Web-based Integrated 2010 & 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
2015 (New): It is reasonable to provide opioid overdose response education, either alone or coupled with naloxone distribution and training, to persons at risk for opioid overdose (or those living with or in frequent contact with such persons). It is reasonable to base this training on first aid and non-HCP BLS recommendations rather than on more advanced practices intended for HCPs.
2015 (New): Empiric administration of IM or IN naloxone to all unresponsive victims of possible opioid-associated life-threatening emergency may be reasonable as an adjunct to standard first aid and non-HCP BLS protocols. For patients with known or suspected opioid overdose who have a definite pulse but no normal breathing or only gasping (ie, a respiratory arrest), in addition to providing standard care, it is reasonable for appropriately trained rescuers to administer IM or IN naloxone to patients with an opioid-associated respiratory emergency (Figure 1). Responders
should not delay access to more advanced medical services while awaiting the patient’s response to naloxone or other interventions.
Empiric administration of IM or IN naloxone to all unresponsive opioid-associated resuscitative emergency patients may be reasonable as an adjunct to standard first aid and non-HCP BLS protocols. Standard resuscitation procedures, including EMS activation, should not be delayed for naloxone administration.
2015 (New): Patients with no definite pulse may be in cardiac arrest or may have an undetected weak or slow pulse. These patients should be managed as cardiac arrest patients. Standard resuscitative measures should take priority over naloxone administration, with a focus on high-quality CPR (compressions plus ventilation). It may be reasonable to administer IM or IN naloxone based on the possibility that the patient is in respiratory arrest, not in cardiac arrest. Responders should not delay access to more-advanced medical services while awaiting the patient’s response to naloxone or other interventions.
Why: Naloxone administration has not previously been recommended for first aid providers, non-HCPs, or BLS providers. However, naloxone administration devices intended for use by lay rescuers are now approved and available for use in the United States, and the successful implementation of lay rescuer naloxone programs has been highlighted by the Centers for Disease Control.1 While it is not expected that naloxone is beneficial in cardiac arrest, whether or not the cause is opioid overdose, it is recognized that it may be difficult to distinguish cardiac arrest from severe respiratory depression in victims of opioid overdose. While there is no evidence that administration of naloxone will help a patient in cardiac arrest, the provision of naloxone may help an unresponsive patient with severe respiratory depression who only appears to be in cardiac arrest (ie, it is difficult to determine if a pulse is present).
2015 (Updated): It may be reasonable to administer ILE, concomitant with standard resuscitative care, to patients who have premonitory neurotoxicity or cardiac arrest due to local anesthetic toxicity. It may be reasonable to administer ILE to patients with other forms of drug toxicity who are failing standard resuscitative measures.
2010 (Old): It may be reasonable to consider ILE for local anesthetic toxicity.
Why: Since 2010, published animal studies and human case reports have examined the use of ILE for patients with drug toxicity that is not the result of local anesthetic infusion. Although the results of these studies and reports are mixed, there may be clinical improvement after ILE administration. As the prognosis of patients who are failing standard resuscitative measures is very poor, empiric administration of ILE in this situation may be reasonable despite the very weak and conflicting evidence.
2015 (Updated): Priorities for the pregnant woman in cardiac arrest are provision of high-quality CPR and relief of aortocaval compression. If the fundus height is at or above the level of the umbilicus, manual left uterine displacement can be beneficial in relieving aortocaval compression during chest compressions.
2010 (Old): To relieve aortocaval compression during chest compressions and optimize the quality of CPR, it is reasonable to perform manual left uterine displacement in the supine position first. If this technique is unsuccessful, and an appropriate wedge is readily available, then providers may consider placing the patient in a left lateral tilt of 27° to 30°, using a firm wedge to support the pelvis and thorax.
Why: Recognition of the critical importance of high-quality CPR and the incompatibility of the lateral tilt with high-quality CPR has prompted the elimination of the recommendation for using the lateral tilt and the strengthening of the recommendation for lateral uterine displacement.
2015 (Updated): In situations such as nonsurvivable maternal trauma or prolonged maternal pulselessness, in which maternal resuscitative efforts are obviously futile, there is no reason to delay performing perimortem cesarean delivery (PMCD). PMCD should be considered at 4 minutes after onset of maternal cardiac arrest or resuscitative efforts (for the unwitnessed arrest) if there is no maternal ROSC. The clinical decision to perform a PMCD—and its timing with respect to maternal cardiac arrest—is complex because of the variability in level of practitioner and team training, patient factors (eg, etiology of arrest, gestational age of the fetus), and system resources.
2010 (Old): Emergency cesarean delivery may be considered at 4 minutes after onset of maternal cardiac arrest if there is no ROSC.
Why: PMCD provides the opportunity for separate resuscitation of the potentially viable fetus and the ultimate relief of aortocaval compression, which may improve maternal resuscitation outcomes. The clinical scenario and circumstances of the arrest should inform the ultimate decision around the timing of emergency cesarean delivery.
These Web-based Integrated Guidelines incorporate the relevant recommendations from 2010 and the new or updated recommendations from 2015.
Part 10 of the 2015 American Heart Association (AHA) Guidelines Update for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) addresses cardiac arrest in situations that require special treatments or procedures other than those provided during basic life support (BLS) and advanced cardiovascular life support (ACLS).
This Part summarizes recommendations for the management of resuscitation in several critical situations, including cardiac arrest associated with pregnancy (Part 10.1), pulmonary embolism (PE) (10.2), and opioid-associated resuscitative emergencies, with or without cardiac arrest (10.3). Part 10.4 provides recommendations on intravenous lipid emulsion (ILE) therapy, an emerging therapy for cardiac arrest due to drug intoxication. Finally, updated guidance for the management of cardiac arrest during percutaneous coronary intervention (PCI) is presented in Part 10.5. A table of all recommendations made in this 2015 Guidelines Update as well as those made in the 2010 Guidelines is contained in the Appendix.
The special situations of resuscitation section (Part 12) of the 2010 AHA Guidelines for CPR and ECC2 covered 15 distinct topic areas. The following topics were last updated in 2010, and are included in this Web-based integrated Guidelines document:
• Management of cardiac arrest associated with asthma (Part 12.1)
• Anaphylaxis (12.2)
• Morbid obesity (12.4)
• Electrolyte imbalance (12.6)
• Trauma (12.8)
• Accidental hypothermia (12.9)
• Avalanche (12.10)
• ACLS treatment of cardiac arrest due to drowning (12.11)
• Electric shock or lightning strikes (12.12)
• Cardiac tamponade (12.14)
• Cardiac surgery (12.15)
• Toxic effects of benzodiazepines, β-blockers, calcium channel blockers, digoxin, cocaine, cyclic antidepressants, carbon monoxide, and cyanide (12.7)
Additional information about drowning is presented in Part 5, “Adult Basic Life Support and Cardiopulmonary Resuscitation Quality.”
The recommendations in the 2015 Guidelines Update are based on an extensive evidence review process that was begun by the International Liaison Committee on Resuscitation (ILCOR) with the publication of the ILCOR 2010 International Consensus on CPR and ECC Science With Treatment Recommendations (CoSTR)3 and was completed with the preparation of the 2015 CoSTR publication.4,5
In the in-depth international evidence review process, the ILCOR task forces examined topics and then generated prioritized lists of questions for systematic review. The process by which topics were prioritized for review are described in the CoSTR publication.6,7 Questions were first formulated in PICO (population, intervention, comparator, outcome) format,8 the search strategy and inclusion and exclusion criteria were defined, and then a search for relevant articles was performed. The evidence was evaluated by using the standardized methodological approach proposed by the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group.9
The quality of the evidence was categorized based on the study methodologies and the 5 core GRADE domains of risk of bias, inconsistency, indirectness, imprecision, and other considerations (including publication bias). Then, where possible, consensus-based treatment recommendations were created. Further information about this international evidence evaluation process can be found in the 2015 CoSTR, “Part 2: Evidence Evaluation and Management of Conflicts of Interest.”10,11
To create the 2015 Guidelines Update, the AHA formed 15 writing groups, with careful attention to avoid or manage conflicts of interest, to assess the ILCOR treatment recommendations and to write AHA treatment recommendations by using the AHA Class of Recommendation and Level of Evidence (LOE) system. The recommendations made in the 2015 Guidelines Update are informed by the ILCOR recommendations and GRADE classification of the systematic reviews in the context of the delivery of medical care in North America. In the online version of this publication, live links are provided so the reader can connect directly to those systematic reviews on the ILCOR Scientific Evidence Evaluation and Review System (SEERS) website. These links are indicated by a combination of letters and numbers (eg, ALS 436). We encourage readers to use the links and review the evidence and appendixes, such as the GRADE tables. Further information about this evidence evaluation process can be found in “Part 2: Evidence Evaluation and Management of Conflicts of Interest” of this 2015 Guidelines Update.
Contemporaneous with the ILCOR evidence-review process, the AHA ECC Committee; Council on Cardiopulmonary, Critical Care, Perioperative, and Resuscitation; Council on Cardiovascular Diseases in the Young; and Council on Clinical Cardiology have developed an AHA Scientific Statement on cardiac arrest in pregnancy.12 While this document provides treatment recommendations for the intra-arrest management of pregnant patients, a full discussion of preparation, prevention, resuscitation, emergency delivery, and postresuscitation care are beyond the scope of this article. Readers are directed to the full Scientific Statement for more complete recommendations.
Cardiac arrest associated with pregnancy is rare in highincome countries. Maternal cardiac arrest occurs in approximately 1:12 000 admissions for delivery in the United States.13 Maternal cardiac arrest rates appear to be increasing in the United States, from 7.2 deaths per 100 000 live births in 1987 to 17.8 deaths per 100 000 live births in 2009.14 Maternal mortality rates are lower in Canada, where maternal mortality is reported as 6.1 deaths per 100 000 deliveries, with a decreasing trend from 2001 until 2011.15,16
The best outcomes for both mother and fetus are likely to be achieved by successful maternal resuscitation. The most common causes of maternal cardiac arrest are hemorrhage, cardiovascular diseases (including myocardial infarction, aortic dissection, and myocarditis), amniotic fluid embolism, sepsis, aspiration pneumonitis, PE, and eclampsia.13,17 Important iatrogenic causes of maternal cardiac arrest include hypermagnesemia from magnesium sulfate administration and anesthetic complications.
The 2015 ILCOR systematic review addressed the questions of patient positioning during CPR and the role of perimortem cesarean delivery (PMCD) in the management of pregnant women in cardiac arrest during the second half of pregnancy.
The evidence regarding advanced treatment strategies for cardiac arrest in pregnancy is largely observational. As a result, the recommendations are based on application of physiologic principles and on close examination of observational studies that are susceptible to bias. The lack of high-quality studies examining treatment of cardiac arrest in late pregnancy represents a major scientific gap.
Patient position has emerged as an important strategy to improve the quality of CPR and resultant compression force and cardiac output. The gravid uterus can compress the inferior vena cava, impeding venous return, thereby reducing stroke volume and cardiac output. In general, aortocaval compression can occur for singleton pregnancies at approximately 20 weeks of gestational age,18 at about the time when the fundus is at or above the umbilicus. Although chest compressions in the left lateral tilt position are feasible in a manikin study,19 they result in decreased CPR quality (less forceful chest compressions) than is possible in the supine position.20 Manual left lateral uterine displacement (LUD) effectively relieves aortocaval pressure in patients with hypotension21 (Figure 2). No cardiac arrest outcome studies have been published examining the effect of LUD or other strategies to relieve aortocaval compression during resuscitation.
Evacuation of the gravid uterus relieves aortocaval compression and may improve resuscitative efforts.22-26 In the latter half of pregnancy, PMCD may be considered part of maternal resuscitation, regardless of fetal viability.27 In a case series, 12 of 20 women for whom maternal outcome was recorded who underwent PMCD during resuscitation had return of spontaneous circulation (ROSC) immediately after delivery, and no cases of worsening maternal status were reported.28 A systematic review of the literature evaluated all case reports of cardiac arrest in pregnancy, but the wide range of case heterogeneity and reporting bias does not allow for any conclusions regarding the timing of PMCD.29 Survival of the mother has been reported up to 15 minutes after the onset of maternal cardiac arrest.22,30-32 Neonatal survival has been documented with PMCD performed up to 30 minutes after the onset of maternal cardiac arrest.22
Priorities for the pregnant woman in cardiac arrest are provision of high-quality CPR and relief of aortocaval compression. (Class I, LOE C-LD)
If the fundus height is at or above the level of the umbilicus, manual LUD can be beneficial in relieving aortocaval compression during chest compressions. (Class IIa, LOE C-LD)
Because immediate ROSC cannot always be achieved, local resources for a PMCD should be summoned as soon as cardiac arrest is recognized in a woman in the second half of pregnancy. (Class I, LOE C-LD)
Systematic preparation and training are the keys to a successful response to such rare and complex events.
