Therapeutic Hypothermia Impacts of Neurological Function of Post Cardiac Arrest Patients - Research Paper Example

? Therapeutic hypothermia impacts of neurological function of post cardiac arrest patients Introduction According to Gal, Slevak and Seidlova (2009), severe neurological impairments because of cardiac arrest with widespread cerebral ischemia are prevalent among residents of the United States today. The use of therapeutic hypothermia to assist patient recover from the post cardiac arrest effects have been extensively studied and established. Therapeutic hypothermia, also known as protective hypothermia is a common treatment used to lower the body temperatures of patients to help them from contracting ischemic injury to their tissues that occurs when the body is predisposed to insufficient blood flow. Cardiac arrest is one of the medical conditions, which are known to result into low or insufficient blood flow into the body of a patient. The process of executing therapeutic hypothermia on patients involves the use of a catheter, which is placed in the inferior vena cava through the femoral veins in the legs through a method known as invasive therapeutic hypothermia. Non-invasive therapeutic hypothermia involves an external application of a blanket that is made extremely cold by water. Strict adherence to the therapeutic hypothermia has been proved to reduce the level of risks for ischemic brain injuries that patients under such conditions of insufficient blood supply are exposed to. The development of therapeutic hypothermia to help reduce the levels of risks that patients recovering from cardiac arrest are exposed was developed by Greek physician Hippocrates when he advocated for the packing of wound soldiers in snow ice, a form of non-invasive therapeutic hypothermia. Studies into the application of therapeutic hypothermia in modern medicine began in 1945 when the first publication on the topic was made as documented by Storm, Steffen and Schefold, (2008). This paper will evaluate how induced therapeutic hypothermia affects the neurological functions and help post cardiac arrest patients recover. The impacts of the practice in reducing the development ischemic injury in cardiac arrest patients will also be evaluated. Literature review The aftermaths of cardiac arrest involves neurological injuries, which results into impairment of oxygen flow into the brain, causes anaerobic metabolism in the brain. As stated by Riana, Abella and Mary, (2006), anaerobic metabolism disrupts adenosine triphosphate dependent cellular pumps, which lead to generation of excess calcium and glutamate in the excretions. This results into excitation of the brain, which magnifies hypoxemia resulting into mitochondrial and cellular death. Disruption of blood brain barrier results into initial injury resulting into increased fluid flow into the brain resulting into worsens state of cerebral edema. This is exactly how persistent cardiac arrest result into increased level of neurological defects, a condition that can be arrested using therapeutic hypothermia. The application of therapeutic hypothermia results into counteractions of the neuroexcitations in the brain cells through process that stabilize the calcium and glutamate release resulting into decreased apoptosis in the brain. It also acts to stabilize the blood brain barrier resulting into reduced flow of fluids into the brain tissues thus reducing the instances of developing cerebral edema. Therapeutic hypothermia thus reduces the destructive mechanisms of cardiac arrest thus reducing the damaging impacts it may produce to the brain and the central nervous system according to Tsai, Barbut and Wang, (2008a). Based on Matthias, Fries and Rossaint (2012), therapeutic hypothermia is done following a three phase procedure, which includes induction, maintenance and re-warming which must be done under controlled environments to prevent potential adverse effects of the procedure. The induction phase enables the attainment of a patient’s target body temperature within the shortest time possible. This is done using solid ice packs, ice lavage or even non-invasive cooling devices such as blankets or wraps. This phase is accompanied by patient sedation and the use of neuromuscular blockers to help reduce shivering when the process approaches the induction phase. During this process of induction, instances of mild dieresis is common, which may result from increased venous return, stemming from vasoconstriction, decreased anti-diuretic hormones or even tubular dysfunctions. This is attributed to the increased urine output among such patients with the first few hours of conducting the procedures. This makes important for volume placement to help arrest possible fluid deficit hypotension, which may occur on the patients. The maintenance phase enables the control of the patient’s temperature within the target range, which lies between 32-34 degrees centigrade, a crucial step in therapeutic hypothermia. In addition, the maintenance phase last for over 24 hours as from the period that the desired temperature is reached and is keenly regulated. This is however dependent on the protocol being used by the physicians and the prevalent condition of cardiac arrest of the patient. At this phase, both automated invasive and non-invasive methods are used to enable the patient’s temperature to remain within the required ranges. Automation of this phase has also been encouraged as it is less laborious and reduces instances of omissions, which may be disastrous during this phase (Polderman, 2009a). Tsai, Barbut and Wang, (2008b) suggested that re-warming phase involves the use of procedures, which are meant to re-warm the patient and enable them regain the normal body temperatures. However, the