Therapeutic hypothermia after cardiac arrest Abdullah Alshimemeri Department of Intensive Care Medicine, College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia
Received: 12‑05‑12 Accepted: 11‑10‑12
Prognosis following out‑of‑hospital cardiac arrest is generally poor, which is mostly due to the severity of neuronal damage. Recently, the use of therapeutic hypothermia has gradually occupied an important role in managing neuronal injuries in some cases of cardiac arrests. Some of the clinical trials conducted in comatose post‑resuscitation cardiac arrest patients within the last decade have shown induced hypothermia to be effective in facilitating neuronal function recovery. This method has since been adopted in a number of guidelines and protocols as the standard method of treatment in carefully selected patient groups. Patient inclusion criteria ensure that hypothermia‑associated complications are kept to a minimum while at the same time maximizing the treatment benefits. In the present work, we have examined different aspects in the use of therapeutic hypothermia as a means of managing comatose patients following cardiac arrest. Key words: Cardiac arrest; Cooling; Hypothermia; Outcome; Ventricular fibrillation
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Cardiac arrest arises from a compromise of the body’s circulatory function resulting from inefficient heart contractions. It differs from cardiac heart failure, which is a condition associated with impaired blood flow to the heart itself. In cardiac arrest (also known as cardiopulmonary arrest) the body organs, the brain in particular, are critically under‑perfused resulting in loss of consciousness which, if not promptly arrested, could lead to brain damage or death. Following a cardiac arrest, cardiopulmonary resuscitation (CPR) is employed to restore blood perfusion. In the presence of a shockable rhythm (ventricular fibrillation and pulseless ventricular tachycardia), defibrillation is employed post‑CPR. Prognosis following out‑of‑hospital cardiac arrest is, in particular, generally poor, especially due to neuronal damage typically associated with the cardiac arrest. The use of artificially induced cooling in therapeutic capacities long predates its recent
clinical application as a neuroprotective agent in post‑cardiac arrests. One of the earliest reports on the use of clinically induced hypothermia came from Hippocrates in the mid‑5 th century, who reportedly was able to control bleeding by packing patients in snow. [1,2] In 1814, Baron Dominique‑Jean Larrey, a battlefield surgeon for Napoleon, observed that the rapid rewarming of injured soldiers placed close to the fireside resulted in their death. He later developed a strategy of more gradual rewarming, which was observed to improve a soldier’s condition.[1,3‑5] In more recent times, results obtained from the application of sub‑systemic temperatures were discouraging, as a number of severe and life‑threatening adverse effects, now understood to have likely resulted from the under‑developed state of medical technology at that time, were observed. This led to the perception in certain circles that therapeutic hypothermia, with respect to clinical relevance, was on a decline. For instance, between 1958 and 1959 small‑scale trials were conducted to investigate the benefits of hypothermia following cardiac arrest. These treatments
Address for correspondence: Dr. Abdullah Alshimemeri, Department of Intensive Care Medicine, College of Medicine, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Kingdom of Saudi Arabia. E‑mail: [email protected]
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gave rise to severe complications[6,7] which were later attributed to inappropriate levels of hypothermia (ca. 30°C, lower than currently employed) and deficient complication management capabilities. Even then, some patients involved in the trials were observed to have their conditions improved. Animal studies also presented encouraging results and formed the basis on which the human trials were designed.[2,9‑11] Further evidence soon began to emerge concerning the human body’s ability to withstand severe thermal conditions, some of which came from grave and near‑fatal circumstances. In 1999, an accident left a woman exposed to critically cold conditions for about 1.5 h, during which her body temperature dropped below 14°C and she suffered a cardiac arrest. However, she survived the incident following an intensive medical resuscitation effort, demonstrating the human body’s inherent ability to tolerate and recover from such extreme thermal trauma.[12,13] Presently, the use of induced hypothermia includes transplantation organ preservation,  open heart surgery,  the surgical management of brain aneurysm, and most importantly, as a neuroprotective in post‑resuscitation cardiac arrest. The application of induced hypothermia in post‑cardiac arrest received encouragement from two independent trials conducted in Europe and Australia (both in 2002). These studies aimed to ascertain the efficacy of controlled cooling in cardiac arrest patients demonstrating shockable rhythms following the return of spontaneous circulation (ROSC). [2,9] In one of the randomized trials (by Bernard et al.), the 77 selected cardiac arrest patients with ROSC were separated into two treatment groups. The group randomized to induced hypothermia treatment had cooling started within 2 h of ROSC and the core body temperature held at 33°C for 12 h. The control group was subjected to normothermia. The resulting pattern suggested a significant improvement in the treatment group with 49% (43 patients) discharged from the hospital with neurologic function sufficiently regained, compared with 26% (9 patients) in the control group. A separate randomized, blinded multicenter trial by the Hypothermia After Cardiac Arrest (HACA) Study Group was designed to determine the effect of mild hypothermia following resuscitation from VF‑triggered cardiac arrest. The degree of regained neurologic function and 6‑month mortality post‑arrest were employed as endpoints. This second trial employed a slightly different target temperature (32‑34°C, bladder temperature) and a specially designed cooling mattress 286
