Part 12: Cardiac Arrest in Special Situations

Pathophysiology

The pathophysiology of asthma consists of 3 key abnormalities:

• Bronchoconstriction

• Airway inflammation

• Mucous plugging

Complications of severe asthma, such as tension pneumothorax, lobar atelectasis, pneumonia, and pulmonary edema, can contribute to fatalities. Severe asthma exacerbations are commonly associated with hypercarbia and acidemia, hypotension due to decreased venous return, and depressed mental status, but the most common cause of death is asphyxia. Cardiac causes of death are less common.⁴

Clinical Aspects of Severe Asthma

Wheezing is a common physical finding, although the severity of wheezing does not correlate with the degree of airway obstruction. The absence of wheezing may indicate critical airway obstruction, whereas increased wheezing may indicate a positive response to bronchodilator therapy.

Oxygen saturation (Sao₂) levels may not reflect progressive alveolar hypoventilation, particularly if oxygen is being administered. Note that Sao₂ may fall initially during therapy because β₂-agonists produce both bronchodilation and vasodilation and initially may increase intrapulmonary shunting.

Other causes of wheezing are pulmonary edema,⁵ chronic obstructive pulmonary disease (COPD), pneumonia, anaphylaxis,⁶ foreign bodies, PE, bronchiectasis, and subglottic mass.⁷

Initial Stabilization

Patients with severe life-threatening asthma require urgent and aggressive treatment with simultaneous administration of oxygen, bronchodilators, and steroids. Healthcare providers must monitor these patients closely for deterioration. Although the pathophysiology of life-threatening asthma consists of bronchoconstriction, inflammation, and mucous plugging, only bronchoconstriction and inflammation are amenable to drug treatment.

Primary Therapy

Adjunctive Therapies

Assisted Ventilation

Troubleshooting After Intubation

When severe bronchoconstriction is present, breath stacking (so-called auto-PEEP) can develop during positive-pressure ventilation, leading to complications such as hyperinflation, tension pneumothorax, and hypotension. During manual or mechanical ventilation, a slower respiratory rate should be used with smaller tidal volumes (eg, 6 to 8 mL/kg),³⁶ shorter inspiratory time (eg, adult inspiratory flow rate 80 to 100 L/min), and longer expiratory time (eg, inspiratory to expiratory ratio 1:4 or 1:5) than generally would be provided to patients without asthma.³⁷ Management of mechanical ventilation will vary based on patient-ventilation characteristics. Expert consultation should be obtained.

Mild hypoventilation (permissive hypercapnia) reduces the risk of barotrauma. Hypercapnia is typically well tolerated.^38,39 Sedation is often required to optimize ventilation, decrease ventilator dyssynchrony (and therefore auto-PEEP), and minimize barotrauma after intubation. Because delivery of inhaled medications may be inadequate before intubation, the provider should continue to administer inhaled albuterol treatments through the endotracheal tube.

Four common causes of acute deterioration in any intubated patient are recalled by the mnemonic DOPE (tube Displacement, tube Obstruction, Pneumothorax, Equipment failure). Auto-PEEP is another common cause of deterioration in patients with asthma. If the asthmatic patient's condition deteriorates or if it is difficult to ventilate the patient, check the ventilator for leaks or malfunction; verify endotracheal tube position; eliminate tube obstruction (eliminate any mucous plugs and kinks); evaluate for auto-PEEP; and rule out a pneumothorax.

High-end expiratory pressure can be reduced quickly by separating the patient from the ventilator circuit; this will allow PEEP to dissipate during passive exhalation. If auto-PEEP results in significant hypotension, assisting with exhalation by pressing on the chest wall after disconnection of the ventilator circuit will allow active exhalation and should lead to immediate resolution of hypotension. To minimize auto-PEEP, decrease the respiratory rate or tidal volume or both. If auto-PEEP persists and the patient displays ventilator dyssynchrony despite adequate sedation, paralytic agents may be considered.

In exceedingly rare circumstances, aggressive treatment for acute respiratory failure due to severe asthma will not provide adequate gas exchange. There are case reports that describe successful use of extracorporeal membrane oxygenation (ECMO) in adult and pediatric patients^40–43 with severe asthma after other aggressive measures have failed to reverse hyoxemia and hypercarbia.

BLS Modifications

BLS treatment of cardiac arrest in asthmatic patients is unchanged.

ACLS Modifications

When cardiac arrest occurs in the patient with acute asthma, standard ACLS guidelines should be followed.

Case series and case reports describe a novel technique of cardiopulmonary resuscitation (CPR) termed “lateral chest compressions”; however, there is insufficient evidence to recommend this technique over standard techniques.^44–50

The adverse effect of auto-PEEP on coronary perfusion pressure and capacity for successful defibrillation has been described in patients in cardiac arrest without asthma.^51,52 Moreover, the adverse effect of auto-PEEP on hemodynamics in asthmatic patients who are not in cardiac arrest has also been well-described.^53–56 Therefore, since the effects of auto-PEEP in an asthmatic patient with cardiac arrest are likely quite severe, a ventilation strategy of low respiratory rate and tidal volume is reasonable (Class IIa, LOE C). During arrest a brief disconnection from the bag mask or ventilator may be considered, and compression of the chest wall to relieve air-trapping can be effective (Class IIa, LOE C).

For all asthmatic patients with cardiac arrest, and especially for patients in whom ventilation is difficult, the possible diagnosis of a tension pneumothorax should be considered and treated (Class I, LOE C).

Signs and Symptoms

The initial symptoms of anaphylaxis are often nonspecific and include tachycardia, faintness, cutaneous flushing, urticaria, diffuse or localized pruritus, and a sensation of impending doom. Urticaria is the most common physical finding. The patient may be agitated or anxious and may appear either flushed or pale.

