Malignant Arrhythmia and Cardiac Arrest in the Operating Room 

Updated: Aug 23, 2017
  • Author: Balazs Horvath, MD; Chief Editor: Sheela Pai Cole, MD  more...
  • Print

Practice Essentials

Key points in the management of malignant arrhythmia (MA) and cardiac arrest in the operating room (OR) include the following:

  • MAs are arrhythmias, primarily ventricular, that result in cardiovascular collapse
  • Ventricular tachycardia (VT), ventricular fibrillation (VF), and torsades de pointes are considered MAs
  • A thorough patient history and a careful review of pertinent diagnostic findings are extremely helpful for both prevention and early recognition of MAs
  • Up-to-date knowledge and utilization of advanced cardiac life support (ACLS)/pediatric advanced life support (PALS) guidelines are required to successfully manage these crisis situations in the OR
  • It is always necessary to consider the influence of a specific surgical procedure or anesthetic technique on cardiac physiology and preexisting pathophysiology
  • Effective communication among the OR team members, including preoperative briefing and clearly defining roles and responsibilities in a crisis situation, is essential
  • It is recommended to conduct cardiopulmonary resuscitation (CPR) drills and simulation with the participation of all OR personnel on a regular basis


Intraoperative events, both surgical and anesthetic, induce several profound homeostatic changes that have diverse manifestations in different organs, including the heart. These changes are further augmented by the preexisting conditions and comorbidities of the patient. Cardiac dysrhythmias can be induced by various triggers. The majority of such arrhythmias have no immediate hemodynamic consequences; they require no emergency treatment, they respond well to pharmacologic interventions, or both.

However, especially in the presence of congenital or acquired structural or conduction abnormalities, a subset of dysrhythmias (ie, sustained VT and VF) may pose an immediate threat to life by causing profound hemodynamic instability. Accordingly, these cardiac rhythm disturbances are labeled as MAs. MAs may be manifested either in hemodynamic collapse or in cardiac arrest: The sudden loss of effective blood flow due to atrial fibrillation (AF) with rapid VT leads to hemodynamic collapse, and VT and VF result in cardiac arrest necessitating CPR or electric defibrillation. [1]

In the general population, about 5% of the arrhythmias are serious, life-threatening MAs. [1] The exact incidence of MA in the general surgical population is not clearly defined. The most common conditions that have the potential to either induce or promote the development of these dysrhythmias are age, myocardial disease, structural cardiac anomaly, Wolff-Parkinson-White (WPW) syndrome, [2] long QT syndrome, [3]  and Brugada syndrome [4]  (see Table 1 below).

Table 1. Structural and Inherited Conditions That Can Cause Malignant Arrhythmias (Open Table in a new window)

Preexisting Condition Mechanism Possible Preoperative Circulatory Signs/Symptoms ECG Changes
Cardiac disease (CAD, CMP, LVEF <40%, myocarditis) Reentry due to scar excitability AsymptomaticChest pain, SOB/DOE, palpitations ST-T changes

Q Waves


AV block

Bundle-branch block
Wolff-Parkinson-White syndrome Presence of one or more accessory pathways Asymptomatic

Paroxysmal SVT, AF; may result in VT/VF and SCD

Shortened PR interval (<120 ms)

Delta wave

Widened QRS complex (>0.12 s)

ST segment–T wave changes reflecting altered depolarization

Long QT syndrome, congenital Congenital mutation of myocardial K+ or Na+ channels Asymptomatic

Palpitations, excessive bradycardia for age, syncope, cardiac arrest

QTc >460 ms (female) or >440 ms (male)

Biphasic or notched T waves 

Long QTc, acquired Drug induced dysfunction of myocardial K+ and Na+ channels Asymptomatic

Palpitations, bradycardia

QTc >460 ms (female) or >440 ms (male)

Biphasic or notched T waves

Brugada syndrome Mutation affecting myocardial Na+ channel function AsymptomaticPalpitations ST elevation of coved type in leads V1-V3 
AV = atrioventricular; CAD = coronary artery disease; CMP = cardiomyopathy; DOE = dyspnea on exertion; ECG = electrocardiography; LVEF = left ventricular ejection fraction; PVC = premature ventricular contraction; QTc = corrected QT interval; SOB = shortness of breath; VF = ventricular fibrillation; VT = ventricular tachycardia.

