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发表于 2009-8-21 18:50:23
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C.I-11. How would you induce anesthesia?
Midazolam, 1 to 2 mg, is given before insertion of an arterial line under local anesthesia. A smooth induction is essential to prevent hypotension, hypertension, and tachycardia. Different techniques may be used to achieve a smooth induction. For patients with good left ventricular function, anesthesia is induced with fentanyl, 5 to 10 μg/kg, and thiopental, 2 to 4 mg/kg. The patient is ventilated by mask with 100% oxygen. After administration of succinylcholine, 1 mg/kg, or pancuronium, 0.1 mg/kg, the patient is intubated. Alternatively, anesthesia is induced with thiopental, 4 mg/kg, and deepened with fentanyl, 5 to 10 μg/kg, and 2.0% isoflurane for 3 to 5 minutes. When adequately anesthetized, the patient is given a muscle relaxant and intubated. If the patient has a history of hypertension or the initial BP is more than 150 mm Hg systolically, fentanyl, 10 μg/kg, is usually required to blunt hypertension and tachycardia from intubation. For patients with poor left ventricular function, potent inhalation agents such as enflurane, isoflurane, and halothane are avoided during induction and maintenance of anesthesia. More midazolam, 2 to 5 mg, and less thiopental, 1 to 2 mg/kg, will be given for induction. Alternatively, etomidate, 0.2 mg, may be administered for induction. (See Chapter 14, section C.6, for other measures to prevent tachycardia and hypertension at the time of intubation.)
C.I-12. How would you maintain anesthesia?
Again, smooth anesthesia is essential to achieve a balance between myocardial oxygen demand and supply. Different agents and techniques may be used to accomplish the same goal. A combination of fentanyl and isoflurane is a popular choice. Alternatively, a neuroleptic technique with a moderate dose of the combination of fentanyl/droperidol/nitrous oxide/oxygen for maintenance of anesthesia may be used safely. After the patient is intubated, a mixture of 60% nitrous oxide and 40% oxygen is administered to keep the patient unconscious.
The depth of anesthesia must be titrated to meet the requirements of the varying intensities of surgical stimulation. Skin incision and sternal splitting are very painful. But the strongest stimulation is usually from sternal retraction with the self-retaining retractor. Fentanyl, 5 μg/kg, is given right before the skin incision. Droperidol, 0.1 mL/kg, is titrated in after the skin incision to keep SBP around 100 to 120 mm Hg. Another dose of fentanyl, 5 μg/kg, is given before sternotomy. Then fentanyl, 5 μg/kg, is given every 30 to 60 minutes to maintain anesthesia. Very high doses of fentanyl or sufentanil, with or without droperidol, and oxygen without nitrous oxide, have been successfully used for cardiac anesthesia. Diazepam or midazolam is administered to achieve unconsciousness and amnesia if droperidol is not used. I prefer droperidol because of its α-blocking effects, which can easily control hypertension when combined with a moderate dose of fentanyl. Meanwhile, at my institution, we believe mild cardiac depression from nitrous oxide may decrease the cardiac oxygen demand in a way similar to the effect of propranolol. The possibility of oxygen toxicity from the use of 100% oxygen should also be kept in mind. Nitrous oxide is not used after CPB, because it will increase potential air embolism in the bypass grafts, coronary circulation, and systemic circulation.
C.I-13. What is the better anesthetic agent for this operation: an inhalation or intravenous agent?
The choice of anesthetic agents is still debatable. Both inhalation and intravenous and combined agents have been used successfully. They both have advantages and disadvantages. Understanding the cardiovascular effects of each anesthetic agent and careful titration of each drug will improve the balance between myocardial oxygen demand and supply. Early detection and appropriate control of the major determinants of myocardial oxygen consumption (i.e., BP, HR, and PCWP) are mandatory if myocardial ischemia is to be avoided. Another consideration is the desirability of early extubation. High-dose narcotic and large doses of sedatives and muscle relaxants should be avoided if early extubation is planned.
Three large-scale outcome studies of patients undergoing CABG surgery reported that anesthetic choice did not affect incidence of perioperative morbidity and mortality.
C.I-14. What are the cardiovascular effects of halothane, enflurane, isoflurane, desflurane, sevoflurane, morphine, and fentanyl?
