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Therapeutic hypothermia (TH) has emerged as an important treatment option for patients resuscitated from cardiac Clinical Application and Management.
Table of contents
- Clinical application of mild therapeutic hypothermia after cardiac arrest.
- Therapeutic hypothermia after cardiac arrest • LITFL • CCC Resuscitation
- Why might I need therapeutic hypothermia after cardiac arrest?
- Recommended for you
Clinical application of mild therapeutic hypothermia after cardiac arrest.
The disadvantages of this method include all the risks associated with placing central venous catheters including injury during placement; infection; and venous thrombosis; in addition to the expense of the units and consumables Seder and Van der Kloot, ; Vaity et al, There are a number of other means by which cooling can be initiated in the comatose post cardiac arrest patient, which are not as widely used in clinical practice as those already discussed within the current article. These include: extra-corporeal circuits via cardiopulmonary bypass or a specific extracorporeal device where blood is circulated by a pump around a circuit that sits outside of the body ; body cavity lavage where cold fluid is infused into the abdominal cavity ; whole-body ice water immersion; continuous renal replacement therapy; and an intranasal cooling system which enables cooling to be commenced prior to ROSC.
Ongoing trials are looking at the safety and efficacy of these methods Seder and Van der Kloot, ; Vaity et al, Initiating TTM can result in physiological side effects for the patient. Several side effects will now be discussed. Shivering occurs in most patients, increasing the metabolic rate and heat production, which in turn can delay cooling and affect temperature control.
Shivering is associated with good neurological outcome when associated with induced hypothermia, as it is a normal physiological response Nolan et al, Shivering usually occurs as the target temperature is being achieved; once the target temperature has been reached, shivering is less common. It is important that shivering is recognised and managed early to prevent the delay in achieving the targeted temperature. Management of shivering is undertaken with the administration of infusions of sedatives and analgesics.
Therapeutic hypothermia after cardiac arrest • LITFL • CCC Resuscitation
If the shivering cannot be controlled following infusion with sedation and analgesics, the use of neuromuscular blockade agents may be considered. Consideration should be given to the half-life of these agents as hypothermia reduces the clearance of sedatives, analgesics and neuromuscular blockade agents; agents with short half-lives will assist in timely neurological assessment of the patient Scirica, Hypothermia can increase systemic vascular resistance as vasoconstriction occurs resulting in hypertension.
The patient may also become tachycardic as the body tries to conserve heat; however, this generally occurs on initiation of cooling Scirica, Once the patients are hypothermic, they may experience bradycardia or arrhythmias. Scirica identifies that although hypertension may occur as a result of vasoconstriction on cooling, it is common to see hypotension in this group of patients. Hypotension can occur as a result of vasodilation caused by a post-resuscitation inflammatory release or directly from cardiac ischaemia that has resulted in cardiac dysfunction.
Hypotension needs to be managed to achieve a mean arterial pressure that ensures there is good cerebral perfusion pressures—usually 80— mmHg. This will avoid cerebral hypotension and hypoperfusion. Post resuscitation, patients are often vasoplegic the patient has a low systemic vascular resistance owing to intravascular depletion; fluid resuscitation should be titrated to a measured central venous pressure.
If the patient continues to have heamodynamic instability and the hypothermia is thought to be contributing, the target temperature can be increased in slow controlled stages until tolerated Scirica, Hypothermia can cause electrolyte imbalance by causing electrolyte loss through increased diuresis Scirica, ; Nolan et al, In addition, hypothermia results in a shift of potassium into the cells, lowering serum levels Scirica, ; Nolan et al, Regular monitoring of electrolyte levels and replacement as required is advised but consideration about pausing replacement prior to the rewarming period should occur as rewarming will result in potassium being released from the cells, elevating serum potassium levels Scirica, ; Nolan et al, Hyperglycaemia is common as hypothermia increases insulin resistance and reduces insulin secretion Scirica, ; Nolan et al, This requires close monitoring and management of blood glucose levels with insulin Scirica, ; Nolan et al, Hypothermia can suppress cellular and antibody immunity making this group of patients more prone to infection Scirica, ; Nolan et al, There is an association with an increased rate of pneumonia in hypothermic post cardiac arrest patients Scirica, ; Nolan et al, , most likely owing to CPR, emergency intubation and mechanical ventilation.
