Secondary Logo

Journal Logo

Cardiac Arrest in the Operating Room: Part 2—Special Situations in the Perioperative Period

McEvoy, Matthew D. MD*; Thies, Karl-Christian MD, FRCA, FERC, DEAA; Einav, Sharon MD; Ruetzler, Kurt MD§,∥; Moitra, Vivek K. MD, FCCM; Nunnally, Mark E. MD, FCCM#; Banerjee, Arna MD*; Weinberg, Guy MD**; Gabrielli, Andrea MD, FCCM††; Maccioli, Gerald A. MD, FCCM‡‡; Dobson, Gregory MD§§; O’Connor, Michael F. MD, FCCM∥∥

doi: 10.1213/ANE.0000000000002595
Critical Care and Resuscitation
Free

As noted in part 1 of this series, periprocedural cardiac arrest (PPCA) can differ greatly in etiology and treatment from what is described by the American Heart Association advanced cardiac life support algorithms, which were largely developed for use in out-of-hospital cardiac arrest and in-hospital cardiac arrest outside of the perioperative space. Specifically, there are several life-threatening causes of PPCA of which the management should be within the skill set of all anesthesiologists. However, previous research has demonstrated that continued review and training in the management of these scenarios is greatly needed and is also associated with improved delivery of care and outcomes during PPCA. There is a growing body of literature describing the incidence, causes, treatment, and outcomes of common causes of PPCA (eg, malignant hyperthermia, massive trauma, and local anesthetic systemic toxicity) and the need for a better awareness of these topics within the anesthesiology community at large. As noted in part 1 of this series, these events are always witnessed by a member of the perioperative team, frequently anticipated, and involve rescuer–providers with knowledge of the patient and the procedure they are undergoing or have had. Formulation of an appropriate differential diagnosis and rapid application of targeted interventions are critical for good patient outcome. Resuscitation algorithms that include the evaluation and management of common causes leading to cardiac in the perioperative setting are presented. Practicing anesthesiologists need a working knowledge of these algorithms to maximize good outcomes.

From the *Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee

Department of Anesthesiology, University Medical Centre Greifswald, Ferdinand-Sauerbruch-Straße, 17475 Greifswald, Germany

Faculty of Medicine, Shaare Zedek Medical Center, Hebrew University, Jerusalem, Israel

Departments of §General Anesthesiology

Outcomes Research, Cleveland Clinic, Cleveland, Ohio

Department of Anesthesiology, Columbia University, College of Physicians and Surgeons, New York, New York

#Department of Anesthesiology, Perioperative Care, and Pain Medicine, New York University, New York, New York

**Department of Anesthesiology, The University of Illinois at Chicago, Chicago, Illinois

††University of Pennsylvania, Philadelphia, Pennsylvania

‡‡Department of Anesthesiology and Critical Care, Sheridan Healthcare, Florida

§§Department of Anesthesia, Dalhousie University, Halifax, Nova Scotia, Canada

∥∥Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois.

Published ahead of print November 30, 2017.

Accepted for publication September 8, 2017.

K.-C. Thies is currently affiliated with the Department of Anesthesiology, University Medical Center Greifswald, Ferdinand-Sauerbruch-Straße, Greifswald, Germany.

Funding: This review was developed from previous iterations on behalf of the American Society of Anesthesiologists and the Society of Critical Care Anesthesiologists. Portions of those documents appear verbatim and are used with the permission of the ASA.

Conflicts of Interest: See Disclosures at the end of the article.

Listen to this Article of the Month podcast and more from OpenAnesthesia.org® by visiting http://journals.lww.com/anesthesia-analgesia/pages/default.aspx.

Implication statement: The spectrum of causes of periprocedural cardiac arrest warrants specific adaptations of the advanced circulatory life support algorithms. A number of rare, life-threatening etiologies of profound hemodynamic and respiratory disturbance leading to cardiac arrest are reviewed. Good patient outcomes in these special situations can be achieved by vigilance, timely formulation of a differential diagnosis for the crisis, and adherence to best practices.

Reprints will not be available from the authors.

Address correspondence to Matthew D. McEvoy, MD, Department of Anesthesiology, Vanderbilt University Medical Center, 1301 Medical Center Dr, TVC 4648, Nashville, TN 37232. Address e-mail to matthew.d.mcevoy@vanderbilt.edu.

Advanced cardiac life support (ACLS) was originally developed as an extension of basic life support with a focus on out-of-hospital cardiac arrest (OHCA).1 OHCA is now recognized as a distinct entity from in-hospital cardiac arrest (IHCA), particularly in relation to more common etiology of arrest, average response rescue time, and survival.2 As noted previously,1 periprocedural cardiac arrest (PPCA) is different from both OHCA and medically related IHCA. The etiologies of the crisis, the perioperative team knowledge of the patient’s comorbidities, the awareness of current physiological state, and the immediate rescue response time significantly improve restoration of spontaneous circulation and survival to discharge when compared to other forms of IHCA.3–6

In addition to these differences in clinical presentation and management, numerous studies have also demonstrated knowledge and skill deficiencies in the proper assessment and management of perioperative crises within the anesthesiology community.7–12 Frequent and concise updates of the knowledge content necessary for managing high-stakes perioperative events is necessary for preparing anesthesiologists and perioperative teams to provide appropriate and timely care.13,14 As noted in part 1, while previous publications have described cardiac arrest and crisis management in the operating room, the most recent update in ACLS prompted a part 1 review of the current literature concerning perioperative life-threatening crisis and cardiac arrest. Accordingly, the goal of this part 2 review is to offer an updated clinical perspective of cardiac arrest during the perioperative period. In part 1, we summarize the causes and outcomes of perioperative cardiac arrest, review concepts in resuscitation of the perioperative patient, and propose a set of algorithms to aid in the prevention and management of cardiac arrest during the perioperative period. In this article, we discuss special anesthesia-related crises and the management thereof.

This review is focused on 8 special circumstances in the perioperative period that, while uncommon, are essential for all practicing anesthesiologists to know. The clinical scenarios presented are severe anaphylaxis, tension pneumothorax, local anesthetic systemic toxicity (LAST), malignant hyperthermia (MH), severe hyperkalemia, hypertensive crisis, trauma-related cardiac arrest, and pulmonary embolism (PE; thrombus or gas). Each scenario will be presented with a brief review of pathophysiology and epidemiology followed by recommendations on proper assessment, initial management, and subsequent management of each perioperative crisis based on a comprehensive review of the literature. The information presented in this article represents the background behind the management recommendations proposed in widely available crisis management checklists such as the Stanford and Harvard crisis checklists that are familiar to many practicing anesthesiologists.15,16 It should be noted that these well-recognized clinical entities are presented as single cause of a life-threatening crisis and out of the clinical contest of more complex condition like septic shock or multiorgan system failure.

Back to Top | Article Outline

METHODS

An international group of 12 experts in the field of perioperative resuscitation has reviewed best available evidence on management of cardiac arrest and periprocedural crises. These experts were selected on the basis of several criteria: (1) clinical experience in anesthesiology and perioperative patient management; (2) expertise in simulation training in perioperative crises; (3) familiarity with the evidence behind current resuscitation guidelines; and (4) international representation (ensure that the recommendations are easily translatable to bedside practice in multiple clinical platforms). The group communicated via email, face-to-face meetings, and telephone. The papers selected for review were those included in the previous iteration of these guidelines1 (which underwent repeat scrutiny) and relevant papers that had been published since 2012 and available in PubMed on the specific topics to be discussed. For part 2, disagreements among committee member were discussed as a group in an attempt to reach consensus, and in case of ongoing dissent, adjudicated by 3 of the authors (M.D.M., V.K.M., and M.F.O.).

The scenarios were chosen through a modified Delphi technique involving several rounds of input from the group. These scenarios were chosen because they represent perioperative emergencies that are likely to be immediately life threatening. Four of the topics briefly covered in a previous publication1 were reanalyzed for a more in-depth discussion and updated knowledge (eg, severe anaphylaxis and hyperkalemia) or landmark publications (eg, trauma-related cardiac arrest). Due to constraints on length for the review article, the number of included scenarios was limited to 7. As such, the scenarios presented are not intended to be an exhaustive list.

Back to Top | Article Outline

Anaphylaxis

Pathophysiology and Epidemiology.

Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction mediated by immunoglobulins IgE and IgG and accounts for about 500–1000 deaths per year in the United States.17,18 The causative agent is usually not obvious, and assigning causality is typically complicated in the periprocedural and hospital setting, where patients are commonly exposed to multiple agents. Furthermore, anaphylactic reactions may occur with no documented prior exposure.19 Hypersensitivity reactions are graded 1–5 corresponding to minor, low severity, life-threatening symptoms, cardiac or respiratory arrest, and death.20,21 The overall incidence of hypersensitivity reactions is about 15 cases per 10,000 operations (95% confidence interval, 13–17 per 10,000).22 The incidence of severe hypersensitivity reactions (grade 3–5) with life-threatening symptoms is about 2 cases per 10,000 operations.22

Back to Top | Article Outline

Presentation and Initial Assessment.

