Induced Therapeutic Hypothermia After Cardiac Arrest - Research Paper Example

?INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST Induced Therapeutic Hypothermia After Cardiac Arrest of INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 2 Abstract Cardiac arrest is quite common in many countries of world including United States, where about 325, 000 reported deaths have been recorded per year according to the study published by Bau P. (2010). Many patients undergoing cardiac arrest, ultimately survive as a result of resuscitation efforts but show a poor quality of neurological functioning due to ischemic injuries following hypoxia especially in brain. Induced therapeutic hypothermia is a technique that can help to prevent brain ischemia and prevent neurological damage in patients who survive the event of cardiac arrest. This technique involves cooling of a patient to about 32 to 34 degrees Centigrade. Although introduced in 1950’s, it was abandoned due to certain difficulties however it was re-introduced in 1980’s after animal studies. After some successful studies, it is now approved by American Heart Association and is a part of their updated resuscitation standards. Given below is an insight into the steps involved, side effects and possible prognosis of induced therapeutic hypothermia. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 3 INTRODUCTION: Therapeutic hypothermia is also known as ‘targeted temperature management’. Michelle E. (2011) has discussed in detail about the induction of therapeutic hypothermia and its outcomes in patients undergoing open cardiac surgery. She defines the therapeutic hypothermia as a ‘deliberate reduction of the core body temperature’ typically to a range of about 32 to 34 degrees Centigrade (89.6 to 93. 2). This is especially true for those patients who are unable to regain consciousness as the blood starts to circulate again following a cardiac arrest. MECHANISM OF CELLULAR INJURY DURING CARDIAC ARREST: During an open heart surgery, there is significant risk of neurological injury on account of the lack of oxygen supply to brain as the circulation comes to a halt. In the absence of oxygen, the brain undergoes anaerobic metabolism as reported by Michelle E. (2011). This leads to damage to ATP dependent cellular functions with a resulting increase in calcium and glutamate excretion. The brain cells thus become more active, consuming more oxygen. With the increasing hypoxemia, further damage occurs leading to cell death. The resultant cerebral edema further enhances the damage. Also, as a result of all these processes, the blood brain barrier also becomes ineffective further contributing to cerebral edema As soon as the circulation returns after the heart starts pumping again, reperfusion injury occurs which adds up to the ongoing damage. Meanwhile, there is already an onset of the inflammatory reaction as a result of cell death leading to a release of neutrophils and macrophages in an attempt to remove the cellular debris. The resultant production of free radicals also catalyses the damaging process thus worsening the cerebral edema. This vicious cycle continues leading to brain death. ROLE OF THERAPEUTIC HYPOTHERMIA IN PREVENTING NEUROLOGICAL DAMAGE: Using the technique of therapeutic hypothermia can be useful to avoid all the above described damage. The therapeutically induced hypothermia after cardiac arrest takes following steps to decrease the extent of neurological damage: 1. It stabilizes the release of calcium and glutamate thus decreasing the degree of cellular death, 2. It stabilizes the blood brain barrier, 3. It causes a suppression of the inflammatory response, 4. It reduces cerebral edema by the help of above actions. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 4 According to the report produced by Michelle E. (2011), there is a reduction in cerebral metabolism from 6% to 10% for every one degree Celcius drop in body temperature. This results in decreased oxygen requirements by the brain cells. Michelle E. (2011) simulates the effects of therapeutic hypothermia to those of cardiac defibrillation which allows the heart to stop functioning and then to reset itself to its original normal rhythm. Likewise, therapeutic hypothermia stops the neurological damage and then helps the brain regain its normal functions. The benefits of therapeutic hypothermia have been under consideration for quite a long period in medical research, but its firm clinical practice has started only after The New England Journal of Medicine published two studies in the year 2002. These were the HACA study (Hypothermia After Cardiac Arrest) and the Bernard study. Only the patients with ventricular tachycardia and ventricular fibrillation were studied in both of these studies. The results of these studies were so fruitful that the American Heart Association (AHA) had to revise its cardiopulmonary resuscitation standards in 2005. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 5 PHASES OF THERAPEUTIC HYPOTHERMIA: According to Michelle E. (2011), there are three phases of therapeutic hypothermia: 1. Induction, 2. Maintenance and 3. Re-warming. All these steps must be carried out in a well controlled manner the risk of side effects still exist. These include: 1. Arrhythmias, 2. Skin break down, 3. Rapid electrolyte shifts. The risk of arrhythmias and skin break down prevails during the first two stages i.e . induction and maintenance collectively known as ‘cold phases’. Rapid electrolyte shifts can occur during the re-warming phase. Throughout the procedure, core temperature measurement is taken by use of an esophageal, pulmonary artery or bladder catheter. 1. INDUCTION PHASE: The induction phase is aimed at bringing the patient to the target temperature as soon as possible. This is accomplished by the use of: a. Ice packs, INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 6 b. Rapid cold-fluid infusion, c. Iced lavage, d. An intravascular catheter to circulate cold fluid in a large vein in closed loop and e. Non invasive cooling devices like gel pads, cooling blankets or wraps. At some instances, it is useful to give sedation and neuromuscular blockage with the commencement of the cooling process. This makes it possible to avoid shivering during induction, thereby helping in reaching the target temperature rapidly. The process of induction requires a careful fluid-balance monitoring both by CVP monitoring and intake/output records. This is important because induction is usually accompanied by mild dieresis owing to an increased venous return as a result of: Vasoconstriction, Tubular dysfunction and Decreased ADH levels. Sometimes volume replacement may be required to prevent hypotension. 