Anesthesia for laser transmyocardial revascularization

Anesthesia for laser transmyocardial revascularization

CASE REPORTS Anesthesia for Laser Transmyocardial Revascularization D a v i d N. T h r u s h , M D NAKE MYOCARDIUM receives its blood supply through...

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CASE REPORTS

Anesthesia for Laser Transmyocardial Revascularization D a v i d N. T h r u s h , M D

NAKE MYOCARDIUM receives its blood supply through a network of channels that communicate directly with the ventricle, rather than through epicardial vessels seen in humans. Transmyocardial revascularization (TMR) is an experimental procedure that attempts to duplicate this anatomy in patients with diffuse distal coronary artery disease unamenable to coronary artery bypass grafting (CABG) or angioplasty. For this reason, the procedure has been called the" snake operation" and was first attempted in 1965 by Sen et al, 1 who used needle acupuncture to create multiple channels through ischemic myocardium. Unfortunately, these channels fibrosed and closed within weeks, offering little long-term benefit. More recently, the carbon dioxide (CO2) and holmium:yttrium-aluminumgarnet (Ho:YAG) lasers are being used as an alternative to needle perforations in the hope that channels created by laser might epithelialize and remain patent longer. 2"4 If successful, this technique would provide an alternative treatment for patients with coronary artery disease refractory to conventional therapies. The following case is presented to illustrate the anesthetic considerations for such a procedure.

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CASE REPORT

A 49-year-old, 80-kg man was experiencing class IV (Canadian Heart Association) angina, despite a four-vessel CABG operation 5 years ago and maximal medical therapy. Medical history was significantfor an inferior myocardial infarction, and medications included nifedipine (20 mg three times daily), metoprolol (50 mg twice daily), isosorbide dinitrate (40 mg four times daily), amiodipine (10 mg/day), and aspirin (375 mg/ day). Recent cardiac angiography showed small, diffusely diseased coronaries, occluded vein grafts, and a patent internal mammary artery graft. Ejection fraction was 40%, and mild pulmonary hypertension was noted. Persantine-thallium scanning showed, on poststress images, defects in the lateral and inferior walls of the left ventricle. Reperfusion of the lateral wall occurred, but the inferior defect was fixed. Wall motion studies showed good motion of the septum, but the other walls showed considerable dyskinesia. Because the patient was not considered an appropriate candidate for repeat CABG or angioplasty and his symptoms were persisting despite medical management, he was enrolled in a protocol for TMR treatment with the holmium laser. Inclusion criteria for the protocol were as follows: class IV angina (Canadian Heart Association); ejection fraction greater than 25%; greater than 10% reversibility in a myocardial defect located in the inferior two thirds of the left ventricle; and unsuitable for CABG or angioplasty. Patients were randomly assigned to either a TMR or medical treatment. In the TMR group, the entire left ventricle was treated with the laser, not just the areas of reversible ischemia.

