anastomosed to the LAD using conventional open instruments. Although experiences at selected single
centers have described satisfactory patency and reduced cost, complications, and postoperative length of
stay,45 the MIDCAB has not achieved widespread application. Technical considerations and exposure
have raised concerns about graft patency, and in the era of increased percutaneous intervention, very
few patients are referred with isolated single-vessel disease. Some groups have advocated for a hybrid
approach, in which the LAD is surgically grafted using the MIDCAB approach and the right coronary and
circumflex branches are treated percutaneously.46 Robotic systems, such as the da Vinci (Intuitive
Surgical, Sunnydale, CA), benefit from high-definition three-dimensional video visualization and precise
remotely controlled instruments with 6- or 7-degree freedom of motion. They have been increasingly
used in noncardiac surgery, particularly in gynecology and urologic specialties. Some centers have
begun using robotic technology to harvest the internal mammary artery along its entire length,
followed by a MIDCAB, also known as robotically assisted CABG (RAS-CAB).47 Others have gone one
step further, performing complete coronary revascularization using robotic instruments: the totally
endoscopic coronary artery bypass (TECAB).48,49 The procedure has been performed with or without
CPB and cardiac arrest. Although in selected centers the procedure appears feasible, the widespread
utilization of minimally invasive coronary artery bypass remains in question because of concerns
regarding patency, particularly in light of recent evidence regarding off-pump surgery in general.
Despite changes in technology, there has been little growth in minimally invasive coronary artery
bypass procedures.
POSTOPERATIVE CARE
Most patients after undergoing coronary bypass grafting require very little physician intervention,
particularly if the operation was conducted according to the preoperative plan. The use of clinical care
pathways is now routine, and they have been demonstrated to reduce morbidity, cost, and length of
hospital stay. However, complications can occur, which must be anticipated for early recognition and
treatment.
Patients after cardiac surgery are routinely admitted to the intensive care setting. Most centers delay
extubation until systemic warming is complete, typically within 4 to 6 hours. This also gives ample
opportunity to ensure adequate hemostasis and hemodynamic stability. Many centers routinely use
pulmonary artery catheters, or Swan–Ganz catheters, for assessment of intracardiac filling pressures as
well as calculation of cardiac output. Cardiac output (CO) can be calculated in one of two ways:
thermodilution or the modified Fick technique. Using thermodilution, room temperature saline of a
known quantity is injected briskly into the right atrium. As the saline mixes with blood traveling
through the right ventricle, blood is cooled. The blood temperature is then recorded in the pulmonary
artery over time. A curve is generated, denoting the change in temperature from baseline, and the area
under this curve is inversely proportional to the cardiac output (e.g., the higher the cardiac output, the
lower the impact the small saline aliquot has on blood temperature). Clinicians should be aware that
severe tricuspid regurgitation can interfere with the validity of the thermodilution technique, typically
underestimating forward flow. The Fick technique relies on the principle of mass balance proposed by
Adolph Fick in 1870. Oxygen consumption (VO2
) must equal the difference in oxygen content of arterial
and venous blood times the cardiac output. Assumptions can be made about oxygen consumption at rest,
and arterial and venous oxygen content (CaO2 and CVO2
) can be calculated by the hemoglobin
concentration and oxyhemoglobin saturation:
CO = VO2/(CaO2
- CVO2
)
Goals for hemodynamic stability generally include maintenance of a mean arterial pressure between
65 and 75 mm Hg and a cardiac index of at least 2 L/min per m2. Outcomes should be individualized, as
a chronically hypertensive patient may require a higher arterial pressure to maintain satisfactory tissue
perfusion, and a postoperative patient with bleeding from a tenuous aortic suture line may benefit from
a more restrictive blood pressure approach. Hypotension is quite common following cardiac surgery and
is often related to hypovolemia, as well as vasodilation from systemic warming and an inflammatory
response from extracorporeal circulation with activation of vasodilatory mediators. Intravascular
hypovolemia is extremely common in the immediate perioperative period. Causes are multifactorial and
include capillary leak from inflammation, venodilation from warming, unrecognized and unreplaced
blood loss, and excessive diuresis, particularly if osmotic diuretics such as mannitol are given during
CPB. Patients may require 2 to 3 L of fluid in the first several hours after surgery. Those with
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ventricular hypertrophy and diastolic dysfunction may reauire additional fluid to maintain cardiac
output. Although not essential, the pulmonary artery catheter can be instrumental in guiding fluid
resuscitation. While colloids, such as albumin and hetastarch, can reduce the total volume required to
maintain stability, there are no prospective randomized data clearly demonstrating its superiority with
regard to outcome benefits.
