Cardiovascular disease is the leading cause of global death with an estimated 17 million deaths per year, and by 2030 this number could be more than 23 million. It is the leading cause of death in the United States. Many of the risk factors identified to predict perioperative fatality are cardiovascular in origin. Coronary artery disease (CAD), peripheral vascular disease (PVD), and risk for CAD increase operative risk. Recent myocardial infarction, the presence of congestive heart failure (CHF), and aortic stenosis are among the most important risk factors. Management of anesthesia for patients with cardiovascular disease requires an understanding of the pathophysiology of the disease process, appropriate preoperative testing, application of perioperative risk reduction strategies, and careful selection of anesthetic, analgesic, neuromuscular, and autonomic blocking drugs. The use of appropriate monitors to match the needs created by cardiovascular disease is very important.
Coronary Artery Disease
CAD (ischemic heart disease), often asymptomatic, is a common accompaniment of aging in the American population (also see Chapter 35 ). Of the adult patients who undergo surgery annually in the United States, about 40% will either have or be at risk for CAD. The presence of CAD in patients who undergo anesthesia for noncardiac surgery may be associated with increased morbidity and mortality rates. History, physical examination with specific attention to cardiac and respiratory disease, and cardiac risk factors are very important. In addition, determination of the presence of the patient’s exercise tolerance, cardiac symptoms, and electrocardiogram (ECG) are important components of the routine preoperative cardiac evaluation (also see Chapter 13 ). The presence of symptoms of cardiac disease include shortness of breath with exercise in men and fatigue in women. People with severe CAD frequently state that they have no chest pain or shortness of breath with walking or activity. When asked about walking up stairs, they readily admit to shortness of breath. The presence of angina, angina at rest, orthopnea, paroxysmal nocturnal dyspnea, and dizziness or fainting can also be signals of cardiovascular disease.
More specialized procedures, such as ambulatory ECG monitoring (Holter monitoring), exercise stress testing, transthoracic or transesophageal echocardiography (TEE), radionuclide ventriculography (determination of ejection fraction), dipyridamole-thallium scintigraphy (mimics the coronary vasodilator response but not the heart rate response associated with exercise), cardiac catheterization, and angiography, are performed on selected patients. There is no evidence that invasive preoperative testing adds appreciably to the information provided by routine history and physical examination and electrocardiographic data for predicting adverse outcomes. For example, echocardiographic determination of ejection fraction may not provide information that improves upon the ability to predict the presence of a preoperative myocardial infarction beyond that provided by a careful preoperative clinical evaluation. Thallium scintigraphy, which evaluates adequacy of coronary blood flow, does not predict patients at risk for perioperative cardiac events. Ultimately, the history and physical examination with specific attention to signs and symptoms of new onset of angina, change in anginal pattern, unstable angina, recent myocardial infarction, CHF, or aortic stenosis, and presence of appropriate medical therapy should determine whether patients are in the best medical condition possible before elective cardiac or noncardiac surgery.
Important aspects of the history taken from patients with CAD before noncardiac surgery include cardiac reserve, characteristics of angina pectoris, the presence of a prior myocardial infarction, and the medical, interventional cardiology, prior percutaneous coronary intervention (PCI), and cardiac surgical therapy for those conditions. Potential interactions of medications used in the treatment of CAD with drugs used to produce anesthesia must also be considered. Coexisting noncardiac diseases that are often present in these patients include hypertension, PVD, chronic obstructive pulmonary disease (COPD) from cigarette smoking, renal dysfunction associated with chronic hypertension, and diabetes mellitus. As stated previously, a thorough evaluation is especially important because patients can remain asymptomatic despite 50% to 70% stenosis of a major coronary artery.
Limited exercise tolerance in the absence of significant pulmonary disease is the most striking evidence of decreased cardiac reserve. Inability to lie flat, awakening from sleep with angina or shortness of breath, or angina at rest or with minimal exertion are evidence of significant cardiac disease. If a patient can climb two to three flights of stairs without symptoms, cardiac reserve is probably adequate. It is very common for patients with severe CAD requiring revascularization to state that they are able to walk as much as they would like but then admit to not being able to climb a single flight of stairs without shortness of breath. The ability to walk slowly on level ground requires only minimal exertion.
Angina pectoris is considered to be stable when no change has occurred for at least 60 days in precipitating factors, frequency, and duration. Chest pain or shortness of breath produced with less than normal activity or at rest, or increasing in frequency, or lasting for increasingly longer periods is considered characteristic of unstable angina pectoris and may signal an impending myocardial infarction. Dyspnea following the onset of angina pectoris may be indicative of acute left ventricular dysfunction due to myocardial ischemia. Angina pectoris due to spasm of the coronary arteries (variant or Prinzmetal angina) differs from classic angina pectoris in that it may occur at rest and then be absent during vigorous exertion. Silent myocardial ischemia does not evoke angina pectoris (asymptomatic) and usually occurs at a heart rate and systemic arterial blood pressure less than those present during exercise-induced myocardial ischemia. About 70% of ischemic episodes are not associated with angina pectoris and as many as 15% of acute myocardial infarctions are silent. Women and diabetics are more likely to have painless myocardial ischemia and infarctions. The most common angina symptom in men is shortness of breath with exertion (e.g., stair climbing), and the most common symptom in women is fatigue.
The heart rate and systolic blood pressure at which angina pectoris or evidence of myocardial ischemia is indicated on the ECG are useful preoperative information. An increased heart rate is more likely than hypertension to produce signs of myocardial ischemia ( Fig. 25.1 ). Tachycardia increases myocardial oxygen requirements while at the same time decreases the duration of diastole, thereby decreasing left ventricular coronary blood flow, which occurs in diastole, and the delivery of oxygen to the left ventricle. Conversely, increased systolic and diastolic blood pressure, while increasing oxygen consumption, simultaneously increases coronary perfusion despite the presence of atherosclerotic coronary arteries.