Before induction of anesthesia, radial arterial and pulmonary artery catheters were inserted. Induction of anesthesia and muscle relaxation were accomplished with fentanyl (50 ~tg/kg), midazolam (0.1 mg/kg), isofurane in 100% oxygen, and pancuronium (0.1 mg/kg). Maintenance of anesthesia was with additional doses of fentanyl (50 pg/kg), pancuronium (0.1 mg), midazolam (0.1 mg/kg), isoflurane, air, and oxygen. The trachea was intubated with a single-lumen 7.5-Fr PVC tube. Hemodynamic values immediately after induction of anesthesia were blood pressure = 105/60 mmHg, pulmonary artery pressure = 32/16 mmHg, pulmonary artery occlusion pressure = 14 mmHg, and cardiac index = 1.8 L/min/m2. Prophylactic lidocaine (100 mg) and magnesiurn (2 g) were administered intravenously followed by a continuous infusion of lidocaine at 2 mg/min. Subsequently, the patient was turned to a 45 ° right lateral decubitus position. The anteriolateral thorax was prepared and draped, and an incision was made in the sixth intercostal space, exposing the apex of the heart. Minimal retraction of the left lung was required, and ventilation of both lungs was continued throughout the procedure. To create the transmyocardial channels, energy from the pulsed Ho:YAG laser (Eclipse Surgical Technology, Inc, Sunnyvale, CA) was applied directly to the epicardium through a l-ram fexible, multistranded quartz-glass fiber, which was advanced through a J-shaped stainless steel guide with a flat, circular pad at the end of the guide (Fig 1). The pad and fiber were oriented perpendicular to the surface of the myocardium. The fiber was advanced through the myocardium as the laser was pulsed. The Ho:YAG laser pulsed at five times/sec with a pulse duration of 250 microseconds. Six to eight pulses were used for each channel. Channels were placed approximately 1 per square centimeter in areas of myocardium at risk for ischemia. Transesophageal echocardiography (TEE) in shortaxis view was used to verify complete perforation of the myocardium. Photomolecular destruction of red blood cells with production of elemental gases occurs when the laser contacts red blood cells, and, during TEE, it appears similar to air bubbles injected into the heart (Figs 2, 3). Once the heart was adequately exposed, the protocol was to make 10 perforations in

From the Department of Anesthesiology, University of South Florida College of Medicine, Tampa, FL. Address reprint requests to David N. Thrush, MD, Department of Anesthesiology, University of South Florida College of Medicine, 12901 Bruce B. Downs Blvd, MDC 59, Tampa, FL 33612-4799. Copyright © 1997 by W.B. Saunders Company 1053-0770/97/1104-0015503.00/0 Key words: myocardial revascularization, laser transmyocardial revascularization, snake myocardium, snake operations.

Journal of Cardiothoracic and Vascular Anesthesia, Vol 11, No 4 (June), 1997: pp 481-484

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Fig 1. Flexible multistranded quartz-glass fiber passing through the J-shaped stainless steel guide with circular pad at end. (Photo courtesy of Eclipse Surgical Technologies, Inc, Sunnyvale, CA. Copyright © 1996 Eclipse Surgical Technologies, Inc. All rights reserved.)

five different areas of the left ventricle: anterolateral, posterolateral, inferior, lateral, and apical. The most difficult areas to reach were treated first. Because the heart had to be lifted to treat posterior aspects of the left ventricle, significant deterioration in blood pressure and cardiac function occurred for short periods during and after this manipulation. Soon after laser therapy was begun, cardiac index decreased to 1.4 L/min/m2 and pulmonary artery pressures increased to 46/24 mmHg. Dobutamine (5 ~g/kg/min) increased cardiac index to 2.5 L/min/m2, but pulmonary artery pressure remained at 48/19 mmHg with an occlusion pressure of 18 mmHg. The original plan was to treat five areas of the left ventricle with 10 perforations each, but after the 41st channel was made, laserinduced ventricular tachycardia degenerated into ventricular fibrillation. The fourth direct defibrillation attempt (30, 40, 50, and 75 joules) was finally successful in converting the rhythm to sinus. Immediately after this incident, blood pressure and cardiac index were 85/45 mmHg and 1.2 L/min/ma, respectively, and 2- to 3-mm ST-segment elevations were noted in leads II and Vs. Similar ST depressions were noted in aVR. The anterior and lateral walls were hypokinetic by TEE. Norepinephrine, 0.05 to 0.10 ~g/kg/min, and nitroglycerin, 1 to 5 ~tg/kg/ min, were titrated with immediate improvement in blood pressure, cardiac output, and regional wall motion. There was a

Fig 3. Photomolecular destruction of red blood cells by the laser appears like bubbles in the left ventricle on TEE.

