Neurocrit Care https://doi.org/10.1007/s12028-019-00817-1

RESUSCITATION FOLLOWING Emergency Neurological Life Support: Following Cardiac Arrest Sarah Livesay1*, Jonathan Elmer2, Matthew Kirschen3 and Sarah Peacock4

© 2019 Neurocritical Care Society

Abstract Cardiac arrest (CA) is the most common cause of in high-income nations. An organized bundle of neurocritical care can improve chances of survival and neurological recovery in patients resuscitated from CA. Therefore, resuscita- tion following CA was chosen as an Emergency Neurological Life Support protocol. Key aspects of successful post- arrest management include identifcation of treatable causes of arrest in need of emergent intervention, prevention of secondary brain injury, and delayed neurological prognostication. Treatable precipitants of arrest that require emergent intervention include, but are not limited to, acute coronary syndrome, intracranial hemorrhage, pulmonary embolism, and major trauma. Secondary brain injury can be attenuated through targeted temperature management, avoidance of hypoxia and hypotension, avoidance of hyperoxia, hyperventilation or hypoventilation, and treatment of seizures. Accurate neurological prognostication is not possible for several days after CA, so early aggressive care should not be limited based on perceived poor neurological prognosis. Keywords: Resuscitation, Cardiac arrest, Targeted temperature management,

Introduction are (1) to identify and treat the suspected cause of the Cardiac arrest (CA) is the most common cause of death arrest, and (2) to stabilize the patient’s cardiopulmonary in both North America and throughout high-income function to prevent re-arrest and provide adequate coro- nations [1]. In the USA, for example, more than 500,000 nary and cerebral perfusion. Patients who achieve ROSC patients sufer a CA each year [2]. With advances in care, and for whom goals of care support aggressive interven- rates of both return of spontaneous circulation (ROSC) tion should be rapidly evaluated for coronary interven- and long-term survival with favorable neurological out- tion and TTM. Transfer to a specialty center that sees come continue to improve over time [2]. Among those a high volume of CA and has experience in post-arrest who survive to hospital treatment after CA, withdrawal cardiac and neurocritical care should be considered for of life-sustaining therapy, based on perceived neurologi- these patients as another strategy to improve outcomes. cal prognosis, is the most common proximate cause of Suggested items to complete within the frst hour of death [3]. resuscitation following CA are shown in Table 1.

Management Protocol Prehospital Care and Immediate Stabilization Te Emergency Neurological Life Support (ENLS) algo- Intra-arrest management should follow the American rithm for initial management following resuscitation Association (AHA) and/or International Liaison from CA is shown in Fig. 1. Early priorities after ROSC Committee on Resuscitation guidelines (ILCOR) [4, 5]. Optimal cardiopulmonary resuscitation (CPR) including chest compressions of adequate rate and depth, few inter- *Correspondence: [email protected] ruptions, and early defbrillation are all associated with 1 Department of Adult and Gerontological Nursing, Rush University College of Nursing, 600 S. Paulina St Suite 1080, Chicago, IL 60612, USA faster ROSC and improved outcomes [6]. Further stud- Full list of author information is available at the end of the article ies are needed to establish the best methods to prevent laryngeal tube arm [13]. Another large randomized trial comparing supraglottic airway placement to endotra- cheal intubation found outcomes were no worse in the supraglottic airway arm [11], while a third found out- comes after bag-valve mask ventilation to be compara- ble to endotracheal intubation [14]. Based on these data, endotracheal intubation should not be viewed as a pri- ority for intra-arrest patient management and can rea- sonably be deferred until after achieving ROSC in most situations. Te optimal timing and method to proceed with endotracheal intubation among patients initially managed with a supraglottic airway are unknown but can likely be deferred until after additional hemodynamic sta- bilization if adequate ventilation and oxygenation can be delivered via the supraglottic airway. Among patients that initially regain pulses after advanced cardiovascular life support (ACLS), re-arrest within minutes is common, occurring in about one in fve cases [15, 16]. Even among those without frank re-arrest, providers should anticipate the potential for clinically important hemodynamic instability. Indeed, both hypo- tension and hypoxia are common and independently associated with worse outcomes [17]. Patients resusci- tated from CA typically require intubation, mechani- cal ventilation, close cardiac and invasive hemodynamic , and attentive general critical care. While cardiopulmonary stabilization is the priority during this phase, volume resuscitation, blood pressure, and