that delivered cold air to the body surface, as against an ice pack used by Bernard et al. to attain a more restrictive core body temperature of 33°C. The outcomes of the two trials were, however, very similar. The HACA group reported a 16% improvement in neurologic function measured within the 6‑month post‑arrest period: 55% of the patients had regained neurologic function in the hypothermia group compared to 39% in the control group. Mild hypothermia was also found to improve mortality within the same time frame by 14%. DEFINITIONS OF HYPOTHERMIA The circumstances surrounding hypothermia can be used to distinguish accidental hypothermia, for instance in drowning victims, from surgical hypothermia employed typically in open‑heart surgery, from its use in transplant tissue preservation and from resuscitative hypothermia employed in post‑resuscitation management of cardiac arrest - the central theme of this review. Hypothermia generally refers to a systemic temperature that is 30°C. This selection criterion rules out the likelihood of existing hypothermia capable of complicating treatment. The American Heart Association recommends therapeutic hypothermia for unconscious/comatose patients after ROSC following out‑of‑hospital cardiac arrest involving VF rhythm (Class IIa) in non‑VF cardiac arrests, and also in both out‑of‑hospital and in‑hospital arrests. The neuroprotective application of therapeutic hypothermia is expected to be explored for other pathologic conditions in the near future. This will require carefully planned randomized trials to investigate the benefits and safety in these other conditions. There are already promising results from animal models suggesting its potential use ischemic stroke and in shock (post‑resuscitation). Therapeutic hypothermia has also been employed in the management of pediatric conditions such as hypoxic ischemic encephalopathy, birth asphyxia, and pediatric cardiac arrest, which in children and infants, results mostly from asphyxia rather than VF, which is the major cause in adult patients. Patients apart from those meeting the general inclusion criteria may also be considered for hypothermia treatment based on expert recommendation and determined on a case‑by‑case basis. Pregnant women are generally excluded as are patients with known cases of coagulopathy or hemodynamic instability. Patients displaying impaired cognition, terminal conditions, a Do‑Not‑Resuscitate status, or for whom resuscitation efforts have lasted longer than 1 h, should also be excluded. TIMING OF COOLING Cooling usually commences with an induction phase during which the core body temperature is lowered at a carefully controlled rate to a target temperature usually between 32°C and 34°C. The employed rates of induction depend on the chosen method of cooling, but generally a method that delivers a cooling rate of 1°C/h will reach a target temperature of 33°C in roughly 4 h, assuming a pre‑induction body temperature of 37°C. 287
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The induction phase is followed by a maintenance phase where the core temperature is maintained for about 12‑24 h, depending on the management plan. Maintaining the target temperature of 33°C for 12 h in the study by Bernard et al., or 24 h (target temperature of 32‑34°C) by the HACA group, reportedly produced similar outcomes.[2,9] It is important that large deviations from the goal temperature be avoided during the maintenance phase in order to ensure positive treatment outcomes. After the patient has been maintained at the goal temperature for the specified duration, a gradual de‑cooling is commenced during which the body is slowly rewarmed (usually passively) at about 0.2‑0.5°C/h until the physiological temperature of about 36.5‑37°C is attained.  Slightly higher rewarming rates have been employed in certain cases, however, it is important to ensure that rewarming is conducted slowly and methodically to reduce the risk of rebound hypothermia, the worsening of brain damage, hypoglycemia, and/or electrolyte imbalance.[8,48] The rate of rewarming has also been indicated to affect the risk and degree of “cold injury”[12,4] and capillary shunting occurring post‑reperfusion.[12,49] The currently high degree of variation in rewarming rates employed by different centers makes it difficult to make categorical statements concerning how well the rewarming rates correlate with management outcomes. There is a need to design trials that will systematically address this question, especially as regards the influence of hypothermia duration and rewarming rate on the recovery of neurologic functions.