Other factors to consider that are more specific to the perioperative period are the type of surgery performed and certain intraoperative events. Perioperative administration of arrhythmogenic medications, including anesthetic agents, must be taken into consideration, especially those that prolong the QT interval (eg, ondansetron, methadone, and sevoflurane). [5] References are available that list medications to avoid with long QT syndrome and Brugada syndrome. [6]

Although MAs are usually related to the well-known etiologies above, there are rare scenarios in which the onset of these dysrhythmias either is related to a previously unknown or new treatable medical condition or is induced by toxicity (eg, a systemic local anesthetic effect) or hyperkalemia (see Table 2 below). In these scenarios, the underlying pathology must be addressed if antiarrhythmic therapies are to succeed. [7]

Table 2. Correctable and Preventable Conditions That May Destabilize Preexisting Proarrhythmogenic Disease or Induce Malignant Arrhythmias Independently During Surgery (Open Table in a new window)

Pathology Early ECG Changes Acute Management
Hypokalemia QT prolongation

ST depression

Short T waves, U wave
Begin K+ replacement, switch to K+ sparing diureticsMagnesium replacement for concomitant hypomagnesemia 
Hyperkalemia Tall peaked T waves

QT shortening

Progressive PR lengthening and QRS widening
IV calcium, dextrose/insulin, beta-adrenergic agonists
Hypomagnesemia Widened QRS complex IV magnesium sulfate
Hypocalcemia QT prolongation IV calcium
Hypercalcemia QT shortening Volume expansion with 0.9% NaClLow-dose loop diuretic
Hypothermia Bradycardia

Osborne (“J”) waves

PT/QT prolongation

QRS widening
Slow, controlled warmingPossible need for CPB
Hyperthermia Nonspecific CoolingIV dantrolene if induced by malignant hyperthermia
Acidosis Nonspecific Verify type of acidosis (respiratory vs metabolic vs mixed)

Manage primary cause

Sodium bicarbonate vs THAM (not available in US)
Hypoxemia Nonspecific Improve oxygenation
Hypocarbia/hypercarbia Nonspecific Optimize ventilation
Pulmonary embolism Nonspecific

P pulmonale

Right-heart catheterization and lysis of thrombusSystemic anticoagulation
Tension pneumothorax Nonspecific Percutaneous release of intrathoracic free air
Pericardial tamponade Nonspecific

Low-voltage PR depression

Direct contact with cardiac structures during procedures Nonspecific


Warn surgeonDiscontinue direct stimulation
Propofol – infusion > single bolus Brugada-type ST changes V1-V3T wave reversal Discontinue
Halogenated inhalation anesthetics QT prolongation Discontinue
Midazolam QT prolongation Discontinue
Fentanyl, sufentanil QT prolongation Discontinue
Dexmedetomidine QT prolongation

Depression of SA and AV nodal function

Bupivacaine QT prolongation IV lipid 20%
AV = atrioventricular; CPB = cardiopulmonary bypass; ECG = electrocardiography; MH = malignant hyperthermia; PAC = premature atrial contraction; PVC = premature ventricular contraction; SA = sinoatrial; THAM = tris-hydroxymethyl-aminomethane (THAM has been discontinued in the United States).


Addressing the problem

Sustained VT, VF, and torsades de pointes are considered MAs. The list of the most common etiologies suggests that it is frequently possible to anticipate the occurrence of these emergencies on the basis of a thorough patient history.

A left ventricular ejection fraction (LVEF) of less than 40%, a history of nonsustained VT, and a previous myocardial infarction (MI) have all been independently associated with a significantly increased 1-year risk of a malignant ventricular arrhythmia. A family history of sudden cardiac death or a need for an implanted cardioversion device (ICD) should raise the index of suspicion for inherited dysrhythmias (eg, long QT, Brugada, and WPW syndromes).

Taking the relevant surgical factors (eg, cardiac procedure, infiltration with local anesthetics, and hyperkalemia) into account, including the drugs used during anesthetic management, allows a proactive approach to MA—that is, avoiding proarrhythmogenic medications and addressing and treating derangements aggressively before they can induce MA and cardiovascular collapse.

