Therapeutic Hypothermia for Neuroprotection in Post Adult Cardiac Arrest - Essay Example

Therapeutic hypothermia for neuroprotection in post adult cardiac arrest Introduction Everyone aspires for good health and vitality but there are several factors that prevent us from achieving this on a constant and periodic basis as we most desire. Encounters with various forms of diseases affect the normal way in which the body should function, taking away that critical element of good health and vitality. Indeed, there are diseases that come and go in no time but there are others that come and stay with us for long, living highly consequential health risks on us. One of such dysfunctions is cardiac arrest in adults, which has been identified to leave most patients with risk of ischemic injury to tissues (quote). Once these ischemic injuries set in, they leave patients with symptoms including high body temperature and other neurological dysfunctions. In such cases, the need to find protective interventions to deal with these aftermath effects becomes highly important and urgent. In this paper, one critical intervention to dealing with post adult cardiac arrest, which has effects like risk of ischemic injury to tissue, which is therapeutic hypothermia discussed for its effectiveness and efficiency as a care approach. Neurological anatomy and physiology Neurological anatomy and physiology is discussed due to the relationship between neurological wellbeing and post cardiac arrest. As Arrich, Holzer, Havel, Müllner and Herkner (2012) note, “Good neurologic outcome after cardiac arrest is hard to achieve”. An understanding of the neurological anatomy and physiology will therefore make it possible to know why this is so and how this situation can effectively be tackled using therapeutic hypothermia. Quote (year) explained that neurological system comprises of two major components, which are the central nervous system (CNS) and the peripheral nervous system (PNS). Whereas the PNS is mainly made up of nerves that exit from the spinal cord, the CNS comprises the brain, the spinal cord, and the cranial nerves. Three major organs can therefore be anatomically and physiologically identified, which are brain, spinal cord and the vertebral column. Functionally, the brain is responsible for functions including “imagination, memory, speech, and limb movements to secretion hormones and control of various organs within the body” (Sehati, 2009). These functions are however made possible by the collective functioning of other cells, tissues and organs including brain cells, meninges, cerebrospinal fluid (csf), ventricles, brainstem, thalamus, cerebellum, lobes, cerebrum, hypothalamus, pituitary gland, basal ganglia, pineal gland, and cranial nerves. Fig 1: Part of the Brain Source: Sehati, 2009 The spinal cord on the other hand is anatomically seen as a long, narrow, tubular bundle of neurons and support cells that expand all the way from the bottom of the brain to the first and second lumbar vertebrae as depicted in figure 2 (quote). The spinal cord plays two major functions, which are to transmit signals from the brain to the remaining part of the body, and allow movement and sensation in all parts of the body (Sehati, 2009). Fig 2: 33 Divisions of the Spinal Cord Source: Sehati (2009) Finally, the vertebral column comprises 33 vertebrae that are well netted to form a flexible and touch column that gives the back body its support. Effects of the neurological system on other body systems Cardiovascular Generally, the cardiovascular system is responsible for pumping oxygenated blood throughout the body, whiles the neurological system is in place to sense the internal and external environments of the body (quote). This means that virtually nothing happens with the cardiovascular system in an effective way that the neurological system can be absent because the neurological system must sense the functioning of the organisations within the cardiovascular system. Through the sensing of the organs, three major effects of the neurological system are felt on the cardiovascular system, which are vagal tone, sympathetic activation, and neurotransmitter effects. Quote (year) notes that there are electrical signals that could make the heart beat up to 110 pulses in a minute though the heart needs only 60 to 80 beats for most activities. The nervous system acts to affect the vagal tone by making the heat slow its pulse rate. In times of stress and exercise however, sympathetic nerves within the neurological system innervates the heart to increase its rate of beating to allow sustenance for the body. Finally, the neurological system releases chemical messengers or neurotransmitters such as epinephrine and once this reaches the heart, it improves the cardiac output and enhances the quantity of blood that reaches all other body tissues (quote). Respiratory The neurological system and respiratory systems are directly related in function, making the neurological system have an effect on the functioning of the respiratory system. The respiratory centres which are responsible for sending signals to the diaphragm and intercostals muscle for these to contrast and relax at periodic intervals to activate breathing are actually located in the brainstem or medulla (quote). In effect, the autonomic nervous system controls the entire act of breathing, making it almost impossible for a person to intentionally hold breath for a certain period of time because once certain times are exceeded, the autonomic nervous system will send signal to the respiratory centre to make you start breathing again. Endocrine The endocrine system and the neurological system actually works hand in hand to make the