oxygen- Fig. 1 ENLS Resuscitation following cardiac arrest protocol ation goals should be chosen to maintain cerebral perfu- sion and prevent secondary brain injury (see “Prevention of Secondary Brain Injury” section). Although TTM may Table 1 Resuscitation following CA checklist for the frst help prevent secondary brain injury, there is evidence of hour harm when TTM induction is begun in the prehospital Checklist setting with aggressive administration of cold crystalloids [18]. Other methods to induce TTM such as endonasal ☐ Initiate hemodynamic and ventilator support cooling may be safer [19], but there is insufcient evi- ☐ Assess for common treatable causes of arrest, consider coronary dence to recommend prehospital induction of TTM at angiography this time. ☐ Assess eligibility for targeted temperature management ☐ Begin induction to target temperature Diagnosis: Identifcation of Treatable Causes of CA ☐ Consider transfer to specialty center During and immediately after a CA, several parallel workfows are necessary to support successful resuscita- primary anoxic brain injury during and immediately after tion. Concurrently with CPR and stabilization, provid- arrest. ers should diligently search for the underlying etiology Tere have been numerous excellent randomized con- of arrest. Cardiac etiologies of arrest are decreasing over trolled trials studying various aspects of prehospital time, and may cause only a minority of arrests in popula- CA management [7–12], most of which have been neu- tion of patients that achieve ROSC and survive to hospi- tral and are beyond the scope of the ENLS curriculum tal care [20]. Initial diagnostic evaluation after ROSC may to review in detail. A large pragmatic trial comparing include a focused history, physical examination, electro- a strategy favoring endotracheal intubation to a strat- cardiogram (EKG) and judicious imaging, and prioritize egy favoring King (King LT-D) laryngeal tube place- identifcation of those etiologies that require specifc ment intra-arrest demonstrated superior survival in the time-sensitive interventions beyond general resuscitative measures. Cardiac Causes transport physician should be considered when arranging Cardiac diseases including acute coronary syndrome interfacility transport of unstable patients resuscitated are common causes of sudden CA. Acute coronary syn- from CA to ensure adequate resources is mobilized for drome may result in myocardial infarction, which may patient transport. cause malignant dysrhythmias and CA. Electrocardiog- raphy should be performed immediately following ROSC Management to evaluate for acute myocardial ischemia, regardless of Prevention of Secondary Brain Injury the primary rhythm associated with the arrest. Signif- In parallel with identifcation and treatment of the CA, cant coronary disease is found in the majority of patients post-resuscitation support should minimize secondary following resuscitation from CA, and percutaneous coro- brain injury. nary intervention is associated with improved neurologi- cal outcome [21–23]. Targeted Temperature Management (TTM) Multiple studies, including two randomized con- Intracranial Hemorrhage trolled trials, have demonstrated that TTM signif- CT imaging of the brain is warranted in the comatose cantly improved outcomes after CA when implemented post-arrest patient. Up to 5-10% of post-arrest patients with a well-defned post-arrest bundle of care [33–36]. demonstrate intracranial hemorrhage, potentially chang- Reducing core body temperature decreases cerebral ing the therapeutic approach [24–26]. In addition to oxygen demand and attenuates multiple cellular path- identifying potential causes of arrest, early brain imag- ways involved in ongoing brain injury in the hours and ing has important prognostic value. Early cerebral edema days after CA [37, 38]. Clinical trials frst demonstrated after CA strongly predicts poor outcomes [24–26]. improved survival and neurological outcomes with induced hypothermia to a core temperature of 32–34 °C Other Causes in selected patients resuscitated from out-of-hospital Other etiologies of CA must also be considered. Pul- CA (OHCA) due to ventricular tachycardia or fbrilla- monary embolism (PE) is a treatable cause of CA, and tion (VT/VF) [33, 34]. Subsequent work has shown that hemodynamic instability defnes a PE as high risk. overall outcomes are equivalent when mild hypother- Clinical suspicion for PE should prompt consideration mia actively targeting a core temperature of 36 °C rather of empiric treatment. If there is rapid hemodynamic than 33 °C is chosen, and that there is no clear beneft improvement, continuous heparin therapy alone may to 48 h of hypothermia compared to 24 h [39, 40]. Te be reasonable. Otherwise, systemic or catheter-directed AHA, ILCOR, the American Academy of , and thrombolysis should be strongly considered [27]. Trauma the Neurocritical Care Society all recommend institut- (e.g., high cervical spine fracture after ground-level falls), ing TTM at a target temperature between 32 and 