Anesthesia advanced circulatory life support
The constellation of advanced cardiac life support (ACLS) events, such as gas embolism, local anesthetic overdose, and spinal bradycardia, in the perioperative setting differs from events in the pre-hospital arena. As a result, modification of traditional ACLS protocols allows for more specific etiology-based resuscitation.
Perioperative arrests are both uncommon and heterogeneous and have not been described or studied to the same extent as cardiac arrest in the community. These crises are usually witnessed, frequently anticipated, and involve a rescuer physician with knowledge of the patient’s comorbidities and coexisting anesthetic or surgically related pathophysiology. When the health care provider identifies the probable cause of arrest, the practitioner has the ability to initiate medical management rapidly.
Recommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community. Adapting ACLS algorithms and considering the differential diagnoses of these perioperative events may prevent cardiac arrest.
Réanimation circulatoire avancée en anesthésie
Le grand ensemble d’événements liés à la réanimation cardiaque avancée (ACLS) tels que les embolies gazeuses, les surdosages d’anesthésiques locaux et la bradycardie sinusale dans un contexte périopératoire est différent des événements que l’on observe à l’extérieur de l’hopital. En conséquence, une modification des protocoles traditionnels d’ACLS permet une réanimation plus spécifique, en fonction de l’étiologie.
Les arrêts cardiaques en période périopératoire sont à la fois rares et hétérogènes; ils n’ont pas été décrits ou étudiés avec la même ampleur que les arrêts cardiaques survenant hors de l’hôpital. Ces crises sont habituellement vécues en direct, souvent anticipées et impliquent l’intervention d’un médecin connaissant les comorbidités du patient ainsi que la physiopathologie en rapport avec l’intervention et les anesthésiques utilisés. Lorsque le professionnel de la santé identifie la cause probable de l’arrêt cardiaque, le praticien a la possibilité d’entreprendre rapidement une prise en charge médicale.
Des recommandations pour la prise en charge doivent être fondées sur les avis d’experts et sur la compréhension de la physiologie plutôt que sur des normes actuellement utilisées pour la création de protocoles d’ACLS hors du milieu hospitalier. L’adaptation des algorithmes d’ACLS et la prise en compte des diagnostics différentiels de ces événements périopératoires peuvent prévenir les arrêts cardiaques.
Advanced cardiac life support (ACLS) was originally developed as an extension of basic life support with a focus on the resuscitation of individuals found unresponsive in the community by providing chest compression and respiratory support. These clinical interventions were later expanded to immediate care in the emergency department and were then exported to unresponsive patients elsewhere in the hospital.
The initiation of cardiopulmonary resuscitation (CPR) is predicated on the discovery of an unresponsive patient who does not have a pulse.1 Advanced cardiac life support is rhythm oriented and specific to sudden manifestations of cardiac and respiratory diseases outside of the hospital. This approach presumes that effective chest compression, adequate ventilation, and electrical and pharmacological management of a pulseless cardiac rhythm will result in the return of spontaneous circulation (ROSC).2,3
Cardiac arrest during anesthesia is distinct from cardiac arrest in other settings because it is usually witnessed and frequently anticipated. Compared with other settings, the response may be both more timely and focused. In the perioperative setting, a patient with a known medical history typically deteriorates into crisis over a period of minutes or hours under circumstances wholly dissimilar to other in-hospital or out-of-hospital scenarios. Consequently, aggressive measures can be taken to support the patient’s physiology and avoid or delay the need for ACLS. Additionally, patients in the perioperative period have a different pathophysiologic milieu. For example, hypovolemia is far more common than a transmural myocardial infarction from plaque rupture. Similarly, prolonged hypoxemia and hypercarbia resulting from the management of unpredictable difficult airways is a well-recognized cause of cardiac arrest in the operating room (OR).4-7 Bradycardiac arrest in the OR is caused or precipitated by vagotonic analgesics, physical manipulations that increase vagal tone, and sympatholysis from anesthetic agents and regional/neuraxial anesthetic techniques.8,9
A large prospective and retrospective case analysis study of all perioperative cardiac arrests occurring during a ten-year period (1989-1999) in a single teaching institution showed an overall incidence of cardiac arrest from all causes of 19.7 per 10,000 anesthetics and a risk of death related to anesthesia-attributable perioperative cardiac arrest of 0.55 per 10,000 anesthetics.4 In a review of cardiac arrests associated with anesthesia, the most common electrocardiogram (ECG) rhythms at the time of arrest were bradycardia (23%), asystole (22%), tachydysrhythmia (including ventricular tachycardia and ventricular fibrillation) (14%), and normal (7%). Remarkably, in 33% of the cases, the heart rhythm was not fully assessed or documented.10 The introduction of worldwide safety standards and improved understanding of the physiologic impact of anesthetic agents is consistent with recent epidemiological data suggesting an improvement of anesthesia-related mortality risk in the United States and abroad, with the highest death rate found in very elderly patients (≥ 85 yr).11
Although the cause of circulatory arrest is usually unknown in patients found in the field, there is a relatively short list of probable causes of circulatory collapse during the perioperative period.4-6,8,9 This certainty produces more focused and etiology-based resuscitation efforts, which frequently do not follow the more generic algorithms of the ACLS guidelines.