In general, halothane, enflurane, isoflurane, desflurane, and sevoflurane produce a dose-related depression in ventricular function and vascular tonus. Halothane sensitizes the heart to catecholamine much more than enflurane, isoflurane, desflurane, and sevoflurane. Isoflurane and desflurane depress cardiac output to a lesser degree than halothane or enflurane secondary to their greater vasodilating capacity. The HR changes least with halothane and increases most with desflurane. Isoflurane may cause tachycardia; the mechanism is unclear. Most studies suggest that halothane, enflurane, and isoflurane decrease coronary vascular resistance. Of these, isoflurane is the most potent coronary vasodilator.
All of the potent drugs decrease arterial pressure in a dose-related manner. The mechanism of the decrease in BP includes vasodilation, decreased cardiac output resulting from myocardial depression, and decreased sympathetic nervous system tone. With halothane, decreased cardiac output is the predominant cause. Halothane also increases venous compliance, and in patients who have high sympathetic tone, such as those with heart failure, halothane decreases systemic vascular resistance. Enflurane causes both vasodilation and decreased myocardial contractility. With isoflurane and desflurane a low peripheral resistance is the major cause of hypotension. Evidence of the relatively greater myocardial depression with halothane and enflurane is the greater increase in right atrial pressure seen with these drugs than with isoflurane.
Narcotics such as morphine and fentanyl at their clinical dose have minimal cardiovascular effects. Both may cause bradycardia. Neither sensitizes the heart to catecholamine or depresses myocardial function. The cardiovascular effects of morphine depend on the dose used. Large doses of morphine sulfate have reportedly caused myocardial lactate production and reduction in coronary blood flow in animals. Sethna and colleagues found that morphine sulfate, 0.25 mg/kg intravenously, did not produce a global myocardial ischemia in patients with CAD. High doses of morphine, 1 mg/kg, produce a significant decrease in arterial BP and systemic vascular resistance accompanied by an average 750% increase in plasma histamine. On the other hand, high doses of fentanyl, 50 file:///H:/images/special/mulower.gifg/kg, do not produce any significant changes in BP, vascular resistance, and plasma histamine levels.
C.I-15. Is isoflurane dangerous for the patient with coronary artery disease?
In patients with CAD, the use of isoflurane is still controversial. Reiz and colleagues reported that 1% isoflurane induced coronary vasodilation that was not related to normal autoregulation and that both decreased coronary perfusion pressure (systemic hypotension) and redistribution of myocardial blood flow (coronary steal) may contribute to the development of regional myocardial ischemia. Another study by Reiz and Ostman, using 1.5 minimum anesthetic concentration (MAC) isoflurane/nitrous oxide anesthesia, concluded that isoflurane may cause coronary steal with myocardial ischemia in patients with CAD. However, Smith and colleagues reported that the substitution of 0.5% to 1.12% isoflurane for 85 μg/kg of fentanyl did not result in an increased incidence of myocardial ischemia, as seen by ST-segment or segmental wall motion changes in patients with CAD. Moreover, Tarnow, Markschies-Hornung, and Schulte-Sasseu demonstrated that 0.5% isoflurane with 50% nitrous oxide improved the tolerance to pacing-induced myocardial ischemia in patients with significant CAD. Two large-scale prospective outcome studies by Slogoff and colleagues and Turman and colleagues could find no evidence that the incidence of ischemia was increased by isoflurane in patients with CAD undergoing CABG surgery. Furthermore, this finding held true even for patients with steal-prone coronary anatomy in the studies by Slogoff and colleagues, Pulley and colleagues, and Leung and colleagues.