A common early sign of respiratory involvement is rhinitis. As respiratory compromise becomes more severe, serious upper airway (laryngeal) edema may cause stridor and lower airway edema (asthma) may cause wheezing. Upper airway edema can also be a sign in angiotensin converting enzyme inhibitor-induced angioedema or C1 esterase inhibitor deficiency with spontaneous laryngeal edema.^58–60

Cardiovascular collapse is common in severe anaphylaxis. If not promptly corrected, vasodilation and increased capillary permeability, causing decreased preload and relative hypovolemia of up to 37% of circulating blood volume, can rapidly lead to cardiac arrest.^61,62 Myocardial ischemia and acute myocardial infarction, malignant arrhythmias, and cardiovascular depression can also contribute to rapid hemodynamic deterioration and cardiac arrest.⁶³ Additionally, cardiac dysfunction may result from underlying disease or development of myocardial ischemia due to hypotension or following administration of epinephrine.^64,65

There are no randomized controlled trials evaluating alternative treatment algorithms for cardiac arrest due to anaphylaxis. Evidence is limited to case reports and extrapolations from nonfatal cases, interpretation of pathophysiology, and consensus opinion. Providers must be aware that urgent support of airway, breathing, and circulation is essential in suspected anaphylactic reactions.

Because of limited evidence, the management of cardiac arrest secondary to anaphylaxis should be treated with standard BLS and ACLS. The following therapies are largely consensus-based but commonly used and widely accepted in the management of the patient with anaphylaxis who is not in cardiac arrest.

BLS Modifications

ACLS Modifications

Scope of the Problem

The Confidential Enquiries into Maternal and Child Health (CEMACH) data set constitutes the largest population-based data set on this target population.⁹² The overall maternal mortality rate was calculated at 13.95 deaths per 100 000 maternities. There were 8 cardiac arrests with a frequency calculated at 0.05 per 1000 maternities, or 1:20 000. The frequency of cardiac arrest in pregnancy is on the rise with previous reports estimating the frequency to be 1:30 000 maternities.⁹³ Despite pregnant women being younger than the traditional cardiac arrest patient, the survival rates are poorer, with one case series reporting a survival rate of 6.9%.^93,94

During attempted resuscitation of a pregnant woman, providers have 2 potential patients: the mother and the fetus. The best hope of fetal survival is maternal survival. For the critically ill pregnant patient, rescuers must provide appropriate resuscitation based on consideration of the physiological changes caused by pregnancy.

Key Interventions to Prevent Arrest

The following interventions are the standard of care for treating the critically ill pregnant patient (Class I, LOE C):

• Place the patient in the full left-lateral position to relieve possible compression of the inferior vena cava. Uterine obstruction of venous return can produce hypotension and may precipitate arrest in the critically ill patient.^95,96

• Give 100% oxygen.

• Establish intravenous (IV) access above the diaphragm.

• Assess for hypotension; maternal hypotension that warrants therapy has been defined as a systolic blood pressure <100 mm Hg or <80% of baseline.^97,98 Maternal hypotension can result in reduced placental perfusion.^99–102 In the patient who is not in arrest, both crystalloid and colloid solutions have been shown to increase preload.¹⁰³

• Consider reversible causes of critical illness and treat conditions that may contribute to clinical deterioration as early as possible.

Resuscitation of the Pregnant Patient in Cardiac Arrest (Figure 1)

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Figure 1.

Maternal cardiac arrest algorithm.

There are no randomized controlled trials evaluating the effect of specialized obstetric resuscitation versus standard care in pregnant patients in cardiac arrest. There are reports in the literature of patients not in arrest that describe the science behind important physiological changes that occur in pregnancy that may influence treatment recommendations and guidelines for resuscitation from cardiac arrest in pregnancy.

BLS Modifications

Patient Positioning

Patient position has emerged as an important strategy to improve the quality of CPR and resultant compression force and output. The pregnant uterus can compress the inferior vena cava, impeding venous return and thereby reducing stroke volume and cardiac output. Reports of noncardiac arrest parturients indicate that left-lateral tilt results in improved maternal hemodynamics of blood pressure, cardiac output, and stroke volume^96,98,104; and improved fetal parameters of oxygenation, nonstress test, and fetal heart rate.^100–102

Although chest compressions in the left-lateral tilt position are feasible in a manikin study,¹⁰⁵ they result in less forceful chest compressions than are possible in the supine position.¹⁰⁶ Two studies found no improvement in maternal hemodynamic or fetal parameters with 10° to 20° left-lateral tilt in patients not in arrest.^107,108 One study reported more aortic compression at 15° left-lateral tilt compared with a full left-lateral tilt.⁹⁷ In addition, aortic compression has been found at >30° of tilt,¹⁰⁹ however the majority of these patients were in labor.

If left-lateral tilt is used to improve maternal hemodynamics during cardiac arrest, the degree of tilt should be maximized. However, at a tilt ≥30° the patient may slide or roll off the inclined plane,¹⁰⁶ so this degree of tilt may not be practical during resuscitation. Although important, the degree of tilt is difficult to estimate reliably; 1 study reported that the degree of table tilt is often overestimated.¹¹⁰ Using a fixed, hard wedge of a predetermined angle may help.

Two studies in pregnant women not in arrest found that manual left uterine displacement, which is done with the patient supine, is as good as or better than left-lateral tilt in relieving aortocaval compression (as assessed by the incidence of hypotension and use of ephedrine).^111,112

Therefore, to relieve aortocaval compression during chest compressions and optimize the quality of CPR, it is reasonable to perform manual left uterine displacement in the supine position first (Class IIa, LOE C). Left uterine displacement can be performed from either the patient's left side with the 2-handed technique (Figure 2) or the patient's right side with the 1-handed technique (Figure 3), depending on the positioning of the resuscitation team. If this technique is unsuccessful, and an appropriate wedge is readily available, then providers may consider placing the patient in a left-lateral tilt of 27° to 30°,¹⁰⁶ using a firm wedge to support the pelvis and thorax (Figure 4) (Class IIb, LOE C).

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Figure 2.

. Left uterine displacement with 2-handed technique.

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Figure 3.

Left uterine displacement using 1-handed technique.

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Figure 4.

Patient in a 30° left-lateral tilt using a firm wedge to support pelvis and thorax.

If chest compressions remain inadequate after lateral uterine displacement or left-lateral tilt, immediate emergency cesarean section should be considered. (See “Emergency Cesarean Section in Cardiac Arrest,” below.)

ACLS Modifications

There should be no delay in delivering usual treatments during the management of cardiac arrest in pregnancy.