36 °C gastrointestinal hemorrhage, overdose, septic , and (strong recommendation, low quality of evidence) [41– anaphylaxis are other possible etiologies of CA. Each 43]. Despite these recommendations, adoption of TTM requires disease-specifc management. If the clinical after CA remains limited [44]. history and initial presentation are suggestive of one of TTM is strongly recommended for patients with an these etiologies, they should be evaluated and managed OHCA of suspected cardiac origin [41]. Data on patients appropriately. with CA from other causes and in the hospital setting are mixed. Patients with initial asystole or pulseless electri- Stabilization and Transfer cal activity (PEA) may also derive some beneft from Post-arrest patients cared for at high-volume centers TTM [45, 46]. While an outcome beneft is less clear in have improved short- and long-term outcomes [28–32]. these populations, TTM is a low-risk intervention and A recent international systematic review and meta- potential benefts likely outweigh the risks. Te AHA and analysis of studies including over 61,000 patients dem- ILCOR guidelines support TTM for adults with OHCA onstrated that transportation to cardiac resuscitation with an initial non-shockable rhythm (weak recommen- centers [with on-site percutaneous coronary interven- dation, very low-quality evidence) [41]. tion (PCI) and TTM capability 24 h a day] was associated Data supporting TTM after in-hospital CA (IHCA) are also mixed. Te AHA and ILCOR guidelines suggest with increased survival (OR = 1.95, 95% CI, 1.47–2.59, P < 0.001) [31]. For this reason, transfer of comatose post- that TTM should be considered for patients who expe- arrest patients to a specialty center ofering PCI, cardiac rience an IHCA (weak recommendation, very low-qual- critical care, TTM, and neurocritical care may be pru- ity evidence) [41]. However, a subsequent cohort study dent. When available, active engagement of a critical care using data from the Get With Te Guidelines-Resusci- tation database suggested worse outcomes when TTM is applied to patients who experienced an IHCA [47]. Tere is some evidence that having a lower core tempera- Tis study should be interpreted with caution given the ture at the moment of coronary reperfusion can mitigate database nature of the study and potential selection bias. myocardial reperfusion injury [54, 55]. Further studies are needed in this patient population to determine the best role of TTM in patients with IHCA. Induction of TTM It is important to note that 36 °C is mild hypothermia After reviewing the contraindications discussed above, and not normothermia and that in the absence of active eligible patients should undergo immediate TTM. All TTM, most post-arrest patients will develop fevers early patients should be intubated at this point. Core tem- after resuscitation [34]. Several studies have suggested perature monitoring is also required. Te route of tem- that a move from a target temperature of 33–36 °C may perature monitoring can be endovascular, esophageal, decrease the proportion of patients receiving active bladder, or rectal. If the urine output is poor, Foley cath- cooling, thus increasing the possibility of fever rates eter-based temperature probes may not give accurate and worse overall outcomes [44, 48]. Te TTM-2 trial readings and an alternate core temperature source should is ongoing and is comparing 33 °C versus normother- be used. Axillary, oral, tympanic, and temporal tempera- mia with early treatment of fever ≥ 37.8 °C. Regardless of ture monitoring are all unreliable during TTM [56–58]. whether 36 °C or a lower target temperature is selected, In patients with a goal core temperature of 32–33 °C, TTM requires active temperature management, shiv- rapid induction of TTM is best accomplished by combin- ering prevention, and a comprehensive bundle of care. ing several cooling induction methods. In patients with- Developing systems to safely and efectively deliver TTM out signifcant left ventricular heart failure, rapid infusion requires signifcant institutional support, particularly to of up to 40 mL/kg of cold (4 °C) saline or Ringer’s lactate ensure that intervention is continuously available [35, decreases the core body temperature by approximately 49]. 1 °C for each liter of fuid administered [57, 59–61]. Some facilities keep saline in refrigerators for this purpose [35, Considerations: When TTM is Not Required 49]. Fluid should be infused rapidly to ensure that the Tere are few absolute contraindications to TTM. fuid does not rewarm during infusion, for example by Patients that rapidly awaken after CA (e.g., they able to using a pressure bag. Of note, one trial found prehospi- follow verbal commands such as “wiggle your toes,” and tal administration of cold fuids increases risk of pulmo- “squeeze my fngers”) are unlikely to derive beneft. Simi- nary edema and re-arrest [18]. Such complications may larly, patients with (DNR) orders or be better managed when the patient is in the emergency preexisting illnesses that