communication function of the body complete. It is not surprising therefore that the endocrine system is at times referred to as the other nervous system. The fact however is that the endocrine system and the neurological system are not the same and have different roles, just that the neurological system complements the roles of the endocrine to a very large extent. For example, the neurological system is active in sending signals that ensures that the chemical signals from the endocrine system move slowly and become long lasting (quote). Again, the functions of the nerves also instigate the action of chemical messengers within the endocrine system that together with the central nervous system tells the body to perform specific physical and mental functions. Assessment of care approach for post adult cardiac arrest Statistics on resuscitated patients of cardiac arrest who die before hospital discharge and in some cases, after hospital discharge is very disturbing. Sandroni, Cavallaro and Antonelli (2013) actually note that over two-thirds of such resuscitated cardiac arrest patients die before hospital discharge. The commonest cause that this situation is attributable to is the fact that post-resuscitation and myocardial dysfunction among post adult cardiac arrest patients is very high (quote). There are several care approaches that may be used in such situations of post-resuscitation mortality but quote (year) admonished that critical assessment of care approaches is needed to address the very cause of mortality. What this means is that the need for care approach for such patients of post adult cardiac arrest must focus on ways of minimising post-resuscitation brain and myocardial dysfunction. Meanwhile, therapeutic hypothermia has been identified as an intervention that directly affects the function of the neurological system in the event of post-resuscitation. What this means is that therapeutic hypothermia has some level of relation in reducing the severity of post-resuscitation brain injury due to its relation with the neurological system (Sandroni, Cavallaro and Antonelli, 2013). In their study, Sandroni, Cavallaro and Antonelli (2013) actually found that in 350 comatose adults resuscitated from out-of-hospital cardiac arrest (OHCA) were cooled to 32-34°C for 12-24 hours after recovery of spontaneous circulation. This is sufficient evidence to the effect that therapeutic hypothermia improves survival in patients who remain comatose after resuscitation from cardiac arrest (quote). Planning therapeutic hypothermia for neuroprotection for post adult cardiac arrest The rationale behind a careful planning session for the use of therapeutic hypothermia for post adult cardiac arrest is in the fact that there are actually several medical uses of therapeutic hypothermia. The session must therefore be planned in such a way that solves specific problems associated with post adult cardiac arrest. Even more, it is important to plan so that neuroprotection can be achieved for patients as the neurological functioning of the body in post adult cardiac arrest has been found to be very important in reducing mortality. Some critical factors to take into consideration in the planning of therapeutic hypothermia for neuroprotection for post adult cardiac arrest include the temperature to work with. Decisions on cooling temperature is very important as there are studies suggesting achieving therapeutic temperatures of 33 °C (91 °F) can actually aid in preventing secondary neurological injuries (Arcure and Harrison, 2009). Successful prevention of further neurological injuries would thus mean that higher levels of neuroprotection can be secured. Another important planning that needs to be done is on the decision whether to cool the patient using return of spontaneous circulation (ROSC) without return of consciousness or whether both ROSC and return of consciousness will be needed (quote). This is because such decisions can largely influence the achievement of improvement in neurological outcomes. This is because both ROSC signs such as breathing, coughing and a palpable pulse, and consciousness signify active functioning of the neurological system as seen above (quote). Implementation of therapeutic hypothermia for neuroprotection for post adult cardiac arrest The implementation of therapeutic hypothermia for neuroprotection for post adult cardiac arrest was undertaken by Sandroni, Cavallaro and Antonelli (2013) who had a control and experimental samples in place for the sake having a comparative judgment of their results. In both cases randomised trials were used for post adult cardiac arrest patients. In the experimental group there was the use of mild therapeutic hypothermia for the treatment of patients resuscitated from non-ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). The control group received the use of isocolemic high volume hemofiltration that was used independently for greater part of the sample, and in some few respondents, in combination with mild therapeutic hypothermia where the need to improve survival after cardiac arrest was eminent (quote). At the end of the study, the researchers recorded outcomes that suggested that the independent use of mild therapeutic hypothermia directly influenced the chances of neuroprotection events and subsequent higher survival rate within a period of six months. The same was not so for the control group who had isocolemic high volume hemofiltration as part of their intervention. The statistical results that the study produced was 5/22 vs. 2/22; risk ratio [RR] for mortality 0.85 [0.65-1.11] p = 0.24. Oddo et al (2012) also emphasised on the direct impact of therapeutic hypothermia on cerebral performance