Anesthesia and cardiac arrest
Common situations associated with perioperative cardiac arrest
Intravenous anesthetic overdose
Inhalation anesthetic overdose
Neuraxial block with high level sympathectomy
Local anesthetic systemic toxicity
Drug administration errors
Hypovolemic and/or hemorrhagic shock
Surgical maneuvers associated with reduced organ blood flow
Acute electrolyte imbalance (high K, low Ca++)
Increased intra-abdominal pressure
Acute coronary syndrome
Severe pulmonary hypertension
Prolonged Q-T syndrome
Epidemiology reviews of cardiac arrest during neuraxial anesthesia suggest an incidence of 1.3-18 per 10,000 patients.9,12-15 A recent review of cardiac arrests during neuraxial anesthesia reports a prevalence of 1.8 cardiac arrests per 10,000 patients, with more arrests occurring in patients receiving spinal anesthesia vs all the other techniques (2.9 vs 0.9 per 10,000 patients, respectively; P = 0.041). In this review, cardiac arrest during neuraxial anesthesia was associated with a greater likelihood of survival compared with cardiac arrest during general anesthesia.9
Although there is a substantial amount of basic science and clinical interest in the effects of high spinal anesthesia on the sympathetic innervation of the heart and circulation,16-22 the pathophysiology of cardiac arrest remains unclear. Various hypotheses have been proposed, invoking factors such as unrecognized respiratory depression, excessive sedation concurrent with a high block, underappreciation of both the direct and indirect circulatory consequences of a high spinal anesthetic, and failure to rescue with airway management and drugs.8,9,23-26 Hypoxemia from hypoventilation is an unlikely etiology because there are case reports documenting adequate oxygen saturation in these patients. Neuraxial cardiac arrests are most likely precipitated by the combination of autonomic imbalance with enhanced vagal tone and an acute decrease in preload from venodilatation.8,9
Treatment of cardiac arrest associated with neuraxial anesthesia
• Discontinue anesthetic or sedation infusion
• Immediate tracheal intubation and ventilation with 100% oxygen
• Treat bradycardia with 1 mg atropine
• Treat bradycardia with severe hypotension with at least 1 mg epinephrine iv
• Consider transcutaneous or intravenous pacemakers for all symptomatic bradycardic rhythms with pulse
• Consider chest compressions at a rate of 100 compressions·min−1 if above measures are ineffective
• Immediate CPR as indicated (no carotid pulse, absence of ECG rhythm, loss of arterial catheter, and pulse oximeter signal)
• Epinephrine 1 mg iv; consider alternative approach to drug therapy, i.e., escalating doses or reducing epinephrine time interval to every 1–2 min
• Consider concurrent treatment with vasopressin 40 U iv
Although the risk of local anesthetic toxicity is difficult to predict, the risk for toxicity increases with dose and site of injection.29 In general, local anesthetics depress the heart in a dose-dependent fashion and can cause bradycardia, asystole, decreased contractility, and hypotension.29-31 Other determinant factors of anesthetic blood level and systemic toxicity are the site of injection and the rate of absorption. Direct intravascular injection of a local anesthetic typically produces an immediate toxic effect, whereas toxicity from absorption over time from well-vascularized peripheral tissue, such as the pleural space, may present in a delayed fashion.29
Bupivacaine, the local anesthetic agent most often associated with cardiac arrest, is a potent and well-described myocardial depressant.30-34 Fortunately, most awake patients who are developing systemic toxicity manifest early neurological symptoms that may suggest impending myocardial dysfunction. In some unfortunate patients, however, these changes presage cardiac arrest.