re-warming process must be controlled as impulsive worming or allowing patients to shiver for results into dangerous electrolyte shift, which has been proved to cause lethal arrhythmias. The process of controlled re-warming is thus done through 0.15-0.5 degrees centigrade process, which results into attaining the normal body temperatures. Depending on the protocol used in therapeutic hypothermia, neuromuscular blockade can be done during the entire process of re-warming to enable the maintenance of tight temperature control. According to Polderman (2009b), Electrolyte monitoring should also be done frequently during this phase as it characterized by frequent electrolyte shift, which results into elevated electrolyte levels. When the re-warming is conducted in a slow and controlled process, the kidney is allowed to excrete excess potassium, which helps in the prevention of hyperkalemia. The monitoring of glucose levels during re-warming phase also prevents the possibility of the patient developing hypoglycemia, which is caused by increased insulin resistance. The period of therapeutic hypothermia is dependent on the facilities of the unit and the protocol being used which is influenced by the available machines and technological devices. Depending on the machines used, the therapeutic hypothermia period can be counted as from the cooling period or even once the target temperature is achieved. Despites its great significant in preventing ischemic infection in patients recovering from cardiac arrest, therapeutic hypothermia has adverse effects on the patients. This stems from the fact that it’s predisposes a patient to electrolyte imbalances, arrhythmias, insulin resistance, shivering from the extremely cold conditions, coagulation problems among other serious conditions. As noted earlier, the process of therapeutic hypothermia is characterized by excessive shifts in electrolytes especially potassium, magnesium and calcium. This has been witnessed during the induction and maintenance stages when intracellular shift in electrolytes is witnessed. Nurses administering this procedure must thus ensure the monitoring and replacement of crucial electrolytes to help in the maintenance of normal electrolyte, which will also help in the prevention of arrhythmias in the patients according to Hassager and Wanscher, (2009). Chamorrow Borrallo and Romera (2010), clarifies that the occurrence of bradycardia, atrioventricular blocks, atrial and ventricular fibrillation increases the patient’s chances of contracting arrhythmias during the process of therapeutic hypothermia. Atropine, a drug commonly used in such a situation may become ineffective in cases of bradycardia making it quite a challenge in controlling this medical condition. Insulin resistance has also been witnessed in patients undergoing therapeutic hypothermia, which predisposes such people to contracting hyperglycemia, which doubles the infection risks of such patients. Caregivers should thus ensure standardized glucose monitoring and administration to help control instances of hyperglycemia in such patients. Polderman (2009a), stated that with the advance low temperatures that the patient is exposed to during the induction phase of therapeutic hypothermia, the body’s natural defense mechanism against cold may initiate increased shivering to increase the metabolic activity and oxygen consumption in the body. Neuromuscular blockages can also be used during the induction and re-warming phase to help control the patient’s temperature. The use of sublingual muscle tone, common neuromuscular blockers also helps in the control of excessive shivering due to its ability to control the body temperatures. The process of shiver prevention is beneficial in the effective control of patient’s temperatures at an early stage to prevent overshooting of body temperatures if neuromuscular blockers are used at advanced and later stages. According to Arpino and Greer (2008) the occurrence of mild platelet dysfunction during therapeutic hypothermia has been proved a reason for possible risk of bleeding to such patients. The blood loss is mostly witnessed when invasive method is applied during the induction phase from the central or the invasive lines. Increase in target temperatures from 33-34 degrees centigrade has been shown to help prevent bleeding due to its ability to alleviate platelet dysfunction that occurs below 34 degrees centigrade. It is therefore prudent that the team responsible for the administration of this process do monitor the coagulation studies to enable them determine the trends and factors which may increase patient’s disposure to coagulation problems. Exposing a patient to highly cold temperatures is considered as a very uncomfortable medical procedure that presents a serious pain and sedation management to the clinical team. During such cold temperatures, the body’s reaction to pain is diminished and therapeutic hypothermia reduces the body’s ability to respond effectively to pain thus presenting a challenge on how one should manage the sedation levels in such a patient. Continuous electroencephalographic monitoring has been extensively used to help in the monitoring of the sedation levels and help detect any seizures, which may develop (Chamorrow Borrallo and Romera, 2010). Therapeutic hypothermia also has an adverse effect on the metabolism of most drugs as has been shown be a number of studies. The clearance of common intensive care unit drugs has been shown in patient undergoing therapeutic hypothermia. As stated by Sunde et al (2007), such drugs include epinephrine, nor epinephrine, morphine, propofol, phenytoin and other beta-blockers. The effects of therapeutic hypothermia in renal functions are believed to play a function in the