Prior Myocardial Infarction
The incidence of myocardial reinfarction in the perioperative period is related to the time elapsed since the previous myocardial infarction ( Table 25.1 ). The incidence of perioperative myocardial reinfarction generally does not stabilize at 5% to 6% until 6 months after the prior myocardial infarction. Thus, a common recommendation is to delay elective surgery, especially thoracic, upper abdominal, or other major procedures, for a period of 2 to 6 months after a myocardial infarction. The exact duration of suggested delay is not clear. Even after 6 months, the 5% to 6% incidence of myocardial reinfarction is about 50 times higher than the 0.13% incidence of perioperative myocardial infarction in patients undergoing similar operations but in the absence of a prior myocardial infarction. Most perioperative myocardial reinfarctions occur in the first 48 to 72 hours postoperatively. However, if ischemia is initiated by the stress of surgery, there can be an increased risk of myocardial infarction for several months after surgery.
|Time Elapsed Since Previous Myocardial Infarction
|Tarhan et al
|Steen et al
|Rao et al
|Shah et al
Several factors influence the incidence of myocardial infarction in the perioperative period. For example, the incidence of myocardial reinfarction is increased in patients undergoing intrathoracic or intra-abdominal operations lasting longer than 3 hours. Factors that do not predispose to a myocardial reinfarction include the (1) site of the previous myocardial infarction, (2) history of prior aortocoronary bypass graft surgery, (3) site of the operative procedure if the duration of the surgery is shorter than 3 hours, and (4) techniques used to produce anesthesia. In patients with CAD or PVD, appropriate use of β-adrenergic blocking drugs reduces the risk of cardiac morbidity (myocardial infarction or cardiac death) (also see Chapter 6 ). Statin therapy with fluvastatin for 30 days before and after surgery, in addition to β-adrenergic blockade, reduces risk of myocardial infarction and death by an additional 50%. Intensive hemodynamic monitoring using an intra-arterial catheter and prompt pharmacologic intervention or fluid infusion to treat physiologic hemodynamic alterations from the normal range may decrease the risk of perioperative cardiac morbidity in high-risk patients (see Table 25.1 ).
Drugs most likely to be taken by patients with CAD are β-adrenergic antagonists, nitrates, calcium channel blockers, angiotensin-converting enzyme inhibitors, drugs that decrease blood lipids, diuretics, antihypertensives, and platelet inhibitors. Knowledge of the pharmacology of these drugs and potential adverse interactions with anesthetics is an important preoperative consideration (see Chapter 6, Chapter 8 ). Accordingly, patients with known CAD, known PVD, or those receiving β-adrenergic blocking drugs should be monitored throughout the perioperative period. Although COPD is not a contraindication to perioperative β-adrenergic blockade, reactive asthma is. Patients with CAD or vascular disease should receive a statin type of drug unless there is a specific contraindication. Despite the potential for adverse drug interactions, cardiac medications being taken preoperatively should be continued without interruption through the perioperative period. Discontinuation of β-adrenergic blockers, calcium channel blockers, nitrates, statins, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers in the perioperative period can increase risk of perioperative morbidity and mortality and should not be discontinued.
Preoperative evaluation of a resting 12-lead ECG is reasonable for patients with known coronary heart disease, significant arrhythmia(s), peripheral arterial disease, cerebrovascular disease, or other significant structural heart disease and may be indicated for some asymptomatic patients without known coronary heart disease (also see Chapter 20 ). Preoperative resting 12-lead ECG is not indicated in patients undergoing low-risk surgery. The preoperative ECG should be examined for evidence of (1) myocardial ischemia, (2) prior myocardial infarction, (3) cardiac hypertrophy, (4) abnormal cardiac rhythm and conduction disturbances, and (5) electrolyte abnormalities. The exercise ECG simulates sympathetic nervous system stimulation as may accompany perioperative events such as direct laryngoscopy, tracheal intubation, surgical incision, postoperative pain, and recovery. The resting ECG in the absence of angina pectoris may be normal despite extensive CAD. Nevertheless, an ECG demonstrating ST-segment depression more than 1 mm, particularly during angina pectoris, confirms the presence of myocardial ischemia. Furthermore, the ECG lead demonstrating changes of myocardial ischemia can help determine the specific diseased coronary artery ( Table 25.2 ). It is of particular importance that a prior myocardial infarction, especially if subendocardial, may not be accompanied by persistent changes on the ECG. The preoperative presence of ventricular premature beats may signal their likely occurrence intraoperatively. A prolonged PR interval on the ECG (longer than 200 ms) may be related to medication therapy such as amiodarone, digoxin, pregabalin, or dolasetron. Conversely, the block of conduction of cardiac impulses below the atrioventricular node (right bundle branch block, left bundle branch block, or intraventricular conduction delay) most likely reflects pathologic changes rather than drug effect.
|Coronary Artery Responsible for Myocardial Ischemia
|Area of Myocardium That May Be Involved
|II, III, aVF
|Right coronary artery
|V 3 -V 5
|Left anterior descending coronary artery
|Anterolateral aspects of the left ventricle
|Circumflex coronary artery
|Lateral aspects of the left ventricle
Risk Stratification Versus Risk Reduction
One of the standard approaches to the perioperative care of patients with cardiac disease is risk stratification. Risk stratification consists of a preoperative history and physical examination followed by some series of tests thought to predict perioperative cardiac morbidity and mortality risks. These tests may include persantine thallium, echocardiography, Holter monitoring, dobutamine stress echocardiography, and angiography and may lead to angioplasty with or without an intracoronary stent or coronary artery bypass surgery. Yet, preoperative risk stratification with invasive testing may not be superior to a careful history and physical examination followed by prophylactic medical therapy. Furthermore, combining the risk of angiography and an intracoronary stent or coronary artery bypass graft (CABG) to a surgical procedure may not reduce total risk. The combined risk of two procedures may exceed that of the original operation. Despite the lack of proven benefit of prophylactic invasive testing combined with either CABG or coronary angioplasty with stenting over medical therapy, the American College of Cardiology (ACC) and American Heart Association (AHA) have developed a protocol entitled ACC/AHA Guideline Perioperative Cardiovascular Evaluation for Noncardiac Surgery. Fig. 25.2 provides a suggested protocol for preoperative evaluation. Unfortunately, the ACC/AHA protocol has been studied and found to be difficult to apply in practice with conflicting guidance on indications for testing with physicians ordering more tests than suggested by the guidelines. Perioperative risk reduction therapy with β-adrenergic blockers and statins may be superior to risk stratification with invasive testing, angioplasty, and CABG.
Perioperative Cardiac Risk Reduction Therapy
There is some controversy after the publication of the POISE study on the use of prophylactic perioperative β-adrenergic blockade. Continuation of anti-ischemic drugs in the perioperative period is recommended. Perioperative use of β-adrenergic blockers in patients with known CAD or PVD is recommended. Prophylactic addition of β-adrenergic blockers to patients at risk for CAD is recommended in patients with significant cardiac risk (revised cardiac risk index [RCRI] ≥ 3) and in those patients with intermediate- or high-risk preoperative tests. If initiation of β-adrenergic blocker administration is planned, it should begin long enough in advance of surgery to assess safety and tolerability, preferably more than 1 day. Large-dose β-adrenergic blocker therapy should not be started on the day of surgery. The following β-adrenergic blocker protocol has been tested in 40,000 patients and has been shown to reduce risk.