Treatment of local anesthetic toxicity
• 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
• Consider chest compressions at rate of 100 compressions·min−1 if above measures are ineffective
• 20% intralipid iv, 1.5 mL·kg−1iv load, then 0.25 mL·kg−1·hr−137,38 (the efficacy of this therapy is still debated and under investigation, and it should complement and not substitute the immediate use of catecholamines39,40)
• Seizures should be treated with benzodiazepines. Small doses of propofol or thiopental may be used if benzodiazepines are not immediately available41
• 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 epinephrine 10-100 μg are preferable to higher doses41
• Vasopressin is not recommended41
• Sodium bicarbonate to maintain a pH > 7.25 in patients without immediate ROSC after CPR and drug therapy
• If ROSC does not occur following the first bolus of lipid emulsion, a second bolus followed by a doubling of the rate of infusion is appropriate41
• Consider therapy with H1 and H2 blockers
• Amiodarone is the drug of choice for ventricular arrhythmias. Lidocaine should be avoided41
• Most important, continue CPR for a prolonged period (we suggest at least 60 minutes) as very good neurologic recovery has been reported in patients after very prolonged cardiac arrests from local anesthetic overdoses
• ECMO may be 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 emulsion41
Anaphylaxis is a rare but important cause of circulatory collapse in the perioperative period.27,42 The reported incidence of anaphylaxis is from one in 10,000 to one in 20,000 anesthetics, with 3-10% of those cases being life-threatening.43-45 Although there is a wide range of minor allergic reactions, hypotension, tachycardia, bronchospasm, and vasoplegic shock may follow when the offending agent is administered as a rapid intravenous bolus - the most common route of drug administration during anesthesia.46 The preponderance of anaphylaxis in perioperative patients is caused by a small number of drugs, particularly neuromuscular blocking agents.43,47
Common causes of anaphylactic shock include nondepolarizing neuromuscular blockers, beta-lactam antibiotics, latex exposure, and intravenous contrast.
Treatment of anaphylaxis
• Stop or remove the inciting agent or drug (e.g., intravenous contrast or latex)
• If feasible, stop surgery or procedure
• Oxygen at FIO2 of 1.0; intubate immediately for respiratory distress
• Epinephrine 0.5-3 μg·kg−1; start epinephrine infusion (5-15 μg·min−1) for a goal SBP 90 mmHg; observe for myocardial ischemia
• Watch for auto-PEEP if severe bronchospasm
• ± Vasopressin 2 U iv
• Intravenous fluids/large bore access
• H1 blocker (diphenhydramine 50 mg iv)
• H2 blocker (famotidine 20 mg iv)
• ± Corticosteroid (e.g., 50-150 mg hydrocortisone iv)
• A tryptase level in the blood can be used to support the diagnosis48
• CPR if no carotid pulse detected for 10 sec
• Epinephrine 1 mg iv, can repeat every 3-5 min or follow by vasopressin 40 U
• Disconnect the ventilator briefly if auto-PEEP suspected
• Consider tension pneumothorax if arrest preceded by severe bronchospasm
• Add adjunctive therapies listed in pre-arrest
Treatment of gas embolism
• Administer 100% oxygen and intubate for significant respiratory distress or refractory hypoxemia. Oxygen may reduce bubble size by increasing the gradient for nitrogen to diffuse out
• Promptly place patient in Trendelenburg (head down) position and rotate toward the left lateral decubitus position. This maneuver helps trap air in the apex of the ventricle, prevents its ejection into the pulmonary arterial system, and maintains right ventricular output
• Maintain systemic arterial pressure with fluid resuscitation and vasopressors/beta-adrenergic agents if necessary. See the algorithm for RV failure
• Consider transfer to a hyperbaric chamber if immediately available. Potential benefits of this therapy include compression of existing air bubbles, establishment of a high diffusion gradient to speed dissolution of existing bubbles, improved oxygenation of ischemic tissues, and lowered intracranial pressure
• Circulatory collapse should be addressed with CPR, and consideration should be given to more invasive procedures as described above
• Early use of TEE to rule out other treatable causes of pulmonary embolism
• Consider the right ventricular shock algorithm
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 pressurized fluid infusion.
