Principles of Cardiovascular Surgery

Principles of Cardiovascular Surgery

CHAPTER 37 Principles of Cardiovascular Surgery ALIREZA ALIZADEH GHAVIDEL, MD  •  SAEID HOSSEINI, MD, FETCS KEY POINTS • Deep hypothermic circula...

2MB Sizes 200 Downloads 114 Views

CHAPTER 37

Principles of Cardiovascular Surgery ALIREZA ALIZADEH GHAVIDEL, MD  •  SAEID HOSSEINI, MD, FETCS

KEY POINTS

• Deep hypothermic circulatory arrest with selective cerebral perfusion provides a safe, bloodless surgical field in selected cardiac surgeries, including aortic arch replacement and pulmonary thromboendarterectomy. • A postoperative hemoglobin (Hgb) level greater than 8 g/L is usually considered sufficient, but for higher risk patients such as older adults or patients with chronic obstructive pulmonary disease or congestive heart failure, higher Hgb levels are useful. • Patients with heart valve replacement on sinus rhythm and good ejection fraction do not require anticoagulation immediately after surgery. • Therapeutic levels of international normalized ratio for patients with mechanical valve replacement are 2 to 3 for aortic valve replacement, 2.5 to 3.5 for mitral valve replacement, and 3 to 4 for eight-sided heart valves. • Because the platelet depletion is consumptive, patients with heparin-induced thrombocytopenia (HIT) usually present with intraarterial or intravenous thrombosis instead of bleeding. • Using heparin in patients with a history of HIT for more than 3 months, normal platelet count, and negative antiplatelet factor 4 who need percutaneous coronary intervention or cardiac surgery may be safe. • Patient–prosthesis mismatch is a challenging issue in aortic valve surgery that can be managed by aortic root enlargement techniques (Manougian and Konno-Rastan procedures), aortic root replacement, low-profile newgeneration valves, or sutureless tissue valves. • Moderate degrees of tricuspid insufficiency would require tricuspid valve repair if the maximum end-systolic diameter is greater than 40 mm or larger than 21 mm/m2 in preoperative echocardiography or over 70 mm in the surgical field of an arrested heart.

EXTRACORPOREAL CIRCULATION Before the invention of the cardiopulmonary bypass (CPB) machine, heart surgery was limited and sporadic. However, this particular invention and its application brought along dramatic advancements, improved outcomes of heart surgery, and established a surprisingly upward trend in the number of cardiac operations. The uniqueness of heart surgery is mainly attributable to the nature of the extracorporeal circulation while using the CPB machine. Also, adding the word “open” in conjunction with heart surgery means that CBP has been used in the course of heart surgery. The machine consists of four or five consoles of roller pumps, one of which is designed to create and provide systemic blood circulation. Sometimes because of safety considerations and higher efficiency, a centrifugal pump is externally attached to the machine, which replaces a roller pump. Two of the other mentioned roller pumps

are for sucking out the blood and returning it to the CPB system (Fig. 37.1). One or two of the remaining roller pumps are used for infusion of cardioplegia solutions and myocardial protection. For promoting CPB system performance, a number of single-use and disposable materials are also consumed, which include oxygenator cannula and corresponding lines and arterial, venous, and cardioplegia cannulas. In fact, the oxygenator is responsible for the function of the lungs during CPB operations. At the beginning, the oxygenator was of the bubble type, and because of its various complications, it became obsolete and was later replaced with membrane oxygenators, which are still in use. This system is designed to exchange gases, remove CO2 and add oxygen to the blood. It consists of very fine hollow fibers made of polypropylene or silicon rubber with a diameter of about 0.3 to 0.8 μm, all of which have tiny pores for gas exchange. Because 647

648

Practical Cardiology

FIG. 37.1  Cardiopulmonary bypass machine and acces-

sories.

blood and gas are somehow in contact with the oxygenator and because of plasma leakage through this membrane, the maximum safe operational time is limited to no more than several hours. Because of the nature of extracorporeal blood flow in CPB, activation of the coagulation system is to be expected. For this reason, before using a cannula and CPB, a high dose of heparin is administered for anticoagulation. The initial heparin dose for injection should be 3 to 4 mg/kg. To monitor heparinization efficacy, two tests, the activated clotting time (ACT) and Hepcon (measuring the concentration of heparin in the blood), are in use. ACT test is more popular and is usually done 3 minutes after heparin injection, when heparinization has taken full effect. When the elapsed time approaches 480 seconds, CPB can be started. During CPB operation, the test is repeated every half hour to every hour, and if the result is lower than expected, more heparin is injected. At the end of surgery and by the end of CPB operation and removal of the cannula, the effect of heparin is neutralized by protamine injection. Recently, as a new technology, manufacturers added disposable CPB materials with heparin-coated parts to reduce the chances of thrombosis and clot formation in CPB, especially the oxygenator. It should be noted that before starting the machine, the CPB reservoir should be primed with crystalloids or colloid solutions, which results in hemodilution. In any case, however, during CPB operation, a hematocrit of about 20% to 25% is acceptable. With the start of CPB operation, natural pulsatile circulation, which was generated by the heart and maintained by the body vessels, temporarily ceases to function and is replaced

with CPB continuous flow. This change in the blood circulation model, which is accompanied by lower than normal average blood pressure, affects organs’ perfusion. To overcome the resulting complications during CPB operation, the patient’s body temperature is lowered, and the patient is in a state of hypothermia. In the early years of heart surgery, patients were operated on at much lower temperatures, and until a few years ago, cardiac surgeries were practiced at temperatures between 25° and 28°C. However, in recent years, a temperature of about 30° to 32°C is more desirable for heart surgeons. Cardiopulmonary bypass blood flow, is based on the patient’s body surface area (BSA) and, of course, adjusted according to body temperature. Usually, a body temperature of 30° to 32°C can be called mild hypothermia. The blood flow rate is adjusted to 2.5 L/m2 of BSA. So accordingly, lower blood flow is possible with lower body temperatures. During CPB operation, the adequacy of blood flow is regulated by monitoring various factors, including urine output and blood gas analysis. At the end of the surgery, when the required procedures have all been accomplished and the patient is being warmed up and ready for weaning from the CPB, it is crucial that it is all done slowly and that its adequacy is determined by different methods of monitoring, including heart transesophageal echocardiography (TEE). 

