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Anesthesia for pulmonary thromboendarterectomy

Anesthesia for pulmonary thromboendarterectomy
Literature review current through: Aug 2023.
This topic last updated: May 13, 2022.

INTRODUCTION — Pulmonary thromboendarterectomy (PTE) is the only definitive and potentially curative therapy for chronic thromboembolic pulmonary hypertension (CTEPH). This topic reviews anesthetic management during surgical PTE procedures. Preparation for PTE, surgical management, postoperative care, and outcomes for PTE procedures are discussed separately. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy".)

Initial management, evaluation, and selection of patients with CTEPH for surgical or medical therapy are also discussed separately. (See "Chronic thromboembolic pulmonary hypertension: Initial management and evaluation for pulmonary artery thromboendarterectomy".)

PREANESTHETIC CONSULTATION — General principles for preanesthetic consultation before cardiac surgical procedures are discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Preanesthetic consultation'.)

Preanesthetic assessment for PTE focuses on the planned surgical approach (table 1), the patient's functional cardiopulmonary status, and any clinically significant comorbidities. Preoperative collaboration among interdisciplinary teams (pulmonology, surgery, cardiology, critical care) is necessary to ensure optimal patient condition. (See "Chronic thromboembolic pulmonary hypertension: Initial management and evaluation for pulmonary artery thromboendarterectomy".)

Overview of surgical techniques for pulmonary thromboendarterectomy

Standard open approach and modifications The standard surgical technique for PTE is performed via a median sternotomy and relies on cardiopulmonary bypass (CPB) with deep hypothermia and elective circulatory arrest (DHCA) to achieve optimal surgical conditions [1]. With relatively short episodes of full circulatory arrest during DHCA, neurologic outcomes are similar to those after use of more moderate hypothermia plus selective antegrade cerebral perfusion (SACP), and visualization in the surgical field is superior with the standard technique [2,3]. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy", section on 'Standardized approach'.)

Alternative techniques to accomplish PTE have been developed in an effort to reduce the neurologic complications of hypothermia and circulatory arrest [1,4]. These include the use of moderate rather than deep hypothermia SACP with or without total circulatory arrest [5]. One report describes a technique using moderate hypothermia without elective circulatory arrest, with use of negative pressure venting of the left heart chambers to maintain a bloodless surgical field and continuous adjustments of CPB pump flow to maintain mixed venous oxygen saturation (SvO2) >65 percent [6]. However, morbidity (eg, neurologic outcomes) and mortality benefits have not been demonstrated for alternative techniques compared with DHCA with elective circulatory arrest. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy", section on 'Alternative techniques'.)

Minimally invasive approach A minimally invasive surgical approach for PTE (MIS PTE) employing bilateral mini-thoracotomies has also been described [7]. For this technique, a double lumen endotracheal tube or bronchial blocker is necessary to achieve lung isolation and sequential one lung ventilation on each side (see "Lung isolation techniques" and "One lung ventilation: General principles"). The arterial cannula is inserted centrally in the ascending aorta, while venous cannulae are inserted peripherally in the femoral vein and right internal jugular vein. Pulmonary arterial, left atrial, and aortic root vents are used to maintain a bloodless surgical field. Standard DHCA with elective circulatory arrest is employed, but periods of circulatory arrest to accomplish thromboendarterectomy on each side are brief. Cross-clamping of the aorta and use of cardioplegia are avoided. Compared with patients undergoing conventional PTE, improvements in pulmonary vascular resistance (PVR) and lung perfusion were similar in those undergoing minimally invasive surgery, while duration of circulatory arrest and length of hospital stay were shorter [7]. However, minimally invasive pulmonary endarterectomy is not considered for patients with obesity, distal thromboembolic disease, or those who are undergoing concomitant cardiac procedures.  

Patient assessment

Cardiopulmonary pathophysiology — Patients scheduled for PTE typically have chronic thromboembolic pulmonary hypertension (CTEPH) resulting in right ventricular (RV) strain or failure [8]. Available electrocardiograms, chest radiographs, pulmonary function tests, ventilation-perfusion (V/Q) scans, computed tomography (CT) angiography, cardiac echocardiography, right heart catheterization, and coronary angiography results are reviewed to understand patient risk (table 2):

Pulmonary pathology

Severity of pulmonary hypertension and increases in PVR. Poor outcomes are associated with preoperative PVR >1200 dynes-second/cm5 or <50 percent relative reduction in postoperative PVR [9,10].  

Other pulmonary pathology, including the degree of pulmonary clot burden, ventilation-perfusion (V/Q) mismatch, and the presence of intimal irregularities or pulmonary vascular webs noted on the VQ scan and/or CT angiography [11].

Some patients with CTEPH develop dilated bronchial arteries with varying degrees of bronchopulmonary collateral arteries to maintain perfusion in the vasculature distal to the pulmonary occlusion [12]. Resulting luxury perfusion in these vessels may predispose these areas to early reperfusion pulmonary edema after sudden relief of obstruction. (See 'Pulmonary complications' below.)

Some centers employ preoperative transcatheter occlusion of bronchopulmonary collateral arteries to improve post-PTE hemodynamics, reduce incidence of reperfusion pulmonary edema, and improve overall outcomes, particularly in patients who have CTEPH with a history of hemoptysis [13,14].

Cardiac pathology

Presence and severity of RV failure, as well as presence of concomitant left ventricular (LV) dysfunction or failure. Significant systolic or diastolic dysfunction of the RV or LV are risk factors for intraoperative hemodynamic instability.

Presence of tricuspid regurgitation or other cardiac valve pathology, which may require concomitant repair (eg, tricuspid valve annuloplasty) [15].

Presence of a patent foramen ovale (PFO) on echocardiography, which may necessitate concomitant PFO repair to avoid postoperative right to left shunting [15].

Presence of coronary artery disease, which may necessitate a concomitant coronary artery bypass grafting procedure to avoid myocardial ischemia [15].