attendant high risk of hypothermia‑induced clotting disorders and dysrhythmias. These shortcomings have been largely addressed in more modern cooling techniques which employ non‑invasive surface cooling with the aid of cooling pads placed over the entire surface of the patient’s body.[8,51,52] The cooling pads are usually coated with hydrogel but they also sometimes take the form of a cooling garment. A temperature drop of between 1.0°C and 1.5°C is achieved with surface cooling in 1 h. However, care should be exercised to avoid the development of skin lesions resulting from the subjection of large skin surface to low temperature. Invasive cooling methods, employing endovascular catheters, have also been recommended for inducing hypothermia.[8,53,54] The catheter is inserted into the inferior vena cava and its surface serves as a platform for cooling, as heat is transferred away from the blood flowing over it. Both cooling pads and catheters are capable of achieving a rapid lowering of the patient’s body temperature to the target value and usually come with a built‑in feedback mechanism to regulate the rate of induced hypothermia, based on instantaneous body temperature. In 1 h, invasive cooling is able to achieve a temperature drop between 2.0°C and 4.5°C, a feature that makes it the preferred method of cooling. The efficiency associated with the use of nasopharyngeal delivery of evaporative coolant has also been reported, while tympanic and core temperature lowering of 2.3°C and 1.1°C (median values) were, respectively, documented in a multicenter study. Lastly, using intravenous infusion of saline at a degree of 4°C, a cooling rate of 2.8°C/h has been achieved.[56,57]
COOLING TECHNIQUES A number of cooling methods currently exist for inducing hypothermia starting with the use of ice packs and cooling blankets to the more sophisticated endovascular cooling techniques. The choice of cooling method should be made after carefully considering the associated cost with respect to derivable benefits and the availability of technical equipment needed to operate the selected method. Whichever method is eventually decided upon, it should be capable of delivering a continuous and regulated cooling and quickly achieving the target temperature, but without the risk of overcooling. Ice packs and cooling blankets usually achieve the target temperature too slowly and are associated with poor control of the cooling rate and a significant risk of overcooling and should therefore be avoided as much as possible. These two methods also lack appropriate temperature feedback control, with an 288
The choice of cooling method ultimately depends on the facilities available at the point of care. For instance, the use of endovascular catheters will understandably be influenced by a consideration of the required expertise and available facilities for handling infections and thrombosis, likely to arise from catheter use. Blankets and cooling pads, as well as ice packs on the other hand, do not require specialized training, a feature that makes them ideal choices in the absence of personnel trained in the use of catheters. HYPOTHERMIA MONITORING The cooling process is typically monitored by measuring the core or peripheral body temperature. Temperature measurements should ideally be commenced prior to starting hypothermia treatment; this additionally ensures that the target temperature is not exceeded Annals of Cardiac Anaesthesia Vol. 17:4 Sep-Dec-2014
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during cooling. Core temperature values often give a better indication of the depth of induced hypothermia and are usually obtained from the pulmonary artery. This is generally considered to be the gold standard of core body temperature measurement. However, esophageal temperature measurements have also been reported to give comparable accuracy  and radiographic scans may be used in guiding catheter insertion while measuring the esophageal temperature. The tympanum is another site where core temperature measurements have been conducted. In many cases, core temperature monitoring is not independent of the cooling process, which facilitates a smooth control of induced hypothermia via feedback sensing. The employed devices are typically capable of rapidly detecting heat changes in the patient’s body as against the measurement of peripheral temperatures, which are often characterized by a lag phase.  