Massive gas embolisms have been characterized by breathlessness, continuous coughing, arrhythmias, myocardial ischemia, acute hypotension with loss of end-tidal carbon dioxide, and cardiac arrest.51
Hyperkalemia can be an elusive but important cause of cardiac arrest in perioperative patients regardless of pre-existing kidney injury. It is important for practitioners to appreciate that many patients who sustain a hyperkalemic cardiac arrest do not appear to undergo the orderly deterioration of cardiac rhythm (peaked T waves followed by a widened QRS complex and eventually the classic sine wave) that has been widely taught. Electrocardiographic changes may be absent in hyperkalemia.52 Life-threatening hyperkalemia (> 6.5 mmol·L−1) can slow atrioventricular conduction or cause asystole, ventricular tachycardia, ventricular fibrillation, and PEA. Several congenital or acquired conditions, including burns and upper/lower motor neuron lesions, can cause upregulation of nicotinic acetylcholine receptors and cardiac arrest via a massive release of potassium, especially when intravenous succinylcholine is used to facilitate intubation.53 The prevalence of hyperkalemia as a cause of cardiac arrest in hospitalized patients is sufficiently high that it should be included in the differential diagnosis of every patient with a new wide-complex arrhythmia. Its treatment has been widely described in the literature.49
Malignant hyperthermia is a rare but potentially fatal manifestation of hypermetabolism which is triggered by exposure to specific drugs in susceptible individuals. The hallmark of this rare syndrome is a sudden and rapid increase of uncompensated oxygen consumption in individuals exposed to succinylcholine and volatile inhalation agents, including enflurane, halothane, isoflurane, sevoflurane, and desflurane. Inherited genetic mutations of the sarcoplasmic reticulum can result in massive release of intracellular calcium after exposure to a triggering agent.54-56 Clinical features of malignant hyperthermia include unexplained tachycardia with hypertension, rapid increase in end-tidal CO2 without hypoventilation, increased minute ventilation if the patient is breathing spontaneously, uncompensated or mixed metabolic acidosis (lactic) with increased PaCO2, a rapid or delayed (up to a few hours) increase in temperature, hyperkalemia from rhabdomyolysis with severe dysrhythmias, myoglobinuria, disseminated intravascular coagulation (DIC) and “nonsurgical” bleeding, localized masseter muscle or generalized muscle rigidity, and massive increase of plasma creatine kinase. A clinician-based diagnosis of DIC substantially increases the risk of cardiac arrest and death.57 The differential diagnosis for malignant hyperthermia includes sepsis, thyrotoxicosis, pheochromocytoma, iatrogenic warming, CO2 rebreathing, and neuroleptic malignant syndrome.
