Cardiac Arrest
Steven A. Robicsek
Joseph A. Layon
Andrea Gabrielli
CASE SUMMARY
A 67-year-old gentleman is scheduled for open elective abdominal aortic aneurysm surgery. Preoperative evaluations and cardiovascular risk stratification highlight a history of stable angina. A recent echocardiogram shows a left ventricular ejection fraction of 50% with left ventricular hypertrophy. He is able to participate in moderate recreational activity, such as golf, and is now chest pain-free for the last 3 months on atenolol and aspirin. He has a mild aortic stenosis but has been told by the family cardiologist that his valve disease is nonamendable to surgery at this time.
Following the induction of anesthesia, and utilizing a balanced technique with opioids and isoflurane, the heart rate increases shortly to 130 bpm with 1.5 mm ST segment depression noted in lead V5. A 60-mg bolus of esmolol decreases the heart rate to 80 bpm, but does not change the ST depression. Transesophageal echocardiography (TEE) is performed. Findings show left ventricular lateral wall hypokinesia. Further reduction of the heart rate with esmolol resolves the wall motion abnormality. The decision is reached to proceed with surgery, which is uneventful.
The patient is transported to the intensive care unit (ICU), still intubated and hemodynamically stable. Upon connecting the patient to the surgical intensive care unit (SICU) ECG leads, you notice that the arterial line goes flat and ventricular fibrillation (VF) is shown on the ECG rhythm strip. The pulse is assessed for 10 seconds, confirming a pulseless rhythm. The best chance to restore spontaneous circulation in this patient is dependent on effective basic and advanced cardiac life support (ACLS):
Chest compressions should be started immediately at a rate of 100 times per minute. A motivated rescuer should achieve at least 1-inch depth with each compression and allow full chest recoil after each stroke.
A defibrillator should be called in immediately.
A second rescuer should provide adequate ventilation. Because this patient remained intubated, ventilation at a rate of eight times per minute, end-tidal volume (VT) to allow chest rise, and inspiratory time of 1 second should be provided.
The airway rescuer should pay attention to avoid hyperventilation while chest compressions are provided.
Defibrillations should be provided as soon as possible, because VF is a shockable rhythm.
Only one 200 J biphasic shock should be provided for each 2-minute cycle of cardiopulmonary resuscitation (CPR).
One mg of epinephrine every CPR cycle or vasopressin, 40 units to replace the first and second dose of epinephrine should be delivered immediately. In shockresistant CPR, IV amiodarone 300 mg should be administered, and followed by repeated IV boluses of 150 mg alternated with a vasopressor.
Postoperative myocardial dysfunction is expected and should be treated with a positive inotrope infusion.
Postoperative neurologic dysfunction (stupor or coma) is expected and should be treated with hemodynamic and general supportive care.
Post-cardiac arrest (CA) hypothermia should be considered in selected cases.
KEY CONCEPTS
Is this an anesthesia-related cardiac arrest (ACA)? Yes, although the most common form of cardiac dysrhythmia during arrest is severe bradycardia followed by asystole (45%). VF is the cause of CA in up to 14% of the cases.
Is there a direct link between the anesthetic management and ventricular defibrillation? Unlikely. The most important predictor of postoperative myocardial infarction (MI) and its complications are the patient’s specific risk and the surgical specific risk.
What are the determinants for successful restoration of spontaneous circulation (ROSC) in these patients? Effective CPR, avoidance of hyperventilation, early defibrillation, and early pharmacologic therapy should be provided to enhance coronary perfusion pressure during chest compressions. Appropriate knowledge
should guide antidysrhythmic therapy after initial failure to restore spontaneous circulation.
The case in the preceding text outlines several important considerations for the management of CA. The American Heart Association published updated guidelines for the management of CPR and emergency cardiovascular care in 2005. These comprehensive guidelines and algorithms were written for a wide variety of scenarios. The operating room and ICU represent unique locations for the management of cardiovascular care because of the immediate availability of medical personnel and equipment. However, successful outcome following intraoperative CA depends on the anesthesiologist’s knowledge of resuscitation guidelines and understanding of the complex interactions between the patient’s coexisting diseases, surgical stress, and anesthetic technique.
