Introduction
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Following the Nielsen study, many hospitals developed two protocols for temperature management after cardiac arrest (33C or 36C). For example, the 36C protocol could be used for patients with contraindications to hypothermia (33C). With ongoing evidence emerging about hypothermia, many hospitals are abandoning their 33C protocols and using 36C for all post-arrest patients. Although this may be old news in some locations, it remains highly controversial in the USA. We present our opinions below, while recognizing that experts and esteemed institutions lie on both sides of this debate.
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Reason #10 Focusing on depth of hypothermia may distract from the importance of duration of temperature management.
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Most of the benefit of temperature management is probably due to avoidance of fever. Thus, the duration of temperature management may be more important than the exact target temperature. Unfortunately, excessive focus on the target temperature often overshadows the importance of the duration of temperature management. In the past we have seen patients cooled to 33C and rewarmed over a 36-hour period, at which point the cooling pads were removed with a subsequent fever. In efforts to maximize the “dose” of temperature management, it may be more beneficial to extend the duration of temperature management rather than lowering the target temperature.
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Reason #9 Therapeutic hypothermia increases the risk of infection.
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Hypothermia suppresses immune function and is associated with increased rates of bacterial infections, particularly pneumonia (Kuchena 2014). This is a real problem, with pneumonia rates as high as 50% in some studies. Although pneumonia has not been linked to mortality or neurologic outcomes, it may prolong the duration of mechanical ventilation and increase ICU length of stay.
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Reason #8 Therapeutic hypothermia may aggravate Torsade de Pointes.
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Although uncommon, some patients present with cardiac arrest due to Torsade de Pointes (TdP). Hypothermia causes bradycardia, QTc prolongation, hypokalemia, and hypomagnesaemia – all of which may promote the recurrence of TdP. We have seen cases where TdP seemed to be aggravated by hypothermia, and this has also been reported in the literature (Huang 2006, Matsuhashi 2010). It is difficult to avoid cooling patients with TdP, because the diagnosis of TdP may not be obvious initially and most hypothermia protocols are silent on this issue.
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Reason #7 Therapeutic hypothermia may compromise hemodynamics.
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Therapeutic hypothermia may cause bradycardia and reduced contractility, causing reduced cardiac output and blood pressure (e.g. table below from the Nielsen study below). Although this can usually be compensated for with vasopressors, it leaves patients with less physiologic reserve if their hemodynamics should deteriorate further. Occasionally patients with refractory shock may require early rewarming.
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The effect of hypotension on cerebral perfusion pressure is concerning. Although hypothermia reduces intracranial pressure, it is likely that many of these patients still suffer from elevated intracranial pressures (ICP). The combination of hypotension and elevated ICP could produce very low cerebral perfusion pressures (CPP). Although hypothermia protocols often prescribe elevated blood pressure targets empirically to support the cerebral perfusion pressure, in practice this is often difficult to achieve.
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Recently a post hoc analysis of the Nielsen trial by Annborn et al. showed a trend towards increased mortality among patients who were cooled to 33C in the presence of shock (figure below). In summary, hypothermia worsens hemodynamics and this could lead to worse outcomes, particularly among patients with shock.
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Recently a post hoc analysis of the Nielsen trial by Annborn et al. showed a trend towards increased mortality among patients who were cooled to 33C in the presence of shock (figure below). In summary, hypothermia worsens hemodynamics and this could lead to worse outcomes, particularly among patients with shock.
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Reason #6 Therapeutic Hypothermia delays accurate neuroprognostication.
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The process of cooling to 33C impairs our ability to accurately neuroprognosticate in nearly every way. Sedatives and analgesics required to facilitate hypothermia and suppress shivering can delay the resumption of consciousness, confounding clinical neuroprognostication and prolonging the duration of mechanical ventilation. Most other diagnostic tools are affected by cooling as well. For example, somatosensory evoked potentials can be suppressed and have been shown in multiple case reports to return to normal several days after rewarming. Biomarkers, particularly neuron specific enolase, are probably attenuated with hypothermia and correlate poorly with outcome in this setting. Delays in neuroprognostication may place an excessive psychological stress on families forced to wait longer to see if their loved one will awaken.
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Reason #5 Withdrawal of care following induced hypothermia can be ethically problematic.
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Having embarked on a course of therapy which temporarily incapacitates the patient, there is an ethical obligation to complete the treatment course. For example, a surgeon would not withdraw care in the middle of an operation. Hypothermia to 33C may delay resumption of consciousness for some days. For example, Mulder et al. 2014 reported that among patients treated with hypothermia who had a good neurologic outcome, 32% required over 72 hours to awaken. If family members wish to withdraw care in the interim, this is ethically problematic. It is possible that our interventionof cooling the patient to 33C could deprive the patient of the opportunity to wake up prior to terminal extubation.
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Reason #4 Cognitive Offloading: Reducing focus on therapeutic hypothermia may allow us to focus more on other aspects of patient care.
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Patients who have cardiac arrest are diverse and extremely ill. These patients may have a variety of underlying processes, including myocardial ischemia, pulmonary embolism, asthma, septic shock, etc. The presence of multiple protocols (33C and 36C) as well as the complexity of the 33C protocol may cause clinicians to focus extensively on the approach to temperature management. This may distract clinicians from other issues, such as diagnosing and managing the underlying cause of cardiac arrest.
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Reason #3 We don't fully understand what happens to the body at 33C.
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Every enzyme in the body is evolutionarily optimized to function best around normal body temperature. Hypothermia will therefore simultaneously affect every metabolic and signaling pathway. Harmful processes will be slowed down, but so will restorative and beneficial processes. The net effect is unclear. The consequence of slowing down every enzyme in the human body defies prediction or understanding.
