Cardiac Surgery

R. Scott Mitchell MD¹

Linda E. Foppiano MD²

Lawrence C. Siegel MD³

Daryl Oakes MD⁴

¹SURGEON

²ANESTHESIOLOGISTS

CARDIOPULMONARY BYPASS

SURGICAL CONSIDERATIONS

The development of cardiopulmonary bypass (CPB) technology has allowed the repair of many congenital and acquired lesions of the heart and great vessels. Designed to replace cardiac and pulmonary functions, full CPB requires a blood pump and oxygenator. The pump may be of the roller-head or centrifugal variety with the latter producing less trauma to formed blood elements. The oxygenator may bubble gases (O2 and CO2) through a blood-filled reservoir (bubble oxygenator) or allow O2 and CO2 to diffuse through a thin membrane into the surrounding blood (membrane oxygenator). Utilization of any blood pump requires at least partial heparinization (ACT > 180 sec), and introduction of an oxygenator mandates full heparinization (ACT > 400 sec).

Full CPB typically drains systemic venous return via the right atrium into a venous reservoir, from which the blood is pumped through an oxygenator and then returned to the aorta or femoral artery, completely bypassing the heart and lungs (Figs 6.1-1 and 6.1-2). Partial CPB usually supports only a portion of the body—typically the infradiaphragmatic portion—and may use the patient’s lungs as an oxygenator (left atrium → femoral artery) or a mechanical oxygenator (femoral vein → femoral artery). Full CPB is utilized during a sternotomy for work on the heart, ascending aorta, and transverse arch. Partial CPB, in which some systemic venous blood returns to the heart and is ejected into the aorta, is normally used for work on the descending or thoracoabdominal aorta. Heparin-coated components, which partially eliminate the necessity for heparin, are available.

After exposure of the relevant organs (heart or descending thoracic aorta), and after heparinization, venous and arterial cannulae must be placed intraluminally. Cannulation of the heart usually involves venous drainage from the right atrium, with either two cannulae inserted through the atrium into the SVC and IVC (bicaval), or via a larger, dual-stage cannula draining the right atria and IVC. Bicaval cannulation reduces venous return (and rewarming) to the heart, and allows caval snares to be placed so that the right atrium can be opened without introducing air into the venous return. Occasionally, atrial manipulation for cannulation can depress CO with resultant hypotension. This usually can be reversed with volume replacement. Aortic cannulation usually is not associated with any physiologic perturbation, although HTN must be avoided to minimize aortic complications. After the cannulae are in place and connections are made to the bypass circuit, CPB may be instituted electively. Most cardiac operations are conducted under mild hypothermia (28°C), unless profound hypothermic circulatory arrest is to be utilized. In that case, a target temperature of 16-18°C is desirable. For operations on the descending thoracic aorta, normothermia is maintained.

Cessation of CPB is accomplished by gradually decreasing pump flows, allowing for right heart filling, and gradually replenishing the circulating blood volume. Pulmonary and coronary vasodilations are mandatory during this phase, as there appears to be heightened vasoreactivity after periods of ischemia and hypothermia. For periods of cardiac arrest, during which the heart is deprived of its arterial blood supply, the metabolic demands of the myocardium must be minimized. This usually is accomplished by achieving diastolic arrest with a hyperkalemic cardioplegic solution and also by lowering myocardial temperature to < 15°C. Frequent reinfusions of cardioplegia maintain hypothermia, prevent lactic acid accumulation, and deliver some minimally available dissolved O2.

The physiologic response to CPB is complex and is associated with a massive catecholamine release that resolves after its cessation. Subsequent changes include abnormal bleeding tendencies, increased capillary permeability, leukocytosis, renal dysfunction, and impairment of the immune response. Hemodilution, nonpulsatile flow, hypothermia, exposure of formed elements to nonendothelial surfaces, complement activation, protein denaturation, cascading effects within the coagulation and fibrinolytic system, and activation of the kallikrein-bradykinin cascade, all contribute to this unphysiologic state, and account for much of the morbidity and mortality after CPB.