more gradual improvement in ST segments. No further channels were created. The apical portion of the left ventricle was not treated. Light digital pressure was necessary to stop the bleeding from the perforation sites in several instances. Estimated blood loss was 800 mL and was primarily from the transmyocardial perforations. The thoracotomy was closed, and the patient was transported to the cardiac surgical intensive care unit. Norepinephrine was discontinued on arrival, but dobutamine (5 pg/kg/min), nitroglycerin (0.5 ~g/kg/min), and lidocaine (2 mg/min) were maintained. Over the following 24 hours, ST segments returned to baseline, and the patient was weaned from mechanical ventilation and inotropic support. Postoperatively, creatine phosphokinase enzymes were 1,300 units with 13% myocardial band, the electrocardiogram was unchanged, and ejection fraction by echo was 50%. The patient was discharged to the nursing floor on postoperative day 3 without further complication. Six months postoperatively, the patients reported greater activity with less pain. Angina class was reduced from IV to II. Repeat persantine-thallium scan showed smaller defects in the lateral and inferior walls of the left ventricle with less redistribution in the lateral wall than previously reported. Gated study showed normal wall motion with the exception of the inferior wall. DISCUSSION

Fig 2. Long-axis view of the left ventricle and aortic outflow tract by TEE before perforation of the ventricle with the laser.

Although the anesthetic considerations for TMR and other maj or cardiac operations share some similarities, special consideration should be given to the type of patient receiving this treatment and the effects of the procedure. For instance, patients selected for TMR are at significant risk for perioperative cardiac complications because of the severity of their coronary artery disease. Many of these patients continue to have unstable angina, despite undergoing multiple CABG or angioplasty procedures and receiving maximal medical therapy. Coronary vasculature is diffusely diseased with marginal blood supply to vulnerable myocardium. Careful attention to myocardial oxygen supply and demand is obviously necessary during the anesthetic course to prevent myocardial ischemia, dysfunction, and infarction. If myocardial ischemia occurs perioperatively, attempts to manipulate vascular tone with vasodilators may be

ANESTHESIA FOR TRANSMYOCARDIAL REVASCULARIZATION

ineffective because of coronary vessels that are already maximally dilated with multiple medications or have fixed coronary lesions. The technical aspects of the TMR operation also affect the anesthetic management. The surgical approach is through an anterolateral thoracotomy at the fifth to sixth intercostal space. Although this approach exposes most of the heart muscle, lifting is necessary so that the laser probe can be positioned behind the heart. This manipulation of the heart can cause transient interruption of coronary blood flow, myocardial dysfunction, ischemia, arrhythmia, and hypotension. Although the transient hypotension and myocardial dysfunction caused by this maneuver improved with sufficient recovery time between treatments and dobutamine, repeated manipulation of the heart in this case probably contributed to the eventual decline in myocardial performance, ventricular irritability, and ventricular fibrillation, which was triggered by the laser. Also, this incision is associated with more postoperative pain than a sternotomy, which is commonly used for other revascularization procedures. Because systemic heparinization is not necessary for TMR, administration uf local anesthetics or opiates in the subarachnoid or epidural space should be considered to provide perioperative analgesia, decrease narcotic requirements, and permit earlier extubation. This patient refused this option. Both CO2 and Ho:YAG lasers have been used for TMR. Both emit energy in the form of invisible infrared light. Because infrared light is strongly absorbed by water, and most tissues are 80% water, tissues are rapidly heated, boiled, and vaporized. Advantages are that energy can be precisely focused on a small discreet area with minimal blood loss and edema. Output from lasers is either continuous wave or pulsed. The CO2 laser emits energy as a continuous wave with intermittent burst delivered by the user. The Ho:YAG laser delivers a pulse of energy for an extremely short period (250 microseconds) to allow finer control and reduce the amount of thermal energy, damage, and edema to adjacent tissues. When using either laser, precautions to protect the patient and operating room personnel are crucial. Medical personnel in the operating room who may enter the hazard zone of the laser energy, including the patient, are required to wear safety eyeglasses or eye patches. Although the goal of TMR is to create channels and improve blood flow to ischemic myocardium, the laser can damage myocardium and transiently impair blood flow. Direct injury can occur if the laser accidentally perforates coronary vasculature, the Purkinje conduction system, or the mitral valve apparatus. This risk is theoretically reduced with the Ho:YAG laser because it vaporizes only the tissue immediately in front of the optical cable. In contrast, energy from the CO2 laser can travel further and injure tissue distal to the intended perforation. For this reason, volume-loading the ventricle has been used to keep it full when the CO2 laser is used; this is not desirable if cardiac function deteriorates. In this case, pulmonary artery occlusion pressure was used to guide fluid administration so that ventricular performance could be maintained while minimizing excessive fluid administration and edema. In addition, the laser can also induce short bouts of ventricular tachycardia that usually spontaneously convert when use of the laser is discontinued. Not surprisingly, repeated episodes of this rhythm with its associated hypotension can impair myocardial function and