Vasoconstrictors are used to treat hypotension, but should only be initiated if the patient has been
adequately fluid resuscitated and myocardial function and cardiac output is preserved. a-Agonists, such
as Neo-Synephrine, will increase vascular tone without increasing contractility or heart rate and do not
exacerbate dysrhythmias. Similarly, vasopressin has no effect on cardiac function, but uniquely will not
increase pulmonary vascular resistance, as there are no vasopressin receptors in the pulmonary vascular
bed. Additionally, vasopressin preferentially constricts efferent renal arterioles rather than afferent
arterioles, resulting in maintained glomerular filtration and urine output. Norepinephrine, epinephrine,
and dopamine are also frequently used to counteract a vasodilatory state. These catecholamines are also
inotropic agents, which can be useful if myocardial function is depressed. However, they all increase
heart rate and myocardial oxygen consumption and can be arrhythmogenic.
Myocardial dysfunction can occur from stunning after cardioplegic arrest, particularly if the crossclamp period was long. This can be problematic if systolic function is severely depressed preoperatively.
Inadequate myocardial protection from insufficient cardioplegia can also result in catastrophic and
unrecoverable postoperative heart failure. Unless the heart is acutely ischemic at the time of surgery, it
is unusual to expect immediate improvement in contractility after surgical revascularization. In fact, the
acutely ischemic heart often tolerates CPB and cardioplegia poorly. Contractility can be globally
severely depressed after emergent coronary bypass grafting in the setting of a sizable STEMI, especially
if the patient was in preoperative shock. If cardiac dysfunction and low cardiac output are detected
intraoperatively, careful assessment of bypass graft position and patency should be undertaken. This is
especially true if new wall motion abnormalities are regional.
Once surgical problems have been corrected, efforts are made to optimize myocardial contractility.
Inotropic agents will improve cardiac function and can be easily titrated to the desired effect.
Catecholamines, such as dopamine, epinephrine, and dobutamine, are frequently used. All of these
agents, through their effects on b receptors, will increase heart rate, predispose to arrhythmias, and
increase myocardial oxygen consumption. Nonetheless, these agents are generally safe, particularly at
low doses. Phosphodiesterase inhibitors, such as milrinone, also improve contractility and have less
effect on heart rate or myocardial contractility. These agents are also vasodilators, and should be used
with caution in patients who are hypotensive. Both catecholamines and phosphodiesterase inhibitors
exert their inotropic effects by increasing cytosolic calcium. For these agents to be effective, there must
be adequate calcium stores. Infusion of supplemental calcium often potentiates the effect of both classes
of drugs. Likewise, acidosis decreases the effectiveness of inotropic agents, and normalization of blood
pH, either by replacement of sodium bicarbonate or hyperventilation, can have an immediate effect on
myocardial function.
When postoperative ventricular dysfunction is entirely related to myocardial stunning, inotropes
should be weaned within the first 24 hours. However, if postoperative cardiogenic shock is severe and
refractory to high-dose inotropic infusions, insertion of an intra-aortic balloon pump should be
considered. Positioned within the thoracic aorta (Fig. 83-14), balloon pump actuation is timed with the
patient’s ECG or arterial pressure tracing. Inflation occurs during diastole, augmenting coronary
perfusion, and deflates during systole, reducing afterload and increasing cardiac output. Insertion of a
ventricular assist device may be beneficial; however, many of these patients subsequently require heart
transplantation, so careful patient selection is essential.
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Figure 83-14. Intra-aortic balloon pump positioned within the descending thoracic aorta. The device must be positioned to not
occlude the left subclavian artery or the abdominal aortic branches.
Postoperative bleeding is infrequent but can occur, especially when patients are taking irreversible
platelet inhibitors. Output from mediastinal chest drains is monitored closely, and markers of
coagulation are assessed. Coagulopathy should be corrected with appropriate blood component
transfusions. Retransfusion of shed blood is generally avoided, as it may exacerbate coagulopathy.
