ACLS Anesthetic Management

Description

The American Heart Association's Advanced Cardiac Life Support (ACLS) course is evidence-based consensus products to assist practitioners with emergency scenarios, in particular cardiac arrest. They are intentionally broad in scope (1).
Algorithms treat distinguishable syndromes to specify care. These are often cardiac rhythm based (e.g., asystole vs. ventricular tachycardia).
ACLS guidelines, however, may not fit the most common arrest scenarios seen in the operating room (OR).
- ACLS treats probabilities; these are not specific to the surgical setting.
- There is no provision in ACLS for a previously ventilated patient.
- Arrest in the OR is witnessed, usually evolves over minutes, and can be treated with a broad range of resources.

Epidemiology

Incidence

Data for arrest or near arrest in the OR are difficult to assess. Best estimates are 4.3–19.7 cardiac arrests per 10,000 anesthetics for adults (approximately 10% of these are directly attributed to anesthesia) and 2.6–11 per 10,000 for children (much higher in infants) (2,4).
Arrest during neuraxial anesthesia is estimated at 1.8 per 10,000 anesthetics and is more common with spinal anesthesia than epidural anesthesia (4).
Most available data on intraoperative cardiac arrest come from registries or closed-claims databases. These are useful tools for studying rare events but cannot be trusted for accurate incidence data.

Prevalence

Arrest is an incident phenomenon, but there are many prevalent factors in the OR that influence the risk and type of arrest.
- Intraoperative hypovolemia is common and an important cause of shock.
- Patient comorbidities contributing to arrest include cardiac and thromboembolic disease.
- Anesthetic agents are potent and their overdose accounts for the majority of arrests attributable to anesthesia. Induction drugs and volatile anesthetic agents are potent vasodilators and negative inotropes.
- Arrest at induction has declined while arrest during maintenance or emergence has remained the same. Esophageal intubation and airway loss are less common since the use of capnography and pulse oximetry became routine (8).
- Complications of intravascular access (e.g., hemorrhage, pneumothorax, tamponade) are rare but serious causes.
The frequency of arrhythmias under anesthesia is different. The most common arrhythmias include (7):
- Bradycardia followed by asystole (45%)
- Unknown (33%)
- Ventricular tachycardia/ventricular fibrillation (14%)
- Pulse-less electrical activity (7%)

Morbidity

Hypoxic neurologic injury is the salient morbidity of cardiac arrest. It is a prominent factor in closed-claims data, associated with some of the highest payments.
Pancreatitis, hepatic dysfunction, renal failure, and the multiple organ dysfunction syndrome (MODS) can follow prolonged shock after cardiac arrest.

Mortality

Estimated mortality from an intraoperative arrest ranges from 20% to 50%, compared with 84–97% for out-of-hospital cardiac arrest (US data) (5).
In one large series from the Mayo Clinic, in-hospital mortality was 21% from arrests directly attributable to anesthesia, versus 71% in those that were not. Other smaller series suggest higher mortality in anesthesia-attributable arrest (up to 80%) (6).
Factors associated with mortality include: ASA patient status, emergency surgery, diabetes mellitus, end-stage organ failure, protracted hypotension or use of vasopressors prior to arrest, invasive monitoring, and type of surgery (cardiac surgery worst).
Unlike other patient populations, asystole is associated with good survival (80% in one series), suggesting it is mediated by autonomic or drug effects, and is therefore reversible in many cases.
Mortality differences suggest that the combination of different etiologies, witnessed arrest, and timely availability of advanced resuscitation techniques make intraoperative arrest different from community arrest.

