Monitoring

Monitoring (Table 35-3) of the patient’s electrocardiogram (ECG) and direct blood pressure (commonly via the radial artery in the nondominant wrist) results is initiated when the patient arrives in the preoperative area. Central lines are usually inserted after transport into the operating room (OR), but occasionally are inserted in another designated location, such as the preoperative area. Whether the patient first undergoes intubation before insertion of central lines (i.e., central venous pressure, pulmonary artery catheter) or after line insertion is at the discretion of the anesthesia provider; the sequence varies among institutions. Increasingly, an anesthesia provider inserts a transesophageal echocardiography (TEE) probe to illustrate cardiac function. Use of TEE for valve surgery and for patients with compromised LV function is routine.^2,3

Table 35-3 Physiologic Monitoring

BP, Blood pressure; CVP, central venous pressure; RA, right atrial; RV, right ventricular; PA, pulmonary artery; LA, left atrial; CO, cardiac output; TEE, transesophageal echocardiography.

Adapted from Lemmer JH, Vlahakes GJ: Handbook of patient care in cardiac surgery, ed 7, Philadelphia, 2010, Lippincott Williams & Wilkins; Bojar RM: Manual of perioperative care in adult cardiac surgery, ed 5, Oxford, 2011, Wiley-Blackwell.

Incisions

After the patient has been anesthetized, positioned, and washed (prepared), the chest is opened. The most commonly used chest incision in cardiac surgery is the median sternotomy; this is the preferred incision when a thorough assessment of, and complete access to, the heart (as with global coronary artery disease) is needed. However, ministernotomy, anterolateral or posterolateral thoracotomy incisions, or transverse sternotomy also may be used (Fig. 35-1). The surgeon splits the sternum with a saw from the sternal notch to the xiphoid process. After the sternum is opened, the exposed pericardial sac is incised anteriorly, and the pericardial edges are tacked up along the chest wall incision to allow complete access to the entire pericardium without the necessity of entering the pleural cavities. Minimally invasive surgery uses smaller incisions and can speed patient recovery, enable the patient to return faster to normal activities, and reduce costs.

FIG. 35-1 Traditional and less invasive thoracic incisions (dotted lines represent chest wall incisions). A, Traditional sternotomy. B, Full sternotomy with limited skin incision. C, Parasternal incision (infrequently used). D and E, Partial lower and upper sternotomy incisions used mainly for valve procedures. F, Right thoracotomy incision can be used for mitral valve procedures. Left anterior thoracotomy (not shown) can be used for single coronary bypass graft to left anterior descending coronary artery.

(From Braunwald E, et al, editors: Heart disease, ed 6, Philadelphia, 2001, Saunders.)

Cardiopulmonary bypass

Systemic venous return to the heart flows by gravity drainage (the level of the patient needs to be above that of the bypass machine to facilitate drainage) into one or two large-bore (e.g., 32F to 36F) cannulas inserted into the right atrium. With the single two-stage cannula (Fig. 35-2), openings in the distal tip drain blood returning from the inferior vena cava (IVC) and openings in the middle portion of the cannula drain venous blood from the superior vena cava (SVC) and the coronary circulation exiting from the coronary sinus. Some blood enters the right atrium (RA) and the pulmonary circulation. With double cannulation (Fig. 35-3), individual cannulas are inserted into the IVC and the SVC, thereby forcing all venous return into the cannulas. Generally the two-stage cannula is used for coronary artery bypass grafting and aortic valve surgery when total right side decompression is not generally needed and blood entering the right side of the heart does not obscure the surgical field. Individual (double) venous cannulation can be used for procedures in the right side (e.g., tricuspid valve repair) to keep the right heart free of blood. Occasionally, two cannulas can be used when greater decompression of the RA is necessary (e.g., mitral valve surgery).

FIG. 35-2 Antegrade cardioplegia infusion catheter is inserted proximal to aortic cross clamp and arterial infusion cannula. Two-stage (single) venous cannula drains sysemic venous return. Openings in distal end of cannula drain blood from lower body; openings in midportion of cannula (within right atrium) drain blood returning from upper body and coronary venous drainage exiting from coronary sinus. Septal temperature probe monitors myocardial septal temperature.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St Louis, 1996, Mosby.)

FIG. 35-3 Double venous cannulation. One cannula is inserted into inferior vena cava, and the other into superior vena cava. Also shown is arterial infusion catheter.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St. Louis, 1996, Mosby.)

After the blood is oxygenated, it is pumped into the systemic circulation via an arterial cannula, commonly located in the aorta (see Fig. 35-3). When aortic pathology (e.g., aortic aneurysm) prevents cannulation, the femoral artery can be cannulated (retrograde flow) for arterial return. The axillary artery may be needed when the aorta or both of the femoral arteries are unavailable.

In addition to the standard cannulation techniques for cardiopulmonary bypass (CPB), minimally invasive systems use endovascular catheters (Fig. 35-4). A venous catheter is inserted into the femoral vein, and the arterial cannula is placed into the femoral artery. The ipsilateral femoral artery is also used for insertion of a multilumen catheter. One lumen serves as an endovascular cross clamp that occludes the aorta with inflation of an intraaortic balloon at the tip of the catheter, and the other lumen can be used for infusion of antegrade cardioplegia. Pressure lines, venting catheters, and a coronary sinus retrograde cardioplegia catheter can be inserted via the jugular vein. This system does not require median sternotomy and is an important adjunct for minimally invasive surgery.⁴

FIG. 35-4 Minimally invasive cardiopulmonary bypass technique. A, Positioning of endovascular catheters). B, Correct positions of endocoronary sinus catheter, endoaortic clamp, endovenous drainage cannula, and endopulmonary vent for port-access cardiopulmonary bypass. EAC, Endoaortic clamp; ECSC, endocoronary sinus catheter; EPV, cardiopulmonary vent.

(A, From Toomasian M, et al: Extracorporeal circulation for port-access cardiac surgery, Perfusion 12:83, 1997. B, From Kaplan J, editor: Kaplan’s cardiac anesthesia, ed 5, Philadelphia, 2006, Saunders.)

A number of risks are associated with the use of CPB (e.g., particulate or air embolus), and some form of checklist is often used before CPB is instituted (Box 35-1) and before the patient is weaned from CPB (Box 35-2). Such checklists help to enhance the safety of CPB. In addition, the clinical sequelae of CPB can affect all body systems. Caregivers in the postoperative period should be aware of the possible effects of CPB (Table 35-4).

Table 35-4 Effects of Cardiopulmonary Bypass

Adapted from Lemmer JH, Vlahakes GJ: Handbook of patient care in cardiac surgery, ed 7, Philadelphia, 2010, Lippincott Williams & Wilkins; Bojar RM: Manual of perioperative care in adult cardiac surgery, ed 5, Oxford, 2011, Wiley-Blackwell.

CPB is not always required. So-called off-pump procedures for myocardial revascularization can be performed while the heart is beating with the use of special devices to isolate the section of the coronary artery to be grafted. For procedures that require entry into the chambers of the heart (e.g., valve replacement), CPB and myocardial protection are necessary for perfusion of the body, avoidance of air emboli that originate from the open cardiac chamber, and myocardial preservation.

