Hypothermia In Post-Cardiac Arrest Patients
Cardiac arrest is the leading cause of debility and unexpected death globally. It can however be managed and patients can gain full recovery if only they get the necessary medical attention expediently. Scientific data collected from numerous researches has proven that elevated temperatures in the brain are the cause of ischemic brain damage in a majority of post cardiac arrest patients. Consequently, studies have revealed that if the temperature of the brain is successfully lowered by induction of mild hypothermia, it mitigates brain damage caused by reperfusion injury following resuscitation.
The induction of mild hypothermia for therapeutic purposes at a temperature of between 28° to 32° Celsius has been practiced in post cardiac arrest patients. Hypothermia has been shown to be effective in ensuring favorable neurological outcomes in the comatose patients who have suffered mild or even massive cardiac arrest. Results from clinical research, dating to as early as the 1950’s confirm the effectiveness of the practice of inducing therapeutic hypothermia in post cardiac arrest to promote favorable neurological outcomes (Bernard, 1996).
The occurrence of cardiac arrest in an out-of-hospital setup is quite common and often leads to unfavorable neurological outcomes. In addition, the inception of induced hypothermia immediately the patient undergoes cardiopulmonary resuscitation is known to diminish the risk of the occurrence of cerebral reperfusion shock. This occurs due to the restoration of the blood flow to the cerebral region following successful cardiopulmonary resuscitation of a patient.
Induction of the cooling of core body temperature following cardiac arrest has also been shown to result in adverse effects in some patients. Ongoing studies have revealed that when hypothermia is induced immediately after the return of spontaneous circulation is associated with a decline in cerebral histological injury in a variety of primate models. It has also been shown to encourage a speedy regain of function after cardiac arrest. However, there is still ongoing research using humans to establish the efficacy, safety and appropriateness of administration of therapeutic hypothermia in regards to ensuring favorable neurologic outcomes (Bernard et al., 2002).
The application of hypothermia is significant only to patients who are eligible for the administration. Patients selection is limited exclusively to those who posses a given medical history or exhibit particular symptoms. The etiology of the cardiac arrest is also a factor that is prominently considered. These strict criteria for selection of those patients who can benefit from induced therapeutic hypothermia can be outlined as follows:
- Post cardiac arrest patients who have been in comatose for not more than six hours to the time of initiation of hypothermia;
- Patients who are capable of regulating their blood pressure, either on their own or upon administration of pressor drugs, following successful cardiopulmonary resuscitation;
- Patients who are comatose during the time of inception of hypothermia;
- The patients must be aged sixteen years and above;
- The initial core body temperature for the patients must be at least 30o Celsius (93o Fahrenheit); and
- If the patients are females within the childbearing age (16-44 years old), they should not test positive for traces of human chorionic gonadotropin hormone (hCG). Absence of HCG confirms that the women are not pregnant.
In the above listed criteria, the term coma denotes a situation where the patient does not respond to stimuli or commands hence, lacking speech and eye movement. However, those exhibiting movements in their posture and weak brainstem reflexes are considered comatose.
In addition, there also exists an equally rigid criterion for the exclusion of patients who are to benefit from this technique. This is because studies have shown that they stand to have elevated risk levels upon induction of hypothermia. This relative criteria upon which patients are discriminated upon is as follows:
- Patients whose reason for comatose is of a non-cardiac arrest nature e.g. victims of severe trauma to the head and uncontrolled bleeding of the cerebral region.
- Patients suffering from gastrointestinal hemorrhage or coagulopathy.
- Patients having unregulated heart beats (arrhythmias)
- Those whose etiology for cardiac arrest is purported to be sepsis or systemic infection as hypothermia is known to block functioning of the immune system and an elevated risk of infection.
- Patients who are pregnant.
- Patients who have undergone major surgery within a fortnight to the development of the cardiac arrest. This is because hypothermia is linked with increased occurrence of infections and hemorrhaging.
- Patients who have suffered a major trauma to their heads, as this is known to result in uncontrollable bleeding of the cerebral region prior to the initiation of hypothermia.