DEEP HYPOTHERMIA AND CIRCULATORY ARREST In a number of cardiac surgeries, we have to take the patient to a deep hypothermia condition (down to about 18°C) to be able to completely stop the CPB blood flow and to operate on the patient in total circulatory arrest (TCA). This group of surgeries is among the surgical procedures in which, because of their nature, blood flow in the body must be cut off (e.g., surgeries on the aortic arch, especially in aortic dissection or the procedures in which the field of operation must be completely free of blood, as in pulmonary endarterectomy or some complex congenital surgeries).1-3 In normal temperatures, the brain can tolerance ischemia for up to 5 minutes maximum, which is definitely not enough time to do these types of procedures. Therefore, to increase this time, we have to cool down the patient’s body. For this purpose, the patient’s body is cooled down to about 18°C, in which organs and especially the brain can tolerate the circulatory arrest more safely. There are a few points to be considered for a safe outcome. The minimum time required from the start

CHAPTER 37  Principles of Cardiovascular Surgery of CPB to reach deep hypothermic circulatory arrest should be 30 minutes to ensure the patient’s body is uniformly cooled down to the desired temperature. However, we are more likely to achieve this goal if this time is extended up to 60 minutes. The temperature gradient difference between heater-cooler device and the patient’s body should be a maximum of 10°C. Brain arteries can selectively be perfused, which can be through either antegrade or retrograde methods. Of course, the antegrade method is more acceptable. 

MYOCARDIAL PROTECTION During heart surgery, to be able to perform surgery on a silent heart or take action on the cardiac chambers, particularly, inside them, the heart must be in an arrested condition. For this purpose, the ascending aorta is clamped, and cardioplegia solution is infused into the aortic root to perfuse the coronary arteries. The main ingredient of this solution is potassium, with a concentration of about 20 mEq/L, as an initial dose for induction to arrest the heart. And for the subsequent doses, the usual potassium concentration is considered to be about 10 mEq/L. The volume of cardioplegia solution for induction in adults is around 750 to 900 cc in a 3-minute -period; this amount is more for enlarged and hypertrophied hearts with perfusion pressure of 30 (mm Hg). Subsequent doses should be 250 cc within a 1-minute period. The safest interval time between doses of cardioplegia solutions is usually about 20 minutes. However, this period has been increased to more than 1 hour with the new cardioplegia HTK solutions. Even though crystalloid solution was primarily used as cardioplegia, in recent years, the most widely used new solution is blood cardioplegia. In terms of optimum temperature, cardioplegia solution used to be applied cold at the beginning of cardiac arrest induction; however, considering that the enzymatic activity of the heart is stopped in cold temperatures yet myocardial cooling does not significantly affect the amount of myocardial oxygen consumption, most cardiac surgeons apply warm to tepid cardioplegic solution. Another delivery method of cardioplegia is retrograde cardioplegia infused through the coronary sinus, which is performed by embedding a special cannula. This method contributes a great deal to heart protection, and it is not usually used as an initial dose of cardiac arrest induction, but it is used in subsequent doses. The injection pressure of the cardioplegic solution must

649

definitely be checked in this method. The acceptable pressure is 20 to 40 mm Hg. A possible complication of this method is a lack of appropriate protection for the right ventricle. 

POSTOPERATIVE CARE Because hemodynamic instability, postoperative bleeding, electrolyte abnormalities, and arrhythmia are common after cardiac surgeries, such patients are usually transferred to the intensive care unit (ICU) under intravenous sedation and intubation for safe postoperative care. Proper circulation must be ensured immediately after the patient is transferred to the ICU bed. Setting up multiple monitors, all intubation and fusion pumps for the patient’s medications by the nursing group can take some time. Natural color and warmth of patient’s feet along with the normal dorsalis pedis and posterior tibialis artery ulses, consistent with the arterial line pressure, can ensure the patient’s sufficient circulation. A low output state with hypotension is one of the most important early complications after open heart surgery that could have various cardiac and noncardiac causes.

Insufficient Preload Vasodilatation secondary to the anesthetics and vasodilators such as nitroglycerin nitroprusside is a common complication. However, hypovolemia is the common cause of low preload after cardiac surgery. Fluid sequestration after open heart surgery, excessive diuresis caused by diuretics, increased insensible loss caused by mechanical ventilation, and subtle or obvious bleeding are the most important causes of hypovolemia. Surgical bleeding has always been one of the challenges for cardiac surgeons. A decrease in the patient’s hematocrit level without evident bleeding maybe secondary to the tamponade or clotted hemothorax and gastrointestinal or retroperitoneal bleeding. The patient’s general appearance and chest bottles should be checked. When the patient is pale and the chest bottle is filled with significant bloody drainage, prompt surgical management should be started. Otherwise if there’s no obvious bleeding and the patient’s hypotension is assured, we need to check for other possible causes. Make sure the administered doses of vasodilator were not excessive. Check the central venous pressure (CVP) and the patient’s hematocrit level, and control the trend of hematocrit level changes. Compensate volume depletion by administrating colloid and crystalloid solutions, and then seek the cause of bleeding, compensate for anemia, and control the bleeding.