Myocardial protection

The goal of myocardial protection is to conserve cardiac energy resources; the goal is achieved with induced hypothermia and rapid diastolic arrest. Hypothermia reduces the metabolic rate (and therefore the energy demands) of the tissue being cooled; effective intraoperative myocardial protection positively affects the patient’s postoperative recovery. For most cardiac procedures of less than 1 hour of induced cardiac arrest (e.g., coronary artery bypass grafting), the perfusionist cools the systemic circulation from a normal temperature of 37° C (98.6° F) to approximately 32° C (89.6° F). The cardioplegia solution is cooled to a lower temperature (near freezing) for intracardiac cooling as a method of myocardial protection. For procedures with a longer cross-clamp time, the systemic temperature may be further reduced to protect the brain, kidneys, and other organs while the heart is arrested by reducing energy demands and limiting ischemic injury. Topical cooling of the heart with cold lavage or frozen “slush” placed on the heart and in the pericardial well helps to achieve transmural cooling. Although induced hypothermia plays an important role in minimization of tissue ischemia during selected portions of cardiac procedures, inadvertant hypothermia has become an important consideration for cardiac patients because of associated risks for perioperative complications. Before surgery, shivering increases myocardial oxygen demands and further taxes hearts that have diminished myocardial energy supplies. During surgery, before and after CPB, inadvertent cooling of the patient is associated with increased surgical bleeding and a diminished immune response. After surgery, hypothermia contributes to patient discomfort, impaired wound healing, prolonged bleeding, longer lengths of stay, and cardiac events such as ischemia and tachyarrhythmias.^2,3 Active measures, such as the application of warm blankets before surgery and during the intraoperative period (before and after induced hypothermia), the postoperative use of forced warm air devices and intravenous fluid warmers, and an increased ambient room temperature, can help to maintain normothermia.

Rapid diastolic arrest conserves existing cellular energy resources (e.g., adenosine triphosphate) by avoiding the energy-expensive state of ventricular fibrillation before the heart achieves an arrested state. Quick arrest of a beating heart (e.g., 10 to 20 seconds) enhances myocardial energy conservation. Potassium is the most commonly used arresting agent, but the solutions may also contain electrolytes, buffers to maintain appropriate pH, glucose, metabolic substrates, calcium antagonists, tromethamine, heparin, and antiarrhythmic agents. The carrying solution can be crystalloid or blood (preferable for its oxygen carrying capacity).⁴

Methods of infusing cardioplegia include the antegrade and retrograde routes and the direct coronary ostial route of infusion. With the antegrade method, a needle catheter is inserted into the anterior aorta proximal to the aortic cross clamp (see Fig. 35-2). The cardioplegia solution is infused with sufficient pressure to close the aortic valve. With the cross clamp applied distally and a competent aortic valve proximally, the only paths for the solution to travel are the right and left coronary ostia lying between the cross-clamped aorta and the closed aortic valve. In patients with aortic valve insufficiency, cardioplegia flow into the coronary ostia is significantly reduced because the incompetent aortic valve provides a lower pressure pathway into the inner ventricular chamber, thereby distending the heart and increasing myocardial wall tension. Retrograde delivery is indicated in the presence of coronary artery lesions that impair the transmural distribution of the cardioplegia when delivered solely by the antegrade route. For the retrograde route, the surgeon inserts a catheter through a stab wound into the right atrial wall and threads the catheter into the coronary sinus. The cardioplegic solution infused into the coronary sinus flows retrograde through the cardiac veins and arteries. The solution exits via the coronary ostia, where it is removed by suction.

In addition to thermal and pharmacologic interventions, other strategies to achieve adequate myocardial energy conservation include implementing actions that consistently maximize myocardial energy supplies and minimizing myocardial energy demands. Surgeons and assistants use caution in touching the heart before bypass to lessen the risk of ventricular fibrillation. Anesthesia providers pharmacologically decrease cellular oxygen demand and increase cellular oxygen supply. Other considerations in protecting the heart include minimization of cross-clamp time with availability of the appropriate supplies and equipment, a plan for surgery (jointly developed by surgeons, anesthesia providers, perfusionists, and nursing personnel), anticipation and ability to respond to potential risks and complications applicable to one’s professional responsibilities and skills, implementation of safety procedures, and frequent and collaborative communication.

Surgery for coronary artery disease

Coronary artery disease remains the leading cause of death among men and women.⁵ Left heart cardiac catheterization is commonly performed for identification of areas affected by obstructive atherosclerotic coronary artery disease. Selective coronary angiography with an injection of contrast medium into the right and left coronary ostia illustrates coronary anatomy, distal coronary perfusion, the location of atherosclerotic lesions, the status of coronary collateral circulation, and the percentage of narrowing of coronary arteries affected by coronary artery disease (CAD). Dye is injected into the LV (ventriculography) to determine wall motion (e.g., hypokinesia, dyskinesia, paradoxic motion), and valvular function (e.g., mitral regurgitation, prosthetic valve function). Generally, a right-heart catheterization yields data concerning the inferior and superior vena cava, the right atrium and ventricle, tricuspid and pulmonary valves, and the pulmonary artery.

Percutaneous coronary interventions, specifically percutaneous coronary interventions angioplasty (PTCA) with stent insertion, can be performed for discrete lesions. Equalized pressure measurements above and below the lesion indicate a successful angioplasty. The restenosis rate for angioplasty at 6 months has been approximately 30%, necessitating additional angioplasties or surgery. Complications from the interventional procedure include prolonged chest pain, myocardial infarction, coronary spasm, or coronary artery dissection that can necessitate emergency coronary artery bypass grafting (CABG). Evidence supports surgical revascularization (i.e., CABG) over percutaneous coronary interventions in patients with left main coronary artery disease.^6,7

When CABG is recommended for patients, the number and type of bypass grafts (e.g., saphenous vein, internal mammary artery) are assessed. Fig. 35-5 illustrates possible arterial and venous autologous conduits. Grafts from cadaver human saphenous vein, human and bovine umbilical vein, and synthetic grafts have been used when other conduits were unavailable. CABG does not cure CAD; its purpose is to increase blood flow to the myocardium beyond the obstructive lesions. CAD is a progressive disease, and retardation of the atherosclerotic process requires life style changes and pharmacologic support (e.g., statins). Gender-based differences in CABG outcomes are under scrutiny, and guidelines have been published to provide evidence for the selection of techniques.⁵

FIG. 35-5 Arterial and venous conduits for coronary bypass surgery.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby.)

Once the sternum is opened, the surgeon dissects the required length of the internal mammary artery (Fig. 35-6). The internal mammary artery (IMA) is dissected from its retrosternal bed to the required length, leaving intact the proximal attachment to the left subclavian artery. The assistant harvests additional bypass conduits, such as the saphenous vein (Fig. 35-7) or the radial artery.⁸ Greater saphenous vein is commonly harvested with video-assisted endoscopic techniques.⁹ Because leg veins have valves that facilitate flow toward the right heart, reversal of the vein is necessary so that flow as a bypass graft is not impeded. After conduit harvesting is completed, or if another procedure is planned (e.g., valve repair), the surgeon proceeds to cannulate for CPB. The body is cooled to the desired temperature, and the heart is arrested with cardioplegia. The surgeon then proceeds to attach the grafts to the heart. The left IMA is commonly used in bypass of the left anterior descending coronary artery. The distal anastomosis is created with attaching the end of the graft conduit to the side of the coronary artery; proximally, the IMA graft remains attached to the subclavian artery. For vein grafts, the surgeon attaches the proximal end of the vein to an opening created in the side of the proximal aorta. Veins grafts may be attached to the diagonal, obtuse marginal, posterior descending, or right coronary arteries, as indicated (Fig. 35-8).

FIG. 35-6 Dissection of left internal mammary artery from retrosternal bed with use of special retractor that elevates sternal border.

(Courtesy Rultract, Inc., Cleveland, Ohio.)

FIG. 35-7 Minimally invasive approach to saphenous vein harvesting. A, Traditional open incision. B, Insertion of endoscopic camera and dissector. C, Venous tributaries cut and clipped, cauterized, or ligated to prevent leaking of blood.

(From Zipes DP, et al: Braunwald’s heart disease: a textbook of cardiovascular medicine, ed 7, Philadelphia, 2005, Saunders.)

FIG. 35-8 Coronary artery bypass grafts with left internal mammary artery to left anterior descending coronary artery, and saphenous vein grafts to obtuse marginal and distal right coronary arteries.

(From Braunwald E, et al, editors: Heart disease, ed 6, Philadelphia, 2001, Saunders.)