preclude meaningful recovery department or ICU, and administration of cold fuids should have discussions with family or proxies regard- may be held until the airway is secure and the patient is ing goals of care early in the hospital course. Some of in the hospital. these patients will move directly to comfort care. Finally, If TTM to 36 °C is the goal, additional eforts may not patients who are more than 12 h after CA are less likely be required to achieve this temperature. Many patients to beneft from TTM and can be ofered active normo- are mildly hypothermic following resuscitation from thermia [50–52]. CA; thus, maintaining this temperature may be all that is required [18, 59, 62]. Regardless of target temperature, Eligibility: When is Targeting 36 °C Preferable to 33 °C? sedation, and management of shivering are required for Because signifcant hypothermia may potentiate coagu- successful induction (see below). In fact, the shivering lopathy and surgical , fndings of intracranial response is likely to be more pronounced because the bleeding, a traumatic etiology of CA, or anticipated patients’ thermoregulatory defenses, which are partly hemorrhagic diathesis should prompt a multidiscipli- suppressed at 32–33 °C, will be much more active at nary risk–beneft discussion. Since mild hypothermia 36 °C [37, 57]. targeting 36 °C does not afect coagulation ability, TTM Targeted temperature management can be achieved to 36 °C is probably advisable in these patients. Tere is using surface, intravascular, intranasal, or esophageal some suggestion that patients maintained at a lower tar- cooling [63]. For patients requiring extracorporeal mem- get temperature may experience more hemodynamic brane oxygenation (ECMO) therapy, body tempera- instability [53]. In patients requiring signifcant vasopres- ture may be strategically managed through this process. sor support after ROSC, a higher target temperature may Automated cooling devices should be started concur- be considered. rently with IV fuid administration or as soon as possible Te need for acute coronary revascularization is not thereafter. Multiple commercially available devices are a contraindication for TTM, and TTM can be initiated available. Air cooling blankets, cooling fans, and cool- prior to or during percutaneous coronary intervention. ing packs are not advised, as they take longer to achieve target temperature and lack a controlled thermoregula- because of prolonged time to onset and risk of hypoten- tion mechanism that is critical for TTM maintenance sion. [57]. and rewarming [63]. Important features of any device are NMB may be used to abate otherwise refractory shiv- good contact to ensure adequate heat exchange (a sim- ering. A single dose of short-acting NMB can be helpful ple cooling blanket is seldom sufcient) and continuous in cases of refractory shivering occurring in patients who input of the patient’s core temperature to ensure temper- are already maximally sedated with continuous infusion ature remains within range. Limited information is avail- agents (i.e., propofol, midazolam). When used, intermit- able regarding comparison of surface and intravascular tent dosing is preferred to continuous infusions. Con- cooling methods. tinuous NMB infusion was not associated with improved outcomes in one small randomized controlled trial [70]. Sedation and Shivering A larger retrospective multicenter cohort study found Many patients shiver vigorously during cooling induction that intermittent as-needed NMB was associated with because the shivering response is maximal at tempera- improved outcomes when compared to continuous NMB tures of approximately 35 °C [37]. Tis problem is pro- [71]. Additionally, NMB obscures any convulsive activ- nounced with lack of adequate sedation (see below). Skin ity that is typically detected by the neurological evalua- counter-warming (i.e., warming of the non-cooled areas tion. Te incidence of non-convulsive status epilepticus of the skin with a warm air blanket) markedly reduces the in the comatose post-arrest patient has been found to shivering response and should be considered, even when range from 12 to 24%, [72–74], and even higher incidence surface cooling methods are used. [57, 64, 65] Initial has been reported in pediatric CA. [75] Of note, seizures drug therapy should include scheduled acetaminophen following CA are associated with increased mortality (650 mg q4 h) and buspirone (30 mg q8 h) per feeding [72–74]. Terefore, continuous EEG should be utilized tube, magnesium therapy (4 g IV q4 h to maintain serum in comatose post-arrest patients, especially if paralysis is levels 3–4 mg/dl or infusion of 0.5–1 mg/h), followed by used. [76]. bolus doses of fentanyl (12.5–100 mcg or 1–2 mcg/kg IV push prn) with or without concomitant infusion of Key Physiological Changes Induced by Hypothermia fentanyl (25–150 mcg/h), or meperidine boluses (12.5– Hypothermia produces a number of predictable, dose- 100 mg IV q4–6 h prn). If shivering is still not controlled, dependent physiological changes. A