Many physiologic variables are now controlled by the anesthesiologist, perfusionist, and surgeon, including systemic flow and perfusion pressure, arterial O2 and CO2, temperature, and Hct. Other physiologic parameters follow either directly or indirectly. Thus, physiologic monitoring for the anesthesiologist and perfusionist include, at a minimum, arterial pressure, CVP, ABG determination (preferably online during CPB), CO, UO, and ECG. Constant communication among surgeons, perfusionist, and anesthesiologist is mandatory for a smooth operation. Transesophageal echocardiography (TEE) is rapidly becoming standard practice for cardiac surgery.

Secondary effects of CPB demand some special considerations during the final stages of the procedure and chest closure. Adverse effects on coagulation have already been mentioned, and vigorous attention to maintenance and replacement of coagulation factors is essential. The capillary leak phenomenon results in interstitial myocardial and pulmonary edema. Decreased myocardial performance and compliance mandate an increased preload, especially
during the physical act of chest closure, where a transient rise in intramediastinal pressure may depress systemic venous return. Similarly, decreased pulmonary compliance and gas exchange mandate vigilance over inspiratory pressures and lung volumes during chest closure because mediastinal volume is physically decreased.

Figure 6.1-1. Detailed schematic diagram of the arrangement of a typical cardiopulmonary bypass circuit using a membrane oxygenator with integral hardshell venous reservoir (lower center) and external cardiotomy reservoir. Venous cannulation is by a cavoatrial cannula, and arterial cannulation is in the ascending aorta. Some circuits do not incorporate a membrane recirculation line; in these cases, the cardioplegia blood source is a separate outlet connector built into the oxygenator near the arterial outlet. The systemic blood pump may be either a roller or centrifugal type. The cardioplegia delivery system (right) is a one-pass combination blood/crystalloid type. The cooler-heater water source may be operated to supply water to both the oxygenator heat exchanger and cardioplegia delivery system. The air bubble detector sensor may be placed on the line between the venous reservoir and systemic pump, between the pump and membrane oxygenator inlet, or between the oxygenator outlet and arterial filter (neither shown), or on the line after the arterial filter (optional position on drawing). One-way valves prevent retrograde flow (some circuits with a centrifugal pump also incorporate a one-way valve after the pump and within the systemic flow line). Other safety devices include an oxygen analyzer placed between the anesthetic vaporizer (if used) and the oxygenator gas inlet and a reservoir level sensor attached to the housing of the hard-shell venous reservoir (on the left center). Arrows, directions of flow; X, placement of tubing clamps; P and T (within circles), pressure and temperature sensors. Hemoconcentrator (described in text) not shown.

Figure 6.1-2. Schematic representation of the CPB circuit. (Reproduced with permission from Hardy JD: Hardy’s Textbook of Surgery, 2nd edition. JB Lippincott, Philadelphia: 1988.)

ANESTHETIC CONSIDERATIONS FOR CARDIOPULMONARY BYPASS (CPB)

This segment is not meant to be a definitive text on CPB, but rather a guide to the anesthetic management of bypass. Communication among surgeons, anesthesiologists, and pump technicians is of vital importance in carrying out this procedure.

▪ PREPARATION FOR BYPASS

Prebypass/anticoagulation	[check mark] baseline ACT (normal = 90-130 sec). Heparin (3 mg [˜300 U]/kg) is administered via a central vein ([check mark] back-bleeding to verify intravascular position) or by the surgeon directly into the atrium (preferred). [check mark] ACT 3 min after heparin. It is essential to ensure adequate anticoagulation (ACT > 400 sec).
Aortic cannulation	Control MAP to ˜70 mm Hg for cannulation to ensure that the aortotomy does not extend. If needed, vasodilators may be used. The arterial line should be inspected for air bubbles.
Venous cannulation	Venous cannulation may be associated with atrial dysrhythmias. Blood loss can be excessive. Be prepared to infuse volume boluses, if necessary.
Pupils	Assess pupil symmetry for later comparison.