Anaphylaxis is characterized by the rapid onset of potentially life-threatening airway, breathing, or circulatory problems. The initial symptoms are nonspecific. Rhinitis, tachycardia, confusion, altered mental status/presyncope, and skin and mucosal changes are common in the awake patient, but not always present.23 In addition, bronchospasm is not present in all cases and does not necessarily precede cardiovascular instability. Extensive vasodilatation and increased vascular permeability lead to decreased cardiac preload with relative hypovolemia, which can in turn cause cardiovascular depression, myocardial ischemia, acute myocardial infarction, and malignant arrhythmias (anaphylactic shock).24,25 When hemodynamic deterioration occurs rapidly and untreated, patients can experience cardiac arrest.24,25 Evidence in the treatment of anaphylaxis is generally limited and is mostly based on case reports and extrapolations from animal models, nonfatal cases, interpretation of pathophysiology, and consensus opinion.19

Back to Top | Article Outline

Assessment and Initial Management Steps.

When anaphylaxis is within the differential diagnosis, surgery should be interrupted, if possible, and the likely triggers of anaphylaxis should be immediately removed (eg, stopping an injection or infusion of medication or blood products).26 Administration of epinephrine is indicated in patients with clinical features of anaphylaxis.27,28 In the setting of signs and symptoms of severe anaphylaxis, 100–300 µg epinephrine should be given intravenously (IV) immediately with repeated and escalating doses as clinically indicated. We do not recommend to use the same epinephrine doses used in pulseless cardiac arrest (1 mg IV) if the patient maintains a cardiac rhythm with a pulse. Caution is warranted, as fatal dysrhythmias to large doses of epinephrine have been reported.27,29 In patients without an IV line, early intramuscular administration of 300–500 µg epinephrine in the anterolateral aspect of the middle third of the thigh is recommended, with this dose being repeated every 5–15 minutes in the absence of clinical improvement.30,31 Inhaled or subcutaneous administration of epinephrine is ineffective for severe anaphylaxis.28 Close hemodynamic monitoring (eg, arterial blood pressure) with a goal systolic blood pressure (SBP) ≥90 mm Hg is indicated.

Immediate endotracheal intubation is critical and should not be delayed, as oropharyngeal and laryngeal edema are likely to occur rapidly.32 If necessary, a surgical airway should be considered.33 Initial fluid resuscitation using 20 mL/kg crystalloid infusions is indicated to treat the vasodilatory component of anaphylactic shock.34,35

Back to Top | Article Outline

Subsequent Assessment and Treatment Steps.

Table 1.

Table 1.

If hemodynamic instability persists after initial epinephrine boluses, this drug should be continued by a carefully titrated continuous IV infusion (0.05–0.3 µg/kg/min) because the plasma half-life of epinephrine is brief (<5 minutes). If epinephrine infusion fails to restore normal hemodynamic variables, continuous infusions of vasopressin,36,37 norepinephrine, methoxamine,38 and metaraminol39 may be considered. Glucagon should be considered in patients who have taken β-blockers and who are unresponsive to combined inotrope and vasopressors management.40 Adjuvant use of antihistamines is appropriate,41–43 and treatment with inhaled β2-adrenergic agents27,44 and IV corticosteroids28,45 should be considered in severe anaphylaxis. Extracorporeal life support (venous–arterial extracorporeal membrane oxygenation) has been successful in isolated cases and may be considered if clinical staff and equipment is immediately available. After stabilization, the patient should be monitored in an intensive care unit (ICU) for at least 24 hours due to the bimodal nature of severe anaphylaxis and a high risk of recrudescence. Finally, laboratory testing for histamine, tryptase, or IgE within 24 hours is indicated for diagnostic purposes.46Table 1 provides a full list of management steps.

Back to Top | Article Outline

Tension Pneumothorax

Epidemiology and Pathophysiology.

A tension pneumothorax occurs when there is a “ball-valve effect” within the lung allowing progressive accumulation of air within the pleural space, which in turn leads to a corresponding increase in intrapleural and intrathoracic pressures. In tension pneumothorax, the intrapleural pressure is positive and exceeds the atmospheric pressure throughout the respiratory cycle. The incidence of tension pneumothorax remains poorly estimated and ranges from 1% to 3% in prehospital, major trauma, and ICU patients.47

The pathophysiology of tension pneumothorax differs between patients who are spontaneously breathing versus those on positive-pressure ventilation. In spontaneously breathing patients, several compensatory mechanisms likely prevent initial hemodynamic compromise. These factors include increasing respiratory rate, decreased tidal volume and negative-pressure contralateral chest excursions. These mechanisms may maintain arterial blood pressure by limiting transmitting pleural pressure to the mediastinum and contralateral hemithorax. In patients receiving positive-pressure ventilation, increased intrapleural pressure throughout the respiratory cycle produces a marked decrease in cardiac venous return, which leads to hypotension, and, if untreated, may result in cardiac arrest.48

Back to Top | Article Outline

Presentation and Initial Assessment.

Spontaneously breathing patients with tension pneumothorax present with shortness of breath, dyspnea, tachypnea, respiratory distress, hypoxemia, and ipsilateral decreased air entry and percussion hyperresonance. In a large systematic review, the reported incidence of respiratory arrest (9%), hypotension (16%), and cardiac arrest (2%) were much lower compared to patients on positive-pressure ventilation.49 Patients on positive-pressure ventilation usually present with hypoxemia, tachycardia, sudden onset of hypotension, subcutaneous emphysema, and ipsilateral decreased air entry. These signs are followed by circulatory collapse and subsequent cardiac arrest with pulseless electrical activity (PEA). Tension pneumothorax should always be in the differential diagnosis of a patient with acute decompensation during laparoscopic surgery.50

Traditionally, diagnosis relies on clinical signs and symptoms although these are unreliable (especially contralateral tracheal deviation and jugular venous distention). Thoracic ultrasonography, which is being used with increasing frequency, may be superior to chest radiography for diagnosing pneumothorax (sensitivity of approximately 80%–90% vs 50%) and can also be performed rapidly at the bedside.51,52

Back to Top | Article Outline

Initial Management Steps.

Initial treatment should focus on maximizing oxygenation. Immediate tube thoracostomy by trained personnel is encouraged as the treatment of choice in both the ventilated and the spontaneously breathing patient.53 However, it should be noted that in situations of high clinical suspicion of tension pneumothorax (eg, high airway pressures, unilateral breath sounds, and circulatory instability in the setting of pneumoperitoneum), immediate needle decompression would be recommended rather than delaying treatment.

Back to Top | Article Outline

Subsequent Assessment and Treatment Steps.

After initial assessment and treatment, the patient should be stabilized to prevent further respiratory or cardiovascular compromise. The tube thoracostomy is left in place until the parenchymal injury that caused the tension pneumothorax has resolved. The underlying cause for the parenchymal injury needs to be ascertained. Occasionally surgical repair may be indicated. Resolution of the pneumothorax is documented with serial chest radiographs.

Back to Top | Article Outline

Local Anesthetic Systemic Toxicity

Epidemiology and Pathophysiology.

While any use of local anesthetic can potentially lead to LAST, peripheral nerve block carries the highest risk, with published rates typically ranging from 1 to 10 per 10,000 qualifying this iatrogenic complication as a “rare event.”54 Nevertheless, the potential for severe, even fatal physiological sequelae demands that measures be taken to reduce the likelihood of LAST and that education/training include detection and treatment of this condition. In addition to using standard monitors and safety measures (eg, frequent aspiration during needle progression incremental injection), there is evidence that the use of ultrasound guidance can reduce the risk of LAST.55

Back to Top | Article Outline

Presentation and Initial Assessment.

A wide range of either neurological symptoms (eg, seizure, agitation, or obtundation) or cardiovascular signs (eg, arrhythmia or conduction block, hypertension, tachycardia, or progressive hypotension and bradycardia) occur with LAST. A study of LAST episodes published from 1979 to 2009 showed that >40% of cases departed from the standard text book presentation (eg, rapid-onset seizure potentially leading to cardiac arrest).56 In 35 of 93 patients (38%), symptoms were delayed >5 minutes, and in 10 patients (11%), cardiovascular signs occurred without a neurological prodrome. Another study from the same group indicated that there is a wide variety of clinical presentations in cases of LAST, including an increase in delayed onset (52%; >5 minutes from injection), which is likely a result of ultrasound guidance.57

Back to Top | Article Outline

Initial Management Steps.

