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*Author of the section on cardiac surgery.
†Author of the section on cardiac transplantation.
Surgical intervention continues to be a mainstay of treatment for acquired heart disease even though catheter-based interventional cardiology techniques have continued to expand and medical management has improved. This chapter focuses on surgical interventions for acquired heart disease, including coronary artery bypass grafting (CABG), minimally invasive cardiac surgery, transmyocardial revascularization, cardiomyoplasty, aortic surgery, and cardiac transplantation. Surgical intervention for valvular heart disease is briefly discussed in this chapter and is more extensively covered in Chapter 29
▪ EVOLVING TRENDS IN CARDIAC SURGERY
Cardiac surgical operative techniques continue to evolve. Arterial bypass conduits such as the internal mammary artery (IMA) are the preferred graft because of excellent long-term patency. Additional arterial conduits have expanded to include radial artery grafts and the gastroepiploic artery (GEA). Spawned by laparoscopic approaches in other surgical subspecialties, minimally invasive cardiac surgery (with and without cardiopulmonary bypass [CPB]) has rapidly developed. Computer-assisted, robotic CABG, and mitral valve surgical procedures have been preformed world wide on highly selected patients.1
Shorter intubation times and “rapid recovery” programs have led to shorter intensive care unit stays with overall reduced length of stay and decreased cost associated with cardiac surgery.
As cardiac surgery techniques evolve, the population changes as well. Interventional cardiology approaches such as coronary angioplasty, atherectomy, and stenting have delayed or replaced surgical revascularization in patients with coronary lesions amenable to catheter-based interventions.
▪ PREOPERATIVE ASSESSMENT AND PREPARATION
Before referral for cardiac surgery, patients complete their cardiac work-up, which includes cardiac catheterization to define coronary artery anatomy and target vessels for revascularization; stress testing to verify areas of ischemia; nuclear scans to identify areas of myocardial viability and ventricular function; and echocardiography to delineate valvular lesions, ventricular function, and focal wall-motion abnormalities. Usually, most of the preoperative medical evaluation is completed before the patient enters the hospital. Prior to cardiac surgery, the patient should have a complete physical examination with special attention given to the cardiovascular examination. A new history and physical examination, chest radiograph, electrocardiogram (ECG), complete blood count, serum electrolytes, coagulation screen, and typing and crossmatching of blood are performed. Preoperative anemia increases the risk of postoperative adverse events.2
These data provide information about other disease conditions and cardiac problems. Patients are admitted to the hospital early on the morning of their surgery. Patients with symptomatic carotid bruits should undergo carotid duplex to assess for carotid stenosis. Patients with pre-existing cerebrovascular disease are at increased risk for neurological complications postoperative.3
Patients with chronic lung disease should undergo pulmonary function testing and arterial blood gas testing because they may have difficulty weaning from the ventilator. Patients undergoing valve surgery should complete a dental evaluation and work before valve repair or replacement to reduce the chance of dental disease being a source of bacteremia and possible prosthetic valve endocarditis. Patients are maintained on antianginal, antihypertensives, and heart failure medications until surgery. Antiplatelet medications are usually discontinued before surgery: aspirin, clopidogrel, and nonsteroidal anti-inflammatory agents should be stopped before surgery to prevent perioperative bleeding. The Society of Thoracic Surgeon’s workforce recommends that for elective patients and for high-risk aspirinsensitive patients that aspirin should be stopped 3 to 5 days before surgery.4
Patients on warfarin usually have their dose withheld 3 to 5 days preoperatively. Patients on warfarin for previous mechanical valve replacements may be admitted 1 to 2 days before surgery for intravenous heparin. Heparin is withheld 1 to 2 hours before surgery, whereas enoxaparin is usually stopped 12 hours beforehand. In a study by Jones et al.,5
patients on preoperative enoxaparin demonstrated a higher rate of bleeding requiring re-exploration for bleeding (7.9% versus 3.7% in the unfractionated heparin group, P
The preoperative nursing assessment should be thorough and well documented because it provides baseline data for postoperative comparison. The history should include a social assessment of family roles and support systems, and a description of the patient’s usual functional level and typical activities. Elderly patients or those with limited social and emotional support may need additional assistance from social service for effective discharge and rehabilitation planning. The patient with acute coronary heart disease (CHD) may be hospitalized for only hours or days before surgery. A myocardial infarction may have occurred, or the patient may be experiencing unstable angina. In either case, if CABG surgery is being considered, then a cardiac catheterization must be performed to determine if surgery is indicated and to define coronary anatomy.
Minimally Invasive Techniques
In standard cardiac surgery, the heart is arrested and circulation is maintained by placing the patient on CPB. Although this procedure has been used successfully for more than three decades, it has drawbacks such as physiologic derangements associated with CPB and long hospital stays. Minimally invasive cardiac surgery has evolved out of laparoscopic techniques originally used in general and gynecologic surgery. The term minimally invasive
covers a variety of techniques rather than referring only to one surgical procedure. Minimally invasive techniques include CABG surgery performed by standard sternotomy but without the use of CPB (off-pump or OPCAB), CABG surgery performed off-pump through a small left anterior thoracotomy (minimally invasive direct coronary artery bypass [MIDCAB]), valve surgery performed on-pump but through “mini-sternotomy,” and computer-enhanced robotic system techniques that allow CABG and valve surgery to be performed on-pump through a small incision with videoscopic assistance and femoral bypass.6
Techniques are rapidly evolving that are geared toward multivessel revascularization through port access on a beating heart. Rather than just one approach for all patients, cardiac surgeons have a variety of surgical techniques available depending on the patient’s anatomy, medical history, and comorbid conditions. Further discussion of these surgical methodologies is found in the coronary bypass and valve surgery sections of this chapter.
CPB comprises an extracorporeal circuit that circulates systemic throughout the body during periods of time the heart and lungs are not functioning during cardiac surgical procedures. CPB has been the standard method used during cardiac surgery for diverting blood from the heart and lungs to provide a stationary, bloodless surgical field and to promote preservation of optimal organ function. Blood is removed from the right atrium or vena cava by one or two cannula, routed through the CPB machine, and returned to the patient by a cannula in the ascending aorta or the femoral artery.