▪ TRANSITION ONTO CPB

Stop ventilation	Commencing bypass is a dangerous period for the patient as a result of the many hemodynamic changes that occur. D/C ventilation once there is no pulmonary blood flow.
Withdraw PA catheter	Withdraw PA catheter 4-5 cm.
Stop infusions	Stop iv drugs and reduce iv fluid infusions to TKO.
Anticoagulation	ACT should be re-3’d after 5 min on CPB to ensure anticoagulation (ACT > 400 sec).
Oxygenation	Verify oxygenation by checking arterial inflow color and inline sensors and by ABG within 5 min of beginning CPB.
Flow	3 for adequate venous drainage (CVP falls to a low level). Ensure adequate arterial inflow. Initial pressures may be very low, but usually will increase. View the descending thoracic aorta on TEE to verify flow (no aortic dissection).
Anesthesia	Anesthetics (e.g., fentanyl and midazolam) may be needed. A repeat dose (e.g., 10 mg pancuronium or 50 mg of rocuronium) should be given to prevent movement or shivering (increases O2 requirements).
Pupils	Assess pupils. Unilateral dilation may indicate arterial inflow into the innominate artery (unilateral carotid perfusion).

▪ BYPASS PERIOD

Anticoagulation	ACT levels should be checked regularly (q 20-30 min) and kept at > 400. Add heparin (5000-10,000 U), if needed.
Pressure/flow	There is controversy about safe flows and pressures. Generally, flows of 1.2-3 L/m2/min are used, with pressures of 30-80 mm Hg. A MAP of 50-60 mm Hg is probably best for cerebral perfusion and does not result in excessive noncoronary blood flow.
Acid-base status	α-stat (ABG measured and interpreted at 37°, regardless of actual patient temperature) regulation of acid-base status is preferred because of maintenance of normal cerebral flow and autoregulation on CPB.
Hct/Electrolytes	Generally, Hct will fall to ˜20, which may be acceptable (however, Hct ≥ 25 is preferable) in most patients. Hypokalemia is common and should be corrected. A K⁺ ˜4.5 mEq/L is desirable. Blood glucose levels should be monitored q 1 h. Treat blood glucose ↑ 125 mg/dl with iv regular insulin. (See Table 6.1-2.)
UO	Keep UO >1 mL/kg/h. If needed, mannitol and/or furosemide should be given (assuming pump flow is adequate).
Temperature	During bypass, T is usually maintained at ˜28°C.

Table 6.1-1. Difference Between α-Stat and pH-Stat Management During CPB

α-Stat (Temperature-uncorrected)	pH Stat (Temperature-corrected)
Plasma pH maintained at 7.4 (when measured at 37°C).	Plasma pH maintained at 7.4 at actual patient temperature.
Arterial PCO₂ maintained at 40 mm Hg (when measured at 37°C).	Arterial PCO₂ maintained at 40 mm Hg at actual patient temperature. Requires addition of CO₂ to inspired gases
Relative respiratory alkalosis during hypothermia	Relative normocapnia during hypothermia
Cerebral autoregulation preserved—CBF maintained.	Results in loss of cerebral autoregulation.

Table 6.1-2. Continuous Insulin Infusion in Intraoperative Adult Cardiac Surgery Patients

1. Bolus and start infusion pump as follows:
	Blood Glucose	Insulin Bolus units		Insulin Drip units/h
	< 125	0		0
	125-175	5		1
	175-225	10		2
	> 225	15		3
2. Frequency of blood glucose determination: every 30 min intraoperatively!
3. Insulin titration:
	Blood Glucose		Action
	< 75		Stop insulin; give D50w and recheck blood glucose in 30 min. When blood glucose > 150, restart with rate 50% of previous rate. 75-100 Stop insulin; recheck blood glucose in 30 min. When blood glucose > 150, restart with rate 50% of previous rate, unless the dose is < 0.25 U/h.
	101-125		If < 10% lower than last test, decrease rate by 0.5 U/h. If > 10% lower than last test, decrease rate by 50%. If neither, continue current rate.
	126-175		Same rate
	176-225		If lower than last test—same rate. If higher than last test—increase rate by 0.5 U/h.
	> 225		If > 19% lower than last test— same rate. If < 10% lower than last test OR if higher than last test increase rate by 1 U/h. If blood glucose > 225 and has not decreased after the third hourly increase in insulin, then double the insulin rate.

▪ TERMINATION OF BYPASS

Rewarming	Prior to discontinuing CPB, the patient should have a core temperature of at least 36°C.
Anesthesia/relaxation	Patient awareness may be a problem during rewarming. Volatile agents ± benzodiazepine (e.g., midazolam 3-5 mg) ± a narcotic to prevent awareness. In addition, a muscle relaxant also should be given.
Acid-base/electrolytes/Hct	[check mark] electrolytes, acid-base status, and Hct. Correct acidosis. K+: 4.5-5.5, normal ionized Ca++, and Hct ≥ 20 should be ensured.
Air maneuvers	Air maneuvers (to remove intracardiac and intraaortic air) are carried out when the heart is opened. Ventilation is commenced after there is pulmonary blood flow and will aid in the evacuation of air. Pleural fluid should be removed.