Care teams that may be called upon to manage these situations should develop and practice standard institutional responses to allow for smooth delivery of resuscitative care. (Class I, LOE C-EO)
During cardiac arrest, if the pregnant woman with a fundus height at or above the umbilicus has not achieved ROSC with usual resuscitation measures plus manual LUD, it is advisable to prepare to evacuate the uterus while resuscitation continues. (Class I, LOE C-LD)
In situations such as nonsurvivable maternal trauma or prolonged pulselessness, in which maternal resuscitative efforts are obviously futile, there is no reason to delay performing PMCD. (Class I, LOE C-LD)
PMCD should be considered at 4 minutes after onset of maternal cardiac arrest or resuscitative efforts (for the unwitnessed arrest) if there is no ROSC. (Class IIa, LOE C-EO)
The clinical decision to perform a PMCD―and its timing with respect to maternal cardiac arrest―is complex because of the variability in level of practitioner and team training, patient factors (eg, etiology of arrest, gestational age), and system resources.
PE is a potentially reversible cause of shock and cardiac arrest. Acute increase in right ventricular pressure due to pulmonary artery obstruction and liberation of vasoactive mediators produces cardiogenic shock that may rapidly progress to cardiovascular collapse. Management of acute PE is determined by disease severity.33 Fulminant PE, characterized by cardiac arrest or severe hemodynamic instability, defines the subset of massive PE that is the focus of these recommendations.34
Less than 5% of patients with acute PE progress to cardiac arrest. Disease of this severity is associated with mortality of 65% to 90%.35-37 PE-related cardiac arrests may occur within hours of symptom onset. Between 5% and 13% of unexplained cardiac arrests are associated with fulminant PE.38,39
Because establishing the diagnosis of acute PE in cardiac arrest situations is often difficult, separate systematic reviews were performed for management of patients with suspected and confirmed PE. Although clinical markers specific to fulminant PE are limited, acute symptoms frequently prompt medical attention before cardiac arrest. Conventional thromboembolism risk factors, prodromal dyspnea or respiratory distress, and witnessed arrest are features associated with cardiac arrest due to PE.38,40 Pulseless electrical activity is the presenting rhythm in 36% to 53% of PE-related cardiac arrests, while primary shockable rhythms are uncommon.38,41,42 Specific recommendations about the use of diagnostic ultrasonography during resuscitation can be found in “Part 7: Adult Advanced Cardiovascular Life Support” in this 2015 Guidelines Update.
Prompt systemic anticoagulation is generally indicated for patients with massive and submassive PE to prevent clot propagation and support endogenous clot dissolution over weeks.43 Anticoagulation alone is inadequate for patients with fulminant PE. Pharmacologic and mechanical therapies to rapidly reverse pulmonary artery occlusion and restore adequate pulmonary and systemic circulation have emerged as primary therapies for massive PE, including fulminant PE.33,44 Current advanced treatment options include systemic thrombolysis, surgical or percutaneous mechanical embolectomy, and extracorporeal cardiopulmonary resuscitation (ECPR).
The 2015 ILCOR systematic review addressed the treatment of PE as the known or suspected cause of cardiac arrest. The role of thrombolytic medications in the management of undifferentiated cardiac arrest was last reviewed in the 2010 Guidelines and is not reviewed again here.45
The evidence regarding advanced treatment strategies for fulminant PE is largely observational. The lack of high-quality studies examining treatment of cardiac arrest due to PE represents a major scientific gap.
There is no consensus on the ideal dose of thrombolytic therapy in PE-associated cardiac arrest. Contemporary examples of accelerated emergency thrombolysis dosing regimens for fulminant PE include alteplase 50 mg intravenous (IV) bolus with an option for repeat bolus in 15 minutes, or single-dose weight-based tenecteplase; thrombolytics are administered with or followed by systemic anticoagulation.56-58 Early administration of systemic thrombolysis is associated with improved resuscitation outcomes compared with use after failure of conventional ACLS.47
Successful surgical and percutaneous mechanical embolectomy in cases of PE-related cardiac arrest have been reported in limited series.59-61 Many of these patients developed cardiac arrest before or during embolectomy. The feasibility of embolectomy under uncontrolled CPR conditions is not known.
No evidence is available to support or refute the effectiveness of empiric thrombolysis in suspected but unconfirmed PE.
In patients with confirmed PE as the precipitant of cardiac arrest, thrombolysis, surgical embolectomy, and mechanical embolectomy are reasonable emergency treatment options. (Class IIa, LOE C-LD)
Comparative data are not available to recommend one strategy over another. Patient location, local intervention options, and patient factors (including thrombolysis contraindications) are recognized elements to be considered.
Thrombolysis can be beneficial even when chest compressions have been provided. (Class IIa, LOE C-LD)
Given the poor outcomes associated with fulminant PE in the absence of clot-directed therapy, standard contraindications to thrombolysis may be superseded by the need for potentially lifesaving intervention.
Thrombolysis may be considered when cardiac arrest is suspected to be caused by PE. (Class IIb, LOE C-LD)
There is no consensus on inclusion criteria (eg, risk factors, signs, or symptoms that constitute suspected PE), thrombolytic timing, drug, or dose in this situation. There are insufficient data on surgical and mechanical embolectomy to evaluate these therapies for cardiac arrest associated with suspected but unconfirmed PE.
In the United States in 2013, 16 235 people died of prescription opioid toxicity, and an additional 8257 died of heroin overdose.64,65 In the United States in 2012, opioid overdose became the leading cause of unintentional injurious death in people aged 25 to 60 years, accounting for more deaths than motor vehicle collisions.66 A majority of these deaths are associated with prescription opioids. Statistics are similar in Canada.67
Isolated opioid toxicity is associated with central nervous system (CNS) and respiratory depression that can progress to respiratory and cardiac arrest. Most opioid deaths involve the co-ingestion of multiple drugs or medical and mental health comorbidities.68-71 In addition, methadone and propoxyphene can cause torsades de pointes, and cardiotoxicity has been reported with other opioids.72-78 Except in specific clinical settings (eg, unintended opioid overdose during a medical procedure), rescuers cannot be certain that the patient’s clinical condition is due to opioidinduced CNS and respiratory depression toxicity alone, and might therefore misidentify opioid-associated cardiac arrest as unconsciousness or vice versa. This is particularly true in the first aid and BLS contexts, where determination of the presence or absence of a pulse is unreliable.79,80 Any treatment recommendations intended for use in the first aid or BLS settings must therefore have benefit that exceeds harm when applied to a mixed patient population that may include people with severe CNS and respiratory depression, respiratory arrest, and cardiac arrest.
In creating the 2015 Guidelines Update, the writing group considered the difficulty in accurately differentiating opioid-associated resuscitative emergencies from other causes of cardiac and respiratory arrest. Opioid-associated resuscitative emergencies are defined by the presence of cardiac arrest; respiratory arrest; or severe life-threatening instability (such as severe CNS or respiratory depression, hypotension, or cardiac arrhythmia) that is suspected to be due to opioid toxicity. The term “opioid-associated life-threatening emergency” is used for first aid and non-healthcare providers.
Naloxone is a potent opioid receptor antagonist in the brain, spinal cord, and gastrointestinal system. Naloxone has an excellent safety profile and can rapidly reverse CNS and respiratory depression in a patient with an opioid-associated resuscitative emergency. Based on the rescuer’s training and clinical circumstance, naloxone can be administered intravenously,81-84 intramuscularly,81,82,85 intranasally,83,85-89 or subcutaneously90; nebulized for inhalation91,92; or instilled into the bronchial tree via endotracheal tube.93 Appropriate dose and concentrations differ by route.
There are no known harms or major clinical effects associated with the administration of naloxone in typical doses to patients who are not opioid-intoxicated or dependent.94,95 Naloxone administration may precipitate acute withdrawal syndrome in patients with opioid dependency, with signs and symptoms including hypertension, tachycardia, piloerection, vomiting, agitation, and drug cravings. These signs and symptoms are rarely life-threatening, and they may be minimized by using the lowest effective dose of naloxone.96 Pulmonary edema has been reported with naloxone administration, but it also may be caused primarily by opioid toxicity.96
The ideal dose of naloxone is not known. In the 2010 Guidelines, an empiric starting dose of 0.04 to 0.4 mg IV or intramuscular (IM) was recommended to avoid provoking severe opioid withdrawal in patients with opioid dependency and to allow for consideration of a range of doses, depending on the clinical scenario.2 Repeat doses or dose escalation to 2 mg IV or IM was recommended if the initial response was inadequate. Few comparative data exist about the appropriate dose of intranasal (IN) naloxone; most studies used a fixed dose of 2 mg, repeated in 3 to 5 minutes if necessary.83,85-89,97 Nebulized naloxone has been studied and well-tolerated in opioid-intoxicated patients at a dose of 2 mg diluted in 3 mL normal saline.91,92 Regardless of the care setting and route of administration, the initial goal of therapy is to restore and maintain patent airway and ventilation, preventing respiratory and cardiac arrest, without provoking severe opioid withdrawal.
The 2015 ILCOR systematic review addressed the questions of whether opioid overdose response education (with or without naloxone distribution) improves outcomes related to opioid overdose and whether naloxone administration or any other therapy improves outcomes in the patients with opioidassociated cardio/respiratory arrest in the first aid, BLS, or ACLS settings.
Several studies have shown that community-based opioid overdose response education and naloxone distribution programs are feasible and that naloxone administration occurs frequently by persons trained by these programs.98 Because patients who have CNS and respiratory depression from opioid overdose cannot self-administer naloxone, naloxone is typically administered in the first aid setting by friends, family, or bystanders.99,100
In 2014, the US Food and Drug Administration approved of the use of a naloxone autoinjector by lay rescuers101 as well as healthcare providers. Both the IM and IN98 routes of administration have been successfully used in first aid settings, with commercially available devices or kits containing a naloxone vial or prefilled syringe and a nasal atomizer or other administration device. IM, IN, and nebulized routes of administration have also been used to treat opioid-associated resuscitative emergencies in the BLS and ACLS settings.82,83,91,102 Recent recommendations by an international working group called for uniform training standards based on simplified (first aid) resuscitation principles for community-based naloxone distribution programs.103
Two clinical trials and 12 observational studies examined outcomes after naloxone treatment for opioid-induced respiratory arrest or severe CNS and respiratory depression. Of these, 5 studies compared routes of naloxone administration,83,85,86,90,104 and 9 assessed the safety of naloxone use or were observational studies of naloxone use alone.82,105-112 All studies reported improvement in level of consciousness and spontaneous breathing after naloxone administration in the majority of patients treated, and complication rates were low. No study compared resuscitation outcomes achieved with naloxone with those achieved through standard therapy alone (eg, manual or mechanical ventilation).
One small observational study noted an improvement in cardiac rhythm in some patients after naloxone administration, but it did not compare outcomes in patients managed with and without naloxone administration.113
It is reasonable to provide opioid overdose response education, either alone or coupled with naloxone distribution and training, to persons at risk for opioid overdose. (Class IIa, LOE C-LD)
Some populations that may benefit from opioid overdose response interventions are listed in Table 1.
It is reasonable to base this training on first aid and non-healthcare provider BLS recommendations rather than on more advanced practices intended for healthcare providers. (Class IIa, LOE C-EO)
Although naloxone has no clear role in the management of confirmed cardiac arrest, first aid and other non-healthcare providers are not instructed to attempt to determine whether an unresponsive person is pulseless.
Empiric administration of IM or IN naloxone to all unresponsive opioid-associated life-threatening emergency patients may be reasonable as an adjunct to standard first aid and non–healthcare provider BLS protocols. (Class IIb, LOE C-EO)
Standard resuscitation, including activation of emergency medical services, should not be delayed for naloxone administration. However, family members and friends of those known to be addicted to opiates are likely to have naloxone available and ready to use if someone known or suspected to be addicted to opiates is found unresponsive and not breathing normally or only gasping (see sequence in Figure 1).
Victims who respond to naloxone administration should access advanced healthcare services. (Class I, LOE C-EO)
For patients with known or suspected opioid overdose who have a definite pulse but no normal breathing or only gasping (ie, a respiratory arrest), in addition to providing standard BLS care, it is reasonable for appropriately trained BLS healthcare providers to administer IM or IN naloxone. (Class IIa, LOE C-LD)
For further information, see “Part 5: Adult Basic Life Support and Cardiopulmonary Resuscitation Quality.”
Patients with no definite pulse may be in cardiac arrest or may have an undetected weak or slow pulse. These patients should be managed as cardiac arrest patients.
Standard resuscitative measures should take priority over naloxone administration, with a focus on high-quality CPR (compressions plus ventilation). (Class I, LOE C-EO)
It may be reasonable to administer IM or IN naloxone based on the possibility that the patient is not in cardiac arrest. (Class IIb, LOE C-EO)
Responders should not delay access to more-advanced medical services while awaiting the patient’s response to naloxone or other interventions. (Class I, LOE C-EO)
Unless the patient refuses further care, victims who respond to naloxone administration should access advanced healthcare services. (Class I, LOE C-EO)
ACLS providers should support ventilation and administer naloxone to patients with a perfusing cardiac rhythm and opioid-associated respiratory arrest or severe respiratory depression. Bag-mask ventilation should be maintained until spontaneous breathing returns, and standard ACLS measures should continue if return of spontaneous breathing does not occur. (Class I, LOE C-LD)
We can make no recommendation regarding the administration of naloxone in confirmed opioid-associated cardiac arrest. Patients with opioid-associated cardiac arrest are managed in accordance with standard ACLS practices.