In addition, when a patient is determined to be susceptible to the development of MAs during a surgical procedure, all necessary equipment, including extended monitoring of right precordial leads and an external defibrillator with transcutaneous electrodes attached, must be deployed to ensure that any MAs can be immediately recognized and treated at an early stage. [8]  

Nevertheless, even with all the prophylactic measures described above, and even in the absence of any known preexisting condition, MAs can still occur suddenly in the OR. Because these events, by definition, lead to cardiovascular collapse, management must follow the ACLS [9] or PALS [10] guidelines for VT/VF.

The ACLS/PALS guidelines emphasize the need for prompt initiation of adequate CPR and discontinuance of all anesthetic medications. Key points include the following:

  • Once the external defibrillator electrodes are attached to the patient, cardiac rhythm must be analyzed
  • Upon verification of VT/VF, a shock must be delivered, followed by 2 minutes of CPR, before the underlying cardiac rhythm is analyzed again
  • Should VT/VF persist, another shock must be delivered, and epinephrine should be administered via the intravenous (IV) or intraosseous (IO) route or through the endotracheal tube (in children, dose and concentration must be adjusted, per PALS guidelines [10] )
  • Should VT/VF persist after these measures, amiodarone should be given IV (in children, lidocaine is an alternative, per PALS guidelines [10] )
  • Any reversible causes of cardiac arrest must be identified and managed 
  • The 2-minute CPR cycle, rhythm analysis, shock delivery, and epinephrine administration must be repeated until either (a) return of spontaneous ventilation (ROSC) is achieved or (b) it is determined that ROSC cannot be achieved despite a prolonged and appropriately executed resuscitation effort
  • If asystole develops, management must then change in accordance with the algorithm for asystole/pulseless electrical activity (PEA)

Treatment options for specific etiologies are highlighted with the help of the common clinical case scenarios described below (see Case Examples 1, 2, 3, and 4). The focus of this article is on emergency situations; however, the reader may also be interested in more broad-based and comprehensive articles on long-term management of these arrhythmias. [11]

The following list is intended as a general step-by-step guide for crisis management in the setting of MA:

  • Maintain vigilance to facilitate early recognition
  • Immediately cease all other patient care activities, including surgical intervention, once appropriate hemostatic control is achieved; the decision whether to complete or abort the procedure once circulation returns depends on the clinical scenario 
  • Discontinue all anesthetics, and ventilate with 100% fraction of inspired oxygen (FiO 2)
  • Have the OR team assume the role of the ACLS team, with the responsible anesthesiologist as the leader
  • Have the surgeon (or another member of the surgical team) start chest compressions immediately; if the patient is prone or the chest is not on a flat, hard surface (eg, a Jackson table or Wilson frame), he or she must be turned supine and placed on a back board
  • Concurrently with the initiation of CPR, call for help, and request that a defibrillator be brought to the OR  
  • Assign a time and record keeper to monitor the timing of CPR cycles and to announce events
  • Ensure airway patency, and confirm the adequacy of ventilation and oxygenation
  • Apply defibrillator pads, and deliver shocks per ACLS/PALS guidelines [9, 10]
  • Continue CPR according to ACLS/PALS guidelines [9, 10]
  • Ensure functional intravenous (IV) access, and administer epinephrine per ACLS/PALS guidelines [9, 10]
  • Obtain arterial blood gas (ABG) values, electrolyte concentrations, hemoglobin (Hb) level, hematocrit (Hct), and any other laboratory tests that are indicated by the clinical situation
  • Administer IV amiodarone for VT that is refractory to direct-current (DC) cardioversion 
  • If hyperthermia is present, manage it by cooling the patient
  • Prepare for postresuscitation management should ROSC be achieved
  • Ensure adequate communication/handoff when transferring the patient to a new clinical unit (eg, the intensive care unit [ICU])

Case Example 1

Clinical scenario

A 62-year-old man with a history of coronary artery disease (CAD) and ischemic cardiomyopathy, an LVEF of 40%, and moderate aortic stenosis (AS), is scheduled to undergo a right total hip arthroplasty. His preoperative heart rate (HR) is 85 beats/min, his preoperative blood pressure (BP) is 162/96 mm Hg, and he has taken his beta blocker on the morning of the procedure.