Potential need for extracorporeal membrane oxygenation (ECMO) – ECMO may be employed in selected patients with cardiopulmonary instability to enable end organ recovery and achieve optimal patient condition before or during PTE surgery. [16]. Insertion of cannulae for initiation of ECMO support is described in a separate topic. (See "Extracorporeal life support in adults in the intensive care unit: The role of transesophageal echocardiography (TEE)".)

For patients already on ECMO, their cannulation sites, vascular access sites, anticoagulation status, ventilator settings, and ECMO flow rates should be carefully recorded to plan a smooth transition to intraoperative care and CPB.

Comorbidities affecting anesthetic management — (table 2)

Hematologic

Hypercoagulable states – Patients with CTEPH often present with coexisting hypercoagulable states such as lupus anticoagulant, antiphospholipid antibodies, protein C and S deficiencies, dysfibrinogenemia, antithrombin III deficiency, or secondary polycythemia. Patients are typically maintained on vitamin K antagonists for life-long thromboprophylaxis; however, some may be taking direct oral anticoagulants (DOACs) [17]. Dosage should be documented and preparations made in case specific reversal agents are needed. (See "Perioperative management of patients receiving anticoagulants".)

Management of these agents in the immediate preoperative period is discussed below. (See 'Preoperative medication management' below.)

Sickle cell disease (SCD) – Patients with SCD have a high risk for sickling crisis during PTE surgery [18,19]. We bring the percentage of hemoglobin S variant (HbS or sickle hemoglobin) level to ≤10 percent with preoperative exchange transfusions before the procedure. It is particularly important to avoid hypoxemia, acidosis, and low-flow states during surgery, to achieve optimal or slightly high pump flow rates during CPB, and to minimize duration of elective circulatory arrest [20-22].

Heparin-induced thrombocytopenia (HIT) – Suspected HIT is particularly challenging in a patient undergoing CPB with DHCA. Perioperative strategies include delaying surgery, preoperative administration of high-dose intravenous immune globulin (IVIG) to reduce the activity of heparin/PF4 antibodies, performing plasmapheresis prior to heparinization, use of a non-heparin anticoagulant instead of heparin, or coadministration of an anti-platelet agent with heparin. These strategies are described in a separate topic. (See "Management of heparin-induced thrombocytopenia (HIT) during cardiac or vascular surgery".)

Data regarding strategies for patients undergoing procedures with DHCA are scant. Although bivalirudin has been used in this setting, unpredictable metabolism and increased bleeding are concerns [23]. Cangrelor is a direct-acting P2Y12 platelet receptor antagonist that provides the benefits of a short half-life, independent clearance in renal impairment, and ability to use point-of-care testing to monitor platelet inhibition during CPB. However, experience with its use during cardiac surgery is limited. There are reports of cangrelor administered in combination with an initial heparin bolus to achieve systemic anticoagulation in several patients requiring DHCA, with one case report in a patient undergoing PTE with DHCA [24,25].

Presence of an inferior vena cava (IVC) filter – If an IVC device was inserted to prevent thromboembolic emboli from the lower extremities, its presence usually precludes placement of lower extremity long venous cannulae for ECMO or CPB, unless fluoroscopy can be used to avoid dislodgement or embolization of the filter [26].

Hepatic – Liver dysfunction with resultant coagulopathy may be present due to RV failure and hepatic congestion. After CPB with DHCA, this coagulopathy is exacerbated. The resultant bleeding diathesis and potential for significant postbypass bleeding necessitate adequate perioperative central and peripheral venous access, as well as availability of blood products. (See 'Availability of blood products' below and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Deep hypothermia'.)

Renal – Chronically reduced renal perfusion and congestive nephropathy predisposes patients to renal dysfunction. A baseline kidney function assessment, preoperative treatment of modifiable risk factors (eg, anemia, thrombocytosis), and avoidance of nephrotoxic drugs are warranted.

Neurologic – CPB, DHCA, and disease-specific factors (eg, hypercoagulable state, polycythemia, chronic hypoxia, presence of patent foramen ovale [PFO] and risk of paradoxical emboli) are risk factors for postoperative delirium stroke [27]. The baseline neurologic exam should be well documented to allow comparative assessments in the postoperative period. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Early postoperative complications'.)

Preoperative medication management — General considerations for management of chronically administered medications are discussed in a separate topic. (See "Perioperative medication management".)

Considerations specific for patients undergoing PTE include:

Medications to treat pulmonary hypertension – It is critically important to continue chronically administered medications for pulmonary hypertension throughout the perioperative period. Interdisciplinary discussions should include plans for ensuring compliance with and perioperative continuation of pulmonary vasodilators. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Management of chronic medications'.)

Bronchodilator therapy – Patients may be receiving bronchodilator therapy, which is continued in the preoperative period at the usual doses up to the time of surgery. Some patients may need additional doses of short-acting inhaled bronchodilators in the perioperative period. (See "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Inhaled bronchodilators and glucocorticoids'.)

Anticoagulant medications Anticoagulation is usually maintained as long as possible preoperatively, due to the inherent thrombotic risk in the CTEPH population. (See "Chronic thromboembolic pulmonary hypertension: Initial management and evaluation for pulmonary artery thromboendarterectomy", section on 'Anticoagulant therapy (indefinite)' and "Perioperative management of patients receiving anticoagulants".)

Warfarin is continued until 24 hours preoperatively and then the patient receives 5 to 10 mg intravenous (IV) vitamin K (typically administered approximately one hour before or during induction of general anesthesia) in order to mitigate risk for intraoperative and postoperative bleeding [18,28].

An alternative strategy is to bridge warfarin with the low-molecular-weight heparin agent enoxaparin five days preoperatively, then hold the dose 24 hours prior to surgery.

Unfractionated heparin infusions can be continued until two hours prior to surgery. Patients who are on DOAC can continue these until 48 hours preoperatively [29].

Diuretics – Assessment of fluid status and need for continuation or titration of diuretics should be individualized.

Availability of blood products — Typing and crossmatching should be performed and an adequate number of blood products (eg, 4 to 6 units of red blood cells and an equal number of fresh frozen plasma units) should be available at the time of the incision. In selected patients with persistent postbypass bleeding and abnormalities on point-of-care coagulation tests, additional blood products may be needed after weaning from CPB (eg, platelets for patients with thrombocytopenia or cryoprecipitate for patients with severe hepatic dysfunction). (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Transfusion of red blood cells'.)