The CPB system has several components, including venous and arterial cannula; a membrane or bubble oxygenator that oxygenates the blood, removal of carbon dioxide, and delivery of anesthetic gases; a heat exchanger that allows the blood to be either heated or cooled by conduction; a pump, which keeps the blood moving at a constant speed; filters, which remove particulate or gas emboli and plasma protein or platelet aggregates; a left ventricular vent to prevent distention of the left ventricle during aortic cross-clamp; cardiotomy suction to aspirate blood from the operative field; and sensors, which detect air bubbles, low levels of oxygen saturation, and low levels of blood in collection chambers.7
Heparin is used for anticoagulation during CPB to prevent clotting in the CPB circuit. Before initiation of CPB, a heparin dose of 3 mg/kg is administered through a central line. Activated clotting time is monitored a minimum of every 30 minutes during CPB. Once CPB is completed, heparin is reversed using protamine sulfate.7
Care is taken to administer protamine slowly and watch for a possible protamine reaction, which may vary from mild hypotension to full-blown anaphylaxis. Patients at greater risk for protamine reaction include those with insulin-dependent diabetes and those with an allergy to fish. While the patient is connected to the CPB machine, the surgeon, anesthetist, and CPB perfusionists control many physiologic variables. Hemodilution with crystalloid solutions is used to reduce hematocrit and the blood’s viscosity. CPB flow rates are controlled to maintain a cardiac index of 2.2 L/min/m2
and a mean arterial pressure around 60 mm Hg. Blood may be cooled to reduce metabolic demands or warmed to normothermia toward the end of the procedure.
CPB produces a systemic inflammatory response that releases biologically active substances that impair coagulation and the immune response. Proinflammatory cytokines contribute to neutrophil adhesion.9
In response to the vascular permeability changes that occur with CPB and to the decrease in plasma oncotic pressure that occurs with hemodilution, large amounts of fluid move from intravascular to interstitial spaces. Movement of fluid into interstitial spaces causes postoperative edema. This generalized edema that occurs after CPB resolves after the first few days postoperative or fluid mobilization may be facilitated with the use of diuretics. The longer the CPB time, the more severe the physiologic derangements during the postoperative recovery.
Systemic warming is started approximately 30 minutes before the anticipated time of discontinuing CPB. If the left atrium, left ventricle, or aorta has been entered, air must be evacuated before aortic cross-clamp removal to prevent air embolism. The heart is warmed and resumes spontaneous rhythm or is paced with epicardial wires. Ventricular fibrillation may occur and is converted with internal defibrillation. Under the direction of the surgeon and anesthesiologist, CPB weaning begins by ventilation of the lungs. CPB is gradually weaned by decreasing the amount of blood diverted through the CPB circuit. When the heart is functioning normally with adequate blood pressure and adequate cardiac index, CPB is discontinued, heparin is reversed, and cannulae are removed. If the heart cannot support an adequate cardiac index and mean arterial pressure after weaning from CPB, the patient may have to be placed back on CPB to rest the heart, and other measures for heart failure may need to be instituted, such as inotropic treatment or intra-aortic balloon pump. In patients who continue to have severe hemodynamic compromise, ventricular assist devices may be used.
is the intraoperative techniques intended to protect the myocardium from damage resultant from the ischemic state that occurs with CPB. In cardiac surgical procedure requiring CPB, cross clamping of the aorta without the use of myocardial protection would result in anaerobic metabolism and depletion of myocardial energy stores. Cross-clamping the aorta without protection for more than 15 to 20 minutes would result in profound myocardial dysfunction.8
Cardioplegia is infused to arrest the heart and provide a bloodless, motionless operative field as well as protect the heart during cardiac surgery. Cardioplegic solution is infused into the aorta or coronary sinus or into the coronary arteries themselves to cause cardiac arrest. Debate continues over the best type of cardioplegia, what is the best temperature (hypothermic vs. normothermic), whether cardioplegia
should be infused antegrade or retrograde, and timing of infusion (intermittent or continuous). Most cardiac surgery programs use a combination of the myocardial protection techniques discussed here.
Cardioplegia solutions are made of crystalloid, oxygenated crystalloid, or crystalloid-blood mixtures. Although cardioplegic solutions vary widely, typical components include potassium, magnesium, or procaine to provide immediate diastolic arrest; oxygen, glucose, glutamate, or aspartate as energy substrate; bicarbonate or phosphate to buffer acidosis; and calcium, steroids, or procaine to stabilize membranes. The solution should be hyperosmolar to edema. Cardioplegia is infused continuously or intermittently.
Cardioplegia can be normothermic or hypothermic. Hypothermic techniques were originally used as a means to reduce metabolic demands during arrest. A cooled nonbeating heart uses less oxygen than a warm-beating or fibrillating heart. Cold cardioplegic solutions are commonly cooled to 15°C to 20°C to reduce oxygen demand. Normothermic cardioplegia has been used at both the induction of cardioplegic arrest and at the termination of arrest. Warm, oxygenated, hyperkalemic blood cardioplegia maintains arrest while supplying oxygenated blood to myocardial cells. “Hot shots” are warm cardioplegic infusions administered at the end of the surgical procedure, before removal of the aortic cross-clamp.
Cardioplegia solution can be delivered antegrade into the ascending aorta, after which it flows through the coronary circulation and returns to the heart through the coronary sinus. Although antegrade cardioplegia has been the standard in cardiac surgery for many years, its delivery may be inadequate. Antegrade cardioplegia infusion through coronary arteries that are severely stenosed or occluded is uneven. Hearts with left ventricular hypertrophy may receive incomplete delivery to the subendocardium. In patients with aortic insufficiency, the left ventricle may become distended because of the retrograde flow of cardioplegia across the valve. Although cardioplegia can be delivered through saphenous vein grafts, it cannot be delivered through IMA grafts. Insufficient delivery of cardioplegia results in poor myocardial protection, which results in postoperative myocardial damage and dysfunction. Because of inadequate delivery using antegrade techniques, retrograde delivery systems were developed. Retrograde cardioplegia is infused under low pressure through catheters inserted directly into the coronary sinus. Cardioplegia flows retrograde through the coronary veins to capillaries to the coronary arterial bed, and exits at the coronary ostia, where effluent is removed by vent and suction. Retrograde and combined retrograde-antegrade techniques allow for optimal delivery and myocardial protection.
