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General, Regional, or Monitored Anesthesia Care for the Cardiac Patient Undergoing Noncardiac Surgery
Key Points
- 1.
With monitored anesthesia care, the stress response to surgery may not be adequately blocked, and the resulting tachycardia may aggravate the patient's underlying cardiac disease.
- 2.
A decrease in minute ventilation and increase in carbon dioxide associated with sedation can have deleterious effects on patients with right heart dysfunction.
- 3.
The recommended dose of epinephrine is reduced to less than 1 µg/kg in the treatment of local anesthetic toxicity; lipid emulsions are preferable.
- 4.
Neuraxial and regional anesthesia may decrease the surgical stress response and can obviate or supplement a general anesthetic, although chronic anticoagulation can impact the safety of these techniques.
- 5.
Epidural anesthesia is often favored over spinal anesthesia for cardiac patients undergoing noncardiac surgery because the level of anesthesia can be incrementally adjusted.
- 6.
Subarachnoid neuraxial catheter placement may permit a safe spinal anesthetic in patients at high risk for complications, with both general anesthesia and traditional spinal anesthesia, by allowing careful titration of the block level.
- 7.
All volatile inhalation agents cause dose-dependent decreases in contractile function, induce arterial and venovasodilation, decrease cardiac myocardial oxygen consumption (Mv o 2 ), and may induce protective myocardial preconditioning.
- 8.
The anesthetic technique for a cardiac patient undergoing noncardiac surgery is dependent on (1) the type of surgery or procedure, (2) the extent of cardiac disease, and (3) the presence of other comorbidities.
Given the increasing prevalence of heart disease, the frequency of patients with significant cardiac disease presenting for noncardiac surgery will likely increase in the future. The anesthetic technique selected for these patients depends on a number of factors, including the type of surgery or procedure, the type and severity of the underlying cardiac disease, and the presence of other comorbidities. Factors influencing the selection of an anesthetic technique (i.e., general, regional, neuraxial, or monitored anesthesia care [MAC]) for cardiac patients undergoing noncardiac surgery are discussed in this chapter.
Patients with cardiac disease undergoing noncardiac surgery are at higher risk of developing perioperative complications. Both surgery and anesthesia can result in adverse cardiac events via sympathetic nervous system stimulation, inflammation, and hypercoagulability that may be induced. Intraoperatively, practitioners caring for the cardiac patient may also encounter hemodynamic instability, acute blood loss, and hypothermia. Therefore choosing the anesthetic technique that will maintain the desired hemodynamic goals ( Table 12.1 ); improve operating conditions; and provide the patient with amnesia, analgesia, or both is crucial.
Table 12.1
Hemodynamic Goals for Common Adult Cardiac Disease
| Cardiac Disease | HR | Preload | Afterload (SVR) | PVR | Contractility | Avoid | Goal |
|---|---|---|---|---|---|---|---|
| AS | Sinus rhythm; 60–80 beats/min | Increased or adequate | Increased | Maintain | Maintain |
|
|
| AR | Fast: 80–100 beats/min | Increased | Decreased | Maintain | Maintain |
|
|
| MS | Sinus rhythm, slower HR to increase diastolic filling time and improve ventricular filling | Normal or increased | Normal | Maintain | Decreased |
|
|
| MR | Increased (normal to increased) | Increased (in some with dilated LA and LV, increased preload can increase regurgitant fraction) | Decreased | Decreased | Maintain |
|
|
| TS | Maintain (depends on sinus rhythm) | Increased | Increased | Maintain | Maintain | ||
| TR | Increased or maintain | Increased | Maintain | Decreased | Maintain | ||
| PS | Increased | Increased | Maintain | Decreased or maintain | Maintain |
|
|
| CAD | Slow: 50–80 beats/min | Decreased | Increased | Maintain | Maintain |
|
|
| HCM | Normal | Increased | Increased | Decrease |
|
|
AR, Aortic regurgitation; AS, aortic stenosis; AV, aortic valve; CAD, coronary artery disease; CO, cardiac output; HCM, hypertrophic cardiomyopathy; HR, heart rate; LA, left atrium, LAP, left atrial pressure; LV, left ventricle; MR, mitral regurgitation; MS, mitral stenosis; MV, mitral valve; PAP, pulmonary artery pressure; PS, pulmonic stenosis; PVR, pulmonary vascular resistance; RV, right ventricle; SV, stroke volume; SVR, systemic vascular resistance; TR, tricuspid regurgitation; TS, tricuspid stenosis.