Several animal studies further confused this issue. Priebe proved that isoflurane was a myocardial depressant and a potent coronary vasodilator in the dog. Sill and colleagues demonstrated that high concentrations of isoflurane (1.5% and 2.5%) dilated intramyocardial arterioles rather than epicardial coronary arteries in the intact dog. Buffington and colleagues reported that isoflurane (1.2% to 1.5%) produced a decrease in collateral flow and a decrement in collateral zone contraction while enhancing flow in the normally perfused zone. They concluded that isoflurane was an arteriolar vasodilator and hence produced coronary steal in dogs with chronic coronary occlusion. On the contrary, Cason and colleagues found that in the dog, isoflurane or halothane at 0.5% MAC and 1.5 MAC had little effect on coronary vascular resistance, and ischemia was precipitated by tachycardia or hypotension rather than by coronary steal. Moreover, Davis and Frank demonstrated that isoflurane decreased myocardial infarct size after left anterior descending coronary artery occlusion in dogs. In addition, Gilbert and colleagues reported greater coronary reserve in swine anesthetized with isoflurane versus halothane at 0.5 to 2.0 MAC. Recently, Hartman and colleagues demonstrated that adenosine but not isoflurane redistributed blood flow away from collateral-dependent myocardium in the presence of a coronary steal-prone anatomy in the chronically instrumented dog. They further found that reductions in myocardial perfusion during isoflurane anesthesia depend on systemic arterial pressure and that isoflurane did not produce coronary steal in this model of multivessel CAD. Furthermore, Cheng and colleagues found that neither isoflurane nor halothane as the sole anesthetic in clinical concentrations caused significant coronary vasodilation or coronary steal from 55 to 30 mm Hg coronary perfusion pressure in a swine model of chronic coronary occlusion with collateral development.
On the basis of recent animal and clinical studies, we can conclude that isoflurane in clinical concentrations may be used safely in patients with CAD provided that hypotension and tachycardia are avoided.
C.I-16. What is the cardiovascular effect of nitrous oxide?
Nitrous oxide is a weak central nervous system depressant. It has been generally considered to have minimal effects on other organ systems. Nitrous oxide has significant cardiovascular effects that may be depressant or stimulatory depending on the anesthetics with which it is used. When high-dose fentanyl is used during coronary surgery, the effects of nitrous oxide depend on the patient's cardiac function. After the administration of 50% nitrous oxide, there are no significant changes in any of the hemodynamic parameters in patients with normal left ventricular function (LVEDP < 15 mm Hg). On the contrary, there is a significant decrease in cardiac index and stroke volume index in patients with left ventricular dysfunction (LVEDP > 15 mm Hg). When added to other inhalational anesthetics, nitrous oxide increases arterial pressure and systemic vascular resistance, suggesting that it has a vasoconstrictive action. Nitrous oxide increases pulmonary vascular resistance in patients with mitral stenosis and pulmonary hypertension.
The pulmonary vascular effects of nitrous oxide are also variable. Patients with elevated PA pressure may have further increases when nitrous oxide is added. Konstadt and colleagues did not corroborate these findings in patients with mitral valvular disease. A study in infants failed to show further increases of pulmonary vascular resistance with the addition of nitrous oxide. It is of interest that the decrease in pulmonary vascular resistance with isoflurane is less than the decrease in systemic vascular resistance.
The contribution of nitrous oxide to myocardial ischemia is controversial. Philbin and colleagues suggested that addition of nitrous oxide to anesthesia with high-dose fentanyl, 100 μg/kg followed by 1 μg/kg per minute, or sufentanil, 30 μg/kg followed by 0.3 μg/kg per minute, can produce clinically inapparent regional myocardial ischemia in the areas supplied by stenotic coronary arteries of dogs. However, using 2D TEE, nitrous oxide added to low-dose fentanyl, 15 μg/kg followed by 0.2 μg/kg per minute, or high-dose sufentanil, 20 μg/kg, did not cause myocardial ischemia in patients with CAD.
Clinically, nitrous oxide may be used before CPB if high-dose narcotics are not used and hypotension does not occur. However, after CPB, nitrous oxide should be avoided because of the possibility of expanding air bubbles in the coronary and cerebral circulation.
C.I-17. What kind of muscle relaxant would you use? Why?