After ROSC or return of spontaneous breathing, patients should be observed in a healthcare setting until the risk of recurrent opioid toxicity is low and the patient’s level of consciousness and vital signs have normalized. (Class I, LOE C-LD)
If recurrent opioid toxicity develops, repeated small doses or an infusion of naloxone can be beneficial in healthcare settings. (Class IIa, LOE C-LD)
Patients who respond to naloxone administration may develop recurrent CNS and/or respiratory depression. Although abbreviated observation periods may be adequate for patients with fentanyl, morphine, or heroin overdose,105,112,114-117 longer periods of observation may be required to safely discharge a patient with life-threatening overdose of a long-acting or sustained-release opioid.96,118,119
Naloxone administration in post–cardiac arrest care may be considered in order to achieve the specific therapeutic goals of reversing the effects of long-acting opioids. (Class IIb, LOE C-EO)
The use of ILE therapy was first developed as a treatment for cardiac arrest resulting from the local anesthetic bupivacaine.120-122 Local anesthetics inhibit voltage at the cell membrane sodium channels, limiting action potential and the conduction of nerve signals. Local anesthetic systemic toxicity (LAST) can present with fulminant cardiovascular collapse that is refractory to standard resuscitative measures. A CNS toxicity phase (agitation evolving to frank seizures or CNS depression) may precede cardiovascular collapse. A recent review of peripheral nerve anesthetic blocks estimated the incidence of LAST equal to 0.87/1000 patients.123 When a local anesthetic is administered, professional organizations recommend continuous neurologic and cardiovascular monitoring, dose fractionation, slow injection, concurrent use of an intravascular marker of systemic absorption (epinephrine 10 to 15 μg), and the use of ultrasound techniques.124
Administration of ILE creates a lipid compartment in the serum, reducing by sequestration the concentration of lipophilic medications in the tissues.125 Administration of ILE also increases cardiac inotropy by other mechanisms.126-128
The 2015 ILCOR systematic review addressed the question of whether administration of lipid emulsion improves outcomes for patients who develop cardiac arrest due to drug toxicity, including that caused by local anesthetics and other drugs.
To date, we identified no human studies that compared outcomes of patients in cardiac arrest treated with ILE plus supportive care versus supportive care alone. A small controlled trial of adults with poisoning from drugs other than local anesthetics showed a more rapid improvement in level of consciousness in the group that received ILE, but all patients survived in both groups.133 Patients with glyphosate-surfactant herbicide ingestion treated with ILE had less hypotension and fewer arrhythmias than historic controls, but there was no difference in survival outcomes.134 Registry studies of patients receiving ILE are difficult to interpret because of a lack of comparison groups.135,136
Animal studies in rats consistently show a benefit of ILE in LAST caused by bupivacaine.131,137 Studies are less consistently positive in porcine models of LAST and from poisoning by drugs other than local anesthetics.132 In a recent systematic review of human case reports, the majority (81/103) reported clinical improvement, such as ROSC, relief of hypotension, resolution of dysrhythmia, improved mental status, or termination of status epilepticus, after ILE administration.132 In this review, all 21 published cases of the use of ILE to treat LAST from bupivacaine demonstrated clinical improvement after ILE administration.
Comparative dose studies are not available. The most commonly reported strategy is to use a 20% emulsion of long-chain triglycerides, giving an initial bolus of 1.5 mL/kg lean body mass over 1 minute followed by an infusion of 0.25 mL/kg per minute for 30 to 60 minutes. The bolus can be repeated once or twice as needed for persistent cardiovascular collapse; the suggested maximum total dose is 10 mL/kg over the first hour.131,138-140 The safety of prolonged infusions (beyond 1 hour) has not been established.141
The most common adverse effect of ILE therapy is interference with diagnostic laboratory testing142; rare cases of pancreatitis142 and pulmonary changes similar to those observed with acute respiratory distress syndrome143 have also been reported. There appear to be complex pharmacodynamic interactions between ILE and epinephrine given during resuscitation, and in some situations, treatment with ILE alters the effectiveness of epinephrine and vasopressin in animal resuscitation studies.144 Although some organizations recommend modification of the pharmacologic treatment of cardiac arrest after ILE administration,145,146 there are no human data to support a modification in ACLS recommendations. More recently, concern has been raised that ILE administration may increase the absorption of lipophilic medications from the gastrointestinal tract147 and interfere with the operation of venoarterial extracorporeal membrane oxygenation circuits.148
It may be reasonable to administer ILE, concomitant with standard resuscitative care, to patients with local anesthetic systemic toxicity and particularly to patients who have premonitory neurotoxicity or cardiac arrest due to bupivacaine toxicity. (Class IIb, LOE C-EO)
It may be reasonable to administer ILE to patients with other forms of drug toxicity who are failing standard resuscitative measures. (Class IIb, LOE C-EO)
Poisoning has been likened to trauma on the cellular level, destroying the natural workings of a victim’s physiology.149 Severe poisoning alters the function of a cellular receptor, ion channel, organelle, or chemical pathway to the extent that critical organ systems can no longer support life.
As with any patient in cardiac arrest, management of the patient with a toxic exposure begins with support of airway, breathing, and circulation. Cardiac arrest due to toxicity is managed in accordance with the current standards of BLS and ACLS. With few exceptions, there are no unique antidotes or toxin-specific interventions that are recommended during resuscitation from cardiac arrest.
Once return of spontaneous circulation is achieved, urgent consultation with a medical toxicologist or certified regional poison center is recommended, as the postarrest management of the critically poisoned patient may benefit from a thorough understanding of the toxic agent. Consultation is also recommended early in the management of a patient with potentially life-threatening poisoning, when appropriate interventions might prevent deterioration to cardiac arrest. In the United States a certified poison center can be reached by calling 1-800-222-1222; in Canada, call 1-800-268-9017.
It is extremely difficult to conduct clinical trials of acute life-threatening poisoning. Challenges include the infrequency with which most specific conditions occur, the heterogeneity of presentation, and ethical challenges related to withholding established care from patients who are unable to provide informed consent because the patient has an altered mental status, the patient is suicidal, or there is a lack of time to explain treatment alternatives.150
The majority of questions addressing cardiac arrest due to drug toxicity remain unanswered. Epidemiological studies are required to document the incidence rate of cardiac arrests secondary to drug toxicity and the safety and efficacy baseline rates for current therapeutic strategies. This section presents recommendations for the care of the patient with a toxicological problem causing cardiac arrest or severe cardiovascular instability (respiratory depression, hypotension, life-threatening alterations of cardiac conduction, etc). Some recommendations are evidence-based, but most research in this area consists of case reports, small case series, animal studies, and pharmacokinetic studies in healthy volunteers. Virtually no toxicology research involves human cardiac arrest. Thus, many of these recommendations are based on expert consensus, and further research is needed to validate them.
Management of the critically poisoned patient begins with airway protection, support of respiration and circulation, and rapid assessment. Patients may or may not be able to provide an accurate history of exposure to a toxic substance. Whenever possible, history gathering should include questioning of persons who accompany the patient, evaluation of containers, review of pharmacy records, and examination of the patient’s prior medical record.151 Many patients who ingest medications in a suicide attempt take more than 1 substance, and the number of substances ingested is greater in fatal than in nonfatal suicide attempts.152 Comprehensive toxicology laboratory testing is virtually never available in a time frame that supports early resuscitation decisions.153
Poisoned patients may deteriorate rapidly. Care for all adult patients who are critically ill or under evaluation for possible toxin exposure or ingestion, particularly when the history is uncertain, should begin in a monitored treatment area where the development of central nervous system depression, hemodynamic instability, or seizures can be rapidly recognized and addressed.154
Gastrointestinal decontamination, once a mainstay in the management of ingested toxins, has a less significant role in poisoning treatment today. With rare exceptions, gastric lavage, whole bowel irrigation, and administration of syrup of ipecac are no longer recommended.155-157 Administration of single-dose activated charcoal to adsorb ingested toxins is generally recommended for the ingestion of life-threatening poisons for which no adequate antidotal therapy is available and when the charcoal can be administered within 1 hour of poisoning.158 Multiple-dose activated charcoal should be considered for patients who have ingested a life-threatening amount of specific toxins (eg, carbamazepine, dapsone, phenobarbital, quinine, or theophylline) for which a benefit of this strategy has been established.159 Charcoal should not be administered for ingestions of caustic substances, metals, or hydrocarbons.158
Charcoal should only be administered to patients with an intact or protected airway. In patients who are at risk for aspiration, endotracheal intubation and head-of-bed elevation should be performed before charcoal administration.159,160 Because the decision to perform gastrointestinal decontamination is complex, multifactorial, and associated with risk, expert advice can be helpful.
A “toxidrome” is a clinical syndrome—a constellation of signs, symptoms, and laboratory findings—suggestive of the effects of a specific toxin. By recognizing these presentations, the clinician can establish a working diagnosis that guides initial management. Some common toxidromes are presented in Table 2: Common Toxidromes. Practically every sign and symptom observed in poisoning can be produced by natural disease, and many clinical presentations associated with natural disease can be mimicked by some poison.161 It is important to maintain a broad differential diagnosis, particularly when the history of toxic chemical exposure is unclear.
There are no data to support the use of specific antidotes in the setting of cardiac arrest due to benzodiazepine overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.
Flumazenil is a potent antagonist of the binding of benzodiazepines to their central nervous system receptors. Administration of flumazenil can reverse central nervous system and respiratory depression caused by benzodiazepine overdose. Flumazenil has no role in the management of cardiac arrest.
The administration of flumazenil to patients with undifferentiated coma confers risk and is not recommended. (Class III, LOE B)
Flumazenil administration can precipitate seizures in benzodiazepine-dependent patients and has been associated with seizures, arrhythmia, and hypotension in patients with coingestion of certain medications, such as tricyclic antidepressants.162,163 However, flumazenil may be used safely to reverse excessive sedation known to be due to the use of benzodiazepines in a patient without known contraindications (eg, procedural sedation).164
There are no data to support the use of specific antidotes in the setting of cardiac arrest due to β-blocker overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.
β-Blocker medication overdose may cause such severe inhibition of β-adrenergic receptors that high-dose vasopressors cannot effectively restore blood pressure, cardiac output, or perfusion. Therapeutic options in the treatment of refractory hemodynamic instability due to β-blocker overdose include administration of glucagon, high-dose insulin, or IV calcium salts.
Administration of glucagon may be helpful for severe cardiovascular instability associated with β-blocker toxicity that is refractory to standard measures, including vasopressors.
The recommended dose of glucagon is a bolus of 3 to 10 mg, administered slowly over 3 to 5 minutes, followed by an infusion of 3 to 5 mg/h (0.05 to 0.15 mg/kg followed by an infusion of 0.05 to 0.10 mg/kg per hour).165-177 (Class IIb, LOE C)
The infusion rate is titrated to achieve an adequate hemodynamic response (appropriate mean arterial pressure and evidence of good perfusion). Because the amount of glucagon required to sustain this therapy may exceed 100 mg in a 24-hour period, plans should be made early to ensure that an adequate supply of glucagon is available. Glucagon commonly causes vomiting. In patients with central nervous system depression, the airway must be protected before glucagon administration. Animal studies have suggested that the concomitant use of dopamine alone or in combination with isoproterenol and milrinone may decrease the effectiveness of glucagon.178-180
Animal studies suggest that high-dose IV insulin, accompanied by IV dextrose supplementation and electrolyte monitoring, may improve hemodynamic stability and survival in β-blocker overdose by improving myocardial energy utilization.181,182 A single human case report183 showed improved hemodynamic stability and survival to discharge following administration of high-dose insulin in refractory shock due to a massive overdose of metoprolol.
Administration of high-dose insulin in patients with shock refractory to other measures may be considered. (ClassIIb, LOE C)
Although the ideal human dose has not been determined, a commonly used protocol calls for IV administration of 1 U/kg regular insulin as a bolus, accompanied by 0.5 g/kg dextrose, followed by continuous infusions of 0.5 to 1 U/kg per hour of insulin and 0.5 g/kg per hour of dextrose.184 The insulin infusion is titrated as needed to achieve adequate hemodynamic response, whereas the dextrose infusion is titrated to maintain serum glucose concentrations of 100 to 250 mg/dL (5.5 to 14 mmol/L). Very frequent serum glucose monitoring (up to every 15 minutes) may be needed during the initial phase of dextrose titration. Sustained infusions of concentrated dextrose solutions (>10%) require central venous access. Insulin causes potassium to shift into the cells. Moderate hypokalemia is common during high-dose insulin-euglycemia therapy, and animals treated with aggressive potassium repletion developed asystole.181 To avoid overly aggressive potassium repletion, 1 human protocol targets potassium levels of 2.5 to 2.8 mEq/L.184
One human case report185 and a large-animal study186 suggest that calcium may be helpful in β-blocker overdose. Administration of calcium in patients with shock refractory to other measures may be considered. (Class IIb, LOE C)
One approach is to administer 0.3 mEq/kg of calcium (0.6 mL/kg of 10% calcium gluconate solution or 0.2 mL/kg of 10% calcium chloride solution) IV over 5 to 10 minutes, followed by an infusion of 0.3 mEq/kg per hour.184 The infusion rate is titrated to adequate hemodynamic response. Serum ionized calcium levels should be monitored, and severe hypercalcemia (ionized calcium levels greater than twice the upper limits of normal) should be avoided. Sustained infusions of IV calcium require central venous access.