Deep Hypothermic Circulatory Arrest
Circulatory arrest (interruption of circulation through the ascending aorta for an extended period of time) may be necessary in procedures involving the ascending aorta and aortic arch. Profound hypothermia is used to protect the brain and other vital organs. The patient’s body temperature is lowered to 18°C and CPB is stopped. Operative procedures are performed expediently because of the interruption of circulation to vital organs. In general, deep hyperthermic arrest can be used up to 60 minutes.8
After repair, the patient is placed back on CPB and is gradually rewarmed.
CARDIAC SURGERY PROCEDURES FOR CORONARY ARTERY REVASCULARIZATION
Coronary Artery Bypass Surgery
Indications for Surgical Revascularization
CABG surgery is done primarily to alleviate anginal symptoms as well as improve survival. CABG surgery is among the most common surgical procedures preformed worldwide. The American College of Cardiology and the American Heart Association Task Force on Practice Guidelines was formed to recommend appropriate use of diagnostic tests and therapies. Based on both literature review and expert opinion, the ACC/AHA updated the guidelines for CABG in 2004. Class I guideline indications for CABG are described as conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective. Class I recommendations for CABG surgery include: significant left main coronary artery stenosis or equivalent; three-vessel coronary disease; two-vessel coronary disease and an ejection fraction less than 50%; one- or two-vessel disease with a large amount of viable myocardium at risk; and one- or two-vessel disease with severe angina despite maximal medical therapy.10
Other class I indications for CABG include failed angioplasty with persistent pain or hemodynamic instability, postinfraction ventricular septal defect (VSD) or postinfarction mitral insufficiency, cardiogenic shock in patients less than age 75.10
In comparison with drug-eluting stents for patients with multivessel coronary disease, CABG is associated with lower mortality rates and lower rates of repeat revascularization.11
Conditions that greatly increase the mortality risk during surgery and anatomic limitations are relative contraindications to CABG surgery. Lack of adequate conduit, coronary arteries distal to the stenosis smaller than 1 to 1.5 mm, and severe aortic atherosclerosis are anatomic abnormalities that may limit the success of the revascularization for technical reasons. Severe left ventricular failure and coexisting pulmonary, renal, carotid, and peripheral vascular disease may significantly increase the risk of surgery by predisposing to complications during the perioperative period. Patients with low ejection fraction are sicker at baseline and more than four times the mortality than patients with high ejection fraction.12
Coronary artery revascularization is accomplished most commonly with the IMA in combination with saphenous vein grafts. Because of the excellent patency associated with IMA grafts, other arterial conduits are now accepted for bypass surgery. Use of the right GEA as a pedicle graft to the right coronary or as a free graft to the left coronary system requires a more extensive surgery because the abdomen must be entered. Radial artery grafts were initially used in the early 1970s but were abandoned because of their tendency to spasm and their poor short-term patency. With the advent of calcium-channel blockers, radial artery grafts have enjoyed renewed interest. Greater saphenous vein from the legs is the most commonly used venous conduit. Because of patient anatomy, history of vein stripping, or previous revascularizations, alternative conduits may be necessary. Veins harvested from the
arms, such as the cephalic or basilic, make poor bypass conduits because of their calibre and high incidence of aneurysm formation. Lesser saphenous vein located on the posterior aspect of the lower leg may be used, but may be small calibre and difficult to harvest. Cadaveric and synthetic bypass grafts have also been attempted but are not commonly used due to poor patency rates. Because of long-term patency, the left IMA is most commonly used to bypass the left anterior descending (LAD) artery. The right IMA may also be used to bypass the LAD, artery as well as the right coronary artery. When multiple grafts are required, single or bilateral IMA grafts in combination with other arterial conduit and saphenous vein grafts can be used to accomplish complete revascularization (Fig. 25-1
). Many authors recommended complete arterial revascularization in young patients in hopes of avoiding additional revascularizations later in life.
▪ Figure 25-1 View of completed internal mammary and saphenous vein grafts. View from the head of the operating table shows: (A) internal mammary graft to left anterior descending coronary artery; (B) temporary epicardial pacing wires inserted into the right ventricle; (C) venous cannula into right atrium; (D) ascending aorta; (E) saphenous vein graft; (F) cardioplegia delivery catheter; (G) aortic cannula. (Photo by D. LeDoux, 2003.)
Saphenous Vein Bypass Grafts.
While the sternal incision is made and the patient is readied for CPB, the saphenous vein is prepared. Traditionally, saphenous vein is harvested using standard incisions. With the advent of minimally invasive surgery, saphenous vein can be harvested using endoscopic techniques and small incisions at the same time that the IMA graft is taken down from the retrosternal bed (Fig. 25-2
). A long segment of vein is carefully exposed, the branches are ligated and divided, and the vein is removed. The vein is flushed with a cold heparinized solution and checked for leaks. One side of the untwisted vein is marked with a surgical pencil, and the vein is filled with and stored in a cold solution. CPB is instituted, a clamp is placed across the distal aorta, and cold cardioplegia is injected into the aortic root. Portions of saphenous vein are sutured to coronary arteries beyond the arterial stenoses. Distal anastomoses to the LAD artery are usually made first, followed by distal anastomoses to the coronary arteries located on the back of the heart. After all distal anastomoses are completed, the aortic cross-clamp is removed and patient warming is begun. Small openings in the ascending aorta are made with a punch, and the proximal end of the saphenous vein is anastomosed to the aorta. After the proximal anastomoses are completed, CPB is discontinued and the chest is closed.
▪ Figure 25-2 Saphenous vein is dissected out by video-assisted endoscopic approach while the internal mammary is dissected down from the retrosternal bed. (Photo by D. LeDoux, 2003.)
IMA Bypass Grafts.
Harvesting the IMA is technically more difficult than harvesting the saphenous vein graft. After the sternum is cut open, the IMA is dissected away from the chest wall. A special retractor is used to expose the IMA in the retrosternal bed.13
A 2-cm-wide pedicle strip is removed from the chest-wall muscle, fat, and pleura that surround the IMA. The pedicle strip, with the IMA lying in the center, is exposed from the IMA origin at the subclavian artery down to the level of the fourth to sixth intercostal space. The branches of the IMA are exposed, divided, and ligated. An incision is made into the coronary artery to be bypassed (usually the LAD) and the distal end of the IMA is sutured into place. The IMA can be used as a free graft rather than a pedicle graft if it is not long enough to reach the target.
Radial Artery Bypass Grafts.