reduction of metabolism of the intensive care unit drugs. It is therefore advisable that lower doses of sedatives and neuromuscular blockers be used on such patients to prevent over accumulation of drugs in the blood. Polderman (2009b) suggested that the process of reduction of neurological injury in cardiac arrest patients using therapeutic hypothermia is done through the reduction of pro-inflammatory mediators, which is part of the reperfusion syndrome. This results into suppression of the immune system, which may result into increased risk of infection in such patients. Therapeutic hypothermia thus increases the patient’s risk of developing new infection because of suppressed body immune systems. The risks levels are increased if the cooling phase is extended beyond 48 hours increasing the patient’s body exposure to infective pathogens. According to Hassager and Wanscher (2009), the determination of a patient’s neurological prognosis has been shown to be a demanding process that requires more sophistication in terms of skills and experience. Attempts to interpret neurological findings and examination require the exercise of caution due to the persistent presence and effects of sedatives and paralytic agents used during the exercise. In an attempt to assess the prognosis of therapeutic hypothermia, neurologist has used the cerebral performance scales. A CPC 1 is known to indicate full recovery from neurological defects, CPC 2 indicate moderate disability while CPC 3 indicates severe disability with preserved consciousness. CPC 5 leads to death or permanent brain damage and loss of neurological functions and coordination in the body. A good outcome out of therapeutic hypothermia is reflected under the CPC 1 and 2 and a poor outcome is reflected by a CPC of four and five where a patient fails to regain consciousness. Assigning a CPC of three as a good or bad outcome has been faced with a number of controversies but severe disability may not be considered with these results, as most patients who are recovering from cardiac arrest would prefer to survive with significant neurological disability but with a preserved consciousness as stated in Varon (2010). Problem analysis The question of whether therapeutic hypothermia has any impacts on the neurological benefits after cardiac arrest has been attempted by various researches and there exist a lot of literature trying to explain the basis of question. It is however believed that the induction of moderate hypothermia before cardiac arrest prevents patients against developing global ischemia, a fact that has been common knowledge since the 50s. Current advanced animal studies have shown improved neurological recovery with therapeutic hypothermia mostly after the body returns to spontaneous circulation after cardiac arrest. In these studies, a complex combination of arrest models, which are laboratory induced, were used in an attempt to resuscitate and apply a variety of induced hypothermia (Chamorrow, Borrallo and Romera, 2010). Varon (2010) indicated that the animal models also lacked uniformity in their outcomes and the level of care provided was low as compared to how it would be in case of human subjects. Since the 1950s, a number of reports have been published on the response of human subjects who were subjected to therapeutic hypothermia immediately after cardiac arrest. The patients posted good neurological outcomes after a period of intensive hospital care and recovery episodes. All these reports are attributed to the subsequent studies that have been conducted to help ascertain the impact of therapeutic hypothermia in patients recovering from cardiac arrest and how this helps in the restoration of their neurological functions. Incidences of sudden cardiac arrest in most countries have risen beyond the figures that were initially postulated and this has contributed a number of deaths or loss of neurological functions due to lack of immediate attention and care. Therapeutic hypothermia has been indicated to improve patient’s chances of surviving cardiac arrest and reducing the levels of brain and nervous injuries that may occur because of cardiac arrest. A study on comatose patients who suffered cardiac arrest and they were subjected to therapeutic hypothermia has also proved its efficiency in reducing the degrading impacts that neurological impairments have on such patients. The effects of therapeutic hypothermia in other patients with hemorrhagic shock and those with severe brain damage have resulted to increased application of the practice in various avenues of hospital setups. Most of these findings have been improved through consistent human trials with variations on the conditions of the patients and the therapeutic hypothermia protocol used on them as suggested by Varon (2010). This dissertation thus seeks to establish the extent to which therapeutic hypothermia helps improving and maintaining neurological functions in patients recovering from cardiac arrest. This determination shall be made based on the analysis of the available literature, which shall be reviewed in line with the dissertation requirements. In making this analysis, a number of questions shall be answered to enable, the paper exhaustively evaluates the impacts of therapeutic hypothermia in the restoration and maintenance of neurological function in post cardiac arrest patients. Cooling is a common procedure during the process of therapeutic hypothermia and the procedure adopted have an impact on the recovery of the patient This paper shall seek to establish the best cooling method and establish the point, which a patient should be cooled and the impacts of each of the methods used in the recovery of the patient. The use of therapeutic hypothermia has been shown to have