Considerations during the COVID-19 pandemic — Non-urgent procedures should be postponed in patients suspected of having coronavirus disease 2019 (COVID-19). Considerations for anesthetic and airway management of patients who might be shedding viral particles are discussed in a separate topic. (See "Overview of infection control during anesthetic care", section on 'Infectious agents transmitted by aerosol (eg, COVID-19)' and "Overview of infection control during anesthetic care", section on 'Considerations with COVID-19 or other agents spread by aerosol'.)

VASCULAR ACCESS AND MONITORS

Intravenous vascular access — Vascular access for patients undergoing PTE includes standard peripheral venous and central venous catheter access (table 3). Notably, the surgical procedure necessitates temporary removal of the pulmonary artery catheter (PAC) by the surgeon, with later repositioning of the PAC before weaning from cardiopulmonary bypass (CPB). During the period the PAC is not in place, continuous infusions of vasoactive agents and other medications should not be connected to the ports of the PAC. The side-ports of the multilumen introducer sheath are used instead, or an additional multilumen central catheter can be inserted to ensure consistent drug delivery throughout the procedure.

In patients undergoing minimally invasive surgical approach for PTE (MIS PTE), a superior vena cava cannula is inserted (either by the anesthesiologist or the surgeon) as part of the cannulation strategy for bicaval venous drainage during CPB [30,31].

Monitors — Monitoring is similar to that for patients undergoing other types of cardiac surgery with CPB, with modifications that are similar to those for the subset of patients who require a period of elective deep hypothermic circulatory arrest (DHCA) (table 3). This includes standard American Society of Anesthesiologists (ASA) monitors as well as intra-arterial and central venous access. Other routine monitoring includes urine output, degree of neuromuscular blockade (using a peripheral nerve stimulator), and temperature (at multiple sites). Point-of-care laboratory testing is employed intermittently. Specialized invasive cardiovascular monitoring includes transesophageal echocardiography (TEE) and a PAC. Also, specialized neuromonitoring such as electroencephalography (EEG) and cerebral oximetry (using near-infrared spectroscopy technology) are usually employed during PTE procedures that include a period of elective DHCA. (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring' and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Monitoring'.)  

Unique aspects of monitoring for PTE procedures are presented below:

Cardiovascular monitoring

Intra-arterial catheters – Discrepancies in peripheral and central arterial blood pressure (BP) often occur after a prolonged period of CPB (particularly if DHCA and rewarming are employed), which may be exacerbated if high doses of vasoactive drugs are administered. In these situations, peripheral (ie, radial) arterial pressure underestimates central aortic pressure (figure 1) [32-35]. Thus, in addition to standard placement of an intra-arterial catheter in the upper extremity prior to induction of general anesthesia, a femoral intra-arterial catheter is also typically inserted by the anesthesiologist after induction of anesthesia, or by the surgeon after incision, to achieve reliable BP monitoring.

If selective antegrade cerebral perfusion (SACP) is to be used for cerebral protection, the right axillary artery is typically cannulated to deliver cerebral perfusion. An arterial cannula in the right radial artery provides the best estimate of cerebral perfusion pressure during SACP. A femoral arterial catheter or left radial arterial catheter is also inserted to simultaneously monitor systemic BP. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Intra-arterial catheter'.)

Pulmonary artery catheter – A PAC is inserted to monitor pulmonary artery pressure (PAP), cardiac output, and mixed venous oximetry throughout the perioperative period, and to note changes in PAP before versus after the surgical intervention.

During insertion of the PAC in the pre-CPB period, balloon position should remain proximal to the diseased portions in the main PA. Once a pulmonary arterial tracing is noted, the balloon is deflated and the PAC is not advanced further. Also, to avoid pulmonary artery injury, the balloon at the tip of the PAC is not inflated to measure pulmonary artery wedge pressure.

Insertion and positioning of the PAC is often challenging in patients with significant tricuspid regurgitation. In such cases, transesophageal echocardiography (TEE) may be used to guide passage through the tricuspid valve, and to confirm that final PAC positioning is optimal. Alternatively, video fluoroscopy can be used to achieve PAC placement in high-risk patients, or used as rescue method when all other approaches fail [36].

During removal of thrombus from the pulmonary arteries, the PAC is temporarily withdrawn into the right ventricle (RV) by the surgeon, then it is replaced (ie, refloated) back into the proximal main pulmonary artery position before separation from CPB. As noted above, the ports of the multilumen introducer sheath cannot be used during the period when the PAC is not in position. (See 'Intravenous vascular access' above.)

Transesophageal echocardiography – Intraoperative TEE examination follows standard guidelines for performance of a comprehensive examination [37]. (See "Anesthesia for cardiac surgery: General principles", section on 'Transesophageal echocardiography'.)

In patients with chronic thromboembolic pulmonary hypertension (CTEPH), TEE examination focuses on pathophysiologic features resulting from longstanding pulmonary artery hypertension with RV strain and subsequent chronic right-sided congestion. RV systolic function and chamber size, presence and direction of interatrial shunting, tricuspid valve pathology (particularly tricuspid regurgitation), and measurement of hepatic vein flow are documented [8,38-42]. Supplemental specific parameters for the assessment of RV systolic function may include 2-dimensional fractional area change of the RV [43], and tricuspid annular plane systolic excursion (TAPSE) [44]. (See "Echocardiographic assessment of the right heart" and "Echocardiographic evaluation of the tricuspid valve" and "Anesthesia for cardiac surgery: General principles", section on 'Transesophageal echocardiography'.)

Neuromonitoring — Neurologic complications are more likely after the PTE procedure than other types of cardiac surgery due to disease-specific factors and procedure-specific factors (particularly DHCA). Thus, we employ neuromonitoring modalities to monitor the functional integrity of the brain and to guide neuroprotective interventions during and after DHCA [2,45].