The radial artery graft is used for bypass conduit only after collateral circulation of the ulnar artery has been assessed by vascular ultrasound or Allen’s test. Although both radial arteries can be used, the radial artery from the patient’s nondominant hand is the usual choice and can be harvested before the chest is opened. Because the radial artery is very thick-walled and prone to spasm, after harvesting, papaverine may be used to flush and dilate the artery before grafting. During and after surgery, nitrates and calcium-channel blockers are used to prevent spasm, although duration of administration of these agents has not been standardized.14
The radial graft is a desirable conduit because of its length and ability to reach most distal targets. Postoperative nursing care includes evaluation of ulnar pulse and distal circulation.
The right GEA is a branch of the gastroduodenal artery that supplies blood to the greater curvature of the stomach. The GEA can be used as an in situ graft on the posterior surfaces of the heart or as a free graft to other vessels. Harvesting of the GEA graft requires laparotomy in addition to the sternotomy or thoracotomy incisions required for CABG. Longer operative times and abdominal surgery increase the complexity of the surgery.
Coronary bypass surgery is done to improve quality of life by relieving anginal symptoms, or to prolong life. Although angina pectoris is relieved in more than 90% of patients who undergo CABG surgery, Canadian Cardiovascular Society class III angina reoccurs in 5% to 10% of patients at 3 years and gradually increases because of graft stenosis or progression of native disease.15
The overall rate is thought to have increased because of the changing population referred for cardiac surgery. In a retrospective cohort study by Guru et al.,16
women had a higher early mortality rate than men although long-term mortality appeared to be equivalent as early as 1 year after surgery.16
The advent of interventional cardiology and improved medical management, patients now referred for CABG surgery are older, sicker, and have more complex disease.
Minimally Invasive Coronary Artery Bypass Surgery
MIDCAB is CABG surgery performed through a left anterior small thoracotomy, a short parasternal incision, or small incisions using port access and video-assisted technology. Because the small incisions limit the surgical approach, MIDCAB is usually confined to proximal disease of the LAD or right coronary artery with IMA as conduits to these sites. Radial artery, GEA, and saphenous vein grafts have also been used if the IMA graft could not be used or if more distal targets required grafting. Surgery is performed on the beating heart. To allow suturing of the graft anastomosis to the beating heart, pharmacologic measures such as adenosine and β-blockers are used to slow or temporarily stop the heart, in conjunction with mechanical stabilizers that immobilize the portion of the coronary artery where the graft anastomosis is sutured (Fig. 25-3
). Transesophageal echocardiography is used to assess for wall-motion abnormalities that would signal ischemia. CPB is on standby during each MIDCAB procedure if emergent conversion to standard sternotomy and CPB is required. The advantages of MIDCAB surgery are coronary revascularization without the physiologic derangements of CPB and avoidance of the traditional sternotomy incision. As a result, patients have less pain, need fewer blood transfusions, and have reduced overall length of hospital stay. Robotic totally endoscopic coronary artery bypass surgery as a totally endoscopic, closed-chest procedure but is limited primarily to the LAD and diagonal branches on the anterior surface of the heart. For patients with multivessel disease, integrated or hybrid revascularization may combine totally endoscopic coronary artery bypass with percutaneous techniques to provide for complete revascularization.17
▪ Figure 25-3 A two-pronged stabilizer immobilizes the surrounding myocardium and coronary artery in off-pump bypass surgery done on a beating heart. A snare is used proximal to the incision on the left anterior descending coronary artery. Forceps hold open the incision on the LAD open, and the internal mammary pedicle will be sewn into place. (Photo by D. LeDoux, 2003.)
Coronary artery bypass surgery performed by median sternotomy but without the use of CPB is known as OPCAB. Like MIDCAB, grafts are performed on the beating heart. Avoidance of CPB and aortic cross clamping may be desirable in patients with poor ventricular function or severe atherosclerosis of the aorta who may not tolerate aortic cross clamping. Median sternotomy allows for better exposure than in MIDCAB techniques. While it has been suggested that OPCAB offers neurologic protection, a randomized controlled trial comparing neurologic outcome of OPCAB to CABG with CPB demonstrated improved neurologic outcomes at 3 months but this difference became negligible at 12 months.18
In a follow-up multicenter randomized controlled trial, avoiding CPB had no effect on 5-year cognitive outcomes.19
Operative Results for MIDCAB and OPCAB
Midterm results in patients undergoing MIDCAB through left anterior small thoracotomy and using the left IMA and OPCAB have been encouraging. In a multicenter, randomized controlled trial comparing OPCAB and CABG with CPB,20
the OPCAB group had less use of blood products (p
< 0.01) and 41% less release of creatinine kinase (CK; p
< 0.01), but otherwise there were no significant differences in complications, quality of life, length of stay, or recurrent angina. A prospective randomized trial was conducted by Drenth et al.21
comparing coronary artery percutaneous transluminal coronary angioplasty with stenting (PCI) to OPCAB in patients for high-grade proximal LAD lesions. In a mean follow-up time of 3 years, angina pectoris class was lower in the OPCAB group (p
= 0.02) as well as the need for antianginal medication (p
= 0.01) when compared to the PCI group. OPCAB is technically more difficult and demanding for surgeons.22
Because operative techniques that involve minimally invasive incisions, port access, and operation on a beating heart have a learning curve, results associated with this newer operative technology are expected to continue to improve over time.
Transmyocardial Laser Revascularization
Transmyocardial laser revascularization (TMLR or TMR) is a technique under investigation in patients with refractory angina. In TMLR, carbon dioxide, holmium-YAG (yttrium-aluminum garnet), or excimer lasers23
are used to produce multiple channels from the endocardial surface of the ventricular wall in an effort directly to improve blood flow to areas of myocardium that cannot be revascularized using traditional techniques. It has also been postulated that myocardial blood flow is enhanced by angiogenesis that occurs with TMLR, although this is still unproven. Left anterolateral thoracotomy is most often used to provide exposure, although TMLR can also be done by standard median sternotomy if it is performed at the same time as standard CABG to other vessels. TMLR is done on a beating heart. The laser is synchronized with the patient’s R-wave. Transesophageal echocardiography is used to detect steam or bubbles that verify channel creation. Epicardial surface seals off with gentle pressure, leaving an endocardial channel in which blood flows. TMLR is recognized by the Society of Thoracic Surgery as acceptable as either sole therapy or as an adjunct to a selected subset of patients with refractory angina be cannot be revascularized by the more traditional methods of bypass surgery or percutaneous intervention.24
CARDIAC SURGERY PROCEDURES FOR ACQUIRED STRUCTURAL HEART DISEASE
Acquired Valvular Heart Disease
Surgical repair of a stenotic or incompetent mitral valve is performed frequently. The reparative surgeries, mitral commissurotomy (in which the fused valve cusps are split open) and annuloplasty (in which the large orifice of an incompetent valve is made smaller) are discussed in Chapter 29
. Care of the patient after surgical repair of valves is similar to that of the patient after CABG surgery.
