Part 10: Special Circumstances of Resuscitation

    Key Words:
  • cardiac arrest
  • defibrillation
  • emergency
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This Part summarizes recommendations for the management of resuscitation in the following special circumstances:

  • cardiac arrest associated with pregnancy
  • cardiac arrest associated with pulmonary embolism
  • cardiac or respiratory arrest associated with opioid overdose
  • role of intravenous lipid emulsion therapy in ACLS management of cardiac arrest due to poisoning/drug overdose
  • cardiac arrest associated with other toxic ingestions (benzodiazepines, β-blockers, calcium channel blockers, digoxin, cocaine, cyclic antidepressants, carbon monoxide, and cyanide)
  • cardiac arrest during percutaneous coronary intervention
  • cardiac arrest associated with asthma
  • cardiac arrest associated with anaphylaxis
  • cardiac arrest in the morbidly obese
  • cardiac arrest associated with life-threatening electrolyte imbalance
  • cardiac arrest associated with trauma
  • commotio cordis
  • cardiac arrest associated with unintentional hypothermia
  • cardiac arrest in avalanche victims
  • cardiac arrest due to drowning
  • cardiac arrest associated with electric shock or lightning strikes
  • cardiac arrest caused by cardiac tamponade
  • cardiac arrest following cardiac surgery
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    Cardiac Arrest Associated With Pregnancy

    Maternal cardiac arrest occurs in approximately 1:12,000 admissions for delivery in the United States; these arrest rates more than doubled between 1989 and 2009.

    BLS Modification: Relief of Aortocaval Compression

    Maternal position has emerged as an important strategy to improve CPR quality, particularly compression force and cardiac output. The gravid uterus can compress the inferior vena cava, impeding venous return and reducing the cardiac output generated by chest compressions. In general, aortocaval compression by the uterus begins to occur for singleton pregnancies at about 20 weeks of gestation, once the fundus is at or above the umbilicus. In the past, the AHA Guidelines recommended positioning the pregnant victim in cardiac arrest on a tilted surface to displace the uterus, but this can compromise the quality of the compressions delivered. Manual uterine displacement effectively relieves aortocaval compression in patients with hypotension (see Figure 1).

    Priorities for the pregnant woman in cardiac arrest are provision of high-quality CPR and relief of aortocaval compression. (Class I, LOE C-LD) (2015 Part 10)

    If the fundus height is at or above the level of the umbilicus, manual lateral uterine displacement can be beneficial in relieving aortocaval compression during chest compressions. (Class IIa, LOE C-LD) (2015 Part 10)

    Figure 1: A, Manual LUD, performed with one-handed technique. B, Two-handed technique during resuscitation
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    ALS Modification: Emergency Cesarean Delivery in Maternal Cardiac Arrest

    Evacuation of the gravid uterus immediately relieves aortocaval pressure and may improve resuscitative efforts. During the latter half of pregnancy, a perimortem caesarean delivery may be considered part of maternal resuscitation. Relatively high maternal survival has been reported following peri-mortem caesarean delivery as late as 15 minutes after cardiac arrest, and newborn survival has been reported when the delivery occurred as late as 30 minutes after maternal cardiac arrest.

    Because immediate return of spontaneous circulation (ROSC) cannot always be achieved [during maternal cardiac arrest], local resources for a perimortem caesarean delivery should be summoned as soon as cardiac arrest is recognized in a woman in the second half of pregnancy. (Class I, LOE C-LD) (2015 Part 10)

    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 maternal cardiac arrest and possible perimortem caesarean delivery should develop and practice standard institutional responses to allow for smooth progression of resuscitative care. (Class I, LOE C-EO) (2015 Part 10)

    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 lateral uterine displacement, it is advisable to prepare to evacuate the uterus while resuscitation continues. (Class I, LOE C-LD) (2015 Part 10)

    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 perimortem caesarean delivery. (Class I, LOE C-LD) (2015 Part 10)

    Perimortem caesarean delivery 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) (2015 Part 10)

    Cardiac Arrest Associated With Pulmonary Embolism

    BLS Modification: Suspected or Confirmed Pulmonary Embolism

    There were no modifications of BLS technique suggested for suspected pulmonary embolism.

    ALS Modifications: Confirmed Pulmonary Embolism

    In patients with confirmed pulmonary embolus as the precipitant of cardiac arrest, thrombolysis, surgical embolectomy, and mechanical embolectomy are reasonable emergency treatment options. (Class IIa, LOE C-LD) (2015 Part 10) There are insufficient data available to recommend one strategy over another.

    Patient location, local intervention options, and patient factors (including thrombolysis contraindications) are some elements to be considered.

    Thrombolysis can be beneficial even when chest compressions have been provided. (Class IIa, LOE C-LD) (2015 Part 10)

    In patients with cardiac arrest and without known pulmonary embolus, routine fibrinolytic treatment given during CPR shows no benefit and is not recommended. (Class III, LOE A) (2010 Part 12)

    ALS Modifications: Suspected Pulmonary Embolism

    Thrombolysis may be considered when cardiac arrest is suspected to be caused by pulmonary embolus. (Class IIb, LOE C-LD) (2015 Part 10)

    Cardiac or Respiratory Arrest Associated With Opioid Overdose

    Opioid Overdose Response Education and Naloxone Training and Distribution

    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) (2015 Part 10)

    Some populations that may benefit from opioid overdose response interventions are listed in the Box.

    It is reasonable to base this opioid overdose response 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) (2015 Part 10)

    Table 1: Groups That May Benefit From Opioid Overdose Response Education and/or Naloxone Distribution and Training

    First Aid and Non–Healthcare Provider BLS Modification: Administration of Naloxone

    Empiric administration of intramuscular or intranasal 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) (2015 Part 10) Standard resuscitation, including activation of emergency medical services, should not be delayed for naloxone administration.