Etiology/Risk Factors

Arrest in the OR is multifactorial.
Ischemic heart disease and conduction abnormalities share etiologies with causes of arrest outside the OR.
Patient comorbidities are the most likely contributors to cardiac arrest, followed by surgical and anesthetic factors.
Anaesthetists cannot prepare for every emergency the same way. Training in arrest management should target 4 specific cause groups:
- Events specific to anesthetic intervention (e.g., pneumothorax, high spinal)
- Reactions to specific agents (e.g., local anesthetic systemic toxicity, malignant hyperthermia)
- Factors that occur more frequently, even though they do not always cause arrest, such as hypovolemic shock and hypoxemia
- Relatively "common" rare causes (somewhere between 0.1 and 1 in 10,000 anesthetics)
Some causes of arrest in the OR that result from direct intervention include:
- Hypoxemia
- Hemorrhage
- Vagal stimulation
- Emboli (e.g., venous air embolism)
- Over-ventilation/auto-PEEP
- Drug reactions (anaphylaxis, malignant hyperpyrexia)

Physiology/Pathophysiology

Since arrest data come from retrospective sources, only correlation can be ascertained. Causation must be speculative.
- Preload (hemorrhage, capillary leak, hypovolemia)
- Afterload (vasoplegia, drug effect)
- Pump function (right heart, left heart, contractility, dysrhythmia)
- Impaired filling (tamponade, auto-PEEP, abdominal compartment syndrome)
Retrospective evaluation of arrests suggests a correlation with preclinical signs.
- Hypotension
- Tachycardia
- Abrupt drops in end-tidal CO₂ are particularly ominous.

Prevantative Measures

MOST of what anaesthetists do involves avoiding arrest scenarios. Skilled anaesthetists proactively avoid disaster before signs of deterioration become apparent.
The time between a problem becoming detectable and arrest can be short as problems escalate.
Rapid treatment is most likely to improve outcomes.

Diagnosis ⬆ ⬇

Disaster evolves quickly; thus, diagnosis and rescue treatment should occur simultaneously.
Monitor failures are far more common than arrest, but must be addressed quickly and arrest scenarios should always be ruled out first.
Factors associated with arrest include:
- Change in ECG to pulse-less rhythm
- Loss of palpable pulse or arterial waveform pulsatility
- Loss of end-tidal CO₂ (very specific, values <10 mm Hg are associated with severe loss of cardiac output and the need for chest compressions).
- Loss of plethysmograph waveform
Do not spend more than 10 seconds seeking a pulse before beginning chest compressions. Return of spontaneous circulation (ROSC) is associated with preserved myocardial oxygen tension, which depletes rapidly without CPR.
Screening for specific risks helps identify sources of arrest (e.g., history of allergy/adverse drug reactions, obstructive airway disease, aortic stenosis, prolonged QT syndrome).
Pulse pressure variation >15%, with a tidal volume of 8–10 mL/kg, predicts fluid responsiveness. In a population at high risk for hypovolemia, this can be very useful.
If available, a focused, rescue transesophageal echocardiography can aid with diagnosis (comparative chamber size, wall motion abnormalities, and signs of embolic phenomena).
Chest radiography may aid with ruling out probable complications of central venous cannulation (e.g., hemorrhage, pneumothorax).

Differential Diagnosis

Pathophysiologic mechanisms are a useful way to organize etiologies and treatments.
Anesthetic causes: Drug overdose, high neuraxial block, local anesthetic systemic toxicity, malignant hyperthermia, drug swap, anaphylactic reaction
Respiratory causes: Hypoxemia, auto-PEEP, hypoxemia, bronchospasm, tension pneumothorax
Cardiovascular causes: Hemorrhage, hypovolemia, acute coronary syndrome, pulmonary hypertension, right heart failure, pulmonary embolism (thrombus, air, fat, etc.), long QT syndrome (Torsades de Pointes), pacemaker failure, oculocardiac syndrome, tamponade, increased intra-abdominal pressure, inferior vena cava (IVC) compression (e.g., flex position, gravid uterus)
Metabolic causes: Electrolyte imbalance (hyperkalemia), transfusion reaction

