Induced Therapeutic Hypothermia

For more than a decade, Targeted Temperature Management (TTM) has been the recommended treatment modality in adult comatose patients following out-of-hospital cardiac arrest (OHCA)[1] in order to improve survival and neurological outcome by minimizing brain injuries due to anoxia and reperfusion injury.

Purpose: The purpose of this speech is to educate and inform my audience of the risks inherent from unintended hypothermia. I’m eager to alert perioperative staff of the potential dangers as well as the preventative measures that can be taken in order to avoid complications associated with unintended hypothermia. My central idea is hypothermia management saves lives.

Cryotherapy is the use of extreme cold in surgery or other medical treatments. Cryotherapy unlike other methods of treatment works in a very specific way in order to stimulate the brain. First a person is put in to The Cryo-sauna, this is a simple shower like machine that uses the gas form of liquid nitrogen to lower the client 's skin surface temperature by 30-50 degrees Fahrenheit over a period of two-three minutes. The chamber is then cooled using liquid nitrogen but clients are not in direct contact with the gas. The skin reacts to the cold and sends messages to the brain that acts as a stimulant to the regulatory functions of the body. This is important because it then makes the brain scan of all areas that may not be working to

The American Heart Association (2011) states that, "Therapeutic hypothermia is the only intervention demonstrated to improve neurologic recovery after cardiac arrest" (Pp 77). Recommendations range between 32 and 36 degrees centigrade for 12 to 36 hours. Cooling may be achieved through either introduction of cooled, isotonic, non-glucose-containing fluid, or surface cooling interventions like ice packs or cold packs. The AHA states, however, that patient core temperature must be monitored by an esophageal thermometer, a pulmonary artery catheter, or a bladder catheter and that peripheral temperature measurements via axillary, aural, or oral thermometers are inadequate for measuring core temperatures in targeted temperature management. Therefore, while the AHA does recommend initiation of therapeutic hypothermia by EMS personnel in certain situations, agencies must carry--and be trained in the use of--equipment to adequately measure the patient 's core temperature. Further, the AHA states that therapeutic hypothermia results in increased neurologic function post-cardiac-arrest but does not identify a timeframe for initiation for these protocols, let alone explore whether or not initiation of post-cardiac-arrest targeted temperature management by EMS influences patient outcomes.

Therapeutic hypothermia, also called targeted temperature management, is a procedure that lowers the body's temperature in order to treat a heart that has suddenly stopped working (cardiac arrest). This procedure is used in emergency situations. During cardiac arrest, the brain cannot get enough oxygen. The brain also starts to swell, which can damage or kill brain cells. Therapeutic hypothermia helps reduce swelling in the brain. It also slows down the body's metabolism and allows the heart and brain to recover.

This article is a example of a foundation of knowledge on the topic of therapeutic hypothermia. Gardner & MacDonald discuss that the typical post cardiac arrest patient does not survive or will recover with severe neurologic deficits as a result of ischemic brain injury from lack of blood flow to the brain (2013). The process of brain death is examined as well as the damange that occurs with reperfusion after ROSC. Damage particularly to the cerebral cortex, cerebellum and hypothalamus can leave the patient in a comatose state if revived (Gardner & MacDonald, 2013). This article is particuarlly valuable as it explains on a physiological level how TH protects the brain from reperfusion injury and improves neurologic outcomes and survivability. The article defends that TH is the best practice for preventing further neurologic damage after ROSC and provides a clinical example. The clinical example recounts a case in which a patient suffered an out of hospital cardiac arrest. Upon admission to the ICU the therapeutic hypothermia protocol was initiated and the patient was cooled below 35 degrees celcius for 24 hours. After rewarming the patient regained consciousness and within ten days was discharged from the hospital with normal neurologic function and as a survivor (Gardner & MacDonald,

A Glasgow Coma Score of 8 or less also is an indication that the patient will need to be intubated soon. Once the tube is placed the ventilation may be useful in controlling the intracranial pressure as an intervention. Hyperventilation is a method used to reduce the carbon dioxide concentration in the vessels causing vasoconstriction which lessens the amount of blood circulating in the brain resulting in a decreased ICP (Zink and McQuillan, 2005). According to Zink and McQuillan, this intervention should only be utilized 24 hours after the initial injury because cerebral blood flow is often reduced at this point and constricting the vessels more may cause ischemia to occur. While using this technique it is important to monitor oxygenation to the brain tissue to assure no irreparable damage is

Treatment of hypothermia focuses on managing and maintaining ABCs, rewarming the patient, correcting dehydration and acidosis, and treating cardiac dysrhythmias.