All patients who have either CAD, PVD, or two risk factors for CAD (age ≥ 60 years, cigarette smoking, diabetes, hypertension, cholesterol ≥ 240 mg/dL) should receive perioperative β-adrenergic blockade unless they have a specific intolerance to β-adrenergic blockers. Patients with renal failure or renal insufficiency may also benefit from therapy.
β-Adrenergic blockade should be started as soon as the patient is identified as having CAD, PVD, or risk factors. If the surgeon identifies the patient as having risk, the surgeon should start the medication. If the anesthesia preoperative clinic identifies the patient, it should be started in the preoperative clinic (also see Chapter 13 ). If the patient is not identified until the morning of surgery, intravenous atenolol or metoprolol should be used. If the drug is started prior to the day of surgery, atenolol 25 mg by mouth (PO) per day (qd) is an appropriate starting dose.
β-Adrenergic blockade should be continued until at least 30 days postoperatively, if not indefinitely, in patients with CAD or PVD. In patients with only risk factors, 7 days may be sufficient.
The optimal time to start β-adrenergic blockade is at the time of identification of the risk. This process should be multitiered to avoid missing patients. The following approach should be used to provide the maximum benefit at the minimum cost.
The surgeon should give a β-adrenergic blocker if the patient has CAD, PVD, or two risk factors. Atenolol 25 mg PO daily is an appropriate starting dose.
If a medical or cardiology consult is requested by surgery, the most common advice is: start a β-adrenergic blocker.
The anesthesia preoperative clinic checks to see if the patients at risk are receiving a β-adrenergic blocker. If the patient is not getting adequate β-adrenergic blockade, the dose is increased.
On the day of surgery, treatment with or increasing the dose of intravenously (IV) administered β-adrenergic blockers should be considered. Intravenous metoprolol in 5-mg boluses is used. Standard dose is 10 mg IV (withhold for heart rate less than 50 beats/min or systolic blood pressure less than 100 mm Hg). Intraoperative doses are used as needed. The patient should receive additional doses in the postanesthesia care unit as needed.
The patient should receive the drug postoperatively for 30 days. If the patient is nil per os (NPO, or nothing by mouth), the patient receives intravenous metoprolol (10 mg IV q12h) unless systolic blood pressure is less than 100 mm Hg or heart rate is less than 50 beats/min. If the patient is taking oral medications, the patient receives atenolol 100 mg PO daily if the heart rate is more rapid than 65 beats/min and the systolic blood pressure is more than 100 mm Hg. If the heart rate is between 55 and 65 beats/min, the dose is 50 mg. There is a hold order for heart rate less than 50 beats/min or systolic blood pressure less than 100 mm Hg.
The patient remains on the drug for at least 30 days postoperatively.
Many patients should remain on the drug for life (patients with known CAD, known PVD, and hypertension).
Preoperative testing and revascularization should only be used as needed for specific indications not prophylaxis. If a patient is identified with new-onset angina, unstable angina, a change in the anginal pattern, or CHF, then further risk stratification is appropriate. If the patient is stable with known CAD, PVD, or two risk factors for CAD, the patient should receive a β-adrenergic blocker.
Care should be taken with patients who have CHF, aortic stenosis, intracoronary stents on platelet inhibitors, or renal failure. All patients who have CHF should be evaluated by a cardiologist for the initiation of β-adrenergic blocker therapy. β-Adrenergic blocker therapy reduces the risk of death from CHF. Many patients with CHF are profoundly improved by β-adrenergic blockade; however, the dose must be titrated slowly and usually under the supervision of a cardiologist. Patients with aortic stenosis should be evaluated by cardiology and β-adrenergic blockade initiated with a cardiologist’s supervision.
Patients with intracoronary stents on platelet inhibitors should be seen by a cardiologist. WARNING: Discontinuation of platelet inhibitors in patients with intracoronary stents can be lethal. Patients with renal failure should be treated with appropriate drugs, but special attention is needed.
Patients with an indication for statin therapy and especially those with known CAD or PVD should be considered for statin therapy. Therapy should be started 30 days prior to surgery and continued for at least 30 days after surgery, possibly indefinitely.
Management of Anesthesia
Anesthesia care for patients with known CAD, known PVD, or two risk factors for CAD (age ≥ 60 years, hypertension, diabetes, significant smoking history, or hyperlipidemia) should begin as soon as the patient is identified as needing surgery. All patients with new-onset angina, a change in anginal pattern, unstable angina, angina without medical therapy, aortic stenosis, CHF, or an intracoronary stent receiving a platelet inhibitor should be referred to cardiology. Patients with recently placed intracoronary stents receiving platelet inhibitors have a high risk of intracoronary thrombosis and death when the platelet inhibitors are discontinued for perioperative care. Patients with bare metal stents may require 3 or more months of antiplatelet therapy. Patients with drug-eluting intracoronary stents may require platelet inhibitors for a year or more. Patients with stable coronary disease on medical therapy with no evidence of CHF or aortic stenosis should receive an oral β-adrenergic blocker (atenolol or metoprolol 25 mg/day PO) and a statin drug. Patients with CHF should have β-adrenergic blockers initiated by cardiology over a prolonged period. The dose of β-adrenergic blockers should be increased as tolerated. β-Adrenergic blockers should be avoided in patients with a history of high-grade atrioventricular (AV) block without a pacemaker, reactive asthma, or an intolerance for β-adrenergic blockers. Diabetes is an indication for perioperative β-adrenergic blockade. For maximal effect, β-adrenergic blockers should be started as soon as the patient is identified as needing surgery. Starting high-dose β-adrenergic blockers on the day of surgery is not indicated. If a patient is identified on the day of surgery, intravenous atenolol or metoprolol can be started in the preoperative area (atenolol or metoprolol 10 mg IV if the heart rate is more rapid than 55 beats/min or systolic blood pressure is higher than 100 mm Hg) and continued postoperatively. Perioperative β-adrenergic blockers should be continued for at least 7 days postoperatively. In patients with higher risks (those with known CAD or PVD), β-adrenergic blockers should be continued at least 30 days if not indefinitely. Esmolol boluses during surgery do not constitute perioperative β-adrenergic blockade and are not adequate to reduce perioperative cardiac risk. Appropriate dosing of β-adrenergic blockers is prudent to avoid sequelae related to hypotension and bradycardia.