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coronary blood flow. Fortunately, only a few seconds of laser are required for each perforation, and recovery time between perforations can be lengthened if myocardial dysfunction or hypotension is prolonged. Indirect injury to the myocardium can occur secondary to edema caused by the laser. As mentioned previously, the Ho:YAG laser attempts to limit edema by delivering energy for brief periods. However, some swelling is bound to occur and may compromise native coronary blood flow because of extrinsic compression, decreased ventricular compliance, and increased irritability. Also, edema may impair blood flow through newly created channels. Small "jets" of blood that initially pulsate through the perforations soon disappear, indicating that blood flow through these channels has stopped secondary to edema or clotting. Consequently, the TMR procedure actually may make blood flow to ischemic myocardium worse before it gets better. In this case, repeated insults to the myocardium probably lead to myocardial ischemia, increased ventricular irritability, and ventricular fibrillation. Obviously, the hope is that after the swelling subsides, these channels will open, become covered with endothelium, and provide blood flow to ischemic myocardium. Endothelialized channels after TMR have been reported, but animal studies of myocardial blood flow using microspheres have failed to show long-term improvement in flow after TMR. 2 However, studies in humans have reported improvement in cardiac function and anginal symptoms after the procedure. 3,4 Horvath et al4 treated 20 patients with class IV angina with laser, creating an average of 21 transmyocardial channels. One patient died of a septal infarct during hospitalization, and one patient died of a presumed arrhythmia at home. One-year follow-up showed a mean angina class of I, and significant improvement in perfusion of areas of reversible ischemia by radionucleotide scanning.3 Cooley et al3 treated 21 patients with laser transmyocardial revascularization and reported a decrease in mean angina class from 3.7 -+ 4 to 1.8 +-- 0.6. At 1-year follow-up, resting mean subendocardial/subepicardial perfusion ratio had increased by 20% -+ 9% in septal regions treated by laser, but decreased by 2% +- 5% in untreated regions. Mean resting left ventricular ejection fraction was not significantly changed after TMR. Perioperative complications included a death from ventricular arrhythmia 5 days after operation, right-sided hemidiaphragmatic paralysis immediately after operation, a brief episode of atrial arrhythmia treated medically, and a death 8 days after operation of pneumonia in a patient with chronic obstructive lung disease. In addition, a 56-year-old man died of an inferior myocardial infarction 94 days after operation, a 77-year-old man died of renal insufficiency 97 days after operation, and a 72-year-old woman died of refractory ventricular fibrillation 287 days after operation. 4 Results from the randomized, prospective investigation in which this patient participated will help determine if this treatment is superior to medical. Bleeding from the perforations is another potential complication. Because heparinization is not needed for this procedure, this risk is somewhat reduced. Usually, bleeding from perforations can be controlled with slight pressure on the epicardium. Pledgetted mattress sutures can be used on each side of the channel if bleeding persists. In preclinical trials with the holmium laser and in this case, significant postoperative