INTRODUCTION
The practice of anesthesiology and perioperative medicine has accumulated much experience in the treatment of CA and accomplished a higher standard of safety than any other medical specialty. Although anesthesiology has become more sophisticated, the potential risks of CA from hypoxemia, dysregulation of the autonomic nervous system, and drug toxicity have increased; however, the field of prevention of CA and the art of resuscitation have expanded as well. The development of complex monitoring systems, safer medications, and the adoption of high clinical standards and in-depth education have contributed to improvements in patient safety.1 Because of these events, the practice of today’s anesthesiology represents an aspect of health care in which the risk of death is extremely low. Another clinical phenomenon that emerged in the last decades is that the anesthesiologist has assumed a leading role in the management of in-hospital CA. The impact on prevention and management of CA by having a qualified anesthesiologist during surgical procedures is evident. In a large retrospective review, the adjusted risk for death and failure to rescue was much lower when the patient was under the care of a physician anesthesiologist (alteration for death = 1.08, p < 0.04; alteration for failure to rescue = 1.10,P < 0.01).2
Such trend of successful prevention and management of CA, however, has been challenged by the increase in the number of invasive procedures, many of them performed in elderly patients with higher cardiovascular risk, and by the practice of anesthesia outside the operating room (e.g., radiology or gastroenterology suite, and ICU). The result is that, although ACA still occurs, prompt recognition and treatment usually leads to a successful outcome. Today’s anesthesiologist is in a unique position to be a key element not only during intraoperative CPR, but also in outside locations. Moreover, the anesthesiologist is expected to extend this role—as is the case in many European emergency systems—to ambulance rescue teams as well.
The purpose of this chapter is to review the multiple causes of perioperative CA, provide evidence-based guidelines for its management, and analyze its outcomes.
What Is the Epidemiology of Cardiac Arrest?
Death directly related to general anesthesia is rare and, when it occurs, it is often unpredictable. Furthermore, the data on anesthesia-related mortality may be misleading because usually only events that occur in the first 24-hour postoperative period are applicable. Although this short-term interval provides near-adequate information on procedural events related to anesthesia, it does not reflect the long-term consequences of therapeutic decisions. This fact is well reflected in the historical aspects of CA in the operating room, which overlaps the history of modern anesthesia.
ACA was first reported in the early 1940s, at the time when general anesthesia predominantly consisted of the administration of chloroform to relatively healthy patients undergoing minor procedures.3 A systematic approach to morbidity and mortality related to anesthesia was developed later in that decade, when a number of unexplained perioperative deaths were reviewed by an ad hoc commission.4 This was followed by extended discussions of CA prevention in the relevant literature, which led to in-depth education and significant quality improvements. A second systematic review, done in the 1950s, listed anesthesia-related mortality rates as one in every 2,700 cases, with approximately two-thirds of them directly attributable to anesthesia. Interestingly, such widespread reporting of anesthesia-related complications, coupled with the increase in older and sicker patients undergoing challenging surgical procedures, led to a paradoxical increase in mortality.5 This was documented in a review conducted by the University of Pittsburgh in 1961, which studied the causes of 536 ACAs in 16,000 patients. Of these, only a single patient was considered an ASA Physical Status classification I (ASA I), and most deaths were attributed to either hypotension or hypoxia.6
The development of modern techniques of CPR in the 1960s significantly improved the rate of successful ROSC. In this process, open chest cardiac massage, then a preferred method of cardiac resuscitation in both inpatients and outside of hospital settings, played an important historical role.7
With the passage of time, it became clear that anesthesia-related events could extend into the postoperative period until at least the first postoperative day. Retrospective reviews of 162 deaths related to general anesthesia identified half of the patients in whom hypoxia, induced by airway manipulation, eventually led to patient demise within the first 24 hours of surgery.8 These, and similar observations in 1960, eventually led to the creation of the postanesthesia care units (PACU) where patients’ vital functions were monitored and primarily managed by anesthesiologists.9
A CA was reviewed systematically again in the early 1980s. At that time, both retrospective and prospective studies indicated a drop in anesthesia-related mortality despite the increased acuity of care in the operating room. However, the degree of urgency as when to operate
emerged as an important factor in the causation of ACA, with most anesthesia mishaps occurring either at the time of induction of anesthesia or during the recovery phase.10 Recent series from Australia11 and from Europe12 confirmed these findings and, in addition, identified ventilatory problems as the most common cause of ACA. Less frequently, prolonged and untreated fluctuations of blood pressure—more frequently hypotension and occasionally accelerated hypertension—were identified to be responsible for episodes of severe bradycardia and eventually asystole. These reports also documented the average patient who experienced ACA to be (i) older, (ii) of male gender, (iii) with a higher ASA physical status score, (iv) undergoing emergency surgery, (v) having a prolonged surgical time, and (vi) surgery performed after 3 Pm. In addition, ACA was often preceded by the administration of medications. Further analysis of these issues introduced obligatory quality control, and outcome reviews by the specialty of anesthesiology, which proved extremely valuable.