Despite this, there is no associated increase in mortality rates and there is no apparent impact on outcome Scirica, ; Nolan et al, Hypothermia does impair coagulation that may result in some minor bleeding but this has yet to be proven in clinical studies according to the ERC Nolan et al, Many clinical areas that undertake TTM do not routinely perform neuromonitoring. Patients post cardiac arrest are at risk of developing secondary neurological injury as identified previously. Seder and Van der Kloot recommend the use of neuromonitoring to detect seizures, elevated intracranial pressure and reduced cerebral blood flow.
The monitoring also aids in deciding on their management as well as that of excessive cerebral and metabolic demands as a result of shivering. Seder and Van der Kloot identify possible mechanisms for neuromonitoring on the intensive care unit and their advantages and disadvantages. These include: continuous electroencephalography EEG that enables immediate recognition of seizures, and shivering in patients who are heavily sedated or where neuromuscular blockade agents have been administered.
It does however require continuous interpretation and associated expertise. Bispectral index BIS monitoring will detect the level of awareness that the patient may have while undergoing TTM, sedation and possible neuromuscular blockade. This will facilitate titration of sedation in less severely injured patients and is easy to use.
If the patient is shivering, it can disrupt the signal. Intracranial pressure monitoring enables clinicians to identify if there is an elevated intracranial pressure, which is common after cardiac arrest. A mean arterial pressure target can then be set and agents administered to ensure an adequate cerebral perfusion pressure. This strategy is invasive and there is an increased risk of procedural bleeding resulting from hypothermia Seder and Van der Kloot, All of the above monitoring can aid in prognostication and can be early indicators, which would prompt further investigations. According to the ERC Nolan et al, , for those patients who have suffered a significant hypoxic brain injury as a result of their cardiac arrest, there is a need to ensure that any prognostication is undertaken to eliminate false positives.
This is especially relevant to TTM as the hypothermia, sedative and neuromuscular blockade agents can interfere with prognostication. For those patients who have received sedation or there is a possibility they may still be paralysed, prognostication should be delayed beyond the 72 hours from ROSC Nolan et al, Occurrence of clinical conditions such as status epilepticus during hypothermia or rewarming are nearly always associated with poor outcome.
When undertaking prognostic clinical examinations or testing such as EEG or short-latency somatosensory evoke potentials SSEP , results should be interpreted in the context of hypothermia or post rewarming, as expected results can differ from those seen in patients who did not undergo TTM Nolan et al, TTM has been shown to provide neuroprotection for comatose post cardiac arrest patients.
Recent clinical trials have led to the publication of guidelines to support the clinical application of TTM as part of the overall management of post cardiac arrest patients. Patients undergoing TTM require close observation and frequent manipulation of treatment strategies to maintain their stability and improve clinical outcome.
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There are multiple ways to deliver TTM and it is the choice of individual clinical areas to determine the targeted temperature; duration of TTM; and initiation of neuromonitoring. This will vary from centre to centre but can be supported in practice by the introduction of standardised protocol-driven care within the intensive care units to avoid delays in therapy or prognostication.
There are areas of TTM that require further clinical trials to provide evidence of efficacy and safety which would support further defined recommendations for clinical practice. A large multi-centered clinical trial is due to be undertaken with the aim of providing further evidence and clarification of what is considered best practice for TTM. Targeted temperature management has replaced therapeutic hypothermia to encompass the management of temperature control. Targeted temperature management is neuroprotective in comatosed post cardiac arrest patients.
Targeted temperature management has three main phases which are interchangeable depending on the target temperature set. There are associated side effects of hypothermia which require close monitoring and management by nursing staff. How could TTM improve the neurological outcome for patients within your clinical area post cardiac arrest? How could TTM be applied within your clinical area currently and in the future taking into consideration resources, training and exposure?
British Journal of Cardiac Nursing Vol.
- Practice Essentials;
- The Picture Show!
