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

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

Disclosures

Anesth Analg. 2018;126(3):889-903.

Abstract and Introduction

Abstract

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.

Introduction

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.

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Abstract and Introduction
Methods
Conclusions
References

Table 1. Assessment and Management of Severe Anaphylaxis
Assessment	Confusion, altered mental status/presyncope Rash and/or rhinitis Perioral/periorbital edema, laryngeal edema, stridor Bronchospasm/dyspnea (not always present) Tachycardia Acute onset hypotension
Initial management	Prearrest Stop or remove the inciting agent or drug (eg, NMBD, antibiotics, blood products, IV contrast, or latex) If feasible, stop surgery or procedure Oxygen at Fio₂ of 1.0; intubate immediately for respiratory distress Watch for auto-PEEP if severe bronchospasm 100–300 μg epinephrine in repeated/escalating doses (or 300–500 μg IM if no IV access present) ±Vasopressin 2 U IV Start epinephrine infusion#8232;(0.05–0.3 μg/kg/min IV) for a goal SBP >90 mm Hg; observe for myocardial ischemia Vasopressin or norepinephrine infusions may be added in patients who are hypotensive in spite of high doses of epinephrine (eg, >2 mg IV) IV fluids/large bore access—initial treatment is bolus of 20 mL/kg IV of LR or PLA H1 blocker (50 mg diphenhydramine IV) H2 blocker (20 mg famotidine IV) ±Corticosteroid (eg, 50–150 mg hydrocortisone IV or methylprednisolone 1–2 mg/kg IV) Continuous arterial blood pressure monitoring as early as possible (systolic blood pressure ≥90 mm Hg)
Initial management	Arrest CPR if no carotid pulse detected for 10 s 100–1000 μg epinephrine IV, can repeat every 3–5 min or replace with 1 dose 40 U vasopressin IV If auto-PEEP suspected, disconnect the ventilator briefly Administer adjunctive therapies listed in prearrest (H1 and H2 blockers and corticosteroids) Consider extracorporeal life support in patients getting good CPR without ROSC
Subsequent management	Send blood for tryptase level to support the diagnosis Monitor in ICU for at least 24 h as there is a risk of recrudescence

Abbreviations: CPR, cardiopulmonary resuscitation; Fio2, fraction of inspired oxygen concentration; ICU, intensive care unit; IM, intramuscular; IV, intravenous; LR, lactated
ringers; NMBD, neuromuscular blocking drug; PEEP, positive end-expiratory pressure; PLA, plasmalyte-A; ROSC, return of spontaneous circulation; SBP, systolic blood pressure.

Table 2. Assessment and Management of Local Anesthetic Systemic Toxicity
Assessment	Seizures, agitation, obtundation Tachycardia Bradycardia or new heart block All in setting of local anesthetic administration
Initial management	Prearrest Stop the administration of local anesthetic Immediate tracheal intubation and ventilation with 100% oxygen Consider transcutaneous or intravenous pacemakers for all symptomatic bradycardic rhythms with pulse If the diagnosis of local anesthetic toxicity is strongly suspected, the use of epinephrine should be avoided as it can worsen outcome 20% lipid emulsion 1.5 mL/kg IV load, then 0.25 mL/kg/min (~20 mL/min) If still with hemodynamic instability, a second bolus followed by a doubling of the rate of infusion is appropriate (0.5 mL/kg/min) Seizures should be treated with benzodiazepines. Small doses of propofol or thiopental may be used if benzodiazepines are not immediately available
Initial management	Cardiac arrest Immediate CPR as indicated (no carotid pulse, ECG, arterial catheter, and pulse oximeter signal) If the diagnosis of local anesthetic toxicity is strongly suspected, small doses of 10–100 μg epinephrine IV are preferable to higher doses Vasopressin is not recommended Sodium bicarbonate to maintain a pH >7.25 in patients without immediate ROSC after CPR and drug therapy If ROSC does not occur after the first bolus of lipid emulsion, a second bolus followed by a doubling of the rate of infusion is appropriate Consider therapy with H1 and H2 blockers Amiodarone is the drug of choice for ventricular arrhythmias Lidocaine should be avoided Most important, continue CPR for a prolonged period (we suggest at least 60 min) as very good neurological recovery has been reported in patients after very prolonged cardiac arrests from local anesthetic overdoses Extracorporeal life support is appropriate in circumstances where the diagnosis is certain, where ECMO is available in a timely fashion, and where there is no ROSC after a second bolus of lipid emulsion
Subsequent management	Monitor for recurrence or delayed progression

Abbreviations: CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ECMO, extracorporeal membrane oxygenation; IV, intravenous; ROSC, return of spontaneous circulation.