Treatment of Reversible Causes

The same reversible causes of cardiac arrest that occur in nonpregnant women can occur during pregnancy. Providers should be familiar with pregnancy-specific diseases and procedural complications and during resuscitation attempts should try to identify common and reversible causes of cardiac arrest in pregnancy.⁹²

Maternal Cardiac Arrest Not Immediately Reversed by BLS and ACLS

Institutional Preparation for Maternal Cardiac Arrest

Experts and organizations have emphasized the importance of preparation.^143,179 Providers at medical centers must review whether performance of an emergency hysterotomy is feasible, and if so, they must identify the best means of accomplishing this procedure rapidly. Team planning should be done in collaboration with the obstetric, neonatal, emergency, anesthesiology, intensive care, and cardiac arrest services (Class I, LOE C).

Post–Cardiac Arrest Care

One case report showed that post–cardiac arrest hypothermia can be used safely and effectively in early pregnancy without emergency cesarean section (with fetal heart monitoring), with favorable maternal and fetal outcome after a term delivery.¹⁵⁹ No cases in the literature have reported the use of therapeutic hypothermia with perimortem cesarean section. Therapeutic hypothermia may be considered on an individual basis after cardiac arrest in a comatose pregnant patient based on current recommendations for the nonpregnant patient (Class IIb, LOE C). During therapeutic hypothermia of the pregnant patient, it is recommended that the fetus be continuously monitored for bradycardia as a potential complication, and obstetric and neonatal consultation should be sought (Class I, LOE C).

BLS and ACLS Modifications

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.

ACLS Modifications

In patients with cardiac arrest and without known PE, routine fibrinolytic treatment given during CPR shows no benefit^185,186 and is not recommended (Class III, LOE A).

In patients with cardiac arrest and presumed PE, however, the use of fibrinolytics during CPR may improve the patient's chance of survival.^187–194 Despite the potential to increase the risk of severe bleeding, fibrinolytics may improve survival to discharge and long-term neurological function in patients with presumed PE-induced cardiac arrest.^193–196 Emergency echocardiography may be helpful in determining the presence of thrombus or PE.

In a small number of patients, percutaneous mechanical thromboembolectomy during CPR has been performed successfully.¹⁸⁹ Surgical embolectomy has also been used successfully in some patients with PE-induced cardiac arrest.^191,197,198

In patients with cardiac arrest due to presumed or known PE, it is reasonable to administer fibrinolytics (Class IIa, LOE B). Survival has been described with percutaneous mechanical thrombectomy or surgical embolectomy with or without prior treatment with fibrinolysis.

Potassium (K+)

Potassium is maintained mainly in the intracellular compartment through the action of the Na+/K+ ATPase pump. The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle cells, including the myocardium.

Potassium is tightly regulated. Under normal conditions potential differences across membranes, especially cardiac, are not affected by alterations in potassium level. Rapid or significant changes in serum concentrations of potassium result from the shifting of potassium from one space to another and may have life-threatening consequences.

Hyperkalemia

Hyperkalemia is one of the few potentially lethal electrolyte disturbances. Severe hyperkalemia (defined as a serum potassium concentration >6.5 mmol/L) occurs most commonly from renal failure or from release of potassium from cells and can cause cardiac arrhythmias and cardiac arrest. In 1 retrospective in-hospital study of 29 063 patients, hyperkalemia was found to be directly responsible for sudden cardiac arrest in 7 cases.¹⁹⁹ Acute kidney injury was present in all the arrest cases, accompanied by acute pancreatitis in 3 cases and acute hepatic failure in 2 cases. Overall renal failure and drug treatment were the most common causes of hyperkalemia, with the most severe cases occurring when excessive IV potassium was administered to a patient with renal insufficiency.

Although severe hyperkalemia may cause flaccid paralysis, paresthesia, depressed deep tendon reflexes, or respiratory difficulties,^200–202 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 5). If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.^203,204

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Figure 5.

ECG changes in hyperkalemia.

Sodium (Na⁺)

Sodium is the major intravascular ion that influences serum osmolality. Sodium abnormalities are unlikely to lead to cardiac arrest, and there are no specific recommendations for either checking or treating sodium during cardiac arrest. Disturbances in sodium level are unlikely to be the primary cause of severe cardiovascular instability.

Magnesium (Mg⁺⁺)

Magnesium is an essential electrolyte and an important cofactor for multiple enzymes, including ATPase. Magnesium is necessary for the movement of sodium, potassium, and calcium into and out of cells and plays an important role in stabilizing excitable membranes. The presence of a low plasma magnesium concentration has been associated with poor prognosis in cardiac arrest patients.^{208,213–216}

Hypermagnesemia

Hypermagnesemia is defined as a serum magnesium concentration >2.2 mEq/L (normal: 1.3 to 2.2 mEq/L). Neurological symptoms of hypermagnesemia include muscular weakness, paralysis, ataxia, drowsiness, and confusion. Hypermagnesemia can produce vasodilation and hypotension.²¹⁷ Extremely high serum magnesium levels may produce a depressed level of consciousness, bradycardia, cardiac arrhythmias, hypoventilation, and cardiorespiratory arrest.^208,215,216

Hypomagnesemia

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.

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. However, empirical use of calcium (calcium chloride [10%] 5 to 10 mL OR calcium gluconate [10%] 15 to 30 mL IV over 2 to 5 minutes) may be considered when hyperkalemia or hypermagnesemia is suspected as the cause of cardiac arrest (Class IIb, LOE C).