Electroencephalography – Full (ie, raw) unprocessed continuous EEG monitoring is the most sensitive method to assess optimal suppression of cerebral metabolic rate of oxygen consumption (CMRO2) during DHCA, as well as to detect cerebral insults. However, this technology typically requires the presence of a neuromonitoring technician [46]. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Electroencephalography' and "Neuromonitoring in surgery and anesthesia", section on 'Electroencephalography'.)

For this reason, a processed EEG monitor such as bispectral index is used in many centers during cardiac surgery with DHCA. Such monitors are familiar to anesthesiologists and prevalent in operating rooms throughout the United States due to ease of data interpretation compared with raw EEG tracings. Although used primarily to assess depth of anesthesia, bispectral index and similar monitors may be used to indicate degree of cerebral burst suppression during cooling and deep hypothermia, and they may provide complementary information regarding cerebral perfusion [47]. However, cautious interpretation is necessary because processed EEG data are more vulnerable to artifacts compared with unprocessed EEG data [48,49]. (See "Accidental awareness during general anesthesia", section on 'Brain monitoring' and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Electroencephalography'.)

Cerebral oximetry – Continuous monitoring of regional cerebral oxygen saturation (rSO2) provides information on regional perfusion of the frontal cortex. This monitor correlates well with physiologic changes in oxygen delivery relative to CMRO2, thereby allowing useful intraoperative hemodynamic and metabolic guidance. For example, an acute unilateral decrease in rSO2 indicates regional decrease in cerebral perfusion that may occur if SACP is inadequate. Bilateral decreases in rSO2 may indicate global cerebral hypoperfusion due to hypoxemia, hypocarbia, anemia, venous hypertension, or inadequate anesthetic depth. However, the etiology of decreases rSO2 is often difficult to determine [50,51]. General interventions to treat decreases in rSO2 that are >20 percent below baseline are noted in the algorithm (algorithm 1). Further discussion regarding cerebral oximetry is available in separate topics. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cerebral oximetry' and "Management of cardiopulmonary bypass", section on 'Neuromonitoring modalities'.)

Temperature monitoring — Continuous multisite temperature monitoring is necessary to optimize cerebral protection during cooling, the period of DHCA, rewarming, and the postbypass period [52]. Tympanic or nasopharyngeal temperature is monitored as a surrogate for brain temperature. A standard bladder temperature probe is used as a surrogate for systemic (ie, core) temperature. Optimal and uniform systemic and brain temperatures must be achieved during cooling for DHCA, and rewarming must be cautious and controlled to avoid cerebral hyperthermia [53,54]. Notably, peripheral temperature is typically discrepant from brain temperature. This discrepancy incurs risk of insufficient brain cooling during DHCA, as well as risk of overheating the brain during subsequent rewarming [55]. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cooling and deep hypothermia' and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Rewarming strategies'.)

Point-of-care testing — Routine intraoperative laboratory point-of-care testing includes intermittent analysis of blood gases, hemoglobin, electrolytes, calcium, glucose, and coagulation assays including activated whole blood clotting time [56,57]. (See "Clinical use of coagulation tests".)

ANESTHETIC MANAGEMENT

Preinduction sedation — Administration of benzodiazepines (eg, midazolam) or opioids (eg, fentanyl) is avoided or minimized in patients with chronic thromboembolic pulmonary hypertension (CTEPH). While mitigation of pain and anxiety may decrease pulmonary vascular resistance (PVR), it is critically important to avoid oversedation and hypoventilation-induced hypercarbia or hypoxemia that may increase PVR and exacerbate right ventricular (RV) dysfunction.

Induction and maintenance of general anesthesia

Induction – The goal for induction of anesthesia is to produce unconsciousness while avoiding hemodynamic instability [18,28]. Sudden increases in sympathetic tone due to noxious stimuli such as endotracheal intubation cause increases in PVR. Conversely, profound hypotension may result from the vasodilatory effects of large doses of sedative-hypnotic or potent volatile inhalation anesthetics, or the sympathectomy caused by a high-dose opioid induction technique. We employ a balanced anesthetic induction technique with lower doses of opioids to blunt the sympathetic responses to noxious stimuli while maintaining some residual intrinsic sympathetic vascular tone and avoiding bradycardia. (See "Anesthesia for cardiac surgery: General principles", section on 'Balanced technique'.)

Notably, some patients require continuous infusion of a vasopressor/inotropic agent (eg, vasopressin, norepinephrine, phenylephrine, dopamine (table 4)) to maintain stable hemodynamics during or after anesthetic induction. (See 'Hemodynamic management' below.)

Maintenance – We typically maintain anesthesia with a relatively constant concentration of a volatile inhalation agent (eg, sevoflurane, isoflurane) as the primary anesthetic, supplemented with an opioid infusion. A total intravenous anesthetic (TIVA) technique is a suitable alternative. (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance techniques'.)

Notably, it is not possible to deliver any IV or inhaled medication during circulatory arrest. Thus, any necessary boluses of anesthetic agents such as propofol or other medications (eg, antibiotic, diuretic, or neuromuscular blocking agent if appropriate) are administered prior to initiation of circulatory arrest. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Anesthetic management'.)

Airway and ventilatory management — Anesthetic goals for airway management include providing optimal ventilation and oxygenation, with immediate availability of rescue therapies for complications such as exacerbation of pulmonary hypertension, unilateral pulmonary hemorrhage, acute reperfusion pulmonary edema, and mucous plugging.

Airway management We insert a larger endotracheal tube (ETT) during induction of anesthesia, typically 8.0 mm internal diameter size in an adult male or 7.5 mm in an adult female, in order to facilitate lung protective ventilation (LPV), use of flexible fiberoptic bronchoscopy, and insertion of a bronchial blocker in the event of pulmonary hemorrhage.

For a minimally invasive surgical approach for PTE, placement of a double lumen endotracheal tube or bronchial blocker is necessary to achieve lung isolation and one lung ventilation. (See "Lung isolation techniques" and "One lung ventilation: General principles".)