detailed discussion propofol (50–75 mcg/kg/min) or midazolam (2–5 mg of these efects is outside the scope of this manuscript IV prn or 1–10 mg/h infusion) may be initiated [37, 57, and has been well reviewed elsewhere [37]. Instead, we 66]. A validated tool such as the Bedside Shiver Assess- focus briefy on selected physiological changes particu- ment Score (BSAS) is useful to monitor shiver response. larly relevant to the frst hours of neurocritical care. A stepwise approach to shiver management that incor- One expected physiologic change that occurs during porates non-pharmacological interventions and non- hypothermia is bradycardia. A heart rate of 35–40 beats sedating medication can help treat shivering while per minute is common at goal temperature of 33 °C and minimizing neuromuscular blockade (NMB) [63]. See the generally does not warrant therapy unless associated with ENLS Pharmacotherapy module for BSAS, a shiver man- hypotension [37]. Bradycardia may be more pronounced agement algorithm, and medications. at lower target temperatures. Atropine is generally inef- While adequate sedation may be provided by bus- fective in hypothermia-induced bradycardia. Instead, pirone, meperidine, dexmedetomidine, or fentanyl, the symptomatic bradycardia may be treated with beta ago- primary purpose of these agents is to prevent shiver- nists [37]. ing. If the patient is hemodynamically stable, propofol Arrhythmias may develop if the core temperature acci- is efective for ensuring adequate sedation and allows dentally falls below 28 °C (30 °C if electrolyte disorders for meaningful serial neurologic examinations due to its are present). Should signifcant arrhythmia develop with short half-life. [67] In patients without signifcant brady- a core temperature less than 30 °C, the patient should cardia, dexmedetomidine is an alternative, and directly be rewarmed rapidly to a core temperature greater than lowers the shivering threshold via central alpha-2 ago- 30 °C, followed by gradual warming to goal temperature. nism. [68] In hemodynamically unstable patients, a Arrhythmias should not be viewed as a reason to dis- midazolam infusion may be used. However, the half-life continue treatment, as mild hypothermia (greater than of midazolam is prolonged by hypothermia and residual 30 °C) does not cause or worsen arrhythmias. QT prolon- sedation may reduce the accuracy of any subsequent neu- gation is common during TH, and concomitant QT pro- rologic examination. [69] Terefore, during TTM, low longing drugs should be used with caution [37]. continuous infusions of midazolam supplemented with During induction of hypothermia, particularly to lower bolus doses are preferred. Morphine should not be used target temperatures, an initial cold diuresis may result in hypokalemia, hypomagnesaemia, and hypophos- 50-55 mmHg was targeted [95]. Although there is insuf- phatemia. Moreover, hypothermia shifts potassium from cient evidence to recommend routine use of mild hyper- the extracellular to intracellular space. Frequent assess- capnia after CA, hyperventilation should be avoided. ment of electrolytes and repletion is indicated. How- Targeting a temperature-corrected PaCO2 ≥ 40 mmHg is ever, overly aggressive repletion of potassium should be reasonable. avoided since serum potassium levels will predictably Both hypoxia and hyperoxia have been independently rise when rewarming is initiated. A goal potassium level associated with adverse outcome after CA, presum- of 3.0–3.5 mmol/L is reasonable during induction and ably because of inadequate cerebral oxygen delivery and maintenance of TTM [63]. Magnesium and phosphorus oxidative stress, respectively [17, 96–98]. Both should should be maintained in the high-normal range. be avoided, and a temperature-corrected PaO2 of 80–120 mmHg is reasonable. Seizure Detection and Treatment Blood gas measurements are afected by body tempera- EEG monitoring is indicated in the comatose post-arrest ture so the clinician needs to correct for these changes patient [75]. Te incidence of non-convulsive status epi- to properly interpret the values. Some blood gas labs ask lepticus ranges from 12 to 24% in adults and up to 47% for patient temperature and make this correction auto- in pediatric CA [72–75]. Other abnormal EEG patterns matically, but many do not. If the lab does not correct for are found in up to 40% of patients, and some are amena- patient temperature, approximate correction is as follows ble to early, aggressive therapy [73]. Seizures may directly (alpha-stat method): [37, 57, 99]. worsen brain injury and should be treated. Continu- ous EEG monitoring during the cooling and rewarming •• For every degree below 37 °C, subtract 5 mmHg from phase should be strongly considered [77]. More details the PaO2 lab value. can be found in the ENLS Status Epilepticus module. •• For every degree below 37 °C, subtract 2 mmHg from the PaCO2 lab value. Hemodynamic Management •• For every degree below 37 °C, add 0.012 units to the After ROSC, protracted cerebral hypoperfusion develops