Monitored Anesthesia Care
Monitored anesthesia care, as defined by the American Society of Anesthesiologists (ASA), involves the preoperative evaluation, intraoperative monitoring and management, and postoperative care of a patient undergoing a surgical procedure without general anesthesia. Intrinsic to MAC is the ability to identify and manage intraoperative physiologic derangements while providing sedation, analgesia, or both to the patient. Sedation and analgesia are often provided during MAC, but they are not required components. However, the practitioner providing MAC must have the ability to convert to a general anesthetic if necessitated by patient or procedural factors.
Monitored anesthesia care, including local anesthesia with or without sedation, is a useful and often successful anesthetic technique for appropriately selected cases. Although MAC may be deemed by some individuals to be the least invasive of all anesthetic techniques because of its association with minor procedures and minimal hemodynamic changes, it is important to acknowledge the challenges, limitations, and potential dangers of MAC. For example, the stress response to surgery may not be adequately attenuated, and the resulting sympathetic stimulation may aggravate the patient's underlying cardiac disease. Patients undergoing procedures under MAC are often pharmacologically sedated; however, because they are not under general anesthesia, they may be aware of their surroundings and will respond to an inadequately blocked surgical stimulus or a stressful operating room (OR) environment. In addition, local anesthetic toxicity can occur with local infiltration of the surgical field and at very high blood levels can lead to cardiovascular collapse. Furthermore, tachycardia induced by the intravascular or subcutaneous injection of local anesthetic with epinephrine can be detrimental for patients with coronary artery disease.
Under MAC, tissue oxygen demand is not significantly decreased from the normal awake state and in fact may be significantly increased if a stress response leads to increased sympathetic tone. Alternatively, hypoxia from excessive sedation and hypoventilation may adversely affect myocardial oxygen supply. Further complicating the scenario, surgeons often request a motionless field to safely complete the procedure. In general, patient movement is more common under MAC and may be even more prevalent in the cardiac population because their physiology may not permit adequate sedation. Close communication with the surgical team is essential for a successful procedure under MAC because it may help prevent or mitigate some of these potential adverse events.
That being said, MAC also has theoretic benefits in patients with underlying cardiac disease. Avoiding the hemodynamic changes often associated with the induction of and emergence from general anesthesia, as well as positive-pressure ventilation, may be desirable in this population. Furthermore, adequate local anesthesia not only minimizes stimulation during a procedure but also can provide for postoperative analgesia and mitigate undesirable increases in sympathetic tone ( Box 12.1 ).
Box 12.1
Monitored Anesthesia Care and Myocardial Oxygen Demand and Delivery
-
Tissue oxygen demand is not significantly decreased from the normal awake state.
-
Hypoxia from sedation and hypoventilation may adversely affect myocardial oxygen supply.
-
Avoidance of the hemodynamic perturbations associated with induction and emergence from general anesthesia may help optimize myocardial supply in select cases.
Unfortunately, no randomized controlled trials have compared outcomes of MAC with outcomes of general anesthesia in cardiac patients. However, the overall goals of MAC and general anesthesia remain the same—minimization of hemodynamic perturbations. Therefore if the adequate administration of local anesthesia, analgesia, or sedatives can mitigate patient stress and hemodynamic perturbations, then MAC may be an optimal anesthetic plan for the cardiac patient undergoing noncardiac surgery.
Monitoring During Monitored Anesthesia Care
As with general anesthesia, standard ASA monitors are required for MAC. Depending on the surgical procedure, expected duration, chance of conversion to general anesthesia, and the potential for hemodynamic fluctuation, more invasive monitors may be indicated. The placement of an arterial catheter may be unnecessary for short, simple procedures. However, in patients with critical valvular heart disease, pulmonary hypertension, severe cardiomyopathy, or other critical cardiac illnesses, an arterial catheter may be indicated. Similarly, the need for invasive arterial monitoring may be determined by the need for deep sedation or a high likelihood of conversion to a general anesthetic. Central venous pressure monitoring is rarely necessary for a planned MAC unless peripheral intravenous (IV) access is unobtainable. Given a lack of airway instrumentation, transesophageal echocardiography (TEE) is often not feasible. However, intermittent TEE examinations are occasionally done for specific procedures (e.g., transcatheter aortic valve replacement done under MAC). Intermittent transthoracic echocardiography may be helpful for challenging cases done under MAC if the windows are accessible.