650

Practical Cardiology

Low-risk patients do not need blood transfusion when the hemoglobin (Hgb) level is more than 8 g/L. For younger patients, we can even wait up to 7 g/L of Hgb. However, an Hgb level higher than 8 g/L is necessary for high-risk patients, such as older adults or patients with congestive heart failure or chronic obstructive pulmonary disease. Unnecessary transfusions may increase the mortality and morbidity rates.4 While compensating for anemia, the origin of the bleeding must also be determined. Check the coagulation tests and patient’s coagulation status with rotational thromboelastometry) (ROTEM) if available, and compensate for coagulation factor deficiency exclusively (target therapy). ROTEM can contribute to proper management of postoperative bleeding.5,6 If there is no important coagulopathy but postoperative blood drainage continues, mediastinal reexploration must be performed after hemodynamic stabilization and resuscitation. There is no reason to continue with conservative management, if the patient has more than 200 cc/hr of drainage or the total bleeding volume is more than 1000 cc (10–15 cc/kg of valves) within the first hours after surgery. For a pale patient who has a sudden drainage of more than 400 cc and hemodynamic instability, no further time should be wasted on the possibility of coagulopathy or other causes. These patients usually have a life-threatening surgical bleeding. Therefore, while resuscitation is done with blood and crystalloid solution, the patient should be transferred to the operating room along with the surgical and anesthetics teams. It should be noted that unusual doses of inotropes without enough resuscitation are not effective. In hypotensive patients with elevated CVP, cardiac tamponade is the most important differential diagnosis. Oliguria can be considered diagnostic for cardiac tamponade in the presence of high CVP, low blood pressure, and tachycardia. Several other factors such as having a Swan-Ganz catheter and bedside echocardiography can also be helpful for the diagnosis of cardiac tamponade. In suspicious cases, chest radiography findings may be useful; a wider or denser mediastinum shadow in comparison with the preoperative chest radiographs may reflect clot formation in the pericardial sac and tamponade. Echocardiographic findings (transthoracic echocardiography, TEE) can be very helpful to differentiate among the various causes of hypotension. Diagnostic delays may result in prolonged hypotension, cardiac arrest, or irreversible organ damage. Therefore, when there is a high suspicion for tamponade clinically, do not wait for imaging. If the patient is

in shock and does not have adequate perfusion pressure, emergent opening of the sternum would be lifesaving secondary to immediate mediastinal pressure removal and venous return improvement. In selected cases, sternal wire removal in the ICU may result in a quick recovery of the patient’s pressure and allows the patient to be transferred to the operating room in a more stable and safer condition. 

Cardiac Causes Low cardiac output syndrome and residual cardiac pathologies are two important causes of postoperative hypotension. Incomplete revascularization, a suboptimal valve repair result, and residual intracardiac shunt may reduce cardiac performance in the postoperative period. Poor myocardial protection during open heart surgeries plays a major role in low-output states. Inappropriate cardioplegic solution dose, content, or infusion route may permanently damage myocytes during the ischemic cardiac arrest period. Temporary functional myocyte damage is more common, so-called stunning that may continue from a few minutes to a few hours, leading to a low-output state in patients. It is a self-limiting condition; however, impaired tissue perfusion requires life support measures and the use of an inotrope or even an intraaortic balloon pump (IABP). Postoperative left ventricular (LV) failure may be caused by perioperative myocardial infarction (MI) or poor myocardial management during open heart surgery. Incomplete revascularization, coronary embolization or thrombosis of the graft, postaortic valve replacement (AVR) damage or functional stenosis of coronary artery ostia, coronary artery damage during other valve surgeries, and severe perioperative hypotension both during induction of anesthesia or during surgery are all of the known causes of postoperative MI. 

Increased Ventricular Afterload Increased ventricular afterload is the other cause of postoperative hypotension. Hypoxia, restlessness, or even aggressive suctioning of the endotracheal tube can easily cause increased LV afterload. These are generally well tolerated by the patients; however, in patients with low cardiac reserve, it can be dangerous. Ventricular septal defect closure or even mitral valve repair (MVr) in patients with severe mitral regurgitation (MR) can increase LV afterload and result in low cardiac output, especially in patients with significant LV dysfunction. Increased right ventricular afterload during a hypertension crisis or pulmonary embolism, in addition to

CHAPTER 37  Principles of Cardiovascular Surgery causing hypoxia through the displacement of ventricular septum and reduced LV preload, can lead to a lowoutput state and hypotension. 

APPROACH TO A LOW-OUTPUT STATE Approaches for dealing with the cases in which reduced preload causes hypotension were explained in the previous pages. Hypotension caused by stunning manifests itself from the very beginning when the CPB machine detachment is done. These types of patients are infused with low to moderate doses of inotrope before being transferred from the operating room to the ICU. Postoperative MI is one of the most important causes of low-output syndrome. MI can manifest itself in a variety of ways after open heart surgery. Unstable hemodynamics or ventricular tachyarrhythmia may be the main clinical presentation of early postoperative MI. The practitioner should check for ST-T changes and other new findings in postoperative electrocardiogram; check the patient’s cardiac enzymes (troponin); and perform bedside echocardiography for the presence of LV dysfunction, wall motion abnormality, or any other internal cardiac pathologies such as MR. If these three diagnostic tools confirm postoperative MI, the patient’s surgeon should be consulted for a further possible surgical procedure (graft revision or additional graft), insertion of a balloon pump, or even insertion of assist devices. During the first hours after coronary artery bypass graft (CABG), MI may be caused by graft thrombosis, poor myocardial protection, technical problems such as shortness of the graft, graft under tension, a long graft or kinking of the graft, a twisted graft, spasm or dissection on arterial conduits, or air or small particle embolism. Early diagnosis and proper management can prevent transmural Q-wave MI. Urgent post-CABG coronary angiography may be helpful and diagnostic in selected stable cases. In this situation, if there is no doubt in doing complete revascularization without any complication, performing emergency angiography and possible intervention can prevent severe myocardial damage, particularly in cases where anatomy of the coronary arteries for CABG is satisfactory. When the patient’s hemodynamics are unstable and there is high suspicion for graft failure, emergent mediastinal reexploration, intraoperative TEE, graft revisions, and a possible additional procedure such as a new graft may be useful in patient management. Additional graft anastomosis and insertion of an IABP can be beneficial in early postoperative graft

651

failure to save the myocardium and prevent obvious LV dysfunction. However, if the patient has diffused atherosclerotic changes and poor coronary artery runoff, conservative management and IABP insertion to reduce afterload and myocardial oxygen demand would be the best options. Sometimes the global ischemia or postoperative MI of the patient is so severe that the conservative or even interventional measures mentioned are not enough. In this case, for patients who have a long life expectancy and if their end organs are not seriously damaged and particularly have no severe brain injury, it is advisable to consult with the patient’s surgeon about the usefulness of using assist devices or extracorporeal membrane oxygenation (ECMO). Considering the availability of assist devices, they can be properly used as a bridge to recovery, or even the bridge to transplant, based on the patient’s condition and the ruling scientific criteria. It must be noted that surgical intervention for hypotension and low cardiac state is only indicated in a small number of patients, and the majority of patients can be managed by supportive measures, including adequate oxygenation, appropriate intravascular volume, enough doses of inotropes, proper acid–base and electrolyte status, appropriate heart rate and rhythm, and even IABP insertion. 