Case reports have suggested that in patients who remain critically hypotensive despite maximal vasopressor therapy, specific interventions using intra-aortic balloon counterpulsation, ventricular assist devices, and extracorporeal membrane oxygenation or other extra corporeal life support (ECLS) devices may be lifesaving.187-189 While evidence remains weak, at least two human case reports indicate a possible benefit from lipid emulsion infusion for overdose by β-blockers.190,191 Animal studies are mixed.192-195 Because this area of therapy is rapidly evolving,196-198 prompt consultation with a medical toxicologist or other specialists with up-to-date knowledge is recommended when managing treatment-refractory hypotension from β-blocker overdosage.
There are no data to support the use of specific antidotes in the setting of cardiac arrest due to calcium channel blocker overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.
Calcium channel blocker overdose also may cause life-threatening hypotension and bradycardia that are refractory to standard agents. Treatment with high-dose insulin has been described in a number of clinical case reports199-210 and animal studies.211-214
High-dose insulin, in the doses listed in the β-blocker section above, may be effective for restoring hemodynamic stability and improving survival in the setting of severe cardiovascular toxicity associated with toxicity from a calcium channel blocker overdose. (Class IIb, LOE B)
Administration of calcium in patients with shock refractory to other measures may be considered. (Class IIb, LOE C)
Digoxin poisoning can cause severe bradycardia and life-threatening arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high degrees of AV nodal blockade. Other plant- and animal-derived cardiac glycosides may produce similar effects, including those found in oleander, lily-of-the-valley, toad skin, and some herbal medications. There are no data to support the use of specific antidotes in the setting of cardiac arrest due to digoxin overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms, with specific antidotes used in the post-cardiac arrest phase if severe cardiotoxicity is encountered.
One vial of antidigoxin Fab is standardized to neutralize 0.5 mg of digoxin. Although the ideal dose is unknown, a reasonable strategy is as follows:
If the ingested dose of digoxin is known, administer 2 vials of Fab for every milligram of digoxin ingested.
In cases of chronic digoxin toxicity or when the ingested dose is not known, calculate the number of vials to administer by using the following formula: serum digoxin concentration (ng/mL)×weight (kg)/100.
In critical cases in which therapy is required before a serum digoxin level can be obtained or in cases of life-threatening toxicity due to cardiac glycosides, administer empirically 10 to 20 vials.
Hyperkalemia is a marker of severity in acute cardiac glycoside poisoning and is associated with poor prognosis.232 Antidigoxin Fab may be administered empirically to patients with acute poisoning from digoxin or related cardiac glycosides whose serum potassium level exceeds 5.0 mEq/L.233
There are no data to support the use of cocaine-specific interventions in the setting of cardiac arrest due to cocaine overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms, with specific antidotes used in the postresuscitation phase if severe cardiotoxicity or neurotoxicity is encountered. A single case series demonstrated excellent overall and neurologically intact survival (55%) in patients with cardiac arrest associated with cocaine overdose who were treated with standard therapy.234
Cocaine-induced tachycardia and hypertension are predominantly caused by central nervous system stimulation. Treatment strategies are extrapolated from acute coronary syndrome studies, small case series, and experiments in cocaine-naïve human volunteers.
It may be reasonable to try agents that have shown efficacy in the management of acute coronary syndrome in patients with severe cardiovascular toxicity. α-Blockers (phentolamine),235 benzodiazepines (lorazepam, diazepam),236 calcium channel blockers (verapamil),237 morphine,238 and sublingual nitroglycerin239,240 may be used as needed to control hypertension, tachycardia, and agitation. (Class IIb, LOE B)
The available data do not support the use of 1 agent over another in the treatment of cardiovascular toxicity due to cocaine. (Class IIb, LOE B)
There is clear evidence that cocaine can precipitate acute coronary syndromes.241 For cocaine-induced hypertension or chest discomfort, benzodiazepines, nitroglycerin, and/or morphine can be beneficial.236,239,242 (Class IIa, LOE B)
Because the effects of cocaine and other stimulant medications are transient, drugs and doses should be chosen carefully to minimize the risk of producing hypotension after the offending agent has been metabolized. Catheterization laboratory studies demonstrate that cocaine administration leads to reduced coronary artery diameter. This effect is reversed by morphine,238 nitroglycerin,240 phentolamine,235 and verapamil237; is not changed by labetalol243; and is exacerbated by propranolol.244 Several studies suggest that administration of β-blockers may worsen cardiac perfusion and/or produce paradoxical hypertension when cocaine is present.244,245
In severe overdose, cocaine acts as a Vaughan-Williams class Ic antiarrhythmic, producing wide-complex tachycardia through several mechanisms, including blockade of cardiac sodium channels.249 Although there is no human evidence in cocaine poisoning, extrapolation from evidence in the treatment of wide-complex tachycardia caused by other class Ic agents (flecainide) and tricyclic antidepressants suggests that administration of hypertonic sodium bicarbonate may be beneficial.250 A typical treatment strategy used for these other sodium channel blockers involves administration of 1 mL/kg of sodium bicarbonate solution (8.4%, 1 mEq/mL) IV as a bolus, repeated as needed until hemodynamic stability is restored and QRS duration is ≤120 ms.251-258 Current evidence neither supports nor refutes a role for lidocaine in the management of wide-complex tachycardia caused by cocaine.
Many drugs can prolong the QRS interval in overdose. These include Vaughan-Williams class Ia and Ic antiarrhythmics (eg, procainamide, quinidine, flecainide), cyclic antidepressants (eg, amitriptyline), and cocaine. Type Ia and Ic antiarrhythmics were not reviewed in 2010. Similar to the type Ia antiarrhythmics, cyclic antidepressants block cardiac sodium channels, leading to hypotension and wide-complex arrhythmia in overdose.
Cardiac arrest caused by cyclic antidepressant toxicity should be managed by current BLS and ACLS treatment guidelines. A small case series of cardiac arrest patients demonstrated improvement with sodium bicarbonate and epinephrine,259 but the concomitant use of physostigmine in the prearrest period in this study reduces the ability to generalize this study.
Administration of sodium bicarbonate for cardiac arrest due to cyclic antidepressant overdose may be considered. (Class IIb, LOE C)
Therapeutic strategies for treatment of severe cyclic antidepressant cardiotoxicity include increasing serum sodium, increasing serum pH, or doing both simultaneously. The relative contributions of hypernatremia and alkalemia are controversial, but in practice most experience involves administration of hypertonic sodium bicarbonate solution (8.4% solution, 1 mEq/mL).
Serum sodium levels and pH should be monitored, and severe hypernatremia (sodium >155 mEq/L) and alkalemia (pH >7.55) should be avoided. A number of vasopressors and inotropes have been associated with improvement in the treatment of tricyclic-induced hypotension, ie, epinephrine,260,261,262 norepinephrine,262-265 dopamine,265-267 and dobutamine.266
Apart from complications from deliberate drug abuse, carbon monoxide is the leading cause of unintentional poisoning death in the United States.268 In addition to reducing the ability of hemoglobin to deliver oxygen, carbon monoxide causes direct cellular damage to the brain and myocardium.269 Survivors of carbon monoxide poisoning are at risk for lasting neurological injury.269
Several studies have suggested that very few patients who develop cardiac arrest from carbon monoxide poisoning survive to hospital discharge, regardless of treatment administered following return of spontaneous circulation.270-272 Routine care of patients in cardiac arrest and severe cardiotoxicity from carbon monoxide poisoning should comply with standard BLS and ACLS recommendations.
Two studies suggest that neurological outcomes were improved in patients with carbon monoxide toxicity of all severity (excluding “moribund” patients)273 and mild to moderate severity (excluding loss of consciousness and cardiac instability)274 who received hyperbaric oxygen therapy for carbon monoxide poisoning. Other studies found no difference in neurologically intact survival.275,276 A systematic review277,278 and a recent evidence-based clinical policy review279 concluded that, based on the available evidence, improvement in neurologically intact survival following treatment for carbon monoxide poisoning with hyperbaric oxygen is possible but unproven.
Hyperbaric oxygen therapy is associated with a low incidence of severe side effects. Because hyperbaric oxygen therapy appears to confer little risk,279 the available data suggest that hyperbaric oxygen therapy may be helpful in treatment of acute carbon monoxide poisoning in patients with severe toxicity. (Class IIb, LOE C)
Patients with carbon monoxide poisoning who develop a cardiac injury have an increased risk of cardiovascular and all-cause mortality for at least 7 years after the event, even if hyperbaric oxygen is administered.280,281 Although data about effective interventions in this population are lacking, it is reasonable to advise enhanced follow-up for these patients.
On the basis of this conflicting evidence, the routine transfer of patients to a hyperbaric treatment facility following resuscitation from severe cardiovascular toxicity should be carefully considered, weighing the risk of transport against the possible improvement in neurologically intact survival.
Cyanide is a surprisingly common chemical. In addition to industrial sources, cyanide can be found in jewelry cleaners, electroplating solutions, and as a metabolic product of the putative antitumor drug amygdalin (laetrile). Cyanide is a major component of fire smoke, and cyanide poisoning must be considered in victims of smoke inhalation who have hypotension, central nervous system depression, metabolic acidosis, or soot in the nares or respiratory secretions.282 Cyanide poisoning causes rapid cardiovascular collapse, which manifests as hypotension, lactic acidosis, central apnea, and seizures.
Patients in cardiac arrest282-284 or those presenting with cardiovascular instability282-288 caused by known or suspected cyanide poisoning should receive cyanide-antidote therapy with a cyanide scavenger (either IV hydroxocobalamin or a nitrate such as IV sodium nitrite and/or inhaled amyl nitrite), followed as soon as possible by IV sodium thiosulfate.286,289,290
Both hydroxocobalamin282-288 and sodium nitrite286,289,290 serve to rapidly and effectively bind cyanide in the serum and reverse the effects of cyanide toxicity. Because nitrites induce methemoglobin formation289 and can cause hypotension,291 hydroxocobalamin has a safety advantage, particularly in children and victims of smoke inhalation who might also have carbon monoxide poisoning. A detailed comparison of these measures has been recently published.292
Sodium thiosulfate serves as a metabolic cofactor, enhancing the detoxification of cyanide to thiocyanate. Thiosulfate administration enhances the effectiveness of cyanide scavengers in animal experimentation293-296 and has been used successfully in humans with both hydroxocobalamin282,288 and sodium nitrite.286,289,290 Sodium thiosulfate is associated with vomiting but has no other significant toxicity.297
Therefore, based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended (Class I, LOE B)
Cardiac arrest during PCI is rare, occurring in approximately 1.3% of catheterization procedures.298,299 Although the risk of cardiac arrest during PCI is present in both elective and emergency procedures, the incidence is higher in emergency cases.300
In general, patients who develop cardiac arrest during PCI have superior outcomes to patients in cardiac arrest that occurs in other settings, including in-hospital units.301 Many patients will respond to standard ACLS resuscitation, including high-quality CPR and rapid defibrillation. Rapid defibrillation (within 1 minute) is associated with survival to hospital discharge rates as high as 100% in this population.302
A subset of patients who develop cardiac arrest during PCI will require prolonged resuscitation efforts. Providing effective prolonged resuscitation in the catheterization laboratory has unique challenges, and a number of interventions and adjuncts for management of cardiac arrest during PCI have been described. Inconsistent availability and lack of comparative studies limit recommendations of one approach over another.
The 2015 ILCOR systematic review addressed the question of whether any special interventions or changes in care, compared with standard ACLS resuscitation alone, can improve outcomes in patients who develop cardiac arrest during PCI.
There are a number of mechanical devices available to provide hemodynamic support during cardiac catheterization in high-risk patients presenting with cardiogenic shock. The use of these devices in cardiogenic shock was not reviewed by ILCOR in 2015. Therefore, the 2015 AHA Guidelines Update for CPR and ECC does not make recommendations on the use of mechanical support devices in patients presenting in cardiogenic shock who undergo PCI. Recent recommendations for the use of mechanical support devices in these situations can be found in the 2013 American College of Cardiology Foundation (ACCF)/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. 303
The feasibility of using mechanical CPR devices during PCI has been demonstrated in both animal304 and human305-308 studies. No comparative studies have examined the use of mechanical CPR devices compared with manual chest compressions during PCI procedures. However, a number of case reports304,305,309 and case series307,308 have reported the use of mechanical CPR devices to facilitate prolonged resuscitation in patients who have a cardiac arrest during PCI. One study demonstrated that the use of a mechanical CPR device for cardiac arrest during PCI was feasible; however, no patients survived to hospital discharge.307 Other studies have reported good patient outcomes, including ROSC, survival to discharge, and functional outcome at hospital discharge, after use of mechanical devices in resuscitation from cardiac arrest during PCI.304,308 Mechanical CPR devices may also allow the use of fluoroscopy during chest compressions without direct irradiation of personnel.