serious impacts in the metabolism and clearance of ICU drugs and thus resulting into reduced dosage. The safety of employing this method on intensive care unit patients will also be established to help ascertain how it affects the health of such patients. This dissertation shall adopt a formal analysis of different medical publications on the topic obtained from medical research databases like EMBASE, Cochrane and Pub Med. The search headlines and keywords used will include hypothermia, hypothermia and cardiac arrest, cardiac arrest and resuscitation, impacts of preventive hypothermia on neurological functions and post cardiac arrest intensive care. Relevant research articles from the American heart association, the American nursing association and other academic journals shall also be reviewed to help tackle the problem. Discussion Cardiac arrest according to Shankaran and McDonald (2012) is medically defined as a sudden circulatory standstill, which predisposes the victim to sudden death especially among those suffering from ischemic heart disease. A number of causes have been advanced for cardiac arrest, which includes pulmonary embolism, electrolyte disturbance, hypoxia, hypotension, electrocution and excessive use of prescription drugs. Patients who recover from cardiac arrest are again exposed to the risks of suffering from neurological injury with research showing that only 10-20% of cardiac arrest patients discharged may not suffer from neurological damage. According to Stammet, Werer and Mertens (2009), cardiac arrest is occasioned by reduced flow of blood into major tissues in the body, a condition that results into anorexia in patients. Reduced or no blood flow into the brain tissues is known to predispose the brain to further damage when perfusion is restored due to overwhelming of the neuronal protective mechanisms. These damages are caused by increased free radical production, increased acidosis, and release of excitatory amino acids, calcium and potassium shifts and expression of apoptotic gene. Therapeutic hypothermia has been proved to slow down most metabolic process and thus inhibiting the deleterious biochemical processes after reperfusion into the brain cells. Based on Deckard, and Ebright (2011), the induction of mild hypothermia as a result reduces the total level of free radicals produced resulting into reduced destructions that such radicals cause. Hypothermia also influences the mechanisms that are known to cause injury during hypoxia and reperfusion making it a preferred treatment for survivors of cardiac arrest. Therapeutic hypothermia after cardiac arrest has also been shown to reduce neurological outcome and is highly recommended for comatose patients admitted at intensive care unit sections following ventricular fibrillation cardiac arrest. According to Chamorrow, Borrallo and Romera (2010) a number of factors however influence the results of treatment against patients who are recovering from cardiac arrest, which include the patient age and the underlying clinical conditions. The causes of circulatory arrest, which I have included in the literature, review section also influence the results of therapeutic hypothermia on the recovery of post cardiac arrest patients. As earlier discussed, there are two cooling devices, which have been shown to post two different results depending on the condition of the patient and availability of the materials. Invasive devices have the ability to maintain the target temperature of patients over time that makes it a better cooling device. However, invasive cooling also poses some disadvantage when compared with the non-invasive method of cooling making it important for the caregivers to evaluate the condition of the patient before deciding on the method to use in every situation. Surface cooling, also known as non-invasive cooling is considered simple and can be used in both preclinical and clinical applications during trials. It also posses rapid induction characteristics and is easy to setup as compared to the invasive method of application thus making it the widely used cooling methods in emergency and field situations. Invasive cooling is also considered to be highly automated and it is thus self-adjusting eliminating the possibility of mistakes that may expose the patient to more risks. Therapeutic hypothermia is also characterized with intensive nursing especially if non-invasive method of cooling is applied. This is however not the case in invasive methods as the automation makes it computerized thus eliminating the need for persistent nursing. All these two methods however possess disadvantages that make it compulsory for caregivers to act with caution in the interest of the patient’s wellbeing as stated by Nicholas and David (2011). Non-invasive methods are not self-maintaining and this makes it prudent for the caregivers to monitor the temperature of the device constantly thus increasing the nursing time. The re-warming phase is also uncontrolled, which may results into spontaneous re-warming of the patients, a process that may predispose the patients to tissues damage. Invasive cooling methods also require expensive machine which are single component use making it uneconomical in emergency based on Sunde et al (2007). The need for puncturing the femoral veins also increases the risks of infections, which may slow the recovery process and result into further complications for the patient. Setting up the invasive cooling method devices may take a long time in a situation where time is of essence if the life and neurological capabilities of the patient is to be regained. It is also immobile and has not been proved better in neurological function recovery when compared to non-invasive making it an expensive procedure that can be