Therapeutic Hypothermia Treatment Following Cardiac Arrest
Category: Stroke
Author: Georgina Tyburski
Posted: Friday - October 2, 2015
19 year old male found unresponsive on the basketball court. EMS called, cardiac resuscitation initiated by his friends and resumed by emergency medical professionals upon arrival. He was taken to the local hospital where he lay comatose, intubated and sedated with occasional purposeful movement noted. The emergency room work up revealed appropriate criteria to implement therapeutic hypothermia.
Cardiac arrest results in over 300,000 deaths per year in North America alone. However, advances in cardiopulmonary resuscitation and post-cardiac arrest care have improved outcomes in a select group of patients. Among these advances are the use of therapeutic hypothermia (TH) and other interventions to improve the care of patients following cardiac arrest.
Immediately following resuscitation from cardiac arrest, the patient can develop a number of problems due to medical comorbidities and the chronic problems of ischemic injury sustained during the arrest. The most immediate threat to survival during the first minutes to hours is cardiovascular collapse. Interventions to optimize blood pressure and maintain end-organ perfusion (e.g., boluses of IV fluid, vasopressors, and inotropes) can help prevent secondary injury from hypotension. Additional short-term goals during the first six hours of care include optimizing oxygenation and ventilation and correcting electrolyte abnormalities. Determination of the cause of cardiac arrest and the initiation of relevant treatments are performed concurrently with resuscitation efforts in order to prevent recurrent arrest and optimize outcome. Evidence supports the use of therapeutic hypothermia (TH) to minimize brain injury and target body temperatures should be achieved within the first few hours following resuscitation.
A physical examination begins with the patient’s airway, breathing and circulation. A baseline neurologic examination should be performed to help determine the possible cause, likely clinical course, and need for neurologic interventions. Brainstem responses, including the pupillary, corneal, gag, and cough response to stimulation, correlate with survival and should be assessed. The Glasgow Coma Score should be determined, with particular attention paid to the motor score, which correlates closely with neurologic outcome. Patients who cannot perform purposeful movements or follow basic commands generally need treatment with induced hypothermia.
Diagnostic tests, including an electrocardiogram, imaging studies, and laboratory tests, are usually required to determine the etiology of cardiac arrest, to confirm endotracheal tube positioning and assess for chest trauma from CPR, and to ascertain the involvement of specific organ systems and gauge the severity of injury.
Imaging studies including chest radiology and CT scans are beneficial to identify common complications from cardiac arrest such as aspiration, pneumothorax and mediastinal abnormalities suggestive of aorta dissection. Bedside emergency ultrasound is helpful to identify causes of arrest that represent ongoing threats to life including pericardial tamponade, pneumothorax, catastrophic pulmonary embolism and intraperitoneal bleeding. CT scan of the brain can detect early cerebral edema or intracranial hemorrhage in the comatose post-cardiac arrest patient.
Labs can provide insight to the cardiac arrest but is also necessary to evaluate the extent and progression of arrest-related injury to organ systems
Neurologic injury is the most common cause of death in patients with out-of-hospital cardiac arrests and contributes to the mortality of in –patients with cardiac arrest. When combined with standard post-cardiac arrest, lowering core body temperature to the range of 32 to 34’ C during the first hours after cardiac arrest improves neurological outcomes compared to not controlling body temperature.
Indication and contraindications: Patient not following commands or showing purposeful movements following resuscitation from cardiac arrest should have their core body temperature managed. The only absolute contraindication for temperature management is an advanced directive that outlines aggressive care. Specific hospital protocols should be directed towards the pregnant and/or hemodynamically unstable patients, and those receiving coronary catheterization or thrombolytics due to the increased risk of bleeding.
The initiation of therapeutic hypothermia in post cardiac arrest patients is recommended that active control of the patient’s core temperature be achieved as soon as possible, with control maintained for at least 48 hours.
The goal temperature is 36’ C for 24 hours in uncomplicated patients who have moderate coma (some motor response) and no evidence of cerebral edema on CT Head scan. It is suggested using 33’ C for at least 24 hours for deep coma (loss of motor response or brainstem reflexes), or early CT Head changes suggesting the development of cerebral edema are detected.
