Updated: Oct 7, 2022
Shivering is a very common occurrence during Targeted Temperature Management after cardiac arrest. Shivering increases metabolic rate and oxygen consumption and makes it difficult to achieve and maintain target temperature. Therefore, combating shivering is an important goal of treatment when applying TTM.
The mechanism of shivering includes the activation of cutaneous cool receptors that send sensory signals to the preoptic area of the hypothalamus (POA). POA serves as an essential brain region to coordinate sleep and body temperature. Signals are transmitted from the cool receptors of the skin through the dorsal horn to reach the lateral parabrachial nucleus, located at the junction of the midbrain and pons. From this nucleus, the GABA neurons in the median preoptic area are activated, which leads to the inhibition of the GABAergic projection neurons and the disinhibition of dorsomedial hypothalamus neurons leading to the activation of neurons in the rostral raphe pallidus nucleus. This nucleus activates the somatomotor output from ventral horn neurons, causing shivering. We suggest this article for a more in-depth understanding of the central efferent pathways for cold-defensive and febrile shivering.
Interventions to prevent shivering should be started prior to the initiation of therapeutic hypothermia protocol and prior to any attempt to lower the patient's core temperature. These interventions include nonpharmacological methods and pharmacological treatments. Numerous studies and protocols have shown that effective control of shivering can be achieved without over-sedation or paralysis. The Columbia anti-shivering protocol was tested in this study.
Cutaneous counterwarming is a non pharmacological method that uses forced warm air on extremities or face with the aim of inhibiting the cutaneous cool receptors from firing signals through the above described pathway. The core temperature is kept at the TTM target, but the skin surface is warmed to prevent the cold receptors from being sensitized.
Medications that are used to control shivering may work by lowering the shivering threshold in the hypothalamus, inhibiting the neural signals or suppressing the muscular response. Acetaminophen, NSAIDS, and buspirone ( 5-HT agonist) lower the shivering threshold in the hypothalamus and prevent shivering. A number of medications can suppress muscular shivering by inhibiting the neural signals from the brain. These medications include fentanyl, alfentanil, meperidine, dexmedetomidine, propofol, clonidine, and magnesium. Paralyzing agents such as atracurium or cis-atracurium are effective medications in suppressing the muscular response and lead to the cessation of shivering. However, these agents will not inhibit the neural signals from the brain that generated the muscular response. In other words, the brain is still shivering, but it is not manifested at the muscular level. These agents may mask insufficient sedation or the presence of seizure and are preferred to be administered in the presence of an adequate amount of sedation and continuous monitoring of EEG.
As detailed in the above protocol, we recommend starting acetaminophen, buspirone, and magnesium along with cutaneous counterwarming on all patients before starting the hypothermia protocol. The Bedside Shivering Assessment Scale (BSAS) is monitored with a score goal of ≤1. Sedative agents are added in a stepwise based on the BSAS and paralytic agents can be used in step 4 only after adequate sedation is achieved.
Van Zanten, Arthur R. H. MD, PhD; Polderman, Kees H. MD, PhD Blowing hot and cold? Skin counter warming to prevent shivering during therapeutic cooling*, Critical Care Medicine: June 2009 - Volume 37 - Issue 6 - p 2106-2108
Choi HA, Ko SA, et al. Prevention of shivering during therapeutic temperature modulation: The Columbia Anti-Shivering Protocol. Neurocrit Care. 2011