In operations that necessitate entry into the heart (valve repair or replacement), CPB is required for perfusion of the body while the heart is arrested and opened. During CABG, the procedure is performed on the epicardial coronary arteries that lie on the surface of the heart, not inside the heart. Coronary bypass surgery can be performed without the use of CPB (off-pump CABG), thereby avoiding the deleterious effects associated with extracorporeal circulation (see Table 35-4). Off-pump surgery may be feasible when pulmonary function is poor but LV function is not severely compromised, and access to the target coronary arteries does not require excessive manipulation of the heart.^2,3 During off-pump procedures, the heart beats to perfuse the systemic, pulmonary, and coronary circulations. This beating heart surgery has been facilitated with the use of stabilizing devices that isolate and reduce the motion of the portion of the artery to be anastomosed (Fig. 35-9, 1). An attachment applies suction to the LV apex and allows the heart to be retracted for access to the lateral (i.e., obtuse marginal branches) and posterior (i.e., posterior descending or distal right coronary artery) portions of the heart (see Fig. 35-9, 2). Patient teaching considerations related to on-pump or off-pump surgery are listed in Table 35-5.

FIG. 35-9 1, Octopus^® Evo AS off-pump cardiac stabilizer minimizes motion at the coronary anastomotic site. 2, Starfish® Evo suction positioning device attaches to the apex of the heart and exposes the lateral and posterior coronary arteries for bypass.

(Courtesy Medtronic Inc., Minneapolis, Minn.)

Table 35-5 Patient Teaching Considerations for Minimally Invasive Surgery (On/Off Pump)

CABG, Coronary artery bypass grafting; CPB, cardiopulmonary bypass; HR, Heart rate; LOS, length of stay; VF, ventricular fibrillation.

Adapted from Rothrock JC: Alexander’s care of the patient in surgery, ed 14, St. Louis, 2011, Mosby; Lemmer JH, Vlahakes GJ: Handbook of patient care in cardiac surgery, ed 7, Philadelphia, 2010, Lippincott Williams & Wilkins; Bojar RM: Manual of perioperative care in adult cardiac surgery, ed 5, Oxford, 2011, Wiley-Blackwell.

Other technical advances have brought together interventional procedures and traditional surgical treatments. This combination is seen in the hybrid cardiovascular suite, which enables patients to receive both percutaneous coronary stent placement and traditional surgical revascularization.¹⁰

Left ventricular aneurysm repair

Another form of myocardial revascularization is repair of an LV aneurysm. An LV aneurysm most often results from a large myocardial infarction or numerous smaller adjacent infarctions that cause a portion of the myocardial wall to become scarred, necrotic, thin, and weak. Scar tissue does not contract during systole but instead bulges outward (paradoxic motion or dyskinesia), which decreases the patient’s cardiac output. Thrombus can form within the trabeculations of the LV, and pieces of thrombus can break off and embolize to the systemic circulation. In addition, the perimeter around the scarred fibrotic aneurysmal area can alter conduction pathways and create reentrant ventricular dysrhythmias. Surgical repair consists of excision of the aneurysmal tissue, removal of existing thrombus, and insertion of a patch into the LV in a manner that restores a more normal (i.e., elliptic) ventricular geometry. If the patient continues to have recurrent ventricular tachycardia, electrophysiologic mapping and possible insertion of an implantable cardioverter-defibrillator (ICD) may be performed after surgery in the electrophysiologic laboratory.³

Valvular heart surgery

Valve surgery is performed more commonly on valves in the left side of the heart (i.e., aortic and mitral valves), because the higher pressures on the left side aggravate traumatic, infectious, or other preexisting injury to the valves and valve components. Repair of the native valve is preferred to replacement when possible. A left heart catheterization yields information concerning the left atrium and ventricle, the proximal aorta, aortic and mitral valves, and the coronary arteries. Echocardiography increasingly is the gold standard for the diagnosis of valvular heart disease. Other imaging processes include aortography that displays the size and function of the aorta and can be used to identify the location of the intimal tear in a dissection. Computed tomographic (CAT) scan and magnetic resonance arteriography have largely replaced aortography for imaging of aortic disease.¹¹

When surgery for valve replacement or repair is indicated, the surgeon selects and inserts the appropriate prosthesis. Valve replacement can be accomplished with biologic (Fig. 35-10) or mechanical (Fig. 35-11) prostheses. Newer, percutaneous aortic valve prostheses (Fig. 35-12) are increasingly available, mainly to patients who may be unable to withstand surgical replacemtnt.¹² Allografts (Fig. 35-13) can serve as biologic valve replacements. Allografts are advantageous because they do not require warfarin anticoagulation, are resistant to infection, and have excellent hemodynamics. They are also useful in patients with small aortic roots, because no sewing ring exists to decrease the size of the aortic valve orifice, unlike prosthetic biologic or mechanical valves. Disadvantages include less availability and technical difficulties associated with insertion. Bioprostheses have the advantage of not requiring chronic anticoagulation postoperatively unless there are other indications, such as chronic atrial fibrillation; their disadvantage is that they do not last as long as mechanical prostheses. Bioprostheses are stored in glutaraldehyde before implantation; the solution must be rinsed off the prosthesis, usually in three baths of normal saline solution.

FIG. 35-10 Biologic valves. A, Medtronic Hancock II® porcine bioprosthesis (side view and top view). B, Freestyle^® Aortic Root bioprosthesis. Stentless porcine aortic root bioprosthesis. Use of porcine stentless valves has reduced demand for cadaver allografts. These valves are especially useful in patients with small aortas.

(Courtesy Medtronic Inc., Minneapolis, Minn.)

FIG. 35-11 Mechanical valves. A, St. Jude Medical bileaflet tilting disk valve prosthesis. B, Medtronic Open Pivot™ mechanical valve. C, Double-ended obturators (left and center) for sizing patient’s valve; probe (right) used to test prosthetic leaflet motion. Sizing obturators are specific to prosthesis.

(A, Courtesy St. Jude Medical, St. Paul, Minn. B and C, Courtesy Medtronic Inc., Minneapolis, Minn.)

FIG. 35-12 Percutaneous aortic valve. A, Diagram of bioprosthesis situated in the aortic valve annulus. B, Valve frame with implanted bioprosthesis.

(Used with permission from Medtronic Inc., Minneapolis, Minn. Copyright Medtronic 2009.)

FIG. 35-13 Aortic valve allograft. Note aortic arch branches (top), tissue from left ventricle (red-brown tissue in lower portion of graft), and attached anterior leaflet of mitral valve (white smooth tissue in lower right portion of graft). Depending on graft material required, surgeon trims excess or unneeded tissue.

(Courtesy CryoLife Inc., Marietta, Ga.)

The advantage of mechanical valves is their durability. The disadvantage is that they require continuous anticoagulation therapy after surgery because mechanical prostheses are thrombogenic.

Minimally invasive techniques are increasingly popular. For example, a catheter-based interventional (i.e., nonsurgical) procedure can be performed in a hybrid suite for percutaneous insertion of a balloon-tipped catheter (commonly inserted into the femoral artery or femoral vein) that is threaded through the aorta or IVC to the intended location to enlarge a (stenotic) valve opening. For aortic valvuloplasty, the balloon tip is positioned across the aortic valve, and the balloon is inflated to dilate the aortic valve orifice. Complications of valvotomy include development of aortic or mitral regurgitation (depending on the affected valve), cardiac perforation, pulmonary edema, and cerebral embolus. Percutaneous aortic valve implantation also can be performed along with traditional aortic valve replacement.¹²

Aortic valve surgery

The closing mechanism of the aortic valve makes repair difficult; aortic stenosis or aortic insufficiency (AI) generally require valve replacement, although some reparative techniques (e.g., suture plicating dilated aortic leaflet commissures) may be performed.