    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 2)

    Victims who respond to naloxone administration should access advanced healthcare services. (Class I, LOE C-EO) (2015 Part 10)

    Figure 2: Opioid-Associated Life-Threatening Emergency (Adult) Algorithm
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    Healthcare Provider BLS Modification: Administration of Naloxone

    Respiratory Arrest

    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 intramuscular or intranasal naloxone. (Class IIa, LOE C-LD) (2015 Part 10)

    Cardiac Arrest

    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) (2015 Part 10)

    It may be reasonable to administer intramuscular or intranasal naloxone based on the possibility that the patient is not in cardiac arrest. (Class IIb, LOE C-EO) (2015 Part 10)

    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) (2015 Part 10)

    Unless the patient refuses further care, victims who respond to naloxone administration should access advanced healthcare services. (Class I, LOE C-EO) (2015 Part 10)

    ACLS Modification: Administration of Naloxone

    Respiratory Arrest

    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) (2015 Part 10)

    Cardiac Arrest

    We can make no recommendation regarding the administration of naloxone in confirmed opioid-associated cardiac arrest. (2015 Part 10)

    Observation and Post-Resuscitation Care

    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) (2015 Part 10)

    If recurrent opioid toxicity develops, repeated small doses or an infusion of naloxone can be beneficial in healthcare settings. (Class IIa, LOE C-LD) (2015 Part 10)

    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, longer periods of observation may be required to safely discharge a patient with life-threatening overdose of a long-acting or sustained-release opioid.

    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) (2015 Part 10)

    Role of Intravenous Lipid Emulsion Therapy in ACLS Management of Cardiac Arrest Due to Poisoning/Drug Overdose

    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.

    Administration of intralipid emulsion creates a lipid compartment in the serum, reducing by sequestration the concentration of lipophilic medications in the tissues.  Administration of intralipid emulsion also increases cardiac inotropy by other mechanisms.

    Case reports of patients with poisonings, including but not limited to bupivacaine anesthetic overdose, reported clinical improvement such as ROSC, relief of hypotension, resolution of arrhythmias, improved mental status or termination of status epilepticus following administration of intravenous lipid emulsion.

    It may be reasonable to administer intralipid emulsion, 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) (2015 Part 10)

    It may be reasonable to administer intralipid emulsion to patients with other forms of drug toxicity who are failing standard resuscitative measures. (Class IIb, LOE C-EO) (2015 Part 10)

    Cardiac Arrest Associated With Other Toxic Ingestions

    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.

    Consultation is recommended early in the management of a patient with potentially life-threatening poisoning, because appropriate interventions might prevent deterioration to cardiac arrest.

    If cardiac arrest develops as the result of toxicity, resuscitation is managed in accordance with the current standards of BLS and ACLS.

    Once return of spontaneous circulation is achieved, urgent consultation with a medical toxicologist or certified regional poison center is recommended.

    To contact a certified poison center in the United States: 1-800-222-1222.

    Initial Approach to the Critically Poisoned Patient

    Protect the airway, provide rapid assessment and support respiration and circulation.

    The patient may not be able to provide an accurate history, so history-taking must include questioning of persons who accompany the patient, evaluation of containers (eg, pill bottles), review of pharmacy records, and examination of the patient’s prior medical record whenever possible.

    Many patients who ingest medications in a suicide attempt take more than 1 substance.

    Poisoned patients may deteriorate rapidly.

    Patients who are critically ill or under evaluation for possible toxin exposure or ingestion, particularly when the history is uncertain, should be cared for in a monitored treatment area where providers can rapidly detect and address the development of central nervous system depression, hemodynamic instability, or seizures.

    With rare exceptions, gastric lavage, whole bowel irrigation, and administration of syrup of ipecac are not recommended.

    Activated Charcoal:

    • Expert advice can be helpful when weighing the complex and multifactorial risks and potential benefits of administration
    • Administration of single dose activated charcoal is generally recommended to adsorb life-threatening poisons for which no adequate antidotal therapy is available and when the charcoal can be administered within 1 hour of poisoning.
    • Consider multiple dose activated charcoal for patients who have ingested a life-threatening amount of specific toxins (eg, carbamazepine, dapsone, phenobarbital, quinine, or theophylline) for which a beneficial effect of this strategy has been established.
    • Activated charcoal should not be administered for ingestions of caustic substances, metals, or hydrocarbons.
    • Activated charcoal should only be administered to patients with an intact or protected airway.
    • In patients at risk for aspiration, endotracheal intubation and elevation of the head of the bed is needed before administration.

    Common Toxidromes

    A toxidrome is a constellation of clinical signs and symptoms and laboratory values suggestive of the effects of a specific toxin. Identification of the presentation of common toxidromes can establish a working diagnosis of the toxin and guide initial management and stabilization.

    Common Toxidromes and their presentations are listed in Table 2.

    Table 2: Common Toxidromes

    Benzodiazepine Toxicity

    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. However, flumazenil has no role in the management of cardiac arrest.

    Flumazenil administration can precipitate seizures in benzodiazepine-dependent patients and has been associated with seizures, arrhythmias, and hypotension in patients with co-ingestion of certain medications, such as tricyclic antidepressants.

    The administration of flumazenil to patients with undifferentiated coma confers risk and is not recommended. (Class III, LOE B) (2010 Part 12)

    Flumazenil may be used safely to reverse excessive sedation known to be caused by the use of benzodiazepines in patients without known contraindications (eg, procedural sedation).

    β-Blocker Toxicity

    Resuscitation from cardiac arrest caused by β-blocker overdose should follow standard BLS and ACLS algorithms.

    Therapeutic options in the treatment of refractory hemodynamic instability caused by β-blocker overdose include administration of glucagon, high-dose insulin, or IV calcium salts.

    Glucagon Administration for β-Blocker Toxicity

    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 (ie, bolus of 0.05 to 0.15 mg/kg followed by an infusion of 0.05 to 0.10 mg/kg per hour). (Class IIb, LOE C) (2010 Part 12)

    Titrate the infusion rate to achieve an adequate hemodynamic response (appropriate mean arterial pressure and evidence of good perfusion).

    Because the amount of glucagon required to sustain 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 secured before glucagon administration.

    Based on animal studies the concomitant use of dopamine alone or in combination with isoproterenol and milrinone may decrease the effectiveness of glucagon.

    High-Dose Insulin Administration for β-Blocker Toxicity

    Very limited data (animal studies and limited human data) suggest that administration of high-dose insulin can be effective for treatment of refractory shock associated with a massive overdose of metoprolol.