- Patients who are comatose due to intoxification because of drug and substance abuse.
The objective of carrying out induced therapeutic cooling is to ensure that a post cardiac arrest, comatose patient have their core temperature affectively lowered to between 32o and 34o Celsius (890 to 93o Fahrenheit). This is accomplished by following the induced hypothermia protocol for at least twenty-four hours from the time of initiation. The cooling should ideally be effected within a six to eight hours window period.
In the practice of induced therapeutical hypothermia, several constraint and adverse effects exist. These pose major challenges towards the implementation of the protocol to ensure favorable outcomes. The sole intervention in reducing the occurrence of brain damage in post cardiac arrest patients is by ensuring that there is minimal time lost between when the patient develops cardiac arrest and the inception of hypothermia. Early induction of the cooling protocol gives the comatose patient a head start as far as favorable neurological outcome is concerned.
Favorable outcome following resuscitation of a comatose post cardiac arrest patient s not easily achieved. The expediency with which the clinical Interventions are performed throughout the resuscitation phase is crucial to averting brain damage or even death. The initiation of therapeutic hypothermia should be prompt, and ideally, it should be done within the first one hour of cardiac arrest (Arrich, Holzer, Herkner and Müllner, 2010).
The hypothesis for this research will be:
- Ho, the nerological outcomes of post cardiac arrest, in out-of-hospital patients, cannot be improved by early initiation of induced therapeutic hypothermia.
- H1 The nerological outcomes of post cardiac arrest, in out-of-hospital patients, can be improved by early initiation of induced therapeutic hypothermia.
Rationale for the proposed hypothetical study
According to results from current research conducted on the use of induced therapeutic hypothermia, it is proven that there exists a direct link between the time of initiation of the cooling and the success rate of averting debility caused by brain damage. The purpose of carrying out this study is to establish this relationship and hence test the hypothesis that, the nerological outcomes of post cardiac arrest, in out-of-hospital patients, can be improved by early initiation of induced therapeutic hypothermia.
Independent variable in this case would be the initiation of therapeutic hypothermia whereas the dependent variable is the improvement of the outcome in post cardiac arrest patients.
From the existing literature concerning research in the field of induced therapeutic hypothermia, it is possible to deduce the benefits that this technique has, challenges facing its application and the progress made in making the technique more effective. Cardiorespiratory arrest is a major cause of lesion and/or ischemia in all body organs and systems. The central nervous system however bears the most brunt even if the attack lasts for a brief moment. Resuscitation that is inevitably followed by hypoperfusion and ischemia have been shown to be particularly injurious to the brain.
This presents the main and pressing concern in the carrying out of cardiopulmonary resuscitation of comatose post cardiac arrest patients or otherwise known as reanimation. Clinical trials seem to suggest that hypothermia enhances survival chances as well as improving the likelihood of complete neurological recovery. This has resulted in the inclusion of hypothermia, as a highly recommended technique in post-resuscitation period for post cardiac arrest comatose patients, in clinical guidelines the world over.
The mechanism of action
The Induction of mild hypothermia in post-resuscitation leads to the improvement of outcomes for patients who have suffered traumatic brain injury and/or cardiac arrest. On the onset of reperfusion, there is always the danger of cerebral reperfusion shock that is injurious to the brain and leads to debility. Hypothermia functions by effectively lowering the metabolism of oxygen in the cerebrum by 6% per 1° Celsius decrease in temperature of the cerebral region; thus, this effect can be attributed to a decline in the normal intra-cerebral electrical activity.
This decline in temperature is also believed to inhibit several biochemical reactions that are responsible for cerebral reperfusion injury. These reactions include drastic shifts in calcium (Ca2+) ions, synthesis of free radicals, and the activation of amino acids secretion. These reactions are responsible for the deleterious effects in mitochondria and for the initiation of apoptosis.