The intraoperative anesthetic management as well as postoperative pain management (also see Chapter 40 ) of patients with CAD should permit the modulation of sympathetic nervous system responses and provide for the rigorous control of hemodynamic variables. Management of anesthesia in these patients is based on a preoperative evaluation of left ventricular function and the maintenance of a favorable balance between myocardial oxygen requirements and myocardial oxygen delivery so as to prevent myocardial ischemia ( Table 25.3 and Box 25.1 ). Any event associated with persistent tachycardia, systolic hypertension, arterial hypoxemia, or diastolic hypotension can adversely influence this delicate balance. Heart rate higher than 100 beats/min increases the risk of postoperative death in patients with risk for CAD; heart rates higher than 120 beats/min significantly increase risk.
|Previous myocardial infarction
|Evidence of congestive heart failure
|Left ventricular end-diastolic pressure
|<12 mm Hg
|>18 mm Hg
|>2.5 L/min/m 2
|<2 L/min/m 2
|Areas of ventricular dyskinesia
Persistent and excessive changes in heart rate and systemic arterial blood pressure should be minimized (see Fig. 25.1 ). Maintaining heart rate and systemic arterial blood pressure within 20% of the awake values is commonly recommended. Monitoring with an intra-arterial catheter greatly improves the ability to maintain stable systemic arterial blood pressures. Nevertheless, an estimated one half of all new perioperative ischemic episodes are not preceded by or associated with significant changes in heart rate or systemic arterial blood pressure. A single 1-minute episode of myocardial ischemia detected by a 1-mm ST-segment elevation or depression increases the risk of cardiac events 10-fold and the risk for death 2-fold. Tachycardia for 5 minutes above 120 beats/min in the postoperative period can increase the risk of death 10-fold. The only clinically proven method to reduce the risk of perioperative myocardial ischemia and associated death is perioperative β-adrenergic blockade (atenolol or metoprolol).
Monitoring (Also See Chapter 20 )
Anticipation of problems and avoidance of potential disasters are key components for successful anesthetic management of patients with cardiovascular disease. Prophylactic therapy and more extensive monitoring reduce risk. Continuous intra-arterial pressure monitoring can reduce the risk of hemodynamic events by early identification of problems. Continuous ECG monitoring rapidly identifies arrhythmias, tachycardia, and myocardial ischemia. Monitoring should be continuous if possible. Rapid changes in hemodynamics can quickly lead to cardiac arrest; monitoring can quickly identify those changes and permits prompt therapy before further complications develop. When operations are completed, monitoring should be continued into the recovery room or intensive care unit (ICU). When patients are transferred from the operating room table to the gurney or ICU bed, or are turned from supine to prone or back to supine, monitoring should be as continuous as possible. Unconscious patients with cardiac disease may have rapid hemodynamic collapse with transfers from the operating room table to the gurney or ICU bed or when turned over and should be monitored during transfers. If arterial blood pressure, ECG, and saturation are monitored, the problem can be quickly identified and corrected prior to serious sequelae. Intravascular volume, vasoconstrictors, β-agonists, β-adrenergic blockers, anticholinergics, and vasodilator drugs should be immediately available. Loss of a pulse oximeter signal or desaturation can imply hypoxia or inadequate arterial blood pressure or cardiac output and should signal an immediate search for a cause and initiation of corrective action. The pulse oximeter is a monitor of both oxygen saturation and perfusion. If the pulse oximeter loses a signal, adequacy of perfusion should be assessed. Loss of the pulse oximeter signal may occur simply from the finger becoming cold, or much more importantly, may be the first warning of hemodynamic collapse. Continuous monitoring and prophylactic therapy can reduce the risk in patients with cardiovascular disease.
The intensity of monitoring in the perioperative period is influenced by the complexity of the operative procedure and the severity of the cardiovascular disease. The five-lead ECG serves as a noninvasive monitor of the balance between myocardial oxygen requirements and myocardial oxygen delivery in unconscious patients (also see Chapter 20 ). When this balance is unfavorably altered, myocardial ischemia occurs, as evidenced on the ECG by at least a 1-mm downsloping of the ST segment from the baseline. A precordial V 5 lead is a useful selection for detecting ST-segment changes characteristic of ischemia of the left ventricle during anesthesia. Intra-arterial pressure monitoring can speed the identification and treatment of hemodynamic changes. Monitoring should be continuous if possible. Ventricular wall motion abnormalities observed by TEE may be the most sensitive indicator of myocardial ischemia, but this monitor is expensive, is invasive, and requires additional training before its use as a routine method for detecting an imbalance between myocardial oxygen delivery and myocardial oxygen requirements. Intraoperative monitoring of pulmonary artery pressures or use of TEE should be reserved for selected high-risk patients (cardiac surgery, recent myocardial infarction, current CHF, unstable angina). Continuous cardiac output monitoring with stroke volume variation (SVV) measurement of fluid responsiveness may improve intravascular fluid management.
Induction of Anesthesia
Preoperative anxiety can lead to preoperative myocardial ischemia. Myocardial ischemia predisposes to subsequent myocardial ischemia. Preoperative β-adrenergic blocker therapy reduces the incidence of myocardial ischemia. Patients should receive their routine medications except for oral hypoglycemic drugs. Preoperative sedative medication is intended to produce sedation and reduce anxiety, which, if unopposed, could lead to secretion of catecholamines and an increase in myocardial oxygen requirements because of an increase in heart rate and systemic arterial blood pressure. Oral administration of benzodiazepines (diazepam or lorazepam PO) is an effective pharmacologic approach to allay severe anxiety. Supplemental oxygen may be needed if narcotics are combined with benzodiazepines for sedation.
Induction of anesthesia is acceptably accomplished with the intravenous administration of rapidly acting drugs. Preinduction placement of an intra-arterial catheter to monitor arterial blood pressure allows rapid pharmacologic manipulations and a very stable induction of anesthesia. An infusion of phenylephrine (0.2 to 0.4 μg/kg/min) started prophylactically stabilizes arterial blood pressure and can eliminate most hemodynamic changes with induction. Etomidate is a popular anesthetic to induce anesthesia because of its limited inhibition of the sympathetic nervous system and limited hemodynamic effects (also see Chapter 8 ). The lack of inhibition of autonomic reflexes by etomidate may lead to hypertension with laryngoscopy and endotracheal intubation. Propofol is popular secondary to its antiemetic effects and rapid recovery, but the dose should be reduced to avoid hypotension with induction. Fentanyl and midazolam in combination with an infusion of phenylephrine and a nondepolarizing muscle relaxant cause minimal associated changes in arterial blood pressure or heart rate.
