Cardiac Arrest in the Operating Room: Resuscitation and Management for the Anesthesiologist: Part 1

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

Disclosures

Anesth Analg. 2018;126(3):876-888. 

In This Article

Acls Operating Room Algorithms

Symptomatic Bradycardia Evolving to Nonshockable Arrest

Perioperative bradycardia, asystole, and PEA have 16 causes (8 Hs and 8 Ts), that build on the differential diagnoses (6 Hs and 6 Ts) proposed by the American Heart Association:[3] hypoxemia, hypovolemia, hyper-/hypokalemia, hydrogen ion excess, hypothermia, hypoglycemia, malignant hyperthermia, hypervagal, toxins (anaphylaxis/anesthetics), tension pneumothorax, pulmonary thrombosis/embolus, coronary thrombosis, tamponade, trauma, QT prolongation, and pulmonary hypertension. These likely causes are listed alongside a suggested approach to perioperative bradycardia in Figure 5. A narrow complex QRS PEA rhythm suggests RV inflow or outflow obstruction (ie, tamponade, tension pneumothorax, auto-PEEP, myocardial ischemia, or pulmonary embolism). A wide complex QRS PEA rhythm may signify a metabolic crisis such as hyperkalemia or local anesthetic toxicity or LV pump failure.[88] Sudden, severe bradycardia in the periprocedural setting is often caused by physical manipulations that increase vagal tone and potentiated by the combination of vagotonic anesthetics and the sympatholysis that accompanies almost all anesthetics.

Figure 5.

Bradycardia. Adaptation of ACLS algorithm for bradycardia. ACLS indicates advanced cardiac life support; AV, atrioventricular; BP, blood pressure; CPR, cardiopulmonary resuscitation; CVL, central venous line or catheter; ECG, electrocardiogram; ECMO, extracorporeal membrane oxygenation; Etco2, end-tidal carbon dioxide; IV, intravenous; PEEP, positive end-expiratory pressure; PTCA, percutaneous transluminal coronary angioplasty; R/O, rule out; ROSC, return of spontaneous circulation; Spo2, pulse oximeter oxygen saturation; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

Treatment with atropine should be considered in any patient who does not become appropriately tachycardic in response to treatment with epinephrine or larger doses of ephedrine.[89] Reports of paradoxical bradycardia and sinus arrest have been described in patients who have received atropine doses of <1 mg. Potential mechanisms include a vagolytic-induced "stress test" of the sinus node; a vagotonic effect at the sinus node and a vagolytic effect at the atrioventricular node to cause a junctional rhythm; atropine-induced peripheral hypotension with a subsequent hypervagotonic reflex; and central nervous system vagotonia via cholinesterase inhibition.[90–93]

The different spectrum of causes of periprocedural bradycardia makes it appropriate to resort to pacing earlier in these patients. Even though we recommend it, there is no evidence to suggest any outcome benefit from the use of pacing (which may delay chest compressions) when full cardiac arrest is in progress.[94–97] Appropriate indications for emergency pacing include hemodynamically unstable bradycardia unresponsive to positive chronotropic agents; symptomatic tissue conduction dysfunction of the sinus node; Mobitz type II second-degree and third-degree block; alternating bundle branch block; or bifascicular block.[3]

Symptomatic Tachycardia Evolving to Pulseless Shockable Arrest (Ventricular Tachycardia, Ventricular Fibrillation, and Torsades De Pointes)

Hypovolemia or a significant imbalance between the depth of anesthesia and the amount of procedural stimulation are the most frequent causes of hypotension in the periprocedural setting. The 8 Hs and 8 Ts can cause a circulatory crisis that can devolve into a PEA arrest.

In general, the evolution of a malignant rhythm is an indicator of a severe process, severe cardiac comorbidities, and/or severe complications. Persistent tachycardia with hemodynamic instability can devolve into symptomatic bradycardia. Tachycardia from any cause other than sinus tachycardia that is associated with significant hypotension is an indication for immediate cardioversion (ventricular rate >150 beats·minute−1).[3] Cardioversion can sometimes convert a patient into a symptomatic bradycardia, which can necessitate emergency pacing. Overdrive pacing of supraventricular or ventricular tachycardia may also be appropriate in perioperative patients, and it should be considered when the rhythm is refractory to drugs or cardioversion.[98]

Figure 4 and Figure 6 outline the practical considerations for the management of symptomatic tachycardia in the perioperative period.

Figure 6.

Tachycardia. Adaptation of the ACLS algorithm for tachycardia. ACLS indicates advanced cardiac life support; AF + WPW, atrial fibrillation and Wolff-Parkinson-White syndrome; BP, blood pressure; EAT, ectopic atrial tachycardia; ECG, electrocardiogram; EF, ejection fraction; EKG, electrocardiogram; IV, intravenous; MAT, multifocal atrial tachycardia; PEEP, positive end-expiratory pressure; R/O, rule out; Spo2, pulse oximeter oxygen saturation; SVT, supraventricular tachycardia; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.

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