The initial focus in treating LAST includes managing the airway to assure adequate oxygenation and ventilation and using a benzodiazepine to suppress seizures. Early treatment of LAST by infusion of lipid emulsion 20% can prevent progression to cardiovascular compromise58 possibly by reducing peak local anesthetic levels.59 Propofol is cardiodepressant, and its lipid content is inadequate to confer benefit. It is important to continue monitoring even after symptoms resolve because recurrence or delayed progression can occur after an interval of apparent stability.60

Back to Top | Article Outline

Subsequent Assessment and Treatment Steps.

Table 2.

Table 2.

If LAST progresses to cardiovascular collapse, it is important to administer high-quality cardiovascular support since improving coronary and cerebral blood flow reduces local anesthetic tissue concentrations both directly and by delivering lipid emulsion to affected sites. The main benefit of infusion of lipid emulsion in reversing LAST is accelerating redistribution of local anesthetic, rapidly shuttling drug from sites of toxicity (brain and heart) to unaffected organs (eg, liver and skeletal muscle). This scavenging effect is the result of both partitioning into the lipid phase and the direct inotropic effect of lipid emulsion infusion.61 The direct inotropy is seen in intact rats and isolated heart without a pharmacotoxic challenge; however, during experimental LAST, it only occurs after myocardial bupivacaine content drops below a specific (eg, channel blocking) threshold. Lipid infusion also exerts a postconditioning effect that might contribute to successful resuscitation.62 It is important to consider extracorporeal life support relatively early in those instances in which the patient does not respond to more conservative measures. Postevent monitoring should occur for at least 6 hours because cardiovascular instability can recur after initial recovery. Table 2 provides a full list of management steps.

Back to Top | Article Outline

Malignant Hyperthermia

Epidemiology and Pathophysiology.

MH is an extreme reaction to volatile anesthetics and succinylcholine, which is attributed to abnormalities of skeletal muscle metabolism and calcium disposition. Its occurrence is rare, ranging between 1:62,000 and 1:500,000 anesthetics, more commonly occurring in men and younger patients, but described in a wide variety of patients.63,64 The pathophysiology of this syndrome involves mainly cytoplasmic proteins participating in the movement of calcium within skeletal muscle, most commonly the ryanodine receptor. However, many genetic abnormalities are associated with MH, both inherited or sporadic. The syndrome is marked by extreme muscle hypermetabolism, leading to muscle necrosis, hyperpyrexia, acidosis, and in extreme cases, cardiac arrest.

Back to Top | Article Outline

Presentation and Initial Assessment.

Because of its rarity, MH can be a once-in-a-career event. Mortality without dantrolene treatment is as high as 80%, but with it, it may be as low as 1.4%.65 Because the time to dantrolene administration correlates with morbidity and mortality, early recognition is crucial to an effective response. The earliest signs of MH are hypercapnia and sinus tachycardia. Masseter muscle spasm, general muscle rigidity, tachypnea, and rising temperature (late) are additional common findings. Blood gas analysis can reveal respiratory and metabolic acidosis, especially when drawn from a vein draining a large muscle bed.

Back to Top | Article Outline

Initial Management Steps.

When MH is suspected, all triggering agents should be immediately discontinued. Dantrolene 2.5 mg/kg IV is the key therapy for MH. Several formulations exist, and providers should be familiar with preparation and administration of a normal adult dose in anticipation of an MH event. Dantrolene should be available at all places that triggering anesthetic agents are available. Regular monitoring of arterial Paco2, temperature, and lactate levels should accompany dantrolene administration, and any abnormalities should be aggressively treated with external and internal cooling, ventilation, and fluid resuscitation.

Back to Top | Article Outline

Subsequent Assessment and Treatment Steps.

Table 3.

Table 3.

After initial recognition and treatment, the goals of care involve the mitigation of ongoing tissue injury, hyperthermia, and their sequelae. With extremes of temperature (median temperature, 40.3°C), disseminated intravascular coagulation may occur.4 Other complications can occur at any temperature, but mortality correlates with temperature.5 Rhabdomyolysis is common; if severe, it can lead to renal failure and hyperkalemia. Cooling and monitoring for these complications should continue for 72 hours after a suspected episode, because of the risk of recrudescence. Because dantrolene interferes with calcium disposition, patients should be monitored for muscle weakness. Importantly, calcium channel blockers are contraindicated in the setting of dysrhythmias. MH resources are available through expert groups in the United States (www.mhaus.org) and in Europe (www.emhg.org). Table 3 provides a full list of management steps.

Back to Top | Article Outline

Severe Hyperkalemia

Epidemiology and Pathophysiology.

The exact cutoff for moderate or severe hyperkalemia is inconsistently described in the literature.66 However, recent reports note that initiation of emergency therapies are recommended for serum potassium levels >6.0 or 6.5 or electrocardiographic (ECG) manifestations of hyperkalemia, regardless of potassium level.67 Of note, a potassium level of ≥6.5 mmol/L occurs in only 0.1% of hospitalized patients.68 Acidosis (primarily metabolic), for example, promotes an extracellular potassium shift; each 0.1 unit decrease in pH is accompanied by an increase of ∼0.6 mmol/L in serum potassium.69,70 The most common causes of hyperkalemia are renal pathology and drug therapy.68,71,72 There are limited data on the prevalence of hyperkalemia in adult patients undergoing surgery and anesthesia. However, hyperkalemia is consistently estimated to be the cause of death in 1%–2% of cases of anesthesia-related cardiac arrests in children.73–75

Back to Top | Article Outline

Presentation and Initial Assessment.

Clinical manifestations of this potentially life-threatening electrolyte disorder are mostly insidious and nonspecific. Thus, preoperative assessment of patients at risk should include timely blood testing. There is a common misconception that the cardiac manifestations of hyperkalemia are well known and occur in an orderly fashion. On the contrary, the cardiac clinical symptoms of hyperkalemia may randomly range from nonexistent to vertigo, chest pain, and presyncope to syncope and cardiac arrest. Physical examination may reveal bradycardia and/or bradyarrhythmia and hypotension.76 Accompanying ECG changes include peaked T-waves, QRS widening, diminished P waves77,78, and/or a range of arrhythmias including bradycardia,79 atrioventricular blocks at different conduction levels,80–82 ventricular tachycardia,83 and ventricular fibrillation.84–86 Absence of ECG changes should not be taken to indicate that blood potassium levels are normal; some patients with end-stage renal disease do not exhibit ECG changes in the presence of hyperkalemia because of a protective effect of calcium fluctuations.87–89 Neurological manifestations include generalized muscle weakness and respiratory failure due to flaccid muscle paralyses.90–92

Abnormal ECG findings should command immediate attention and treatment when highly suggestive of severe hyperkalemia. Cardiac arrest caused by hyperkalemia has been shown to be associated with accompanying ECG changes, multiorgan system failure, and emergent admission.93 Therefore, perioperative management of life-threatening hyperkalemia depends on whether surgery is elective or urgent and on the perioperative timing of the finding. With the widespread availability of sugammadex, succinylcholine should be avoided or used with great caution if there is any concern for the acute development of hyperkalemia (eg, patients with muscle wasting from neurological injury or those who have been immobile for days in the ICU).94

Back to Top | Article Outline

Initial Management Steps.

The first management step is avoidance of hyperkalemia and thus postponing of elective surgical cases in the setting of this condition and avoiding succinylcholine and prolonged propofol infusions for urgent/emergent cases with known hyperkalemia.86,95–97 Respiratory acidosis should be corrected normalizing ventilation. Acute hyperventilation is to be avoided because it can contribute to hypotension by reducing venous return. Treatment with β-2 agonists (eg, salbuterol) and glucose with insulin can be initiated to promote potassium shift toward the intracellular compartment.98–101 Combined therapy with β-2 agonists and insulin is more effective than a single agent.102 The literature supports administration of calcium as a membrane stabilizer when ECG changes are present.102 In the setting of ongoing hemorrhage and blood administration (with citrate), preventative therapy with calcium may also be deemed justifiable.

Back to Top | Article Outline

Subsequent Assessment and Treatment Steps.

Table 4.

Table 4.

If patient volume status is considered adequate and his or her renal function permits, loop diuretics may be administered in the hope of inducing potassium loss. Early and aggressive correction of potassium is important to avoid deterioration to cardiac arrest.93 Moderate quality evidence (retrospective observation) supports treatment with IV calcium chloride during adult hyperkalemic cardiac arrest.103 The use of bicarbonate to enhance intracellular shift of potassium is controversial.103,104 Selection bias may underlie the association of both therapies with poor cardiopulmonary resuscitation (CPR) outcomes, since both drugs are more likely to be used in critically ill patients and after prolonged CPR.104 If hyperkalemia is considered reversible, bridging therapy with extracorporeal life support should be considered.105 Hemodialysis should be initiated as soon as possible after return of spontaneous circulation.106,107 There have been reports of successful outcome from hyperkalemic cardiac arrest with hemodialysis being initiated even during CPR.108–111 Given that vascular access is often easily available in the operating room, blood purification is a pertinent option should hyperkalemic cardiac arrest occur perioperatively. Table 4 provides a full list of management steps.