Initial Approach to the Critically Poisoned Patient

Management of the critically poisoned patient begins with airway protection, support of respiration and circulation, and rapid assessment. Patients may or may not be able to provide an accurate history of exposure to a toxic substance. Whenever possible, history gathering should include questioning of persons who accompany the patient, evaluation of containers, review of pharmacy records, and examination of the patient's prior medical record.²²⁰ Many patients who ingest medications in a suicide attempt take more than 1 substance, and the number of substances ingested is greater in fatal than in nonfatal suicide attempts.²²¹ Comprehensive toxicology laboratory testing is virtually never available in a time frame that supports early resuscitation decisions.²²²

Poisoned patients may deteriorate rapidly. Care for all adult patients who are critically ill or under evaluation for possible toxin exposure or ingestion, particularly when the history is uncertain, should begin in a monitored treatment area where the development of central nervous system depression, hemodynamic instability, or seizures can be rapidly recognized and addressed.²²³

Gastrointestinal decontamination, once a mainstay in the management of ingested toxins, has a less significant role in poisoning treatment today. With rare exceptions, gastric lavage, whole bowel irrigation, and administration of syrup of ipecac are no longer recommended.^224–226 Administration of single-dose activated charcoal to adsorb ingested toxins is generally recommended for the ingestion of life-threatening poisons for which no adequate antidotal therapy is available and when the charcoal can be administered within 1 hour of poisoning.²²⁸ Multiple-dose activated charcoal should be considered for patients who have ingested a life-threatening amount of specific toxins (eg, carbamazepine, dapsone, phenobarbital, quinine, or theophylline) for which a benefit of this strategy has been established.²²⁹ Charcoal should not be administered for ingestions of caustic substances, metals, or hydrocarbons.²²⁸

Charcoal should only be administered to patients with an intact or protected airway. In patients who are at risk for aspiration, endotracheal intubation and head-of-bed elevation should be performed before charcoal administration.^229,230 Because the decision to perform gastrointestinal decontamination is complex, multifactorial, and associated with risk, expert advice can be helpful.

Toxidromes

A “toxidrome” is a clinical syndrome—a constellation of signs, symptoms, and laboratory findings—suggestive of the effects of a specific toxin. By recognizing these presentations, the clinician can establish a working diagnosis that guides initial management. Some common toxidromes are presented in the Table. Practically every sign and symptom observed in poisoning can be produced by natural disease, and many clinical presentations associated with natural disease can be mimicked by some poison.²³¹ It is important to maintain a broad differential diagnosis, particularly when the history of toxic chemical exposure is unclear.

Opioid Toxicity

There are no data to support the use of specific antidotes in the setting of cardiac arrest due to opioid overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.

Naloxone is a potent antagonist of the binding of opioid medications to their receptors in the brain and spinal cord. Administration of naloxone can reverse central nervous system and respiratory depression caused by opioid overdose. Naloxone has no role in the management of cardiac arrest.

In the patient with known or suspected opioid overdose with respiratory depression who is not in cardiac arrest, ventilation should be assisted by a bag mask,^232–238 followed by administration of naloxone and placement of an advanced airway if there is no response to naloxone (Class I, LOE A).

Administration of naloxone can produce fulminate opioid withdrawal in opioid-dependent individuals, leading to agitation, hypertension, and violent behavior. For this reason, naloxone administration should begin with a low dose (0.04 to 0.4 mg), with repeat dosing or dose escalation to 2 mg if the initial response is inadequate.²³⁹ Some patients may require much higher doses to reverse intoxication with atypical opioids, such as propoxyphene, or following massive overdose ingestions.^240,241 Naloxone can be given IV,^{235,236,242,243} IM,^232,235,236 intranasally,^232,242 and into the trachea.²⁴⁴

The duration of action of naloxone is approximately 45 to 70 minutes, but respiratory depression caused by ingestion of a long-acting opioid (eg, methadone) may last longer. Thus, the clinical effects of naloxone may not last as long as those of the opioid, and repeat doses of naloxone may be needed.

Patients with life-threatening central nervous system or respiratory depression reversed by naloxone administration should be observed for resedation. Although a brief period of observation may be appropriate for patients with morphine or heroin overdose,²⁴⁵ a longer period of observation may be required to safely discharge a patient with life-threatening overdose of a long-acting or sustained-release opioid.^239,246

Benzodiazepines

There are no data to support the use of specific antidotes in the setting of cardiac arrest due to benzodiazepine overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.

Flumazenil is a potent antagonist of the binding of benzodiazepines to their central nervous system receptors. Administration of flumazenil can reverse central nervous system and respiratory depression caused by benzodiazepine overdose. Flumazenil has no role in the management of cardiac arrest.

The administration of flumazenil to patients with undifferentiated coma confers risk and is not recommended (Class III, LOE B). Flumazenil administration can precipitate seizures in benzodiazepine-dependent patients and has been associated with seizures, arrhythmia, and hypotension in patients with coingestion of certain medications, such as tricyclic antidepressants.^247,248 However, flumazenil may be used safely to reverse excessive sedation known to be due to the use of benzodiazepines in a patient without known contraindications (eg, procedural sedation).²⁴⁹

β-Blockers

There are no data to support the use of specific antidotes in the setting of cardiac arrest due to β-blocker overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.

β-Blocker medication overdose may cause such severe inhibition of β-adrenergic receptors that high-dose vasopressors cannot effectively restore blood pressure, cardiac output, or perfusion. Therapeutic options in the treatment of refractory hemodynamic instability due to β-blocker overdose include administration of glucagon, high-dose insulin, or IV calcium salts.

Calcium Channel Blockers

There are no data to support the use of specific antidotes in the setting of cardiac arrest due to calcium channel blocker overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms.

Calcium channel blocker overdose also may cause life-threatening hypotension and bradycardia that are refractory to standard agents. Treatment with high-dose insulin has been described in a number of clinical case reports^284–295 and animal studies.^296–299 High-dose insulin, in the doses listed in the β-blocker section above, may be effective for restoring hemodynamic stability and improving survival in the setting of severe cardiovascular toxicity associated with toxicity from a calcium channel blocker overdose (Class IIb, LOE B).

Limited evidence supports the use of calcium in the treatment of hemodynamically unstable calcium channel blocker overdose refractory to other treatments.^{285,286,289,290,292–294,297,300–303} Administration of calcium in patients with shock refractory to other measures may be considered (Class IIb, LOE C).

There is insufficient and conflicting evidence to recommend the use of glucagon^{289,290,294,296,297,300,303–306} in the treatment of hemodynamically unstable calcium channel blocker overdose.

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 blockade. Other plant- and animal-derived cardiac glycosides may produce similar effects, including those found in oleander, lily-of-the-valley, toad skin, and some herbal medications. There are no data to support the use of specific antidotes in the setting of cardiac arrest due to digoxin overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms, with specific antidotes used in the post-cardiac arrest phase if severe cardiotoxicity is encountered.