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Reason #2 Therapeutic hypothermia to 33C may be less effective in real-world settings than in clinical trials.
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Cooling to 33C is a very complex and context-dependent intervention. Its efficacy and safety depend on how well it is performed. For example, in a small community hospital induction of hypothermia may consist of packing a patient in ice before loading them in an ambulance to transfer to a referral center. Alternatively, at a regional referral ICU, induction of hypothermia may be accomplished with sophisticated temperature-management devices, precise electrolyte control, and careful attention to hemodynamics and cardiac rhythm.
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The studies demonstrating mortality benefit from cooling to 33C (HACA and Bernard et al.) were both performed at top research hospitals on patients presenting initially through the emergency department. It is unclear how this may generalize to other hospitals, or to patients who are cooled prior to inter-hospital transfer. Kim 2014showed that prehospital cooling caused higher rates of re-arrest in the field, suggesting a potential danger if cooling is not done correctly. Morrison et al. just released a study showing that a quality improvement project which increased utilization of cooling to 33C correlated with a trend towards reduced survival to hospital discharge. These studies raise questions about how safe cooling to 33C is outside of major clinical trials. Since cooling to 36C is easier and safer, it probably performs better across various settings.
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Reason #1 The main reason that 33C is still being used may be status quo bias.
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Currently there is no clinical evidence that 33C is superior to 36C. Compared to 36C, 33C has a variety of additional risks and is more technically challenging. The continued use of cooling to 33C is an example of status quo bias (discussed further by the Medical Evidence Blog). There is a tendency to stick with established treatments, the tried-and-true. We have worked hard for years establishing protocols and expertise in cooling patients to 33C. When patients did well we attributed it to the hypothermia, but when they did poorly we said “well, they would have done poorly anyway” (circular logic reinforcing the status quo). It is hard to challenge this status quo that we have strived so hard to achieve.
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Imagine, for a moment, how history might have been different if the Nielsen, HACA, and Bernard studies had all been published simultaneously in 2002. The accompanying editorial surely would have concluded that avoidance of fever was the critical intervention. It is difficult to imagine that there would have been any enthusiasm for cooling to 33C in that scenario. Thus, our current practice is shaped more by inertia than by an unbiased accounting of all available evidence.
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Lack of status quo bias might also help explain why every center involved in the Nielsen trial immediately moved to a 36C target after the conclusion of the trial (Nielsen 2015). During the trial, the status quo of cooling every patient to 33C was inadvertently destroyed. This might have freed these centers to make a decision without bias based on prior practice patterns.
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Conclusions
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The initial studies which launched therapeutic hypothermia (the HACA trial and Bernard et al.) did for post-arrest patients what the Rivers trial did for septic patients. Instead of being ignored for a few days on the ventilator, post-arrest patients became the focus of intensive multidisciplinary management with a focus on preventing secondary brain injury. We have seen this aggressive management approach improve outcomes.
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Over time, our approach to critical care has evolved. The PROCESS, ARISE, and PROMISE trials have informed us that many components of the Rivers protocol are unnecessary. Similarly, the Nielsen study has informed us that we can obtain the same results while targeting a more physiologic temperature.
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We remain steadfast in our dedication to immediate, precise, and intensive resuscitation of post-arrest patients. We are not suggesting a reduction in the energy invested in these patients, but rather that such energy may be invested more wisely in other aspects of patient care. Rather than focusing excessively on the target temperature, it may be more important to thoroughly investigate and manage the etiology of the arrest. It is possible that the duration of temperature management could be more important than the actual target temperature, but this aspect often receives less attention. Meanwhile impeccable supportive care must be maintained with close attention to all organ systems.
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Coauthored with Ryan Clouser (@neurocritguy), a colleague with expertise and board certification in Neurocritical Care. This post is based on a presentation by Dr. Clouser at Medicine Grand Rounds.
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Disclaimer: These are our personal opinions and do not reflect our employers or institution (full disclaimers here).
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Conflicts of interest: None.
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Conflicts of interest: None.
Josh is the creator of PulmCrit.org. He is an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont.
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Good questions: (1) In-hospital arrests are a different population of patients compared to out-of-hospital arrests. For example, out-of-hospital arrest may occur in people who are otherwise doing OK, versus in-hospital arrest which may occur in patients with multiple active disease processes who are deteriorating despite active medical therapy. (2) Patients with VT/VF often have immediate-onset cardiac arrest without hypoxemia or hypoperfusion prior to the event. In contrast, for example, a patient with asthma and respiratory arrest with subsequent cardiac arrest has a prolonged period of hypoxemia and hypoperfusion occuring even before the cardiac arrest itself. (3) When we were using… Read more »
Another excellent post as usual. As a future intensivist I always look forward to your thoughtful posts.Can you comment on the fact that cooling seemed to help in previous trials more so for out-of-hospital arrest and not for in-hospital arrest, I would suppose the time it takes to reach the patient for CPR is something which adds another layer of complexity to this issue, and why just VF/VT and not asystole/PEA?Also with respect to keeping pts at 36 degrees, these pts are still undergoing a cooling protocol-their temperature is just different than the traditional 33, but at times they still… Read more »
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My brother in law is currently undergoing this cooling procedure at U of M Hospital in Michigan. We pray it works, he was found with no pulse laying in a house, the chest compressions caused bleeding around his heart and they put in a drainage tube to relieve the pressure. They are now cooling him down. We will know in a matter of days what the outcome is for his brain activity. We are praying he has an encounter with Jesus while he is in the coma.