    Administration of high-dose intravenous insulin may be considered in patients with β-blocker overdose and shock refractory to other measures. (Class IIb, LOE C) (2010 Part 12)

    A commonly used insulin administration 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.

    Titrate the insulin infusion as needed to achieve adequate hemodynamic response.

    Titrate the dextrose infusion to maintain serum glucose concentration 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 from the extracellular (including the intravascular) to the intracellular space. As a result, moderate hypokalemia is common. To avoid overly aggressive potassium repletion,1 human protocol targeted potassium concentration of 2.5 to 2.8 mEq/L.

    Calcium Administration for β-Blocker Toxicity

    Calcium administration may be helpful in the treatment of shock caused by β-blocker toxicity.

    Administration of calcium may be considered in patients with shock related to β-blocker overdosethat is refractory to other measures. (Class IIb, LOE C) (2010 Part 12)

    One approach is to administer 0.3 mEq/kg of IV calcium (0.6 mL/kg of 10% calcium gluconate solution or 0.2 mL/kg of 10% calcium chloride solution) over 5 to 10 minutes, followed by an infusion of 0.3 mEq/kg per hour.

    Titrate the infusion rate to adequate hemodynamic response.

    Monitor serum ionized calcium concentration, and taper the infusion if necessary to prevent severe hypercalcemia (ionized calcium levels greater than twice the upper limits of normal).

    Sustained infusions of IV calcium require central venous access.

    Other Therapies for β-blocker Toxicity

    When managing treatment-refractory hypotension. it is important to promptly consult with a medical toxicologist or other specialist with current knowledge regarding management of β-blocker overdose.

    Calcium Channel Blocker Toxicity

    Resuscitation from cardiac arrest caused by calcium channel blocker overdose should follow standard BLS and ACLS algorithms.

    Calcium channel blocker overdose can cause life-threatening hypotension and bradycardia that are refractory to standard agents.

    In the setting of severe cardiovascular toxicity associated with toxicity from a calcium channel blocker overdose, high-dose insulin, may be effective for restoring hemodynamic stability and improving survival. (Class IIb, LOE B) (2010 Part 12) See doses above (see Insulin section of β-blocker overdose, above).

    In patients with shock refractory to other measures, administration of calcium may be considered. (Class IIb, LOE C) (2010 Part 12)

    There is conflicting evidence regarding the use/effectveness of glucagon in the treatment of hemodynamically unstable calcium channel blocker overdose.

    Toxicity of Digoxin and Related Cardiac Glycosides

    Digoxin poisoning can cause severe bradycardia and life-threatening arrhythmias, including ventricular tachycardia, ventricular fibrillation, and high degrees of AV nodal block.

    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.

    Antidigoxin Fab antibodies should be administered to patients with severe life-threatening cardiac glycoside toxicity. (Class I, LOE B) (2010 Part 12)

    One vial of antidigoxin Fab is standardized to neutralize 0.5 mg of digoxin.

    A reasonable dosing strategy for antidigoxin Fab antibodies is:

    • 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 the severity of acute cardiac glycoside toxicity and is associated with poor prognosis.

    Antidigoxin Fab may be administered empirically to patients with acute poisoning from digoxin or related cardiac glycosides and a serum potassium concentration exceeding 5.0 mEq/L.

    Cocaine Overdose

    Resuscitation from cocaine-related cardiac arrest should follow standard BLS and ACLS algorithms, with specific antidotes used in the post-cardiac arrest phase if severe cardiotoxicity or neurotoxicity is encountered.

    Cocaine-induced tachycardia and hypertension are predominantly caused by central nervous system stimulation.

    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) benzodiazepines (lorazepam, diazepam), calcium channel blockers (verapamil), morphine, and sublingual nitroglycerin may be used as needed to control hypertension, tachycardia, and agitation[associated with cocaine overdose].
    (Class IIb, LOE B) (2010 Part 12)

    The available data do not support the use of [any] 1 agent over another in the treatment of cardiovascular toxicity due to cocaine. (Class IIb, LOE B)  (2010 Part 12)

    For cocaine-induced hypertension or chest discomfort, benzodiazepines, nitroglycerin, and/or morphine can be beneficial. (Class IIa, LOE B) (2010 Part 12)

    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 is metabolized.

    Cocaine-induce reduction of coronary artery diameter is reversed by morphine, nitroglycerin, phentolamine, and verapamil. The cocaine-induced reduction in coronary artery diameter is not changed by labetalol and it is exacerbated by propranolol.

    β- blockers may worsen cardiac perfusion and/or produce paradoxical hypertension when cocaine is present.

    In the setting of cocaine, pure β-blocker medications are not indicated.
    (Class IIb, LOE C) (2010 Part 12)

    Extrapolation from evidence in the treatment of wide-complex tachycardia caused by other class Ic anti-arrhythmic agents (flecainide) and tricyclic antidepressants suggests that administration of hypertonic sodium bicarbonate may be beneficial.

    A typical treatment strategy used for other overdoses of 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.

    Cyclic Antidepressant Toxicity

    Cardiac arrest caused by cyclic antidepressant toxicity should be managed by current BLS and ACLS treatment guidelines.

    Administration of sodium bicarbonate for cardiac arrest due to cyclic antidepressant overdose may be considered. (Class IIb, LOE C) (2010 Part 12)

    Therapeutic strategies for treatment of severe cyclic antidepressant cardiotoxicity include increasing serum sodium, increasing serum pH, or doing both simultaneously.

    In the management of severe cardiotoxicity from cyclic antidepressant overdose, sodium bicarbonate boluses of 1 mL/kg may be administered as needed to achieve hemodynamic stability (adequate mean arterial blood pressure and perfusion) and QRS narrowing. (Class IIb, LOE C) (2010 Part 12)

    Monitor serum sodium concentration and pH and avoid severe hypernatremia (sodium >155 mEq/L) and alkalemia (pH >7.55).

    A number of vasopressors and inotropes (epinephrine, norepinephrine, dopamine, and dobutamine) have been associated with improvement in tricyclic-induced hypotension.

    Carbon Monoxide Poisoning

    Carbon monoxide poisoning is a leading cause of unintentional poisoning death in the United States.

    Routine care of patients in cardiac arrest and severe cardiotoxicity from carbon monoxide poisoning should comply with standard BLS and ACLS recommendations. However, if cardiac arrest develops from carbon monoxide poisoning, morbidity and mortality are high.