Antidigoxin Fab antibodies should be administered to patients with severe life-threatening cardiac glycoside toxicity (Class I, LOE B).^307–316 One vial of antidigoxin Fab is standardized to neutralize 0.5 mg of digoxin. Although the ideal dose is unknown, a reasonable strategy is as follows:

• If the ingested dose of digoxin is known, administer 2 vials of Fab for every milligram of digoxin ingested.

• In cases of chronic digoxin toxicity or when the ingested dose is not known, calculate the number of vials to administer by using the following formula: serum digoxin concentration (ng/mL)×weight (kg)/100.

• In critical cases in which therapy is required before a serum digoxin level can be obtained or in cases of life-threatening toxicity due to cardiac glycosides, administer empirically 10 to 20 vials.

Hyperkalemia is a marker of severity in acute cardiac glycoside poisoning and is associated with poor prognosis.³¹⁷ Antidigoxin Fab may be administered empirically to patients with acute poisoning from digoxin or related cardiac glycosides whose serum potassium level exceeds 5.0 mEq/L.³¹⁸

Cocaine

There are no data to support the use of cocaine-specific interventions in the setting of cardiac arrest due to cocaine overdose. Resuscitation from cardiac arrest should follow standard BLS and ACLS algorithms, with specific antidotes used in the postresuscitation phase if severe cardiotoxicity or neurotoxicity is encountered. A single case series demonstrated excellent overall and neurologically intact survival (55%) in patients with cardiac arrest associated with cocaine overdose who were treated with standard therapy.³¹⁹

Cocaine-induced tachycardia and hypertension are predominantly caused by central nervous system stimulation. Treatment strategies are extrapolated from acute coronary syndrome studies, small case series, and experiments in cocaine-naïve human volunteers. It may be reasonable to try agents that have shown efficacy in the management of acute coronary syndrome in patients with severe cardiovascular toxicity. α-Blockers (phentolamine),³²⁰ benzodiazepines (lorazepam, diazepam),³²¹ calcium channel blockers (verapamil),³²² morphine,³²³ and sublingual nitroglycerin^324,325 may be used as needed to control hypertension, tachycardia, and agitation (Class IIb, LOE B). The available data do not support the use of 1 agent over another in the treatment of cardiovascular toxicity due to cocaine (Class IIb, LOE B).

There is clear evidence that cocaine can precipitate acute coronary syndromes.³²⁶ For cocaine-induced hypertension or chest discomfort, benzodiazepines, nitroglycerin, and/or morphine can be beneficial (Class IIa, LOE B).^321,324,327 Because the effects of cocaine and other stimulant medications are transient, drugs and doses should be chosen carefully to minimize the risk of producing hypotension after the offending agent has been metabolized. Catheterization laboratory studies demonstrate that cocaine administration leads to reduced coronary artery diameter. This effect is reversed by morphine,³²³ nitroglycerin,³²⁵ phentolamine,³²⁰ and verapamil³²²; is not changed by labetalol³²⁸; and is exacerbated by propranolol.³²⁹ Several studies suggest that administration of β-blockers may worsen cardiac perfusion and/or produce paradoxical hypertension when cocaine is present.^329,330 Although contradictory evidence exists,^331,332 current recommendations are that pure β-blocker medications in the setting of cocaine are not indicated (Class IIb, LOE C).³³³

In severe overdose, cocaine acts as a Vaughan-Williams class Ic antiarrhythmic, producing wide-complex tachycardia through several mechanisms, including blockade of cardiac sodium channels.¹⁰⁷ Although there is no human evidence in cocaine poisoning, extrapolation from evidence in the treatment of wide-complex tachycardia caused by other class Ic agents (flecainide) and tricyclic antidepressants suggests that administration of hypertonic sodium bicarbonate may be beneficial.³³⁴ A typical treatment strategy used for these other sodium channel blockers involves administration of 1 mL/kg of sodium bicarbonate solution (8.4%, 1 mEq/mL) IV as a bolus, repeated as needed until hemodynamic stability is restored and QRS duration is ≤120 ms.^335–342 Current evidence neither supports nor refutes a role for lidocaine in the management of wide-complex tachycardia caused by cocaine.

Cyclic Antidepressants

Many drugs can prolong the QRS interval in overdose. These include Vaughan-Williams class Ia and Ic antiarrhythmics (eg, procainamide, quinidine, flecainide), cyclic antidepressants (eg, amitriptyline), and cocaine. Type Ia and Ic antiarrhythmics were not reviewed in 2010. Similar to the type Ia antiarrhythmics, cyclic antidepressants block cardiac sodium channels, leading to hypotension and wide-complex arrhythmia in overdose.

Cardiac arrest caused by cyclic antidepressant toxicity should be managed by current BLS and ACLS treatment guidelines. A small case series of cardiac arrest patients demonstrated improvement with sodium bicarbonate and epinephrine,³⁴³ but the concomitant use of physostigmine in the prearrest period in this study reduces the ability to generalize this study. Administration of sodium bicarbonate for cardiac arrest due to cyclic antidepressant overdose may be considered (Class IIb, LOE C).

Therapeutic strategies for treatment of severe cyclic antidepressant cardiotoxicity include increasing serum sodium, increasing serum pH, or doing both simultaneously. The relative contributions of hypernatremia and alkalemia are controversial, but in practice most experience involves administration of hypertonic sodium bicarbonate solution (8.4% solution, 1 mEq/mL). 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).^335–342 Serum sodium levels and pH should be monitored, and severe hypernatremia (sodium >155 mEq/L) and alkalemia (pH >7.55) should be avoided. A number of vasopressors and inotropes have been associated with improvement in the treatment of tricyclic-induced hypotension, ie, epinephrine,^239,344,345 norepinephrine,^345–348 dopamine,^348–350 and dobutamine.³⁴⁹

Local Anesthetic Toxicity

Inadvertent intravascular administration of local anesthetics, such as bupivacaine, mepivacaine, or lidocaine, can produce refractory seizures and rapid cardiovascular collapse leading to cardiac arrest. Clinical case reports^351–355 and controlled animal studies^356–360 have suggested that rapid IV infusion of lipids may reverse this toxicity either by redistributing the local anesthetic away from its site of action or by augmenting metabolic pathways within the cardiac myocyte.