Treatment ⬆ ⬇

CPR should be initiated quickly (allow no more than 10 seconds to find a pulse in suspected arrest) [C].
Compression rate should be 100/minute and each compression should be at last 51 mm in depth (1).
Respiratory rate should be no more than 10 breaths/minute (1).
Local anesthetic systemic toxicity: Intralipid^™ rescue is associate with ROSC (1) and good outcomes have been reported even after 60 minutes of CPR (7).
Fluid responsiveness should be immediately assessed. Fluids are beneficial in most cases (7).
Amiodarone is a first-line agent in ventricular tachycardia and ventricular fibrillation (1).
Consider pacing for hemodynamically significant bradycardia (1).
In right heart failure, physiologic considerations include adequate filling, perfusion pressure (both systolic and diastolic systemic pressures), and inotropic support (7).
Embolic arrests, including venous air embolism, should be treated as right heart failure (7).
Wide-complex bradycardia and asystole are consistent with hyperkalemia. Early treatment with an IV calcium chloride bolus is indicated (7).
Emergency pacing is indicated for:
- Bradycardia unresponsive to chronotropes (7)
- Escape rhythms, drug overdose, acidosis, electrolyte abnormalities (7)
- Significant sinus node dysfunction, Mobitz type II 2nd degree, 3rd degree heart block, alternating bundle branch block, or bifascicular block (1).
- Overdrive pacing of tachycardias (supraventricular tachycardia or ventricular tachycardia) (7).

Follow-Up ⬆ ⬇

During post-arrest care, one should consider: Targeted temperature management (therapeutic cooling) (1) and avoidance of hyperoxia (PaO₂ >100 mm Hg) (7).
Patients surviving anaphylaxis or malignant hyperthermia, or those with a difficult airway, should be given documentation they can bring for future operative encounters (7).

Closed Claims Data

Death or brain damage was associated with induction of anesthesia in 62% of cases during 1985–1992, versus 35% of cases from 1993 to 1999 (8).
Caplan et al. describe 14 cases of high spinal, suggesting that bradycardia is an important early warning sign and that epinephrine is associated with ROSC (3).

Pregnancy Considerations

The gravid uterus can compress the aorta and IVC after the 20th week of gestation.

Resuscitation of the mother may not be possible until the fetus is delivered by emergency hysterotomy.

During arrest, hysterotomy should be performed at the bedside since there is insufficient time to transport the patient to the OR.

Pediatric Considerations

CPR recommendations in pediatric patients vary by the patient's age.

Resuscitation drugs should be dosed according to the patient's weight.

Intravenous access can be uniquely difficult in pediatric patients. Intraosseous lines are a method to get quick reliable access to the circulation.

Cardiac output in children frequently depends on heart rate (rather than on contractility), making the treatment of bradycardia an important part of pediatric resuscitation.

References ⬆ ⬇

American Heart Association . ACLS Provider Manual, 2010.
Newland MC , Ellis SJ , Lydiatt CA , et al. Anesthetic-related cardiac arrest and its mortality: A report covering 72,959 anesthetics over 10 years from a US teaching hospital. Anesthesiology. 2002;97:108–115.
Zuercher M , Ummenhofer W. Cardiac arrest during anesthesia. Curr Opin Crit Care. 2008;14:269–274.
Peterson GN , Domino KB , Caplan RA , et al. Management of the difficult airway: A closed claims analysis. Anesthesiology. 2005;103:33–39.
Gabrielli A , O’Connor MF , Maccioli GA. Anesthesia-centric ACLS. Available at: .
Nichol G , Thomas E , Callaway CW , et al. Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA. 2008;300:1423–1431.
Sprung J , Warner ME , Contreras MG , et al. Predictors of survival following cardiac arrest in patients undergoing noncardiac surgery: A study of 518,294 patients at a tertiary referral center. Anesthesiology. 2003;99:259–269.
Caplan RA , Ward RJ , Posner K , et al. Unexpected cardiac arrest during spinal anesthesia: A closed claims analysis of predisposing factors. Anesthesiology. 1988;68:5–11.

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Basics ⬇