ANTICOAGULATION Postoperative prophylactic heparin can significantly reduce the risk of thromboembolic events in patients undergoing cardiac surgeries similar to other major surgeries. For patients undergoing nonvalvular surgeries, the use of low-molecular-weight heparin (LMWH) is recommended postoperatively, but the administration of 5000 to 7500 units of unfractionated heparin (UFH) has its own advocates. The concomitant use of mechanical prophylaxis has been demonstrated.6 In patients undergoing CABG, the use of heparin prophylaxis during the first postoperative 48 hours can prevent thromboembolic complications in patients with new-onset atrial fibrillation (AF). If postoperative AF is transient, some surgeons recommend carefully continuing anticoagulation for 6 to 12 months postoperatively.

Mitral Valve Repair Patients on sinus rhythm with good ejection fraction do not require heparin immediately after surgery. Heparin can be started on the first day after surgery. Oral

652

Practical Cardiology

anticoagulation for 6 to 8 weeks in high-risk patients with thromboembolic complications can be useful, and international normalized ratio (INR) ranging from 2 to 2.5 is sufficient.7-9 Then aspirin 80 to 100 mg/day should be continued for 1 year. The use of a single antiplatelet can be an acceptable alternative for low-risk patients.7,9,10,11 

from 3 to 4. Mechanical valve dysfunction secondary to thrombosis usually leads to critical clinical conditions because the lower pressure gradient beyond these valves prevents opening of limited motion of valve leaflets.8,9 

Mitral Valve Replacement

Heparin-induced thrombocytopenia (HIT) is a lifethreatening adverse event that results from immune system activation caused by the heparin molecule and leads to platelet activation. HIT has two types. In type I, the immune system is not involved, and it is caused by interaction between heparin and platelets, leading to platelet sequestration and aggregation. It is also called heparin-associated thrombocytopenia. This event develops in 10% of patients, and the platelet count decreases by 30% to 50%. In type I, the platelet count usually falls below 100,000 mm3. However, it returns to normal ranges a few days after heparin discontinuation.12,13 Type II HIT develops as a result of antiplatelet factor 4 in the presence of heparin, and it is dangerous, leading to systemic intraarterial or intravenous thrombosis. It should be considered that bleeding is not common in HIT, and thrombocytopenia is consumptive. This type is referred to as the immunologic type. About 10% of patients receiving heparin may develop HIT antibody, but only 1% to 5% of them develop HIT, and 30% of these patients will have lifethreatening thrombotic complications. The probability of HIT is higher in patients receiving UFH than in those receiving LMWH (about 10 times higher). In a study, it has been shown that 1.2% of patients receiving heparin for more than 4 days develop HIT. In any patient receiving heparin, the possibility of HIT should be kept in mind, and the platelet count should be checked every 2 to 3 days. If the platelet count decreases more than 50%, especially 5 to 14 days after heparin administration, and there is no reason for thrombocytopenia such as sepsis, HIT should be strongly suspected.12,13 Systemic arterial or venous thrombosis may be the first clinical presentation of HIT. In such situations, the heparin infusion should be stopped, and another anticoagulation agent should be started along with a test for antiplatelet factor 4 in serum. Argatroban, danaparoid, and bivalirudin are direct thrombin inhibitors that may be used as an alternative to heparin. The U.S. Food and Drug Administration (FDA) has not approved dabigatran for use in patients with HIT. Bivalirudin infusion (0.15 mg/kg/hr) should be started

Heparin should be administered during the first 24 hours after surgery in patients with a history of valve thrombosis, deep vein thrombosis, and previous thromboembolic events, LV dysfunction, and large left atrium (LA). Moreover, warfarin is prescribed with 5 to 7.5 mg/day on the second postoperative day and is adjusted based on INR checking. The therapeutic range of INR in patients undergoing mechanical mitral valve replacement (MVR) without severe LV dysfunction and a lack of above-mentioned risk factors is 2.5 to 3.5. It is better to consider INR ranges 0.5 above these values in patients with old-generation mechanical valves such as Starr-Edwards valves, having a large LA, or having a low ejection fraction.6-9 In patients with a biologic mitral valve, warfarin is used for 3 months after surgery.9,10 The therapeutic INR range for high-risk patients is considered 2.5 to 3. In patients with contraindications of warfarin use, an antiplatelet is an acceptable alternative. 

Aortic Valve Replacement Patients undergoing aortic valve replacement (AVR) do not need an immediate postoperative anticoagulation during the first 24 hours unless it is for other indications such as AF. If the patient does not have a risk of bleeding, warfarin can be begun on the second postoperative day. The therapeutic range of INR for a mechanical aortic valve is usually recommended to be 2 to 3. If a patient has old-generation mechanical aortic valves, the range of INR should be higher than these values (2.5–3.5). Patients with biologic valves in the aortic position do not usually need oral anticoagulation, and using an antiplatelet is sufficient.7-9 Also, patients with aortic valve repair or aortic valve–sparing surgeries have no need for anticoagulation, and use of an antiplatelet is sufficient.9 

Pulmonary and Tricuspid Valves The use of warfarin for tissue valves in pulmonary or tricuspid positions is reasonable for 3 months. Mechanical valves in the right side of the heart need higher INR values because of lower pressures and a high probability of thrombosis, and it should range

HEPARIN-INDUCED THROMBOCYTOPENIA

CHAPTER 37  Principles of Cardiovascular Surgery and adjusted so that the activated partial thromboplastin time ranges 1.5 to 2.5 times higher than normal ranges. It should be kept in mind that the use of warfarin in patients with HIT can result in microthrombosis and consequent skin necrosis and fingertip gangrene caused by lower levels of protein C. Therefore, it is necessary to wait for some days until the platelet count is above 150,000/mm3 before warfarin therapy is started. Intravenous vitamin K should be used if the patient is already taking warfarin when diagnosed with HIT.13 Warfarin should be initiated with a dosage of less than 5 mg/day. Alternative anticoagulation should be continued for the first 3 to 5 days. If a patient with HIT has a thrombotic complication, it is better to use argatroban because it is approved by the FDA for such cases. The usual dose of this agent is 2 mcg/kg/min, but it should be adjusted for patients with liver failure or heart failure and after cardiac surgeries (0.5–1.2 mcg/kg/min). For patients with HIT after percutaneous coronary intervention (PCI) or patients with HIT requiring cardiac surgery or a cardiopulmonary pump, bivalirudin is the drug of choice.13 In patients with HIT 3 months ago and normal platelet count and negative antiplatelet factor 4 who need PCI or cardiac surgery, the use of UFH may not be problematic.