Mortality from malignant hyperthermia was as high as 70% before the widespread awareness of this complication, its early recognition, and its timely treatment with intravenous dantrolene.54 The mortality from malignant hyperthermia has decreased, and a recent study of patients in the United States reports a mortality rate of 11.7%.58 Malignant hyperthermia with cardiac arrest carries a mortality of 50% in healthy young individuals under anesthesia.57 The most effective way to prevent malignant hyperthermia is to avoid use of triggering agents in patients suspected or known to be susceptible.55
Treatment of malignant hyperthermia
• Discontinue all anesthetic and switch from the anesthesia ventilator to manual Ambu bag ventilation from a separate source of oxygen. Switch to a dedicated clean anesthesia ventilator or transport or ICU ventilator when feasible. Continue ETCO2 monitoring if feasible
• Stop surgery when feasible
• Switch to intravenous anesthetic if necessary
• Sodium dantrolene (be sure you know where it is in your hospital and how to prepare it): give 2.5 mg·kg−1 or 1 mg·lb−1 initial dose. Repeat bolus of Na dantrolene, titrating to tachycardia and hypercarbia (10 mg·kg−1 suggested upper limit, but more may be given as needed, up to 30 mg·kg−1)
• 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: calcium chloride 10 mg·kg−1, insulin 0.1 U·kg−1 + 50 mL D50w for adult or 1 mL·kg−1 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, CPK 10,000 IU·L−1)
• 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 mmHg)
• 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 (DIC)
• Call for help, including the MH hotline, if feasible (www.mhaus.org) call 1-800-644-9737 or 1-800-MH-HYPER in the USA and Canada; outside the USA, call 00113144647079
• 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%)
Complications of central venous access
In the category of equipment-related damaging events, the ASA Closed Claims Project found that central venous placement is the most frequent event associated with death and permanent brain damage during anesthesia.7 Although a pneumothorax is a well-described and relatively rare complication of central venous catheter placement or removal, an analysis from the ASA closed-claims database suggests that hemothorax and tamponade are also important though sometimes unrecognized fatal complications of patients who undergo attempts at central venous cannulation.58,59 If a patient’s hemodynamic situation deteriorates following central venous catheter placement, expeditious focused echocardiography should be considered in addition to chest radiography.60
When ACLS was first introduced, it was the consensus product of a multidisciplinary group with a common interest in ACLS. At the time, there was little scientific evidence to guide and shape the guidelines that the group eventually authored. Fortunately, there was an interest in scenarios that were sufficiently common to permit systematic study, which facilitated subsequent revisions of the ACLS guidelines.61 However, given that cardiac arrest occurs rarely in the perioperative period, it is difficult, or impossible, to perform large epidemiological studies and generate evidence-based guidelines.
Recent surveys among anesthesiologists suggest a lack of awareness of both basic and anesthesia-related knowledge regarding resuscitation from cardiac arrest.62,63 One recent study has documented delay in the cardioversion and defibrillation of patients with shockable rhythms in the perioperative setting.64 Despite these challenges, detailed reviews of this topic are now available,65 and there is a wealth of expertise and experience among anesthesiologists in managing both circulatory crisis and cardiac arrest in perioperative patients.
After performing a review of the relevant literature, we offer these suggestions, hoping that they will inspire systematic studies and more formal guidelines to manage these rare perioperative events.
Pre-cardiac arrest issues
Rescuing a patient from an intraoperative crisis requires two separate and very distinct components: comprehension that the patient is in crisis and effective action.66-68 Some clinicians may not recognize the early signs and symptoms of physiological deterioration that often precede adverse events.66Failure to rescue may be a misidentified “cause” of cardiac arrest. Regrettably, in some instances, failure to rescue is really the inability to rescue a patient from an underlying process that becomes so severe (after delayed recognition of a crisis in evolution) that an adverse event, including death, is inevitable despite the timely institution of maximal support.66,69
In addition to initiating therapies during crisis, it is also appropriate to consider escalating the level of monitoring to correspond with the level of supportive care. Clinicians should assess the patient’s known comorbidities, surgical logistics, hemodynamic effects of the anesthetics used, and ongoing autonomic nervous system modulation (e.g., tachydysrhythmias with hypotension vs bradydysrhythmias with hypotension). The timely insertion of both an arterial catheter and a central venous catheter will likely be very helpful in the serial evaluation and management of patients (outlined below).70 Insertion of invasive monitors should not take precedence over supportive measures. The decision to escalate the level of monitoring, similar to the decision to escalate therapies, is ultimately a clinical decision that considers a large number of patient and surgical factors and is beyond the scope of these recommendations.