Patients in cardiogenic shock or with other high-risk features (eg, multivessel coronary disease) may be at increased risk for adverse outcomes during or after PCI. Ventricular assist devices, intraaortic balloon pumps (IABP), and ECPR are all rescue treatment options available to support circulation and permit completion of the PCI. Not all interventions are available or can be rapidly deployed in all centers.
Rapid initiation of ECPR or cardiopulmonary bypass is associated with good patient outcomes in patients with hemodynamic collapse and cardiac arrest in the catheterization lab.310-316 The use of ECPR is also feasible and associated with good outcomes when used as a bridge to coronary artery bypass grafting.310,316-318 The combination of ECPR and IABP has been associated with increased survival when compared with IABP alone for patients who present with cardiogenic shock, including those who have a cardiac arrest while undergoing PCI.311,315,319 Available observational studies often implement ECPR 20 to 30 minutes after cardiac arrest.311,313
IABP counterpulsation increases coronary perfusion, decreases myocardial oxygen demand, and improves hemodynamics in cardiogenic shock states, but it is not associated with improved patient survival in cardiogenic shock.320-328 The role of IABP in patients who have a cardiac arrest in the catheterization laboratory is not known.
Several case series have reported on the use of emergency coronary artery bypass graft surgery after failed PCI.329,330 In patients with cardiogenic shock or cardiac arrest and failed PCI, mechanical CPR devices and/ or ECPR have been used as rescue bridges to coronary artery bypass graft. Although no comparison studies have examined the use of this therapy as an adjunct to PCI, survival to hospital discharge rates as high as 64% have been reported.310,311,316,318
It may be reasonable to use mechanical CPR devices to provide chest compressions to patients in cardiac arrest during PCI. (Class IIb, LOE C-EO)
It may be reasonable to use ECPR as a rescue treatment when initial therapy is failing for cardiac arrest that occurs during PCI. (Class IIb, LOE C-LD)
Because patients can remain on ECPR support for extended periods of time without possibility of recovery, practical and ethical considerations must be taken into account in determining which victims of cardiac arrest should receive ECPR support.
Institutional guidelines should include the selection of appropriate candidates for use of mechanical support devices to ensure that these devices are used as a bridge to recovery, surgery or transplant, or other device. (Class I, LOE C-EO)
Due to a lack of comparative studies, it is not possible to recommend one approach (manual CPR, mechanical CPR, or ECPR) over another when options exist.
Asthma is responsible for more than 2 million visits to the emergency department (ED) in the United States each year, with 1 in 4 patients requiring admission to a hospital.331 Annually there are 5,000 to 6,000 asthma-related deaths in the United States, many occurring in the prehospital setting.332 Severe asthma accounts for approximately 2% to 20% of admissions to intensive care units, with up to one third of these patients requiring intubation and mechanical ventilation.333 This section focuses on the evaluation and treatment of patients with near-fatal asthma.
Several consensus groups have developed excellent guidelines for the management of asthma that are available on the World Wide Web:
The pathophysiology of asthma consists of 3 key abnormalities:
Complications of severe asthma, such as tension pneumothorax, lobar atelectasis, pneumonia, and pulmonary edema, can contribute to fatalities. Severe asthma exacerbations are commonly associated with hypercarbia and acidemia, hypotension due to decreased venous return, and depressed mental status, but the most common cause of death is asphyxia. Cardiac causes of death are less common.334
Wheezing is a common physical finding, although the severity of wheezing does not correlate with the degree of airway obstruction. The absence of wheezing may indicate critical airway obstruction, whereas increased wheezing may indicate a positive response to bronchodilator therapy.
Oxygen saturation (SaO2) levels may not reflect progressive alveolar hypoventilation, particularly if oxygen is being administered. Note that SaO2 may fall initially during therapy because β2-agonists produce both bronchodilation and vasodilation and initially may increase intrapulmonary shunting.
Patients with severe life-threatening asthma require urgent and aggressive treatment with simultaneous administration of oxygen, bronchodilators, and steroids. Healthcare providers must monitor these patients closely for deterioration. Although the pathophysiology of life-threatening asthma consists of bronchoconstriction, inflammation, and mucous plugging, only bronchoconstriction and inflammation are amenable to drug treatment.
Oxygen should be provided to all patients with severe asthma, even those with normal oxygenation. As noted above, successful treatment with β2-agonists may cause an initial decrease in oxygen saturation because the resultant bronchodilation can initially increase the ventilation-perfusion mismatch.
Short-acting β-agonists provide rapid, dose-dependent bronchodilation with minimal side effects. Because the dose delivered depends on the patient’s lung volume and inspiratory flow rate, the same dose can be used in most patients regardless of age or size. Studies have shown no difference in the effects of continuous versus intermittent administration of nebulized albuterol338,339; however, continuous administration was more effective in a subset of patients with severe exacerbations of asthma.338 A Cochrane meta-analysis showed no overall difference between the effects of albuterol delivered by metered-dose inhaler spacer or nebulizer.340 If prior use of a metered-dose inhaler has not been effective, use of a nebulizer is reasonable.
Although albuterol is sometimes administered intravenously (IV) in severe asthma, a systematic review of 15 clinical trials found that IV β2-agonists, administered by either bolus or infusion, did not lead to significant improvements in any clinical outcome measure.339
Levalbuterol is the R-isomer of albuterol. Comparisons with albuterol have produced mixed results, with some studies showing a slightly improved bronchodilator effect in the treatment of acute asthma in the ED.341 There is no evidence that levalbuterol should be favored over albuterol.
One of the most common adjuncts used with β-agonist treatment, particularly in the first hours of treatment, include anticholinergic agents (see “Adjunctive Therapies” below for more detail). When combined with short-acting β-agonists, anticholinergic agents such as ipratropium can produce a clinically modest improvement in lung function compared with short-acting β-agonists alone.342,343
Systemic corticosteroids are the only treatment for the inflammatory component of asthma proven to be effective for acute asthma exacerbations. Because the antiinflammatory effects after administration may not be apparent for 6 to 12 hours, corticosteroids should be administered early. The early use of systemic steroids hastens the resolution of airflow obstruction and may reduce admission to the hospital.344 Although there may be no difference in clinical effects between oral and IV formulations of corticosteroids,345,346 the IV route is preferable in patients with severe asthma. In adults a typical initial dose of methylprednisolone is 125 mg (dose range: 40 mg to 250 mg); a typical dose of dexamethasone is 10 mg.
Ipratropium bromide is an anticholinergic bronchodilator pharmacologically related to atropine. The nebulizer dose is 500 mcg.345,346 Ipratropium bromide has a slow onset of action (approximately 20 minutes), with peak effectiveness at 60 to 90 minutes and no systemic side effects. The drug is typically given only once because of its prolonged onset of action, but some studies have shown that repeat doses of 250 mcg or 500 mcg every 20 minutes may be beneficial.347 A recent meta-analysis indicated a reduced number of hospital admissions associated with treatment with ipratropium bromide, particularly in patients with severe exacerbations.348
When combined with nebulized β-adrenergic agents and corticosteroids, IV magnesium sulfate can moderately improve pulmonary function in patients with asthma.349 Magnesium causes relaxation of bronchial smooth muscle independent of serum magnesium level, with only minor side effects (flushing, lightheadedness). A Cochrane meta-analysis of 7 studies concluded that IV magnesium sulfate improves pulmonary function and reduces hospital admissions, particularly for patients with the most severe exacerbations of asthma.350 The use of nebulized magnesium sulfate as an adjunct to nebulized β-adrenergic agents has been reported in a small case series to improve FEV1 and SpO2,351 although a prior meta-analysis demonstrated only a trend toward improved pulmonary function with nebulized magnesium.352 For those with severe refractory asthma, providers may consider IV magnesium at the standard adult dose of 2 g administered over 20 minutes.
Epinephrine and terbutaline are adrenergic agents that can be given subcutaneously to patients with acute severe asthma. The dose of subcutaneous epinephrine (concentration 1:1000) is 0.01 mg/kg, divided into 3 doses of approximately 0.3 mg administered at 20-minute intervals. Although the nonselective adrenergic properties of epinephrine may cause an increase in heart rate, myocardial irritability, and increased oxygen demand, its use is well-tolerated, even in patients >35 years of age.353 Terbutaline is given in a subcutaneous dose of 0.25 mg, which can be repeated every 20 minutes for 3 doses. There is no evidence that subcutaneous epinephrine or terbutaline has advantages over inhaled β2-agonists. Epinephrine has been administered IV (initiated at 0.25 mcg/min to 1 mcg/min continuous infusion) in severe asthma; however, 1 retrospective investigation indicated a 4% incidence of serious side effects. There is no evidence of improved outcomes with IV epinephrine compared with selective inhaled β2-agonists.354
Ketamine is a parenteral, dissociative anesthetic with bronchodilatory properties that also can stimulate copious bronchial secretions. One case series355 suggested substantial efficacy, whereas 2 published randomized trials in children356,357 found no benefit of ketamine when compared with standard care. Ketamine has sedative and analgesic properties that may be useful if intubation is planned.
Heliox is a mixture of helium and oxygen (usually a 70:30 helium to oxygen ratio mix) that is less viscous than ambient air. Heliox has been shown to improve the delivery and deposition of nebulized albuterol358; however, a recent meta-analysis of clinical trials did not support its use as initial treatment for patients with acute asthma.359 Because the heliox mixture requires at least 70% helium for effect, it cannot be used if the patient requires >30% oxygen.
Although once considered a mainstay in the treatment of acute asthma, methylxanthines are no longer recommended because of their erratic pharmacokinetics, known side effects, and lack of evidence of benefit.360
Leukotriene antagonists improve lung function and decrease the need for short-acting β2-agonists for long-term asthma therapy, but their effectiveness during acute exacerbations of asthma is unproven.
Case reports in adults361 and children362 suggest a benefit of the potent inhalation anesthetics sevoflurane and isoflurane for patients with life-threatening asthma unresponsive to maximal conventional therapy. These agents may have direct bronchodilator effects. In addition, the anesthetic effect of these drugs increases the ease of mechanical ventilation and reduces oxygen demand and carbon dioxide production. This therapy requires expert consultation in an intensive care setting, and its effectiveness has not been evaluated in randomized clinical studies.
Noninvasive positive-pressure ventilation (NIPPV) may offer short-term support for patients with acute respiratory failure and may delay or eliminate the need for endotracheal intubation.363-365 This therapy requires that the patient is alert and has adequate spontaneous respiratory effort. Bilevel positive airway pressure (BiPAP), the most common method of delivering NIPPV, allows for separate control of inspiratory and expiratory pressures.
Endotracheal intubation is indicated for patients who present with apnea, coma, persistent or increasing hypercapnia, exhaustion, severe distress, and depression of mental status. Clinical judgment is necessary to assess the need for immediate endotracheal intubation for these critically ill patients. Endotracheal intubation does not solve the problem of small airway constriction in patients with severe asthma; thus, therapy directed toward relief of bronchoconstriction should be continued. Mechanical ventilation in the asthmatic patient can be difficult and associated risks require careful management. Intubation and positive-pressure ventilation can trigger further bronchoconstriction and complications such as breath stacking that result from incomplete expiration, air trapping, and buildup of positive end-expiratory pressure (ie, intrinsic or auto-PEEP). This breath stacking can cause barotrauma. Decreasing tidal volume may avoid auto-PEEP and high peak airway pressures. Optimal ventilator management requires expert consultation and ongoing careful review of ventilation flow and pressure curves. Although endotracheal intubation introduces risks, it should be performed when necessary based on clinical condition.
Rapid sequence intubation is the technique of choice and should be performed by an expert in airway management. The provider should use the largest endotracheal tube available (usually 8 or 9 mm) to decrease airway resistance. Immediately after intubation, endotracheal tube placement should be confirmed by clinical examination and waveform capnography. A chest radiograph should then be performed.
When severe bronchoconstriction is present, breath stacking (so-called auto-PEEP) can develop during positive-pressure ventilation, leading to complications such as hyperinflation, tension pneumothorax, and hypotension. During manual or mechanical ventilation, a slower respiratory rate should be used with smaller tidal volumes (eg, 6 to 8 mL/kg),366 shorter inspiratory time (eg, adult inspiratory flow rate 80 to 100 L/min), and longer expiratory time (eg, inspiratory to expiratory ratio 1:4 or 1:5) than generally would be provided to patients without asthma.367 Management of mechanical ventilation will vary based on patient-ventilation characteristics. Expert consultation should be obtained.
Mild hypoventilation (permissive hypercapnia) reduces the risk of barotrauma. Hypercapnia is typically well tolerated.368,369 Sedation is often required to optimize ventilation, decrease ventilator dyssynchrony (and therefore auto-PEEP), and minimize barotrauma after intubation. Because delivery of inhaled medications may be inadequate before intubation, the provider should continue to administer inhaled albuterol treatments through the endotracheal tube.