emerged as an important factor in the causation of ACA, with most anesthesia mishaps occurring either at the time of induction of anesthesia or during the recovery phase.10 Recent series from Australia11 and from Europe12 confirmed these findings and, in addition, identified ventilatory problems as the most common cause of ACA. Less frequently, prolonged and untreated fluctuations of blood pressure—more frequently hypotension and occasionally accelerated hypertension—were identified to be responsible for episodes of severe bradycardia and eventually asystole. These reports also documented the average patient who experienced ACA to be (i) older, (ii) of male gender, (iii) with a higher ASA physical status score, (iv) undergoing emergency surgery, (v) having a prolonged surgical time, and (vi) surgery performed after 3 Pm. In addition, ACA was often preceded by the administration of medications. Further analysis of these issues introduced obligatory quality control, and outcome reviews by the specialty of anesthesiology, which proved extremely valuable.
A 10-year retrospective review published in 2002 showed the overall ACA rate in a large academic institution in the United States to vary from 1.37 per 10,000 to 0.69 per 10,000 anesthetics.13 Further trends were observed overseas where, after a temporary increase in anesthesia-related deaths (associated with twofold increase of major cardiovascular and neurosurgical operations), the mortality from ACA sharply declined.14
Even after the results of these studies became generally known, the direct cause-effect relationship between the choice of anesthesia and ACA was difficult to identify. The pieces of the puzzle, however, fell into place at the end of the 1980s when confidentiality agreements between investigators and government agencies allowed the development of a massive database on ACAs.15 These surveys showed that most cardiac deaths were multifactorial and/or related to inefficient control of the airway and asphyxia. Respiratory complications have also been noted as important contributors to morbidity and ACAs.16
About the same time, the American Society of Anesthesiologists began reporting nationwide insurance claims arising from anesthetic complications. Even with the limitations of voluntary reporting, these reports reliably confirmed that unrecognized airway obstructions were the cause of ACA in approximately 25% of the cases. With the introduction of pulse oximetry as a standard of care in 1984, the number of ACAs caused by unrecognized airway obstruction decreased significantly. Additionally, such a registry also documented the prevalence of spinal anesthesia overdose as a common cause of ACA. This type of survey became essential to provide insight17,18 and formulate policies aimed at improving the quality of anesthesia care.17,19 This eventually resulted in the formulation of the American Society of Anesthesiologists’ (ASA) Practice Guidelines for Management of the Difficult Airway.20 A byproduct of this process was the development of “safety-first mentality” of anesthesiologists, with a consequential decrease in their professional liability premiums. These registries listed the following several event categories that were frequently associated with ACAs:
Inadequate ventilation leading to hypoxia
Severe dysrhythmias, mostly bradycardia induced by hypoxia or drug management, usually narcotics or succinylcholine
Unrecognized hypovolemia resulting in prolonged severe hypotension
This grouping of patients according to the above seems to be valid up to 12 hours post anesthesia on the wards, in the recovery room and the ICU, and on the wards.12
Further studies on anesthesia-related mortality include the retrospective, single institution review of 250,000 anesthetic records,21 which shows the mortality of ACA to be relatively low, ranging from 0.55:10,000 to 2.4:10,000 procedures. In a similar study conducted by the Mayo Clinic,22 ACA is defined as a condition requiring either closed chest compression or open cardiac massage performed between the onset of anesthesia or during transport to the ICU. The two outcome variables observed in the survey were survival for at least 1 hour after resuscitation and survival to discharge from the hospital. Probable causes of ACA were grouped into the following three categories:
Intraoperative hemorrhage
Preexisting cardiac disease and
Hypoxia, either at intubation or at extubation
What Is the Pathophysiology of Cardiac Arrest?