Left ventricular failure
Right ventricular failure
Clinical progression to shock
Some patients will continue to deteriorate despite volume infusions. In these cases, anesthesiologists may administer small boluses of vasopressor drugs or initiate inotropic support.
If therapy with catecholamines does not improve hemodynamics, small boluses of vasopressin (arginine vasopressin [AVP] 0.5-2 U iv) may work where other catecholamines have failed. Extensive literature documents the use of AVP and its analogs in low-flow states, cardiopulmonary arrest, and general and regional anesthesia.75-78 Given the autonomic imbalance of the perioperative period, consideration should be given to the use of atropine in any patient who does not manifest the anticipated tachycardic response in a crisis.79
Corrective measures for clinical progression to shock and a modified stepwise approach for cardiac arrest in the operating room based on the American Heart Association’s 2010 ACLS Guidelines and the 2008 International Liaison Committee on Resuscitation Consensus Statement on post-cardiac arrest syndrome
Corrective Measures for Clinical Progression to Shock
• Recognize a true crisis
• Call for help
• Call for defibrillator
• Hold surgery and anesthetic if feasible
• Administer FIO2 of 1.0
• Confirm airway positioning and functioning
• Assess oxygen source and anesthetic circuit integrity
• Review ETCO2 trends before hemodynamic instability
Generate a Differential Diagnosis
• Evaluate procedure and consult with procedural colleagues
• Review recently administered medications
• Obtain chest radiograph to rule out tension pneumothorax if airway resistance acutely increased
• Obtain echocardiogram (transesophageal echocardiogram if patient’s trachea is intubated or if patient has a surgically prepped chest) to evaluate ventricular filling, ventricular function, and valvular function, and to exclude pericardial tamponade (Focused Echocardiographic Evaluation and Resuscitation [FEER] exam80)
• Empiric replacement therapy with corticosteroids (in patients who have not been previously treated with steroids, hydrocortisone 50 mg iv and fludrocortisone 50 μg po/nasogastric is an appropriate dose81,82)
Perioperative Cardiac Arrest
• Check pulse for 10 sec
• Effective two-rescuer CPR:
1. Minimize interruptions
2. Chest compression rate 100 compressions·min−1
3. Depth 2 in, full decompression, real-time feedback.
4. Titrate CPR to A-line BP diastolic 40 mmHg or ETCO2 20 mmHg
• Drug Rx
• Attempt CVL placement
• Bag mask ventilation until intubation
• Endotracheal intubation
• Difficult airway algorithm
• Respiratory rate 10 breaths·min−1
• VT to visible chest rise
• TI 1 sec
• Consider inspiratory threshold valve (ITV)
• Defibrillation if shockable rhythm
• Repeat defibrillation every 2 min if shockable rhythm
Post Cardiac Arrest
• Invasive monitoring
• Final surgical anesthetic plan
• Transfer to ICU
Ventilation during severe shock or cardiac arrest
Practitioners may be concerned that reducing ventilation in a patient in shock or in severe respiratory failure will have deleterious effects. Although this has been the conventional wisdom in anesthesia and medicine, studies from the past 15 years suggest a survival benefit from moderate hypoventilation and respiratory acidosis. For example, hypoventilation is associated with a lower incidence of barotrauma in patients with acute respiratory distress syndrome (ARDS) or COPD and is rarely a cause of hypoxemia. Patients with severe lung disease can tolerate hypercarbia and respiratory acidosis.83-88
Hyperventilation is deleterious in all conditions of low-flow state. Studies of ventilation during shock emphasize the following principle: In a low-flow state, the duration of increased intrathoracic pressure is proportional to the ventilation rate, tidal volume, inspiratory time, and delayed chest decompression and is inversely proportional to coronary and cerebral artery perfusion.84,89-91 For example, ventilation at 20 breaths·min−1 during CPR is associated with significantly lower survival than ventilation at 10 breaths·min−1. The most recent ACLS guidelines emphasize avoiding hyperventilation during CPR until an advanced airway device (endotracheal tube, laryngeal mask airway device, or esophageal airway) is inserted. This can be achieved via a higher compression:ventilation ratio (30:2) for single-rescuer CPR for victims of all ages (except newborns) and for two-rescuer CPR for adult victims. Once an advanced airway is in place, the respiratory rate should be maintained at no more than 10 breaths·min−1 with an inspiratory time of one second and the tidal volume limited to “chest rise” (approximately 500 mL in an average 70 kg adult).3 Capnography is usually a more reliable indicator of ROSC than carotid or femoral arterial pulse palpation.3 If rescuers are concerned that the capnograph is malfunctioning, blowing into the sidestream CO2 collecting tube is a quick way to assess this.