▪ WEANING FROM BYPASS

Prior to weaning	Prior to weaning from CPB, the aortic cross-clamp should have been off for 30 min to allow rewarming and reperfusion of the heart. Defibrillation is often needed, and pacing may be required. NSR or AV pacing is preferred. Vasoactive drugs should be available. After normal T, ventilation, cardiac rhythm, and reperfusion are established, bypass may be terminated. The heart is gradually volume-loaded (transfused from oxygenator) to adequate filling pressures and bypass flow slowly decreased over 15-45 sec until it is off. Return to bypass in the event of progressive cardiac distension or dysfunction. Assess CO and BP and adjust vascular resistance as necessary. Inotropic agents often are required at this stage.
Reversal of anticoagulation	After the patient is off CPB, anticoagulation must be reversed with protamine (1-1.3 mg/100 U heparin), administered slowly over 10-20 min because rapid administration can be associated with ↓ BP (treat with volume, calcium, α-agonists as necessary). Other reactions include pulmonary HTN and true allergic reactions. [check mark] ACT to ensure that it has returned to control (90-130 sec).
BP management	Vasoactive support often is needed in the postbypass period; the need varies with surgical procedure, disease process, and underlying cardiac function. In general, SBP should be limited to 120 mm Hg to avoid stress on the aortotomy site.

▪ COAGULATION AND CPB

General	Bleeding is common post-CPB and may be considerable. Both preop and intraop factors contribute to this. Knowledge of these factors and the tests involved will aid with the management of these patients (Table 6.1-3).
Preop factors	Hx of previous bleeding during surgery is important. Many drugs may contribute to bleeding: aspirin/NSAIDs/clopidogrel (Plt dysfunction), anticoagulants (heparin, Coumadin) and fibrinolytic agents. These should be stopped preop, if possible, or their action reversed. Other pathological processes (e.g., liver failure/congestion, renal failure, or hemophilia) also play a role. Preop testing is important and should include PT, PTT, Plt count, and bleeding time, as a minimum.
Intraop factors	CPB is associated with ↓ Plt count and function. Circulating clotting factors are decreased, and fibrinolysis occurs. Many surgical teams routinely use either Amicar (5-10 g loading dose; 1 g/h, maintenance) or Aprotinin (1 mL, test dose; 1-2 million KIU, loading; 0.25-0.5 million KIU/h, maintenance) prophylactically during cardiac surgery to inhibit the fibrinolytic process. Aprotinin also has anti-inflammatory properties that may offset the inflammatory response to CPB. Recent studies have associated aprotinin (and not aminocaproic acid or tranexamic acid) with increased risk of CV events, including MI and heart failure, cerebrovascular events and renal dysfunction/failure in patients undergoing CABG surgery.
Post-CPB bleeding	The common causes of post-CPB bleeding are surgical causes, inadequate heparin reversal, ↓ number of Plt and Plt dysfunction, ↓ clotting factors, fibrinolysis, DIC, excessive BP, and hypothermia. Surgical causes and inadequate heparin reversal ([check mark] ACT) should be ruled out. If no surgical cause is found and ACT is normal, Plt (1-2 plateletpheresis units) should be infused. PT, PTT, Plt count, TT, reptilase time, fibrinogen, and FSP should be checked. TEG may prove very useful. (See Fig 7.12-9 and Table 7.12-3 in Liver/Kidney Transplantation, p. 717.)