653

and papillary muscles remain intact. However, for MVR in a patient with degenerative mitral valve pathology and failed MVr during an MVR for degenerative MR, it is better to save both leaflets or at least posterior leaflets along with the corresponding chordae, and then the prosthetic valve is placed in the native valve and sutured to the annulus of the native valve (valve-invalve technique). The latter technique better saves LV function and decreases atrioventricular groove rupture. It has been also demonstrated that saving the subvalvular apparatus does not lead to an increase in thromboembolic events.14 Continuous and interrupted suturing are the two main techniques used for suturing the prosthetic valve to the annulus of the native valve; however, there is no superiority of one technique over another, and they are selected based on surgeon’s preference and experience. The selection of valve type is based on the patient’s age, sex, background of diseases, life expectancy and survival, pregnancy, valve position, and socioeconomic status. Obviously the final decision should be made after the patient and family members have gone through a complete description and are enlightened regarding the advantages and disadvantages of their choices (Table 37.1). MVr is the standard

Mitral Valve Surgery The standard approach for mitral valve (MV) surgery is via midsternotomy. After CPB and arresting the heart with cardioplegic solution, the LA is opened longitudinally through the entrance of the right pulmonary veins. A transseptal approach is another option to expose the MV through an iatrogenic atrial septal defect. This option can be used in patients with concomitant tricuspid surgery or redo mitral surgeries. The third technique for exposing the MV is incision in the roof of the LA (between the ascending aorta and superior vena cava [SVC]) that gives good exposure to the MV. The use of less invasive procedures for the MV is increasing in daily practice. There are two main techniques of minimally invasive procedures, including da Vinci robot and video thoracoscopic access. A right mini-thoracotomy and peripheral arterial cannulation (i.e., femoral vein and artery) is used in both techniques for CPB establishment and valve surgery. MVr and MVR are the two main and common procedures for MV disease. MVR is generally limited for patients with dominant mitral stenosis in which thickened, calcified, and inflexible leaflets prevent the surgeon from doing an appropriate MVr. During an MVR procedure in rheumatic MV with high scores, both leaflets and thickened chordae are resected completely,

TABLE 37.1

Different Types Prosthetic Heart Valves Type of Prosthesis Mechanical valve

Tissue valves

Group

Brand (Examples)

Caged-ball

Starr-Edwards

Tilting disc (mono-leaflet) Bileaflet

Bjork-Shiely Medtronic-Hall St. Jude On-X Sorin (Carbomedics)

Stented

Carpentier-Edwards Edwards-Perimount Edwards-Magna Pericarbon More St. Jude Trifecta Biocore (Epic) FreeStyle Toronto SPV

Stentless (only for aortic ­position) Sutureless (only for aortic position)

Sorin (Perceval) Medtronic (3F Enable) Edwards (Intuity Elite)

654

Practical Cardiology

TABLE 37.2

Carpentier Mitral Regurgitation Classification Classification

Type I

Type II

Type IIIa

Type IIIb

Leaflet motion status

Normal

Increased

Restricted Systolic and diastolic

Restricted in systole And tattered in diastole

Pathology

Annular dilatation Leaflet cleft or ­perforation

Leaflet prolapse Chorda or PM rupture

Commissural fusion Thickened/calcified leaflet +/- subvalvular apparatus

PM displacement and chorda tattering

Clinical diagnosis

FMR Endocarditis Congenital MV cleft

Degenerative MR Barlow disease Flail MV

Rheumatic disease

IMR LV aneurysm

Schematic MR jet mechanism

FMR, functional mitral regurgitation; IMR, ischemic mitral regurgitation; LV, left ventricular; MR, mitral regurgitation; MV, mitral valve; PM, papillary muscle.

operation for degenerative diseases of the MV and some congenital MV diseases. Selection of the MVr technique is based on the Carpenter classification (Table 37.2). Generally, type II cases, which are MV prolapse caused by elongated or ruptured chordae of at least one scallop of the MV, are generally repaired by neochordae. The neochorda is usually a PTFE (polytetrafluoroethylene) suture that comes from papillary muscle to the free edge of the prolaptic leaflet to create good coaptation depth between two mitral leaflets. Resection or plication of the prolaptic scallop of the MV is another technique that is generally used for a prolaptic posterior leaflet. An annuloplasty ring with a complete ring or band is a part of the MVr that is chosen by the surgeon’s preference and the pathology of the MV. In type I MR, the repair technique is mainly focused on minimizing and repairing the annulus, which is usually performed by complete and rigid rings. MVr in type III is more complex and may include different techniques and a combination of augmentation by a pericardial patch, resection of secondary chordae, and papillary muscle approximation. 

Aortic Valve Surgery Patient–prosthesis mismatch (PPM) remains a challenging issue in aortic surgery and is defined as iEOA (indexed effective orifice area/BSA) less than 0.85. When the iEOA is less than 0.75, the PPM is severe, and the patient is usually symptomatic.15,16 Despite new-generation prostheses with good EOA, some patients still need aortic root

FIG. 37.2  Aortic valve replacement with aortic root

­ nlargement with the Manougian technique using autoloe gous pericardial patch.

enlargement. A posterior root enlargement (Manougian procedure) technique is widely used and is effective with good surgical outcomes.17 In this method, the aortotomy incision is extended toward the aortic annulus and anterior mitral leaflet, and the aortic annulus is enlarged by reconstruction, creating a gap using an autologous pericardial or synthetic Dacron patch (Fig. 37.2).