New technologies and devices providing automatic CPR92,93 and an airway in-line negative inspiratory valve providing increased venous return during chest decompression94 have all been associated with an increased rate of ROSC, although no clear increase in hospital discharges has been observed.
Auto-positive end-expiratory pressure
Auto-positive end-expiratory pressure (auto-PEEP), also known as intrinsic PEEP or gas trapping, is a well-described cause of circulatory collapse and may be difficult to recognize as a cause of PEA/electromechanical dissociation.95 It occurs almost exclusively in patients with obstructive lung disease, including asthma and COPD (emphysema), and is exacerbated by hyperventilation. In these patients, patterns of ventilation that do not allow sufficient time for complete exhalation produce a gradual increase in the end-expiratory volume and pressure in the lung. This pressure is transmitted to the great veins in the thorax, which depresses both venous return and cardiac output. As auto-PEEP increases, venous return declines.96,97 Auto-positive end-expiratory pressure should be considered a cause of rapid hemodynamic deterioration in an anesthetized patient with acute bronchospasm.
If auto-PEEP is suspected as the cause of circulatory crisis, disconnecting a patient’s tracheal tube from the ventilator for a brief time (5-10 sec) can produce a dramatic improvement in the circulation. Patients who demonstrate dramatic improvement in response to this maneuver will benefit from maximal therapy for obstruction/bronchospasm and will likely fare best with a reduced respiratory rate, short inspiratory time (to promote a longer expiratory time), and lower tidal volumes (no more than 8 mL·kg−1).
Hypovolemia and systolic and pulse pressure variation
The corollary is also true: Minimal or absent systolic and pulse pressure variation with respiration strongly suggests that interventions, other than the infusion of volume or increasing venous return via vasopressors, will be required to support the circulation (e.g., adding positive inotrope agents or eliminating negative inotrope agents). Importantly, excessive tidal volumes (>10 mL·kg−1), increased residual volume and lung compliance (emphysema), and decreased chest wall compliance (3rd degree chest burn, obesity, prone position) will also cause an increase in systolic pressure variation requiring practitioners to make incremental adjustments to their criteria for volume responsiveness.99 Additional indices of fluid responsiveness include the passive leg raise (a quick, reversible, and easy to perform maneuver in which the patient’s legs are raised and a change in blood pressure is assessed—useful in spontaneously ventilating patients), variation in inferior vena cava diameter with respiration via ultrasonography (if access to the abdomen is possible), and esophageal Doppler assessment of aortic velocity.100,106-112
In the setting of severe hypotension, it is reasonable for practitioners to provide volume resuscitation, as long as there is an increase in blood pressure and/or cardiac output without an increased requirement of FIO2 or worsening of total lung compliance (both possible signs of cardiogenic pulmonary edema).