Table 6.1-3. A Treatment Plan for Excessive Bleeding after Cardiac Surgery

Action	Dosage	Indication
Rule out surgical cause	—	Absence of oozing at puncture sites and incision
More protamine	0.5-1 mg/kg	ACT > 150 sec or aPTT > 1.5 times control
Warm the patient	—	“Core” temperature < 35°C
Apply positive end-expiratory pressure (PEEP)^* Desmopressin	5-10 cm H₂O 0.3 mcg/kg iv	Prolonged bleeding time
Aminocaproic acid	50 mg/kg, then 25 mg/kg/h	Elevated D-dimer or teardrop shaped TEG tracing
Tranexamic acid	10 mg/kg, then 1 mg/kg/h	Elevated D-dimer or teardrop shaped TEG tracing
Platelet transfusion	1 U/10 kg	Platelet count < 100,000/mm³
Fresh frozen plasma	15 mL/kg	PT or aPTT > 1.5 times control
Cryoprecipitate	1 U/4 kg	Fibrinogen < 1 g/L or 100 mg/dL
^*PEEP is contraindicated in hypovolemia.

Suggested Readings

1. Conlon N, Grocott HP, Mackensen GB: Neuroprotection during cardiac surgery. Expert Rev Cardiovasc Ther 2008; 6(4):503-20.

2. De Somer F: What is optimal flow and how to validate this? J Extra Corpor Technol 2007; 39(4):278-80.

3. Entwistle JWC III, Boateng P, Wechsler AS: Intraoperative myocardial protection. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 5th edition. Lippincott Williams & Wilkins: 2013, 648-67.

4. Gibbs NM, Larach DR: Anesthetic management during cardiopulmonary bypass. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 5th edition. Lippincott Williams & Wilkins: 2013, 214-37.

5. Hessell EA II, Murphy GS, Groom RC et al: Cardiopulmonary bypass: equipment, circuits, and pathophysiology. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 5th edition. Lippincott Williams & Wilkins: 2012, 587-629.

6. Mangano DT, Tudor IC, Dietzel C, et al: The risk associated with aprotinin in cardiac surgery. N Engl J Med 2006; 336(4):353-65.

7. Morris BN, Romanoff ME, Royster RL. The postcardiopulmonary bypass period. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 5th edition. Lippincott Williams & Wilkins: 2013, 238-64.

8. Shore-Lesserson L, Malayaman SN, Harrow JC et al: Coagulation management during and after cardiopulmonary bypass. In: Hensley FA, Martin DE, Gravlee GP, eds. A Practical Approach to Cardiac Anesthesia, 5th edition. Lippincott Williams & Wilkins: 2012, 548-70.

CORONARY ARTERY BYPASS GRAFT SURGERY

SURGICAL CONSIDERATIONS

Description: Coronary artery bypass grafting (CABG) is the most frequently performed cardiac operation. Since the discovery that coronary thrombosis is the causative event for MI, many schemes have been devised to augment the restricted coronary blood flow, including collateral pericardial blood flow to epicardial arteries and implantation of the internal mammary artery (IMA) with unligated side branches into the LV muscle. With the discovery by Favalaro that saphenous veins can be anastomosed to the epicardial coronary arteries, a new era of myocardial revascularization began. Basically, the technique involves bypass to a narrowed or occluded epicardial coronary > 1 mm in diameter with a small-diameter conduit (usually reversed saphenous vein or IMA) distal to the narrowed segment, with the proximal arterial inflow source being the ascending aorta. The IMA may be mobilized from the chest wall, leaving its proximal origin with the subclavian artery intact (pedicled graft), or the IMA may be transected and its proximal end anastomosed to the aorta or saphenous vein as a “free mammary graft.” An “all-arterial revascularization,” using the right IMA and nondominant RA, is being utilized with increasing frequency.

Figure 6.1-3. Coronary artery circulation—anterior view. (Reproduced with permission from Edwards EA, Malone PD, Collins JJ Jr: Operative Anatomy of the Thorax. Lea & Febiger, Philadelphia: 1972.)

The heart is approached through a median sternotomy, with the patient supported on full CPB (see separate section on CPB, p. 348). Although various operative strategies may be used, the most common regimen is for all distal (epicardial) anastomoses to be performed during a single period of aortic cross-clamping and cardiac arrest. During that period of induced asystole, myocardial protection is achieved by hypothermia and occasional reperfusion via antegrade or retrograde cardioplegia. Cardiac standstill and a bloodless field are mandatory to allow these very demanding small-diameter anastomoses to be constructed, with no obstruction to flow, in a minimal amount of time. The cross-clamp is then removed and the heart allowed to resume beating. A partially occluding aortic cross-clamp can then be applied to allow construction of the proximal aortic anastomoses. After a sufficient period of resuscitation, the patient is weaned from CPB, and decannulation, heparin reversal, and chest closure are allowed to proceed as previously noted.