Four common causes of acute deterioration in any intubated patient are recalled by the mnemonic DOPE (tube Displacement, tube Obstruction, Pneumothorax, Equipment failure). Auto-PEEP is another common cause of deterioration in patients with asthma. If the asthmatic patient’s condition deteriorates or if it is difficult to ventilate the patient, check the ventilator for leaks or malfunction; verify endotracheal tube position; eliminate tube obstruction (eliminate any mucous plugs and kinks); evaluate for auto-PEEP; and rule out a pneumothorax.
High-end expiratory pressure can be reduced quickly by separating the patient from the ventilator circuit; this will allow PEEP to dissipate during passive exhalation. If auto-PEEP results in significant hypotension, assisting with exhalation by pressing on the chest wall after disconnection of the ventilator circuit will allow active exhalation and should lead to immediate resolution of hypotension. To minimize auto-PEEP, decrease the respiratory rate or tidal volume or both. If auto-PEEP persists and the patient displays ventilator dyssynchrony despite adequate sedation, paralytic agents may be considered.
In exceedingly rare circumstances, aggressive treatment for acute respiratory failure due to severe asthma will not provide adequate gas exchange. There are case reports that describe successful use of extracorporeal membrane oxygenation (ECMO) in adult and pediatric patients370-373 with severe asthma after other aggressive measures have failed to reverse hyoxemia and hypercarbia.
BLS treatment of cardiac arrest in asthmatic patients is unchanged.
When cardiac arrest occurs in the patient with acute asthma, standard ACLS guidelines should be followed.
Case series and case reports describe a novel technique of cardiopulmonary resuscitation (CPR) termed “lateral chest compressions”; however, there is insufficient evidence to recommend this technique over standard techniques.374-380
The adverse effect of auto-PEEP on coronary perfusion pressure and capacity for successful defibrillation has been described in patients in cardiac arrest without asthma.381,382 Moreover, the adverse effect of auto-PEEP on hemodynamics in asthmatic patients who are not in cardiac arrest has also been well-described.383-386
Therefore, since the effects of auto-PEEP in an asthmatic patient with cardiac arrest are likely quite severe, a ventilation strategy of low respiratory rate and tidal volume is reasonable. (Class IIa, LOE C)
During arrest a brief disconnection from the bag mask or ventilator may be considered, and compression of the chest wall to relieve air-trapping can be effective. (Class IIa, LOE C)
For all asthmatic patients with cardiac arrest, and especially for patients in whom ventilation is difficult, the possible diagnosis of a tension pneumothorax should be considered and treated. (Class I, LOE C)
Anaphylaxis is an allergic reaction characterized by multisystem involvement, including skin, airway, vascular system, and gastrointestinal tract. Severe cases may result in complete obstruction of the airway and cardiovascular collapse from vasogenic shock. Anaphylaxis accounts for about 500 to 1000 deaths per year in the United States.387
The term classic anaphylaxis refers to hypersensitivity reactions mediated by the immunoglobulins IgE and IgG. Prior sensitization to an allergen produces antigen-specific immunoglobulins. Subsequent reexposure to the allergen provokes the anaphylactic reaction, although many anaphylactic reactions occur with no documented prior exposure. Pharmacological agents, latex, foods, and stinging insects are among the most common causes of anaphylaxis described.
The initial symptoms of anaphylaxis are often nonspecific and include tachycardia, faintness, cutaneous flushing, urticaria, diffuse or localized pruritus, and a sensation of impending doom. Urticaria is the most common physical finding. The patient may be agitated or anxious and may appear either flushed or pale.
A common early sign of respiratory involvement is rhinitis. As respiratory compromise becomes more severe, serious upper airway (laryngeal) edema may cause stridor and lower airway edema (asthma) may cause wheezing. Upper airway edema can also be a sign in angiotensin converting enzyme inhibitor-induced angioedema or C1 esterase inhibitor deficiency with spontaneous laryngeal edema.388-390
Cardiovascular collapse is common in severe anaphylaxis. If not promptly corrected, vasodilation and increased capillary permeability, causing decreased preload and relative hypovolemia of up to 37% of circulating blood volume, can rapidly lead to cardiac arrest.391,392 Myocardial ischemia and acute myocardial infarction, malignant arrhythmias, and cardiovascular depression can also contribute to rapid hemodynamic deterioration and cardiac arrest.393 Additionally, cardiac dysfunction may result from underlying disease or development of myocardial ischemia due to hypotension or following administration of epinephrine.394,395
There are no randomized controlled trials evaluating alternative treatment algorithms for cardiac arrest due to anaphylaxis. Evidence is limited to case reports and extrapolations from nonfatal cases, interpretation of pathophysiology, and consensus opinion. Providers must be aware that urgent support of airway, breathing, and circulation is essential in suspected anaphylactic reactions.
Because of limited evidence, the management of cardiac arrest secondary to anaphylaxis should be treated with standard BLS and ACLS. The following therapies are largely consensus-based but commonly used and widely accepted in the management of the patient with anaphylaxis who is not in cardiac arrest.
Early and rapid advanced airway management is critical and should not be unnecessarily delayed.
Given the potential for the rapid development of oropharyngeal or laryngeal edema,396 immediate referral to a health professional with expertise in advanced airway placement is recommended. (Class I, LOE C)
The intramuscular (IM) administration of epinephrine (epinephrine autoinjectors, eg, the EpiPen™) in the anterolateral aspect of the middle third of the thigh provides the highest peak blood levels.397 Absorption and subsequent achievement of maximum plasma concentration after subcutaneous administration is slower than the IM route and may be significantly delayed with shock.397
Epinephrine398 should be administered early by IM injection to all patients with signs of a systemic allergic reaction, especially hypotension, airway swelling, or difficulty breathing. (Class I, LOE C))
The adult epinephrine IM auto-injector will deliver 0.3 mg of epinephrine and the pediatric epinephrine IM auto-injector will deliver 0.15 mg of epinephrine.
In both anaphylaxis and cardiac arrest the immediate use of an epinephrine autoinjector is recommended if available. (Class I, LOE C)
In both anaphylaxis and cardiac arrest the immediate use of an epinephrine autoinjector is recommended if available. (Class I, LOE C)
Early recognition of the potential for a difficult airway in anaphylaxis is paramount in patients who develop hoarseness, lingual edema, stridor, or oropharyngeal swelling.
In a prospective evaluation of volume resuscitation after diagnostic sting challenge, repeated administration of 1000-mL bolus doses of isotonic crystalloid (eg, normal saline) titrated to systolic blood pressure above 90 mm Hg was used successfully in patients whose hypotension did not respond immediately to vasoactive drugs.391,401
Vasogenic shock from anaphylaxis may require aggressive fluid resuscitation. (Class IIa, LOE C)
There are no human trials establishing the role of epinephrine or preferred route of administration in anaphylactic shock managed by ACLS providers.398 In an animal study of profound anaphylactic shock, IV epinephrine restored blood pressure to baseline; however, the effect was limited to the first 15 minutes after shock, and no therapeutic effect was observed with the same dose of epinephrine administered IM or subcutaneously.402
Therefore, when an IV line is in place, it is reasonable to consider the IV route as an alternative to IM administration of epinephrine in anaphylactic shock. (Class IIa, LOE C)
For patients not in cardiac arrest, IV epinephrine 0.05 to 0.1 mg (5% to 10% of the epinephrine dose used routinely in cardiac arrest) has been used successfully in patients with anaphylactic shock.403
In a study of animals sensitized by ragweed, a continuous IV infusion of epinephrine maintained a mean arterial pressure at 70% of preshock levels better than no treatment or bolus epinephrine treatment (IV, subcutaneous, or IM).406 Furthermore, a recent human study suggests that careful titration of a continuous infusion of IV epinephrine (5 to 15 mcg/min), based on severity of reaction and in addition to crystalloid infusion, may be considered in treatment of anaphylactic shock.401
Therefore, IV infusion of epinephrine is a reasonable alternative to IV boluses for treatment of anaphylaxis in patients not in cardiac arrest (Class IIa, LOE C) and may be considered in postarrest management. (Class IIb, LOE C)
Recently vasopressin has been used successfully in patients with anaphylaxis (with or without cardiac arrest) who did not respond to standard therapy.407-409 Other small case series described successful results with administration of alternative α-agonists such as norepinephrine,410 methoxamine,411,412 and metaraminol.413-415
Alternative vasoactive drugs (vasopressin, norepinephrine, methoxamine, and metaraminol) may be considered in cardiac arrest secondary to anaphylaxis that does not respond to epinephrine. (Class IIb, LOE C)
No randomized controlled trials have evaluated epinephrine versus the use of alternative vasoactive drugs for cardiac arrest due to anaphylaxis.
There are no prospective randomized clinical studies evaluating the use of other therapeutic agents in anaphylactic shock or cardiac arrest.
Adjuvant use of antihistamines (H1 and H2 antagonist),416,417 inhaled β-adrenergic agents,418 and IV corticosteroids 419 has been successful in management of the patient with anaphylaxis and may be considered in cardiac arrest due to anaphylaxis. (Class IIb, LOE C)
Use of these advanced techniques may be considered in clinical situations where the required professional skills and equipment are immediately available. (Class IIb, LOE C)
Morbid obesity can provide challenges during the resuscitation attempt. Airway management may be more challenging, and changes to the thorax may make resuscitative efforts more demanding. Evidence from 2 case studies,422,423 1 case series,424 and 1 related clinical study425 indicated no differences in survival based on patient weight. However, one large case series demonstrated lower survival for morbidly obese children who required in-hospital pediatric CPR.426
No modifications to standard BLS or ACLS care have been proven efficacious, although techniques may need to be adjusted due to the physical attributes of individual patients.
Electrolyte abnormalities can be associated with cardiovascular emergencies and may cause or contribute to cardiac arrest, hinder resuscitative efforts, and affect hemodynamic recovery after cardiac arrest. An evidence-based review in 2010 focused on electrolyte abnormalities most often associated with cardiac arrest.
Early consideration may be given to using selective methods of therapeutic management in addition to standard ACLS protocols that can be provided rapidly and have been shown to be effective in patients with cardiovascular instability as outlined below. Current BLS and ACLS should be used to manage cardiac arrest associated with all electrolyte disturbances.
Potassium is maintained mainly in the intracellular compartment through the action of the Na+/K+ ATPase pump. The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle cells, including the myocardium.
Potassium is tightly regulated. Under normal conditions potential differences across membranes, especially cardiac, are not affected by alterations in potassium level. Rapid or significant changes in serum concentrations of potassium result from the shifting of potassium from one space to another and may have life-threatening consequences.
Hyperkalemia is one of the few potentially lethal electrolyte disturbances. Severe hyperkalemia (defined as a serum potassium concentration >6.5 mmol/L) occurs most commonly from renal failure or from release of potassium from cells and can cause cardiac arrhythmias and cardiac arrest. In 1 retrospective in-hospital study of 29 063 patients, hyperkalemia was found to be directly responsible for sudden cardiac arrest in 7 cases.427 Acute kidney injury was present in all the arrest cases, accompanied by acute pancreatitis in 3 cases and acute hepatic failure in 2 cases. Overall renal failure and drug treatment were the most common causes of hyperkalemia, with the most severe cases occurring when excessive IV potassium was administered to a patient with renal insufficiency.
Although severe hyperkalemia may cause flaccid paralysis, paresthesia, depressed deep tendon reflexes, or respiratory difficulties,428-430 the first indicator of hyperkalemia may be the presence of peaked T waves (tenting) on the electrocardiogram (ECG). As serum potassium rises, the ECG may progressively develop flattened or absent P waves, a prolonged PR interval, widened QRS complex, deepened S waves, and merging of S and T waves (Figure 3). If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.431,432
Treatment of severe hyperkalemia aims at protecting the heart from the effects of hyperkalemia by antagonizing the effect of potassium on excitable cell membranes, forcing potassium into cells to remove it promptly from the circulation, and removing potassium from the body. Therapies that shift potassium will act rapidly but are temporary and thus may need to be repeated. In order of urgency, treatment includes the following:
· Stabilize myocardial cell membrane:
· Calcium chloride (10%): 5 to 10 mL (500 to 1000 mg) IV over 2 to 5 minutes or calcium gluconate (10%): 15 to 30 mL IV over 2 to 5 minutes
· Shift potassium into cells:
· Sodium bicarbonate: 50 mEq IV over 5 minutes
· Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10 U regular insulin and give IV over 15 to 30 minutes
· Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes
· Promote potassium excretion:
· Diuresis: furosemide 40 to 80 mg IV
· Kayexalate: 15 to 50 g plus sorbitol per oral or per rectum
When cardiac arrest occurs secondary to hyperkalemia, it may be reasonable to administer adjuvant IV therapy as outlined above for cardiotoxicity in addition to standard ACLS. (Class IIb, LOE C)
Life-threatening hypokalemia is uncommon but can occur in the setting of gastrointestinal and renal losses and is associated with hypomagnesemia. Severe hypokalemia will alter cardiac tissue excitability and conduction. Hypokalemia can produce ECG changes such as U waves, T-wave flattening, and arrhythmias (especially if the patient is taking digoxin), particularly ventricular arrhythmias,433,434 which, if left untreated, deteriorate to PEA or asystole.