    Carbon monoxide not only reduces the ability of hemoglobin to carry oxygen, it also can cause direct brain and myocardial cellular damage, and lasting myocardial and neurologic injury.

    Pulse oximetry will not accurately reflect oxy-hemoglobin saturation in the presence of carbon monoxide poisoning.

    Hyperbaric Oxygen

    Hyperbaric oxygen therapy may be helpful in treatment of acute carbon monoxide poisoning in patients with severe toxicity. (Class IIb, LOE C) (2010 Part 12)

    Although there is limited data about effective interventions in this population, it is reasonable to provide enhanced follow-up for them. Hyperbaric oxygen appears to confer little risk and may be beneficial.

    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 Toxicity

    Cyanide can be found in jewelry cleaners, electroplating solutions, as a metabolic product of the some drugs (eg, the putative antitumor drug amygdalin [laetrile]) and is a major component of fire smoke.

    Consider cyanide poisoning in victims of smoke inhalation who have:

    • hypotension
    • central nervous system depression
    • metabolic acidosis
    • soot in the nares or respiratory secretions

    Cyanide poisoning causes rapid cardiovascular collapse, which manifests as hypotension, lactic acidosis, central apnea, and seizures.

    Patients in cardiac arrest or those presenting with cardiovascular instability 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.

    Hydroxocobalamin and sodium nitrite rapidly and effectively bind serum cyanide to reverse the effects of cyanide toxicity. Nitrites can induce methemoglobin formation and they can cause hypotension. Hydroxocobalamin does have a safety advantage, especially for children and victims of smoke inhalation. Note that in the presence of methemoglobinemia, the oxygen saturation reported by pulse oximetry will be inaccurate.

    Sodium thiosulfate can enhance the detoxification of cyanide to thiocyanate and enhances the effectiveness of cyanide scavengers. Vomiting is the only known complication, so the patient’s airway must be kept clear.

    A treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning (Class I, LOE B) (2010 Part 12)

    Cardiac Arrest During Percutaneous Coronary Intervention

    Many patients who develop cardiac arrest during PCI will respond to standard ACLS resuscitation, including high-quality CPR and rapid defibrillation. See, also, 2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for Patients With ST-Elevation Myocardial Infarction, the 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction, and the 2014 NSTEMI Guidelines.

    A subset of patients who develop cardiac arrest during percutaneous coronary intervention will require prolonged resuscitation efforts. Mechanical devices may be useful to provide hemodynamic support during cardiac catheterization, especially those presenting in cardiogenic shock or those requiring percutaneous coronary intervention during or after cardiac arrest.

    ACLS Modifications

    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) (2015 Part 10)

    It may be reasonable to use Extracorporeal CPR as a rescue treatment when initial therapy is failing for cardiac arrest that occurs during PCI. (Class IIb, LOE C-LD) (2015 Part 10)

    Institutional guidelines should address 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 another device. (Class I, LOE C-EO) (2015 Part 10)

    It is not possible to recommend one approach (manual CPR, mechanical CPR, or ECPR) over another when options exist.

    Cardiac Arrest Associated With Asthma

    Patients with severe life-threatening asthma require urgent and aggressive treatment with simultaneous administration of oxygen, bronchodilators, and steroids, and the possible addition of anticholinergics.

    Monitor these patients closely for deterioration.

    Primary Therapy


    Provide oxygen to all patients with severe asthma, even those with normal oxygenation.

    Successful treatment with β-2-agonists (ie, bronchodilators) may cause an initial decrease in oxygen saturation.

    Inhaled β-2-Agonists

    There is no evidence that levalbuterol should be favored over albuterol.

    When combined with short- acting β-agonists, anticholinergic agents such as ipratropium can produce a clinically modest improvement in lung function over use of β-agonists alone.


    Systemic corticosteroids are the only proven effective treatment for the inflammatory component of asthma during acute exacerbations. They should be administered early, because it may take as long as 6 hours before the onset of effect in improving forced expiratory volume in 1 second.

    Although there may be no difference in clinical effects between oral and IV corticosteroids, the IV route is preferable for patients with severe asthma.

    In adults a typical initial dose of methylprednisolone is 125 mg (range: 40 mg to 250 mg); a typical dose of dexamethasone is 10 mg.


    Ipratropium bromide is an anticholinergic bronchodilator that is pharmacologically related to atropine. In combination with β-adrenergic bronchodilators, ipratropium can be particularly effective for severe exacerbations of asthma. The nebulizer dose is 500 mcg. Ipratropium bromide has a slow onset of action (approximately 20 minutes), with peak effect in 60 to 90 minutes, with no systemic side effects. Although the drug is typically given once because it has prolonged effects, some beneficial effects have been reported in repeat doses (250 mcg or 500 mcg every 20 minutes).

    Adjunctive Therapies

    Magnesium Sulfate

    When combined with nebulized β-adrenergic agonists and corticosteroids, IV magnesium sulfate (standard adult dose: 2 g administered over 20 minutes) can moderately improve pulmonary function in patients with asthma. Magnesium relaxes bronchial smooth muscle and improves pulmonary function independent of serum magnesium level, with only minor side effects (flushing, lightheadedness). Nebulized magnesium sulfate, when used as an adjunct to nebulized β-adrenergic agents for acute severe asthma can improve forced expiratory volume in 1 second and oxyhemoglobin saturation (SpO2).

    Epinephrine or Terbutaline

    Epinephrine and terbutaline are adrenergic agents that can be given subcutaneously to patients with acute severe asthma. It is not clear that either agent has advantages over inhaled β-2-agonists.

    Subcutaneous epinephrine (concentration 1:1000) is given in total dose of 0.01 mg/kg, divided into 3 doses of approximately 0.3 mg administered at 20-minute intervals. It may be administered IV (0.25 mcg/min to 1 mcg/min continuous infusion), although it is not clear that the IV route is more effective than the subcutaneous route. Adrenergic effects may cause an increase in heart rate, myocardial irritability, and increased oxygen demand that may be more severe when the drug is given intravenously.

    Terbutaline is given in a subcutaneous dose of 0.25 mg, which can be repeated every 20 minutes for 3 doses.