The choice of conduit depends on availability and durability. Historically, the saphenous vein was the first small vessel conduit with acceptable patencies but with prolonged experience, it appears that 50% of vein grafts will be significantly diseased or occluded at 10 yr. The IMA appears to have superior long-term performance with ˜90% 10-yr patency rates. Other arterial conduits, such as the left gastroepiploic artery, superficial epigastric artery, and the radial artery, are being investigated as to their long- and short-term durability. Typical target arteries include the distal right coronary and its major terminal branch, the posterior descending artery. From the left circulation, the left anterior descending (LAD), with its diagonal and septal branches, is the most important, having been estimated to supply blood to 60% of the left ventricle.

The left circumflex coronary artery courses in the posterior atrioventricular groove and is not easily accessible for bypass, which is usually performed to its obtuse marginal or posterolateral branches.

In a randomized study on coronary artery surgery (CASS), coronary bypass was noted to be superior to medical management for relief of angina and to prolong life in patients with left main CAD and in those with three-vessel disease and impaired LV function. Other patients may receive bypass for intractable angina refractory to medical management.

Variant procedure or approaches: port access coronary artery revascularization (see p. 389); off-pump and minimally invasive coronary artery bypass (see p. 389).

Usual preop diagnosis: CAD with Class 3 or 4 angina (angina with minimal exertion or at rest)

▪ SUMMARY OF PROCEDURE

Position	Supine
Incision	Median sternotomy with legs prepped for saphenous vein harvest
Special instrumentation	Complete hemodynamic monitoring; TEE
Unique considerations	CPB
Antibiotics	Cefazolin 2 g iv prior to incision, then 1 g q 4 h
Surgical time	3.5-4.5 h
Closing considerations	Prevention of coagulopathy; maintenance of preload
EBL	500-600 mL
Postop care	ICU: 1-3 d, intubated 6-24 h.
Mortality	2-4%
Morbidity	Cognitive decline in patients > 60 yr: 26% MI: 3-6% Pneumonia: 5% CVA/stroke: 2-4% ↓ renal function
Pain score	7-8

ANESTHETIC CONSIDERATIONS

(Procedures covered: CABG; LV aneurysmectomy)

PREOPERATIVE

H&P and tests will divide these patients broadly into two groups: (a) high-risk, characterized by poor LV function (cardiac failure; EF < 40%; LVEDP > 18 mm Hg; CI < 2.0 L/min/m2; ventricular dyskinesia; three-vessel disease; occlusion of left main or left main equivalent; valvular disease; recent MI; ventricular aneurysm; VSD; MI in progress; and old age); and (b) low-risk, characterized by good LV function. The type of monitoring chosen will depend on the patient’s group.