We usually use pancuronium. When full paralyzing doses are given in a bolus, D-tubocurarine tends to produce bradycardia and hypotension from ganglionic blockade and histamine release, whereas pancuronium and gallamine generally produce tachycardia and hypertension caused by vagolytic effect and norepinephrine released from cardiac sympathetic nerves. D-Tubocurarine may be given in increments of 6 mg every 5 to 10 minutes until patients are fully paralyzed (0.3 mg/kg). BP and HR are usually not changed by this small dose and slow injection rate. Pancuronium is a better choice if hypotension (BP < 80 mm Hg systolically) and bradycardia (HR < 50 beats per minute) are present. Theoretically, pancuronium may increase myocardial oxygen consumption caused by tachycardia and hypertension. However, pancuronium is the most commonly used muscle relaxant for CABG. In practice, most patients with CAD take file:///H:/images/special/betalower.gif-adrenergic blocking agents, which can decrease the vagolytic effect of pancuronium. Also, the bradycardia associated with the popular narcotic anesthetic techniques can attenuate the tachycardia induced by pancuronium. Vecuronium and cisatracurium have no major cardiovascular effects, but their intermediate duration of action necessitates frequent administration of the relaxant. Pipecuronium and doxacurium are two new long-acting, nondepolarizing muscle relaxants. They seem to have no hemodynamic side effects associated with neuromuscular blockade. They can be used in large bolus doses.
C.I-18. If ST-segment depression is seen during surgery, how would you treat it? What is the relationship between perioperative myocardial ischemia and postoperative myocardial infarction?
ST-segment depression indicates myocardial ischemia, either from increased oxygen demand or decreased oxygen supply. The treatment includes the following: - Increase oxygen supply: Correct hypotension and hypoxemia.
- Decrease oxygen demand: Correct hypertension, tachycardia, and increased PCWP or CVP by deepening anesthesia or by using vasodilators and propranolol. All the major determinants must be considered and corrected to their normal levels.
Gerson, Hickey, and Bainton (in experimental dogs) found that elevation of ST segments induced by occlusion of the coronary artery was more limited with halothane than with a combination of nitroprusside and propranolol. The more favorable effect of halothane was explained by its effects on coronary vascular reserve and the known effect of nitroprusside to reduce myocardial blood flow to ischemic myocardium.
If there are no obvious changes in BP, HR, and pulmonary wedge pressure, nitroglycerin is indicated for coronary spasm. Nitroglycerin may be given by intravenous drip. Sublingual nifedipine or intravenous nicardipine or diltiazem may be given to relieve coronary spasm.
In 1985, Slogoff and Keats reported that perioperative myocardial ischemia occurred in 37% of all patients undergoing CABG. They proved that perioperative myocardial infarction was almost three times as frequent in patients with ischemia (6.9%) compared with patients without ischemia (2.5%). Intraoperative tachycardia was associated with a higher incidence of myocardial ischemia and infarction. However, Knight and colleagues demonstrated that 42% of patients undergoing CABG had preoperative episodes of myocardial ischemia, 87% of which were clinically silent. They further found that anesthesia and surgery did not worsen the preoperative ischemic pattern. Furthermore, in another study in 1989, Slogoff and Keats postulated that approximately 90% of new myocardial ischemia observed during anesthesia was the manifestation of silent ischemia observed in the patient before the operation and only 10% was related to anesthetic management. Therefore, the relationship between intraoperative ischemia and postoperative outcome is still unsolved.
C.I-19. Would you use prophylactic nitroglycerin during coronary artery bypass grafting to prevent intraoperative myocardial ischemia or perioperative myocardial infarction?
No. It has been reported that prophylactic administration of nitroglycerin, 0.5 or 1.0 mg/kg per minute, during fentanyl anesthesia in patients undergoing CABG did not prevent myocardial ischemia or reduce the incidence of perioperative myocardial infarction.
C.I-20. How would you correct hypertension?
BP=blood flow/resistance
Hypertension is usually due to inadequate depth of anesthesia. Occasionally, it is due to fluid overloading. The treatment of hypertension includes the following: - Deepen the anesthesia. Inhalation agents, such as halothane, enflurane, and isoflurane are more effective than narcotics because of their vasodilator effect.
Vasodilators, when inhalation agents are not used: - Sodium nitroprusside produces more arteriolar dilation than venodilation. Dose: 10- to 100-μg per minute intravenous drip titration.
- Nitroglycerin produces more venodilation than arteriolar dilation. Dose: 20- to 200-μg per minute intravenous drip titration, or bolus in 20-μg increments.
C.I-21. How would you treat hypotension?
Hypotension is usually caused by hypovolemia, deep anesthesia, bradycardia, or CHF. The treatments are as follows: - Increase fluid infusion and put the patient in a head-down position when CVP or PCWP is low.
- Lighten the level of anesthesia or use a vasoconstrictor: phenylephrine, 0.1-mg intravenous increments, to correct vasodilation produced by anesthesia.