▪ HYPOXIA
Irreversible hypoxic or ischemic brain damage is a devastating complication, which may occur when, at normal body temperatures, the brain is deprived of its oxygen supply for more than 5 to 7 minutes.23 Such a situation may develop in the context of a “cannot intubate-cannot ventilate” scenario. Such airway management failure may be caused by misplacement of the endotracheal tube, airway obstruction, airway collapse, accidental extubation, or aspiration of gastric contents. Laryngospasm induced by mechanical irritation during inadequate depth of anesthesia or bronchospasm of anaphylactic or intrinsic origin may also cause severe episodes of hypoxia. Errors in oxygen supply seldom occur but, when they do, are devastating.24 The proportion of ACAs caused by failure of adequate ventilation remained relatively constant at approximately 35% in the 1980s.10 This increased somewhat in the 1990s25 when airway- and ventilation-related CA during intubation or extubation amounted to approximately 45% of all ACAs, with the
cause of most of these mishaps being either lack of proper monitoring and/or underestimation of the level of sedation.
cause of most of these mishaps being either lack of proper monitoring and/or underestimation of the level of sedation.
At present, the low reported incidence of ACA from hypoxia or hypercarbia is in large part due to the introduction of pulse oximetry and capnography into the daily practice of anesthesia. In fact, the ASA Closed Claims Study reported that 57% of hypoxia-related deaths could have probably been avoided simply with the use of pulse oximetry and capnography.26 Hypoxic brain damage may also occur during prolonged hypotension. In general, although older age and comorbidities have been associated with a worse outcome, they did not seem to influence, per se, the occurrence of hypoxemic CA.
Hyperventilation frequently results from the prevention and treatment of hypoxia, caused by occasional inability to intubate and ventilate; however, if used indiscriminately, it may be harmful. Anesthesiologists, in the presence of adequate lung compliance, have traditionally learned to link the phenomenon of cyclic blood pressure variation—when positive pressure ventilation is applied—to hypovolemia or lung overinflation.27 Recent evidence supports the knowledge that inadvertent hyperventilation is common during CPR. Unnecessary hyperventilation, that is, too many breaths or too large VTs given during CPR, is an inherent risk for death because it may raise intrathoracic pressure to levels high enough to impede venous return and decrease coronary and cerebral perfusion, thereby compromising the success of CPR.28
The aforementioned clinical and laboratory observations led to an important change in the resuscitation guidelines for CA for adult victims with an advanced airway device (ETT, LMA and Combitube) in place—that is, to maintain a respiratory rate no >10 breaths per minute, with an inspiratory time of 1 second and a VT limited to “chest rise”, (estimated ≈ 500 mL in the adult patient).29
Pharmaceuticals such as neuromuscular blocking agents12,13 with the potential to decrease respiratory drive can also be associated with hypoxemic CA. Human and environmental factors may also contribute to the occurrence of hypoxemic CA, especially by performing ineffective CPR. CPR is more likely ineffective if CA occurs after the typical hospital working hours—after 5 Pm or during the weekends—probably secondary to the reduced number of specialists present in the hospital after hours, as well as the emergent nature of procedures. It is also no surprise that the outcome of ACAs is the best in tertiary referral centers where personnel with airway skills are available throughout the night.30
Pregnant women and children, especially neonates, are highly susceptible to hypoxemic CA. Both, respiratory and circulatory events are equally distributed in children and infants, occurring in 19 per 10,000 and 2.1 per 10,000 respectively.31 The adjusted ACA is approximately ninefold higher compared to adults. However, because of the low incidence of comorbidities, as well as the neuronal plasticity in the very young, the outcome of ACA is generally better in this population. Anesthetic mishaps causing hypoxic CA in infants are also possible during the maintenance of anesthesia. Relative hypovolemia from preoperative fasting may be a contributing event.