Measurements taken from the bladder are commonly affected by bladder conditions (for instance, how full the bladder is) which, especially in oliguria, should be taken into account in determining peripheral temperature values. Apart from the bladder, the mouth and the rectum are additional sites that have been employed for peripheral measurements. MANAGEMENT OF COMPLICATIONS OF THERAPEUTIC HYPOTHERMIA Concerns regarding the development of hypothermia‑associated complications are usually based on projections of biochemical events expected from cold treatment, which include effects on cardiac and immune functions, coagulopathy and the disruption of electrolyte balance. There are, however, indications that the associated risks of adverse effects are comparable with those reported for the control group. Nevertheless, the expected adverse effects are usually factored in while determining eligibility criteria and selecting patients for treatment. Complications likely to result from induced hypothermia include reduction in heart rate and cardiac output, prolongation of clotting time, electrolyte imbalance, overcooling, vasoconstriction, and shivering.[50,59] The last two effects exemplify the body’s natural homeostatic response to temperatures below physiologic thresholds, 36.5°C for vasoconstriction and 35.5°C for shivering. Hypothermia‑induced reduction in cardiac output and heart rate are interdependent and often offset by a reduction in metabolic rates, which in turn reduces Annals of Cardiac Anaesthesia Vol. 17:4 Sep-Dec-2014
the body’s metabolic demand.  Cold diuresis resulting from peripheral vasoconstriction and elevated venous return, however, may constitute a challenge when maintaining blood volume and should be effectively managed to avoid a precipitous drop in blood pressure and increase in vascular viscosity. These are generally associated with the early stages of hypothermia induction (i.e. the induction phase), but are not normally serious complications, except when they are accompanied by shivering. By increasing oxygen consumption along with metabolic rate, inadequately managed shivering may overwork the heart (tachycardia) and increase morbidity.[8,61,62] For this reason, the management of shivering during therapeutic cooling should be addressed aggressively. There are different ways by which hypothermia‑induced shivering is managed at different hospitals. The use of threshold‑lowering drugs is associated with doubtful efficacies and involves the use of non‑steroidal anti‑inflammatory drugs (NSAIDs) and analgesics. Sedatives (e.g. midazolam between 5 mg/h and 20 mg/h for a 70‑kg adult) and opiates (meperidine, fentanyl, and morphine) have been administered for their anti‑shivering effects. A recent review shows that some protocols employ propofol at 6 mg/kg/h after midazolam administration. Although neuromuscular blocking drugs have also been employed, their administration should proceed with extreme caution as they are likely to make the early detection of seizures difficult and have been associated with polyneuromyopathy. A counter‑warming of face and limbs is a good idea for managing hypothermia‑induced shivering. It has been observed that every degree drop in core body temperature may be compensated for by a 4°C increase of the skin temperature. Post‑arrest syndrome and nosocomial infections have been associated with hyperthermia complications during treatment.[12,8] Normothermia for 72 h following ROSC is the recommended intervention strategy in these cases. Other likely side effects include respiratory infections, which are associated with immune suppression resulting from hypothermia. CONCLUSION Evidence has emerged from clinical trials that demonstrates the efficacy of induced hypothermia in restoring neuronal function and reducing mortality associated with cardiac arrest. To optimize 289
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treatment outcomes, however, patient recruitment should be carefully conducted to minimize risks of hypothermia‑associated complications. Therapeutic hypothermia is recommended in post‑resuscitation cardiac arrest patients with a shockable rhythm, and also in cases of asphyxia cardiac arrest in children and infants. It is important, however, that therapeutic hypothermia be administered in a setting where complications from treatment and worsening symptoms of the patient’s status can be immediately and efficiently handled. In a general sense, this will entail the availability of a cardiac defibrillator and medications such as anti‑arrhythmic drugs, sedatives, muscle relaxants, and electrolytes in case of electrolyte imbalance. However, further studies are required to understand better and correlate aspects of hypothermic treatment, such as the rate of induction, the duration of the maintenance phase, and the rate of rewarming, with clinical outcomes. REFERENCES 1. 2.
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Cite this article as: Alshimemeri A. Therapeutic hypothermia after cardiac arrest. Ann Card Anaesth 2014;17:285-91. Source of Support: Nil, Conflict of Interest: None declared.
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