Sedation
Patients undergoing procedures with MAC commonly receive some form of sedation, analgesia, or both, with the goal being the relief of pain and anxiety during the procedure. Modulation of pain and anxiety during a procedure is especially important in patients with underlying cardiac disease given the risks posed by any increase in sympathetic tone. Most medications commonly used for sedation during routine anesthetics may be used safely and effectively in patients with cardiac disease, provided potential side effects are monitored for and managed appropriately ( Table 12.2 ).
Table 12.2
Sedatives and Analgesics for Monitored Anesthesia Care
| Drug | Dose |
|---|---|
| Propofol | Bolus: 0.25–1 mg/kg Infusion: 25–75 µg/kg/min |
| Midazolam | Bolus: 0.02–0.1 mg/kg |
| Fentanyl | Bolus: 25–100 µg |
| Remifentanil | Infusion: 0.02–0.05 µg/kg/min |
| Dexmedetomidine | Bolus: 0.5–1 µg/kg over 10 min Infusion: 0.3–1 µg/kg/h |
Propofol
Propofol is a lipid-soluble alkylphenol derivative that has become widely used for the induction and maintenance of sedation because of its rapid onset and redistribution, titratability, potential for amnesia, and antiemetic properties. It is rapidly redistributed after bolus administration, with an initial distribution half-life of 2 to 8 minutes and is rapidly metabolized by the liver. Because of lipid solubility, prolonged use via infusion increases the context-sensitive half-time; however, the decline in serum levels remains relatively rapid compared with other IV anesthetics. Sedation with propofol may be accomplished via several techniques: (1) single bolus dose (or titrated bolus doses) for short procedures, (2) bolus followed by infusion or repeated boluses for longer procedures, and (3) infusion alone without bolus.
Although it has many beneficial properties, propofol has significant effects on the cardiovascular system that should be considered in patients with underlying cardiac disease. Although the direct action of propofol on the myocardium is controversial, it likely has some direct myocardial depressant effects via L-type Ca 2+ channels or sarcolemma calcium release modulation. This depressant effect may be more pronounced in the failing myocardium and may result in a significant reduction in cardiac output. Propofol also causes reliable decreases in preload and systemic vascular resistance (SVR) by a multifactorial process that includes decreased sympathetic tone, decreased calcium mobilization in smooth muscle, and inhibition of prostacyclin synthesis. The net result is decreases in arterial blood pressure, SVR, and potentially cardiac output that may be more pronounced in patients with cardiac disease. Heart rate is reported to be relatively unchanged.
Despite the aforementioned effects, propofol sedation during MAC can be safely accomplished in patients with cardiac disease as long as these cardiovascular effects are carefully considered. Patients with poor left ventricular (LV) function and slow circulation times take longer to show an effect from a propofol bolus or change in infusion rate. Therefore a cumulative overdose may occur in this patient population if adequate dosing intervals are not maintained. Further compounding this issue, older adult patients who frequently have cardiac disease also require lower doses for the same clinical effect. Given these characteristics and propofol's narrow therapeutic index, it is possible to transition rapidly from light sedation to general anesthesia and apnea. The risk of hypoventilation and apnea must be considered in patients who are sensitive to changes in partial pressure of CO 2 (e.g., severe pulmonary hypertension).
Patients with valvular disease who are sensitive to changes in SVR (e.g., aortic stenosis) must be treated with extreme caution, and in severe cases, propofol may be best avoided. However, propofol may be safely used for patients with valvular heart disease if reduced doses are used and the drug is carefully titrated to effect. In higher risk patients, sedation with an infusion only rather than a bolus followed by an infusion may lead to greater hemodynamic stability at the expense of longer time to an adequate sedation depth.
Fentanyl
Fentanyl is a synthetic opioid that is 50 to 100 times more potent than morphine and significantly more lipid soluble. It is a common component of MAC and general anesthesia because of its rapid onset, short half-life, and minimal systemic side effects (e.g., histamine release, venodilation) compared with morphine. After IV administration, fentanyl demonstrates an initial effect in 1 to 2 minutes and maximum effect at 6 minutes, with an expected duration of action of 30 to 60 minutes. Termination of action is due to redistribution from the central nervous system (CNS) to the muscle and fat compartments. These properties make it useful for procedures under MAC; however, it has no amnestic properties, and if amnesia is desired, it must be combined with another agent.