    Ketamine is a parenteral, dissociative anesthetic with bronchodilatory properties that can stimulate copious bronchial secretions. It also has sedative and analgesic properties that may be useful if intubation is planned. Studies comparing ketamine with standard care for severe asthma have yielded inconsistent results.


    Heliox is a mixture of helium and oxygen (usually a 70:30 helium to oxygen ratio mix) that is less viscous than ambient air; it has been shown to improve the delivery and deposition of nebulized albuterol. However, it is not yet been shown to improve the effect of initial therapies. 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.

    Leukotriene Antagonists

    Leukotriene antagonists improve lung function and decrease the need for short-acting β2-agonists for chronic  asthma therapy, but their effectiveness during acute exacerbations of asthma is unproven.

    Inhaled Anesthetics

    Potent inhalation anesthetics sevoflurane and isoflurane may be effective for patients with life-threatening asthma unresponsive to maximal conventional therapy. These agents may have direct bronchodilator effects, and their anesthetic effects increase the ease of mechanical ventilation and reduce oxygen demand and carbon dioxide production. This therapy requires expert consultation in an intensive care setting, and its effectiveness has not been evaluated in prospective randomized clinical studies.

    Assisted Ventilation

    Noninvasive positive-pressure ventilation may offer short-term support for alert patients with adequate spontaneous respiratory effort during acute respiratory failure. It may delay or eliminate the need for endotracheal intubation.

    Endotracheal intubation is indicated for patients who present with:

    • apnea
    • coma
    • persistent or increasing hypercapnia
    • severe distress
    • increased respiratory effort with evidence of fatigue
    • depression of mental status

    Clinical judgment is necessary to assess the need for immediate endotracheal intubation for critically ill patients with status asthmaticus, because intubation and positive-pressure ventilation are high-risk procedures that can trigger:

    • further bronchoconstriction
    • breath stacking (that results from incomplete exhalation) and subsequent barotrauma
    • air trapping
    • buildup of positive end-expiratory pressure (ie, intrinsic or “auto-PEEP”)

    Rapid sequence intubation is the technique of choice for endotracheal tube placement and should be performed by an expert in airway management.

    Use the largest endotracheal tube available (usually 8 or 9 mm) to attempt to minimize resistance to airflow provided by the tube itself.

    Immediately after intubation, tube placement should be confirmed by clinical examination and waveform capnography and should be followed by a chest radiograph to evaluate depth of insertion.

    Optimal ventilator management requires expert consultation and ongoing careful review of ventilation flow and pressure curves. Use of a small tidal volume may avoid auto-PEEP and high peak airway pressures.

    Troubleshooting After Intubation

    During manual or mechanical ventilation use:

    • a slower respiratory rate with smaller tidal volumes (eg, 6 to 8 mL/kg)
    • a shorter inspiratory time (eg, adult inspiratory flow rate 80 to 100 L/min),
    • longer expiratory time (eg, inspiratory to expiratory ratio 1:4 or 1:5) than generally would be provided to patients without asthma. Note: mild hypoventilation (permissive hypercapnia) reduces the risk of barotrauma.

    Management with mechanical ventilation will vary based on patient-ventilation characteristics. Obtain expert consultation.

    Sedation is often required to optimize ventilation, decrease ventilator dyssynchrony (and therefore auto-PEEP), and minimize barotrauma after intubation.

    Continue to administer inhaled albuterol treatments through the endotracheal tube.

    If the 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 tubing kinks)
    • evaluate for auto-PEEP
      • quickly reduce high-end expiratory pressure by separating the patient from the ventilator circuit
      • to minimize auto-PEEP, decrease the respiratory rate or tidal volume or both.
      • consider use of neuromuscular blocking agents (with sedation) if auto-PEEP persists and the patient displays ventilator dyssynchrony despite adequate sedation
    • rule out a pneumothorax

    In exceedingly rare circumstances, aggressive treatment for acute asthma-related respiratory failure will not provide adequate gas exchange.

    There are case reports that describe successful use of extracorporeal membrane oxygenation (ECMO) in adult and pediatric patients with severe asthma after other aggressive measures have failed to reverse hypoxemia and hypercarbia.

    BLS and ACLS Modifications

    BLS treatment of cardiac arrest in asthmatic patients is unchanged.

    Standard ACLS guidelines should be followed.

    Additional measures are needed if cardiac arrest develops in patient who is intubated and mechanically ventilated.

    • auto-PEEP adversely affects coronary perfusion pressure and capacity for successful defibrillation
    • auto-PEEP has also been shown to adversely affect hemodynamics in patients with asthma who are not in cardiac arrest

    Since the effects of auto-PEEP in the asthmatic patient with cardiac arrest are likely to be quite severe, it is reasonable to use a ventilation strategy of low respiratory rate and tidal volume. (Class IIa, LOE C) (2010 Part 12)

    During cardiac arrest, providers may consider briefly disconnecting the patient from the bag mask device or the ventilator, and compression of the chest wall may then be effective to relieve air-trapping. (Class IIa, LOE C) (2010 Part 12)

    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) (2010 Part 12)

    Cardiac Arrest Associated With Anaphylaxis

    Anaphylaxis is an allergic reaction characterized by multisystem involvement, including skin, airway, vascular space, and gastrointestinal tract.

    Severe cases of anaphylaxis may result in complete obstruction of the airway and cardiovascular collapse from vasogenic shock.

    Pharmacological agents, latex, foods (eg, peanuts), and stinging insects are among the most common causes of anaphylaxis described.

    Signs and Symptoms

    Initial symptoms of anaphylaxis can include:

    • tachycardia,
    • faintness,
    • cutaneous flushing,
    • urticaria,
    • diffuse or localized pruritus,
    • a sensation of impending doom.

    The patient may be agitated or anxious and may appear either flushed or pale.

    A common early sign of respiratory involvement with anaphylaxis 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.

    Cardiovascular collapse is common in severe anaphylaxis. If not promptly corrected, vasodilation and increased capillary permeability will cause decreased circulating blood volume, decreased cardiac preload and relative hypovolemia, and can rapidly lead to cardiac arrest.

    Myocardial ischemia and acute myocardial infarction, malignant arrhythmias, and cardiovascular depression can also contribute to rapid hemodynamic deterioration and cardiac arrest.