Ventilatory strategies We employ a LPV strategy with low tidal volume (6 mL/kg) and we maintain plateau pressures <30 mmHg, with initial positive end-expiratory pressure (PEEP) set at 5 cm H2O [58]. Adjustments of the fraction of inspired oxygen (FiO2) are made with the goal of maintaining oxygen saturation 94 to 96 percent. Carbon dioxide tension (PaCO2) is maintained in the low normal range (ie, 30 to 40 mmHg). Although specific evidence for patients with CTEPH is scant, improved or noninferior outcomes after PTE have been noted with use of LPV compared with historic ventilation strategies employing higher tidal volumes (ie, 10 to 15 mL/kg) [58,59]. Details regarding LPV strategies are discussed in other topics. (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Low tidal volume ventilation: Initial settings'.)

Assessment for pulmonary hemorrhage in the postbypass period Shortly before and after separation from cardiopulmonary bypass (CPB), the patient is assessed for the possibility of pulmonary hemorrhage, which can be fatal. This includes checking and suctioning the ETT for evidence of bleeding, and manual lung inflation to qualitatively check for abnormally low lung compliance. Further evidence for pulmonary hemorrhage includes marked reductions in lung compliance compared with prebypass values. (See 'Pulmonary complications' below.)

Hemodynamic management — Most patients with CTEPH presenting for PTE have significant RV dilation, functional tricuspid regurgitation, and severely depressed RV systolic function. Such patients are at risk for acute RV failure and are exquisitely sensitive to sudden loss of adequate heart rate, hypotension-induced ischemia, or increases in either RV preload or afterload. Coexisting cardiovascular pathology such as left ventricular (LV) dysfunction or a vasodilatory state also influences hemodynamic management. In patients with milder CTEPH disease, the RV has adapted to increased RV afterload, with RV hypertrophy but normal RV systolic function. Such patients may tolerate increased PVR, but are nevertheless vulnerable to hypovolemia, hypotension, and arrhythmias.

Key hemodynamic goals during PTE include:

Avoid increases in PVR by:

Avoiding hypoxemia, hypercarbia, and increases in sympathetic tone or intrathoracic pressure.

Continuing preoperative or chronically administered IV infusions of pulmonary vasodilators as well as any inhaled pulmonary vasodilators initiated before or after anesthetic induction (eg, nitric oxide 20 to 40 ppm) until onset of CPB. However, prophylactic use of pulmonary vasodilators is avoided since most patients with CTEPH have a limited response to these agents.

Avoid exacerbation of RV dysfunction by:

Optimizing RV preload with judicious administration of fluid throughout the prebypass period. Either overfilling or underfilling the right heart may be detrimental in a patient with a hypertrophied or dysfunctional RV. We monitor real time TEE to detect changes in RV volume and maintain optimal RV filling. Trends in central venous pressure (CVP) are also used to guide fluid management.

Maintaining myocardial perfusion by maintaining systemic mean arterial pressure in the range of 65 to 80 mmHg), and avoiding even brief episodes of hypotension. Although inotropic support is not initiated prophylactically, a norepinephrine or vasopressin infusion is administered if necessary (table 4).

Maintain RV output and forward flow by:

-Maintaining adequate HR. Typically, a faster heart rate (eg, 80 to 100 beats/minute) is optimal for RV cardiac output. Bradycardia is avoided.

-Maintaining sinus rhythm. Arrhythmias such as atrial fibrillation or atrioventricular block are treated promptly to avoid rapid hemodynamic decompensation. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Treatment of arrhythmias'.)

-Administering inotropic support when RV systolic function is significantly compromised. In patients with severe preoperative RV dysfunction, inotropic support with a vasopressor/inotropic agent such as epinephrine or dopamine may be initiated before induction of general anesthesia (table 4).

Blood and hemostasis management — Detailed discussions of general principles for blood management during cardiac surgery with CPB and deep hypothermia with elective circulatory arrest (DHCA) are available in other topics. (See "Blood management and anticoagulation for cardiopulmonary bypass" and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Anticoagulation'.)

Specific management considerations for patients with CTEPH during PTE include:

Acute normovolemic hemodilution (ANH) – Since hemoglobin level is typically elevated due to chronic hypoxemia in patients with CTEPH, autologous blood harvesting of 500 to 1500 mL (1 to 3 units) before CPB can be performed in most patients, with reinfusion after CPB to minimize allogenic blood transfusions [60,61]. ANH is avoided if the hemoglobin level is <11 g/dL or if the patient is hemodynamically unstable and cannot tolerate blood removal. Details regarding this technique are described separately. (See "Surgical blood conservation: Acute normovolemic hemodilution".)

Antifibrinolytic use – We employ standard dosing of an antifibrinolytic agent for patients undergoing PTE (epsilon-aminocaproic acid), while other centers use tranexamic acid, as described separately. (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Antifibrinolytic administration'.)

While evidence indicates that risk of thrombosis and thromboembolic events is not increased by use of antifibrinolytic agents during CPB with DHCA [62,63], use for PTE procedures varies among institutions because effects in patients with CTEPH are unknown [8].

Cerebral protection — Patients undergoing PTE have a high risk for perioperative neurologic complications (with reports as high as 16 percent) due to the need for CPB with DHCA, as well as pre-existing associated comorbidities [2,26,45,64]. (See 'Comorbidities affecting anesthetic management' above.)

The following strategies for cerebral protection are based on evidence and experience derived from DHCA in aortic surgery [65-67] (see "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cerebral protection'):

Hypothermia

DHCA – We employ deep hypothermia with a period of elective circulatory arrest to maintain a bloodless surgical field during PTE [8,11]. Cooling to a temperature of 18 to 20°C is based on the goal of achieving electrocortical silence on the electroencephalogram (EEG), rather than aiming for a specific temperature goal prior to initiation of circulatory arrest [68]. In addition to systemic cooling via the CPB circuit, we apply ice packs or a cooling jacket to the head throughout the arrest period to achieve regional surface cooling of the brain [69]. Although the maximal acceptable duration of circulatory arrest time is uncertain [26,66,70], we aim for a period less than 30 to 40 minutes total to accomplish bilateral PTE, with 15 to 20 minutes allotted for each side [45]. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Cooling and deep hypothermia'.)