CHAPTER 37  Principles of Cardiovascular Surgery

A

655

B

FIG. 37.3  A, Calcified aortic valve stenosis. B, Placement of a sutureless tissue valve (Perceval).

Normal ascending aorta

A

Aorta aneurysm

B

Ascending aorta dissection

C

FIG. 37.4  Surgical views of different forms of ascending aorta disease. A, Normal ascending aorta. B,

Aortic aneurysm. C, Ascending aorta dissection.

An anterior root enlargement technique (KonoRastan procedure) is used on complex congenital LV outflow tract obstruction with higher mortality and morbidity rates. In this technique, the aortotomy incision is extended in the right side or right coronary artery orifice toward the ventricular septum and the RV outflow tract. Then defect repair is done with two separate patches.18 Sutureless tissue valves are a good alternative for older patients with calcified aortic stenosis and a small aortic root. These valves (Perceval/Sorin, Intuity/ Edwards, 3f enable/Medtronic) can be implanted by minimally invasive approaches (Fig. 37.3).

Surgery of the aortic root aneurysm is the other challenging issue in cardiac surgery (Fig. 37.4). Because it is performed in a high-pressure area and the patients usually have underlying connective tissue disorders or old ages, the high probability of postoperative bleeding and its consequent problems may affect the patient outcome.19 The Bentall operation is a well-known procedure for some patients with ascending aorta aneurysm or type A aortic dissection, in which the entire aortic valve and aneurysmal tissues are resected and coronary ostia are prepared as a button. Then a suitable

656

Practical Cardiology

size of composite graft (prosthetic valve plus Dacron tube graft) is implanted and end-to-side anastomosis is done for both coronary artery buttons on the proper side of the composite grafts (Fig. 37.5). Valve-preserving methods (David and Yacoub operation) are usually used for patients who have normal aortic leaflets and aortic annulus size of less than 30 mm. In the David operation, the diseased aortic wall, including the Valsalva sinuses, is resected and the coronary artery buttons prepared. Then the preserved native aortic valve is reimplanted inside a cylindrical Dacron tube graft, and coronary buttons

Intramural hematoma

A

are implanted the same as for the Bentall procedure. In the Yacoub technique, the aortic resection and coronary ostia implantation are the same, but instead of valve resuspension, the rim of the remnants of the native Valsalva sinuses are anastomosed to a prefashioned cylindrical Dacron graft to create new Valsalva sinuses (Fig. 37.6). These techniques can be used for type A aortic dissection; however, because of various extensions of dissection, the distal-end anastomosis of the Dacron graft maybe different. If the side branches of the aortic arch are intact and the dissection flap only involves

Right coronary ostium

Implanted composite graft

Left coronary ostium

B

FIG. 37.5  A and B, Bentall procedure with a composite graft.

Right coronary ostium

Chronic dissecting flap

Right coronary ostium

Aortic valve

A

Native aortic valve

Dissected aortic wall

B

Left coronary ostium

Preserved aortic valve

C

FIG. 37.6  A to C, Valve-sparing aortic root reconstruction with the David technique.

Dacron tube graft

CHAPTER 37  Principles of Cardiovascular Surgery the lesser curvature of the arch, the diseased aortic wall is resected, and the distal end of the tube graft is tailored into a beveled shape and anastomosed to the arch remnant (hemi-arch techniques). If the aortic arch branches are involved with dissection, each branch can be interposed with a smaller Dacron graft, or different anastomosis technique can be specialized for each case. TCA is mandatory for arch replacement, and the antegrade (exclusive cerebral perfusion via the arterial route) or retrograde (exclusive cerebral perfusion via the SVC route) techniques may improve brain protection and increase the safe circulatory arrest time. 

Tricuspid Valve Surgery Functional tricuspid regurgitation (TR) is the main cause of tricuspid valve (TV) involvement that is secondary to left-sided heart valve diseases. During the surgical treatment of MV, when there is severe TR or moderate TR associated with a dilated annulus (i.e., maximum end-systolic diameter >40 mm or >21 mm/m2), TV repair is strongly recommended.20 Suture annuloplasty and ring annuloplasty are the two main TV repair techniques. In suture annuloplasty, the diameter of the TV annulus is minimized using a twolayered suture thread. The well-known technique of suture annuloplasty is the De-vega technique, during which the suture thread is passed through the periphery of the annulus except for half of the septal leaflet that is close to the conductive pathway. In ring annuloplasty, a specialized incomplete ring for TV is used to minimize and stabilize the TV annulus (Fig. 37.7). This technique is more common nowadays. TV rings have three types similar to MV rings, including flexible (e.g., Cosgrove band), semirigid (e.g., classic Carpentier Edwards), and rigid (e.g., Edwards/ MC3). Acceptable results have been reported using all

FIG. 37.7  Tricuspid valve ring annuloplasty with a rigid

ring.

657

ring types. There are acceptable outcomes of three types for repairing the TV. The repair of TV cannot be always performed by only applying a ring, and it sometimes needs to use neochordae, patch augmentation, resection, and plication. In cases with thickened and calcified TV leaflets such as rheumatic diseases and when the repair’s result is undesirable, the TV should be replaced by a large-sized prosthetic valve. There are some controversies regarding the selection of valve type. Advocates of biologic valves believe that the pace of degeneration is lower in the right side because of lower pressures, and when the valve destructs, it is not an emergent situation, and there is enough time to make an intervention; however, thrombosis in right-sided mechanical valves is an emergent condition. Another benefit of biologic valves is that another biologic valve can be implanted percutaneously with the “valve-in-valve” technique. On one hand, advocates of mechanical valves believe that most patients requiring TV replacement have undergone MV or aortic valve replacements by mechanical valves, and they need to take warfarin. On the other hand, right-sided mechanical valve thrombosis, either of the tricuspid or pulmonary valve, can be treated with thrombotic agents.21,22 Isolated TV surgery is done in rare cases of endocarditis or Ebstein anomaly. 