    Additionally, cardiac dysfunction may result from underlying disease or development of myocardial ischemia from hypotension or following administration of epinephrine.

    To prevent cardiac arrest in suspected anaphylactic reactions, urgent treatment of the cause of the anaphylaxis, and support of airway, breathing, and circulation are essential.

    Standard BLS and ACLS therapies are appropriate into the management of cardiac arrest secondary to anaphylaxis.

    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.

    First Aid and BLS Therapy

    Given the potential for the rapid development of oropharyngeal or laryngeal edema in the patient with anaphylaxis, immediate referral to a health professional with expertise in advanced airway placement is recommended. (Class I, LOE C) (2010 Part 12)

    In both anaphylaxis and cardiac arrest, the immediate use of an epinephrine autoinjector is recommended if available. (Class I, LOE C) (2010 Part 12)

    The intramuscular (IM) administration of epinephrine (ie, with an epinephrine autoinjector) in the anterolateral aspect of the middle third of the thigh provides the highest peak epinephrine concentration in the blood.

    Absorption and subsequent achievement of maximum epinephrine plasma concentration after subcutaneous administration is slower than the IM route and may be significantly delayed with shock.

    Epinephrine 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) (2010 Part 12)

    The recommended [adult] dose of epinephrine is 0.2 to 0.5 mg (1:1000) IM to be repeated every 5 to 15 minutes in the absence of clinical improvement. (Class I, LOE C) (2010 Part 12)

    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.

    ACLS Modifications


    For patients with anaphylaxis, providers must recognize that patients who develop hoarseness, lingual edema, stridor, or oropharyngeal swelling are at risk for the development of a difficult airway and providers must have the equipment and personnel ready to respond.

    For patients with anaphylaxis, we recommend that ACLS providers plan for advanced airway management, including use of a surgical airway if needed. (Class I, LOE C) (2010 Part 12)

    Early and rapid advanced airway management is critical and should not be unnecessarily delayed.

    Fluid Resuscitation

    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 successful in treating hypotension.

    Vasogenic shock from anaphylaxis may require aggressive fluid resuscitation. (Class IIa, LOE C) (2010 Part 12)

    Vasopressors for Anaphylactic Shock

    When intravenous access 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) (2010 Part 12)

    For patients not in cardiac arrest, IV epinephrine 0.05 to 0.1 mg (ie, 5% to 10% of the epinephrine dose used routinely in cardiac arrest) has been used successfully in patients with anaphylactic shock.

    Because fatal overdose of epinephrine has been reported, close hemodynamic monitoring is recommended. (Class I, LOE B) (2010 Part 12)

    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 also be considered in post-cardiac arrest management. (Class IIb, LOE C) (2010 Part 12)

    Vasopressors for Anaphylactic Cardiac Arrest

    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) (2010 Part 12)

    This recommendation was made on the basis of reports of use of alternative vasopressor therapy, and did not include direct comparisons of alternative vasopressors to epinephrine.

    Other Potential Interventions for Anaphylaxis

    Adjuvant use of antihistamines (H1 and H2 antagonist), inhaled β-adrenergic agents, and IV corticosteroids has been successful in management of the patient with anaphylaxis and may be considered in cardiac arrest due to anaphylaxis. (Class IIb, LOE C) (2010 Part 12)

    Extracorporeal CPR [ie, initiation of cardiopulmonary bypass during the resuscitation of the patient in cardiac arrest] may be considered for selected patients as rescue therapy when conventional CPR efforts are failing in settings in which it can be expeditiously implemented and supported by skilled providers. (Class IIb, LOE C-LD) (2019 ACLS)

    Cardiac Arrest in the Morbidly Obese

    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. In addition, it may be difficult to estimate appropriate resuscitation drugs doses.

    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.

    Cardiac Arrest Associated With Life-Threatening Electrolyte Imbalances

    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.

    Current BLS and ACLS strategies should be used to manage cardiac arrest associated with all electrolyte disturbances.

    Potassium (K+) Imbalance

    Potassium is maintained primarily 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 myocardial cells.

    Potassium concentration is tightly regulated. Under normal conditions potential differences across membranes, especially myocardial cells, are not affected by mild or gradual alterations in serum potassium concentration. Rapid or significant changes in serum potassium concentration can result from the shifting of potassium between the intra-cellular and the extracellular (including intravascular) spaces and may have life-threatening consequences.

    A number of conditions can cause potassium shifts into and out of the cellular space. For example, the serum potassium changes when the serum pH changes; acidosis or a fall in serum pH will produce a shift of potassium out of the cells into the extracellular space, including the vascular space, causing a rise in the serum potassium. Alkalosis or a rise in serum pH will produce the opposite effect, causing a shift of potassium back into the cells (and a lowering of the serum potassium concentration).

    Hypothermia will cause a fall in serum potassium but, in addition, the myocardium becomes more sensitive to the potassium, so it can develop signs of toxicity at relatively low serum potassium concentrations.


    Severe hyperkalemia (defined as a serum potassium concentration >6.5 mEq/L or 6.5 mmol/L) most commonly develops in patients with renal failure or following release of potassium from cells (eg, in acute tumor lysis syndrome). Hyperkalemia can cause cardiac arrhythmias and cardiac arrest.

    Although severe hyperkalemia may cause flaccid paralysis, paresthesia, depressed deep tendon reflexes, or respiratory difficulties, 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 rhythm, and asystolic cardiac arrest may develop.

    Figure 3: 2010 ECG Changes Hyperkalemia
    This is a preview, select a link below to view this image in a variety of formats, including a full text description.
    ACLS Modifications in Management of Severe Hyperkalemic Cardiotoxicity or Cardiac Arrest

    Treatment of severe hyperkalemia aims at protecting the heart from the effects of hyperkalemia by antagonizing the effect of potassium on excitable cell membranes, shifting potassium from the extracellular/intravascular space into cells, 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 of severe hyperkalemia 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 or prevent potassium absorption:
      • Diuresis: furosemide 40 to 80 mg IV
      • Kayexalate: 15 to 50 g plus sorbitol orally or per rectum
      • Dialysis

    Note that the level of evidence supporting these recommendations is very low (limited to case series) but the therapies are widely accepted.