Ketamine is not often used to induce anesthesia for patients with coronary disease because of the associated increase in heart rate and systemic arterial blood pressure, which may increase myocardial oxygen requirements. When giving desflurane, the inspired concentration should be slowly increased to avoid sympathetic stimulation and associated tachycardia, pulmonary hypertension, myocardial ischemia, and bronchospasm. Tracheal intubation is facilitated by the administration of succinylcholine or a nondepolarizing neuromuscular blocking drug (also see Chapter 11 ).
Myocardial ischemia may accompany the tachycardia and hypertension that result from the stimulation of direct laryngoscopy as necessary for tracheal intubation. Adequate anesthesia and a brief duration of direct laryngoscopy are important in minimizing the magnitude of these circulatory changes. When the duration of direct laryngoscopy is not likely to be brief, or when hypertension coexists, the addition of other drugs to minimize the pressor response produced by tracheal intubation should be considered. For example, laryngotracheal lidocaine (2 mg/kg) administered just before placing the tube in the trachea produces rapid topical anesthesia of the tracheal mucosa and minimizes the magnitude and duration of the systemic arterial blood pressure increase. Alternatively, lidocaine (1.5 mg/kg IV), administered just before initiating direct laryngoscopy, is efficacious (also see Chapter 16 ).
Administration of opioids (fentanyl, sufentanil, alfentanil, or remifentanil) before initiating direct laryngoscopy reduces the stimulation produced by tracheal intubation. β-Adrenergic blockers are effective in attenuating heart rate increases associated with tracheal intubation. Tachycardia should be avoided in all patients with coronary disease, vascular disease, or risk factors for coronary disease.
Maintenance of Anesthesia
The choice of anesthesia is often based on the patient’s left ventricular function (see Table 25.3 ). For example, patients with CAD but normal left ventricular function may develop tachycardia and hypertension in response to intense stimulation. Controlled myocardial depression produced by a volatile anesthetic with or without nitrous oxide may be appropriate if the primary goal is to prevent increased myocardial oxygen requirements. Equally acceptable for maintenance of anesthesia is the use of a nitrous oxide–opioid technique with the addition of a volatile anesthetic as necessary to treat acute increases in systemic arterial blood pressure as produced by a change in the level of surgical stimulation. When hypertension is treated with a volatile anesthetic (isoflurane, desflurane, sevoflurane), the drug-induced decrease in systemic vascular resistance (SVR) is more responsible for decreases in systemic arterial blood pressure than is drug-induced myocardial depression. The ability to rapidly increase the alveolar concentration of sevoflurane makes this drug uniquely efficacious for treating sudden increases in systemic arterial blood pressure. Abrupt and large increases in the delivered concentrations of desflurane may be accompanied by stimulation of the sympathetic nervous system and transient increases in systemic arterial blood pressure, heart rate, pulmonary hypertension, and myocardial ischemia (also see Chapter 7 ).
Volatile anesthetics are vasodilators. Under unusual clinical circumstances, potent coronary vasodilators can divert blood flow from ischemic areas of myocardium (blood vessels already fully dilated) to nonischemic areas of myocardium supplied by vessels capable of vasodilation. Regional myocardial ischemia associated with drug-induced vasodilation is known as coronary artery steal. There are reports that the incidence of myocardial ischemia is either unchanged or increased in patients with CAD and anesthetized with isoflurane compared with those receiving a different volatile anesthetic or an opioid-based anesthetic. Volatile anesthetics to varying degrees (halothane, isoflurane, sevoflurane, and desflurane) induce ischemic preconditioning and may protect the myocardium from subsequent ischemia. All facts considered, volatile anesthetics may be either beneficial in patients with CAD because they decrease myocardial oxygen requirements and induce ischemic preconditioning, or detrimental because they decrease systemic arterial blood pressure and coronary perfusion pressure or produce coronary artery steal (isoflurane) or tachycardia (desflurane). A large clinical trial in patients undergoing cardiac surgery failed to demonstrate a difference between halothane, enflurane, isoflurane, and narcotic-based anesthetics. Avoiding tachycardia with the use of long-acting β-adrenergic blockers (metoprolol or atenolol) is more important than anesthetic choice. Intraoperative bolus doses of short-acting β-adrenergic blockers (esmolol) have not been shown to be effective in reducing perioperative cardiac risk. Prophylactic perioperative administration of long-acting β-adrenergic blockers (metoprolol or atenolol) is needed to reduce perioperative risk.
Patients with impaired left ventricular function, as associated with a prior myocardial infarction, may not tolerate direct myocardial depression produced by volatile anesthetics. In these patients, the use of short-acting opioids with nitrous oxide may be a more acceptable selection. Nitrous oxide, when administered to patients who have received opioids for anesthesia, may produce undesirable decreases in systemic arterial blood pressure and cardiac output. High-dose fentanyl (50 to 100 μg/kg IV) or equivalent doses of sufentanil or alfentanil as the primary anesthetic with benzodiazepines added to ensure amnesia may be useful for patients who cannot tolerate the myocardial depression from even low concentrations of anesthesia. Yet, this technique is not clearly better than moderate dose narcotics with an inhaled or intravenous anesthetic. Infusions of dexmedetomidine combined with smaller-dose fentanyl (1-10 μg/kg) and inhaled anesthetics work well and apparently reduce postoperative delirium in patients undergoing CABG.
A regional anesthetic is an excellent technique in patients with CAD (also see Chapter 17, Chapter 18 ). Regional anesthesia for peripheral surgery (orthopedic, podiatric, peripheral vascular) and lower abdominal surgery (gynecologic and urologic) is a very safe technique for patients with cardiac risk. However, flow through critically narrowed coronary arteries is pressure-dependent. Therefore, decreases in systemic arterial blood pressure associated with a regional anesthetic that are more than 20% of the preblock value probably should be treated with an intravenous infusion of crystalloid solutions or a vasoconstrictor such as phenylephrine. Phenylephrine improves coronary perfusion pressure but at the expense of increasing afterload and myocardial oxygen requirements. Nevertheless, the increase in coronary perfusion pressure is likely to more than offset any increase in myocardial oxygen requirements. Perioperative β-adrenergic blockers should be used in patients with cardiac risk undergoing surgery using regional anesthesia.