pH lab value. within hours and may last hours to days [78–81]. Dur- ing this time, cerebral vascular resistance is increased TTM Duration and Rewarming and pressure autoregulation is right-shifted or absent, ENLS focuses primarily on the frst few hours of patient resulting in decreased blood fow oxygen delivery, and management. Discussion of the duration and particu- increased perfusion pressure needed to sustain microvas- lar considerations for slow and controlled rewarming cular fow [81–86]. Observational studies show a consist- are beyond the scope of this paper. We refer readers to ent association between lower post-arrest blood pressure guidelines and reviews on TTM for detailed discussion of and mortality [17, 87, 88]. Moreover, maintaining a mean the entire course of TTM [63, 100]. Generally speaking, arterial pressure (MAP) > 80 mmHg is associated with interventions are expedited to achieve target tempera- improved outcomes, even if achieved at the expense of ture as quickly as possible. Tis is commonly referred vasopressor dependence [36, 87, 89, 90]. Transient left to as the induction phase. Patients are then maintained ventricular systolic and diastolic dysfunction early after at target temperature for 24 h. Studies range in duration ROSC are also common, but may be less clinically signif- from 12–48 h and 24 h is generally recommended. [63] cant and can usually be managed conservatively [91–93]. Tis is commonly referred to as the maintenance phase. In patients with suspicion of acute coronary syndrome as Te rewarming phase follows maintenance and should be the inciting etiology of CA, urgent or emergent coronary slow and controlled in order to avoid critical complica- angiography and revascularization should be consid- tions. Active normothermia is typically maintained for ered unless there is evidence of devastating neurological 24–48 h after rewarming is completed. injury [94]. Delayed Neurological Prognostication Pulmonary Management As in many neurocritical care conditions, accurate neu- Comatose post-arrest patients should be intubated rological prognostication after CA is challenging. A and mechanically ventilated. Although cerebral pres- detailed discussion of post-arrest prognostication is sure autoregulation may be impaired after resuscitation, beyond the scope of this manuscript. Critical to the initial response to carbon dioxide (CO­ 2) usually remains intact. evaluation and management of the post-arrest patient are Hyperventilation may result in cerebral vasoconstriction an understanding that in the frst 72 h after CA, no sign, and inadequate blood fow, and a Phase II randomized symptom, or combination of fndings short of controlled trial showed better outcomes when a PaCO­ 2 of precludes favorable recovery [42, 101]. Even clinical fndings compatible with brain death are not defnitive arterial pressure should be monitored continuously for at least 24 h following resuscitation or rewarming, [116]. should be titrated to avoid whichever comes later [102]. Premature withdrawal of extremes of oxygenation and ventilation, with hypoxemia life-sustaining therapy based on perceived neurologi- strictly avoided (goal SaO2 < 100%, but > 94%), and tar- cal prognosis has been linked to thousands of prevent- geting a PaCO2 that is appropriate to the specifc patient able after CA annually [3, 103]. Early limitations condition [116, 131, 132]. Tere is insufcient evidence in care may be appropriate in some patients, for example regarding glucose management in children after ROSC. those with preexisting advanced directives or severe con- In general, blood glucose concentrations should be moni- comitant medical comorbidities. However, early aggres- tored carefully, avoiding both hyperglycemia (> 180 mg/ sive care should not be limited or withheld based only on dL) and hypoglycemia (< 80 mg/dL). Seizures and status perceived poor neurological prognosis. epilepticus are common (47% and 32%, respectively) in the post-ROSC period. Seizures should be treated with Pediatric Considerations careful attention to potential hemodynamic side efects Pediatric CA afects nearly 20,000 children each year of anticonvulsants, although it remains unclear whether in the USA. Overall, survival to hospital discharge has treatment improves outcomes [75]. improved over the last two decades for IHCA, but not Hyperthermia after pediatric CA is common and asso- for OHCA [104, 105]. IHCA occurs primarily in pediat- ciated with poor neurologic outcomes [133]. Two large ric ICUs [106]. Te incidence of IHCA is 1.4–1.8% with prospective, randomized studies of comatose children 78% of children achieving return of circulation and 45% post-ROSC from both IHCA and OHCA (i.e., Terapeu- surviving to hospital discharge. Nearly 90% of survivors tic Hypothermia After CA (THAPCA) trials) found no of IHCA have favorable neurologic outcomes [107, 108]. beneft in survival with favorable functional outcomes at Although longer durations of CPR are associated with 1 year in patients treated with therapeutic hypothermia lower