Although the number of maternal deaths due to general anesthesia shows a substantial decrease, airway management failures in obstetric anesthesia still occur. This may be associated with displacement of the stomach by the gravid uterus and high risk of aspiration. Other pregnancy related, physiologic changes may also contribute to adverse outcomes, including ACA. These changes include diaphragmatic elevation and decreased functional residual capacity, both of which reduce oxygen lung reserves. The oxyhemoglobin dissociation curve is shifted to the left, thereby resulting in less oxygen release. Hemodilution decreases hemoglobin concentration, and oxygen consumption is increased, factors that contribute to the development of ACA approximately 10-fold. Many of these patients are subjected to general anesthesia on an emergency basis, secondary to “fetal distress.” A confidential review in the early 1980s attributed general anesthesia-related maternal mortality to difficult intubation in 40% of cases, equipment failure in 18%, and postoperative hypoventilation in 5%.32 Although the danger of hypoxia in the pregnant woman still persists, recent reports show that anesthesia for cesarean section is now 30 times safer than it was 50 years ago. This is most likely due to the widespread use of regional anesthesia and improved monitoring.33,34
▪ ANESTHESIA-RELATED CARDIAC ARREST
Life-threatening dysrhythmias occur during anesthesia in approximately 0.4% of the patient population.35 Their occurrence may be related to the anesthetic technique, which in turn impacts on the hemodynamic variables and may eventually cause CA.
The most common forms of cardiac dysrrhythmias during anesthesia are bradycardia or asystole (45%), ventricular tachycardia or fibrillation (14%), and pulseless electrical activity (PEA) (7%). In the presence of dysrrhythmias, a high index of suspicion for undetected hypoxia should be the rule, and resuscitation should be performed keeping in mind the pathophysiology of local, general, and neuraxial anesthesia and their effect on resuscitation efforts. The physician or other health care provider’s prior knowledge of the patient’s medical history, their immediate awareness of the probable cause of arrest, and the initiation of medical management within seconds also influence survival. Unfortunately, failure to increase the Fio2 to 1.0, forgetting to close the vaporizer with the inhalational anesthetic, and unnecessarily delayed defibrillation or pharmacologic interventions still occur in the operating room.
The cardiovascular effects of inhaled anesthetic agents may include myocardial depression, parasympathetic or sympathetic stimulation, increased myocardial excitability, and severe hypotension. The latter is most likely to occur in patients with valvular heart disease, heart block, constrictive pericarditis, or anaphylactic reaction. Inhalational anesthetics may also hinder atrioventricular conduction, and have a direct negative inotropic effect
that can sensitize the myocardium to the arrhythmic effects of catecholamines.36 In animal studies, overdose with inhalational agents has been found to interfere with coronary autoregulation and create transient episodes of sympathetic hyperactivity, both of which may result in myocardial ischemia. This usually resolves when the anesthetic is terminated; low ejection fraction may persist and contribute to postoperative cardiovascular instability. Previously unrecognized coronary artery disease may also lead to fatal arrhythmias and to the failure of resuscitation.37
that can sensitize the myocardium to the arrhythmic effects of catecholamines.36 In animal studies, overdose with inhalational agents has been found to interfere with coronary autoregulation and create transient episodes of sympathetic hyperactivity, both of which may result in myocardial ischemia. This usually resolves when the anesthetic is terminated; low ejection fraction may persist and contribute to postoperative cardiovascular instability. Previously unrecognized coronary artery disease may also lead to fatal arrhythmias and to the failure of resuscitation.37