Neuromuscular Blocking Drugs (Also See Chapter 11 )
The choice of nondepolarizing neuromuscular blocking drugs during maintenance of anesthesia for patients with CAD may be influenced by the circulatory effects of these drugs. Vecuronium, rocuronium, and cisatracurium do not evoke histamine release and associated decreases in systemic arterial blood pressure, even with the rapid intravenous administration of large doses. Likewise, the systemic arterial blood pressure lowering effects of atracurium and mivacurium are usually modest, especially if the drug is injected over 30 to 45 seconds to minimize the likelihood of drug-induced histamine release. None of these neuromuscular blocking drugs will adversely alter myocardial oxygen requirements. Pancuronium increases heart rate and systemic arterial blood pressure, but these changes are usually less than 15% above predrug values, making this drug a possible choice for administration to patients with CAD. Furthermore, circulatory changes produced by pancuronium can be used to offset negative inotropic or chronotropic effects of drugs being used for anesthesia. In contrast to pancuronium, the other nondepolarizing neuromuscular blocking drugs would not be expected to offset decreases in systemic arterial blood pressure or heart rate as associated with the administration of large doses of opioids. With the increased use of more selective neuromuscular blocking drugs (vecuronium, rocuronium, and cisatracurium), use of pancuronium has markedly decreased and in some cases has been eliminated.
Nondepolarizing neuromuscular blockade in patients with CAD can be safely antagonized with anticholinesterase drugs (i.e., neostigmine) combined with an anticholinergic drug. Glycopyrrolate has more titratable chronotropic effects than atropine. Tachycardia after reversal of nondepolarizing muscle relaxants can still occur. One of the common causes of postoperative myocardial ischemia and infarction is tachycardia after emergence, which may be the result of the combination of emergence, surgical pain, and reversal of nondepolarizing muscle relaxants. The addition of long-acting intravenous β-adrenergic blockers should be used to avoid tachycardia, which may lead to myocardial ischemia in this period.
Sugammadex has been used in many countries and now the United States (also see Chapter 11 for details). Sugammadex does not have significant cardiovascular effects. Readers are advised to read the Food and Drug Administration (FDA) prescribing information, which provides an excellent description of its pharmacology.
Treatment of Myocardial Ischemia
The appearance of signs of myocardial ischemia on the ECG supports the aggressive treatment of adverse changes in heart rate or systemic arterial blood pressure. Only 5% of perioperative myocardial ischemia found on Holter ECG is identified by clinicians. Prophylactic therapy with long-acting β-adrenergic blockers is essential to reduce perioperative risk. Tachycardia is treated with the administration of atenolol, metoprolol, propranolol, or esmolol. Excessive increases in systemic arterial blood pressure respond to narcotics, increases in inhaled anesthetics, β-adrenergic blockers, or continuous intravenous infusion of nitroprusside. Nitroglycerin is a more appropriate choice than nitroprusside when myocardial ischemia is associated with a normal systemic arterial blood pressure. Hypotension should be treated with a phenylephrine infusion to rapidly restore pressure-dependent perfusion through atherosclerotic coronary arteries. In addition to drugs, the intravenous infusion of fluids to restore systemic arterial blood pressure can improve myocardial oxygen supply. A disadvantage of this approach is the time necessary for intravenous fluid treatment to be effective.
Although few or no data support the use of pulmonary artery catheters, in selected patients a pulmonary artery catheter in combination with a TEE probe may be helpful for monitoring responses to intravenous fluid replacement and the therapeutic effects of drugs on left ventricular function and cardiac output. Continuous measurement of SVV or pulse pressure variation (PPV) can predict fluid responsiveness and be used to optimize fluid administration as part of goal-directed therapy. Right atrial (central venous) pressure does not predict left-sided heart volume status. In healthy patients who have a reduced need for monitoring and in patients with CAD when the ejection fraction is higher than 0.5 and when there is no evidence of left ventricular dysfunction, right atrial pressure is more likely to correlate with pulmonary artery occlusion pressure. Pressures measured with pulmonary artery catheters correlate poorly with volume status in patients with diastolic dysfunction, myocardial ischemia, mitral regurgitation or stenosis, pulmonary hypertension, positive end-expiratory pressure (PEEP), pulmonary stenosis, or tricuspid regurgitation. Abrupt increases in the pulmonary artery pressure may also reflect acute myocardial ischemia or acute mitral regurgitation. When compared with TEE, monitoring with a pulmonary artery catheter is not a highly sensitive approach for detecting myocardial ischemia. TEE also provides an assessment of regional wall motion, global ventricular function, valvular function, intravascular fluid volume, and associated ventricular filling. TEE is more expensive than pulmonary artery catheterization, but the information is more accurate and useful than pulmonary artery catheter data.
Decreases in body temperature that occur intraoperatively may predispose to shivering on awakening, leading to abrupt increases in myocardial oxygen requirements. Attempts to minimize decreases in body temperature and provision of supplemental oxygen are of obvious importance. Postoperative pain relief is important as pain-induced activation of the sympathetic nervous system can increase myocardial oxygen requirements.
Postoperative care of the patient with CAD is based on provision of perioperative anti-ischemic drugs (β-adrenergic blockers, or statins), analgesia, and, if needed, sedation to blunt excessive sympathetic nervous system activity and facilitate rigorous control of hemodynamic variables (also see Chapter 39 ). Intensive and continuous postoperative monitoring is useful for detecting myocardial ischemia, which is often asymptomatic. Episodes of myocardial ischemia lead to increased risk and increasingly frequent occurrences. Reducing the incidence of myocardial ischemia with β-adrenergic blockers reduces 30-day and 2-year mortality rates. Patients with known CAD, known PVD, or two risk factors for CAD (≥60 years of age, hypertension, vascular disease, diabetes, significant smoking history, or hyperlipidemia) should be placed on a perioperative β-adrenergic blocker unless there is a specific contraindication. They should receive β-adrenergic blockers as soon as they are identified as being at risk for cardiac complications. Patients with a lower risk should take the drug for at least 7 days postoperatively. Patients with known coronary disease or vascular disease should remain on the drug for at least 30 days if not permanently. COPD is not a contraindication to perioperative β-adrenergic blockade, but reactive asthma is. Diabetes is not a contraindication for perioperative β-adrenergic blockade; it is an indication. All medications have a therapeutic index and β-adrenergic blockers are no exception. The dose of perioperative β-adrenergic blockers should follow standard manufacturer guidelines to avoid hypotension, bradycardia, morbidity, and death.
The major determinant of pulmonary complications (atelectasis, pneumonia) after cardiac surgery is poor cardiac function. Early mobilization and pain control are likely to minimize the incidence of clinically significant pulmonary complications.