Case reports have shown return of spontaneous circulation in patients with prolonged cardiac arrest unresponsive to standard ACLS measures,^361,362 suggesting a role for administration of IV lipids during cardiac arrest. Although ideal dosing has not been determined, because dosage varied across all studies, it may be reasonable to consider 1.5 mL/kg of 20% long-chain fatty acid emulsion as an initial bolus, repeated every 5 minutes until cardiovascular stability is restored (Class IIb, LOE C).³⁶³ After the patient is stabilized, some papers suggest a maintenance infusion of 0.25 mL/kg per minute for at least 30 to 60 minutes. A maximum cumulative dose of 12 mL/kg has been proposed.³⁶³

Some animal data suggest that lipid infusion alone may be more effective than standard doses of epinephrine or vasopressin.^357,360 Although there is limited evidence to change routine care for severe cardiotoxicity, several professional societies advocate protocolized clinical use.^364–366 Because this is a rapidly evolving clinical area,^367,368 prompt consultation with a medical toxicologist, anesthesiologist, or other specialist with up-to-date knowledge is strongly recommended.

Carbon Monoxide

Apart from complications from deliberate drug abuse, carbon monoxide is the leading cause of unintentional poisoning death in the United States.³⁶⁹ In addition to reducing the ability of hemoglobin to deliver oxygen, carbon monoxide causes direct cellular damage to the brain and myocardium.³⁷⁰ Survivors of carbon monoxide poisoning are at risk for lasting neurological injury.³⁷⁰

Several studies have suggested that very few patients who develop cardiac arrest from carbon monoxide poisoning survive to hospital discharge, regardless of treatment administered following return of spontaneous circulation.^371–373 Routine care of patients in cardiac arrest and severe cardiotoxicity from carbon monoxide poisoning should comply with standard BLS and ACLS recommendations.

Cyanide

Cyanide is a surprisingly common chemical. In addition to industrial sources, cyanide can be found in jewelry cleaners, electroplating solutions, and as a metabolic product of the putative antitumor drug amygdalin (laetrile). Cyanide is a major component of fire smoke, and cyanide poisoning must be considered in victims of smoke inhalation who have hypotension, central nervous system depression, metabolic acidosis, or soot in the nares or respiratory secretions.³⁸³ Cyanide poisoning causes rapid cardiovascular collapse, which manifests as hypotension, lactic acidosis, central apnea, and seizures.

Patients in cardiac arrest^383–385 or those presenting with cardiovascular instability^383–389 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.^387,390,391

Both hydroxocobalamin^383–389 and sodium nitrite^387,390,391 serve to rapidly and effectively bind cyanide in the serum and reverse the effects of cyanide toxicity. Because nitrites induce methemoglobin formation³⁹⁰ and can cause hypotension,³⁹² hydroxocobalamin has a safety advantage, particularly in children and victims of smoke inhalation who might also have carbon monoxide poisoning. A detailed comparison of these measures has been recently published.³⁹³

Sodium thiosulfate serves as a metabolic cofactor, enhancing the detoxification of cyanide to thiocyanate. Thiosulfate administration enhances the effectiveness of cyanide scavengers in animal experimentation^394–397 and has been used successfully in humans with both hydroxocobalamin^383,389 and sodium nitrite.^387,390,391 Sodium thiosulfate is associated with vomiting but has no other significant toxicity.³⁹⁸ Therefore, based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended (Class I, LOE B).

BLS Modifications

When multisystem trauma is present or trauma involves the head and neck, the cervical spine must be stabilized. A jaw thrust should be used instead of a head tilt–chin lift to establish a patent airway. If breathing is inadequate and the patient's face is bloody, ventilation should be provided with a barrier device, a pocket mask, or a bag-mask device while maintaining cervical spine stabilization. Stop any visible hemorrhage using direct compression and appropriate dressings. If the patient is completely unresponsive despite rescue breathing, provide standard CPR and defibrillation as indicated.

ACLS Modifications

After initiation of BLS care, if bag-mask ventilation is inadequate, an advanced airway should be inserted while maintaining cervical spine stabilization. If insertion of an advanced airway is not possible and ventilation remains inadequate, experienced providers should consider a cricothyrotomy.

A unilateral decrease in breath sounds during positive-pressure ventilation should prompt the rescuer to consider the possibility of pneumothorax, hemothorax, or rupture of the diaphragm.

When the airway, oxygenation, and ventilation are adequate, evaluate and support circulation. Control ongoing bleeding where possible and replace lost volume if the losses appear to have significantly compromised circulating blood volume. Cardiac arrest resuscitation will likely be ineffective in the presence of uncorrected severe hypovolemia.

Treatment of PEA requires identification and treatment of reversible causes, such as severe hypovolemia, hypothermia, cardiac tamponade, or tension pneumothorax.³⁹⁹ Development of bradyasystolic rhythms often indicates the presence of severe hypovolemia, severe hypoxemia, or cardiorespiratory failure. Ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT) are treated with CPR and defibrillation. For treatment recommendations regarding cardiac tamponade in traumatic cardiac arrest, see Part 12.14: “Cardiac Arrest Caused by Cardiac Tamponade.”

Resuscitative thoracotomy may be indicated in selected patients. A review of the literature from 1966 to 1999, carried out by the American College of Surgeons Committee on Trauma, found a survival rate of 7.8% (11.2% for penetrating injuries and 1.6% for blunt lesions) in trauma victims who would otherwise have 100% mortality.⁴⁰⁰ Practitioners should consult the guidelines for withholding or terminating resuscitation, which were developed for victims of traumatic cardiac arrest by a joint committee of the National Association of EMS Physicians and the American College of Surgeons Committee on Trauma.^401,402

Commotio Cordis

Commotio cordis is VF triggered by a blow to the anterior chest during a cardiac repolarization.^403,404 Blunt cardiac injury may result in cardiac contusion with injured myocardium and risk of ECG changes and arrhythmias. Even a small blow to the anterior chest during a cardiac repolarization, such as that imparted by the strike of a baseball or hockey puck, may trigger VF, so-called commotio cordis.⁴⁰⁵ Events causing commotio cordis are most commonly seen in young persons up to 18 years of age who are engaged in sports but may occur during daily activities. Prompt recognition that a precordial blow may cause VF is critical. Rapid defibrillation is often life-saving for these frequently young victims of cardiac arrest. Provision of immediate BLS care using an automated external defibrillator (AED) and ACLS for VF in this setting is appropriate.