survival and worse neurologic outcome, 90% of (32–34 °C) compared to those treated with normother- children who survive after receiving more than 30 min mia (36–37.5 °C) [134, 135]. Tus, PALS guidelines for of CPR still have favorable outcomes [107, 109, 110]. temperature management in comatose children after CA Te initial rhythm in pediatric IHCA is most commonly recommend either maintenance of 5 days of continuous bradycardia with poor perfusion, or PEA which is often normothermia (36–37.5 °C) or maintenance of 2 days of preceded by tissue hypoxia from or initial continuous hypothermia (32–34 °C) followed by shock [107, 111]. Shockable rhythms (VF or pulseless 3 days of continuous normothermia. Continuous tem- VT) are less common and occur only in 10–15% of pedi- perature monitoring and aggressive treatment of fever atric CAs [111–113]. Improved outcomes after IHCA are (temperature of ≥38 °C) post-ROSC are Class I recom- in part due to a focus on delivering high-quality CPR in mendations [116]. compliance with pediatric advanced life support (PALS) While respiratory failure is the most common etiol- guidelines and advances in post-resuscitation care [114– ogy of pediatric CA, children can have other primary 117]. Improved outcomes have also been associated with causative mechanisms [112, 124, 136]. Children with an the use of individualized physiologic monitoring to guide unclear etiology of cardiac should undergo evaluation for intra-arrest therapies [6, 118], interdisciplinary debrief- the cause of CA including EKG and ECHO, neuroimag- ing programs [119], and ECMO as a rescue therapy for ing with CT, toxicology screens, infectious work-up, and refractory CA [120, 121]. Survival rates from OHCA are occult trauma. Patients with an arrhythmogenic cause of lower than IHCA and range from 3 to 16% with higher CA should be evaluated for channelopathies and cardio- survival rates for older children [117, 122, 123]. Favorable myopathy [137]. neurologic outcomes are present in 37–62% of survivors Similar to adults, accurate neurological prognostication [112, 123–125]. after CA is challenging and no single variable for prog- Similar to adults, the post-resuscitation phase should nostication has been established and validated. PALS focus on limiting secondary end-organ injury. Myocardial guidelines recommend that providers consider multiple dysfunction and arterial hypotension are common after factors when predicting outcomes after pediatric CA. pediatric CA [126–128], and hypotension (i.e., SBP < 5th percentile for age) is associated with increased mortality Nursing Considerations and lower rates of survival with favorable neurologic out- Nursing care for a patient with CA includes delivery of come [129, 130]. Te PALS guidelines recommend that high-quality CPR. After ROSC, the goals of care are to hypotension (i.e., SBP < 5th percentile for age) be treated maintain cerebral perfusion and prevent secondary brain with parenteral fuids, inotropes, and vasopressors, injury. Patients who sufer CA generally require admis- and when appropriate resources are available, invasive sion to an ICU with nursing care that includes close Table 2 Resuscitation following CA communication regarding assessment and referral Communication

☐ Patient age, pre-arrest circumstances ☐ Duration of CA and initial arrest rhythm ☐ Most likely etiology of arrest, if known ☐ Neurological examination on frst assessment ☐ PCI eligibility ☐ Time hypothermia started and/or target temperature reached ☐ Current core temperature ☐ Current drug infusions (especially sedative and vasoactive agents) Sample Sign-of Narrative Prehospital to ER: “I am signing out a 58-year-old man with known hypertension who collapsed with co-workers while walking to lunch.” “CPR was started by co-workers, an AED was applied and patient found to have a shockable rhythm. He was shocked once by the AED. EMS arrived approxi- mately 10 min later. He was found to be in ventricular tachycardia, and he received 1 mg of epinephrine and was shocked again. ROSC after approxi- mately 18 min.” After ROSC, we obtained an EKG and the patient was found to have ST elevation in leads V3-V6. He has an LMA and oxygen saturation is 100%. Blood pressure is 130/85 mm Hg and he is now in sinus tachycardia at 108 beats/min ER to ICU 58-year-old man with out of hospital CA with ROSC obtained at 18 min. “He was found to have a STEMI, and underwent PCI with stenting of a proximal LAD occlusion. He received heparin, aspirin, and prasugrel in the cath lab. On his initial neurological examination post-cath GCS was 5 (E1V1M3).” “TTM was started with a target temperature of 36 °C. Target temperature was achieved 45 min later at 14:10. Current temperature is 36.1 °C with a gel adhesive pad cooling device applied.” “The patient is currently on 2mcg/kg/min of norepinephrine. He received a single dose of cisatracurium at the initiation of TTM with 2gm of magne- sium and 150mcg of fentanyl. Fentanyl is ordered PRN for shivering along with the TTM and shivering management order set.”