category (CPC) so as to confirm an established relationship between therapeutic hypothermia and neuroprotaction for post adult cardiac arrest. This study also made use of non-VF/VT patients. Quite significantly, the patients used in this case were those receiving care from an intensive care unit (ICU). The results of the study showed very impressive neurological outcomes in terms of the cerebral performance category of respondents. The rates of observational improvements were considered to be impressive and result oriented as against those in the historical controls were statistical results of 2/12 vs. 1/11; p = 0.99 was produced (Otto et al, 2012). This is sufficient evidence on the relevance of using therapeutic hypothermia in post adult cardiac arrest patients for the sake of achieving neuroprotection of these people, most of who risk increased chances of mortality if no timely interventions are provided (quote). Relationship between SIRS/sepsis/MODS and neurological system 2 Evaluation of interventional treatment for post adult cardiac arrest José G. C, Jane H. B, Valerie J. M, Brent M. And Hinchey P. R (2011) noted that there remains much work to do in understanding the effectiveness and timing of early therapeutic hypothermia in pre-hospital environments. Indeed, the validity of this argument remains very significant till date because there continues to be high mortality rates associated with adult post cardiac arrest; even for patients who receive therapeutic hypothermia. For example, Sandroni, Cavallaro and Antonelli (2013) noted that mortality from cardiac arrest goes beyond levels of 90% for out-of-hosptal cardiac arrest and 70% for in-hospital cardiac arrest. By implication, continuous evaluation of interventional treatments for post adult cardiac arrest, including interventions that make use of therapeutic hypothermia is very important. In such evaluation processes, there are two major things that must be looked out for. These are initial post care evaluation and subsequent post care evaluation. In each of these forms of evaluations, the health provider must ensure that adequate measures and structures are put in place to measure levels of improvement, especially in neurological activity. More specifically, the functions and areas of concern for the care giver have been provided by Peberdy et al. (2010) in the table below. Initial post care evaluation Subsequent post care evaluation Ensure increased cardiopulmonary function and vital organ perfusion. Monitor functioning of post–cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, and hypothermia. Assess outcome of critical-care unit results on post–cardiac arrest care. Identify and treat the precipitating causes of the arrest and prevent recurrent arrest. Continue to keep body temperature under check to optimize survival and neurological recovery Identify and treat acute coronary syndromes (ACS) Improve mechanical ventilation to minimize lung injury Ensure there is decreased risk of multi-organ injury by supporting organ function where necessary Objectively assess prognosis for recovery Give periodic rehabilitation services when required Source: Peberdy et al. (2010) Conclusion From the discussions, there is sufficient evidence to the fact that it is difficult to gain effective neurological functionality after a cardiac arrest. However, this is not impossibility. Certainly, adult post cardiac arrest patients have the right to benefit from maximum neuroprotection so that the remaining number of days they have to spend can be guaranteed with safe and secure neurological activity. The discussion has actually showed why the need for neuroprotection should be a priority achievement for every post adult cardiac arrest. This is because of the link or effect of the neurological system on the remaining parts of the body. Because of this influence and important role that the neurological system has on the remaining parts of the body, a refusal to give these patients neuroprotection would mean other future complications for them that deals with other systems such as cardiovascular system, endocrine system, and of course the respiratory system. Having said this, the need to approach neuroprotection from a very proactive perspective would also be emphasised. This is because most often than not, enuroprotection interventions that cannot guarantee long lasting improvement in neurological functions of the body has been selected. Using therapeutic hypothermia can guarantee that a multi-facet approach to neuroprotection that is made up of secured improvement in the functionality of several body organs is achieved. Finally, the need to constantly evaluate and assess the effect of therapeutic hypothermia must not be overlooked as this holds the key to comprehensive care. References José G. C, Jane H. B, Valerie J. M, Brent M. And Hinchey P. R (2011). Field-induced Therapeutic Hypothermia for Neuroprotection after Out-of Hospital Cardiac Arrest. J Emerg Med. 2011;40(4):400-409. Arcure, J and Harrison, E. E. (2009). "Review Article of the Use of Early Hypothermia in the Treatment of Traumatic Brain Injuries". Journal of Special Operations Medicine 10 (3): 22–5. Sandroni C, Cavallaro F and Antonelli M (2013). Therapeutic hypothermia: is it effective for non-VF/VT cardiac arrest? Critical Care 2013, 17:215 Arrich J, Holzer M, Havel C, Müllner M, Herkner H. (2012). Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev. 2012 Sep 12;9:CD004128 Peberdy et al. (2010). 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. http://circ.ahajournals.org/content/122/18_suppl_3/S768.full Sehati N (2009). Nervous System Anatomy and Physiology. http://sehati.org/index/patientresources/normalanatomy.html Read More