Initiation of therapeutic hypothermia
The cooling of the core body temperature should effectively be induced as early as possible, from the time of onset of the cardiac arrest. Research findings also indicate that there is still need to ascertain the optimal cooling temperature, period for induced therapeutic hypothermia and the ideal rate for cooling and rewarming if need be. Available data from clinical research findings using non-human primate models suggest that the earlier hypothermia is induced, following reperfusion resulting from cardiac arrest, the higher the chances for obtaining favorable neurological outcomes.
As further studies are conducted on the subject, it has been found out that the therapeutic advantages of hypothermia increase as more and more findings are made on improvement of the physical as well as the pharmacological methods employed. The newly discovered techniques that are currently still undergoing further experimental tests make it possible for the rapid lowering of a patient’s body temperature.
Cooling Techniques and Monitoring
There is a variety of cooling techniques in use for the induction of hypothermia. Nevertheless, none of these methods has been found to combine efficacy and ease of application. The techniques for the induction and maintenance of hypothermia can be largely classified into two, i.e. invasive and non-invasive methods. The monitoring of the cooling is the most important consideration as opposed to choice of method to be used in the induction of hypothermia.
The invasive techniques include the extracorporeal, venovenous and arteriovenous cooling of blood. The venovenous cooling mostly involves the use of a pump and refrigerating equipment. Extracorporeal cooling is an efficient and safe way of inducing therapeutic mild hypothermia rapidly, and it is potentially viable for conducting research into new frontiers as far as hypothermia is concerned (Holzer et al, 2005). These methods of inducing hypothermia are rarely employed today owing to their cumbersomeness, high risk of infections and logistic difficulties. Research and development of new methods of cooling blood has also considerably contributed to the obsoleteness of the invasive techniques (Bigelow, 1959).
The non-invasive or external techniques for cooling include use of a cold-water bath, use of cooling blankets, and infusion of cold saline into the pleural cavity and the placing of ice packs. The application of external cooling techniques is quite simple to use although they are slack in decreasing the core temperature. They include methods such as the use of ice packs, cooling blankets, wet towels, use of a cooling helmet and fanning. In addition, cooling by means of peritoneal and pleural irrigation is very feasible although it is rarely employed.
With the recent discovery of new extracorporeal, cooling techniques have been shown to be highly efficient; however, most practitioners find them to be too invasive for application and especially in an out-of-hospital environment or in casualty departments. For these methods, the main component is an intravascular heat exchange device that works like a refrigerator to provide faster cooling of core temperature alongside a more accurate regulation and monitoring of temperature.
During induced therapeutic hypothermia, shivering of the patient occurs. This is as a result of the body responding to the cooling and it results in a gradual rise of the core temperature. The consequence here is an overall increase in the metabolic rate of consumption of oxygen in the cerebrum and its associated deleterious effects. Therefore, involuntary shivering is addressed by the administration of a combination of sedative and neuromuscular blocker drugs (Bigelow, 1959).
During induced therapeutic hypothermia, precise monitoring and regulation of the core temperature is critical. When the core temperature falls to under 32o Celsius, it introduces a much higher risk of the development of certain complications such as infections, coagulopathy and arrhythmias. Persistent and accurate monitoring of core temperature is important, although some temperature-monitoring methods such as use of tympanic temperature measurements have proved to be less reliable.
Relevance of the study to the existing scientific knowledge
The research studies included in this review are relevant and current and this can be attested to the several ongoing clinical studies to probe the use of therapeutic hypothermia. During the last decade, substantial data has been collected which vouches for the use of prophylactic hypothermia for the treatment of traumatic brain injury (Fox et al., 2010).
To date, the most credible knowledge base on the subject strongly advocates for the earliest possible initiation of the hypothermia protocol for cardiac arrest cases. Prompt and early initiation of mild to moderate hypothermia in the patients is linked with the declining cases of debility and death. It is also proven to significantly promote favorable neurologic outcomes. Most of the research done on the subject also seems to supports the commencement of the hypothermia as soon as possible.