Respiratory	Hx of smoking or COPD—patient should be encouraged to stop smoking at least 2 wk before surgery. Treat COPD and optimize therapy before surgery. Tests: CXR; PFTs; as indicated by H&P
Cardiovascular	In the preop assessment, the following factors will affect patient management and surgical outcome: Hx of angina (stable, unstable at rest, and precipitating factors) Patient’s exercise tolerance will provide a clue to LV functions and surgical outcome. The presence of CHF (Sx: SOB, PND, orthopnea, DOE, pulmonary edema, JVD, 3rdheart sound). Recent (< 6 mo) MI, dysrhythmias, HTN, vascular disease (particularly carotid stenosis, aortic disease). Valvular disease (particularly MR or AS) or the presence of a VSD or LV aneurysm may portend increased risk of periop complications. Tests: 12-lead ECG: [check mark] ischemia (area involved), LVH, previous MI, dysrhythmias. Exercise stress testing: [check mark] exercise tolerance, area of ischemia, maximal HR and BP before ischemia occurs, dysrhythmias. Thallium scan: [check mark] component of reversible ischemia. ECHO (may be combined with stress ECHO): [check mark] LV function, wall motion abnormalities, valvular disease, VSD. Cardiac catheterization: [check mark] extent and location of disease, LV function, valvular pathology, VSD, LVEDP, LV aneurysm.
Postinfarction VSD	The development of a postinfarction VSD is associated with high operative morbidity and mortality because of the difficulty in repairing the lesion due to friable tissue, difficulty in obtaining hemostasis, emergent nature of the condition, and possible pulmonary edema. These patients effectively have poor LV function and should be considered as high-risk patients. They often require support, including IABP, during induction, prebypass, and postbypass.
LV aneurysm	LV aneurysm is usually a late complication of infarction; however, it can occur early, when it usually is associated with cardiac rupture (and high mortality). These patients usually have poor myocardial function and should be anesthetized with full monitoring, including PA catheterization. Postbypass, the LV cavity is reduced in size and compliance. To ensure an adequate CO, maintain adequate preload, a higher than normal HR (A-V pacing if needed), and sinus rhythm, and consider the use of inotropes. LV aneurysms are often associated with dysrhythmias and may require cardiac mapping. Hemostasis is often difficult to obtain, and adequate iv access is a necessity. Treatment usually entails the use of blood and blood products.
Emergency revascularization	Emergency revascularization occurs in the setting of acute MI, often with acute LV failure or after failed PTCA, where the patient may be stable, suffering from acute ischemia and hemodynamically unstable, or even in full cardiac arrest. Factors to consider in these cases are full stomach (and the need for rapid-sequence induction [p. B-5] in the face of ischemia); the prior use of fibrinolytic agents (with increased risk of hemorrhage); need for inotropes; antianginals; IABP; and dysrhythmias. These patients have a higher morbidity and mortality. In patients who have received fibrinolytic agents, consider postbypass use of antifibrinolytic agents (e.g., aminocaproic acid).
Neurological	Previous stroke or Hx/Sx of carotid artery disease should be documented and evaluated.
Endocrine	Diabetes is common and periop control of blood glucose is important. Tests: Blood glucose
Renal	[check mark] baseline renal function, as CPB places these patients at risk for renal failure. Tests: Cr; BUN; electrolytes (particularly K+)
Hematologic	Patients are often on aspirin or other antiplatelet therapy, which may lead to increased intraop hemorrhage. These agents should be stopped 7-10 d before surgery, if possible. Some patients may be on anticoagulants (usually heparin in the immediate preop period). Heparin should be stopped 6-8 h preop; however, in some patients, heparin infusion is continued into the OR. Other patients may have received thrombolytic agents that put them at increased risk for intraop hemorrhage. Tests: Consider Plt count, PTT, if indicated.
Laboratory	Hb/Hct; other tests as indicated from H&P. T&C 2-4 U PRBCs.
Premedication	Patients should be instructed to continue all medications (e.g., nitrates, β-blockers; Ca++ antagonists, antidysrhythmics, and antihypertensives) before surgery, with the exception of diuretics on the day of surgery. Allaying anxiety may decrease the incidence of periop ischemia and help with the preinduction placement of lines. If necessary, preop sedation may include diazepam (10 mg po) or lorazepam (1-2 mg po) the night before and again 1-2 h before arrival in the OR with the addition of morphine (0.1 mg/kg im) and scopolamine (0.3 mg im). Most often midazolam (1-5 mg iv) immediately prior to OR is used. Severely compromised patients will require less premedication.

INTRAOPERATIVE

Anesthetic technique: GETA. An arterial line should be inserted, using liberal amounts of local anesthetic, before induction. The presence of real-time BP monitoring can be critical in the care of these patients, especially during induction. Although it is helpful to have a CVP line before induction for preload monitoring and drug infusion, it is not essential. This line usually is inserted after the patient is intubated. If infused drugs are necessary before the CVP catheter is in place, they can be administered through a separate peripheral iv.