If a dysfunctional mitral or aortic valve is not suitable for repair, valve replacement is undertaken. Valvular heart surgery can be accomplished through a standard median sternotomy incision, through a small parasternal incision, or through port access using small incisions and endoscopic techniques. Because valve surgery requires an arrested, open heart, CPB must be used and can be done by the standard method or by femorofemoral cannulation. Surgical techniques for mitral valve replacement (MVR) and aortic valve replacement (AVR), types of prosthetic heart valves, and indications for valvular replacement are discussed in Chapter 29
Mitral Valve Repair or Replacement.
The routine medical care after MVR surgery is similar to that after CABG surgery. Early after MVR surgery, a patient is more likely to have important cardiovascular or pulmonary dysfunction than a patient who has undergone CABG surgery. Late after surgery, problems related to the prosthetic device may occur. Prognosis and outcome after MVR are related to severity of the left ventricular and right ventricular dysfunction before surgery.
Aortic Valve Replacement.
The routine medical care after AVR surgery is similar to that after CABG surgery. Early after AVR surgery, a patient is more likely to have arrhythmia, decreased cardiac output, or neurologic dysfunction than a patient who has undergone CABG surgery. Late after surgery, arrhythmia, heart failure, or problems related to the prosthetic device may occur. Prognosis and outcome after AVR are related to severity of left ventricular dysfunction before surgery.
Surgical Techniques for the Failing Heart
As an alternative to cardiac transplant, number surgical techniques are evolving. In the Dor procedure, the left ventricular cavity is opened and monofilament sutures placed circumferentially above the boarder of the diseased muscle, restoring the normal contour of the ventricle.25
The reduction ventriculoplasty was pioneered by Batitista as a surgical option for patients with cardiomyopathy who cannot undergo cardiac transplantation. To decrease wall tension and ventricular size in the dilated left ventricular, an oval-shaped portion of myocardium is removed from apex to base. Although Batitista reported encouraging results in his own series, this procedure after being introduced in the United States has had mixed results.25
While the Cleveland Clinic series reported midterm results with a 30-day mortality rate of 3.2%,26 other series have reported high mortality rates.25
Dynamic cardiomyoplasty is an alternative to heart transplantation for patients with end-stage heart failure. Surgery is accomplished through a left thoracotomy incision, and CPB is not required. The latissimus dorsi muscle is placed into the thoracic cavity through a space where the second rib has been resected. Intramuscular pacing electrodes are inserted in the proximal portion of the muscle. The patient is then repositioned, and a sternal incision is made to complete the muscle wrap around the heart. A cardiomyostimulator (a pacemaker especially designed for cardiomyoplasty) is implanted beneath the rectus muscle and activated 2 weeks after surgery, allowing the muscle to rest and
develop collateral circulation before pacing is started. Stimulation is gradually introduced by a stimulated pulse synchronized to every other cardiac cycle. Long-term survival after cardiomyoplasty has been reported as high as 50% at 8 years.27
Although cardiomyoplasty is not a replacement for cardiac transplantation, it may have a limited role in patients who would not be candidates for transplantation.
Acquired VSD Repair
Rupture of the intraventricular septum after MI is a rare complication that can occur with acute MI. The infarct that accompanies VSD is usually extensive and transmural. Thinning and dilatation of the infarcted portion of septum, which evolves to rupture 1 to 7 days after MI, causes biventricular failure as the left ventricle shunts blood into the right ventricle, causing right-sided heart failure and pulmonary edema. Clinical signs of acquired VSD include rapid-onset biventricular failure or cardiogenic shock, pansystolic murmur, and a sequential increase in venous oxygen saturation from the right atrium to the pulmonary artery. Bedside cardiac output measures done with the pulmonary artery catheter by thermodilution are falsely elevated because of the left-to-right ventricular shunt. The anatomy and size of the septal rupture is diagnosed by echocardiography and cardiac catheterization.
Stabilization of the patient with septal rupture is aimed at afterload reduction. Using pharmacologic vasodilators and intraaortic balloon pumping, forward flow is improved and the left-to-right shunt fraction is reduced. The VSD is repaired by patching the defect with a Dacron-covered patch, which is then lined, if possible, with pericardium to make it leak proof. In patients with significant coronary artery stenosis, CABG surgery may also be added to the operative procedure. Even with surgical repair, the hospital mortality rate after VSD repair remains 10% to 40%.28 The important risk factors associated with early death are poor preoperative hemodynamic state and acute right ventricular dysfunction.
Repair of Ascending Aortic Aneurysm or Dissection
Aortic aneurysm is used to describe localized dilatation of the aorta. Causes of ascending aortic aneurysm include hypertension, Marfan’s syndrome, and cystic medial necrosis. The likelihood of aortic aneurysm rupture is related to size. The more the aorta is stretched, the greater the tension and wall stress forces. If the ascending aorta is aneurysmal, the cusps of the aorta may be distorted, resulting in aortic insufficiency and acute or chronic heart failure.
Aortic dissection occurs secondary to disruption of the intimal layer of the aorta and is a true medical emergency. Blood enters the intimal tear and dissects a false lumen in the abnormal medial layer, with blood flowing retrograde and antegrade, separating layers of the intimal and adventitial layers. The dissection is propagated by hypertension and elevated force of contraction. In the Stanford classification, type A describes dissection of the ascending aorta and transverse arch, whereas type B is used to describe dissections of the descending thoracic aorta. Aortic dissection has a grave prognosis and requires prompt surgical intervention.