Fentanyl provides excellent pain control during invasive procedures and can be used via intermittent bolus with titration to the desired effect. Alternatively, it may be administered as an infusion, but this is rarely indicated for procedures under MAC. Redistribution to secondary compartments and a terminal half-life of 2 to 4 hours lead to progressively increasing serum concentration during a continuous infusion and increase the chance of adverse events.
In general, opiates have a favorable cardiovascular profile and have been used successfully in cardiac surgery for decades. The major hemodynamic effects of bradycardia and decreases in arterial blood pressure, which are usually mild, are attributed to decreased sympathetic tone. The main problems associated with opioid use during MAC are related to hypoventilation and apnea. Careful monitoring is indicated, especially in at-risk populations (e.g., older adults) that will respond poorly to elevated CO 2 and atelectasis.
Remifentanil
Although remifentanil is a synthetic opioid like fentanyl, it is structurally unique in that it contains ester linkages. It is therefore metabolized by blood- and tissue-nonspecific esterases, resulting in a very short half-life of 5 to 20 minutes. It is not affected by liver or kidney dysfunction, nor is the half-life prolonged in pseudocholinesterase deficiency.
Remifentanil has been used successfully in MAC anesthesia, including procedures done in the cardiac catheterization suite. The most common technique for remifentanil-based MAC is a low-dose infusion that is titrated to analgesia and sedation. Bolus administration is possible, but infusion is often preferred because of the rapid onset and short duration of action. It has been administered in intermittent bolus form for short painful events such as uterine contractions during labor, but for procedures with relatively constant stimulation levels, an infusion provides more stable analgesia.
Major side effects include intense pruritus, dizziness, and respiratory depression. Otherwise, the cardiovascular profile is similar to that of other opiates (e.g., fentanyl), and as with other opiates, dose-related side effects such as respiratory depression may be more common in elderly patients.
Dexmedetomidine
Dexmedetomidine is a highly specific α 2 agonist useful for both procedural and intensive care unit (ICU) sedation. It produces a sedative–hypnotic effect with associated analgesia and sympatholysis via agonism at central presynaptic α 2 receptors. It redistributes rapidly after short-term administration, with a context-sensitive half-time of 4 minutes after a 10-minute infusion. However, it demonstrates a prolonged duration of action with longer infusions because of an elimination half-life of 2 to 3 hours.
Dexmedetomidine may be administered as a bolus or as an infusion with or without a loading dose for procedural sedation during MAC. The method of administration determines the hemodynamic effects, with bolus administration producing a biphasic cardiovascular profile. After a bolus, there is an initial increase in blood pressure and decrease in heart rate that are likely due to stimulation of peripheral postsynaptic α 2 receptors. After 15 minutes, the heart rate returns to baseline, and arterial blood pressure decreases to approximately 15% below baseline. Avoiding a loading dose and relying solely on an infusion may avoid this biphasic response.
The overall cardiovascular effects of dexmedetomidine are generally well tolerated by patients with cardiac disease. However, there is some indirect decrease in contractility and reduction in SVR caused by sympatholysis, which may have adverse consequences for critically ill patients. Compared with propofol, dexmedetomidine has a slower onset and offset, making it more difficult to titrate during MAC anesthesia. However, it has minimal respiratory depressant effects, which is a significant advantage compared with propofol. In addition, dexmedetomidine has analgesic properties. Dexmedetomidine does not appear to be as amnestic as propofol, and patients are more easily arousable, which may be an advantage or disadvantage depending on the surgical procedure.
Midazolam
A water-soluble benzodiazepine, midazolam has a long history of use in patients with cardiac disease. As a γ-aminobutyric acid type A (GABA A ) agonist, benzodiazepines such as midazolam have hypnotic, amnestic, anxiolytic, and anticonvulsant effects that make them very useful for a variety of surgical procedures. There are also minimal hemodynamic changes associated with the administration of midazolam, the most significant being a small decrease in blood pressure with an unchanged cardiac index. It has been used safely in patients with ischemic heart disease, as well as valvular heart disease.
Because it has no analgesic properties, midazolam is often combined with an opiate for procedural sedation. Given as a bolus, it has an effect within 2 to 3 minutes and lasts 1 to 6 hours. Infusions may be used for prolonged sedation or as part of a general anesthetic but are rarely indicated for MAC.
Midazolam with or without fentanyl remains a valuable tool for procedures under MAC, especially minimally invasive procedures. Low doses of midazolam and fentanyl titrated to effect generally produce little hemodynamic change and are well tolerated by patients with severe cardiac disease or other significant comorbidities. However, patients receiving benzodiazepines typically remain sedated longer after completion of the procedure than those given propofol. Therefore undesirable prolonged postoperative amnesia or sedation is a potential adverse effect of midazolam. In addition, adverse effects are more common and may persist for a longer period of time in the older adult patient population.