Selective antegrade cerebral perfusion (SACP) – Some centers employ more moderate hypothermia (20 to 28°C), relying on SACP to provide cerebral protection during the period of elective circulatory arrest [71-73]. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Deep hypothermia with selective antegrade cerebral perfusion'.)

With relatively short episodes of full circulatory arrest, neurologic outcomes are similar after DHCA compared with more moderate hypothermia plus SACP [2,3]. With any hypothermic technique, it is critically important to avoid cerebral hyperthermia during rewarming [74-76]. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Rewarming strategies'.)

Pharmacologic agents – There is scant evidence of efficacy for any pharmacologic agent to improve cerebral protection during CPB with DHCA. (See "Anesthesia for aortic surgery requiring deep hypothermia", section on 'Pharmacologic agents'.)

Many institutions do administer a pharmacologic adjunct for patients undergoing PTE with DHCA [65,67,75]. The most commonly used agents are:

Steroids – Evidence does not support the use of steroids for cerebral protection, although they are widely used for this purpose. Traditional regimens vary (eg, administration of preoperative oral prednisolone or administration of methylprednisolone during anesthetic induction or as bolus in the CPB pump prime). Concerns regarding adverse effects including abnormal glucose metabolism and immune system modulation have been reported, particularly with use of a high-dose regimen. [8,66,77,78].

Barbiturate or propofol anesthetics – Evidence does not support administration of barbiturates or high doses of propofol to further suppress cerebral electrocortical activity and decrease the cerebral metabolic rate of oxygen consumption (CMRO2) prior to initiation of DHCA. Furthermore, concerns regarding adverse effects include myocardial depression and, in the case of long-acting barbiturates, the likelihood of delayed emergence from anesthesia [79,80]. However, some centers do administer such agents to further suppress cerebral metabolic activity. Since the short-acting barbiturate thiopental has become unavailable in most countries, these centers use either the long-acting barbiturate pentobarbital (eg, 100 mg), or substitute propofol (eg, 2.5 mg/kg) due to its minimal effects on cardiac function [8,18]. Dosing of either agent should be guided by the goal of achieving cerebral isoelectricity during DHCA rather than using a fixed dose.

Mannitol – While mannitol is often a component of the CPB prime solution because of its diuretic effects and theoretical free radical scavenging properties, there is insufficient evidence supporting its use for cerebral (or renal) protection [81]. (See 'Renal protection' below.)

Other agents used in some institutions include antiinflammatory or anticonvulsant agents, lidocaine, magnesium, calcium channel blocker [65,75].

Renal protection — The incidence of postoperative acute renal failure (AKI) is higher after PTE with DHCA (45 percent) [82], compared with aortic surgery with DHCA (17 to 50 percent) [83,84], or cardiac surgical procedures without DHCA (18 to 30 percent) [85,86]. To minimize AKI risk, we avoid nephrotoxic agents; employ best practices during CPB including maintenance of adequate pump flow, perfusion pressure, and oxygen delivery; and minimize duration of CPB and the period of DHCA [82]. Evidence does not support the common practice of administration of intraoperative diuretics (eg, mannitol, furosemide), which may actually increase risk of AKI [87-89]. (See "Management of cardiopulmonary bypass".)

MANAGEMENT OF POSTBYPASS COMPLICATIONS

Pulmonary complications — In the postbypass and early postoperative periods after PTE, persistent hypoxemia and compromised pulmonary function may occur due to acute pathophysiologic changes superimposed on chronic thromboembolic pulmonary hypertension (CTEPH) disease [90].

Hypoxemia – Common causes of hypoxemia shortly after separation from cardiopulmonary bypass (CPB) include atelectasis, decreased lung and chest wall compliance, pulmonary edema, mainstem bronchial intubation, diaphragmatic paralysis, and pneumothorax [91]. While removal of pulmonary thromboemboli typically decreases the ratio of dead space to tidal volume and improves local pulmonary blood flow in the endarterectomized regions, surgery-induced increases in atelectasis may cause prolonged worsening of intrapulmonary shunting with consequent hypoxemia. Furthermore, loss of vasoregulatory mechanisms in the endarterectomized vasculature exacerbates hypoxemia, particularly in the lower lobes that are primarily affected in most patients with CTEPH [92,93]. In particular, patients with obesity are likely to have increased ventilation/perfusion (V/Q) mismatch and significant hypoxemia after PTE.

Treatment strategies for hypoxemia include the following:

Although positive end-expiratory pressure (PEEP) of only 5 to 10 mmHg is generally recommended during intraoperative mechanical ventilation, higher PEEP settings may be warranted for the postbypass and early postoperative periods.

Although inhaled pulmonary vasodilators are not routinely used after PTE, these may be beneficial to achieve adequate oxygenation in the postbypass period in selected patients with severe hypoxemia [94-98]. Improvements are thought to be due to improved V/Q matching in the non-diseased portions of the lung. However, despite short-term improvements in oxygenation or RV function, these treatments are not associated with better long-term outcomes.

Pulmonary artery steal syndrome Pulmonary steal syndrome is a temporary redistribution of pulmonary blood flow towards the newly opened pulmonary segments and away from previously well-perfused areas, which increases V/Q mismatching in the non-diseased lung [91,99]. Although this phenomenon occurs angiographically in up to 80 percent of patients in the immediate post-procedure period, 96 percent improve or resolve in follow-up imaging [100]. Postbypass management focuses on supportive therapies for hypoxemia such as increasing the fraction of inspired oxygen (FiO2). As noted above, inhaled nitric oxide may improve hypoxemia by improving perfusion of the non-diseased lung, but is reserved for patients with severe hypoxemia or hemodynamic compromise due to severe RV dysfunction.

Reperfusion lung injury – Reperfusion lung injury (RLI), also termed reperfusion pulmonary edema, may occur within 72 hours after surgery, but usually not in the immediate postbypass period. Diagnostic criteria are hypoxemia with arterial oxygen tension (PaO2) to FiO2 ratio <300, and sterile infiltrates affecting the reperfused lung segment(s) on chest radiography. The underlying multifactorial pathophysiology includes inflammatory responses to the surgical procedure with cytokine release and increased vascular permeability, blunted hypoxic pulmonary vasoconstriction, and reperfusion-induced accumulation of extravascular lung water [77,90,101,102].