2. MAINTENANCE PHASE: This phase comprises of maintaining the patient’s body temperature within the target range which lies usually lies between 32 to 34 degrees Centigrade. This may last for about 24 hours or as per requirements. Using the automated methods may be helpful to keep the patient’s body temperature within required range. 3. RE-WARMING PHASE: This is a carefully monitored stage which can’t be allowed to go on too rapidly or too slowly due to the risks involved, especially the risk of potentially lethal arrhythmias following electrolyte shifts. The recommendations suggest a controlled re-warming of 0.15 to 0.5 degrees Centigrade per hour as reported in the study by Michelle E. (2011). This can be achieved by an assisted neuromuscular blockade throughout the phase of re-warming. Critically elevated levels of electrolytes can be prevented by frequent electrolyte monitoring. Slow re-warming allows kidneys sufficient time to excrete excessive potassium from the body which prevents hyperkalemia thereby reducing the risk of arrhythmias. The re-warming phase also requires frequent glucose monitoring due to a risk of hypoglycemia. This is because during the earlier phase of hypothermia, insulin resistance develops which diminishes later on thus increasing the risk for hypoglycemia. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 7 Again, this phase also requires a very careful fluid monitoring via CVP and fluid intake/output records due to vasodilation occurring during temperature rise. Volume replacement may be required. The duration of therapeutic hypothermia differs according to the facility protocols. No direct recommendations are available for it. ADVERSE EFFECTS OF THERAPEUTIC HYPOTHERMIA: Some of the possible adverse effects of therapeutic hypothermia include: 1. Fluid and electrolyte imbalances, 2. Coagulation problems, 3. Insulin resistance, 4. Arrhythmias and 5. Shivering. FLUID AND ELECTROLYTE IMBALANCES: Fluid and electrolyte imbalances are particularly important regarding potassium, calcium and magnesium during therapeutic hypothermia. These changes mainly take place during the induction and maintenance phases. Potassium shifts carry a risk of developing arrhythmias. Such problems can be prevented by careful monitoring of electrolytes and appropriate replacement where required. COAGULATION PROBLEMS: During induced therapeutic hypothermia, there may arise some degree of platelet dysfunction increasing the risk for bleeding which is different for different patients. To control the bleeding problems, sometimes it is useful to increase the target temperature from 33 to 34 degrees Centigrade. Blood products may be required in some cases. INSULIN RESISTANCE: Insulin resistance can lead to hyperglycemia, which exacerbates the chances of infection. This adverse effect can be prevented by glucose monitoring and insulin administration. ARRYTHMIAS: There is an increased of arrhythmias during induced therapeutic hypothermia owing to the electrolyte shifts which occur mainly during the induction and maintenance phases. These include: 1. Atrial fibrillation, INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 8 2. Ventricular fibrillation, 3. Bradycardia and 4. Atrioventricular blocks 5. Skin break down. During induced hypothermia, Atropine usually becomes ineffective for bradycardia, however, transvenous or transcutaneous bradycardia is a helpful technique. SHIVERING: It is obvious that shivering may increase during induced therapeutic hypothermia as a natural defense mechanism for cold. Shivering helps to re-warm the body increasing the metabolic activity and thus the oxygen requirements. This can be kept under safe limits by providing adequate sedation and counter warming of body extremities. Another good way is to use a neuromuscular blockade technique during the induction and re-warming phases. If shivering continues through the maintenance phase as well, a bolus dose of neuromuscular blockers is helpful which effectively controls the subclinical muscle tone or ‘microshivering’ as well, as described by Michelle E. (2011). Taking the above measures can provide a fruitful control of shivering thereby keeping the patient well within the range of targeted temperature which also reduces the risk for developing arrhythmias. Arrhythmias are particularly a risk if the temperature drops up to less than 30 degrees Centigrade. SKIN BREAKDOWN: Induced therapeutic hypothermia can lead to skin breakdown owing to the vasoconstriction caused by reduced temperature. This side effect can be prevented by using waffle boots and low-airloss bed. CONTINUOUS EEG MONITORING: Continuous EEG monitoring is important and helpful during induced therapeutic hypothermia as it helps to determine any level of consciousness on part of the patient at any time. DRUG METABOLISM: Hypothermia also affects the drug metabolism. So, the anesthetic drugs given for the purpose of sedation and pain relief take time to clear off the body once the patient attains a normal temperature; thus their effects may be prolonged. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 9 PROGNOSIS OF INDUCED THERAPEUTIC HYPOTHERMIA: Induced therapeutic hypothermia technique has shown proven beneficial effects on survival of the patients undergoing open heart surgery and preventing their brain damage. According to the report published by the Central Florida Health Alliance; Leesburg Regional Medical Center, about 30% of patients with induced hypothermia go home intact neurologically. (“Induced Hypothermia,” 2013). CONCLUSION: Induced therapeutic hypothermia is a life saving technique with proven results as discussed above and its role in preventing neurological damage during cardiac arrest cannot be ignored. INDUCED THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST 10 REFERENCES Induced Hypothermia (2013) Retrieved April 14, 2013 from: http://www.cfhalliance.org/svc-induced-hypothermia.htm Michelle E. Deckard, Patricia R, Ebright (July 2011) Therapeutic Hypothermia After Cardiac Arrest: What, Why, Who and How. American Nurse Today Vol 6. No. 7. Retrieved from: http://owl.english.purdue.edu/owl/resource/560/10/ Bau P. , Courtney V., McGuire, Marie A., Maloney (March 01, 2010) Use of Mild Therapeutic Hypothermia to Treat Cardiac Arrest. Journal of The American Academy of Physician Assistants. Retrieved from: http://www.jaapa.com/use-of-mild-therapeutic-hypothermia-to-treat-cardiac-arrest/article/164767/ Read More