Back to Top | Article Outline

Traumatic Cardiac Arrest

Epidemiology and Pathophysiology.

Traumatic cardiac arrest (TCA) carries a high mortality rate, but in survivors, the neurological outcome appears to be much better than in other causes of cardiac arrest.112,113 Uncontrolled hemorrhage is the main cause of death (48%), followed by tension pneumothorax (13%), asphyxia (13%), and pericardial tamponade (10%).114 A large systematic review reported an overall survival rate of 3.3% in blunt and 3.7% in penetrating trauma, with good neurological outcome in 1.6% of all cases.112

Back to Top | Article Outline

Presentation and Initial Assessment.

Figure 1.

Figure 1.

Patients in TCA present with loss of consciousness, agonal or absent spontaneous respiration, and absence of a femoral or carotid pulse. The prearrest state is characterized by tachycardia, tachypnea, decreased pulse pressure, and a deteriorating conscious level. Hypotension may present late and beyond 1500 mL of blood loss. Beyond this stage (class III hemorrhagic shock), peripheral pulses will become absent, and the patient left untreated will typically proceed to pulseless electrical dissociation or asystolic cardiac arrest. Resuscitative efforts in TCA should focus on immediate assessment and simultaneous treatment of the hemorrhage and surgical control of the reversible causes (Figure 1).113,115

Back to Top | Article Outline

Initial Management Steps.

Short prehospital times are associated with increased survival rates for major trauma and TCA. The time elapsed between injury and surgical control of bleeding should be minimized. When feasible, the patient should be immediately transferred to a designated trauma center for damage control resuscitation (DCR).116 “Scoop and run” for these patients may be a better choice for survival than engaging on a long resuscitation on the field. While anesthesiologists in many international settings may be involved with prehospital care, being prepared to manage the airway and provide aggressive fluid resuscitation on patient arrival to the emergency room is also paramount. Successful treatment of TCA requires a team approach with all measures carried out rather in parallel than sequentially. The emphasis lies on rapid treatment of all potentially reversible pathology. In cardiac arrest caused by hypovolemia, cardiac tamponade, or tension pneumothorax, chest compressions alone are unlikely to be as effective as in normovolemic cardiac arrest.115,117–119 Therefore, chest compressions take a lower priority than the immediate treatment of reversible causes.

Ultrasonography should be used in the evaluation of the compromised trauma patient to target life-saving interventions if the cause of shock cannot be established clinically.116,120 Hemoperitoneum, hemothorax or pneumothorax, and cardiac tamponade can be diagnosed reliably in minutes. Early whole-body computed tomography scanning as part of the primary survey may improve outcome in major trauma.121 Whole-body computed tomography is increasingly employed to identify the source of shock and to guide subsequent hemorrhage control. Figure 1 shows the traumatic cardiac (peri-) arrest algorithm of the European Resuscitation Council, which is based on the universal ALS algorithm.122

Back to Top | Article Outline
Hypovolemia.

The treatment of severe hypovolemic shock has several elements. The main principle is to achieve immediate hemostasis. Temporary hemorrhage source control can be lifesaving. External hemorrhage can be treated with direct or indirect compression, pressure dressings, tourniquets, and topical hemostatic agents.116 Noncompressible hemorrhage is more difficult to control. External splints/pressure, blood and blood products, IV fluids, and tranexamic acid (TXA) can be used during patient transport and until hemorrhage is controlled surgically. Resuscitative endovascular balloon occlusion is a promising alternative to aortic cross-clamping or manual aortic compression in patients exsanguinating from noncompressible torso injuries and can serve as a bridge to definitive hemorrhage control.123,124 If the patient is in hypovolemic TCA, immediate restoration of the circulating blood volume with blood products is mandatory. Hyperventilation should be avoided in hypovolemic patients since positive-pressure ventilation may worsen hypotension by impeding venous return to the heart.125 Therefore, low tidal volumes and slow respiratory rates may be associated with a more acceptable circulation.

Back to Top | Article Outline
Hypoxemia.

Hypoxemia due to airway obstruction and loss of ventilator drive has been reported as the cause of 13% of all TCAs.114 Immediate control of the airway and effective invasive ventilation can reverse hypoxic cardiac arrest. However, positive-pressure ventilation should be applied with caution to limit its deleterious effect on venous return. Oxygen should be delivered at a fraction of 1.0, and ventilation should be monitored with capnography to avoid hyperventilation.116

Back to Top | Article Outline
Cardiac Tamponade and Resuscitative Thoracotomy.

Cardiac tamponade is the underlying cause of approximately 10% of cardiac arrests in trauma.114 Where there is TCA and penetrating trauma to the chest or epigastrium, immediate resuscitative thoracotomy (RT; via a clamshell incision) can be life saving.126,127 The chance of survival from cardiac injury is about 4 times higher for stab wounds than for a gunshot wounds.128 In 2012, an evidence review with resultant guidelines stated that RT should also be applied for 3 other categories of life-threatening injuries after arrival in hospital, which include blunt trauma with <10 minutes of prehospital CPR, penetrating torso trauma with <15 minutes of CPR, and penetrating trauma to the neck or extremity with <5 minutes of prehospital CPR.129 The guidelines estimate survival rates of approximately 15% for RT in patients with penetrating wounds and 35% for patients with a penetrating cardiac wound. In contrast, survival from RT after blunt trauma is dismal, with reported survival rates of 0%–2%.129,130 In the setting of the above presentation (ie, cardiac arrest with penetrating trauma), the prerequisites for a successful RT can be summarized as “4 Es rule” (4E):

  • (1) Expertise: RT teams must be led by a highly trained and competent health care practitioner.
  • (2) Equipment: adequate equipment to carry out RT and to deal with the intrathoracic findings is mandatory.
  • (3) Environment: ideally, RT should be carried out in an operating theatre; RT should not be carried out if there is inadequate physical access to the patient or if the receiving hospital is not easy to reach.
  • (4) Elapsed time: the time from loss of vital signs to commencing an RT should not be >10 minutes.

If any of the 4 criteria are not met, RT is likely less effective and exposes the team to unnecessary risks.131

Back to Top | Article Outline

Subsequent Management and Treatment.

Damage control resuscitation is a term recently adopted in trauma resuscitation to improve outcome of uncontrolled hemorrhages. DCR combines permissive hypotension and hemostatic resuscitation with limited (damage control) surgical repair. Limited evidence and general consensus (https://www.nice.org.uk/guidance/ta74) have supported a conservative approach to IV fluid infusion, with permissive hypotension until surgical hemostasis is achieved.132 In the absence of invasive monitoring, fluid resuscitation is titrated to maintain a radial pulse.133,134 Hemostatic resuscitation with blood and blood products is used as primary resuscitation fluids to prevent exsanguination, dilution of hemostatic blood components, and trauma-induced coagulopathy.135 The typical massive transfusion protocol recommends packed red blood cells, fresh frozen plasma, and platelets ratio of 1–2:1:1.136

Simultaneous damage control surgery and hemostatic resuscitation using massive transfusion protocol are the principles of DCR in patients with exsanguinating injuries.116,135 Although the evidence for permissive hypotension during resuscitation is limited, particularly with regards to blunt trauma, permissive hypotension has been endorsed in both civilian (https://www.nice.org.uk/guidance/ta74) and military care, generally aiming for an SBP of 80–90 mm Hg.137 Caution is advised for patients with traumatic brain injury in whom a raised intracranial pressure may require a higher cerebral perfusion pressure. Specifically, the most recent Brain Trauma Foundation Guidelines for severe traumatic brain injury recommend maintaining an SBP ≥100 mm Hg for patients 50–69 years of age or ≥110 mm Hg for patients 15–49 years of age or older than 70 to improve outcomes and reduce mortality.138

Finally, TXA (loading dose 1 g over 10 minutes followed by infusion of 1 g over 8 hours) increases survival from traumatic hemorrhage.139,140 It is effective when administered within the first 3 hours after trauma; however, TXA should not be started any later than 4 hours after the injury because late dosing is associated with increased mortality.

Back to Top | Article Outline

Pulmonary Embolism

Epidemiology and Pathophysiology.

