Circulation, Airway, and Breathing

Any intraoperative emergency can quickly become an intraoperative cardiac arrest. Accordingly, the anesthesiologist must be familiar with ACLS, especially as it applies to the operating room [Reference Moitra, Gabrielli, Maccioli and O’Connor2].

ACLS was initially developed for the resuscitation of patients found unresponsive, in contrast to patients in the operating room where the cardiac arrest is both witnessed, and sometimes predicted. Therefore, ACLS should be modified in the operating room, as discussed by Moitra et al. [Reference Moitra, Gabrielli, Maccioli and O’Connor2].

Although the management of cardiac arrest is similar both in and outside the operating room, there are unique considerations for the surgical patient. In contrast to the various causes of cardiac arrest outside the operating room, intraoperative cardiac arrests frequently stem from induced bradycardias, hypoxemia, and hypovolemia, whereas etiologies such as transmural myocardial infarctions (MIs) from plaque rupture are relatively uncommon [Reference Moitra, Gabrielli, Maccioli and O’Connor2].

Because many intraoperative emergencies require resuscitation, it is important to be aware of the priorities during resuscitation: circulation, airway, breathing. During an intraoperative emergency that has degraded into a cardiac arrest, the anesthesiologist must first assess the patient’s circulation. If the patient is pulseless, chest compressions should be initiated immediately at a rate of 100–120 compressions per minute. If end-tidal carbon dioxide (ETCO₂) is present via an endotracheal tube (ETT), the anesthesiologist should target chest compressions to an ETCO₂ >10 mmHg, to ensure adequate circulation. Chest compression depth should be the lesser of 2 inches or one-third the anterior–posterior diameter of the patient [Reference Panchal, Berg and Kudenchuk1]. While a noninvasive cuff can be used initially, an arterial line is preferred to allow for closer monitoring. The anesthesiologist should assess the ECG rhythm as soon as possible to identify whether there is a perfusing rhythm or if the rhythm should be cardioverted or defibrillated. Every anesthesiologist should be comfortable identifying arrhythmias and their individual management.

Once circulation is assessed, the anesthesiologist should turn to the airway and begin ventilation. The provider must assess the adequacy of ventilation and establish an advanced airway if noninvasive ventilation is inadequate. If an ETT is indicated, chest compressions should not be interrupted for >10 seconds at a time. Once an advanced airway is placed, a rate of one breath every 6–8 seconds should be administered, with caution to avoid hyperventilation [Reference Sutherasan, Vargas, Brunetti and Pelosi3].

Beyond the standard American Society of Anesthesiologists’ (ASA) monitors, there are multiple monitoring modalities available to the anesthesiologist during an emergency. Perhaps the most important from a diagnostic perspective is the ultrasound, which allows the anesthesiologist to diagnose a number of conditions, including pulmonary pathologies (pneumothoraces, pleural effusions, hemothoraces), abdominal pathologies such as hemorrhage, and cardiac pathologies (acute valvulopathies, pericardial effusions, MI, ventricular failure). Another important monitoring modality is an arterial catheter, which is critical to trending and correcting blood gas abnormalities, monitoring blood pressure, and identifying/treating electrolyte abnormalities that may contribute to lethal arrhythmias.

After stabilization, obtaining additional information in the form of labs and imaging is of prime importance and the patient will need to be transported to either the postanesthesia care unit (PACU) or the intensive care unit (ICU). If the patient’s surgery took place at an outpatient surgical facility, the facility may need to arrange for an ambulance to transport the patient to a nearby hospital.

Extracorporeal Cardiopulmonary Resuscitation

Patients presenting with sudden cardiac arrest or respiratory impairment refractory to conventional medical therapy may be candidates for extracorporeal membrane oxygenation (ECMO). However, there are currently no guidelines for when ECMO is indicated. The American Heart Association (AHA) recognizes that there is insufficient evidence to recommend the routine use of extracorporeal cardiopulmonary resuscitation (eCPR) for patients with cardiac arrest [Reference Panchal, Berg and Hirsch4]. Accordingly, the use of ECMO during ACLS depends on institution-specific processes and procedures.

Hypovolemia

Hypoxia

Hypoxia and respiratory failure are frequent occurrences in monitored anesthesia care due to use of sedatives, hypnotics, and narcotics without a secured airway. The primary treatment for hypoxia in this setting is noninvasive and includes the use of jaw thrust, chin lift, oral/nasal airway, and placement of a supraglottic airway or an ETT. If hypoxia persists after the airway is secured, further investigation is required since the patient may be experiencing an issue other than airway obstruction, such as hypoxic delivery of oxygen, hypoventilation, shunt, ventilation/perfusion mismatch, or diffusion impairment.

Management of the difficult airway will be discussed in Chapter 2.