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bleeding and pericardial tamponade were not a problem. 2-4 Another potential risk associated with operating the fiberoptically guided laser system is fiber breakage and embolization. Magnesium and lidocaine were administered prophylactically to prevent ventricular arrhythmias during TMR. Although this regimen was not successful in preventing ventricular fibrillation, it is difficult not to use some type of antiarrhythmic medication during a procedure that induces multiple episodes of ventricular tachycardia in a potentially ischemic heart. Lidocaine is probably a better choice than magnesium because minimal side effects occur at therapeutic doses. 5 The rationale for giving magnesium is less clear. Unless a deficiency of magnesium is present, administration of magnesium is probably not indicated. 6,7 Also, magnesium elimination depends on intact renal function, which, if impaired, can lead to hypermagnesemia. Symptoms include sedation, decreased deep tendon reflexes, and respiratory depression. Based on these considerations, the following anesthetic plan was followed. Besides routine monitors, computerized STsegment analysis and trending and TEE were used to detect perioperative ischemia. This seemed particulary important because myocardial swelling from thermal injury could further compromise coronary blood flow. Direct measurement of radial artery blood pressure was used to detect sudden changes in blood pressure that can occur in this procedure. Significant hypotension can occur, with laser-induced ventricular arrhythmias, manipulation of the heart, and failure. A pulmonary artery catheter was used to measure cardiac output and filling pressures because of the likelihood of myocardial dysfunction. A high-dose narcotic/benzodiazepine/relaxant technique supple-

mented with low concentrations of isoflurane was chosen. The goal was to provide the necessary anesthesia and avoid any unnecessary myocardial depression, especially during manipulation of the heart or creation of the transmyocardial perforations when significant myocardial depression and hypotension could occur. For this reason, isoflurance was used to blunt the response to induction and incision, but was discontinued once the laser therapy was begun. Prolonged (at least 24 hours) intubation and mechanical ventilation were planned and considered desirable in this case, because it was believed that myocardial swelling and the risk of fatal arrhythmias and failure were high in the immediate postoperative period. If these concerns are later found to be less of a problem than originally anticipated, the technique could be modified to facilitate earlier extubation. Cardiac function probably deteriorated during the operation because of multiple factors, including manipulation of the heart, myocardial swelling, and repeated episodes of ventricular arrhythmia. Regardless of the cause, it was treated successfully with dobutamine, which increased contractility, lowered pulmonary artery pressures, and had minimal effect on heart rate. Norepinephrine was chosen for its ability to increase diastolic perfusion pressure and improve blood pressure, cardiac output, and coronary blood flow, and nitroglycerin because it dilates coronary arteries and is the drug of choice for spasm. In conclusion, the anesthetic management for TMR is unique because of the severity of the ischemic heart disease and the potential problems that can occur secondary to burning holes in the heart with a laser. Further experience with this new procedure will provide valuable information regarding the perioperative management of these patients.

REFERENCES

1. Sen PK, Udwadia TE, Kinare SG, et al: Transmyocardial acupuncture, a new approach to myocardial revascularization. J Thorac Cardiovasc Surg 50:181-189, 1965 2. Kohmoto T, Fisher PE, Gu A, et al: Does blood flow through holmium: YAG transmyocardial laser channels? Ann Thorac Surg 61:861-868, 1996 3. Cooley DA, Frazier OH, Kadipasaoglu AK, et al: Transmyocardial laser revascularization: Clinical experience with twelve-month follow-up. J Thorac Cardiovasc Surg 1t 1:791-799, 1996 4. Horvath KA, Mannting F, Cummings N, et al: Transmyocardial

laser revascularization: Operative techniques and clinical results at two years. J Thorac Cardiovasc Surg 111:1047-1053, 1996 5. Ritchie JM, Greene NM: Local Anesthetics, in Goodman and Gilman's The Pharmacological Basis of Therapeutics (ed 6). New York, NY, MacMillan Publishing, 1980, pp 300-320 6. Knopes KD, Hecker BR: Magnesium is not a valuable therapy in cardiac surgical patient. J Cardiothorac Vas Anes 5:522-524, 1991 7. Birch RF, Lake CL: Magnesium is a valuable therapy in the cardiac surgical patient. J Cardiothorac Vas Anes 5:518-520, 1991