- Atropine, 0.2 to 2.0 mg, for bradycardia, or isoproterenol, 1 mg/100 mL of 5% dextrose intravenous drip titration, rarely indicated.
- Treat CHF when PCWP is high and TEE shows hypokinesia:
- Lighten the level of anesthesia.
- Restrict fluids.
- Diuretics: furosemide (Lasix) 20 to 40 mg intravenously
- Inotropic agents
- CaCl2 (0.5 to 1.0 g)
- Epinephrine: 2 to 8 μg per minute intravenous drip
- Dobutamine or dopamine: 5 to 20 μg/kg per minute intravenous drip
- Amrinone, 0.75 to 1.5 mg/kg, then 5 to 10 μg/kg per minute intravenous drip, or
- Milrinone, 0.05 mg/kg, then 0.5 to 0.7 μg/kg per minute intravenous drip
- Norepinephrine if peripheral vascular resistance is low
- Intraaortic balloon pump (IABP)
C.I-22. What are the indications for intravenous propranolol or esmolol during surgery? How much would you give? What are the relative contraindications?
Indications
- ST-segment depression associated with tachycardia; no response to deepening the level of anesthesia
- Supraventricular tachycardia more than 120 per minute
- Recurrent ventricular arrhythmias
Contraindications
- CHF
- Asthma, chronic obstructive pulmonary disease
However, esmolol is cardioselective and appears to have little effect on bronchial or vascular tone at doses that decrease HR in humans. It has been used successfully in low doses in patients with asthma. Esmolol is metabolized rapidly in the blood by an esterase located in the erythrocyte cytoplasm. Esmolol is a short-acting β-blocker with an elimination half-life of 9 minutes and a pharmacologic half-life of 10 to 20 minutes.
Dosages
Propranolol, 0.25-mg increments every 1 to 2 minutes, total dose 2 to 3 mg
Esmolol, 10-mg increments up to 0.5 mg/kg followed by 50- to 300-μg/kg per minute intravenous drip
C.I-23. How would you correct increased pulmonary capillary wedge pressure?
It is important to treat the patient as a whole. All monitors must be considered together, not only one single parameter. Increased PCWP is usually due to a light level of anesthesia or CHF. Combining the readings of PCWP and BP will produce a differential diagnosis. Occasionally, an increased PCWP with hypotension and low cardiac output is caused by HOCM. HOCM can be diagnosed by TEE, which demonstrates SAM of mitral valve, mitral regurgitation, and usually good left ventricular contractility.
Inadequate Anesthesia: Increased PCWP with Hypertension
- Deepen the level of anesthesia with inhalation agents, such as isoflurane, halothane, or enflurane, which also have a vasodilator effect.
- Give a vasodilator. Nitroglycerin is a better venodilator than nitroprusside.
Congestive Heart Failure: Increased Pulmonary Capillary Wedge Pressure with Hypotension and Low Cardiac Output
- Lighten the level of anesthesia.
- Restrict fluids.
- Use vasodilators.
- Give diuretics.
- Use inotropic agents.
Hypertrophic Obstructive Cardiomyopathy (Idiopathic Hypertrophic Subaortic Stenosis)
- β-Blocker to decrease HR and contractility
- Fluid loading to keep left ventricle full and decrease left ventricular outflow tract obstruction
- Increase afterload to keep left ventricle full
C.I-24. During sternal splitting, would you do something?
Stop ventilation and deflate the lungs to prevent lung injury from the electric saw.
C.I-25. Would you monitor pulmonary capillary wedge pressure continuously? Why?
No, if the Swan–Ganz catheter balloon is inflated continuously, pulmonary infarction distal to the occlusion may ensue. Usually PA diastolic pressure (PADP) is monitored continuously because PADP is very close to PCWP.
C.I-26. Discuss autologous transfusion and blood conservation for cardiac surgery.
Autologous transfusion is the collection and reinfusion of the patient's own blood or blood components. The realization that homologous blood is responsible for transmission of acquired immune deficiency syndrome (AIDS), hepatitis, transfusion reaction, and autosensitization has led to increased interest in autologous transfusion and blood conservation. There are several options for autologous transfusion: preoperative autologous blood donation, preoperative use of erythropoietin, intraoperative normovolemic hemodilution, intraoperative plasmapheresis, pharmacologic treatment, and perioperative blood salvage.