Large-bore peripheral IV access is obtained before induction of general anesthesia, and a right radial artery catheter is placed after induction. Endotracheal intubation is easy; however, HR increases to 110 beats/min and BP to 207/110 mm Hg. Labetalol 30 mg IV returns HR and BP to their preoperative values.

During positioning and preparation for surgery, BP drops to 70/41 mm Hg and responds slowly to IV boluses of lactated Ringer solution (LRS) 500 mL, ephedrine, and phenylephrine. After the skin incision, HR rises to 105 beats/min and BP to 200/115 mm Hg. At the same time, five-lead ECG shows ST-T elevation in leads I-aVL-V5. Surgery is halted, and while labetalol 10 mg IV is given, ECG shows wide, polymorphic QRS complexes at a rate of 140/min, BP falls to 0 mm Hg, and end-tidal carbon dioxide (EtCO2) falls from 36 mm Hg to 12 mm Hg.


The surgeon was instructed to start chest compressions at a rate of 100/min, bilateral breath sounds were verified, and controlled ventilation was continued with 100% FiO2 at a rate of 12/min. The circulating nurse was assigned to start recording time and CPR events, and the code was called per hospital policy.

One minute after the initiation of CPR, additional personnel arrived with a biphasic defibrillator that was connected to the patient. After all personnel were cleared, a 200-J asynchronous shock was delivered, and chest compressions were resumed for 2 minutes. At this point, ECG showed VF. Epinephrine 1 mg IV was given, and another 200 J shock was delivered. While CPR was continuing, ABG values, electrolyte concentrations, and Hb level were determined. Besides a mixed metabolic and respiratory acidosis with a base excess (BE) of –8, no abnormalities were revealed.

After a third shock, a second dose of epinephrine, and administration of amiodarone 300 mg IV, sinus rhythm with ST elevation returned, BP was 100/62 mm Hg, and HR was 92 beats/min. The incision was closed with staples, and the patient was transferred to the cardiac catheter suite, where a 90% stenosis of the left anterior descending artery was found. A stent was placed, and the patient recovered with no neurologic complications.

The known preexisting cardiac conditions predisposed this patient to a recurrent ischemic cardiac event. Attention to the patient's history and immediate initiation of management according to the ACLS VT/VF guidelines [9] resulted in a favorable outcome.


Case Example 2

Clinical scenario

A 35-year-old woman who is a former heroin user is scheduled to undergo laparoscopic cholecystectomy for recurrent cholelithiasis. She has been on methadone 120 mg/day PO, and she has taken her regular dose on the morning of the procedure. Her body mass index (BMI) is 35 kg/m2, she smokes 10 cigarettes per day, and she states that she has no other medical problems. Preoperative laboratory findings are significant for a potassium concentration of 3.1 mmol/L. No preoperative ECG is available.

After an uneventful induction, surgery is under way with sevoflurane maintenance and ondansetron for prophylaxis of postoperative nausea and vomiting. When the cystic artery is clamped, polymorphic wide-complex ECG changes are suddenly noted at an HR of 200 beats/min, BP drops to 50/29 mm Hg, and EtCO2 falls from 42 mm Hg to 19 mm Hg.


The surgeon was notified, chest compressions were started, and help (including a defibrillator) was called. Because of the methadone treatment and the morphology of the ECG changes, torsades de pointes caused by acquired prolonged QTc was suspected. Magnesium sulfate 2 g IV was given over a period of 1 minute. ECG showed immediate return of sinus rhythm, and BP rose to 112/68 mm Hg. Potassium 20 mEq was added to 1 L of LRS, and surgery continued.

Ten minutes later, another episode of torsades de pointes occurred that responded to asynchronous defibrillation with 120 J, as well as a second IV bolus of magnesium sulfate 2 g. Subsequent ECG showed long QTc. Magnesium sulfate infusion was started at a rate of 5 g/hr, and the surgical procedure was completed without further complications.  The patient was extubated, ECG showed a QTc of 480 ms, and the patient was transitioned from methadone to buprenorphine-naloxone for opioid-dependence maintenance therapy.