“H⁺” Acidosis

Malignant hyperthermia (MH) is typically caused by an autosomal dominant mutation in RYR1 (ryanodine receptor, or less commonly, CACNA1S). MH susceptibility may also be inherited with various myopathies [Reference De Wel and Claeys9]. Exposure to triggering agents (volatile anesthetics and succinylcholine) results in the release of calcium from the sarcoplasmic reticulum of primarily myocytes, leading to a hypercatabolic and hypermetabolic state. Signs and symptoms include tachycardia, hyperthermia, hypercarbia, muscle rigidity, and metabolic acidosis. Treatment includes the following: removing the triggering agent, utilizing a charcoal filter (with hourly replacement), and replacing the ventilator circuit while maintaining high oxygen flow and minute ventilation to accommodate increased production of carbon dioxide [Reference Cieniewicz, Trzebicki, Mayzner-Zawadzka, Kostera-Pruszczyk and Owczuk10]. If it is not possible to cancel the procedure, total intravenous anesthesia should be utilized. Dantrolene should be administered and repeated as frequently as necessary until PaCO₂, heart rate, and muscle rigidity are reduced. Bicarbonate should be considered for base excess (BE) <−8. Active cooling should be utilized. Dysrhythmias should be treated with caution, and calcium channel blockers should be avoided. Potassium levels should be monitored and hyperkalemia should be promptly treated. After the patient is stabilized, creatine kinase levels should be monitored (as they are a presumptive sign of rhabdomyolysis and myoglobinuria) [Reference Rosenberg, Davis, James, Pollock and Stowell11].

Tension Pneumothorax

A pneumothorax is a collection of air or fluid between the parietal and visceral pleura, resulting in the compression of pulmonary and/or vascular systems. Tension pneumothorax refers specifically to a one-way inlet allowing for an acute compromise of the thoracic anatomical structures. A pneumothorax may present as an intraoperative emergency with hemodynamic instability and difficulty ventilating. Causes of a pneumothorax include penetrating chest trauma, iatrogenic injury during central line placement or peripheral nerve block, any other procedures near the lungs, or rupture of bullae. Alternatively, the accumulation of fluids (blood, lymph, or malignant effusions) may result in a hemothorax, chylothorax, or large pleural effusion, and cardiopulmonary resuscitation (CPR) causing rib fractures and perforation of the pleura [Reference Childs12]. A pneumothorax may present with dyspnea, pleuritic chest pain, tachycardia, tachypnea, and, in the case of tension pneumothorax, acute hemodynamic collapse. Identification of a pneumothorax in an anesthetized patient is more challenging, but the diagnosis should be considered when there is hemodynamic instability during abdominal or thoracic surgeries, elevated airway pressure, deviation of the trachea from the midline, decreased breath sounds, jugular venous distension, elevated airway pressures, loss of lung sliding on lung ultrasound, loss of comet tails or B-lines, and the presence of A-lines on ultrasound [Reference Blaivas, Lyon and Duggal13]. Treatment involves needle decompression. If needle decompression on the second mid-clavicular line is not effective, decompression on the fourth or fifth mid-axillary line (just cranial to the ribs) may be attempted. If neither of these relieves the obstruction, then conversion to open thoracotomy may be indicated. Regardless, tube thoracostomy should be performed following these maneuvers.

“Thrombosis”/Embolism

Emboli of various etiologies can occur intraoperatively or postoperatively, and cause hemodynamic instability. In this section, we briefly go through the commonly encountered emboli in anesthesia.

Pulmonary emboli (PEs) are divided into either massive or submassive, depending on the presence of hemodynamic instability. Clinically, only a massive PE is likely to be apparent to the anesthesiologist. Mechanistically, a blood clot, amniotic fluid, or fat embolism gets dislodged from the venous system and becomes wedged in the pulmonary vascular tree, increasing right ventricular (RV) afterload and causing RV dilation and reduced function, ultimately resulting in reduced cardiac output and potentially cardiogenic shock. Diagnosis depends on recognition of clinical signs and risk factors such as recent major surgery, high body mass index, use of contraceptive pills, immobility, etc. Treatment depends on the severity and stability of the patient and must take into consideration the risks and benefits of various treatment options. Treatment generally includes systemic anticoagulation, catheter-based thrombolysis, and an open-heart embolectomy.

Venous air emboli (VAEs) can occur in almost any procedure but is commonly seen in craniotomies, especially in the sitting position [Reference Palmon, Moore, Lundberg and Toung14]. VAEs occur when room air is entrained with the venous system (typically when venous access is above the heart). Hemodynamic collapse can occur by obstructing the right ventricular outflow tract (RVOT), for which 100–300 mL of air is generally required [Reference Yeakel15]. Detection depends on the device utilized, but transesophageal echocardiography (TEE) is the most sensitive and capable of detecting 0.02 mL kg⁻¹. Clinically, there is an acute drop in ETCO₂ and arterial oxygen saturation, as dead space increases, dysrhythmias occur, and RV strain is seen on imaging. If VAE is suspected, the surgical field should be flooded with saline to minimize further entrainment. To maintain oxygenation and facilitate reabsorption of the entrained air, 100% oxygen should be administered. Aspiration from a pulmonary artery (PA) catheter may aid in reducing the volume of obstructing air by as much as 50%, and bilateral jugular venous compression should be applied to increase venous pressure, allowing for detection of sites of air entrainment and interrupting ongoing VAEs. Positional changes, such as left lateral decubitus and the Trendelenburg position, to decrease RVOT obstruction may be beneficial. The best treatment of VAEs is prevention, which can be achieved by meticulous line placement, patient positioning, and liberal use of bone wax, as the intramedullary venous system may be a possible source of VAEs [Reference Sato, Toya, Ohira, Mine and Greig16].