Aortic insufficiency

The regurgitating blood in AI creates an increased volume load on the LV. Mild chronic AI can be tolerated by the LV for almost 20 years with more forceful dilation and contraction to eject the additional regurgitant volume. Eventually the LV is stimulated to hypertrophy and decompensates if corrective therapy is not implemented. Symptoms include dyspnea from pulmonary edema and fatigue and other symptoms associated with LV failure. Sudden acute AI (e.g., from bacterial endocarditis that causes tearing of the leaflets [Fig. 35-14] or acute aortic dissection that dilates the aortic annulus) is poorly tolerated, because the normal-sized LV cannot accommodate the sudden increased volume and the lowered diastolic pressure that results from a portion of the cardiac output (CO) being regurgitated into the LV impairs coronary filling. Emergency aortic valve replacement is indicated for acute AI. Aortic valve replacement (see the definition of valve replacement) is generally indicated for AI; some reparative techniques are available for the aortic valve, but they tend to have less successful outcomes.

FIG. 35-14 Perforated aortic valve leaflets resulting from bacterial endocarditis. Patient had aortic insufficiency.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby. Courtesy Edward A. Lefrak, Md.)

Aortic stenosis

Aortic stenosis (AS) can occur as a congenital process, as in the bicuspid valve (a common congenital anomaly first diagnosed in adulthood),¹³ as an acquired disease process related to a history of rheumatic heart disease, or as calcific AS (Fig. 35-15). An inflammatory process has been associated also with the development of aortic stenosis.²

FIG. 35-15 A, Bicuspid aortic valve with calcified stiffened leaflets producing stenosis. Note greatly reduced orifice area. B, Rheumatic trileaflet (e.g., morphologically normal) aortic valve. Thickened, glistened, and smooth leaflets are typical of rheumatic changes. C, Calcific aortic stenosis of trileaflet aortic valve.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby. Courtesy William C. Roberts, MD; Michael Spencer, photographer.)

AS represents an increased pressure load on the LV (increased afterload). The LV responds by developing LV hypertrophy, which results in decreased LV compliance. The LV cavity becomes reduced because of the hypertrophying muscle invading the ventricular cavity. During cardiac catheterization for study of the aortic valve stenosis, calculated pressure gradients between the LV and the aorta may exceed 50 mm Hg. As an example, the aortic pressure may be 100 mm Hg, but the LV pressure may be 150 mm Hg, which shows the work required by the LV to eject an adequate cardiac output. LV dilatation and failure can develop when the myocardium is no longer capable of generating sufficient pressure to eject an adequate CO.

Other forms of AS include narrowing of the outflow tract below or above the valve. Subvalvular stenosis occurs when the intraventricular septum becomes hypertrophied and creates an obstruction to LV outflow. This lesion is known as idiopathic hypertrophic subaortic stenosis or hypertrophic obstructive cardiomyopathy; surgical treatment for subaortic stenosis with a hypertrophied septum involves excision of a portion of the hypertrophied septum; cardiomyopathy may require heart transplantation. Supraaortic valvular stenosis occurs when the aorta above the valve is narrowed from a congenital anomaly. Repair involves opening the affected portion of the aorta and inserting a patch graft to enlarge the narrowed vessel.

Procedure

For aortic valve replacement (Fig. 35-16), the leaflets are excised, the annulus is sized with obturators (i.e., sizers) specific to the prosthesis desired (Fig. 35-17), and the selected prosthesis is implanted. After surgery, anticoagulation therapy is usually initiated 3 to 5 days after surgery, when the patient’s intravascular lines and chest tubes are discontinued and immediate postoperative hemorrhage is no longer a concern. Oral warfarin therapy is then started and titrated appropriately to achieve an international normalized ratio of 2.0 to 3.0 times normal (target, 2.5 for mechanical valves); a target international normalized ratio of 2.5 to 3.5 may be sought in the first 3 months following mechanical valve replacement.^3,14

FIG. 35-16 A, Aortic valve replacement. Cardiopulmonary bypass cannulation, retrograde cardioplegia, and left ventricular vent (inserted via right superior pulmonary vein) are shown. Note incision site on aorta (dotted line). B, If retrograde cardioplegia is not used, handheld ostial catheters may be used for cardioplegia infusion. C, Valve leaflets are completely excised. D, Sutures are placed in aortic annulus and prosthetic sewing ring. E, Stitches are tied and cut. F, Aorta is closed.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St. Louis, 1996, Mosby.)

FIG. 35-17 Valve sizers in use. A, Obturator/sizer is screwed onto handle. B, Obturator used to size aortic annulus. C, Sizing mitral valve annulus. Ao, Aorta; LA, left atrium; RV, right ventricle.

(Courtesy Medtronic Inc., Minneapolis, Minn.)

Mitral valve surgery

The structure of the mitral valve often enables the surgeon to repair rather than replace the valve. Most of the components of the mitral valve—the annulus, leaflets, chordate tendineae, papillary muscles, and the endoventricular wall—are amenable to repair. Reparative procedures may be performed for either mitral valve regurgitation or stenosis.

Mitral regurgitation (MR)

Any of the mitral valve components may be affected. An enlarged annulus is a common cause of mitral regurgitation (MR). The valve leaflets may be normal, but they are unable to coapt and create a competent valve because the dilated annulus pulls the leaflet edges away from one another. The causes of MR may be inflammatory, degenerative, infective, ischemic, structural, or congenital.^15–17 The myxomatous mitral valve (Fig. 35-18) reflects leaflet degeneration from fibroelastic changes. MR also may be related to fibrosis, calcification, or tears in a previously implanted valve prosthesis (Fig. 35-19). Chordae tendineae may be ruptured or excessively elongated or shortened and fused from bacterial endocarditis, one or more papillary muscle heads may have ruptured as a result of ischemic heart disease, or the ventricular endocardium may be dilated.

FIG. 35-18 Myxomatous mitral valve producing regurgitation. Thin elongated leaflets are rarely amenable to valve repair and usually require valve replacement.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby. Courtesy Edward A. Lefrak, MD.)

FIG. 35-19 Explanted porcine mitral valve prosthesis. Leaflets are torn and calcified.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby. Courtesy Edward A. Lefrak, MD.)

Chronic MR produces an enlarged atria where stasis of blood can lead to thrombus formation and subsequent thromboembolism; the dilated atrium can also lead to conduction disturbances such as atrial fibrillation. Pulmonary overloading occurs and eventually can produce pulmonary hypertension; the subsequent increased pulmonary pressures may produce functional tricuspid valve regurgitation. Acute MR is poorly tolerated because the left atrium is unable to contain the sudden regurgitant volume overload and pulmonary overload ensues rapidly; emergency valve replacement or repair (if possible) is indicated.

Mitral stenosis (MS)

Unlike AS, AI, or MR, stenosis of the mitral valve is the only lesion that does not place either a volume or a pressure load on the LV. However, chronic mitral stenosis (MS; like MR) produces an enlarged atria and stasis of blood (with the risk of thromboembolism) and frequently leads to atrial fibrillation. Functional tricuspid regurgitation may develop. MS is the result of changes in one or more of the components of the mitral apparatus. The causes of MS may be inflammation, calcification, tumors (i.e., left atrial myxoma), and infection. Bacterial vegetations and the sequelae of rheumatic fever continue to be significant causes of MS.¹⁵ With MS the leaflets become progressively more fibrotic and stenotic. Fig. 35-20 illustrates the classic “fish mouth” appearance of a rheumatic mitral valve: smooth fibrotic thickened leaflets, commissural fusion, and shortened thickened chordae tendineae.

FIG. 35-20 Stenotic rheumatic mitral valve with classic “fish mouth” appearance. Leaflets are smooth and thickened; chordae tendineae arising from papillary muscle tips are shortened and fused.

(From Seifert PC: Cardiac surgery, St. Louis, 2002, Mosby. Courtesy William C. Roberts, MD; Michael Spencer, photographer.)