Local Anesthesia
Local anesthetics are membrane-stabilizing drugs that inhibit sodium influx through voltage-gated sodium channels in the neuron cell membrane and decrease the rate of depolarization, thus inhibiting the generation of action potentials. They are divided into two classes (amides and esters), with amides being used most commonly for surgical local anesthesia. Commonly used drugs include lidocaine, mepivacaine, bupivacaine, or ropivacaine with or without epinephrine ( Table 12.3 ). These medications can provide excellent pain control in appropriate procedures as long as the surgical field is adequately blocked.
Table 12.3
Commonly Used Local Anesthetics
| Drug | Maximum Dose | Duration of Action |
|---|---|---|
| Lidocaine | Without epinephrine: 4.5 mg/kg (maximum, 300 mg) With epinephrine: 7 mg/kg (maximum, 500 mg) |
90–200 min |
| Mepivacaine | Without epinephrine: 5 mg/kg (maximum, 400 mg) With epinephrine: 7 mg/kg (maximum, 550 mg) |
120–240 min |
| Chloroprocaine | Without epinephrine: 15 mg/kg With epinephrine: 20 mg/kg |
30–60 min |
| Bupivacaine | Without epinephrine: 2 mg/kg (maximum, 175 mg) With epinephrine: 3 mg/kg (maximum, 225 mg) |
180–360 min |
| Ropivacaine | 2–3 mg/kg (maximum, 250 mg) | 180–360 min |
| Tetracaine | Without epinephrine: 1.5 mg/kg With epinephrine: 2.5 mg/kg |
180–600 min |
Cardiac patients presenting for noncardiac surgery under MAC may be at higher risk of developing local anesthetic systemic toxicity given that they often have multiple known risk factors (e.g., advanced age, heart failure, ischemic cardiomyopathy, conduction abnormalities, or concurrent medications that inhibit sodium channels) ( Table 12.4 ). Local anesthetic toxicity is related to elevated plasma concentrations of unbound drug. Risk factors for increased plasma levels include intravascular injection, excessive dose or rate of administration, delayed clearance, and injection in highly vascular tissue. Amide local anesthetics are hepatically metabolized and may have decreased clearance in patients with liver disease, including liver disease secondary to cardiac dysfunction (e.g., hepatic congestion from right-sided heart failure). Liver disease also results in a decrease in production of proteins that bind local anesthetics, which leads to an increased unbound drug fraction. Acidosis, which may be present in patients with severe cardiac disease and reduced oxygen delivery, also lead to an increase in unbound drug fraction caused by dissociation from binding proteins. Furthermore, patients with very low ejection fractions are more likely to receive higher total doses of local anesthetic because of “stacked” injections. This is because of their slow circulation time and the delayed clinical effect or signs of toxicity.
Table 12.4
Medications That Inhibit Sodium Channels
| Drug | Uses |
|---|---|
| Class IA Antiarrhythmics | |
|
AF, atrial flutter, SVT, and VT |
| Class IB Antiarrhythmics | |
|
Ventricular tachyarrhythmias |
| Class IC Antiarrhythmics | |
|
Life-threatening SVT and VT |
| Anticonvulsants | |
|
|
AF, Atrial fibrillation; SVT, supraventricular tachycardia; VT, ventricular tachycardia.
Another consideration is the inclusion of epinephrine in the local anesthetic solution. For example, for every 20 mL of local anesthetic with epinephrine 1 : 200,000, a patient will receive 100 µg of subcutaneous epinephrine. If large volumes of local anesthetic with epinephrine are used, the total epinephrine dose administered may be enough to cause hypertension and tachycardia. This may even occur without accidental IV injection. As previously stated, hypertension and tachycardia may be problematic in patients with ischemic heart disease or pulmonary hypertension. Therefore it is important to remain vigilant and closely monitor these patients during and after injections ( Box 12.2 ).
Box 12.2
Risk Factors for Local Anesthetic Systemic Toxicity
-
Advanced age, heart failure, ischemic cardiomyopathy, conduction abnormalities, and medications that inhibit sodium channels
-
The total epinephrine dose should be considered when epinephrine-containing local anesthetics are administered to patients who may poorly tolerate tachycardia.
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