Atrial Fibrillation Surgery In this surgery, the aberrant pathways are blocked to restore sinus rhythm. James Cox has innovated this technique by implementing incision and suturing of these incisions in the LA and right atrium. The development of fibrosis in the location of cut and sew leads to the blockage of pathologic aberrant pathways. Because this technique requires experience and proficiency and the incisions are located in potentially hazardous parts such as adjacent to the MV and coronary sinus, there have been some modifications of incision number and energy source for this technique. Nowadays, during MV surgeries that require ablation of the AF, a combination of cut and sew, radiofrequency, and cryoablation is used so that in addition to desirable outcomes, the incidence of complications and bleeding is decreased. Pulmonary vein isolation is a technique limited to the pulmonary vein orifices and does not need cutting. It can be performed in some minutes using different sources of energies, and according to our experience, its success rate to restore sinus rhythm is about 65%.23 Given the minimally invasive surgeries, AF can be performed as an isolated and an off-pump surgery with acceptable results. 

658

Practical Cardiology

Pericardium Surgery Subxiphoid pericardial drainage along with pericardial window creation by a left thoracotomy are two usual approaches to massive pericardial effusion or tamponade. Radical pericardiotomy, when possible, is the classic surgical management of constrictive pericarditis (CP). The major part of the thickened (or even calcified) parietal pericardium should be resected using an off- or onpump technique. It is also important that the thickened epicardium is removed as much as possible. Two stripes of pericardium adjacent to the phrenic nerves should be preserved on each side to prevent diaphragmatic paresis. Total pericardiectomy is not possible in some cases of postoperative or tuberculosis CP because of dense adherence of diseased pericardium to the epicardium in critical locations such as the atrioventricular groove, vena cava, or coronary artery course. Despite the technical difficulties and surgical complications such as bleeding myocardial damages or even perforation of the fragile portion of the heart, patients’ late survival outcomes are usually good after total pericardiectomy.24 

CORONARY ARTERY BYPASS GRAFT The routine approach for CABG is midsternotomy, which is performed in most cardiac surgery centers. Thereafter, the left internal mammary artery (LIMA) is routinely, and almost as an essential component of CABG, harvested. LIMA harvest is recommended in the form of skeletonization because it provides more length while at the same time causing less impaired blood supply to the sternum and thereby increasing the probability of mediastinitis. Care must be taken to harvest the LIMA carefully because even an intimal injury decreases the longevity of this graft. If desired, the right internal mammary artery is used immediately after LIMA harvest is finished. If more conduits, such as the saphenous vein or radial artery, are required simultaneously with midsternotomy and LIMA harvesting, they are also open or endoscopically harvested. However, in certain cases, if the patient only has single-vessel coronary artery disease, particularly of the left anterior descending coronary artery (LAD), a small left anterior thoracotomy incision is used, which is known as minimally invasive direct coronary artery bypass (MIDCAB). In certain cases, a left lateral thoracotomy incision is used, especially in redo surgeries in which the previous LIMA graft opens into the LAD and the patient needs a graft on the obtuse marginal branch. After the conduit harvest, heparinization, and cannulation, the patient is placed on CPB. Subsequently, based on the diseased coronary artery, suitable sites for graft are reviewed and preferably marked with a knife

superficially. The main strategy for complete revascularization, which means graft bypassing all coronary arteries with a diameter of more than 1 mm and a constriction of more than 50%. After clamping the aorta and cardioplegic arrest, the prepared conduits are anastomosed to the selected targets. A suitable segment that is free of atheroma should be chosen for grafting. An incision of about 5 mm is made. Then for saphenous vein graft (SVG) or radial artery anastomosis, 7-0 polypropylene sutures are used. For LIMA anastomosis, 8-0 sutures of the same suture material are used. In the sequential bypass method, one conduit is anastomosed to more than one coronary artery. In this method, after finishing with distal anastomosis, the aortic clamp is released, and the proximal end(s) is anastomosed on the ascending aorta with a side clamp. In some patients with extensive atherosclerotic involvement endothelium must be removed along with atheroma tissues (coronary endarterectomy) in order to create an appropriate lumen for anastomosis. Usually the longevity of this type of anastomosis is less than grafts on vessels without endarterectomy.25 Thus, endarterectomy is usually avoided in our surgeries unless for poor run-off targets or when the coronary artery is opened in an inappropriate segment and there are no lumens for anastomosis. To perform endarterectomy, an incision of approximately 6 to 8 mm is made on a completely occluded coronary artery, and then with the help of an endarterectomy probe, the atheroma tissue on the opened section of vessel is removed from the adjacent walls. Maximum precision is applied to completely remove the atheroma tissue distal to the anastomosis position. To perform this, it is usually sufficient to separate the anterior part of atheroma from the remaining wall of the vessel with the help of an endarterectomy probe. Complete and precise endarterectomy may lead to better graft patency. 

OFF-PUMP CORONARY ARTERY BYPASS GRAFT With the introduction of off-pump coronary artery bypass (OPCAB), to avoid the complications of CPB, many cardiac surgeons favored this method. However, after gaining experience, they noticed the possibility of incomplete revascularization, and perhaps the quality of the anastomosis is not as desirable as with the on-pump method. Also, the complications of CPB are not significant. Most surgeons are returning to the onpump method, and presently, only about one fifth of surgeons routinely perform the OPCAB technique, with associated good results.26