Procedure

Most of the components of the mitral valve apparatus—valve leaflets, the annulus, chordae tendineae, papillary muscles, and the endoventricular wall—are amenable to repair. The tricuspid valve is similarly configured. Open commissurotomy can be performed by exposing the affected valve (with the use of CPB and induced cardiac arrest) and sharply incising the fused commissures. The procedure is performed often for children or young adults with a history of rheumatic fever. Performed at an earlier age, commissurotomy can delay the inevitable future need for more extensive valve repair or replacement; this is a significant consideration because the patient can avoid the potential complication of prosthetic valve replacement. Balloon valvulotomy also may be performed in some instances.

Annuloplasty and valvuloplasty may be performed on the affected component. An annuloplasty procedure commonly is performed on the mitral or tricuspid valve or both. A cloth-covered prosthetic annuloplasty ring (Fig. 35-21) in a size smaller than the dilated native annulus is sutured to the valve annulus (Fig. 35-22). When the stitches are tied, excess annular tissue is pulled up against the ring, thereby reducing the overall circumference of the valve orifice and allowing the valve leaflets to coapt properly. Annuloplasty rings have different configurations (e.g., circular, almond shaped, C shaped) and are flexible, rigid, or semirigid. The surgeon’s selection of the prosthesis is based on factors such as the underlying pathology, anatomy, annular dynamics, remodeling of the annular geometry, and preservation of valve function. Prosthetic valvular annuloplasty itself does not require postoperative long-term anticoagulation therapy.

FIG. 35-21 Annuloplasty rings. A, Duran AnCore^® ring. B, CG Future^® ring.

(Courtesy Medtronic Inc., Minneapolis, Minn.)

FIG. 35-22 A, Annuloplasty ring bean-shaped sizer with handle used to measure annulus (note retraction of chordae tendineae to facilitate sizing). B, Stitches are inserted into annulus and into prosthetic ring. C, Sutures are tied and cut; bulb syringe squirts saline solution into orifice to determine whether repair has produced competent valve. Portion of excess posterior leaflet tissue has been resected.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St. Louis, 1996, Mosby.)

In addition to insertion of a prosthetic annuloplasty ring for annular dilation (see Figs. 35-21 and 35-22), valvuloplasty can be performed. Excess portions of the posterior leaflet of the mitral valve are excised, and the remaining edges are sewn together to promote leaflet coaptation and to reduce the annular circumference. Torn leaflets can be repaired with a patch of pericardium. Ruptured chordae tendineae can be replaced with suture or reattached to the valve leaflet; shortened thickened chordae can be incised to increase length and improve flexibility; and excessively lengthened chordae can be shortened by implanting a portion of the chord into a papillary muscle head. Debridement of calcific nodules can be done, although valve replacement may be needed with severe calcification.

Balloon valvotomy for the mitral valve is performed with a catheter percutaneously inserted into a large vein and threaded to the RA, where a septal puncture is made to allow access into the left atrium and to the mitral valve. This technique is useful for children, young adults, and patients who are too elderly or medically compromised to withstand an operation. Occasionally the catheter is threaded up the aorta and through the aortic valve into the LV and then placed across the mitral valve where the balloon is inflated. Percutaneous mitral valve repair can be performed, but the procedure is less effective than surgery for reducing mitral regurgitation.¹⁸

When valvular deformation injury is severe, prosthetic replacement may be required. For mitral valve replacement (Fig. 35-23), the anterior leaflet is usually excised, but often all or part of the posterior leaflet and its attached chordae are retained to preserve the LV geometry and enhance LV function. Although valve replacement improves cardiac function by removing the stresses associated with volume or pressure overloading, transient symptoms of ventricular failure can exist after mitral valve replacement for chronic MR because the LV no longer has the release valve represented by the incompetent valve. With the insertion of a competent mitral prosthetic valve, the LV must develop sufficient pressure to push all the LV end-diastolic volume forward through the aortic valve. Afterload reduction (e.g., with sodium nitroprusside) assists LV ejection. Potential complications associated with prosthetic valve replacement are thromboembolism, anticoagulation-related hemorrhage, prosthetic valve endocarditis, perivalvular leak, and prosthetic failure.^2,3

FIG. 35-23 Mitral valve replacement. A, Incision (dotted) line in left atrium, exposure of mitral valve, and illustration of relationship between mitral and aortic valves and atrioventricular node. Double venous cannulas shown for cardiopulmonary bypass; antegrade cardioplegia catheter inserted into aorta below the cross clamp and aortic cannula are shown. B, Sutures are placed in native valve annulus and then prosthetic. C, Completed valve replacement.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St. Louis, 1996, Mosby.)

Tricuspid valve repair

Tricuspid regurgitation may be the result of severe mitral stenosis that produces significant back pressure that affects the right side of the heart. It can develop also as a result of rheumatic changes, a right ventricle (RV) infarction, infection, or annular dilatation from right atrial remodeling that occurs with RV failure. Although tricuspid stenosis occurs infrequently in adults, it can occur as a result of rheumatic heart disease or bacterial endocarditis.

Annuloplasty repair is generally performed, although tricuspid valve replacement is performed if a repair to the native valve cannot be accomplished. During ring insertion for tricuspid annulus repair (Fig. 35-24), the surgeon is especially cautious when inserting stitches near the atrioventricular node and the bundle of His (in the area of the tricuspid septal leaflet) to avoid creating complete heart block or other injury to the conduction system. A suture annuloplasty (i.e., without the insertion of a prosthetic ring) can be used also for some tricuspid valve repairs (see also the definition of valvuloplasty).

FIG. 35-24 A, Tricuspid valve repair is similar to mitral valve repair. Note that stitches are not inserted in area of atrioventricular conduction tissue (see text). B, Completion of tricuspid valve repair.

(Courtesy Medtronic Inc., Minneapolis, Minn.)

Surgery for thoracic aortic aneurysms and dissections

Localized or diffuse dilation of the aortic wall leads to progressive enlargement of all layers of the aorta. Surrounding tissue may be compressed by the enlarging vessel, and eventual rupture with exsanguination can occur without treatment. Diagnosis is made with CT scan and magnetic resonance arteriography, which display the size and shape of the aorta and can be used to identify the location of the intimal tear in a dissection.¹⁹ Surgical treatment consists of excision of the aneurysmal tissue with insertion of a prosthetic graft (e.g., Dacron; Fig. 35-25). An endovascular stented graft made from expanded polytetrafluoroethylene (PTFE) can be used to repair f descending (and abdominal) aortic aneurysms. The prosthesis is initially compressed, inserted percutaneously into the femoral artery, and guided into the aorta where it is expanded and deployed in the desired position.

FIG. 35-25 Resection of aneurysmal portion of ascending aorta and transverse arch and insertion of prosthetic patch. Circulatory arrest is instituted until arch vessels are repaired. A, Graft anastomosed to distal portion of aorta. B, Arch vessels are anastomosed as island to prosthetic graft. C, After arch vessels are connected, cross clamp is placed on graft, cardiopulmonary bypass is resumed, and proximal anastomosis is completed.

(From Waldhausen JA, et al: Surgery of the chest, ed 6, St. Louis, 1996, Mosby.)