Ascending aortic dissection and aneurysm are treated with surgical resection of the involved portion of aorta and replacement with prosthetic tubular graft. In ascending aortic aneurysm or type A dissection, if the aortic valve is regurgitant, it is replaced. In the case of aneurysm alone, it may be possible to spare the aortic valve by resuspending it within the prosthetic graft of the ascending aorta (David procedure). If surgery involves the aortic arch, deep hypothermic circulatory arrest is used (see the “Surgical Techniques
Routine Postoperative Care
Immediate postoperative care is similar for patients undergoing any cardiac surgical procedure, including CABG, MIDCAB, valve repair or replacement, and cardiac transplantation. After cardiac surgery, the patient is admitted to an intensive care unit for close monitoring for 6 to 24 hours after surgery. On arrival in the intensive care unit, the critical care nurse performs a number of rapid assessments to ensure patient stability. Routine care includes continuous ECG monitoring, measurement of blood pressure by arterial line, pulse oximetry, pulmonary artery pressures, and body temperature measurement. Intermittent parameters may include cardiac output measurement as well as calculation of derived hemodynamic parameters, such as afterload, cardiac index, and contractility indices. Specialty pulmonary artery catheters, such as the continuous cardiac output pulmonary artery catheter, may be used to evaluate minute-to-minute changes in cardiac output. Oximetry pulmonary artery catheters may be used continuously to monitor mixed venous oxygen concentration, and values can be used to calculate oxygen consumption and delivery parameters during periods of critical illness.
Sinus bradycardia or other hemodynamically significant bradycardic dysrhythmias such as accelerated junctional rhythm can occur postoperatively and may be treated with an atrial or atrioventricular pacemaker set at a rate of 70 or 100 beats/min. Heart block may occur after valve repair or replacement because of edema and trauma at the suture lines close to the conduction system. Hypertension may be treated with either intravenous nitrates or sodium nitroprusside. Hypotension occurs often during the first 12 hours after surgery as the patient warms and as systemic vascular resistance decreases to normal levels. Hypovolemia (right or left atrial or pulmonary artery wedge pressure of less than 8 to 10 mm Hg) may be present because of the fluid volume alterations that occur with CPB or if diuretic was administration at the end of CPB. Hypovolemia may be treated with crystalloid or colloid volume expanders such as 5% albumin or hetastarch, or with crystalloid. If the patient’s hemoglobin is less than 8 g/dL, packed red blood cells or whole blood may be administered. Blood may be recovered through the chest tubes for autotransfusion during the first 4 to 12 hours after surgery. If patients are normovolemic, they are usually placed on a salt and free-water restriction. Potassium replacement is often necessary. Patients are usually maintained on a respirator for the first 1 or 2 hours after surgery, until the effects of anesthesia have reversed. Patients are on prophylactic antibiotics, usually a second-generation cephalosporin, to prevent wound infection for 48 hours or less. Antibiotic prophylaxis beyond 48 hours is not associated with decreased infections.29
Because of improved anesthesia and surgical techniques and a shift from acute care resulting from changes in reimbursement, cardiac surgery has evolved to include same day admission and shortened length of stay. Stable, uncomplicated patients are earmarked to “fast track” by extubating early and minimizing their intensive care unit and hospital stay. Patient care is directed by an
established care map or “roadmap.” In the operating room, patients receive lower doses of opioids with the aim of extubation within 1 or 2 hours after arrival in the intensive care unit. The patient is kept sedated with short-acting agents such as propofol or midazolam intravenous infusions. When the patient is hemodynamically stable and bleeding is under control, the patient can be extubated. As a result, cardiac surgery patients may stay in the intensive care unit as little as 8 to 12 hours, thus freeing up critical care beds and reducing costs to the patient. Patients who are “fast tracked” in rapid recovery programs are discharged 3 to 5 days after surgery. Nurse practitioners or physician assistants in collaboration may manage cardiac surgery patients with the physician. Atrial arrhythmias and pulmonary complications are the most common variances that keep patients in hospital longer than planned by the care map.
Early Complications After Cardiac Surgery
Cardiovascular dysfunction or low cardiac output syndrome can occur after cardiac surgery. Low cardiac output syndrome may be related to reduced preload, increased afterload, arrhythmias, cardiac tamponade, or myocardial depression with or without myocardial necrosis. Excessive bleeding can occur secondary to coagulopathy, uncontrolled hypertension, or inadequate hemostasis. Perioperative MI and pericarditis can occur as a result of cardiac surgery.
Pleural and mediastinal tubes are attached to water-seal and 20-cm suction to drain mediastinal shed blood. Although blood may clot in these chest tubes, they should not be stripped because stripping may cause excessive suction, which may increase bleeding or cause damage to grafts.30
Excessive postoperative bleeding (mediastinal drainage of more than >500 mL for the first hour after surgery or drainage, totaling >200 mL/h thereafter) usually is mechanical in nature and caused by bleeding from suture lines, but it may be caused by the presence of pericardial adhesions from an earlier surgery or to a coagulopathy. Postoperative bleeding is usually venous rather than arterial. Coagulopathies may occur in patients with prolonged CPB times or excessive intraoperative bleeding. If patients are bleeding excessively, coagulation panels should be obtained immediately to evaluate for coagulopathy. Coagulopathies caused by depletion of factors should be treated with administration of depleted factors, such as fresh-frozen plasma, platelets, and cryoprecipitate. Autotransfusion may be used to replace red blood cells, but filtered blood lacks adequate clotting factors. In an observational study of 8004 coronary artery bypass patients,31
having a lower nadir hematocrit is associated with increased risk of developing low output heart failure and that risk was increased further with transfusion of packed red blood cells as a significant independent predictor of low output heart failure (adjusted odds ratio, 1.27; 95% CI, 1.00 to 1.61; p
Pharmacologic means of controlling postoperative hemorrhage include a variety of nonhematogenous therapies. Aminocaproic acid is an antifibrinolytic medication that inhibits conversion of plasminogen to plasmin. Desmopressin (DDAVP) may be infused intravenously in patients with severe platelet dysfunction after prolonged CPB or uremia. DDAVP shortens bleeding time and improves platelet function by increasing circulating levels of von Willebrand factor. DDAVP also increases factor VIII C levels, which shorten the partial prothrombin time. In the past, aprotinin had been used extensively to limit bleeding especially in redo operations, the safety of aprotinin came under scrutiny. An observational study by Mangano et al.32
of 4,374 patient undergoing revascularization found a doubling of the risk of renal failure (95% CI), 55% increased risk of MI or heart failure (p
< 0.001), and 181% increase in risk of stroke or encephalopathy (p
= 0.001). In a retrospective analysis by Shaw et al.,33
patients who received aprotinin had higher mortality rate and larger increase in serum creatinine than those who received Aminocaproic or no antifibrinolytic agent.