Thromboembolism, venous gas embolism, and fat embolism are all well-recognized complications that can occur during anesthesia and surgery. Venous thromboembolism is the most common cause of PE in periprocedural patients. Prophylaxis reduces its incidence, but cannot entirely prevent its occurrence.141 Thromboembolism causes circulatory crisis via a combination of mechanical obstruction and the release of inflammatory mediators, both of which increase the right ventricular (RV) afterload.142 In severe cases, the associated increase in pulmonary vascular resistance is so great that the right ventricle is unable to maintain the cardiac output. As the RV fails, it typically dilates, and the interventricular septum flattens and shifts toward the left ventricle.

Back to Top | Article Outline

Presentation and Initial Assessment.

Signs of PE under general anesthesia include the following: unexplained hypotension with concurrent decrease in Etco2; desaturation that is only moderately responsive to increased Fio2; transitory bronchospasm with increased airway resistance; rapid changes of heart rhythm (often dysrhythmias or bradycardia after a transitory tachycardia); unexplained increased of central venous pressure or all pulmonary pressures; and rapid progression to nonshockable cardiac arrest (usually PEA).

Back to Top | Article Outline

Management Steps.

A strategy for managing RV shock in this situation is proposed in Figure 2. In approximately 5% of cases, acute thromboembolism causes cardiac arrest, most often PEA.143,144 Echocardiography of the patient with RV shock will typically reveal RV dilation and dysfunction, with an underfilled left ventricle.145

Figure 2.

Figure 2.

The management of intraoperative or perioperative thromboembolism is highly dependent on the procedure and patient. Therapeutic options range from supportive measures only to anticoagulation to thrombolysis.143,144,146,147

Back to Top | Article Outline

Epidemiology and Pathophysiology.

Gas embolism is an important cause of circulatory crisis and cardiac arrest in perioperative patients. As the number of procedures in which minimally invasive techniques involving gas insufflation increases, the frequency of intraoperative gas embolisms will likely increase.148 The risk for a venous air embolism increases when the surgical field is above the right atrium, particularly in patients with central venous pressure. The focus of hemodynamic support is on improving RV function.52

Common causes of gas embolism include laparoscopy, endobronchial laser procedures, central venous catheterization or catheter removal, hysteroscopy, pressurized wound irrigation, prone spinal surgery, posterior fossa surgery in the sitting position, and endoscopic retrograde cholangiopancreatography. Nonoperative cause of vascular air embolism includes direct vascular access procedures and pressurized hemoperfusion.

Back to Top | Article Outline

Management Steps.

Table 5.

Table 5.

All surgical procedures at risk of venous gas embolism should be specifically monitored. Right parasternal precordial Doppler ultrasound has very high sensitivity for air embolism (88%).149 Transesophageal echocardiography allows for recognition of air embolism size and location and assessment of ventricular function, but can be difficult or impossible to perform with some patient positions (eg, sitting) or procedures (eg, endoscopic retrograde cholangiopancreatography).150 Massive gas embolisms in awake patients have been characterized by breathlessness, continuous coughing, arrhythmias, myocardial ischemia, acute hypotension with loss of end-tidal carbon dioxide, and cardiac arrest. Patients who survive any kind of an embolic event are likely to require continued evaluation and management for several hours in an ICU setting. Table 5 provides a full list of management steps.

Back to Top | Article Outline

Postresuscitation Management

It is beyond the scope of this article to detail the appropriate steps of postresuscitation management. Current guidelines are available that specify the appropriate management steps to maximize discharge from the hospital with a favorable neurological function as most important outcome parameters. Neurological, cardiovascular, and respiratory dysfunction are best managed in specialized ICUs where monitoring of electroencephalogram, targeted temperature management, glucose management, correction of electrolytes, and management of blood gas parameters are all promptly available.151–153

Back to Top | Article Outline

CONCLUSIONS

The causes, logistics, and management of periprocedural crises and arrest differ substantially from those taught in the American Heart Association ACLS guidelines. Furthermore, current evidence illustrates the need for educational updates on concerning PPCA among the anesthesiology community, including review of current evidence, use of checklists, and simulation.11,154–157 The purpose of this review is to present the latest evidence and practical recommendations for managing 7 high-stakes perioperative events that can lead to significant circulatory disturbance and PPCA. These are core topics for all practitioners who care for patients in the periprocedural setting, but they by no means represent an exhaustive list of emergency conditions. It is incumbent upon all anesthesiologists to have a working knowledge of these clinical scenario and understanding of the current therapeutic options to maximize patient outcomes.

Back to Top | Article Outline

DISCLOSURES

Name: Matthew D. McEvoy, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: M. D. McEvoy received funding from GE Foundation, Edwards Life Sciences, and Cheetah Medical, all unrelated to this manuscript.

Name: Karl-Christian Thies, MD, FRCA, FERC, DEAA.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Sharon Einav, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Kurt Ruetzler, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Vivek K. Moitra, MD, FCCM.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: V. K. Moitra declares the following conflicts of interest: liaison between the American Society of Anesthesiologists and the American Heart Association; expert testimony.

Name: Mark E. Nunnally, MD, FCCM.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Arna Banerjee, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Guy Weinberg, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: G. Weinberg is an equity holder, a member of the board of directors, and received consulting fees from ResQ Pharma, Inc.

Name: Andrea Gabrielli, MD, FCCM.

Contribution: This author helped edit the final manuscript and approve the manuscript.

Conflicts of Interest: None.

Name: Gerald A. Maccioli, MD, FCCM.

Contribution: This author helped in the conception, and helped edit the final manuscript and approve the manuscript.

Conflicts of Interest: None.

Name: Gregory Dobson, MD.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

Name: Michael F. O’Connor, MD, FCCM.

Contribution: This author helped in the conception, and helped write the manuscript, edit the manuscript, and finally approve the manuscript.

Conflicts of Interest: None.

This manuscript was handled by: Avery Tung, MD, FCCM.