Aortic dissection is a unique condition affecting the aortic media. Surgery is indicated for ascending aortic and transverse aortic arch dissections and involves excising the portion of the aorta that contains the tear and replacing excised tissue with a graft. Uncomplicated descending thoracic aortic dissections are more commonly managed medically with antihypertensive medications and analgesics. Surgery, with a traditional incision or an endovascular prosthesis, is indicated with impending rupture.^20,21

Blunt trauma to the thoracic aorta can lead to aortic rupture. Newer imaging techniques have enabled clinicians to intervene more promptly in these cases, thereby improving survival.¹¹ Endovascular graft insertion or traditional repair may be performed.²²

Ventricular assistance

Ventricular assist devices (VADs) decrease the workload of the heart by diverting blood from the ventricle to an artificial pump that maintains systemic (left VAD [LVAD]) or pulmonary (right VAD [RVAD]) perfusion. A BiVAD supports both right and left ventricles. Placement of a cardiac transplant candidate on a VAD enhances anabolism, ambulation, and improved organ function; these physiologic improvements enable the patient to become a stronger transplant candidate. In this case, the VAD is used as a bridge to transplantation. Improvements in VAD therapy have significantly reduced the incidence rate of infection and thromboembolism. VADs have been especially valuable in the treatment of heart failure.^23,24 A vented electric LVAD for destination therapy or permanent replacement for the LV enables patients to be relatively independent by reducing the reliance on in-line power sources.²⁵

Short-term assist devices include the intraaortic balloon pump (IABP), a sausage-shaped balloon mounted on a catheter percutaneously inserted into the aorta distal to the left subclavian artery via the femoral artery. The balloon inflates during diastole, propelling blood proximally to the aortic root and into the coronary ostia to enhance coronary perfusion. Distally, blood is propelled into the peripheral vascular bed to enhance organ blood flow. When the balloon deflates during LV systole, LV afterload is reduced by the movement of blood during balloon inflation. With the increase in coronary blood flow and the decrease in afterload, the total work of the heart is reduced, thereby providing an environment that supports the recovery of a failing myocardium and improves peripheral vascular perfusion.²⁴

Transplantation

With the improvement in pharmacologic therapy, comorbidity management and infection prophylaxis, cardiac transplantation 1-year survival rates approach 90%.²⁶ Potential candidates are patients who are considered to be in the New York Heart Association Functional Classification System’s class IV, which denotes the most compromised cardiac status, and who have less than a 10% chance of survival for 6 months. Heart donors are persons with irreversible catastrophic brain injury who do not have atherosclerotic heart disease. Age limitations have become less restrictive, and donors and recipients may be 60 years or older in certain cases.

Removal of the donor heart is accomplished with transection of the venae cavae, the pulmonary artery, the left atrium, and the aorta. The donor heart is placed in a sterile bag with cold preservation fluid and transported to the recipient’s institution. The surgeon places the recipient on CPB and removes the recipient’s heart surgically after the donor heart has been judged acceptable and has arrived in the recipient’s operating room. The pulmonary artery, the SVC and the IVC, the pulmonary veins, and the aorta of the donor are anastomosed to the comparable tissue of the recipient. This technique has been modified from the traditional technique, in which a right atrial anastomosis was performed. The newer technique reduces some of the dysrhythmias and tricuspid valve dysfunction associated with the previously created RA connections. After surgery, transplant patients receive the same care provided other cardiac surgery patients with the addition of immunosuppression-related infection and rejection monitoring.

Two new cardiac transplantation subpopulations include patients with previously repaired congenital heart disease and transplantation recipients requiring retransplantation. Ten-year survival after transplantation in the former group is excellent.²⁶ Retransplantation patient survival improves in the absence of primary allograft failure and refractory rejection within the first 6 months after retransplantation. Guidelines for this subpopulation remain vague and are undergoing refinement.^26,27

Lung transplantation involves replacement of one or both lungs with lungs from a donor or a single lung from a living donor. Newer allograft organ protective strategies have contributed to improved outcomes in lung transplantation candidates. Contraindications for transplantation include significant pulmonary hypertension, the presence of systemic disease, a recent pulmonary infarction, or active systemic infection.^28,29

Surgery for adult congenital heart disease

A number of congenital anomalies might not be treated until adulthood. These congenital lesions tend to be less severe and therefore asymptomatic (or mildly symptomatic) in childhood. Some of the most common are listed in the following sections.³⁰

Atrial septal defect

A frequently seen congenital anomaly in adulthood is the atrial septal defect (Fig. 35-26).³¹ The most common form of atrial septal defect in the adult is the ostium secundum defect, located in the midportion of the septum in the vicinity of the fossa ovalis (formerly the intrauterine shunt known as the foramen ovale). Less common is the sinus venosus defect located near the entrance of the SVC in the high RA. Sinus venosus defects are associated with partial anomalous pulmonary venous return (commonly of the right superior pulmonary vein), whereby the anomalous pulmonary vein enters the RA (rather than the left atrium) and returns oxygenated blood from the lungs into the SVC or the upper RA. Closure of the secundum and sinus venosus septal defects is accomplished with suturing or patching the defect with a patch of pericardium or prosthetic material. During repair of a sinus venosus defect, the patch is placed in such a way that anomalous pulmonary venous drainage is diverted into the left atrium.

FIG. 35-26 Location of three types of atrial septal defect. Sinus venosus defect (I) is shown with anomalous drainage of right upper pulmonary vein. Ostium secundum defect (II) is in midportion of septum in area of fossa ovalis. Ostium primum defect (III) is located in base of septum, with its inferior edge formed by continuity of tricuspid and mitral valves. Often a cleftlike anomaly is seen in anterior leaflet of mitral valve visible through defect.

(From Miller TA, editor: Physiologic basis of modern surgical care, St. Louis, 1988, Mosby.)

Completion of surgery

After the cardiac repair is completed, temporary pacing wires are attached to the right atrial and ventricular surface, brought out through the chest below the sternal incision, and connected to an external pacemaker generator. One or more chest tubes are placed anteriorly, laterally, or posteriorly in the pericardium to facilitate drainage. The tubes exit via stab wounds below the sternal incision. If either of the pleurae were opened during the procedure, the tip of one of the pericardial chest tubes is inserted into the affected pleura. The pericardial sac is rarely closed so that any remaining blood or fluid can drain freely into the chest tubes, avoiding the creation of a cardiac tamponade. Occasionally, when a repeated operation is anticipated (e.g., after a biologic valve replacement in a young person), the upper (cephalad) portion of the pericardium may be closed so that less scar tissue forms over the cannulation sites for CPB (e.g., the aorta). The lower portion of the sac remains open to drain fluid. The sternum is closed with stainless steel wires, and the fascia, subcutaneous tissue, and skin are closed with suture. Before transfer from the OR to the postanesthesia care unit (or intensive care unit [ICU]), portable monitoring lines for heart rate and rhythm, arterial blood pressure, and oxygen saturation are connected for transport to the postoperative unit. Patients can have acute circulatory instability develop, because of either the normal recovering physiologic state or inadvertent movement or displacement of the numerous invasive lines and tubes needed. A portable defibrillator is often placed on the transport bed for use if ventricular tachycardia or ventricular fibrillation develops during transport.

Postanesthesia care

Cardiac surgery patients commonly go to a specialized cardiovascular surgery ICU or postanesthesia care unit (PACU). Whether a critical care nurse or a postanesthesia nurse, a caregiver should be aware of the level of knowledge, understanding, and anxieties of both the patient and the family before surgery. When possible, and depending on the individual institution’s policies and procedures, the postoperative caregiver nurse can provide preoperative instruction for the patient and family or make an introductory visit before surgery. Teaching content for coronary or valve surgery (see Table 35-1) can be initiated in the preoperative period and reinforced after surgery. Discharge from the cardiovascular surgery ICU or open heart PACU to a step-down unit increasingly occurs within hours. A reduction has also been seen in the overall length of stay (LOS) from 1 or longer to a few days. The movement toward rapid postoperative endotracheal extubation and shortened LOS has been spurred not just by costs but also by improved pain control that facilitates earlier extubation and by fundamental shifts in anesthetic management from a high-dose opioid technique to a more balanced approach with moderate-dose opioids, shorter acting muscle relaxants, and volatile anesthetics. The so-called fast-track approach (i.e., extubation immediately after or within a few hours of surgery)² is becoming a standard of care in a number of centers.³ The longer LOS sometimes seen in the rapidly growing number of patients 80 years and older may be the result of comorbid conditions such as peripheral vascular disease, renal pathology, diabetes mellitus, hyperlipidemia, and hypertension, but advances in anesthetic techniques and myocardial protection during surgery have improved morbidity and mortality rates in older and younger patients. This chapter is designed to familiarize the PACU nurse with the perioperative care for the adult cardiac patient. Understanding what the patient has experienced before and during surgery assists the nurse to tailor care after surgery to the patient’s needs and to strengthen the continuity of that care.