Several studies reported an association with hypokalemia and development of ventricular fibrillation,435-438 whereas a single animal study reported that hypokalemia lowered the ventricular fibrillation threshold.439 However, the management of hypokalemia in the setting of cardiotoxicity, specifically torsades de pointes, is largely based on historical case reports that report slow infusion of potassium over hours.440
The effect of bolus administration of potassium for cardiac arrest suspected to be secondary to hypokalemia is unknown and ill advised. (Class III, LOE C)
Sodium is the major intravascular ion that influences serum osmolality. Sodium abnormalities are unlikely to lead to cardiac arrest, and there are no specific recommendations for either checking or treating sodium during cardiac arrest. Disturbances in sodium level are unlikely to be the primary cause of severe cardiovascular instability.
Magnesium is an essential electrolyte and an important cofactor for multiple enzymes, including ATPase. Magnesium is necessary for the movement of sodium, potassium, and calcium into and out of cells and plays an important role in stabilizing excitable membranes. The presence of a low plasma magnesium concentration has been associated with poor prognosis in cardiac arrest patients.436,441-444
Hypermagnesemia is defined as a serum magnesium concentration >2.2 mEq/L (normal: 1.3 to 2.2 mEq/L). Neurological symptoms of hypermagnesemia include muscular weakness, paralysis, ataxia, drowsiness, and confusion. Hypermagnesemia can produce vasodilation and hypotension.445 Extremely high serum magnesium levels may produce a depressed level of consciousness, bradycardia, cardiac arrhythmias, hypoventilation, and cardiorespiratory arrest.436,443,444
Hypomagnesemia, defined as a serum magnesium concentration <1.3 mEq/L, is far more common than hypermagnesemia. Hypomagnesemia usually results from decreased absorption or increased loss of magnesium from either the kidneys or intestines (diarrhea). Alterations in thyroid hormone function, certain medications (eg, pentamidine, diuretics, alcohol), and malnourishment can also induce hypomagnesemia.
Hypomagnesemia can be associated with polymorphic ventricular tachycardia, including torsades de pointes, a pulseless form (polymorphic) of ventricular tachycardia. For cardiotoxicity and cardiac arrest, IV magnesium 1 to 2 g of MgSO4 bolus IV push is recommended. (Class I, LOE C)
Calcium abnormality as an etiology of cardiac arrest is rare. There are no studies evaluating the treatment of hypercalcemia or hypocalcemia during arrest.
However, empirical use of calcium (calcium chloride [10%] 5 to 10 mL OR calcium gluconate [10%] 15 to 30 mL IV over 2 to 5 minutes) may be considered when hyperkalemia or hypermagnesemia is suspected as the cause of cardiac arrest. (Class IIb, LOE C)
BLS and ACLS for the trauma patient are fundamentally the same as that for the patient with primary cardiac arrest, with focus on support of airway, breathing, and circulation. In addition, reversible causes of cardiac arrest need to considered. While CPR in the pulseless trauma patient has overall been considered futile, several reversible causes of cardiac arrest in the context of trauma are correctible and their prompt treatment could be life-saving. These include hypoxia, hypovolemia, diminished cardiac output secondary to pneumothorax or pericardial tamponade, and hypothermia.
When multisystem trauma is present or trauma involves the head and neck, the cervical spine must be stabilized. A jaw thrust should be used instead of a head tilt–chin lift to establish a patent airway. If breathing is inadequate and the patient’s face is bloody, ventilation should be provided with a barrier device, a pocket mask, or a bag-mask device while maintaining cervical spine stabilization. Stop any visible hemorrhage using direct compression and appropriate dressings. If the patient is completely unresponsive despite rescue breathing, provide standard CPR and defibrillation as indicated.
After initiation of BLS care, if bag-mask ventilation is inadequate, an advanced airway should be inserted while maintaining cervical spine stabilization. If insertion of an advanced airway is not possible and ventilation remains inadequate, experienced providers should consider a cricothyrotomy.
A unilateral decrease in breath sounds during positive-pressure ventilation should prompt the rescuer to consider the possibility of pneumothorax, hemothorax, or rupture of the diaphragm.
When the airway, oxygenation, and ventilation are adequate, evaluate and support circulation. Control ongoing bleeding where possible and replace lost volume if the losses appear to have significantly compromised circulating blood volume. Cardiac arrest resuscitation will likely be ineffective in the presence of uncorrected severe hypovolemia.
Treatment of PEA requires identification and treatment of reversible causes, such as severe hypovolemia, hypothermia, cardiac tamponade, or tension pneumothorax.446 Development of bradyasystolic rhythms often indicates the presence of severe hypovolemia, severe hypoxemia, or cardiorespiratory failure. Ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT) are treated with CPR and defibrillation. For treatment recommendations regarding cardiac tamponade in traumatic cardiac arrest, see “Cardiac Arrest Caused by Cardiac Tamponade.”
Resuscitative thoracotomy may be indicated in selected patients. A review of the literature from 1966 to 1999, carried out by the American College of Surgeons Committee on Trauma, found a survival rate of 7.8% (11.2% for penetrating injuries and 1.6% for blunt lesions) in trauma victims who would otherwise have 100% mortality.447 Practitioners should consult the guidelines for withholding or terminating resuscitation, which were developed for victims of traumatic cardiac arrest by a joint committee of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma.448,449
Commotio cordis is VF triggered by a blow to the anterior chest during a cardiac repolarization.450,451 Blunt cardiac injury may result in cardiac contusion with injured myocardium and risk of ECG changes and arrhythmias. Even a small blow to the anterior chest during a cardiac repolarization, such as that imparted by the strike of a baseball or hockey puck, may trigger VF, so-called commotio cordis.452 Events causing commotio cordis are most commonly seen in young persons up to 18 years of age who are engaged in sports but may occur during daily activities. Prompt recognition that a precordial blow may cause VF is critical. Rapid defibrillation is often life-saving for these frequently young victims of cardiac arrest. Provision of immediate BLS care using an automated external defibrillator (AED) and ACLS for VF in this setting is appropriate.
Unintentional or accidental hypothermia is a serious and preventable health problem. Severe hypothermia (body temperature <30°C [86°F]) is associated with marked depression of critical body functions, which may make the victim appear clinically dead during the initial assessment. Therefore, lifesaving procedures should be initiated unless the victim is obviously dead (eg, rigor mortis, decomposition, hemisection, decapitation). The victim should be transported as soon as possible to a center where aggressive rewarming during resuscitation is possible.
When the victim is extremely cold but has maintained a perfusing rhythm, the rescuer should focus on interventions that prevent further loss of heat and begin to rewarm the victim immediately. Additional interventions include the following:
Prevent additional evaporative heat loss by removing wet garments and insulating the victim from further environmental exposures. Passive rewarming is generally adequate for patients with mild hypothermia (temperature >34°C [93.2°F]).
For patients with moderate (30°C to 34°C [86°F to 93.2°F]) hypothermia with a perfusing rhythm, external warming techniques are appropriate.453 Passive rewarming alone will be inadequate for these patients.454
For patients with severe hypothermia (<30°C [86°F]) with a perfusing rhythm, core rewarming is often used, although some have reported successful rewarming with active external warming techniques.455,456 Active external warming techniques include forced air or other efficient surface-warming devices.
Patients with severe hypothermia and cardiac arrest can be rewarmed most rapidly with cardiopulmonary bypass.453,457-462 Alternative effective core rewarming techniques include warm-water lavage of the thoracic cavity460,463-467 and extracorporeal blood warming with partial bypass.468-470
Adjunctive core rewarming techniques include warmed IV or intraosseous (IO) fluids and warm humidified oxygen.471 Heat transfer with these measures is not rapid, and should be considered supplementary to active warming techniques.
Do not delay urgent procedures such as airway management and insertion of vascular catheters. Although these patients may exhibit cardiac irritability, this concern should not delay necessary interventions.
Beyond these critical initial steps, the treatment of severe hypothermia (temperature <30°C [86°F]) in the field remains controversial. Many providers do not have the time or equipment to assess core body temperature or to institute aggressive rewarming techniques, although these methods should be initiated when available.
When the victim is hypothermic, pulse and respiratory rates may be slow or difficult to detect,472,473 and the ECG may even show asystole. If the hypothermic victim has no signs of life, begin CPR without delay. If the victim is not breathing, start rescue breathing immediately.
The temperature at which defibrillation should first be attempted in the severely hypothermic patient and the number of defibrillation attempts that should be made have not been established. There are case reports of refractory ventricular arrhythmias with severe hypothermia; however, in a recent animal model it was found that an animal with a temperature of as low as 30°C had a better response to defibrillation than did normothermic animals in arrest.474,475
If VT or VF is present, defibrillation should be attempted. If VT or VF persists after a single shock, the value of deferring subsequent defibrillations until a target temperature is achieved is uncertain.
It may be reasonable to perform further defibrillation attempts according to the standard BLS algorithm concurrent with rewarming strategies. (Class IIb, LOE C)
To prevent further loss of core heat, remove wet garments and protect the victim from additional environmental exposure. Insofar as possible, this should be done while providing initial BLS therapies. Rewarming should be attempted when feasible.
For unresponsive patients or those in arrest, advanced airway insertion is appropriate as recommended in the standard ACLS guidelines. Advanced airway management enables effective ventilation with warm, humidified oxygen and reduces the likelihood of aspiration in patients in periarrest.
ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality. Conventional wisdom indicates that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical.476 In addition, drug metabolism may be reduced, and there is a theoretical concern that medications could accumulate to toxic levels in the peripheral circulation if given repeatedly to the severely hypothermic victim. For these reasons, previous guidelines suggest withholding IV drugs if the victim’s core body temperature is <30°C (86°F).
In the last decade a number of animal investigations have been performed evaluating both vasopressors and antiarrhythmic medications that could challenge some of this conventional wisdom.477-482 In a meta-analysis of these studies, Wira et al483 found that vasopressor medications (ie, epinephrine or vasopressin) increased rates of return of spontaneous circulation (ROSC) when compared with placebo (62% versus 17%; P<0.0001, n=77). Coronary perfusion pressures were increased in groups that received vasopressors compared with placebo. But groups given antiarrhythmics showed no improvement in ROSC when compared with control groups, although sample sizes were relatively small (n=34 and n=40, respectively).
One small-animal investigation suggested that the application of standard normothermic ACLS algorithms using both drugs (ie, epinephrine and amiodarone) and defibrillation improved ROSC compared with a placebo arm of defibrillation only (91% versus 30%; P<0.01; n=21). Human trials of medication use in accidental hypothermia do not exist, although case reports of survival with use of intra-arrest medication have been reported.461,465,484
Given the lack of human evidence and relatively small number of animal investigations, the recommendation for administration or withholding of medications is not clear.
It may be reasonable to consider administration of a vasopressor during cardiac arrest according to the standard ACLS algorithm concurrent with rewarming strategies. (Class IIb, LOE C)
After ROSC, patients should continue to be warmed to a goal temperature of approximately 32° to 34°C; this can be maintained according to standard postarrest guidelines for mild to moderate hypothermia in patients for whom induced hypothermia is appropriate. For those with contraindications to induced hypothermia, rewarming can continue to normal temperatures.
Because severe hypothermia is frequently preceded by other disorders (eg, drug overdose, alcohol use, or trauma), the clinician must look for and treat these underlying conditions while simultaneously treating hypothermia.
Multiple case reports indicate survival from accidental hypothermia even with prolonged CPR and downtimes.457,469 Thus, patients with severe accidental hypothermia and cardiac arrest may benefit from resuscitation even in cases of prolonged downtime and prolonged CPR. Low serum potassium may indicate hypothermia, and not hypoxemia, as the primary cause of the arrest.485 Patients should not be considered dead before warming has been provided.
Avalanche-related deaths are on the rise in North America due to winter recreational activities, including backcountry skiing and snowboarding, helicopter and snowcat skiing, snowmobiling, out-of-bounds skiing, ice climbing, mountaineering, and snowshoeing. The most common causes of avalanche-related death are asphyxia, trauma, and hypothermia, or combinations of the 3. Rescue and resuscitation strategies focus on management of asphyxia and hypothermia, because most field research has been done on these 2 conditions.
Avalanches occur in areas that are difficult to access by rescuers in a timely manner, and burials frequently involve multiple victims. The decision to initiate full resuscitative measures should be determined by the number of victims, resources available, and likelihood of survival. Studies of avalanche victims demonstrate a progressive nonlinear reduction in survival as the time of avalanche burial lengthens.486-489 The likelihood of survival is minimal when avalanche victims are buried >35 minutes with an obstructed airway and in cardiac arrest on extrication487,488,490-496 or are buried for any length of time and in cardiac arrest on extrication with an obstructed airway and an initial core temperature of <32°C.488-490,494,497
It may be difficult to know with any certainty how long an avalanche victim has been buried. The core temperature at time of extrication provides a proxy for duration of burial. A case series497 of buried avalanche victims showed a maximum cooling rate of 8°C per hour, whereas a case report494 described a maximum cooling rate of 9°C per hour. These cooling rates suggest that at 35 minutes of burial, the core temperature may drop as low as 32°C.