Rescue sequence for cardiac arrest in the operating room
For a variety of reasons, recognizing the time to commence CPR in the OR is more difficult than it may appear to outsiders. First, false alarms vastly outnumber real events because disconnection of sensors (“asystole”), blood draws, and electrocautery are more common than cardiac arrest in most ORs.113,114 Monitoring devices can also fail from heavy use. Second, hypotension and bradycardia are relatively common occurrences in the OR, and most patients recover to an adequate hemodynamic status with minimal intervention. Third, it can be difficult or impossible to obtain satisfactory monitoring in many patients, especially those with vasculopathy, hypothermia, burns, vasoconstriction, or morbid obesity.115
The features of cardiac arrest in the OR include ECG with pulseless rhythm (ventricular tachycardia [V-tach], ventricular fibrillation [V-fib], severe bradycardia, and asystole), loss of carotid pulse > ten seconds, loss of end-tidal CO2 with loss of plethysmograph, and/or loss of arterial line tracing. Once cardiac arrest is confirmed, effective CPR should be initiated immediately in the OR. More important, the rescuer should provide physiological feedback and monitor the data from the ECG, pulse oximetry, end-tidal CO2 (ETCO2), CVP, and arterial catheter. Effective chest compression is indicated by an ETCO2 close to or above 20 mmHg. In 100% of cases, an ETCO2 <10 mmHg after 20 min of standard ACLS is associated with failure of ROSC.116-119 A relaxation (diastolic) pressure (calculated at the time of full chest decompression) of 30-40 mmHg in the presence of an arterial catheter has been associated with a higher rate of ROSC, even after prolonged CPR.120-122 Feedback on the quality of chest compressions can be provided by some of the new defibrillators.123
In the presence of a CVP, the estimate of coronary perfusion pressure (CPP) during CPR is more accurate than by aortic relaxation only. Coronary perfusion pressure can be estimated by briefly freezing the monitoring screen with the arterial line and synchronizing the CVP waveforms. Coronary perfusion pressure is calculated at the time of full chest decompression and is equal to the arterial catheter pressure minus CVP. A CPP > 15 mmHg is associated with an increased rate of ROSC.124,125
ACLS operating room algorithms
Symptomatic bradycardia evolving to nonshockable arrest
Amnemonic approach to the differential diagnosis of bradycardia and nonshockable cardiac arrest
Hydrogen ion (acidemia)
Trauma (hemorrhagic shock, CV injury)
Symptomatic tachycardia evolving to pulseless shockable arrest (ventricular tachycardia, ventricular fibrillation, and torsades de pointes)
Although symptomatic tachycardia, often triggered by severe hypovolemia or an imbalance between surgical stimulus and anesthetic depth, is frequent in the perioperative arena, data regarding its incidence and management are lacking.131 The differential diagnosis for nonshockable tachycardia includes the 8Hs and 8Ts.
Evolution to a malignant rhythm is unlikely in the absence of severe cardiac comorbidities and/or anesthesia complications. Persistent hemodynamic instability with tachycardia can sometimes degenerate rapidly to symptomatic bradycardia. Immediate cardioversion is indicated for a patient with hemodynamic instability from tachycardia (ventricular rate > 150 beats·min−1).3 Cardiac pacing may be necessary in patients after cardioversion because some patients’ rhythms will convert to symptomatic bradycardia. Overdrive pacing of supraventricular or ventricular tachycardia refractory to drugs or electrical cardioversion is also appropriate in perioperative patients.132
Pharmacological approach to shockable rhythm post defibrillation and recommended infusion doses
Torsades de pointes
Cardiac arrest in the perioperative setting is rare and has a different spectrum of causes that compel situation-specific adaptations of ACLS algorithms. In fact, there are intuitive differences in patient management when the health care provider has prior knowledge of a patient’s medical history, is immediately aware of the probable cause of arrest, and initiates medical management within seconds. Since it is both uncommon and heterogeneous, perioperative cardiac arrest has not been described or studied to the same extent as cardiac arrest in the community; thus, recommendations for management must be predicated on expert opinion and physiological understanding rather than on the standards currently being used in the generation of ACLS protocols in the community.
The authors extend their deepest gratitude to the following practitioners who read various drafts of these guidelines and provided useful feedback: Avery Tung MD, Karen Domino MD, Mark Nunnally MD, Heidi Kummer MD, Steven Robicsek PhD MD, Eugene Y. Cheng MD, Daniel Brown MD PhD, Sheila E. Cohen MB, ChB, FRCA, and Patricia A. Dailey MD.
These guidelines were developed from our previous Society of Critical Care Anesthesiologists (SOCCA) and American Society of Anesthesiologists (ASA) monograph reported in 2008. Portions of those guidelines appear verbatim and are used with the permission of the ASA and SOCCA.
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