The aim of the final phase of this therapy is to gradually rewarm the patient to the normal body temperature of 37 °C. Gradual rewarming of the patient is strongly recommended as rewarming the patient too quickly can cause a number of adverse side effects such as a sudden arrhythmia that can cause electrolyte shifts, hypoglycemia, and hypotension. Neuromuscular blockers are often administered in conjunction with rewarming to prevent shivering thermogenesis, which can lead to sudden electrolyte disturbances. An ideal rate of rewarming of 0.15 °C to 0.25 °C per hour is recommended in order to minimize the adverse side effects associated with this phase (Peberdy et al., 2010, S770).

Malignant hypothermia is a disease, caused by a bad reaction of anesthetics. This disease causes an immensely rapid temperature rise and extreme muscle contractions. MH (malignant hypothermia) is passed down through families and inherited by one parent carrying it giving it to the child. “Malignant hyperthermia occurs in 1 in 5,000 to 50,000 instances in which people are given anesthetic gases” (NIH, 2007). Most people aren’t aware that they are prone to this disease/reaction because they have never been under anesthesia drugs, or have never received surgery.

The lack or delay in appropriate treatment for individuals who experience a sudden cardiac arrest has created a major public health disparity. Research into pre-hospital treatment and subsequent implementation has historically seen neglect by the medical and scientific community creating vast differences in survivability of cardiac arrests between demographic groups. In 2010, the American Heart Association and Emergency Cardiovascular Care program developed the 2020 impact goal to reduce death from cardiovascular disease and stroke by 20% and double out-of-hospital cardiac arrest (OHCA) survival rates (http://circ.ahajournals.org/content/121/4/586#sec-1). This has prompted a massive influx of research into the disparities that exist and an

○ Important details include the duration of the anoxic episode prior to initiation of cardiopulmonary resuscitation, and the duration of the cardiopulmonary resuscitation (longer imparts poorer prognosis); as well as the cognitive state of the victim prior to the event

Hypothermia has two main types of causes. It classically occurs from exposure to extreme cold. Commonly this includes alcohol intoxication but may also include low blood sugar, anorexia, and advanced age. Hypothermia may be diagnosed based on either a person's symptoms in the presence of risk factors or by measuring a person's core temperature. One of the lowest documented body temperatures from which someone with accidental hypothermia has survived is in a near-drowning of a 7-year-old girl in Sweden. Survival after more than six hours of CPR has been described. Symptoms of mild hypothermia may be vague, Increased urine production due to cold, mental confusion, and hepatic dysfunction may also be present. Hyperglycemia may be present, as glucose consumption by cells and insulin secretion both decrease, and tissue sensitivity to insulin may be blunted. Sympathetic activation also releases glucose from the liver. In many cases, however, especially in alcoholic patients, hypoglycemia appears to be a more common presentation. Low body temperature results in shivering becoming more violent. Muscle mis-coordination becomes apparent. Movements are slow and labored, accompanied by a stumbling pace and mild confusion, although the person may appear alert. Surface blood

Without early intervention on average 360,000 people out of the hospital succumb to cardiac arrest. “ Cardiac arrest and sudden death account for 60 percent of all deaths from coronary artery disease”,(Bledsoe, Porter, & Cherry, 2011,2007,2004, p. 1229)There are several causes of sudden cardiac arrest. Most are caused by ventricular fibrillation. “During ventricular fibrillation, the ventricles do not beat normally. Instead they quiver rapidly and irregularly.” When this occurs, the heart pumps very little and blood does not get circulated throughout the body. “ Most of the cases found with sudden cardiac death are related to undetected cardiovascular disease.("Sudden Cardiac Death," 2015, para. 2)Sudden cardiac arrest are immediate and drastic that includes sudden collapse, no pulse, not breathing, and loss of consciousness. “Four rhythms produce pulseless cardiac arrest: ventricular fibrillation, rapid ventricular tachycardia, pulseless electrical activity and asystole.”("Circulation ," 2005, p. IV-58)Other signs and symptoms that could occur prior to sudden cardiac arrest, include fatigue,

Furthermore, it can be argued that there may be no point in testing for EEG reactivity since studies had shown that some specific EEG patterns seen in anoxic brain injury following cardiac arrest suggests a poor outcome and these patterns do not react to external stimuli such as in alpha coma (Misra and Kalita 2005; Kaplan and Sutter 2012), generalised burst suppression (Blum and Rutkove 2007; Sandroni, C et al 2014) and status epilepticus (Sandroni, C et al., 2014). However, the specificity of these EEG patterns in the determination of prognosis is low (63%) according to Thenayan et al (2010). They found four patients with malignant EEG pattern recovered awareness. However, evaluation of EEG reactivity has significantly improved prognostification