Table 3. Assessment and Management of Malignant Hyperthermia
Assessment	Hypercapnia Tachycardia Tachypnea in nonparalyzed patients Muscle rigidity/masseter spasm Hyperthermia
Initial management	Discontinue triggering volatile anesthetics and switch from the anesthesia ventilator to manual Ambu bag ventilation from a separate source of oxygen. If available, switch to a dedicated clean anesthesia ventilator or transport or ICU ventilator when feasible. Continue Etco₂ monitoring Stop surgery or procedure when feasible If necessary, switch to intravenous anesthetic Sodium dantrolene: give 2.5 mg/kg or 1 mg/lb initial dose. Repeat bolus of Na dantrolene, titrating to tachycardia and hypercarbia (10 mg/kg suggested upper limit, but more may be given as needed, up to 30 mg/kg) Begin active cooling: ice packs to groin, axilla, and neck; cold intravenous solutions into the peritoneal cavity when feasible; nasogastric or peritoneal lavage when feasible Stop cooling measures at 38°C to avoid overshooting If hyperkalemia suspected by peaked ECG T waves or intraventricular conduction delay confirmed by high K serum level: 10 mg/kg calcium chloride, 0.1 U/kg insulin, 50 mL D50w for adult or 1 mL/kg for pediatrics. Repeat as necessary Metabolic acidosis: 100 mEq of HCO3− in adults, then titrate to pH 7.2. Normalize pH if confirmed rhabdomyolysis (suggested threshold, 10,000 IU/L CPK)#8232; Respiratory acidosis: treatment is controversial due to adverse hemodynamic effects of hyperventilation if low-flow state is confirmed. (We suggest an initial goal of modest permissive hypercarbia with a goal Etco2 of 50–60 mm Hg) Dysrhythmias: avoid calcium antagonists after Na dantrolene, potential for worsening hyperkalemia Myoglobinuria with oliguria: place Foley catheter; increase rate of fluid resuscitation Invasive pressure monitoring when feasible, more HCO3− to neutralize urine pH, consider intravenous mannitol Supportive measures for disseminated intravascular coagulation Call for help, including the MH hotline, if feasible (www.mhaus.org), call 1–800-644-9737 or 1–800-MH-HYPER in the United States and Canada; outside the United States, call 00113144647079
Subsequent management	Monitor for recrudescence for 72 h and treat/cool as required When the crisis is resolved: consider caffeine–halothane muscle biopsy in vitro contracture test, molecular genetic testing for genetic mutation analysis for patient's relatives (sensitivity 25%)

Adapted from https://www.mhaus.org/.
Abbreviations: CPK, creatine phosphokinase; D50w, dextrose in water (50%); ECG, electrocardiogram; Etco2, end-tidal carbon dioxide; ICU, intensive care unit;
K, potassium; MH, malignant hyperthermia.

Table 4. Assessment and Management of Severe Hyperkalemia
Assessment	Vertigo Chest pain Syncope Bradycardia Diminished p-waves on ECG Peaked T-waves on ECG Wide complex QRS on ECG Heart block on ECG Ventricular tachycardia Ventricular fibrillation
Initial management	Cardiac protection Administer calcium chloride or calcium gluconate 1–2 g IV. Repeat as required for ECG signs of hyperkalemia
	Interventions to drive potassium into intracellular space (these are temporizing interventions) Administer 1 ampule of D50 and 10 units of insulin IV Administer 50 mEq of sodium bicarbonate Administer 4–10 puffs albuterol
	Interventions to eliminate potassium or increase corporeal capacity Administer 20–40 mg furosemide IV, monitor urine output in response. Increase to 1–1.5 mg/kg if oliguric response Administer 30 or 60 g of kayexalate OG/NG/PR. Repeat as needed Initiate renal replacement therapy Transfuse washed pRBC (these units are hypokalemic and will avidly absorb serum potassium) In patients with hyperkalemic cardiac arrest, extracorporeal life support is appropriate while the cause of hyperkalemia is being treated and the patient is undergoing treatment to definitively lower their serum potassium
Subsequent management	Monitor serum potassium serially, continue to treat cause(s) of hyperkalemia

Abbreviations: ECG, electrocardiogram; IV, intravenous; OG, orogastric; NG, nasogastric; PR, per rectum; pRBC, packed red blood cell.

Table 5. Assessment and Management of Massive or Submassive Pulmonary Embolism
Assessment	Significant hemodynamic instability or collapse during cases with high risk of thrombotic or air embolus Etco₂ that suddenly declines Increased airway pressures Consider early use of TEE to confirm diagnosis/rule out other treatable causes of pulmonary embolism
Initial management	Prearrest If possible, stop the infusion of the gas or ask the surgeon to flood the surgical field Administer 100% oxygen and intubate for significant respiratory distress or refractory hypoxemia Place patient in Trendelenburg (head down) position and rotate toward the left lateral decubitus position Maintain BP with fluid resuscitation and vasopressors/β-adrenergic agents if necessary. (See the algorithm for RV failure) Consider transfer to a hyperbaric chamber if immediately available
	Cardiac arrest Circulatory collapse should be addressed with CPR and consideration of CPB/emergent thrombectomy if available
Subsequent management	Consider the right ventricular shock algorithm

Abbreviations: BP, blood pressure; CPB, cardiopulmonary bypass; RV, right ventricular; CPR, cardiopulmonary resuscitation; TEE, transesophageal echocardiography.

Authors and Disclosures

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

*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 and ^‖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; and ^‖‖Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois.

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

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.