Intraoperative management is directed at preventing RLI by employing nonspecific measures such as lung-protective ventilation (LPV) with optimal use of PEEP and FiO2 (see 'Airway and ventilatory management' above). Interruptions of positive pressure ventilation are avoided. Fluid management is conservative.

Treatment of acute pulmonary edema is not usually necessary during the intraoperative period. However, if edema does develops shortly after weaning from CPB, then higher PEEP levels are employed, and a diuretic (typically furosemide) is administered [103]. Little evidence is available to support the efficacy of interventions that manipulate pulmonary blood flow (eg, inotropes, pulmonary vasodilators) in decreasing the incidence or severity of RLI [59]. Details regarding further treatment of RLI in the postoperative period are described separately. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy", section on 'Postoperative management' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Notably, pulmonary edema fluid often appears pink or red in color. Differentiation from airway or intrapulmonary hemorrhage while the patient is still in the operative room is important since active bleeding requires specific intervention.

Intrapulmonary hemorrhage Postbypass assessment for pulmonary hemorrhage is described above. (See 'Airway and ventilatory management' above.)

Intrapulmonary hemorrhage after PTE is a potentially fatal complication occurring in up to 13.6 percent of patients. Risk factors include advanced age, preoperative hemoptysis, unfavorable preoperative hemodynamics (eg, high pulmonary vascular resistance [PVR], low RV output), greater distal disease burden, and residual postoperative pulmonary hypertension [104]. Disruptions of the intima layer in the pulmonary artery and distal segments are the most common source of bleeding.

Management depends on severity of hemorrhage and the associated degree of compromise in gas exchange (algorithm 2) [105-107]. Mild to moderate bleeding can be managed by applying positive airway pressure, treating coagulopathy, and surgical application of topical vasoconstrictors such as phenylephrine, vasopressin, or epinephrine. Significant ongoing bleeding may require selective or complete lung isolation using a bronchial blocker or double lumen endotracheal tube.

More aggressive surgical measures such as embolization of the bleeding source, clamping of the pulmonary artery, or selective lung resection may be necessary in some patients. Temporary venovenous or venoarterial extracorporeal membrane oxygenation (ECMO) can be used in severe cases [108]. (See "Extracorporeal life support in adults in the intensive care unit: The role of transesophageal echocardiography (TEE)".)

Other measures to treat refractory pulmonary hemorrhage include topical application of antifibrinolytic agents or recombinant factor VII administered via bronchoscopy or by inhalation of a nebulized form. Although these treatments have been used to treat diffuse alveolar hemorrhage from other causes [109-113], they are controversial for patients with CTEPH due to concerns that systemic absorption may lead to a hypercoagulable state and recurrence of pulmonary thromboemboli. One case report describes application of activated factor VII via bronchoscopy to successfully treat refractory pulmonary hemorrhage in a patient on ECMO support after PTE surgery [114].

Hemodynamic instability — Postbypass hemodynamic instability is associated with preoperative severity of CTEPH disease, RV dysfunction, and other comorbidities. Despite beneficial reductions in PVR due to clot removal from the pulmonary artery and CPB-induced vasodilation that tends to promote forward cardiac output and end-organ perfusion, hemodynamic instability may still occur. Typical causes include underlying RV dysfunction, residual pulmonary hypertension, CPB-induced myocardial stunning, hypotension-induced RV ischemia, or persistent bleeding with consequent hypovolemia.

Key postbypass hemodynamic goals are to ensure adequate RV preload and provide sufficient RV perfusion pressure. We avoid prophylactic use of inotropic agents or pulmonary vasodilators in the postbypass period as some data suggest this may increase risks for RLI and other postoperative morbidity and mortality in patients undergoing PTE compared with risks after other types of cardiac surgery [59] (see "Intraoperative problems after cardiopulmonary bypass", section on 'Controversies regarding use of inotropic drug therapy'). Nevertheless, patients with severe RV dysfunction will likely need inotropic and/or vasopressor support. We typically administer epinephrine alone, or a combination of epinephrine and milrinone, with or without vasopressin in order to further increase systemic vascular resistance (table 4). Inhaled pulmonary vasodilator therapy may also be necessary. Further discussion regarding selection of vasoactive agents and pulmonary vasodilators in patients with severe RV dysfunction is available in a separate topic. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Vasopressors and inotropes' and "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Chronic targeted therapy for pulmonary hypertension: Patient selection'.)

If separation from CPB is not possible, temporary mechanical circulatory support with venoarterial extracorporeal membrane oxygenation (ECMO) may be employed as rescue therapy. Successful weaning from ECMO after PTE ranges from 50 to 70 percent [115,116]. Discussions regarding initiation and management of ECMO are available in separate topics:

(See "Intraoperative problems after cardiopulmonary bypass", section on 'Extracorporeal membrane oxygenation'.)

(See "Extracorporeal life support in adults in the intensive care unit: The role of transesophageal echocardiography (TEE)".)

(See "Extracorporeal life support in adults in the intensive care unit: Overview".)

Bleeding and coagulopathy — Establishing postbypass hemostasis is typically challenging after cardiac surgery with deep hypothermia and elective circulatory arrest (DHCA). Surgical bleeding is exacerbated by coagulopathy due to the anti-hemostatic effects of CPB and deep hypothermia (table 5). Chronic preoperative anticoagulation therapy, hepatic congestion, renal dysfunction, and prolonged intraoperative durations of CPB and DHCA worsen postbypass coagulopathy. General principles for management of coagulopathy and postbypass bleeding after CPB and DHCA are discussed in detail in other topics. (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Achieving hemostasis and management of bleeding' and "Anesthesia for aortic surgery requiring deep hypothermia", section on 'The postbypass period'.)