Protamine also may be administered intravenously in patients who had inadequate reversal of heparin or in those with heparin rebound. Protamine must be administered as a slow intravenous infusion to prevent hypotension. Patients with insulin-dependent diabetes or allergy to fish are more likely to have allergic reactions to protamine. If postoperative bleeding continues and coagulation tests are normal, bleeding may be mechanical or may result from suture line or venous bleeding. Adequate control of hypertension with sodium nitroprusside may also help control bleeding. If coagulopathies were corrected and bleeding continues, mediastinal re-exploration is advised to decrease the risk of cardiac tamponade.
Cardiac tamponade is a life-threatening emergency that may occur immediately postoperative. Compression of the right heart with blood and/or clot decreases left ventricular preload and consequently, cardiac output that results in causes hemodynamic deterioration.34
Cardiac tamponade is suspected as a cause of low cardiac output if right and left heart pressures increase and equalize. Physical exam findings, hemodynamic parameters, and diagnostic tests for tamponade include: decreased cardiac index, mediastinal drainage that may increase as well as decrease or stop, radiography shows widening of the cardiac silhouette, neck vein distention, a pulsus paradoxus is noted by arterial line or by auscultation, or narrow pulse pressure is present. Although tachycardia is a sign of classic tamponade, the cardiac surgical patient may be unable to generate a compensatory tachycardia because of heart block or previously administered β-blockers or calcium-channel blockers. Echocardiography provides rapid confirmation of pericardial fluid and tamponade physiology, facilitating intervention with echo-guided pericardiocentesis, or open pericardial drainage in the operating room.
Myocardial depression (impaired myocardial contractility) may be reversible or irreversible after cardiac surgery. If a patient is not acidotic or hypoxemic and has evidence of decreased cardiac contractility, myocardial cell dysfunction or necrosis is suspected. Treatment of low cardiac output secondary to myocardial dysfunction first involves treatment of hypoxemia, acidosis, heart rate and rhythm abnormalities, decreased preload, and increased afterload. If a patient continues to have a low cardiac output after these maneuvers, inotropes or intraaortic balloon pump therapy is instituted. A variety of inotropes and vasoactive medications may be employed postoperatively (Table 25-1
). Dobutamine, dopamine, epinephrine, norepinephrine, and milrinone intravenous infusions are frequently used for inotropic support of myocardial depression after cardiac surgery. If the patient’s cardiac index is normal to high and hypotension is related to vasodilation, pressers such as vasopressin
and phenylephrine may be used A variety of vasodilating agents such as sodium nitroprusside, nitroglycerin, and angiotensin-converting enzyme inhibitors may be used to reduce afterload in low cardiac output syndrome as well as hypertension. Intra-aortic balloon pump therapy is frequently used in patients with severe cardiac dysfunction that is not adequately supported with medications alone.
Table 25-1 ▪ INOTROPES AND VASODILATOR INTRAVENOUS INFUSIONS COMMONLY USED AFTER CARDIAC SURGERY
Mechanism of Action
Primarily β1-adrenergic receptor stimulation
Low cardiac output after cardiac surgery
1-2 mcg/kg/min for renal effect 5-20 mcg/kg/min for inotropy and increased vascular resistance
Stimulation of dopaminergic and a drenergic receptors
Treatment of shock and hypotension after cardiac surgery in patient who has been volume resuscitated
0.01-0.1 mcg/kg/min to high dose 0.3-0.3 mcg/kg/min
Stimulation of α- and β1- and β2-adrenergic receptors
Treatment of low cardiac output and shock after cardiac surgery
Stimulation of β1- and β2-adrenergic receptors
Used after heart transplantation and in patients with severe bradycardia to stimulate heart rate
Phosphodiesterase inhibition resulting in increase inotropy and vasodilation
Low cardiac output after cardiac surgery; may require use of adrenergic agent to maintain blood pressure
Dilates coronary arteries and reduces myocardial oxygen demand, reduce ventricular pressures
Used to prevent spasm in arterial grafts after cardiac surgery as well as may be used to reduce preload and afterload
0.3-5 mcg/kg/min (high doses may result in thiocyanate toxicity)
Cause peripheral vasodilation by acting directly on smooth muscle in the venous and arterial circulation
Used to decreased blood pressure and afterload
Stimulation of α- and β-adrenergic receptors (α effects are predominate)
Used for shock and low systemic vascular resistance after cardiac surgery
Potent α-adrenergic stimulator
Used to increase systemic vascular resistance and blood pressure cardiac output is maintained but blood pressure is low
Used to treat shock and increase systemic vascular resistance and blood pressure cardiac output is maintained but blood pressure is low
+, increase; 0, no change; −, decrease.
Perioperative Myocardial Infarction.
Despite improved methods of myocardial protection, perioperative MI continues to be a serious complication. Diagnosis of perioperative MI is made from a variety of diagnostic tests including ECG, echocardiography, and cardiac enzymes. MI related to cardiac surgery may be secondary to spasm of grafts, emboli of air or debris, or insufficient myocardial protection. CK is routinely elevated immediately after cardiac surgery and usually drops after 12 to 16 hours. CK peaks associated with perioperative MI occur 16 to 24 hours after surgery. More recently, troponin I has been used for the diagnosis of perioperative MI. Postoperative troponin I levels in patients without perioperative MI peak at 8 to 10 hours, whereas in patients with perioperative MI, troponin I levels peak in 20 hours and at higher concentrations.35
A study by Lasocki et al.36
found that elevated troponin I levels more than 13 ng/mL was an independent predictor of in-hospital mortality. The interpretation of troponin release is complex due to a variety of potential underlying reasons.37
New wall-motion abnormalities noted on echocardiography are another way to verify perioperative MI. Postoperative pericarditis may mimic myocardial ischemia with chest pain and widespread ST-segment elevation. ECG changes associated with pericarditis are J-point changes, concave rather than convex, and do not result in pathologic Q waves.