Back to Top | Article Outline

REFERENCES

1. Moitra VK, Gabrielli A, Maccioli GA, O’Connor MF. Anesthesia advanced circulatory life support. Can J Anaesth. 2012;59:586–603.
2. Chan PS, Krumholz HM, Nichol G, Nallamothu BK; American Heart Association National Registry of Cardiopulmonary Resuscitation Investigators. Delayed time to defibrillation after in-hospital cardiac arrest. N Engl J Med. 2008;358:9–17.
3. Koga FA, El Dib R, Wakasugui W, et al. Anesthesia-related and perioperative cardiac arrest in low- and high-income countries: a systematic review with meta-regression and proportional meta-analysis. Medicine (Baltimore). 2015;94:e1465.
4. Nunnally ME, O’Connor MF, Kordylewski H, Westlake B, Dutton RP. The incidence and risk factors for perioperative cardiac arrest observed in the national anesthesia clinical outcomes registry. Anesth Analg. 2015;120:364–370.
5. Siriphuwanun V, Punjasawadwong Y, Lapisatepun W, Charuluxananan S, Uerpairojkit K. Incidence of and factors associated with perioperative cardiac arrest within 24 hours of anesthesia for emergency surgery. Risk Manag Healthc Policy. 2014;7:155–162.
6. Xue FS, Li RP, Wang SY. Factors affecting survival and neurologic outcome of patient with perioperative cardiac arrest. Anesthesiology. 2014;121:201–202.
7. Harrison TK, Manser T, Howard SK, Gaba DM. Use of cognitive aids in a simulated anesthetic crisis. Anesth Analg. 2006;103:551–556.
8. Burden AR, Carr ZJ, Staman GW, Littman JJ, Torjman MC. Does every code need a “reader?” improvement of rare event management with a cognitive aid “reader” during a simulated emergency: a pilot study. Simul Healthc. 2012;7:1–9.
9. Arriaga AF, Bader AM, Wong JM, et al. Simulation-based trial of surgical-crisis checklists. N Engl J Med. 2013;368:246–253.
10. Murray DJ, Boulet JR, Kras JF, Woodhouse JA, Cox T, McAllister JD. Acute care skills in anesthesia practice: a simulation-based resident performance assessment. Anesthesiology. 2004;101:1084–1095.
11. Murray DJ, Boulet JR, Avidan M, et al. Performance of residents and anesthesiologists in a simulation-based skill assessment. Anesthesiology. 2007;107:705–713.
12. McIntosh CA. Lake Wobegon for anesthesia…where everyone is above average except those who aren’t: variability in the management of simulated intraoperative critical incidents. Anesth Analg. 2009;108:6–9.
13. Goldhaber-Fiebert SN, Lei V, Nandagopal K, Bereknyei S. Emergency manual implementation: can brief simulation-based or staff trainings increase familiarity and planned clinical use? Jt Comm J Qual Patient Saf. 2015;41:212–220.
14. Goldhaber-Fiebert SN, Howard SK. Implementing emergency manuals: can cognitive aids help translate best practices for patient care during acute events? Anesth Analg. 2013;117:1149–1161.
15. Available at: http://emergencymanual.stanford.edu/. Accessed August 16, 2017.
16. Available at: http://www.projectcheck.org/checklists.html. Accessed August 16, 2017.
17. Johansson SG, Bieber T, Dahl R, et al. Revised nomenclature for allergy for global use: report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. J Allergy Clin Immunol. 2004;113:832–836.
18. Neugut AI, Ghatak AT, Miller RL. Anaphylaxis in the United States: an investigation into its epidemiology. Arch Intern Med. 2001;161:15–21.
19. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S829–S861.
20. Fasting S, Gisvold SE. [Serious intraoperative problems—a five-year review of 83,844 anesthetics]. Can J Anaesth. 2002;49:545–553.
21. Mertes PM, Laxenaire MC. Allergy and anaphylaxis in anaesthesia. Minerva Anestesiol. 2004;70:285–291.
22. Saager L, Turan A, Egan C, et al. Incidence of intraoperative hypersensitivity reactions: a registry analysis: a registry analysis. Anesthesiology. 2015;122:551–559.
23. Soar J, Pumphrey R, Cant A, et al.; Working Group of the Resuscitation Council (UK). Emergency treatment of anaphylactic reactions—guidelines for healthcare providers. Resuscitation. 2008;77:157–169.
24. Raper RF, Fisher MM. Profound reversible myocardial depression after anaphylaxis. Lancet. 1988;1:386–388.
25. Nicolas F, Villers D, Blanloeil Y. Hemodynamic pattern in anaphylactic shock with cardiac arrest. Crit Care Med. 1984;12:144–145.
26. Simons FE, Sheikh A. Anaphylaxis: the acute episode and beyond. BMJ. 2013;346:f602.
27. Pumphrey RS. Lessons for management of anaphylaxis from a study of fatal reactions. Clin Exp Allergy. 2000;30:1144–1150.
28. Muraro A, Roberts G, Worm M, et al.; EAACI Food Allergy and Anaphylaxis Guidelines Group. Anaphylaxis: guidelines from the European Academy of Allergy and Clinical Immunology. Allergy. 2014;69:1026–1045.
29. Johnston SL, Unsworth J, Gompels MM. Adrenaline given outside the context of life threatening allergic reactions. BMJ. 2003;326:589–590.
30. Sheikh A, Shehata YA, Brown SG, Simons FE. Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock. Cochrane Database Syst Rev. 2008:CD006312.
31. Korenblat P, Lundie MJ, Dankner RE, Day JH. A retrospective study of epinephrine administration for anaphylaxis: how many doses are needed? Allergy Asthma Proc. 1999;20:383–386.
32. Yilmaz R, Yuksekbas O, Erkol Z, Bulut ER, Arslan MN. Postmortem findings after anaphylactic reactions to drugs in Turkey. Am J Forensic Med Pathol. 2009;30:346–349.
33. Yunginger JW, Sweeney KG, Sturner WQ, et al. Fatal food-induced anaphylaxis. JAMA. 1988;260:1450–1452.
34. Brown SG, Blackman KE, Stenlake V, Heddle RJ. Insect sting anaphylaxis; prospective evaluation of treatment with intravenous adrenaline and volume resuscitation. Emerg Med J. 2004;21:149–154.
35. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2012:CD000567.
36. Schummer C, Wirsing M, Schummer W. The pivotal role of vasopressin in refractory anaphylactic shock. Anesth Analg. 2008;107:620–624.
37. Williams SR, Denault AY, Pellerin M, Martineau R. Vasopressin for treatment of shock following aprotinin administration. Can J Anaesth. 2004;51:169–172.
38. Rocq N, Favier JC, Plancade D, Steiner T, Mertes PM. Successful use of terlipressin in post-cardiac arrest resuscitation after an epinephrine-resistant anaphylactic shock to suxamethonium. Anesthesiology. 2007;107:166–167.
39. Green R, Ball A. Alpha-agonists for the treatment of anaphylactic shock. Anaesthesia. 2005;60:621–622.
40. Thomas M, Crawford I. Best evidence topic report. Glucagon infusion in refractory anaphylactic shock in patients on beta-blockers. Emerg Med J. 2005;22:272–273.
41. Simons FE. Advances in H1-antihistamines. N Engl J Med. 2004;351:2203–2217.
42. Sheikh A, Ten Broek V, Brown SG, Simons FE. H1-antihistamines for the treatment of anaphylaxis: Cochrane systematic review. Allergy. 2007;62:830–837.
43. Lin RY, Curry A, Pesola GR, et al. Improved outcomes in patients with acute allergic syndromes who are treated with combined H1 and H2 antagonists. Ann Emerg Med. 2000;36:462–468.
44. Gibbs MW, Kuczkowski KM, Benumof JL. Complete recovery from prolonged cardio-pulmonary resuscitation following anaphylactic reaction to readministered intravenous cefazolin. Acta Anaesthesiol Scand. 2003;47:230–232.
45. Choo KJ, Simons E, Sheikh A. Glucocorticoids for the treatment of anaphylaxis: Cochrane systematic review. Allergy. 2010;65:1205–1211.
46. Tole JW, Lieberman P. Biphasic anaphylaxis: review of incidence, clinical predictors, and observation recommendations. Immunol Allergy Clin North Am. 2007;27:309–326, viii.
47. Roberts DJ, Leigh-Smith S, Faris PD, et al. Clinical presentation of patients with tension pneumothorax: a systematic review. Ann Surg. 2015;261:1068–1078.
48. Barton ED. Tension pneumothorax. Curr Opin Pulm Med. 1999;5:269–274.
49. Leigh-Smith S, Harris T. Tension pneumothorax—time for a re-think? Emerg Med J. 2005;22:8–16.
50. Phillips S, Falk GL. Surgical tension pneumothorax during laparoscopic repair of massive hiatus hernia: a different situation requiring different management. Anaesth Intensive Care. 2011;39:1120–1123.
51. Leigh-Smith S, Davies G. Tension pneumothorax: eyes may be more diagnostic than ears. Emerg Med J. 2003;20:495–496.
52. Roberts DJ, Niven DJ, James MT, Ball CG, Kirkpatrick AW. Thoracic ultrasonography versus chest radiography for detection of pneumothoraces: challenges in deriving and interpreting summary diagnostic accuracy estimates. Crit Care. 2014;18:416.
53. Kenny L, Teasdale R, Marsh M, McElnay P. Techniques of training in the management of tension pneumothorax: bridging the gap between confidence and competence. Ann Transl Med. 2016;4:233.
54. Weinberg G, Barron G. Local anesthetic systemic toxicity (LAST): not gone, hopefully not forgotten. Reg Anesth Pain Med. 2016;41:1–2.
55. Barrington MJ, Kluger R. Ultrasound guidance reduces the risk of local anesthetic systemic toxicity following peripheral nerve blockade. Reg Anesth Pain Med. 2013;38:289–299.