Methods used to implement therapeutic hypothermia include using intravascular or surface methods to control temperature. Intravenous infusion of 30ml/kg of cold (4’ C / 39’F) isotonic saline, using a pressure bag to increase the rate of administration reduces the core temperature by >2’ C per hour. One liter of saline infused via pressure bag over approximately 15 minutes can drop the core temperature by approximately 1’C. Use with isotonic solutions must be used cautiously due to the risk of pulmonary edema and increased need for diuretic use.
Surface cooling methods, including ice packs, cooling blankets, and cooling vests can reduce the cord body temperature by 0.5 to 1’C per hour. In patients who cannot tolerate rapid fluid administration, cool water and fans can be used as an alternative method to induce hypothermia. Therapeutic hypothermia is usually induced by infusing 1 to 2 liters of cold saline using a pressure bag, while simultaneously implementing surface cooling using cooling blankets and or ice packs applied to the axillae, groin, and neck (adjacent to major blood vessels).
Both surface and intravascular cooling devices are effective at maintaining a goal temperature for 12 to 24 hours. However, the effect of mild temperature fluctuations and excessive hypothermia on patient outcomes is unknown, and thermostatically controlled devices provide the most precise minute-to-minute temperature regulation.
Shivering raises body temperature and must be suppressed in patients being treated with therapeutic hypothermia. Failure to suppress shivering is a common reason for delays in achieving goal temperatures while cooling patients. Titrating sedation is recommended and many times high doses of sedation are required to accomplish shivering suppression. A continuous infusion of medications such as propofol and Fentanyl with or without the use of benzodiazepines (eg. Midazolam) is one effective approach to sedation.
Temperature monitoring and re-warming, the core body temperature must be monitored continuously during the therapeutic hypothermia procedure. The gold standard for temperature measurement is central venous temperature. Other alternatives are available to use such as monitoring methods including esophageal, bladder and rectal probes. During the re-warming process the temperature should be raised gradually, with the rate of increase not to exceed 0.5’C per hour. It requires close monitoring of the patient due to the re-warming process causing electrolyte abnormalities such as hyperkalemia (high potassium), cerebral edema, and seizure to name a few.
Several available approaches to the re-warming process include manual re-warming by increasing the set point for the patient’s temperature when a cooling blanket has been used for cooling. By increasing the set point of the patient’s temperature by 0.5’C every three hours until a normal temperature is reached. In the situation where ice packs were used, a few ice packs can be removed each hour and the rate of re-warming can be used to determine when additional ice pack are applied if the patient’s temperature is increasing to quickly. Other alternatives to re-warm patients include increasing the room temperature, applying a convective heating device, heat lamps, or warming inspired air via the ventilator heating circuit on the humidifier.
Potential adverse effects of therapeutic hypothermia in clued impaired coagulation due to clotting enzymes operating slower and more platelets function less effectively during therapeutic hypothermia. Also and increased risk of infection related to therapeutic hypothermia impairs leukocyte function. Other adverse effects include cardiac arrhythmias such as bradycardia and QT interval prolongation. Hyperglycemia due to insulin resistance has been observed in some cases. Hypothermia can also lead to a “cold dieresis” resulting in numerous electrolyte imbalances such as hypovolemia, hypokalemia, hypomagnesaemia and hypophosphatemia. It is extremely important to monitor these patient’s volume status and basic electrolyte labs frequently during temperature management.
Numerous studies are ongoing regarding the benefit of therapeutic hypothermia. It has been proven for the treatment of post cardiac arrest coma therapeutic hypothermia can be successfully implemented in intensive care practice with major benefits on patient outcomes. The outcomes appear to be related to the type and duration of initial cardiac arrest.
In the scenario of the 19 year old patient suffering cardiac arrest, the therapeutic hypothermia intervention was a benefit in preserving brain tissue. The flight team immediately implemented therapeutic hypothermia protocol by using chilled IV isotonic solutions, ice bags and tracheal temperature monitoring. This young man suffered a catastrophic event. Aggressive intervention, immediate recognition and implementation of therapeutic hypothermia this patient was able to be discharged and lead a normal life without neurological deficit.
Did your client receive aggressive appropriate interventions post cardiac arrest?