avoided in Kasey and Samuel (2013). Implication of the practice Therapeutic hypothermia has a number of physiological effects whose impacts on the health of the patient recovering from cardiac arrest should be known before the process can be continued. The length of cooling which depends on the age of the subject also influences the psychological effects of the hypothermia on patients, a parameter which is dependent on the ages of the patients and the severity of their attack. Hypothermia affects the myocardial functions depending on the level of cooling used on the patient. Che, Li and Liu (2011), state that therapeutic hypothermia also have a number of implications on the renal functions of the patient, a factor that has been attributed to decreased drug metabolism and retention in intensive care unit patients. During the cooling period, an increase in the urinary output occurs, a condition that is known as dieresis, which is caused, by a combination of an increase in venous return and a decrease in the production of ADH hormone. Furthermore, the alteration of electrolyte balance by therapeutic hypothermia results into changes in the levels of magnesium, calcium, and potassium and phosphate ions in the blood. This is due to the shift and migration of the electrolytes from the bloodstream into the intracellular compartments, a situation that predisposes a patient to hypokalemia (Rossetti, Oddo and Logroscino, 2011). According to Hassager and Wanscher (2009), however, re-warming results into a reverse reaction in which the electrolytes migrate from the intracellular compartments into the bloodstream predisposing the patients to risks of hyperkalemia. A slow and consistent re-warming is therefore advisable to help control the impacts of hyperkalemia on the patient’s health. This allows for excess excretion of the electrolytes by the kidney which results to reduction of potassium to the required intracellular levels in the body. Preventive hypothermia also has a number of implications on the body drug clearance and metabolism, a situation that has been proved more prevalent in intensive care unit drugs. Propofol, opiates, and morphine drugs among other neuromuscular blockers experience reduced metabolism and clearance in patients undergoing therapeutic hypothermia. This results into increased drug levels, which is harmful to the patient and makes it mandatory to reduce the dosage and frequencies of administration of such drugs to post cardiac arrest recovery patients. GIT motility also decreases with mild hypothermia, which is common within the mild temperatures of 32 degrees centigrade. Drug absorption across the intestinal membranes is also reduced in patients undergoing therapeutic hypothermia making it mandatory to use intravenous and intramuscular routes of drug administration for increased effects according to Freeman (2013). Recommendations for future studies The benefits of therapeutic hypothermia in protecting cardiac arrest patients has been extensively demonstrated especially how this medical procedure can help protect post cardiac arrest patients recover without being affected by neurological defects. However, as Peberdy, Callaway and Neumar (2010) opined, many studies still need to be conducted to ascertain the positive and negative impacts of this practice on patients and how it can be improved to reduce the negative effects that were earlier highlighted. The impacts of hypothermia in elevating drug concentration in intensive care unit patients because of reduced or impaired drug metabolism should be well studied. This should involve the study on other drugs that are used on such patients including analgesics, sedatives and paralytics to ascertain how hypothermia affects their pharmacokinetics and pharmacodynamic properties. This should be done using a multi-centered approach of clinical trials to enable the study includes the effect of drug variations found in different individuals and how this affects this process. The presence of different protocols used by different facility based on individual judgments also makes it impossible to have a standard basis to ascertain the benefits of the difference approaches used. There is thus a need for a trial study to help optimize the different protocols currently used by the different hospitals to come up with a standard protocol, which can guide the entire process and help in the development of better conclusions. As Che, Li and Liu (20110 indicated, lack of any research to differentiate the potential benefits of the two cooling methods and the implications of each on the recovery of cardiac arrest patient has resulted into shifting of the two protocols depending on the situation and availability of resources. However, for standard protocol to be developed, research findings that support the benefits of invasive cooling method and non-invasive cooling methods should be conducted. This will provide basis for practitioners to choose the method of preference depending on the situations and availability of the facilities. Therapeutic hypothermia has however proved its significance in mitigating the effects of neurological damage on post cardiac arrest patients. It is thus accurate to conclude that research has proved that induced therapeutic hypothermia increases the neurological functions thus reduces the levels of damage to the brain and the nervous system in post cardiac arrest patients. 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Intra-arrest rapid head cooling improves post-resuscitation myocardial function in comparison with delayed post-resuscitation surface cooling. Critical Care Medicine, 36, 434-439 Varon, J. (2010). Therapeutic hypothermia: implications for acute care practitioners. Postgraduate medicine, 1, 19-27. Read More