Valvular Heart Disease
The most frequently encountered forms of valvular heart disease produce pressure overload (mitral stenosis, aortic stenosis) or volume overload (mitral regurgitation, aortic regurgitation). The net effect of valvular heart disease is interference with forward flow of blood from the heart into the systemic circulation. TEE has revolutionized the evaluation and intraoperative management of valvular heart disease ( Box 25.2 ). Selection of anesthetic drugs for patients with valvular heart disease is often based on the likely effects of drug-induced changes in cardiac rhythm, heart rate, systemic arterial blood pressure, SVR, and pulmonary vascular resistance (PVR) relative to maintenance of cardiac output in these patients. Although no specific general anesthetic is superior, when cardiac reserve is minimal, an anesthetic combination of opioids, an amnestic benzodiazepine, and an inhaled anesthetic is common. Dexmedetomidine infusions may be extremely useful in combination with other drugs. Patients with valvular heart disease should receive appropriate antibiotics in the perioperative period for protection against infective endocarditis. Monitoring intra-arterial pressure is helpful in patients with clinically significant valvular heart disease.
Determine significance of cardiac murmurs (most often aortic stenosis).
Identify hemodynamic abnormalities associated with physical findings (most often mitral regurgitation).
Determine transvalvular pressure gradient.
Determine cardiac valve regurgitation.
Evaluate prosthetic valve function.
Mitral stenosis is characterized by mechanical obstruction of left ventricular diastolic filling secondary to a progressive decrease in the orifice of the mitral valve. The obstruction produces an increase in left atrial and pulmonary venous pressure. Increased PVR is likely when the left atrial pressure is chronically higher than 25 mm Hg. Distention of the left atrium predisposes to atrial fibrillation, which can result in stasis of blood, the formation of thrombi, and systemic emboli. Chronic anticoagulation or antiplatelet therapy (or both) of patients with atrial fibrillation can reduce the risk of systemic embolic events. Mitral stenosis is commonly due to the fusion of the mitral valve leaflets during the healing process of acute rheumatic carditis. Symptoms of mitral stenosis do not usually develop until about 20 years after the initial episode of rheumatic fever. A sudden increase in the demand for cardiac output as produced by pregnancy or sepsis, however, may unmask previously asymptomatic mitral stenosis.
Patients with mitral stenosis who are being chronically treated with digitalis for the control of heart rate should continue to take this drug throughout the perioperative period. Adequate digitalis effect for heart rate control is generally reflected by a ventricular rate less than 80 beats/min. Because diuretic therapy is common in these patients, the serum potassium concentration should be measured preoperatively. Other common antiarrhythmic drugs such as β-adrenergic blockers should also be continued. The discontinuation of anticoagulant or antiplatelet therapy should be discussed with the surgeon and cardiologist. Patients should be switched from warfarin (Coumadin) therapy to heparin therapy prior to surgery depending on the type of case. Also, patients with mitral stenosis can be more susceptible than normal individuals to the ventilatory depressant effects of sedative drugs used for preoperative medication. If patients are given sedative drugs, supplemental oxygen may increase the margin of safety. Most medications that patients are taking, except anticoagulants, antiplatelet drugs, and oral hypoglycemic agents, should be continued throughout the preoperative period.
Management of Anesthesia
Preinduction of anesthesia placement of an intra-arterial pressure monitoring line can speed the identification and treatment of hemodynamic changes in patients with clinically significant valvular disease. Induction of anesthesia in the presence of mitral stenosis can be achieved with intravenous drugs, with the possible exception of ketamine, which may be avoided because of its propensity to increase the heart rate. Tracheal intubation is facilitated by the administration of a neuromuscular blocking drug. Drugs used for maintenance of anesthesia should cause minimal changes in heart rate and in SVR and PVR. Furthermore, these drugs should not greatly decrease myocardial contractility. No one anesthetic has been proved to be superior. These goals can be achieved with combinations of an opioid and low concentrations of a volatile anesthetic or intravenous anesthetics such as propofol or dexmedetomidine. Although nitrous oxide can increase PVR, this increase is not sufficient to justify avoiding this drug in all patients with mitral stenosis. The effect of nitrous oxide on PVR, however, seems to be accentuated when coexisting pulmonary hypertension is severe. Avoiding the use of nitrous oxide allows higher inspired oxygen concentrations and may reduce pulmonary vasoconstriction. Rapid increases in the concentration of desflurane may cause tachycardia, bronchospasm, and pulmonary hypertension and should be avoided. Control of arterial blood pressure with a prophylactic intravenous infusion of the vasoconstrictor phenylephrine can reduce hemodynamic changes with induction of anesthesia.
Nondepolarizing neuromuscular blocking drugs with minimal circulatory effects are useful in patients with mitral stenosis. The adverse effects of drug-induced tachycardia in response to drug-assisted antagonism of nondepolarizing neuromuscular blocking drugs should be avoided ( Box 25.3 ). Sugammadex, which can replace neostigmine, does not cause cardiovascular changes. If cases are prolonged and neuromuscular blockade is not required for the conduct of the case, allowing the nondepolarizing neuromuscular blockade to be eliminated through metabolism may reduce the risk of tachycardia with drug-assisted antagonism. Intraoperative intravenous fluid therapy must be carefully titrated because these patients are susceptible to intravascular volume overload and to the development of left ventricular failure and pulmonary edema. Likewise, the head-down position may not be well tolerated because the pulmonary blood volume is already increased.
Avoid sinus tachycardia or rapid ventricular response rate during atrial fibrillation.
Avoid marked increases in central blood volume associated with overtransfusion or head-down position.
Avoid drug-induced decreases in systemic vascular resistance.
Avoid events such as arterial hypoxemia or hypoventilation that may exacerbate pulmonary hypertension and evoke right ventricular failure.
Monitoring intra-arterial pressure and SVV or PPV is a helpful guide to the adequacy of intravascular fluid replacement. If central pressures are measured, an increase in right atrial pressure could also reflect pulmonary vasoconstriction, suggesting the need to check for causes, which may include nitrous oxide, desflurane, acidosis, hypoxia, increased mitral regurgitation, or light anesthesia.
Postoperatively, patients with mitral stenosis are at high risk for developing pulmonary edema and right-sided heart failure. Mechanical ventilation may be necessary, particularly after major thoracic or abdominal surgery. The shift from positive-pressure ventilation to spontaneous ventilation with weaning and extubation may lead to increased venous return and increased central venous pressures with worsening of heart failure.