Induction	Generally, a moderate- to high-dose narcotic technique (e.g., fentanyl 10-100 mcg/kg or sufentanil 2.5-20 mcg/kg), supplemented by etomidate (0.1-0.3 mg/kg) or midazolam (50-350 mcg/kg), is appropriate. As with all cardiac cases, the speed of induction and total drug dose depend on the patient’s cardiac function and pathology. Muscle relaxation may be obtained using pancuronium (0.1 mg/kg), given slowly to avoid tachycardia, or vecuronium (possibility of bradycardia, especially if the patient is β-blocked). It is important to avoid the sympathetic response to laryngoscopy. The use of high-dose narcotics (see above), esmolol (100-500 mcg/kg over 1 min, followed by 40-100 mcg/kg/min infusion), SNP (0.5-3 mcg/kg/min), lidocaine (1-2 mg/kg), or a combination of these agents, may decrease or ablate this response. NTG (0.5-2 mcg/kg/min) also may be used during induction if evidence of ischemia occurs.
Maintenance	Usually narcotic (total: fentanyl 10-100 mcg/kg or sufentanil 5-20 mcg/kg) with midazolam (50-350 mcg/kg) for amnesia. Patients with good LV function may benefit from the decreased myocardial O₂ demand associated with the use of volatile agents (2° ↓ contractility). N₂O is generally avoided. Propofol infusion may be used while rewarming and postbypass.
Emergence	Transported to ICU, sedated, intubated, and ventilated. Extubate when able—often < 6 h if lower-dose narcotic technique used (fast-track).
Blood and fluid requirements	IV: 14 ga × 1-2 NS/LR @ 6-8 mL/kg/h UO 0.5-1 mL/kg/h Warm all fluids. Humidify gases.
Monitoring	Standard monitors (p. B-1) Arterial line CVP or PA catheter ECG TEE	Standard monitors and an A-line are placed before induction. [check mark] BP in both arms. Right radial preferred if left IMA graft, because retraction of the sternum may compress the left subclavian. CVP (and/or PA line, if indicated), usually is placed after intubation. In the low-risk/good LV function group, CVP is adequate; in high-risk/poor LV function, a PA catheter is useful for hemodynamic monitoring, weaning from bypass, and vasoactive therapy. Some groups use routine PA catheterization for all patients undergoing CABG surgery. Five-lead monitoring using leads II and V5 (or area most at risk for ischemia). Will reflect regional wall motion abnormalities, papillary muscle dysfunction, and MR.
Myocardial O₂ balance	Supply—Coronary blood flow: Perfusion pressure (DBP-LVEDP) Diastolic filling time (HR) blood viscosity (optimal Hct = 30) Coronary vasoconstriction: Spasm PaCO₂ (hypocapnia → constriction) α-sympathetic activity Supply—O₂ delivery: O₂ sat Hct Oxyhemoglobin dissociation curve Demand—O₂ consumption: BP (afterload) Ventricular volume (preload) Wall thickness (↓ subendocardial perfusion) HR Contractility	The balance of myocardial O2 supply vs demand is important in the management of these patients. The goal of anesthesia is to ensure that this balance remains in equilibrium and that no ischemia occurs, or, if it does, that it is treated promptly. Those patients with poor LV function or complicated disease will benefit from maintenance of contractility (avoid volatile agents) and a high FiO2, whereas those with good LV function may benefit from mild cardiac depression (↓ demand associated with the addition of low-dose volatile agents). Certain events are associated with increased risk of intraop ischemia: intubation, incision, sternotomy, cannulation, tachycardia, ↑ BP or ↓ BP, ventricular fibrillation or distension, inadequate cardioplegia, emboli, spasm, or inadequate revascularization. Care should be taken to avoid these complications and to ablate responses to stimuli.
Detection of ischemia	ECG PA catheter TEE	ST segment depression or elevation or a new T-wave alteration may suggest ischemia. Monitoring two leads—one lateral (e.g., V5) and one inferior (e.g., II)—gives the best detection rate. Elevations of PCWP may be indicative of ischemia. A new V-wave on the PCWP trace is a better sign of possible ischemia (papillary muscle dysfunction). The appearance of a new regional wall motion abnormality is the most sensitive indicator of ischemia, but it requires constant monitoring.
Treatment of ischemia	Caused by tachycardia: Esmolol (100-500 mcg/kg) ↑ anesthesia Verapamil (2.5-10 mg iv) Caused by ↑ BP: NTG (0.5-4 mcg/kg/min) ↑ anesthesia Caused by ↓ BP: Phenylephrine (0.2-0.75 mcg/kg/min) ↑ preload Caused by ↓↓ HR: A-V pacing	Although avoidance of ischemia is the goal, when it does occur it should be treated aggressively. Treatment may include inotropic support (e.g., dopamine 1-5 mcg/kg/min, epinephrine 25-150 ng/kg/min or milrinone 0.375-0.75 mcg/kg/min). If LV failure persists despite other therapy, an IABP or VAD may be inserted.
Positioning	[check mark] and pad pressure points [check mark] eyes