All patients in the cardiac PACU or cardiovascular surgery ICU need intensive continuous hemodynamic monitoring and rapid intervention to prevent complications from the surgery and CPB. Patients are routinely monitored for dysrhythmias, pleural effusion, bleeding, and cardiovascular, neurologic, renal, pulmonary, respiratory, and temperature alterations. The nurse’s role is critical to ensure that anticipated clinical changes (e.g., temperature, fluid shifts) do not progress to more serious complications that can jeopardize optimal patient outcomes. In addition, nurses in the postoperative unit and the step-down unit educate patients about the plan of care and involve patients and family members to implement the plan designed for patients and their families.

On admission to the postoperative unit, the nurse immediately assesses the parameters currently monitored. If any of these parameters indicates circulatory or ventilatory dysfunction, immediate resuscitative measures are instituted. If circulatory and ventilatory statuses appear adequate on entry to the postoperative unit, then admission routines are initiated. The respiratory therapist or anesthesia care provider usually attaches the patient to the ventilator, establishes the initial ventilator settings, and sets the alarms. After the patient is attached to the ventilator, the nurse auscultates both lung fields and repeats the assessment often until discharge from the PACU.

Invasive monitoring lines are attached to transducers or manometers. Patency is ascertained, and values and wave tracings are continuously displayed and recorded. Commonly measured intravascular parameters include mean arterial, right atrial, mean pulmonary artery, pulmonary artery systolic, pulmonary artery diastolic, pulmonary capillary wedge, and left atrial pressures. In addition to these directly measured parameters, these values assist in calculation of indirect or derived hemodynamic parameters, such as cardiac output and cardiac index, systemic vascular resistance, and pulmonary vascular resistance. These parameters assist in the assessment of both LV and RV status and are used in determination of pharmacologic, fluid, and mechanical therapies for the postoperative patient. Once these invasive lines are connected, the nurse reviews and assesses with the anesthesia provider the intravascular lines and solutions in regard to type, drugs infused, flow rates, patency, and expiration times. Intake and output recordings with running totals are made and documented hourly or more often as clinically indicated. Volume administration and replacement treatments are largely determined by the individual patient’s hemodynamic parameters, and responses can vary greatly from hour to hour.

Chest tube drainage systems inserted in the OR are connected in the postoperative unit to suction systems to achieve 15 to 20 cm of negative suction. The amount and the type of chest tube drainage are frequently assessed and recorded on an hourly basis. Drainage that exceeds 100 mL/h should be brought to the attention of the physician (e.g., intensivist, surgeon, or anesthesiologist, depending on institutional practice). Chest tubes are usually removed on the first or second postoperative day, as long as intracardiac lines have been removed, no evidence of fluid accumulation is present on chest radiograph results, and drainage has been less than 200 mL in the last 6 hours. Most patients have one or two mediastinal chest tubes that facilitate pericardial drainage after surgery. If the pleural spaces were opened during the procedure or the internal mammary arteries were dissected off the chest wall, or both, then pleural chest tubes are also present to facilitate drainage and to prevent a pneumothorax.

Arterial blood gas values are determined on admission and as needed thereafter. Intubated patients retain their breathing tubes until the effects of anesthesia subside and hemodynamic stability is achieved and maintained. Controlled ventilation is used initially. As patients begin to generate their own respirations, they are switched to intermittent mandatory ventilation modes, in which they gradually increase their spontaneous respirations to maintain adequate minute ventilations. Once patients maintain an adequate respiratory rate, they are switched to continuous positive airway pressure (CPAP) systems. With CPAP, the patient determines the respiratory rate, and the ventilator provides the positive pressure to the airway that the glottis normally provides when the patient is not intubated. The use of CPAP prevents microatelectasis and increases the functional residual capacity of the lung by increasing lung expansion. Once the patient maintains adequate arterial blood gas levels on CPAP, extubation usually follows quickly. After extubation, face masks or nasal cannulas are used to deliver supplemental oxygen.

A continuous ECG recording is established, alarm limits are set, and a strip recording is obtained. A 12-lead ECG may be obtained for complex or unusual dysrhythmias. Cardiac rhythm is assessed frequently and documented at least every 2 hours. Lead selection varies, but modified chest lead one (MCL₁), in which the left-atrial and right-atrial leads are in their respective places and the third lead is placed on the fourth right intercostal space, is commonly used. Electrode placement with this lead does not interfere with defibrillation procedures or with mediastinal or chest tube dressing placement. The apical pulse is auscultated and validated with the ECG recording. Most patients have a temporary external pacer, and the nurse checks and records the type of pacer, the mode, the rate, and the milliamperage and determines whether the pacer is functioning adequately. If the patient is not being paced, the nurse needs to ensure that the unused pacemaker wires are covered with gauze, placed in a plastic covering (e.g., a finger cot), and securely dressed and attached to the chest to protect the patient from electrical hazard. Usually two ventricular and two atrial pacing wires are attached to the epicardium with a fine suture before the chest is closed. These wires then exit the chest via stab wounds on either side of the sternal incision. Wires are most often left in place for a few days after surgery and may be used to assist in cardiac rate and rhythm control. Before the patient is discharged from the hospital, the wires are totally removed with gentle traction or they are clipped off at the skin level (with a portion left attached to the epicardium and residing in the subcutaneous tissues).

The patient’s neurologic status is assessed on admission and every 30 to 60 minutes and thereafter until arousal from anesthesia. Neurologic complications can affect the central or the peripheral nervous system and include cerebral or peripheral thromboembolism, encephalopathy, coma, impaired intellectual function. Use of off-pump (versus on-pump) techniques for patients undergoing CABG have not shown improvements in neurocognitive outcomes.^3,36 Once the patient has been aroused, neurologic assessments are decreased to every 2 hours.

An admission temperature is obtained and active rewarming therapies are instituted. Temperatures are recorded hourly during this period, and rewarming devices are discontinued when the patient’s condition reaches normothermia. One temperature-related condition is hypothermia-related hypocarbia. The body temperature usually remains lower than normal during the early postoperative hours. The body temperature returns to normal slowly; rebound hyperthermia occurs occasionally. As rewarming takes place, carbon dioxide is produced. Consequently, hypercarbia can develop, and ventilator settings should be adjusted to produce a minute volume necessary to facilitate normocarbia. In addition, if rebound hyperthermia occurs or if rewarming devices are not regulated and monitored appropriately, a hyperthermic overshoot can occur, which increases myocardial oxygen demand and consumption.³

An abdominal assessment is performed on admission and every 2 hours thereafter until bowel sounds return. A nasogastric or orogastric tube inserted after induction of anesthesia relieves gastric distention and facilitates removal of gastric contents.² It is usually attached to low intermittent suction or gravity drainage and removed at the time of extubation. Analysis of pH and tests for the presence of occult blood can be performed on gastric secretions if they begin to resemble coffee grounds. After the nasogastric tube is removed, the patient is given ice chips and resumes a clear liquid diet within the first 24 hours.

Urinary drainage from the catheter inserted in the OR should be recorded on admission to the PACU and then hourly. The appearance of the urine is also monitored closely. During the first few hours after surgery, massive diuresis of 2 to 3 L of pale dilute urine is usually common from diuretics that are generally administered during the discontinuation of CPB to facilitate the removal of fluid that has sequestered during surgery in the interstitial space. When this initial diuresis resolves, urine color and consistency return to normal. Urinary output should be more than 0.5 mL/kg/h; a lower urine output is commonly the result of decreased renal perfusion.³

Peripheral pulses and skin color and temperature are assessed and recorded hourly. All incisions and intravascular and tube insertion sites are observed. The patient is placed in a 30-degree position with the legs supported at the knees and the calves slightly elevated to reduce the incidence of ventilator associated pneumonia. This position facilitates venous return from the legs and limits swelling, particularly in patients with saphenous vein excision. Legs are wrapped from toes to hips with elastic leg wraps or antiembolism stockings.