Arrhythmias are common after cardiac surgery and are a prevalent cause of increased length of stay after cardiac surgery. Bradyarrhythmias are common after CABG and valve surgeries and may require temporary pacing via epicardial pacing wires placed at the time of surgery. Bradycardia or heart block following cardiac surgery is often hemodynamically significant may require placement of permanent transvenous pacers before discharge. Atrial arrhythmias are the most common after cardiac
surgery. Contributing factors of atrial fibrillation (AF) may include electrolyte or metabolic disturbances, increased circulating catecholamines, volume overload, hypoxia, and myocardial ischemia or MI. Although atrial tachyarrhythmias may occur any time during the first few days to weeks after cardiac surgery, they frequently peak around the second or third day postoperative. Atrial fibrillation after cardiac surgery may be associated with important complications including stroke, renal dysfunction, and prolonged hospitalization.38
Risk factors for postoperative AF include advanced age, history of congestive heart failure or AF, chronic obstructive lung disease, male sex, history of rheumatic heart disease, prolonged aortic cross-clamp time, and bicaval cannulation.39
The onset of tachyarrhythmias is often preceded by frequent premature atrial contractions. Medications commonly used to control the ventricular response in AF and flutter include diltiazem (either intravenous drip or orally), digoxin, and β-blockers (orally or by intravenous drip, such as esmolol). Medications used to promote conversion of AF include procainamide, amiodarone, and sotalol. While multiple medications have been studied, β-blockers have been the only medication consistently shown across clinical studies that reduce the frequency of postoperative AF.40
β-Blockers should be considered early during the postoperative course, especially if the patient was on β-blockers preoperatively. Although β-blockers, atrial pacing, antiarrhythmic medications, or a combination of these therapies may reduce the incidence or duration of AF, optimal strategies are still being defined.41
Postoperative arrhythmia diagnosis and treatment is facilitated by the presence of atrial epicardial pacemaker wires. Atrial activity is more pronounced when recorded in atrial ECGs than when recorded in a normal surface ECG (Fig. 25-4
). When atrial activity is accentuated, differentiation between supraventricular and ventricular arrhythmias, and AF and flutter is made easier. If the ventricular response to AF exceeds 110 beats/min, then the patient’s rate should be controlled.
If pharmacologic modalities fail to convert the patient to a sinus rhythm, electrical therapies may be used. Atrial flutter may be converted using rapid atrial pacing. To perform rapid atrial pacing, both atrial epicardial wires are connected to the rapid atrial pacemaker. The pacemaker output is set between 10 and 20, and the pacemaker rate is set approximately 20% faster than the existing atrial rate (atrial rate can be determined on the atrial ECG). Rapid atrial pacing continues for 30 seconds or until the atrial ECG complex changes from a negative to a positive deflection in lead II. Rapid atrial pacing is then abruptly discontinued, which allows the atria to resume a normal sinus rhythm (Fig. 25-5
). Patients with chronic AF may be refractory to either pharmacologic or electrical conversion. If the AF is new in onset (<1 year), the patient may be successfully cardioverted by synchronized cardioversion. If the patient has been in AF or flutter longer than 48 hours or the AF remains paroxysmal, it is desirable to anticoagulate for 3 to 4 weeks to prevent thromboembolism, and then have the patient return for elective cardioversion if they remain in AF or flutter.
▪ Figure 25-4 Atrial electrocardiography is done by attaching limb leads and V1 in standard fashion and then attaching V2 and V3 directly to the atrial pacing wires with alligator clips. Simultaneous surface lead and unipolar atrial lead ECG recordings are obtained. (A) Lead V1 is the surface or reference lead. There is no atrial enhancement. (B, C) Leads V2 and V3 are unipolar atrial leads that accentuate the atrial activity and demonstrate an atrial rate of approximately 300 beats/min that was not apparent on the surface lead or standard 12-lead ECG.
▪ Figure 25-5 Recording of a burst of rapid atrial pacing used to overdrive and convert this atrial flutter to sinus rhythm. Arrows denote atrial pacing spikes.
While premature ventricular contractions and nonsustained runs of ventricular tachycardia may occur commonly after cardiac surgery, sustained ventricular tachycardia and ventricular fibrillation are rare but associated with a poor prognosis.42
Premature ventricular contractions and nonsustained runs of ventricular tachycardia should be treated with correction of electrolytes, reduction or elimination of arrhythmogenic drugs such as catecholamines, and ruled out for ischemia. Sustained ventricular tachycardia should be cardioverted and antiarrhythmic agents such as amiodarone or lidocaine should be instituted.42
Electrophysiology studies and implantable defibrillators may be used in selected cases.
Routinely, patients are intubated and ventilated for 2 to 4 hours after cardiac surgery. Pulmonary function is monitored with continuous pulse oximetry as well as intermittent arterial blood gases and chest radiographs. Mild pulmonary dysfunction is common after cardiac surgery. Pathophysiologic changes that occur after CPB include increased capillary permeability, increased pulmonary vascular resistance, and intrapulmonary aggregation of leukocytes and platelets. A noncardiac pulmonary edema may occur immediately after CPB or during the first several days after surgery. Comparative studies between OPCAB and CABG with CPB suggest that CPB alone may not be the major cause of the development of postoperative pulmonary dysfunction.9
In a prospective, controlled trial by Roosens et al.,43
both patients with and without CPB had dramatic impairment of respiratory system mechanic postoperatively. Severe pulmonary dysfunction is uncommon and may be related to preexisting lung disease. Although severe lung injury after cardiac surgery is rare, it continues to be a major impact on morbidity and mortality as well as related cost of hospitalization.9
In a case controlled study by Milot et al.44
in 3,278 patients, adult respiratory distress syndrome after cardiac surgery was rare (0.4%) but carried a 15% mortality rate. Independent predicators of adult respiratory distress syndrome in cardiac surgery patients include number of blood products transfused, shock, and previous cardiac surgery.44
Chest radiographs should be performed as part of the fever work-up to rule out atelectasis and pneumonia. Atelectasis may occur secondary to hypoventilation related to sternal incision discomfort. Pain from chest tubes and sternotomy incision interferes with normal respiration and pulmonary toilet, making adequate pain control a high priority. Diminished breath sounds and lung fields at the bases that are dull to percussion indicate significant pleural effusions. Pneumothorax may occur any time during the postoperative period or at the time of pleural chest tube removal. Phrenic nerve damage may result in diaphragmatic paralysis or dysfunction but is uncommon with today’s surgical techniques.
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