Mitral regurgitation is characterized by left atrial volume overload and decreased left ventricular forward stroke volume due to the backflow of part of each stroke volume through the incompetent mitral valve back into the left atrium. This regurgitant flow is responsible for the characteristic V waves seen on the recording of the pulmonary artery occlusion pressure. Mitral regurgitation secondary to rheumatic fever usually has a component of mitral stenosis. Dilated cardiomyopathy, which may be from ischemia, multiple myocardial infarctions, viral or parasitic infections, or other causes, may cause mitral regurgitation. Isolated mitral regurgitation may be acute, reflecting papillary muscle dysfunction after a myocardial infarction or rupture of chordae tendineae secondary to infective endocarditis.
Management of Anesthesia
Management of anesthesia in patients with mitral regurgitation should avoid decreases in the forward left ventricular stroke volume. Conversely, cardiac output can be improved by mild increases in heart rate and mild decreases in SVR ( Box 25.4 ). Preinduction placement of intra-arterial pressure monitoring can speed the identification and treatment of hemodynamic changes in patients with clinically significant valvular disease.
Avoid sudden decreases in heart rate.
Avoid sudden decreases in systemic vascular resistance.
Minimize drug-induced myocardial depression.
Monitor the magnitude of the V wave as a reflection of mitral regurgitant flow.
Maintain sinus rhythm.
Maintain diastolic pressure if possible.
A general anesthetic is the usual choice for patients with significant mitral regurgitation. Although decreases in SVR are theoretically beneficial, the rapid onset and uncontrolled nature of this response with a spinal anesthetic may detract from the use of this technique. Local or regional anesthesia may be used safely for surgery on peripheral body sites. Continuous spinal anesthetics may allow a slow titration of the regional block and can be a good choice of anesthetic. Maintenance of general anesthesia can be provided with volatile anesthetic, with or without nitrous oxide, or a continuous infusion of intravenous anesthetic. The concentration of volatile anesthetic can be adjusted to attenuate undesirable increases in systemic arterial blood pressure and SVR that can accompany surgical stimulation. Avoiding the use of nitrous oxide allows higher inspired oxygen concentrations and may reduce pulmonary vasoconstriction. Rapid increases in the concentration of desflurane may cause tachycardia, bronchospasm, and pulmonary hypertension and should be avoided. Control of arterial blood pressure with a prophylactic intravenous infusion of the vasoconstrictor phenylephrine can reduce hemodynamic changes with induction. Intravascular fluid volume must be maintained by prompt replacement of blood loss to ensure adequate venous return and ejection of an optimal forward left ventricular stroke volume.
Aortic stenosis is characterized by increased left ventricular systolic pressure to maintain the forward stroke volume through a narrowed aortic valve. The magnitude of the pressure gradient across the valve serves as an estimate of the severity of valvular stenosis. Hemodynamically significant aortic stenosis is associated with pressure gradients more than 50 mm Hg or valve areas less than 1.2 cm 2 . A peak systolic gradient exceeding 50 mm Hg in the presence of a normal cardiac output or an effective aortic orifice less than about 0.75 cm 2 in an average-sized adult (i.e., 0.4 cm 2 /m 2 of body surface area or less than approximately one fourth of the normal orifice) is generally considered to represent critical aortic stenosis. The combination of symptoms (angina, congestive failure, or fainting), signs (serious left ventricular dysfunction and progressive cardiomegaly), and a reduced valve area also indicate the diagnosis of critical aortic stenosis requiring surgical replacement. Increased intraventricular pressures are accompanied by compensatory increases in the thickness of the left ventricular wall. Angina pectoris occurs often in these patients in the absence of CAD, reflecting an increased myocardial oxygen demand because of the increased amounts of ventricular muscle associated with myocardial hypertrophy in combination with higher intraventricular pressures. There is a decrease in oxygen delivery secondary to the aortic valve pressure gradient in combination with an increase in oxygen requirements from the increase in left ventricular pressure and stroke work. Thus, aortic stenosis results in an increase in left ventricular stroke work and oxygen requirements (increased demand) while reducing coronary blood flow (reduced supply). The factors determining coronary blood flow are described by the following equation:
Isolated nonrheumatic aortic stenosis usually results from progressive calcification and stenosis of a congenitally abnormal (usually bicuspid) valve. Aortic stenosis due to rheumatic fever almost always occurs in association with mitral valve disease. Likewise, aortic stenosis is usually accompanied by some degree of aortic regurgitation. Regardless of the cause of aortic stenosis, the natural history of the disease includes a long latent period, often 30 years or more, before symptoms occur. Because aortic stenosis may be asymptomatic, it is important to listen for this cardiac murmur (systolic murmur in the second right intercostal space that may radiate to the right carotid) in patients scheduled for surgery. The incidence of sudden death is increased in patients with aortic stenosis.
Management of Anesthesia
With the advent of transcatheter aortic valve replacement (TAVR) the indications for aortic valve replacement (AVR) have changed, and many patients previously thought too high risk for surgical AVR (SAVR) are now considered candidates for TAVR. Patients with critical aortic stenosis or aortic stenosis with reduced left ventricular function or symptoms of angina or CHF should be evaluated for AVR prior to elective surgery.
Goals during management of anesthesia in patients with aortic stenosis are avoidance of arterial hypotension, maintenance of normal sinus rhythm, and avoidance of extreme and prolonged alterations in heart rate, SVR, and intravascular fluid volume ( Box 25.5 ). Hypotension on induction can rapidly lead to myocardial ischemia from high myocardial oxygen requirements secondary to a constant load on the left ventricle from the stenotic valve combined with a decrease in coronary perfusion pressure secondary to an increase in left ventricular end-diastolic pressure and a relative diastolic hypotension. The most critical issue on induction of anesthesia is the avoidance of hypotension. Preservation of normal sinus rhythm is critical because the left ventricle is dependent on properly timed atrial contractions to ensure optimal left ventricular filling and stroke volume. Marked increases in heart rate (more than 100 beats/min) decrease the time for left ventricular filling and ejection and decrease coronary blood flow while increasing myocardial oxygen consumption. Coronary blood flow to the left ventricle occurs during diastole, and changes in heart rate primarily affect diastolic time. Bradycardia (less than 50 beats/min) can lead to acute overdistention of the left ventricle. Tachycardia may lead to myocardial ischemia and ventricular dysfunction. In view of the obstruction to left ventricular ejection, decreases in SVR may be associated with large decreases in systemic arterial blood pressure and coronary blood flow and result in myocardial ischemia. Intra-arterial pressure monitoring is essential prior to induction of anesthesia and throughout the anesthetic period and can speed identification and treatment of hemodynamic changes. Prophylactic infusions of vasoconstrictors such as phenylephrine started prior to induction, may reduce hemodynamic changes.