Cardiopulmonary bypass affects every body system, and a brief review of some of the effects on the patient seen in the postoperative period is useful to the nurse. For example, epinephrine and norepinephrine levels are markedly elevated during CPB. Hyperglycemia and impaired insulin responses are present and result in use of fat stores for energy until carbohydrate metabolism returns to normal levels. Secretion of antidiuretic hormone and aldosterone is also increased, stimulated by different mechanisms associated with the physiologic components of stress. Serum complement that is activated when blood contacts the inner surfaces of the bypass circuit cause an inflammatory response with a marked increase in total body water and interstitial edema. Postoperative fluid requirements are affected by rewarming because rewarming itself causes fluid shifts. This excess fluid usually redistributes itself by the second or third day after surgery and is excreted spontaneously or with diuretic therapy. CPB and hypothermia also alter coagulation factors, platelet formation, and the immune system.²

In addition, when exposed to the foreign surfaces of the CPB circuit, platelets clump together. A decrease in the number of functional platelets occurs along with a decrease in the aggregative and adhesive functions of remaining platelets. Release of vasoactive substances occurs as platelets are destroyed. In addition, exposure to the CPB circuit (and suctioning devices) causes a breakdown of plasma proteins, including gamma globulin, which in turn can cause fat microemboli release, microcoagulation, clotting factor consumption, and increased vascular permeability. The shear stresses caused by suction catheters and the tubing and connectors within the circuit also damage the formed elements of the blood (e.g., erythrocytes, leukocytes).

A written assessment is performed after admission routines. The frequency of assessment and documentation of the hemodynamic parameters and routines is dictated by the patient’s response to and recovery from surgery. Recovery time varies from among patients but generally occurs within 12 to 24 hours, except with impaired cardiac, pulmonary, renal, or other organ function. During that time numerous expected postoperative physiologic alterations occur, largely because of the techniques of CPB, hypothermia, anesthesia, and surgical manipulation of the myocardium. With correct interventions, these physiologic responses are short lived and reversible; however, two problems exist. First, although these alterations are reversible, they can lead to complications if not identified early and treated quickly. Such is the case with uncontrolled hypertension, which can develop into hemorrhage if fresh suture lines are disrupted. Second, these alterations often resemble complications and thus may be missed in the early stages. For example, the initial absence of a pedal pulse may be attributed to hypothermia and vasoconstriction only to be traced later to a vascular embolism. For these reasons, the PACU nurse must be knowledgeable about the causes, assessment factors, and interventions for both expected physiologic alterations and complications that can occur after cardiac surgery. These alterations and potential complications are reviewed briefly in the following section.

Cardiovascular system

A number of predisposing factors are known to increase the incidence rates of postoperative complication and early mortality. These factors include preoperative cardiac conditions, such as myocardial dysfunction, recent MI, and previous CABG surgery or systemic conditions such as advanced age, obesity, diabetes mellitus, and chronic obstructive pulmonary disease. The surgical risks of CABG can be assessed before surgery, and complications can be anticipated with these preoperative risk factors taken into consideration.

Complications related to CABG and valvular surgery can generally be classified as either cardiac or noncardiac. Cardiac complications include myocardial infarction, congestive heart failure, tamponade, dysrhythmias, and postoperative hypertension. Each of these complications can contribute to decreased cardiac output.

These complications also contribute to increased costs. One multiyear, statewide study of isolated CABG patients demonstrated the greatest additive costs for prolonged ventilation ($40,704), renal failure ($49,128), and mediastinitis ($62,773).³⁷ Noncardiac complications include hemorrhage, wound dehiscence and infection, and neurologic, renal, pulmonary, and gastrointestinal problems. Each complication is addressed individually.

Cardiac complications of coronary artery bypass grafting and valvular surgery

Noncardiac complications of coronary artery bypass grafting and valvular surgery

Respiratory system

The effects of anesthesia, sedation, and the deflation of the lungs during CPB commonly create moderate episodes of impaired gas exchange with concurrent alterations in the arterial blood gas values. These episodes, largely atelectatic in nature, are usually self limiting or easily resolved with sustained maximal inspiration, chest physiotherapy, and administration of supplemental oxygen. If a hemothorax or a pneumothorax develops, more negative pressure may be added to the drainage systems, or additional chest tubes may be inserted. A volume overload from overaggressive replacement or mobilization of fluid from the third spaces may exist and can hamper gas exchange; diuretic therapy is indicated.^2,3

Nervous system

Temporary and permanent sensory, motor, perceptual, and cognitive deficits can occur during the perioperative period. Permanent deficits can usually be attributed to a low cerebral perfusion state from inadequate cardiac output or to an embolic phenomenon from intracardiac thrombi, calcified valve fragments, aortic plaque dislodgement and subsequent embolization from application of the aortic crossclamp, or air embolization from intracardiac chambers of invasive lines. The magnitude of the deficit is determined by the degree of neurologic involvement. Deficits are usually identified early in the postoperative period when the effects of anesthesia have resolved. Some of these deficits may not be identified until after extubation. Transient deficits, lasting from hours to days, can range in degree from slowness to arousal to confusion and delirium. Deficits can be caused by microemboli from tissue debris, air bubbles, or platelet aggregation and are associated with CPB.³

Renal system

Prerenal and acute renal failure states can develop after cardiac surgery. Inadequate CO from myocardial depression or inadequate volume replacement can lead to prerenal oliguria. Blood urea nitrogen and serum sodium levels increase, and serum creatinine levels remain the same. Low sodium content is seen in the urine as the body attempts to save sodium and thus increase its intravascular volume. If these states continue for prolonged periods, acute renal failure can ensue. Treatment focuses on maintenance of adequate volume replacement and increase in CO, with an inotropic agent if necessary. In addition, renal emboli from intracardiac thrombi or hemolysis from blood transfusions or prolonged CPB runs (from trauma to the formed elements of the blood producing hematuria) can also lead to the development of acute renal failure. In acute renal failure, serum creatinine and urea levels elevate and remain in a 10:1 ratio, urine sodium levels increase, and the plasma urine osmolality ratio falls to 1:1. Transient hematuria is usually short lived and may resolve after infusion of an osmotic diuretic (e.g., mannitol).^2,3

Gastrointestinal system

Gastrointestinal complications are similar to those for general surgery.⁴¹ After extubation, the patient may remain on nothing by mouth (i.e., NPO) status for a few hours. Small amounts of ice or water are then allowed. Gastric distention can occur if air enters the stomach and can cause cardiac problems and pulmonary complications. A nasogastric tube can be inserted to decompress the stomach. Rarely, mesenteric or splenic ischemia or infarction from intracardiac thrombi or air emboli may occur; surgical revascularization can be performed.

Peripheral vascular system

Vascular complications can include both venous and arterial thrombus formation and embolism development. Venous thrombus can develop as a result of blood stasis from immobilization and inactivity in the immediate postoperative period. Arterial complications are largely associated with various intravascular devices such as intraarterial lines and intraaortic balloon catheters, when present. Assessment of pulses should be ongoing, and a Doppler pencil may be used to confirm the patency of the radial artery after removal of the intraarterial pressure monitoring line. The status of lower extremity pulses, skin color and temperature, and motor activity should be monitored closely, particularly in the presence of an intraaortic balloon catheter and particularly during insertion and removal. Passive and active range-of-motion exercises and early ambulation are advocated and encouraged in these patients to prevent complications. Patients are instructed and assisted in performing active dorsiflexion and extension of the feet and ankles. These maneuvers facilitate venous return and decrease stasis.^2,3