This Part summarizes recommendations for the management of resuscitation in the following special circumstances:
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.
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).
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)
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)
There were no modifications of BLS technique suggested for suspected 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.
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)
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)
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)
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.
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)
We can make no recommendation regarding the administration of naloxone in confirmed opioid-associated cardiac arrest. (2015 Part 10)
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)
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)
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)
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.
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.
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.
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.
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).
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 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.
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.
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 may be helpful in the treatment of shock caused by β-blocker toxicity.
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.
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.
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).
There is conflicting evidence regarding the use/effectveness of glucagon in the treatment of hemodynamically unstable calcium channel blocker overdose.
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.
One vial of antidigoxin Fab is standardized to neutralize 0.5 mg of digoxin.
A reasonable dosing strategy for antidigoxin Fab antibodies is:
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.
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)
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.
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.
Cardiac arrest caused by cyclic antidepressant toxicity should be managed by current BLS and ACLS treatment guidelines.
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 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.
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 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:
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.
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.
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.
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.
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.
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).
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 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 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.
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.
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:
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:
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.
During manual or mechanical ventilation use:
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:
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 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.
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)
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.
Initial symptoms of anaphylaxis can include:
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.
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)
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 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.
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.
Early and rapid advanced airway management is critical and should not be unnecessarily delayed.
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.
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.
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)
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.
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)
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.
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 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.
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:
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)
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.
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 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 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)
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:
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.
Airway and Ventilation:
When the airway, oxygenation, and ventilation are adequate, evaluate and support circulation.
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: https://doi.org/10.1016/S1072-7515(02)01668-X.)
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.
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.
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.
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.
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.
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)
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.
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.
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)
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)
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.
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.
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.
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.
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 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.
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.
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.
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)
Causes of cardiac arrest following cardiac surgery include conditions that may be readily reversed such as:
Pacing wires, if present, may reverse symptomatic bradycardia or asystole.
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)
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.