In this case, recognizing the ECG pattern characteristic of torsades de pointes was the key to initiation of appropriate treatment. However, a preoperative ECG would have revealed the methadone-induced QT prolongation. If this had been known, it would have been possible to avoid administering drugs known to prolong the QT interval (in this case, ondansetron and sevoflurane) during general anesthesia.

Whenever a patient is taking a medication that prolongs the QT interval, it is recommended to obtain a preoperative 12-lead ECG and to be judicious in administering additional medications known to prolong the QT interval.  


Case Example 3

Clinical scenario

A 55-year-old man is scheduled to receive an orthotopic deceased donor liver graft. He has alcohol-induced end-stage liver disease (ESLD) with hepatorenal and hepatopulmonary syndromes. One minute after unclamping of the portal vein and reperfusion of the graft, BP falls to 48/29 mm Hg, HR drops to 40 beats/min, ECG shows peaked T waves, and VF is suddenly seen on the monitor. The potassium concentration is determined to be 8.2 mmol/L, and metabolic acidosis is present with a BE of –14.


A 500-mg IV bolus of calcium chloride was given with sodium bicarbonate 50 mEq IV, followed by dextrose 25 g and regular insulin 10 units. There was no immediate response. In view of the extensive retraction required to expose the surgical field, effective chest compressions and transcutaneous cardioversion were deemed unlikely to be successful. The surgeon performed cardiac compression using a bimanual technique, in which the diaphragmatic surface of the heart was stabilized with the palm of one hand and the sternum was compressed with the heel of the other.

After the arrival of sterile cardiac defibrillator paddles, one paddle was placed above the left liver and beneath the heart, and the other paddle was placed on the anterior surface of the heart. A 50-J shock was delivered, and normal sinus rhythm resumed. Furosemide 20 mg IV, albuterol 10 mg IV, and another 50 mEq IV dose of sodium bicarbonate were added to the management of initial hyperkalemia following reperfusion. The serum potassium level was normalized, and metabolic acidosis was corrected.

Postreperfusion syndrome during orthotopic liver transplantation is a result of multiple factors. [12] One prominent cause of bradycardia/asystole or various cardiac dysrhythmias is hyperkalemia. First-line treatment of acute symptomatic hyperkalemia consists of stabilizing the cardiac cell membranes with calcium and correcting metabolic acidosis. It is also important to facilitate the drive of extracellular potassium into the myocytes with dextrose/insulin and beta adrenergic medications. The next step is to augmenting excretion of excess potassium using loop diuretics.

Because of the retractor used for surgical exposure, the distance between the chest wall and the heart may render chest compressions and delivery of cardioversion ineffective. The surgical team must be prepared to employ the alternative methods described here to ensure adequate CPR. [13]


Case Example 4

Clinical scenario

A 14-year-old girl is brought to the cardiac laboratory suite for electrophysiologic (EP) study and ablation of the accessory reentry pathway of WPW syndrome. She has a history of frequent palpitations and has lost consciousness on two occasions. Her vital signs on admission are within normal limits. General anesthesia is planned, and she requests inhalation induction because she has a severe needle phobia. During preparation for monitoring, she suddenly becomes pale, diaphoretic, and unconscious.


ECG monitors were applied immediately, and VT at a rate of 144 beats/min was revealed. Chest compressions were immediately started at a rate of 100/min. Bag-mask ventilation was initiated with an FiO2 of 100%. The compression-to-ventilation ratio was 15:2. Biphasic DC cardioversion with 120 J was delivered, to no effect.

CPR was resumed, and peripheral IV access was established while endotracheal intubation was also performed. After 2 minutes of chest compressions and controlled ventilation with 100% FiO2 at a rate of 12/min, a second, larger shock of 200 J was delivered and immediately followed by administration of adenosine 12 mg IV. Normal sinus rhythm was restored, and the EP study was completed successfully.

WPW syndrome may cause ventricular preexcitation, and the resulting ventricular tachyarrhythmia can lead to fatal cardiovascular collapse. [2] In addition to the nonspecific management of that complication, the underlying conduction anomaly must be addressed so as to block the reentry mechanism that is responsible for the ventricular preexcitation. In this case, given that the planned procedure aimed to eliminate the abnormal pathway and that the patient’s condition responded well to therapy, it was prudent to proceed with the EP study.