Initial Care for Victims of Accidental Hypothermia

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

• Preventing additional evaporative heat loss by removing wet garments and insulating the victim from further environmental exposures. Passive rewarming is generally adequate for patients with mild hypothermia (temperature >34°C [93.2°F]).

• For patients with moderate (30°C to 34°C [86°F to 93.2°F]) hypothermia with a perfusing rhythm, external warming techniques are appropriate.⁴⁰⁶ Passive rewarming alone will be inadequate for these patients.⁴⁰⁷

• For patients with severe hypothermia (<30°C [86°F]) with a perfusing rhythm, core rewarming is often used, although some have reported successful rewarming with active external warming techniques.^408,409 Active external warming techniques include forced air or other efficient surface-warming devices.

• Patients with severe hypothermia and cardiac arrest can be rewarmed most rapidly with cardiopulmonary bypass.^{406,410–415} Alternative effective core rewarming techniques include warm-water lavage of the thoracic cavity^{413,416–420} and extracorporeal blood warming with partial bypass.^421–423

• Adjunctive core rewarming techniques include warmed IV or intraosseous (IO) fluids and warm humidified oxygen.⁴²⁴ Heat transfer with these measures is not rapid, and should be considered supplementary to active warming techniques.

• Do not delay urgent procedures such as airway management and insertion of vascular catheters. Although these patients may exhibit cardiac irritability, this concern should not delay necessary interventions.

Beyond these critical initial steps, the treatment of severe hypothermia (temperature <30°C [86°F]) in the field remains controversial. Many providers do not have the time or equipment to assess core body temperature or to institute aggressive rewarming techniques, although these methods should be initiated when available.

BLS Modifications

The most important and detrimental consequence of submersion is hypoxia; therefore, oxygenation, ventilation, and perfusion should be restored as rapidly as possible. This will require immediate bystander CPR plus activation of the EMS system. With the 2010 AHA Guidelines for CPR and ECC, CPR now begins with chest compressions in a C-A-B sequence. However, the guidelines recommend that healthcare providers tailor the sequence based upon the presumed etiology of the arrest. Healthcare provider CPR for drowning victims should use the traditional A-B-C approach in view of the hypoxic nature of the arrest. Victims with only respiratory arrest usually respond after a few artificial breaths are given.

Recovery From the Water

When attempting to rescue a drowning victim, the rescuer should get to the victim as quickly as possible. It is crucial, however, that the rescuer pays constant attention to his or her own personal safety during the rescue process.

The reported incidence of cervical spine injury in drowning victims is low (0.009%).^472,473 Unnecessary cervical spine immobilization can impede adequate opening of the airway and delay delivery of rescue breaths. Routine stabilization of the cervical spine in the absence of circumstances that suggest a spinal injury is not recommended (Class III, LOE B).^473,474

Rescue Breathing

The first and most important treatment of the drowning victim is the immediate provision of ventilation. Prompt initiation of rescue breathing increases the victim's chance of survival.⁴⁷⁵ Rescue breathing is usually performed once the unresponsive victim is in shallow water or out of the water. Mouth-to-nose ventilation may be used as an alternative to mouth-to-mouth ventilation if it is difficult for the rescuer to pinch the victim's nose, support the head, and open the airway in the water.

Management of the drowning victim's airway and breathing is similar to that recommended for any victim of cardiopulmonary arrest. Some victims aspirate no water because they develop laryngospasm or breath-holding.^465,476 Even if water is aspirated, there is no need to clear the airway of aspirated water, because only a modest amount of water is aspirated by the majority of drowning victims, and aspirated water is rapidly absorbed into the central circulation.^465,477 Attempts to remove water from the breathing passages by any means other than suction (eg, abdominal thrusts or the Heimlich maneuver) are unnecessary and potentially dangerous.⁴⁷⁷ The routine use of abdominal thrusts or the Heimlich maneuver for drowning victims is not recommended (Class III, LOE C).

Chest Compressions

As soon as the unresponsive victim is removed from the water, the rescuer should open the airway, check for breathing, and if there is no breathing, give 2 rescue breaths that make the chest rise (if this was not done previously in the water). After delivery of 2 effective breaths, if a pulse is not definitely felt, the healthcare provider should begin chest compressions and provide cycles of compressions and ventilations according to the BLS guidelines. Once the victim is out of the water, if he or she is unresponsive and not breathing after delivery of 2 rescue breaths and is pulseless, rescuers should attach an AED and attempt defibrillation if a shockable rhythm is identified. It is only necessary to dry the chest area before applying the defibrillation pads and using the AED. If hypothermia is present, follow the recommendations in Part 12.9: “Cardiac Arrest in Accidental Hypothermia.”

Vomiting by the Victim During Resuscitation

The victim may vomit when the rescuer performs chest compressions or rescue breathing. In fact, in a 10-year study in Australia, two thirds of victims who received rescue breathing and 86% of those who required compressions and ventilations vomited.⁴⁷⁸ If vomiting occurs, turn the victim to the side and remove the vomitus using your finger, a cloth, or suction. If spinal cord injury is suspected, the victim should be logrolled so that the head, neck, and torso are turned as a unit to protect the cervical spine.