    When cardiac arrest occurs secondary to hyperkalemia, it may be reasonable, in addition to standard ACLS, to administer adjuvant IV therapy as outlined above for cardiotoxicity. (Class IIb, LOE C) (2010 Part 12)

    ACLS Modifications in Management of Severe Hypokalemic Cardiotoxicity

    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, which, if left untreated, deteriorate to PEA or asystole.

    When cardiac arrest is suspected to be secondary to hypokalemia, the effect of bolus administration of potassium is unknown and is not advised. (Class IIb, LOE C) (2010 Part 12)

    Sodium (Na+) Imbalance

    Sodium abnormalities are unlikely to be the primary cause of severe cardiovascular instability or cardiac arrest, and there are no specific recommendations for either checking or treating sodium concentration during cardiac arrest.

    Magnesium (Mg++)

    Magnesium plays an important role in nerve and muscle conduction. In addition, serum magnesium concentration affects serum calcium concentration.


    Hypermagnesemia is defined as a serum magnesium concentration >2.2 mEq/L (normal: 1.3 to 2.2 mEq/L). Hypermagnesemia can cause neurologic changes as well as cardiac arrhythmias, hypoventilation and cardiorespiratory arrest.

    Neurological symptoms of hypermagnesemia include muscular weakness, paralysis, ataxia, drowsiness, and confusion. Hypermagnesemia can produce vasodilation and hypotension. Extremely hypermagnesemia may produce a depressed level of consciousness, bradycardia, cardiac arrhythmias, hypoventilation, and cardiorespiratory arrest.

    Administration 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 during cardiac arrest associated with hypermagnesemia. (Class IIb, LOE C) (2010 Part 12)


    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.

    The presence of a low serum magnesium concentration has been associated with poor prognosis in cardiac arrest patients.

    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) (2010 Part 12)

    Calcium (Ca++)

    Calcium abnormality as an etiology of cardiac arrest is rare. There are no studies evaluating the treatment of hypercalcemia or hypocalcemia during arrest.

    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) (2010 Part 12)

    Cardiac Arrest Associated With Trauma

    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. However, management of the patient with trauma requires rapid assessment and vigilance for signs of hidden injuries and ongoing hemorrhage.

    Reversible causes of cardiac arrest in the context of trauma include:

    • hypoxia,
    • hypovolemia,
    • diminished cardiac output secondary to pneumothorax or pericardial tamponade, and
    • hypothermia.

    BLS Modifications

    When multisystem trauma is present or trauma involves the head and neck, stabilize the cervical spine.

    Use a jaw thrust instead of a head tilt–chin lift to establish a patent airway.

    If breathing is inadequate and the patient’s face is bloody, provide ventilation 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 delivery of rescue breaths, provide standard CPR and defibrillation as indicated.

    ACLS Modifications

    Airway and Ventilation:

    • If bag-mask ventilation is inadequate, an advanced airway should be inserted while maintaining cervical spine stabilization if indicated.
    • If insertion of an advanced airway is not possible and ventilation remains inadequate, experienced providers should consider a cricothyrotomy.
    • When there is a unilateral decrease in breath sounds during positive-pressure ventilation 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.
    • 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 attempted defibrillation.
    • Resuscitative thoracotomy may be indicated in selected patients.

    Consult the guidelines for withholding or terminating resuscitation, which was 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 (DOI:

    Commotio Cordis

    Commotio cordis a blow to the anterior chest, such as that imparted by the strike of a baseball or hockey puck, that occurs during cardiac repolarization with the effect of triggering ventricular fibrillation.

    Prompt recognition is critical to successful treatment of those with sudden collapse and cardiac arrest.

    Provide immediate BLS care with high-quality CPR and attempt defibrillation using an automated external defibrillator. Provide ACLS care if required.

    Cardiac Arrest in Unintentional Hypothermia

    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.

    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.

    Initial Care for Victims of Unintentional Hypothermia

    When the victim is extremely cold but has maintained a perfusing rhythm, focus on interventions that prevent further loss of heat and begin to rewarm the victim immediately.

    • Passive rewarming is generally adequate for patients with mild hypothermia (temperature >34°C [93.2°F]). Remove wet garments and insulate the victim from further environmental exposures to prevent additional evaporative heat loss.
    • External warming techniques such as forced air or other efficient surface-warming devices are appropriate for patients with moderate (30°C to 34°C [86°F to 93.2°F]) hypothermia with a perfusing rhythm. Passive rewarming alone will be inadequate for these patients.
    • Core rewarming is often used for patients with severe hypothermia (<30°C [86°F]) with a perfusing rhythm. Some have reported successful rewarming with active external warming techniques.
    • Patients with severe hypothermia and cardiac arrest can be rewarmed most rapidly with cardiopulmonary bypass.
    • Alternative effective core rewarming techniques include warm-water lavage of the thoracic cavity and extracorporeal blood warming with partial bypass.
    • Adjunctive core rewarming techniques include warmed intravenous or intraosseous fluids and warm humidified oxygen. Heat transfer with these measures is not rapid and should be considered supplementary to active warming techniques.

    Do not delay urgent interventions such as airway management and insertion of vascular catheters regardless of evidence of cardiac irritability.

    In the field, providers who have the time and equipment to assess core body temperature or to institute aggressive rewarming techniques should do so.

    BLS Modifications

    When the victim is hypothermic, pulse and respiratory rates may be slow or difficult to detect, 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.

    If VF or pulseless VT is present, attempt defibrillation.

    If VF or pulseless VT persists after a single shock, the value of deferring subsequent defibrillation attempts 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) (2010 Part 12)

    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.

    ACLS Modifications

    For unresponsive patients or those in arrest, advanced airway insertion is appropriate as recommended in the ACLS guidelines. Advanced airway management enables effective ventilation with warm, humidified oxygen and reduces the likelihood of aspiration in patients in prearrest.

    ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality.

    The serum potassium will fall as hypothermia develops and rise as the patient is rewarmed. Severe hypothermia and resultant tissue damage, by contrast, may cause a subsequent rise in the serum potassium,

    During cardiac arrest, it may be reasonable, concurrent with rewarming strategies, to consider administration of a vasopressor according to the standard ACLS algorithm. (Class IIb, LOE C) (2010 Part 12)

    Post-Cardiac Arrest Care

    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 post-cardiac arrest 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/baseline temperatures.