Intravenous drugs, such as etomidate,38 succinylcholine,39 and propofol,40,41 by their ability to increase vagal activity, may predispose to asystole. Dexmedetomidine, an α-2 adrenergic receptor agonist with sedativeanalgesic and anxiolytic properties and a full agonist to the α-2 adrenergic receptor, may act synergistically with general anesthesia to cause severe bradycardia and hemodynamic instability. This occurs primarily by potentiation of the effects of other negative chronotropic drugs, such as digoxin and pyridostigmine, or with the effects of a neuraxial block. The resulting asystole is usually brief and responds well to parasympatholytic agents. Hypoxemiainduced sympathetic stimulation may be followed by severe bradycardia and asystole.1 This may be facilitated by increased serum potassium, acute metabolic and respiratory acidosis, or by the cardiovascular depressant effect of the anesthetic itself. Hypercapnia from hypoventilation leads to an increase in circulating catecholamines. The combination of succinylcholine and dexmetomidine is commonly associated with initial bradycardia followed by asystole. This is more likely to occur with repeated administration.42 The mechanism is probably competition for available cholinergic receptors by succinylcholine, direct stimulation of the carotid baroreceptors, and accumulation of acetylcholine. Remifentanil, a short-acting, potent narcotic has also been associated with severe cardiac depression.43
Surgical manipulation of different organs, such as the rectum, uterus, cervix, larynx, bronchial tree, bladder and urethra, mesentery, the carotid sinus, heart, dura, biliary tract, extraocular muscles, and testicles all could lead to severe bradyarrhythmias by enhancing an unopposed vagal tone.
Abnormalities of potassium and calcium metabolism are often seen in patients undergoing either elective or emergent surgical interventions. Studies on the dysrhythmic effects of hypokalemia not only confirmed that hypokalemia may endanger patients with MI,44 but also conclusively linked rapid correction of chronic hypokalemia to ACA. An occasional side effect of succinylcholine is the acute onset of hyperkalemia and consequent cardiovascular instability. This usually occurs in patients with thermal injuries, upper or lower motor neuron damage, or other critical illness resulting in immobilization. The manifestation is usually late, approximately 1 month after the initial injury, and is related to extrajunctional neuromuscular receptor upregulation.
Air embolism, as well as pulmonary thromboembolism, may also induce bradycardia and asystole, the latter because of increase in right ventricular afterload and decrease in cardiac output. “Mixed” CA, caused by hypoxia and dysrhythmias, as well as metabolic-induced CA, may occur in special clinical situations. Massive hemorrhage and cardiac diseases, such as cardiomyopathy, myocardial ischemia, and acute myocarditis may also lead to ACA by causing decreased systemic oxygen delivery and coronary perfusion. Hypothermia during the course of surgery or intracardiac diagnostic procedures may increase myocardial irritability and evoke physiologic responses, leading to severe dysrhythmias. Interestingly, hypoxic ACA actually has a better prognosis than ACAs from other causes. For example, a recent series showed that 16 out of 20 patients having suffered hypoxic ACA survived to hospital discharge.30
How Can Regional Anesthesia Lead to Cardiac Arrest?
Up to 50% of CAs occurring during local or regional anesthesia may be avoided by timely recognition and correction of inadequate ventilation.45 In this respect, the database of the American Society of Anesthesiology Closed Claim Study, a project of the ASA Committee on Professional Liability,18 revealed surprising clinical trends. In each case, CA occurring from local or regional anesthesia was unexpected, as the patient’s ASA status was low; additionally, the outcome was, in general, poor. In 30% of the 14 cases reviewed, a spinal anesthetic was applied in the course of an emergency procedure, and the use of tetracaine seemed to be the drug most commonly associated with CA. Most anesthesiologists involved in these cases were experienced.
Despite the obvious selection biases resultant from self-reporting, there were some special features of patients suffering CA in local or regional anesthesia (see Table 21.1). These findings indicate that, despite the presence or immediate availability of an anesthesiologist, the crisis situation was often appreciated too late, the treatment ineffective, and the neurologic recovery limited; indeed, only four patients regained consciousness. Even those patients were left with various degrees of cognitive dysfunction. One may conclude that hypoventilation induced by opioids, benzodiazepines, or hypnotics may have enhanced a preexistent sympathetic blockade produced by a relatively high spinal anesthesia, and that the anesthesiologist’s level of awareness of this potential interaction was low.33,46
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