- Side-effects of induced hypothermia;
Andrea McDonnell Search for more papers by this author. Table 1. Proposed causes of hyperthermia Mechanisms of hyperthermia post cardiac arrest Increased heat production of endogenous catecholamines Decreased heat loss or altered distribution of body heat owing to vasoconstriction Loss of thermoregulatory mechanisms seen in patients with stroke as a result of damage in the anterior region of the hypothalamus Infection following cardiopulmonary resuscitation CPR which can be secondary to pulmonary aspiration or gut translocation of bacteria and toxins following global ischaemia during and after CPR Affect of hyperthermia on the ischaemic brain Release of neurotransmitters is increased Production of oxygen radicals during the reperfusion phase is increased Adenosine triphosphate ATP depletion Enhanced calpain activation associated with irreversible neuronal damage.
Source: Vaity et al Proposed causes of hyperthermia. View as image HTML. Table 2. Source: Nolan et al, TTM mechanism of neuroprotection. Table 3. Recommendations for clinical practice. Table 4. Methods of achieving TTM Conventional cooling techniques Ice packs Cold Intravenous fluid administration Wet towels Crushed ice Surface cooling systems Cooling blankets or pads Water- or air-circulating blankets Water-circulating gel-coated pads Intravascular cooling systems Less commonly used techniques Extra-corporeal circuits Body cavity lavage Whole-body ice water immersion Continuous renal replacement therapy Intranasal cooling system.
Source: Seder and Van der Kloot, ; Vaity et al, Methods of achieving TTM. References Amey C. Tailored Temperature Management in Neurocritical Care. Eur Neurol Rev. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. New Engl J Med. Inducing hypothermia after out of hospital cardiac arrest.
European Resuscitation Council Guidelines for Resuscitation. Erratum in: Resuscitation. Therapeutic hypothermia following cardiac arrest [IPG ]. Therapeutic hypothermia after cardiac arrest. Crit Care Med. Crit Care. This is a safe and effective method, as the temperature range is better controlled both during induction and rewarming. Currently, the most effective method to induce hypothermia is the use of endovascular catheters that provide optimized temperature control for induction, maintenance or rewarming.
This system uses a special coated metal central venous catheter where water circulates from an external cooler system. The catheter may be installed either via femoral, subclavia or jugular accesses. The experience with these devices is still limited as they are more expensive but, on the other hand, less troublesome to the team than conventional methods. Mean blood pressure levels above 80 mmHg are recommended for cardiac arrest survivors, and volume replacement and vasopressors may be required to keep these values.
The most commonly used vasopressor during TH is norepinephrine. Hypothermia causes insulin resistance. Blood glucose monitoring should be performed with venous blood measures, as skin vasoconstriction may change the results. Laboratory tests may be scheduled every 6 or 12 hours, depending on previous results, and include the same tests as during the induction phase.
Why might I need therapeutic hypothermia after cardiac arrest?
Pulse oxymetry is not a suitable parameter during hypothermia, and the mechanic ventilation parameters should be set based on gasometry values. Feeding is not indicated during TH, as stomach emptying is delayed in these patients. Additionally, there is an increased mechanic ventilation associated pneumonia VAP risk for possible aspiration during CA.
Strict VAP prevention measures are thus recommended.
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Another fundamental aspect for this phase management is sedation and analgesia. In addition to continued midazolam and phentanyl infusions, additional doses may be needed to maintain appropriate sedation. Seizures activity may be masked by sedation and muscular blockade, so continued electroencephalogram is indicated, if available. BIS and electroencephalogram uses are protocol refinements, and are not indispensable. Convulsive seizures and shivering require aggressive therapy in any phase, as they increase metabolic oxygen demands.
Neuromuscular blockers should be reevaluated after 12 hours and stopped if there is no evidence of shivering. Severe arrhythmias and bleeding during this phase require cooling discontinuation. Continued electrocardiogram monitoring is fundamental during the entire treatment period. Bradycardia or Osborne waves do not indicate TH discontinuation.
Rewarming fase: this phase takes place 24 hours after cooling was started, and should be slow, by 0.