If information on the duration of burial or the state of the airway on extrication is not available to the receiving physician, a serum potassium level of <8 mmol/L on hospital admission is a prognostic marker for ROSC491 and survival to hospital discharge.490,497 High potassium values are associated with asphyxia,490,497-499 and there is an inverse correlation between admission K+ and survival to discharge in all-cause hypothermic patients.490,500-503 In a series of 32 avalanche survivors the highest serum K+ was 6.4 mmol/L,497 but there is a single case report of a 31- month-old child with a K+ of 11.8 mmol/L presenting with hypothermia from exposure unrelated to an avalanche who survived.504 This suggests that the upper survivable limit of potassium is unknown for children who are hypothermic and victims of avalanche.
Full resuscitative measures, including extracorporeal rewarming when available, are recommended for all avalanche victims without the characteristics outlined above that deem them unlikely to survive or with any obvious lethal traumatic injury. (Class I, LOE C)
All victims of drowning who require any form of resuscitation (including rescue breathing alone) should be transported to the hospital for evaluation and monitoring, even if they appear to be alert and demonstrate effective cardiorespiratory function at the scene. (Class I, LOE C)
A number of terms are used to describe drowning.508 To aid in use of consistent terminology and uniform reporting of data, use of the Utstein definitions and style of data reporting specific to drowning is recommended.509,510
Although survival is uncommon in victims who have undergone prolonged submersion and require prolonged resuscitation,511,512 successful resuscitation with full neurological recovery has occurred occasionally after prolonged submersion in icy water513-516 and, in some instances, warm water.517,518 For this reason, scene resuscitation should be initiated and the victim transported to the ED unless there is obvious death (eg, rigor mortis, decomposition, hemisection, decapitation, lividity).
The most important and detrimental consequence of submersion is hypoxia; therefore, oxygenation, ventilation, and perfusion should be restored as rapidly as possible. This will require immediate bystander CPR plus activation of the EMS system. With the 2010 AHA Guidelines for CPR and ECC, CPR now begins with chest compressions in a C-A-B sequence. However, the guidelines recommend that healthcare providers tailor the sequence based upon the presumed etiology of the arrest. Healthcare provider CPR for drowning victims should use the traditional A-B-C approach in view of the hypoxic nature of the arrest. Victims with only respiratory arrest usually respond after a few artificial breaths are given.
When attempting to rescue a drowning victim, the rescuer should get to the victim as quickly as possible. It is crucial, however, that the rescuer pays constant attention to his or her own personal safety during the rescue process.
The reported incidence of cervical spine injury in drowning victims is low (0.009%).519,520 Unnecessary cervical spine immobilization can impede adequate opening of the airway and delay delivery of rescue breaths.
The first and most important treatment of the drowning victim is the immediate provision of ventilation. Prompt initiation of rescue breathing increases the victim’s chance of survival.522 Rescue breathing is usually performed once the unresponsive victim is in shallow water or out of the water. Mouth-to-nose ventilation may be used as an alternative to mouth-to-mouth ventilation if it is difficult for the rescuer to pinch the victim’s nose, support the head, and open the airway in the water.
Management of the drowning victim’s airway and breathing is similar to that recommended for any victim of cardiopulmonary arrest. Some victims aspirate no water because they develop laryngospasm or breath-holding.512,523 Even if water is aspirated, there is no need to clear the airway of aspirated water, because only a modest amount of water is aspirated by the majority of drowning victims, and aspirated water is rapidly absorbed into the central circulation.512,524 Attempts to remove water from the breathing passages by any means other than suction (eg, abdominal thrusts or the Heimlich maneuver) are unnecessary and potentially dangerous.524
The routine use of abdominal thrusts or the Heimlich maneuver for drowning victims is not recommended. (Class III, LOE C)
As soon as the unresponsive victim is removed from the water, the rescuer should open the airway, check for breathing, and if there is no breathing, give 2 rescue breaths that make the chest rise (if this was not done previously in the water). After delivery of 2 effective breaths, if a pulse is not definitely felt, the healthcare provider should begin chest compressions and provide cycles of compressions and ventilations according to the BLS guidelines. Once the victim is out of the water, if he or she is unresponsive and not breathing after delivery of 2 rescue breaths and is pulseless, rescuers should attach an AED and attempt defibrillation if a shockable rhythm is identified. It is only necessary to dry the chest area before applying the defibrillation pads and using the AED. If hypothermia is present, follow the recommendations in “Cardiac Arrest in Accidental Hypothermia.”
The victim may vomit when the rescuer performs chest compressions or rescue breathing. In fact, in a 10-year study in Australia, two thirds of victims who received rescue breathing and 86% of those who required compressions and ventilations vomited.525 If vomiting occurs, turn the victim to the side and remove the vomitus using your finger, a cloth, or suction. If spinal cord injury is suspected, the victim should be logrolled so that the head, neck, and torso are turned as a unit to protect the cervical spine.
Victims in cardiac arrest may present with asystole, PEA, or pulseless VT/VF. For treatment of these rhythms, follow the appropriate PALS or ACLS guidelines. Case reports of pediatric patients document the use of surfactant for fresh water–induced respiratory distress, but further research is needed.526-529 The use of extracorporeal membrane oxygenation in patients with severe hypothermia after submersion has been documented in case reports.515,516,530
Injuries from electric shock and lightning strike result from the direct effects of current on the heart and brain, cell membranes, and vascular smooth muscle. Additional injuries result from the conversion of electric energy into heat energy as current passes through body tissues.531
Fatal electrocutions may occur with household current; however, high-tension current generally causes the most serious injuries.532 Contact with alternating current (the type of current commonly present in most North American households and commercial settings) may cause tetanic skeletal muscle contractions, “locking” the victim to the source of the electricity and thereby leading to prolonged exposure. The frequency of alternating current increases the likelihood of current flow through the heart during the relative refractory period, which is the “vulnerable period” of the cardiac cycle. This exposure can precipitate VF, which is analogous to the R-on-T phenomenon that occurs in nonsynchronized cardioversion.533
The National Weather Service estimates that an average of 70 deaths and 630 injuries occur due to lightning strikes in the United States each year.534 Lightning strike injuries can vary widely, even among groups of people struck at the same time. Symptoms are mild in some victims, whereas fatal injuries occur in others.535,536
The primary cause of death in victims of lightning strike is cardiac arrest, which may be associated with primary VF or asystole.535-538 Lightning acts as an instantaneous, massive direct-current shock, simultaneously depolarizing the entire myocardium.536,539 In many cases intrinsic cardiac automaticity may spontaneously restore organized cardiac activity and a perfusing rhythm. However, concomitant respiratory arrest due to thoracic muscle spasm and suppression of the respiratory center may continue after ROSC. Unless ventilation is supported, a secondary hypoxic (asphyxial) cardiac arrest will develop.540
Lightning also can have myriad effects on the cardiovascular system, producing extensive catecholamine release or autonomic stimulation. The victim may develop hypertension, tachycardia, nonspecific ECG changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with release of creatinine kinase-MB fraction.
Lightning can produce a wide spectrum of peripheral and central neurological injuries. The current can produce brain hemorrhages, edema, and small-vessel and neuronal injury. Hypoxic encephalopathy can result from cardiac arrest.
Victims are most likely to die of lightning injury if they experience immediate respiratory or cardiac arrest and no treatment is provided. Patients who do not suffer respiratory or cardiac arrest, and those who respond to immediate treatment, have an excellent chance of recovery. Therefore, when multiple victims are struck simultaneously by lightning, rescuers should give the highest priority to patients in respiratory or cardiac arrest.
For victims in cardiac arrest, treatment should be early, aggressive, and persistent. Victims with respiratory arrest may require only ventilation and oxygenation to avoid secondary hypoxic cardiac arrest. Resuscitation attempts may have high success rates and efforts may be effective even when the interval before the resuscitation attempt is prolonged.540
The rescuer must first be certain that rescue efforts will not put him or her in danger of electric shock. When the scene is safe (ie, the danger of shock has been removed), determine the victim’s cardiorespiratory status. If spontaneous respiration or circulation is absent, immediately initiate standard BLS resuscitation care, including the use of an AED to identify and treat VT or VF.
Maintain spinal stabilization during extrication and treatment if there is a likelihood of head or neck trauma.541,542 Both lightning and electric shock often cause multiple trauma, including injury to the spine,542 muscular strains, internal injuries from being thrown, and fractures caused by the tetanic response of skeletal muscles.543 Remove smoldering clothing, shoes, and belts to prevent further thermal damage.
No modification of standard ACLS care is required for victims of electric injury or lightning strike, with the exception of paying attention to possible cervical spine injury. Establishing an airway may be difficult for patients with electric burns of the face, mouth, or anterior neck. Extensive soft-tissue swelling may develop rapidly, complicating airway control measures. Thus, early intubation should be performed for patients with evidence of extensive burns even if the patient has begun to breathe spontaneously.
For victims with significant tissue destruction and in whom a pulse is regained, rapid IV fluid administration is indicated to counteract distributive/hypovolemic shock and to correct ongoing fluid losses due to third spacing. Fluid administration should be adequate to maintain diuresis and facilitate excretion of myoglobin, potassium, and other byproducts of tissue destruction (this is particularly true for patients with electric injury).539 Regardless of the extent of external injuries after electrothermal shock, the underlying tissue damage can be far more extensive.
Cardiac tamponade can be a life-threatening event. Increasing fluid and pressure in the pericardium reduces atrial and ventricular filling. As filling is reduced, stroke volume and cardiac output fall, with associated hypotension leading to cardiac arrest. Rapid diagnosis and drainage of the pericardial fluid are required to avoid cardiovascular collapse.
Pericardiocentesis guided by echocardiography is a safe and effective method of relieving tamponade in a nonarrest setting, especially when used in conjunction with a pericardial drain, and may obviate the need for subsequent operating room treatment.544-548
In the arrest setting, in the absence of echocardiography, emergency pericardiocentesis without imaging guidance can be beneficial. (Class IIa, LOE C)
Emergency department thoracotomy may improve survival compared with pericardiocentesis in patients with pericardial tamponade secondary to trauma who are in cardiac arrest or who are prearrest,549-551 especially if gross blood causes clotting that blocks a pericardiocentesis needle.552 (Class IIb, LOE C)
The incidence of cardiac arrest following cardiac surgery is in the range of 1–3%. Causes include conditions that may be readily reversed such as ventricular fibrillation, hypovolemia, cardiac tamponade, or tension pneumothorax. Pacing wires, if present, may reverse symptomatic bradycardia or asystole. A recent review may be helpful for those seeking additional information.553
Studies of patients with cardiac arrest after cardiac surgery who are treated with resternotomy and internal cardiac compression have reported improved outcome compared with a standard protocol554-564 when patients are treated by experienced personnel in intensive care units. Findings of similar quality studies565-569 reported no difference in outcomes when resternotomy was compared with standard management of cardiac arrest after cardiac surgery. Resternotomy performed outside an intensive care unit generally has a very poor outcome.554,561,568
For patients with cardiac arrest following cardiac surgery, it is reasonable to perform resternotomy in an appropriately staffed and equipped intensive care unit. (Class IIa, LOE B)
Despite rare case reports describing damage to the heart possibly due to external chest compressions,570,571 chest compressions should not be withheld if emergency resternotomy is not immediately available. (Class IIa, LOE C)
Despite rare case reports describing damage to the heart possibly due to external chest compressions,570,571 chest compressions should not be withheld if emergency resternotomy is not immediately available. (Class IIa, LOE C)
Nine case series have reported survival of some post–cardiac surgery patients during cardiac arrest refractory to standard resuscitation measures following the use of extracorporeal membrane oxygenation572-576and cardiopulmonary bypass.564,577-579
In post-cardiac surgery patients who are refractory to standard resuscitation procedures, mechanical circulatory support (eg, extracorporeal membrane oxygenation and cardiopulmonary bypass) may be effective in improving outcome. (Class IIb, LOE B)
Rebound hypertension following administration of pressors during resuscitation has the potential to induce significant bleeding in this group of patients. Results from a single study of epinephrine580 and another study evaluating the choice of antiarrhythmics581 in patients with cardiac arrest following cardiac surgery were neutral. There is insufficient evidence on epinephrine dose, antiarrhythmic use, and other routine pharmacological interventions to recommend deviating from standard resuscitation guidelines when cardiac arrest occurs after cardiac surgery.
Eric J. Lavonas, Chair; Ian R. Drennan; Andrea Gabrielli; Alan C. Heffner; Christopher O. Hoyte; Aaron M. Orkin; Kelly N. Sawyer; Michael W. Donnino
Terry L. Vanden Hoek, Chair; Laurie J. Morrison; Michael Shuster; Michael Donnino; Elizabeth Sinz; Eric J. Lavonas; Farida M. Jeejeebhoy; Andrea Gabrielli
The American Heart Association requests that this document be cited as follows:
American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 10: Special Circumstances of Resuscitation. ECCguidelines.heart.org.
© Copyright 2015 American Heart Association, Inc.