This concurs with the hypothesis that would be put to test in this research. In addition, there exists a large and potent area for conducting further research on the initiation of hypo therapy for cardiac arrest patients especially during response to emergencies in an out-of-hospital setting. These findings from all the past, recent and ongoing studies, are important since they form the basis for the formulation of this research’s hypothesis. They were all carried out in different locations and in pursuit of equally unique objectives. However, they all staunchly support the development of the hypothesis in this study (Bigham et al., 2010).
Existing gaps in knowledge
The application of therapeutic hypothermia as a method of mitigating traumatic brain injury is still faced by many unanswered questions. This has resulted in the omission of the method as standard procedure in the post-resuscitation of cardiac arrest. This is despite all the established positive effects of the induction of mild hypothermia immediately after cardiopulmonary resuscitation, especially in post cardiac arrest patients. Sustained controversy looms especially on what long-term effects this method has on the patients. Moreover, little is known about the consequences of the duration, depth and rate of rewarming after completion of hypothermia on both death and debility (McIntyre et al, 2003).
In yet another separate study, it was established that the success rate of therapeutic hypothermia, in effectively minimizing unfavorable neurologic outcome and mortality largely depends on duration, and depth of cooling and the rewarming rate. This was found to be the case especially so for patients monitored for not more than twenty-four hours after hypothermia. In a nutshell, the experimental findings are not significant enough to warrant the routine application of hypothermia as a standard procedure for the management of traumatic brain injury (Shafi and Mariscalco, 2006).
This research aims at filling the existing gaps in knowledge as far as the optimal time of induction of hypothermia for therapeutic purposes is concerned.
Induced therapeutic hypothermia is a tried and tested method of reducing the risk of death and adverse neurologic outcomes after resuscitation of post cardiac arrest patients. It is a highly potential neuroprotective intervention for comatose patients who risk suffering traumatic brain injury occasioned by cardiac arrest.
For the achievement of its beneficial purposes, therapeutic hypothermia should ideally be initiated at the early stages, immediately after and ischemic shock, or cardiac arrest. If otherwise administered, all its beneficial effects will most probably be minimized or all together lost (Holzer et al, 2005).
The optimal time for induction of therapeutic hypothermia remains elusive. This research seeks to establish if early induction is correlated with higher chances of obtaining favorable neurological outcomes. This proposed study will also aim at establishing if the nerological outcomes of post cardiac arrest, in out-of-hospital patients, can be improved by early initiation of induced therapeutic hypothermia. This implies that cooling, for out-of-hospital cardiac arrest cases, should be initiated in the ambulance, en-route to the hospital, instead of waiting till the patient arrives there.
Arrich, J., Holzer, M., Herkner, H. & Müllner, M. (2010). Cochrane corner: hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Anesth Analg, Vol. 110(4):1239. Web.
Bernard, S. (1996) Induced hypothermia in intensive care medicine. Anaesth Intensive Care, Vol. 24(3):382-8. Web.
Bernard, S. A., et al. (2002). Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med, Vol. 21; 346 (8):557-63. Web.
Bigelow, W.C. (1959). Methods for Inducing Hypothermia and Rewarming. Annals of the New York Academy of Sciences, X Issue, Vol. 80, Hypothermia pg 522–532. Web.
Bigham, B. L., et al. (2010). Predictors of adopting therapeutic hypothermia for post-cardiac arrest patients among Canadian emergency and critical care physicians. Resuscitation. Vol. 81(1):20-4. Web.
Fox, J. L., et al. (2010). Prophylactic hypothermia for traumatic brain injury: a quantitative systematic review. CJEM, Vol. 12(4):355-64. Web.
Holzer, M., et al. (2005). Extracorporeal venovenous cooling for induction of mild hypothermia in human-sized swine. Crit Care Med, Vol. 33(6):1452-3. Web.
McIntyre, L.A. et al. (2003). Prolonged therapeutic hypothermia after traumatic brain injury in adults: a systematic review. JAMA, Vol. 289 (22):2992-9. Web.
Shafi, N. I. & Mariscalco, M. M. (2006). Considering the use of induced hypothermia in a pediatric patient with traumatic brain injury: a critical appraisal of two meta-analyses. Pediatr Crit Care Med, Vol. 7(5):468-72. Web.