    Because severe hypothermia is frequently preceded by other disorders (eg, drug overdose, alcohol use, or trauma), look for and treat these underlying conditions while simultaneously treating hypothermia.

    Withholding and Cessation of Resuscitative Efforts

    Multiple case reports have documented survival from unintentional hypothermia even with prolonged CPR and prolonged arrest times. Thus, patients with severe unintentional hypothermia and cardiac arrest may benefit from longer attempted resuscitation even in cases of prolonged arrest time and prolonged CPR. Low serum potassium may be associated with hypothermia, and not hypoxemia, as the primary cause of the arrest. Patients should not be considered dead before warming has been provided.

    Cardiac Arrest in Avalanche Victims

    The most common causes of avalanche-related death are asphyxia, trauma, and hypothermia, or combinations of these 3 problems.

    The likelihood of survival is minimal when avalanche victims are buried >35 minutes with an obstructed airway and in cardiac arrest on extrication 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.

    A serum potassium concentration of <8 mmol/L on hospital admission is a prognostic marker for ROSC and survival to hospital discharge. High potassium concentration is associated with asphyxia, and there is an inverse correlation between admission K+ and survival to discharge in all-cause hypothermic patients.

    Full resuscitative measures, including extracorporeal rewarming when available, are recommended for all avalanche victims who do not have obvious lethal traumatic injury and who do not have the characteristics associated with very poor survival. (Class I, LOE C) (2010 Part 12)

    Cardiac Arrest Due to Drowning

    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) (2010 Part 12)

    BLS Modifications

    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 rescue breaths are given.

    Recovery From the Water

    Routine stabilization of the cervical spine in the absence of circumstances that suggest a spinal injury is not recommended. (Class III, LOE B) (2010 Part 12)

    Rescue Breathing

    The routine use of abdominal thrusts or the Heimlich maneuver for drowning victims is not recommended. (Class III, LOE C) (2010 Part 12) This maneuver can be harmful.

    Victims of drowning do not have airway obstruction; they have hypoxia and require immediate CPR including rescue breaths. Abdominal thrusts are not needed and will likely result in expulsion of water and other stomach contents, with risk of aspiration. If the abdominal thrusts cause expulsion of stomach contents, that can then cause airway obstruction that interferes with the delivery of rescue breaths.

    Chest Compressions

    As soon as the unresponsive victim is removed from the water, shout for nearby help, 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 send someone to activate the emergency response and retrieve an AED (if not already done) and begin chest compressions and provide cycles of compressions and breaths according to the BLS guidelines.

    Rescuers should attach an AED as soon as one is available and follow the prompts, attempting defibrillation if a shockable rhythm is identified.

    It is only necessary to quickly wipe the chest area before applying the defibrillation pads and using the AED.

    If hypothermia is present, follow the recommendations in “Cardiac Arrest in Unintentional Hypothermia,” above.

    Vomiting by the Victim During Resuscitation

    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 log rolled so that the head, neck, and torso are turned as a unit to prevent twisting of the cervical spine.

    Cardiac Arrest Associated With Electric Shock and Lightning Strikes

    Electric Shock

    Current flow (ie electric shock) through the heart during the relative refractory period can precipitate VF, which is analogous to the R-on-T phenomenon that occurs in nonsynchronized cardioversion.

    Lightning Strike

    Lightning acts as an instantaneous, massive direct-current shock, simultaneously depolarizing the entire myocardium. 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.

    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.

    BLS Modifications

    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 VF or pulseless VT.

    Maintain spinal stabilization during extrication and treatment if there is a likelihood of head or neck trauma.

    Both lightning and electric shock often cause multiple trauma, including injury to the spine, muscle strains, internal injuries from being thrown, and fractures caused by the tetanic response of skeletal muscles.

    Remove smoldering clothing, shoes, and belts to prevent further thermal damage.

    ACLS Modifications

    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.

    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). Regardless of the extent of external injuries after electrothermal shock, the underlying tissue damage can be far more extensive.

    Cardiac Arrest Caused by Cardiac Tamponade

    When cardiac tamponade is suspected in the patient in cardiac arrest, in the absence of echocardiography, emergency pericardiocentesis without imaging guidance can be beneficial. (Class IIa, LOE C) (2010 Part 12)

    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, especially if gross blood causes clotting that blocks a pericardiocentesis needle. (Class IIb, LOE C) (2010 Part 12)

    Cardiac Arrest Following Cardiac Surgery

    Causes of cardiac arrest following cardiac surgery include conditions that may be readily reversed such as:

    • ventricular fibrillation,
    • hypovolemia,
    • cardiac tamponade,
    • tension pneumothorax.

    Pacing wires, if present, may reverse symptomatic bradycardia or asystole.


    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) (2010 Part 12)

    Despite rare case reports describing damage to the heart possibly due to external chest compressions, chest compressions should not be withheld if emergency resternotomy is not immediately available. (Class IIa, LOE C) (2010 Part 12)

    Mechanical Circulatory Support

    In post-cardiac surgery patients who are refractory to standard resuscitation procedures, mechanical circulatory support (eg, extracorporeal CPR). (Class IIb, LOE B) (2010 Part 12)

    Authorship and Disclosures

    2015 Writing Team

    Eric J. Lavonas, Chair; Ian R. Drennan; Andrea Gabrielli; Alan C. Heffner; Christopher O. Hoyte; Aaron M. Orkin; Kelly N. Sawyer; Michael W. Donnino

    Table 3: Part 10: Special Circumstances of Resuscitation: 2015 Guidelines Update Writing Group Disclosures

    2010 Writing Team

    Terry L. Vanden Hoek, Chair; Laurie J. Morrison; Michael Shuster; Michael Donnino; Elizabeth Sinz; Eric J. Lavonas; Farida M. Jeejeebhoy; Andrea Gabrielli

    Table 4: 2010 - Guidelines Part 12: Cardiac Arrest in Special Situations: Writing Group Disclosures


    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.

    © Copyright 2015 American Heart Association, Inc.


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    Part 10: Special Circumstances of Resuscitation