Return to the operating room should be considered if drainage exceeds 600 to 800 mL in 4 to 5 hours,
without signs of slowing.
Inhibitors of plasminogen can be helpful in reducing postoperative coagulopathy and bleeding
complications. There are three agents in this class of drug: ε-aminocaproic acid (Amicar, Xanodyne
Pharmaceuticals, New Port, KY), tranexamic acid, and aprotinin (Trasylol, Bayer Leverkusen,
Germany). The first two agents are synthetic binders of plasminogen or plasmin. Aprotinin is a naturally
occurring serine protease inhibitor that can inhibit plasminogen, as well as many other proteases.
Although meta-analysis suggested that aprotinin was superior to the other agents,50 concerns regarding
the safety of aprotinin have been raised, suggesting a higher incidence of renal failure51 and even
mortality.52 A subsequent prospective randomized trial concluded that aprotinin was independently
associated with a higher rate of death,53 and as such its approval has been halted by the U.S. Food and
Drug Administration.
There has recently been great enthusiasm for using a blood conservation strategy. Transfusion of as
little as a single unit of packed red cells is independently associated with increased morbidity after
coronary bypass surgery.54 Efforts to minimize hemodilution using retrograde priming and
hemofiltration can be very effective at reducing transfusion rates, but the most important adjunct to
reduce blood usage is reduced transfusion triggers. Evidence exists that hemoglobin concentrations as
low as 7 g/dL can be safe and are very well tolerated in intensive care unit patients.55
Cardiac tamponade is an infrequent but feared complication that can be fatal and is often difficult to
diagnose. The classic scenario is a patient with initially high chest drainage that suddenly ceases. The
patient then insidiously develops oliguria, followed by low cardiac output and refractory hypotension.
Signs such as bulging neck veins, elevated central venous pressure, pulsus paradoxus, and widened
mediastinal silhouette on chest radiography may be variably present. Echocardiography can establish
the diagnosis by demonstrating a pericardial effusion with right atrial and right ventricular
compression. However, it is important to note that echocardiography cannot rule out the diagnosis.
Timely diagnosis usually requires experience and a low index of suspicion. Treatment involves
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immediate return to the operating room, where removal of the obstructing fluid and clot results in
immediate relief of constriction and normalization of hemodynamic parameters. When tamponade
occurs late, it may be treatable with percutaneous drains if the pericardial fluid content is thin and
without significant clot burden.
Atrial fibrillation is extremely common following CABG, with a frequency of 25% to 30%. Its
occurrence is higher for older patients and those with lung disease, and after combined CABG and valve
surgery, decreased ventricular function, prolonged aortic cross-clamp period, and more severe
hypothermia. Interestingly, the rate of atrial fibrillation does not appear to be reduced after off-pump
CABG.56 It most frequently occurs between the second and the fourth postoperative day, and can be
precipitated by electrolyte imbalances, particularly hypokalemia or hypomagnesemia. If the rate is
excessively high or the patient has significant ventricular hypertrophy, atrial fibrillation can result in
hemodynamic compromise producing hypotension and oliguria. The most frequently used treatment for
postoperative atrial fibrillation is amiodarone. It can achieve adequate rate control after an intravenous
load of 150 mg in the majority of patients, with minimal effect on blood pressure or contractility. As a
class III antiarrhythmic, amiodarone is also very effective at facilitating conversion to sinus rhythm.
When given preoperatively, amiodarone can also reduce the rate of postoperative atrial fibrillation,
although bradycardia is more common in protocols that use higher doses.57 Beta-blocking agents are
also effective at achieving rate control, and when given routinely preoperatively and reinitiated
immediately after surgery, they have reduced the occurrence of atrial fibrillation.58 Diltiazem is
immediately effective at controlling rapid atrial fibrillation, and is typically given as a 5- to 10-mg load,
followed by a continuous infusion of 5 to 10 mg/hr. Although it is associated with hypotension, its short
half-life makes this complication quite manageable. For atrial fibrillation with rapid ventricular
response refractory to amiodarone, beta blockers, and diltiazem, it may be reasonable to add digoxin.
