
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