CHAPTER 37  Principles of Cardiovascular Surgery

REFERENCES 1. Pouard P, Bojan M. Neonatal cardiopulmonary bypass. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2013;16(1):59–61. 2. Rice RD, Sandhu HK, Leake SS, et al. Is Total Arch Replacement Associated With Worse Outcomes During Repair of Acute Type A Aortic Dissection? Ann Thorac Surg. 2015 Dec;100(6):2159–2165. 3. Kim NH, Delcroix M, Jenkins DP, et al. Chronic thromboembolic pulmonary hypertension. J Am Coll Cardiol. 2013 Dec 24;62(suppl 25). 4. Murphy Gavin J, Reeves Barnaby C, Rogers Chris A, Rizvi Syed IA, Culliford Lucy, Gianni D. Angelini Increased Mortality, Postoperative Morbidity, and Cost After Red Blood Cell Transfusion in Patients Having Cardiac Surgery. Circulation. 2007;116:2544–2552. http://dx.doi.org/10.1161/ CIRCULATIONAHA.107.698977. Originally published online Nov 12, 2007. 5. Alizadeh Ghavidel A, Toutounchi Z, Shahandashti FJalili, Mirmesdagh Y. Rotational thromboelastometry in prediction of bleeding after cardiac surgery. Asian Cardiovasc Thorac Ann. 2015 Jun;23(5):525–529. http://dx.doi.org/ 10.1177/0218492314566330. 6. Jamieson WR, Cartier CP, Allard M. Surgical management of valvular heart disease. Can J Cardiol. 2004;20(suppl E): 7–120. 7. Dunninga J, Versteeghb M, Fabbric A, et al. Nashefg, on behalf of the EACTS Audit and Guidelines Committee. Guideline on antiplatelet and anticoagulation management in cardiac surgery. Eur J Cardiothorac Surg. 2008; 34(iss.1):73–92. 8. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease (version 2012). Eur Heart J. 2012;33:2451–2496. http://dx.doi.org/10.1093/ eurheartj/ehs109. 9. Nishimura RA, Otto CM, Bonow RO, et al. American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014 Jun 10;63(22): e57–e185. http://dx.doi.org/10.1016/j.jacc.2014.02.536. Epub 2014 Mar 3. 10. El-Husseiny M, Salhiyyah K, Raja SG, Dunning J. Should warfarin be routinely prescribed for the first three months after a bioprosthetic valve replacement? Interact Cardiovasc Thorac Surg. 2006;5:616–623. 11. Asopa S, Patel A, Dunning J. Is short term anticoagulation necessary after mitral valve repair? Interactive J Thorac Cardiovasc Surg. 2006;5:761–765. 12. Watson H, Davidson S, Keeling D. Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology. Guidelines on the diagnosis and management of heparin-induced thrombocytopenia: second edition. Br J Haematol. 2012 Dec;159(5):528–540. http://dx.doi.org/10.1111/bjh.12059. Epub 2012 Oct 9.

659

13. Ahmed I, Majeed A, Powell R. Heparin induced thrombocytopenia: diagnosis and management update. Postgrad Med J. 2007;83:575–582. http://dx.doi.org/10.1136/ pgmj.2007.059188. 14. Alizadeh Ghavidel A, Mirmesdagh Y, Harifi M, Sadeghpour An, Nakhaeizadeh R, Omrani G. The Impact of Sub-valvular Apparatus Preservation on Prosthetic Valve Dysfunction During Mitral Valve Replacement. Res Cardiovasc Med. 2012 September;1(2):55–61. 15. Alizadeh-Ghavidel A, Azarfarin R, Alizadehasl A, Sadeghpour-Tabaei A, Totonchi Z. Moderate Patient-Prosthesis Mismatch Has No Negative Effect on Patients’ Functional Status After Aortic Valve Replacement With CarboMedics Prosthesis. Res Cardiovasc Med. 2016 May;5(2):e29038. 16. Alizadeh Ghavidel A. Surgical Management of Small Aortic Root (Review article). Iran J Cardiac Surg. 2007;3: 15–22. 17. Alizadeh Ghavidel A, Omrani G, Chitsazan M, Totonchi Z, Givtaj N. Long-term results of aortic valve replacement with posterior root enlargement. Asian Cardiovasc Thorac Ann. 2014;22:1059. http://dx.doi.org/10.1177/0218492314528923. 18. Tabatabaie MB, Alizadeh Ghavidel A, Yousefnia MA, Hoseini S, Javadpour SH, Raesi K. Classic konno-rastan procedure: indications and results in the current era. Asian Cardiovasc Thorac Ann. 2006 Oct;14(5):377–381. 19. Alizadeh Ghavidel A, Tabatabaei MB, Yousefnia MA, Omrani GR, Givtaj N, Raesi K. Mortality and morbidity after aortic root replacement: 10-year experience. Asian Cardiovasc Thorac Ann. 2006 Dec;14(6):462–466. 20. Dreyfus GD, Martin RP, Chan K, Dulguerov F, Alexandrescu C. Functional Tricuspid Regurgitation: A Need to Revise Our Understanding. J Am Coll Cardiol. 2015;65(21):2331– 2336. http://dx.doi.org/10.1016/j.jacc.2015.04.011. 21. Khajali Zahra, Mohammadzadeh Shabnam, Maleki Majid, et al. Fibrinolytic therapy for Mechanical Pulmonary Valve Thrombosis. Pediatr Cardiol. 2014 Aug 22. 101007/00246-014. 22. Dehaki MG, Alizadeh Ghavidel A, Omrani G, Javadikasgari H. Long-Term Outcome of Mechanical Pulmonary Valve Replacement in 121 Patients with Congenital Heart Disease. Thorac Cardiovasc Surg. 2015 Aug;63(5):367–372. http:// dx.doi.org/10.1055/s-0034-1387129. Epub 2014 Sep. 23. Alizadeh Ghavidel A, Javadpour H, Shafiee M, Tabatabaie MB, Raiesi K, Hosseini S. Cryoablation for surgical treatment of chronic atrial fibrillation combined with mitral valve surgery: a clinical observation. Eur J Cardiothorac Surg. 2008 Jun;33(6):1043–1048. 24. Alizadeh Ghavidel A, Gholampour M, Kyavar M, Mirmesdagh Y, Tabatabaie MB. Constrictive pericarditis treated by surgery. Tex Heart Inst J. 2012;39(2):199–205. 25. Wang J, Gu c, Yu W. Short- and Long-Term Patient Outcomes From Combined Coronary Endarterectomy and Coronary Artery Bypass Grafting: A Meta-Analysis of 63,730 Patients (PRISMA). Medicine (Baltimore). 2015 Oct;94(41):e1781. 26. Polomsky M, He X, O’Brien SM, et al. Outcomes of offpump versus on-pump coronary artery bypass grafting: impact of preoperative risk. J Thorac Cardiovasc Surg. 2013 May;145(5):1193–1198.