This drug should be used with caution, because it is proarrhythmic. Drug concentrations should be
followed and potassium levels maintained aggressively. If rapid ventricular response results in
significant hemodynamic instability, electrical cardioversion should be performed. Cardioversion may
also be considered if atrial fibrillation persists after 24 to 36 hours because of the risk of clot formation
within the left atrial appendage. Cardioversion should not be performed if atrial fibrillation has been
present for more than 48 hours. If atrial fibrillation is persistent, anticoagulation must be considered
and weighed against the potential for postoperative bleeding complications. The vast majority of
patients who develop atrial fibrillation after CABG will revert to sinus rhythm, and the complication
rate is generally low. However, atrial fibrillation does increase the length of stay and cost of
hospitalization, so efforts to reduce its incidence are necessary.
Deep sternal wound infection involving the bone occurs in approximately 0.5% to 1% of patients.
Independent risk factors are obesity, diabetes, immunosuppression, use of both internal mammary
arteries, chronic lung disease, and malnutrition. The most frequent organism is Staphylococcus aureus,
although gram negatives can be seen in diabetics and immunosuppressed patients. Helpful preventative
strategies include decontamination of nasal Staphylococcus species with mupirocin, preoperative
Hibiclens wash, and tight postoperative glucose control. The diagnosis is established with sternal wound
drainage and palpable sternal instability. Systemic antibiotics should be initiated and the patient
returned to the operating room expeditiously for sternal débridement. Delay could result in
mediastinitis with sepsis and shock. Under most circumstances, the chest wall is reconstructed with
myocutaneous flaps based on the pectoralis and rectus abdominus muscles.
RESULTS OF CORONARY BYPASS GRAFTING
Overall, the mortality rate following coronary bypass grafting is between 2% and 3%. This number has
been progressively declining despite rising median age and worsening severity of disease (Fig. 83-15).
Improved outcomes can be attributed to advances in surgical technique, anesthetic approaches,
preoperative timing and patient selection, sophistication of intensive care systems, and superior
pharmacology, including antiplatelet agents, beta blockers, and statins. Increased competition, both
between cardiac surgeons and with percutaneous interventionalists, and public reporting of data have
undoubtedly improved efficiency and contributed significantly to better outcomes. Major morbidity is
estimated to be 10% to 12%. Risk of stroke is approximately 1% to 2%, renal failure requiring renal
replacement therapy is 0.5% to 1%, deep sternal wound infection is 0.5% to 1%, and need for urgent
reoperation is 3% to 5%. Overall, median length of hospital stay is approximately 6 days.
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Figure 83-15. Unadjusted isolated coronary artery bypass operative mortality: 2000–2009. (This graph is reprinted from the
Society of Thoracic Surgeons adult cardiac database 4th 2009 harvest report executive summary. © The Society of Thoracic
Surgeons. Used with permission. All rights reserved.)
Table 83-2 Independent Predictors of Mortality Following Coronary Bypass
Procedures
The STS maintains a voluntary registry for cardiac surgery outcomes. Participation throughout the
United States is extremely high, and the database is generally considered an excellent representation of
cardiac surgery outcomes. Overall, coronary bypass procedures have increased in volume, although at a
slower pace in recent years, presumably as a result of expanded medical and percutaneous treatments.
In 2008, 163,000 isolated coronary bypass procedures were submitted to the STS database. With over
1.4 million individual cases embedded in the dataset, enormous information can be obtained regarding
risk factors for mortality and morbidity. Independent predictors of death are listed in Table 83-2 and
include coronary reoperation, preoperative shock, dialysis dependence, immunosuppressed state,
advanced age, diabetes mellitus, nonwhite race, female gender, previous stroke, advanced heart failure
symptoms, peripheral vascular disease, and chronic lung disease. While the presence of these predictors
are not contraindications for coronary bypass grafting, these prognostic tools are helpful both in
balancing potential benefits from predicted risks and in correctly informing patients, families, and
referring physicians. There are two well-described predictive models that can be used to estimate risk of
death following coronary bypass surgery. Each model has been created using large voluntary registry
data, one from the STS, and one created from the European registry from 128 hospitals across eight
countries. Both models incorporate features related to the patients, the nature of their clinical
presentation, and the planned operative intervention. Although far from perfect, both models can be
very helpful in determining patient selection and preoperative optimization and in tailoring the therapy
to the unique clinical circumstances.
Another risk factor for death after coronary bypass grafting that is not included in either stratification
model is incomplete revascularization. Incomplete revascularization refers to failure to construct a
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