56. Di Gregorio G, Neal JM, Rosenquist RW, Weinberg GL. Clinical presentation of local anesthetic systemic toxicity: a review of published cases, 1979 to 2009. Reg Anesth Pain Med. 2010;35:181–187.
57. Vasques F, Behr AU, Weinberg G, Ori C, Di Gregorio G. A review of local anesthetic systemic toxicity cases since publication of the American Society of Regional Anesthesia recommendations: to whom it may concern. Reg Anesth Pain Med. 2015;40:698–705.
58. McCutchen T, Gerancher JC. Early intralipid therapy may have prevented bupivacaine-associated cardiac arrest. Reg Anesth Pain Med. 2008;33:178–180.
59. Dureau P, Charbit B, Nicolas N, Benhamou D, Mazoit JX. Effect of Intralipid® on the dose of ropivacaine or levobupivacaine tolerated by volunteers: a clinical and pharmacokinetic study. Anesthesiology. 2016;125:474–483.
60. Marwick PC, Levin AI, Coetzee AR. Recurrence of cardiotoxicity after lipid rescue from bupivacaine-induced cardiac arrest. Anesth Analg. 2009;108:1344–1346.
61. Fettiplace MR, Lis K, Ripper R, et al. Multi-modal contributions to detoxification of acute pharmacotoxicity by a triglyceride micro-emulsion. J Control Release. 2015;198:62–70.
62. Rahman S, Li J, Bopassa JC, et al. Phosphorylation of GSK-3β mediates intralipid-induced cardioprotection against ischemia/reperfusion injury. Anesthesiology. 2011;115:242–253.
63. Ording H. Incidence of malignant hyperthermia in Denmark. Anesth Analg. 1985;64:700–704.
64. Lu Z, Rosenberg H, Brady JE, Li G. Prevalence of malignant hyperthermia diagnosis in New York State Ambulatory Surgery Center discharge records 2002 to 2011. Anesth Analg. 2016;122:449–453.
65. Larach MG, Brandom BW, Allen GC, Gronert GA, Lehman EB. Cardiac arrests and deaths associated with malignant hyperthermia in North America from 1987 to 2006: a report from the North American malignant hyperthermia registry of the malignant hyperthermia association of the United States. Anesthesiology. 2008;108:603–611.
66. Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: something old, something new. Kidney Int. 2016;89:546–554.
67. Rossignol P, Legrand M, Kosiborod M, et al. Emergency management of severe hyperkalemia: guideline for best practice and opportunities for the future. Pharmacol Res. 2016;113:585–591.
68. Phillips BM, Milner S, Zouwail S, et al. Severe hyperkalaemia: demographics and outcome. Clin Kidney J. 2014;7:127–133.
69. Simmons DH, Avedon M. Acid-base alterations and plasma potassium concentration. Am J Physiol. 1959;197:319–326.
70. Pertersen BD, Jackson JA, Buckley JJ, Van Bergen FH. Influence of alterations in arterial blood pH and carbon dioxide tension on plasma potassium levels in humans anesthetized with nitrous oxide, thiopental and succinyldicholine. J Appl Physiol. 1957;11:93–96.
71. Acker CG, Johnson JP, Palevsky PM, Greenberg A. Hyperkalemia in hospitalized patients: causes, adequacy of treatment, and results of an attempt to improve physician compliance with published therapy guidelines. Arch Intern Med. 1998;158:917–924.
72. Rimmer JM, Horn JF, Gennari FJ. Hyperkalemia as a complication of drug therapy. Arch Intern Med. 1987;147:867–869.
73. Ramamoorthy C, Haberkern CM, Bhananker SM, et al. Anesthesia-related cardiac arrest in children with heart disease: data from the Pediatric Perioperative Cardiac Arrest (POCA) registry. Anesth Analg. 2010;110:1376–1382.
74. Bhananker SM, Ramamoorthy C, Geiduschek JM, et al. Anesthesia-related cardiac arrest in children: update from the Pediatric Perioperative Cardiac Arrest Registry. Anesth Analg. 2007;105:344–350.
75. Morray JP, Geiduschek JM, Ramamoorthy C, et al. Anesthesia-related cardiac arrest in children: initial findings of the Pediatric Perioperative Cardiac Arrest (POCA) Registry. Anesthesiology. 2000;93:6–14.
76. Chon SB, Kwak YH, Hwang SS, Oh WS, Bae JH. Severe hyperkalemia can be detected immediately by quantitative electrocardiography and clinical history in patients with symptomatic or extreme bradycardia: a retrospective cross-sectional study. J Crit Care. 2013;28:1112.e7–1112.e13.
77. Browning JJ, Channer KS. Hyperkalaemic cardiac arrhythmia caused by potassium citrate mixture. Br Med J (Clin Res Ed). 1981;283:1366.
78. Oh PC, Koh KK, Kim JH, Park H, Kim SJ. Life threatening severe hyperkalemia presenting typical electrocardiographic changes—rapid recovery following medical, temporary pacing, and hemodialysis treatments. Int J Cardiol. 2014;177:27–29.
79. Slade TJ, Grover J, Benger J. Atropine-resistant bradycardia due to hyperkalaemia. Emerg Med J. 2008;25:611–612.
80. Sohoni A, Perez B, Singh A. Wenckebach block due to hyperkalemia: a case report. Emerg Med Int. 2010;2010:879751.
81. Kim NH, Oh SK, Jeong JW. Hyperkalaemia induced complete atrioventricular block with a narrow QRS complex. Heart. 2005;91:e5.
82. Tiberti G, Bana G, Bossi M. Complete atrioventricular block with unwidened QRS complex during hyperkalemia. Pacing Clin Electrophysiol. 1998;21:1480–1482.
83. Maeda H, Uramatsu M, Nakajima S, Yoshida KI. Lethal ventricular tachycardia triggered after femoral fracture repair in an obese man with insulin-resistant diabetes. Int J Legal Med. 2016;130:1587–1591.
84. Yin Y, Zhu T. Ventricular fibrillation during anesthesia in a Wenchuan earthquake victim with crush syndrome. Anesth Analg. 2010;110:916–917.
85. Woodforth IJ. Resuscitation from transfusion-associated hyperkalaemic ventricular fibrillation. Anaesth Intensive Care. 2007;35:110–113.
86. Chakravarty EF, Kirsch CM, Jensen WA, Kagawa FT. Cardiac arrest due to succinylcholine-induced hyperkalemia in a patient with wound botulism. J Clin Anesth. 2000;12:80–82.
87. Khattak HK, Khalid S, Manzoor K, Stein PK. Recurrent life-threatening hyperkalemia without typical electrocardiographic changes. J Electrocardiol. 2014;47:95–97.
88. Cobo Sánchez JL, Alconero Camarero AR, Casaus Pérez M, et al. Hyperkalaemia and haemodialysis patients: eletrocardiographic changes. J Ren Care. 2007;33:124–129.
89. Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant. 2002;17:1639–1642.
90. Freeman SJ, Fale AD. Muscular paralysis and ventilatory failure caused by hyperkalaemia. Br J Anaesth. 1993;70:226–227.
91. Jayawardena S, Burzyantseva O, Shetty S, Niranjan S, Khanna A. Hyperkalaemic paralysis presenting as ST-elevation myocardial infarction: a case report. Cases J. 2008;1:232.
92. Evers S, Engelien A, Karsch V, Hund M. Secondary hyperkalaemic paralysis. J Neurol Neurosurg Psychiatry. 1998;64:249–252.
93. An JN, Lee JP, Jeon HJ, et al. Severe hyperkalemia requiring hospitalization: predictors of mortality. Crit Care. 2012;16:R225.
94. Blanié A, Ract C, Leblanc PE, et al. The limits of succinylcholine for critically ill patients. Anesth Analg. 2012;115:873–879.
95. Piotrowski AJ, Fendler WM. Hyperkalemia and cardiac arrest following succinylcholine administration in a 16-year-old boy with acute nonlymphoblastic leukemia and sepsis. Pediatr Crit Care Med. 2007;8:183–185.
96. Mali AR, Patil VP, Pramesh CS, Mistry RC. Hyperkalemia during surgery: is it an early warning of propofol infusion syndrome? J Anesth. 2009;23:421–423.
97. Lee JH, Ko YS, Shin HJ, Yi JH, Han SW, Kim HJ. Is there a relationship between hyperkalemia and propofol? Electrolyte Blood Press. 2011;9:27–31.
98. DeFronzo RA, Felig P, Ferrannini E, Wahren J. Effect of graded doses of insulin on splanchnic and peripheral potassium metabolism in man. Am J Physiol. 1980;238:E421–E427.
99. Kaminer B, Bernstein RE. The electrocardiographic and plasma potassium changes after adrenalin and insulin injections. S Afr J Med Sci. 1952;17:35.
100. Clausen T, Kohn PG. The effect of insulin on the transport of sodium and potassium in rat soleus muscle. J Physiol. 1977;265:19–42.
101. Clausen T, Flatman JA. The effect of catecholamines on Na-K transport and membrane potential in rat soleus muscle. J Physiol. 1977;270:383–414.
102. Mahoney BA, Smith WA, Lo DS, Tsoi K, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005:CD003235.
103. Wang CH, Huang CH, Chang WT, et al. The effects of calcium and sodium bicarbonate on severe hyperkalaemia during cardiopulmonary resuscitation: a retrospective cohort study of adult in-hospital cardiac arrest. Resuscitation. 2016;98:105–111.
104. Raymond TT, Stromberg D, Stigall W, Burton G, Zaritsky A; American Heart Association’s Get With the Guidelines-Resuscitation Investigators. Sodium bicarbonate use during in-hospital pediatric pulseless cardiac arrest—a report from the American Heart Association Get With The Guidelines(®)-Resuscitation. Resuscitation. 2015;89:106–113.
105. Chiu CC, Yen HH, Chen YL, Siao FY. Severe hyperkalemia with refractory ventricular fibrillation: successful resuscitation using extracorporeal membrane oxygenation. Am J Emerg Med. 2014;32:943.e5–943.e6.