Notably, considerations for treatment of coagulopathy after PTE in patients with CTEPH is balanced against the presence of any preexisting hypercoagulable state. In one retrospective study of 351 patients receiving chronic preoperative warfarin therapy, unactivated prothrombin complex concentrate was successfully used as an alternative to fresh frozen plasma to treat refractory postbypass bleeding after PTE [117]. However, we avoid activated products such as factor eight inhibitor bypassing activity and recombinant activated factor VII.

EARLY POSTOPERATIVE MANAGEMENT — After PTE, patients remain intubated with controlled mechanical ventilation during the immediate postoperative period. Management of transport from the operating room to the intensive care unit (ICU) is similar to that for other types of cardiac surgery. (See "Anesthesia for cardiac surgery: General principles", section on 'Transport and handoff in the intensive care unit'.)

In selected patients with significant compromise of pulmonary function, optimal mechanical ventilation can be achieved prior to transport to the ICU by using an advanced ICU ventilator while the patient is still in the operating room.  

Postoperative multidisciplinary care includes expert management of underlying chronic thromboembolic pulmonary hypertension (CTEPH) disease. Patients with an uncomplicated ICU course are typically extubated within 12 hours and discharged from the ICU on the second or third postoperative day (table 6) [118]. (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy", section on 'Postoperative management'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pulmonary hypertension in adults".)

SUMMARY AND RECOMMENDATIONS

Preanesthetic assessment for pulmonary thromboendarterectomy (PTE) in patients with chronic thromboembolic pulmonary hypertension (CTEPH) focuses on:

The planned surgical approach (eg, standard approach with median sternotomy, cardiopulmonary bypass [CPB], and elective deep hypothermic circulatory arrest [DHCA]; or a minimally invasive approach). (See 'Overview of surgical techniques for pulmonary thromboendarterectomy' above.)

Severity of pulmonary hypertension (pulmonary vascular resistance [PVR]), right ventricular (RV) failure, and other pulmonary pathology (eg, pulmonary clot burden, ventilation-perfusion [V/Q] mismatch, presence of bronchopulmonary collateral arteries). Selected patients benefit from perioperative extracorporeal membrane oxygenation (ECMO). (See 'Cardiopulmonary pathophysiology' above.)

Comorbidities affecting anesthetic management (eg, hematologic abnormalities such as hypercoagulability, coagulopathy due to liver dysfunction, renal dysfunction, neurologic conditions). (See 'Comorbidities affecting anesthetic management' above.)

Continue anticoagulants and bronchodilators in the preoperative period. Continue intravenous (IV) or inhaled pulmonary vasodilators until onset of CPB. (See 'Preoperative medication management' above.)

Monitoring includes:

Cardiovascular monitoring (see 'Cardiovascular monitoring' above)

-Central venous catheter

-Pulmonary artery catheter (PAC; temporarily removed by the surgeon, with repositioning before weaning from CPB)

-Transesophageal echocardiography to assess RV function, right atrium for interatrial septal shunting, and tricuspid valve (eg, tricuspid regurgitation)

Neuromonitoring (see 'Neuromonitoring' above)

-Unprocessed or processed electroencephalography (EEG) to assess optimal suppression of cerebral metabolic rate of oxygen consumption (CMRO2) during DHCA

-Cerebral oximetry to recognize and treat decreases in regional cerebral oxygen saturation (rSO2) (algorithm 1).

Temperature (see 'Temperature monitoring' above)

-Tympanic or nasopharyngeal probe as a surrogate for brain temperature

-Bladder probe as a surrogate for systemic (ie, core) temperature

Point-of-care testing (blood gases, hemoglobin, electrolytes, calcium, glucose, coagulation assays) (see 'Point-of-care testing' above)

We typically employ a balanced induction technique, and maintain anesthesia primarily with a relatively constant concentration of a volatile inhalation agent (eg, sevoflurane, isoflurane) supplemented with an opioid infusion. All anesthetics are discontinued during DHCA. (See 'Induction and maintenance of general anesthesia' above.)

We insert a large endotracheal tube (ETT; 8.0 mm [males]; 7.5 mm [females]). We employ a lung protective ventilation strategy. (See 'Airway and ventilatory management' above.)

Key hemodynamic goals include (see 'Hemodynamic management' above):

Avoid increasing PVR

-Avoid hypoxemia, hypercarbia, increases in sympathetic tone or intrathoracic pressure

-Continue previously initiated IV and inhaled pulmonary vasodilators

Avoid exacerbating RV dysfunction

-Minimize RV preload with judicious fluid administration.

-Maintain myocardial perfusion (mean arterial pressure 65 to 80 mmHg); avoid hypotension (using vasopressin or norepinephrine if necessary (table 4)).

-Maintain RV output with adequate heart rate (eg, 60 to 80 beats/minute) and sinus rhythm. Administer inotropic support with dopamine and/or epinephrine if necessary (table 4).

Blood management includes:

Prebypass – Acute normovolemic hemodilution is often feasible. An antifibrinolytic agent is administered. (See "Surgical blood conservation: Acute normovolemic hemodilution" and 'Blood and hemostasis management' above.)

Postbypass – Surgical bleeding is exacerbated by anti-hemostatic effects of deep hypothermia (table 5), ischemia and reperfusion injury, fibrinolysis, and platelet activation. (See 'Bleeding and coagulopathy' above.)

Cerebral protection is achieved by cooling to 18 to 20°C. Some centers employ more moderate hypothermia (20 to 28°C) with selective antegrade cerebral perfusion (SACP). (See 'Cerebral protection' above.)  

Common etiologies for postbypass hypoxemia include atelectasis, decreased lung and chest wall compliance, pulmonary edema, mainstem intubation, diaphragmatic paralysis, and pneumothorax. Procedure-specific pulmonary complications include redistribution of blood flow (ie, pulmonary steal syndrome), increased permeability of the pulmonary vasculature, lack of hypoxic pulmonary vasoconstriction in endarterectomized segments, reperfusion lung injury (RLI), and pulmonary hemorrhage. (See 'Pulmonary complications' above.)

Patients remain intubated with controlled mechanical ventilation in the immediate postoperative period. (See 'Early postoperative management' above.)

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Topic 131633 Version 9.0

References

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