INTRODUCTION: Definition, Parameters & Methodologies of Induction and Maintenance
Targeted temperature management (TTM), also referred to as iatrogenically induced hypothermia, is a deliberate core body temperature reduction below normothermia devised to assist in the preservation of patient neurological function after cardiac arrest (CA) (Kasper, 2015; Oh et al., 2015).
Several means of cooling the core body temperature may be employed including both internal and external. These include temperature depression through cold normal saline infusions [internally], cold packs and blankets [externally] as well as other methods to temporarily lower patient body temperature to a controlled steady range (Oh, 2015).
The term TTM may be applied in a literal sense to any desired therapeutic temperature range as defined by the term “targeted,” including normo/hypo/hyperthermic methods of patient management. However, clinically, the term TTM, particularly in the context of CA, generally implies thermoregulatory temperature depression and maintenance, or induced hypothermia.
The current standard recommendations for therapeutic hypothermia are induction <12hrs post-return of spontaneous circulation (post-ROSC), target temperature between 32degC – 36degC for a duration of 12-24hrs (Kasper, 2015; Callaway et al., 2015).
Therefore, for the scope of this article, TTM will be defined by the suggested guidelines’ target temperatures of 32degC – 36degC.
THERAPEUTIC MECHANISM
As a thermoregulatory intervention, it has been theorized TTM therapy addresses the decrease in cerebral perfusion by decreasing the brains metabolic requirement (Sahuquillo, 2007; Kasper, 2015; Li, 2017). The physiology underlying TTMs therapeutic effects isn’t fully understood, currently. There are however several theories regarding plausible mechanisms to explain the efficaciousness of the novel therapy.
A study by Li, J et al. (2017) revealed TTM was effective in helping mitigate the degree of cerebral edema in pigs by way of blood brain barrier tight junction attenuation (Li et al., 2017). In addition, several other neuroprotective functions were cited in their study including decreases in inflammatory cytokine release, brain metabolism, mitochondrial membrane permeability and oxidative stress (Li, 2017).
Generally, as observed in most living systems, a decrease in cell temperature leads to decreases in cellular metabolism. In turn, requirements in cellular energy and nutrients are decreased. A decrease in demand for respiratory oxygen and overall metabolic requirements, in a decreased perfusion state, serves as a significant alleviation of burden for all cells of the body- particularly for high demanding organs such as the brain.
ADVERSE EFFECTS & CONTRAINDICATIONS
TTM serves as a disruption in homeostasis, and has several effects on human physiology that require careful patient monitoring. These effects include depressions in platelet function and immune system responses (Pang et al., 2016).
As such, there are several co-morbidities which may be contraindications of treatment. Patients with known platelet pathologies, of quantity and/or quality, candidacies must be carefully considered and require close monitoring by practitioners to avoid bleeding complications. As well, immunocompromised patients may be at higher risk of nosocomial infection development as a result of TTM.
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LITERATURE CITED
Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L. 1., Jameson, J. L., & Loscalzo, J. (2015). Harrison’s principles of internal medicine (19th edition.). New York: McGraw Hill Education.
Oh, S. H., Oh, J. S., Kim, Y. M., Park, K. N., Choi, S. P., Kim, G. W., … Korean Hypothermia Network Investigators (2015). An observational study of surface versus endovascular cooling techniques in cardiac arrest patients: a propensity-matched analysis. Critical care (London, England), 19(1), 85. doi:10.1186/s13054-015-0819-7.
Callaway, C. W., Donnino, M. W., Fink, E. L., Geocadin, R. G., Golan, E., Kern, K. B., … Zimmerman, J. L. (2015). Part 8: Post-Cardiac Arrest Care: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 132(18 Suppl 2), S465–S482. doi:10.1161/CIR.0000000000000262.
Li, J., Li, C., Yuan, W., Wu, J., Li, J., Li, Z., & Zhao, Y. (2017). Mild hypothermia alleviates brain oedema and blood-brain barrier disruption by attenuating tight junction and adherens junction breakdown in a swine model of cardiopulmonary resuscitation. PloS one, 12(3), e0174596. doi:10.1371/journal.pone.0174596.
Sahuquillo J, Vilalta A. (2007). Cooling the injured brain: how does moderate hypothermia influence the pathophysiology of traumatic brain injury. Current Pharmaceutical Design. 13(22), 2310-22.
Pang, P. Y., Wee, G. H., Hoo, A. E., Sheriff, I. M., Lim, S. L., Tan, T. E., … Lim, C. H. (2016). Therapeutic hypothermia in adult patients receiving extracorporeal life support: early results of a randomized controlled study. Journal of cardiothoracic surgery, 11, 43. doi:10.1186/s13019-016-0437-8
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