106. Ncomanzi D, Sicat RM, Sundararajan K. Metformin-associated lactic acidosis presenting as an ischemic gut in a patient who then survived a cardiac arrest: a case report. J Med Case Rep. 2014;8:159.
107. Tay S, Lee IL. Survival after cardiopulmonary arrest with extreme hyperkalaemia and hypothermia in a patient with metformin-associated lactic acidosis. BMJ Case Rep. 2012;:piibcr2012007804.
108. Costa P, Visetti E, Canavese C. Double simultaneous hemodialysis during prolonged cardio-pulmonary resuscitation for hyperkalemic cardiac arrest. Case report. Minerva Anestesiol. 1994;60:143–144.
109. Lin JL, Huang CC. Successful initiation of hemodialysis during cardiopulmonary resuscitation due to lethal hyperkalemia. Crit Care Med. 1990;18:342–343.
110. Lin JL, Lim PS, Leu ML, Huang CC. Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis. Intensive Care Med. 1994;20:287–290.
111. Torrecilla C, de la Serna JL. Hyperkalemic cardiac arrest, prolonged heart massage and simultaneous hemodialysis. Intensive Care Med. 1989;15:325–326.
112. Zwingmann J, Mehlhorn AT, Hammer T, Bayer J, Südkamp NP, Strohm PC. Survival and neurologic outcome after traumatic out-of-hospital cardiopulmonary arrest in a pediatric and adult population: a systematic review. Crit Care. 2012;16:R117.
113. Leis CC, Hernández CC, Blanco MJ, Paterna PC, Hernández Rde E, Torres EC. Traumatic cardiac arrest: should advanced life support be initiated? J Trauma Acute Care Surg. 2013;74:634–638.
114. Kleber C, Giesecke MT, Lindner T, Haas NP, Buschmann CT. Requirement for a structured algorithm in cardiac arrest following major trauma: epidemiology, management errors, and preventability of traumatic deaths in Berlin. Resuscitation. 2014;85:405–410.
115. Willis CD, Cameron PA, Bernard SA, Fitzgerald M. Cardiopulmonary resuscitation after traumatic cardiac arrest is not always futile. Injury. 2006;37:448–454.
116. Spahn DR, Bouillon B, Cerny V, et al. Management of bleeding and coagulopathy following major trauma: an updated European guideline. Crit Care. 2013;17:R76.
117. Lockey D, Crewdson K, Davies G. Traumatic cardiac arrest: who are the survivors? Ann Emerg Med. 2006;48:240–244.
118. Luna GK, Pavlin EG, Kirkman T, Copass MK, Rice CL. Hemodynamic effects of external cardiac massage in trauma shock. J Trauma. 1989;29:1430–1433.
119. Crewdson K, Lockey D, Davies G. Outcome from paediatric cardiac arrest associated with trauma. Resuscitation. 2007;75:29–34.
120. Ferrada P, Evans D, Wolfe L, et al. Findings of a randomized controlled trial using limited transthoracic echocardiogram (LTTE) as a hemodynamic monitoring tool in the trauma bay. J Trauma Acute Care Surg. 2014;76:31–37.
121. Huber-Wagner S, Lefering R, Qvick LM, et al.; Working Group on Polytrauma of the German Trauma Society. Effect of whole-body CT during trauma resuscitation on survival: a retrospective, multicentre study. Lancet. 2009;373:1455–1461.
122. Truhlář A, Deakin CD, Soar J, et al.; Cardiac Arrest in Special Circumstances Section Collaborators. European Resuscitation Council Guidelines for Resuscitation 2015: Section 4. Cardiac arrest in special circumstances. Resuscitation. 2015;95:148–201.
123. Manzano Nunez R, Naranjo MP, Foianini E, et al. A meta-analysis of resuscitative endovascular balloon occlusion of the aorta (REBOA) or open aortic cross-clamping by resuscitative thoracotomy in non-compressible torso hemorrhage patients. World J Emerg Surg. 2017;12:30.
124. Sridhar S, Gumbert SD, Stephens C, Moore LJ, Pivalizza EG. Resuscitative endovascular balloon occlusion of the aorta: principles, initial clinical experience, and considerations for the anesthesiologist. Anesth Analg. 2017;125:884–890.
125. Pepe PE, Roppolo LP, Fowler RL. The detrimental effects of ventilation during low-blood-flow states. Curr Opin Crit Care. 2005;11:212–218.
126. Wise D, Davies G, Coats T, Lockey D, Hyde J, Good A. Emergency thoracotomy: “how to do it”. Emerg Med J. 2005;22:22–24.
127. Flaris AN, Simms ER, Prat N, Reynard F, Caillot JL, Voiglio EJ. Clamshell incision versus left anterolateral thoracotomy. Which one is faster when performing a resuscitative thoracotomy? The tortoise and the hare revisited. World J Surg. 2015;39:1306–1311.
128. Arreola-Risa C, Rhee P, Boyle EM, Maier RV, Jurkovich GG, Foy HM. Factors influencing outcome in stab wounds of the heart. Am J Surg. 1995;169:553–556.
129. Burlew CC, Moore EE, Moore FA, et al. Western Trauma Association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012;73:1359–1363.
130. Tamura M, Oda M, Matsumoto I, Fujimori H, Shimizu Y, Watanabe G. Double-barrel reconstruction for complex bronchial disruption due to blunt thoracic trauma. Ann Thorac Surg. 2009;88:2008–2010.
131. Seamon MJ, Chovanes J, Fox N, et al. The use of emergency department thoracotomy for traumatic cardiopulmonary arrest. Injury. 2012;43:1355–1361.
132. Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994;331:1105–1109.
133. Harris T, Thomas GO, Brohi K. Early fluid resuscitation in severe trauma. BMJ. 2012;345:e5752.
134. Harris T, Davenport R, Hurst T, Jones J. Improving outcome in severe trauma: trauma systems and initial management: intubation, ventilation and resuscitation. Postgrad Med J. 2012;88:588–594.
135. Jansen JO, Thomas R, Loudon MA, Brooks A. Damage control resuscitation for patients with major trauma. BMJ. 2009;338:b1778.
136. Holcomb JB, Tilley BC, Baraniuk S, et al.; PROPPR Study Group. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313:471–482.
137. Eastridge BJ, Salinas J, McManus JG, et al. Hypotension begins at 110 mm Hg: redefining “hypotension” with data. J Trauma. 2007;63:291–297.
138. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80:6–15.
139. Crash-2 Collaborators IBS. Effect of tranexamic acid in traumatic brain injury: a nested randomised, placebo controlled trial (CRASH-2 Intracranial Bleeding Study). BMJ. 2011;343:d3795.
140. Roberts I, Shakur H, Afolabi A, et al.; CRASH-2 Collaborators. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial. Lancet. 2011;377:1096–1101, 1101.e1.
141. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999;353:1386–1389.
142. Tapson VF. Acute pulmonary embolism. N Engl J Med. 2008;358:1037–1052.
143. Comess KA, DeRook FA, Russell ML, Tognazzi-Evans TA, Beach KW. The incidence of pulmonary embolism in unexplained sudden cardiac arrest with pulseless electrical activity. Am J Med. 2000;109:351–356.
144. Lavonas EJ, Drennan IR, Gabrielli A, et al. Part 10: special circumstances of resuscitation: 2015 American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132:S501–S518.
145. Price S, Uddin S, Quinn T. Echocardiography in cardiac arrest. Curr Opin Crit Care. 2010;16:211–215.
146. Abu-Laban RB, Christenson JM, Innes GD, et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346:1522–1528.
147. Böttiger BW, Arntz HR, Chamberlain DA, et al.; TROICA Trial Investigators; European Resuscitation Council Study Group. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359:2651–2662.
148. Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164–177.
149. Schubert A, Deogaonkar A, Drummond JC. Precordial Doppler probe placement for optimal detection of venous air embolism during craniotomy. Anesth Analg. 2006;102:1543–1547.
150. Pandia MP, Bithal PK, Dash HH, Chaturvedi A. Comparative incidence of cardiovascular changes during venous air embolism as detected by transesophageal echocardiography alone or in combination with end tidal carbon dioxide tension monitoring. J Clin Neurosci. 2011;18:1206–1209.
151. Nolan JP, Soar J, Cariou A, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines for Post-resuscitation Care 2015: section 5 of the European Resuscitation Council Guidelines for Resuscitation 2015. Resuscitation. 2015;95:202–222.
152. Girotra S, Chan PS, Bradley SM. Post-resuscitation care following out-of-hospital and in-hospital cardiac arrest. Heart. 2015;101:1943–1949.
153. Callaway CW, Donnino MW, Fink EL, et al. Part 8: post-cardiac arrest care: 2015 American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132:S465–S482.
154. Weinger MB, Banerjee A, Burden AR, et al. Simulation-based assessment of the management of critical events by board-certified anesthesiologists. Anesthesiology. 2017;127:475–489.
155. Murray DJ, Freeman BD, Boulet JR, Woodhouse J, Fehr JJ, Klingensmith ME. Decision making in trauma settings: simulation to improve diagnostic skills. Simul Healthc. 2015;10:139–145.
156. Henrichs BM, Avidan MS, Murray DJ, et al. Performance of certified registered nurse anesthetists and anesthesiologists in a simulation-based skills assessment. Anesth Analg. 2009;108:255–262.
157. Murray D. Clinical skills in acute care: a role for simulation training. Crit Care Med. 2006;34:252–253.
Copyright © 2017 International Anesthesia Research Society