Preoperative Autologous Blood Donation
Donations are appropriate for properly selected patients with stable CAD, stable valvular disease, and congenital heart disease. The risk of blood donation may be higher for patients with unstable angina or severe aortic stenosis; these patients are usually not considered good candidates for autologous blood donation. The patient should have a hemoglobin level of more than 11 g/dL to donate blood.
The optimal donation period begins 4 to 6 weeks before surgery, and the last donation is usually collected no later than 72 hours before surgery.
Preoperative Use of Erythropoietin
This is an established and efficacious but relatively expensive therapy to reduce blood transfusions. To optimize the hemoglobin response, oral or intravenous iron supplementation is recommended.
Intraoperative Normovolemic Hemodilution
This is the removal of blood through an arterial or venous catheter immediately after induction of anesthesia, before CPB or the administration of heparin. Depending on the patient's size and hematocrit level, 500 to 1,000 mL of blood is collected into blood bags containing CPDA-1 anticoagulant and is kept at room temperature.
This blood is spared the rigors of CPB, including hemolysis, platelet destruction, and clotting factor degradation. The autologous blood is transfused after reversal of the heparin with protamine. It has been demonstrated that the effect of 1 unit of fresh whole blood on platelet aggregation after CPB is at least equal, if not superior, to the effect of 8 to 10 stored platelet units. However, if the patient's hematocrit level is less than 33% or the hemoglobin level is less than 11 g/dL, normovolemic hemodilution is not recommended because further decreasing the oxygen-carrying capacity may worsen myocardial ischemia. In addition, hemodilution during CPB will further decrease the hematocrit to levels that require homologous blood transfusion. Normovolemic hemodilution should be performed cautiously in patients with critical left main coronary stenosis and aortic stenosis because sudden cardiac arrest has been observed during the procedure.
Intraoperative Plasmapheresis
Coagulopathy associated with hypothermia, shock, CPB, multiple transfusions, and the blood salvage technique, which removes clotting factors and platelets, often necessitates use of fresh frozen plasma and platelet packs to control postoperative bleeding and clotting problems. Recently a plasma-collection system has been developed to salvage up to 1,000 mL of platelet-rich plasma before CPB. This technique does not cause hemodilution, so it can be used in all patients, including those with anemia. The platelet-rich plasma can be stored at room temperature until transfused, usually after protamine reversal of the heparin. It is recommended that the collected product be placed on a rocker until infusion and that the pH level be held constant.
Pharmacologic Treatment
The prophylactic use of aprotinin, ε-aminocaproic acid (EACA) and tranexamic acid reduces blood transfusions in cardiac surgery. Aprotinin inhibits a host of proteases, including trypsin, plasmin, kallikrein, and factor XIIa activation of complement. The adult dose is 2 million kallikrein-inhibition units (KIU) for the patient and bypass pump, followed by 500,000 KIU per hour for 4 hours. The synthetic antifibrinolytics, EACA and tranexamic acid, bind to plasminogen and plasmin, thus inhibiting binding of plasminogen at the lysine residues of fibrinogen. Effective antifibrinolysis requires a loading dose of 100 to 150 mg/kg for EACA or 10 mg/kg for tranexamic acid and a constant infusion for each at one tenth the loading dose each hour.
Perioperative Blood Salvage
This is the collection and reinfusion of blood lost during and immediately after surgery. The posttransfusion survival of perioperatively salvaged red blood cells has been shown to be comparable to that of allogeneic red blood cells. At the conclusion of CPB, all blood remaining in the oxygenator and bypass circuits should be salvaged and if needed infused. Blood salvaged intraoperatively may be transfused directly (unwashed) or processed (washed) before infusion. Commercially available equipment exists for each option. Blood collected by intraoperative salvage represents an excellent source of red blood cell support. However, salvaged blood is deficient in coagulation factors and platelets.
Postoperative blood salvage is another technique of autologous blood transfusion using blood lost after surgery. Blood salvaged after cardiac surgery is generally collected from mediastinal and chest drains and transfused without washing. Because it is usually defibrinated, it does not require anticoagulation before transfusion. Though dilute, the blood is sterile and contains viable red cells. |
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