neurologic, hemodynamic, and respiratory monitoring. Clinical Pearls Te role of the nurse includes initiation of TTM, close • Intra-arrest management (CPR) should follow AHA/ILCOR guidelines monitoring of vital signs, neurological examination and • Early re-arrest is common and should be prepared for in all patients who monitoring for seizures, and cardiac arrhythmias. It is achieve ROSC important for the nurse to monitor patients for complica- • Early after ROSC, time-sensitive etiologies of arrest should be actively tions that may arise from TTM including hemodynamic investigated, including acute myocardial infarction, , pulmonary embolism, etc. changes such as bradycardia, shivering, bleeding, and • Patient outcomes after CA may be improved by transfer to a high- electrolyte abnormalities [138]. Care of patients under- volume CA center. going TTM also includes minimizing immobility, pro- • Comatose post-arrest patients should undergo TTM to 33 °C or 36 °C longed sedation, and mechanical ventilation. Te nurse with few exceptions. should closely monitor the route of temperature moni- • Careful attention to electrolytes, shiver monitoring and prevention, and toring to ensure that the monitor of choice is in the cor- hemodynamic and pulmonary management during TTM is critical rect position to obtain accurate measurements. Nursing • Additional post-arrest care should minimize secondary injury through optimizing cerebral perfusion, avoiding hyperoxia, and detecting and staf should closely follow the TTM algorithm including treating seizures ensuring that the temperature and duration of cooling are as prescribed. Te nurse should use the BSAS scoring tool to incorporate interventions and countermeasures to prevent and treat shivering. Frequent skin assessments Author details 1 Department of Adult and Gerontological Nursing, Rush University College should be performed to prevent injury relating to cooling of Nursing, 600 S. Paulina St Suite 1080, Chicago, IL 60612, USA. 2 Departments devices and immobility. of , Critical Care Medicine and Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 3 Departments of Anes- Communication thesiology and Critical Care Medicine, Neurology, and Pediatrics, Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Penn- When communicating to an accepting or referring phy- sylvania, Philadelphia, PA, USA. 4 Department of Critical Care Medicine, Mayo sician about this patient, consider including the key ele- Clinic, Jacksonville, FL, USA. ments listed in Table 2. Acknowledgements 13. Wang HE, Schmicker RH, Daya MR, et al. Efect of a strategy of initial The authors are grateful for the contributions and insight provided by the laryngeal tube insertion vs endotracheal intubation on 72-hour survival following reviewers: Jason McMullan, MD; Scott Thomas May, PharmD, BCPS, in adults with out-of-hospital cardiac arrest: a randomized clinical trial. J BCCCP; and Victoria McCredie, MBChB, PhD, FRCPC, MRCPUK, UNCS. Am Med Assoc. 2018;320(8):769–78. 14. Jabre P, Penaloza A, Pinero D, et al. Efect of bag-mask ventilation vs Author contributions endotracheal intubation during cardiopulmonary resuscitation on SL, JE, MK, SP contributed in writing the manuscript. neurological outcome after out-of-hospital cardiorespiratory arrest: a randomized clinical trial. JAMA. 2018;319(8):779–87. Source of Support 15. Salcido DD, Sundermann ML, Koller AC, Menegazzi JJ. Incidence and None. outcomes of rearrest following out-of-hospital cardiac arrest. Resuscita- tion. 2015;86:19–24. Conflict of interest 16. Salcido DD, Stephenson AM, Condle JP, Callaway CW, Menegazzi JJ. Sarah Livesay being the owner/consultant at Sarah Livesay LLC/Stroke Chal- Incidence of rearrest after return of spontaneous circulation in out-of- lenges, consultant at Lombardi Hill and also a speakers Bureau at Stryker hospital cardiac arrest. Prehosp Emerg Care. 2010;14(4):413–8. NV. Jonathan Elmer, Matthew Kirschen, and Sarah Peacock have nothing to 17. Hartke A, Mumma BE, Rittenberger JC, Callaway CW, Guyette FX. disclose. Incidence of re-arrest and critical events during prolonged transport of post-cardiac arrest patients. Resuscitation. 2010;81(8):938–42. 18. Kim F, Nichol G, Maynard C, et al. Efect of prehospital induction of Publisher’s Note mild hypothermia on survival and neurological status among adults Springer Nature remains neutral with regard to jurisdictional claims in pub- with cardiac arrest: a randomized clinical trial. J Am Med Assoc. lished maps and institutional afliations. 2014;311(1):45–52. 19. 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