ACLS Modifications

Victims in cardiac arrest may present with asystole, PEA, or pulseless VT/VF. For treatment of these rhythms, follow the appropriate PALS or ACLS guidelines. Case reports of pediatric patients document the use of surfactant for fresh water–induced respiratory distress, but further research is needed.^479–482 The use of extracorporeal membrane oxygenation in patients with severe hypothermia after submersion has been documented in case reports.^468,469,483

Electric Shock

Fatal electrocutions may occur with household current; however, high-tension current generally causes the most serious injuries.⁴⁸⁵ Contact with alternating current (the type of current commonly present in most North American households and commercial settings) may cause tetanic skeletal muscle contractions, “locking” the victim to the source of the electricity and thereby leading to prolonged exposure. The frequency of alternating current increases the likelihood of current flow through the heart during the relative refractory period, which is the “vulnerable period” of the cardiac cycle. This exposure can precipitate VF, which is analogous to the R-on-T phenomenon that occurs in nonsynchronized cardioversion.⁴⁸⁶

Lightning Strike

The National Weather Service estimates that an average of 70 deaths and 630 injuries occur due to lightning strikes in the United States each year.⁴⁸⁷ Lightning strike injuries can vary widely, even among groups of people struck at the same time. Symptoms are mild in some victims, whereas fatal injuries occur in others.^488,489

The primary cause of death in victims of lightning strike is cardiac arrest, which may be associated with primary VF or asystole.^488–491 Lightning acts as an instantaneous, massive direct-current shock, simultaneously depolarizing the entire myocardium.^489,492 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.⁴⁹³

Lightning also can have myriad effects on the cardiovascular system, producing extensive catecholamine release or autonomic stimulation. The victim may develop hypertension, tachycardia, nonspecific ECG changes (including prolongation of the QT interval and transient T-wave inversion), and myocardial necrosis with release of creatinine kinase-MB fraction.

Lightning can produce a wide spectrum of peripheral and central neurological injuries. The current can produce brain hemorrhages, edema, and small-vessel and neuronal injury. Hypoxic encephalopathy can result from cardiac arrest.

Victims are most likely to die of lightning injury if they experience immediate respiratory or cardiac arrest and no treatment is provided. Patients who do not suffer respiratory or cardiac arrest, and those who respond to immediate treatment, have an excellent chance of recovery. Therefore, when multiple victims are struck simultaneously by lightning, rescuers should give the highest priority to patients in respiratory or cardiac arrest.

For victims in cardiac arrest, treatment should be early, aggressive, and persistent. Victims with respiratory arrest may require only ventilation and oxygenation to avoid secondary hypoxic cardiac arrest. Resuscitation attempts may have high success rates and efforts may be effective even when the interval before the resuscitation attempt is prolonged.⁴⁹³

BLS Modifications

The rescuer must first be certain that rescue efforts will not put him or her in danger of electric shock. When the scene is safe (ie, the danger of shock has been removed), determine the victim's cardiorespiratory status. If spontaneous respiration or circulation is absent, immediately initiate standard BLS resuscitation care, including the use of an AED to identify and treat VT or VF.

Maintain spinal stabilization during extrication and treatment if there is a likelihood of head or neck trauma.^494,495 Both lightning and electric shock often cause multiple trauma, including injury to the spine,⁴⁹⁵ muscular strains, internal injuries from being thrown, and fractures caused by the tetanic response of skeletal muscles.⁴⁹⁶ 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. Establishing an airway may be difficult for patients with electric burns of the face, mouth, or anterior neck. Extensive soft-tissue swelling may develop rapidly, complicating airway control measures. Thus, early intubation should be performed for patients with evidence of extensive burns even if the patient has begun to breathe spontaneously.

For victims with significant tissue destruction and in whom a pulse is regained, rapid IV fluid administration is indicated to counteract distributive/hypovolemic shock and to correct ongoing fluid losses due to third spacing. Fluid administration should be adequate to maintain diuresis and facilitate excretion of myoglobin, potassium, and other byproducts of tissue destruction (this is particularly true for patients with electric injury).⁴⁹² Regardless of the extent of external injuries after electrothermal shock, the underlying tissue damage can be far more extensive.

Mechanical CPR During PCI

Mechanical chest compression devices have been used successfully in an animal model⁴⁹⁷ and adult humans^497–501 to provide maintenance of circulation in cardiac arrest while continuing a percutaneous coronary procedure. It is reasonable to use mechanical CPR during PCI (Class IIa, LOE C).

Emergency Cardiopulmonary Bypass

One case series⁵⁰² describes the use of emergency cardiopulmonary bypass to stabilize and facilitate emergency coronary angioplasty in patients with cardiac arrest unresponsive to ACLS during PCI. It is reasonable to use emergency cardiopulmonary bypass during PCI (Class IIb, LOE C).

Cough CPR

Multiple case reports^503–507 describe the use of cough CPR to temporarily maintain adequate blood pressure and level of consciousness in patients who develop ventricular arrhythmias during PCI while definitive therapy for malignant arrhythmias is instituted. It is reasonable to use cough CPR during PCI (Class IIa, LOE C).

Intracoronary Verapamil

One large case series⁵⁰⁸ describes the successful use of intracoronary verapamil to terminate reperfusion-induced VT following mechanical revascularization therapy. Verapamil was not successful in terminating VF.

Resternotomy

Studies of patients with cardiac arrest after cardiac surgery who are treated with resternotomy and internal cardiac compression have reported improved outcome compared with a standard protocol^519–529 when patients are treated by experienced personnel in intensive care units. Findings of similar quality studies^530–534 reported no difference in outcomes when resternotomy was compared with standard management of cardiac arrest after cardiac surgery. Resternotomy performed outside an intensive care unit generally has a very poor outcome.^519,526,533

For patients with cardiac arrest following cardiac surgery, it is reasonable to perform resternotomy in an appropriately staffed and equipped intensive care unit (Class IIa, LOE B). Despite rare case reports describing damage to the heart possibly due to external chest compressions,^535,536 chest compressions should not be withheld if emergency resternotomy is not immediately available (Class IIa, LOE C).

Mechanical Circulatory Support

Nine case series have reported survival of some post–cardiac surgery patients during cardiac arrest refractory to standard resuscitation measures following the use of extracorporeal membrane oxygenation^537–541 and cardiopulmonary bypass.^{529,542–544} In post–cardiac surgery patients who are refractory to standard resuscitation procedures, mechanical circulatory support (eg, extracorporeal membrane oxygenation and cardiopulmonary bypass) may be effective in improving outcome (Class IIb, LOE B).

Pharmacological Intervention

Rebound hypertension following administration of pressors during resuscitation has the potential to induce significant bleeding in this group of patients. Results from a single study of epinephrine⁵⁴⁵ and another study evaluating the choice of antiarrhythmics⁵⁴⁶ in patients with cardiac arrest following cardiac surgery were neutral. There is insufficient evidence on epinephrine dose, antiarrhythmic use, and other routine pharmacological interventions to recommend deviating from standard resuscitation guidelines when cardiac arrest occurs after cardiac surgery.