Anesthesia for aortic surgery requiring deep hypothermia

INTRODUCTION — Open surgical repair of portions of the ascending aorta or aortic arch may require temporary interruption of cerebral and systemic blood flow [1]. Deliberate hypothermia is induced with the aid of cardiopulmonary bypass (CPB) to protect the brain and other vital organs from ischemia during this period of elective circulatory arrest. Deep hypothermic circulatory arrest (DHCA) permits surgical reconstruction of the aortic arch without crossclamping a diseased aorta or instrumenting and possibly injuring aortic arch branch vessels. Selective antegrade cerebral perfusion (SACP) is a technique to perfuse the brain using the CPB circuit by direct cannulation of the axillary artery or aortic arch branch vessels. Retrograde cerebral perfusion (RCP) is a technique to improve the safety of DHCA by providing partial perfusion to the brain using the cardiopulmonary bypass circuit during interruption of antegrade cerebral perfusion.

This topic discusses anesthetic management and strategies for cerebral protection during cardiac surgical procedures requiring CPB with a period of DHCA, RCP, or SACP. Management of routine CPB and weaning from CPB are discussed separately. (See "Management of cardiopulmonary bypass" and "Weaning from cardiopulmonary bypass".)

Surgical indications and techniques to accomplish repairs of the ascending aorta and aortic arch are reviewed in other topics. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta' and "Overview of open surgical repair of the thoracic aorta", section on 'Aortic arch'.)

PREANESTHETIC CONSULTATION AND PLANNING — The preanesthetic consultation for patients undergoing cardiac surgical procedures is discussed separately. (See "Preoperative evaluation for anesthesia for cardiac surgery".)

If emergency surgical repair of acute ascending aortic dissection (Stanford type A) is necessary, surgical and preanesthetic evaluation and preparation are expedited so that induction of general anesthesia can proceed without delay [2]. Risk of mortality due to complications (eg, acute aortic regurgitation, cardiac tamponade, stroke, myocardial infarction) is estimated to be as high as 1 to 2 percent per hour after symptom onset (figure 1). (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Emergency surgery' and "Surgical and endovascular management of acute type A aortic dissection".)

Comorbidities due to ascending aortic or arch disease — The anesthesiologist's review of the preoperative surgical evaluation and plan, as well as the preoperative aortic imaging studies, is particularly important for patients undergoing surgery of the ascending aorta and arch. Anesthetic care is dependent on the surgical approach, including vascular cannulation plans that guide monitoring choices (eg, site[s] for direct arterial pressure monitoring). (See "Overview of open surgical repair of the thoracic aorta", section on 'Preoperative evaluation and preparation'.)

With either chronic or acute disease of the ascending aorta or arch, coexisting conditions that may affect anesthetic and surgical management include:

Aortic regurgitation — Aortic regurgitation (AR; also called aortic insufficiency) may be present due to a dilated aortic root or dissection that involves the aortic root. This condition is often associated with signs and symptoms of congestive heart failure. Diagnosis with preoperative transthoracic or transesophageal echocardiography (TEE) is confirmed by intraoperative TEE examination during the prebypass period. (See 'Transesophageal echocardiography' below.)

Preparation for modifications in cardioplegia delivery technique and/or left ventricular (LV) venting during cardiopulmonary bypass (CPB) may be necessary if significant AR is present. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'.)

Atherosclerotic disease — Severe thoracic aortic atherosclerosis or carotid artery disease may be present. Thoracic aortic atherosclerosis increases the risk of cerebral and systemic thromboembolic complications. Although mean arterial pressure (MAP) is generally targeted between 50 and 80 mmHg (or ≥65 mmHg), a slightly higher MAP (typically ≥75 mmHg) is often maintained during CPB in patients with significant cerebrovascular disease, particularly if longstanding hypertension may have caused a shift in the cerebral autoregulation threshold (table 1) [3-5]. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Cerebrovascular disease'.)

Also, the presence of significant occlusive cerebrovascular disease may impact the choice of techniques for delivery of selective antegrade cerebral perfusion (SACP) due to limited effectiveness of retrograde cerebral perfusion (RCP). (See 'Deep hypothermia with selective antegrade cerebral perfusion' below and 'Deep hypothermia with retrograde cerebral perfusion' below.)

Mediastinal mass effect — A mediastinal mass effect may be present due to compression of the right ventricular outflow track, trachea, right pulmonary artery, or left mainstem bronchus by a large ascending aortic aneurysm (image 1) [6-9]. This may result in hemodynamic or airway compromise during induction. (See "Anesthesia for patients with an anterior mediastinal mass".)

Acute aortic dissection — With acute aortic dissection, complications that increase risk and affect anesthetic and surgical management include (movie 1) [2,10] (see "Surgical and endovascular management of acute type A aortic dissection"):

●Acute AR – Acute AR may occur as a consequence of dissection involving the aortic root. In the preoperative period, patients with acute AR typically present with tachycardia and decompensated heart failure due to a sudden increase in LV diastolic pressure. Beta-blocker therapy to control heart rate (HR) or blood pressure (BP) should be withheld or administered cautiously to prevent cardiogenic shock in a patient with acute AR (or cardiac tamponade, as noted below). (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Anti-impulse therapy'.)

Additional considerations for patients with significant AR are applicable during CPB. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'.)

●Cardiac tamponade – Cardiac tamponade is a common complication of Stanford type A aortic dissection (figure 1). The aortic root and the first 11 cm of the ascending aorta lie within the pericardial sac; thus, a contained rupture of the aortic root or proximal ascending aorta may result in hemopericardium with tamponade. Presence of blood in the pericardial space on the preoperative computed tomography (CT) scan or echocardiogram or signs of cardiac tamponade on physical examination should be noted. Severity of pericardial tamponade is assessed with preoperative transthoracic echocardiography (TTE) but may worsen during the course of a preoperative evaluation. Thus, severity is reassessed with intraoperative TEE after induction of general anesthesia.

Similar to patients with acute AR, beta-blocker therapy should be withheld or administered cautiously to prevent cardiogenic shock in a patient with cardiac tamponade. Other anesthetic management considerations for a patient with cardiac tamponade are described separately. (See "Anesthesia for thoracic trauma in adults", section on 'Cardiac tamponade' and "Anesthesia for thoracic trauma in adults", section on 'Anesthetic considerations for specific procedures'.)

●Malperfusion of extremities – Aortic branch vessels that are dissected or perfused from the false lumen of the aorta may result in limb malperfusion that determines which site(s) should be used for arterial cannulation for CPB, as well as for intra-arterial catheter insertion for continuous monitoring of BP (see 'Intra-arterial catheter' below). Malperfusion may manifest as a pulse deficit on physical examination or be noted as decreased flow on the arterial phase of the preoperative CT angiogram (CTA).

●Acute stroke – Acute stroke may develop due to malperfusion or dissection of the aortic arch vessels [11]. Intraoperative surface vascular ultrasound or carotid artery Duplex imaging, if available, is employed by the anesthesiologist to diagnose extension of the dissection into the common carotid arteries and to assess blood flow in these arteries in patients with suspected acute stroke. (See 'Surface vascular ultrasound of the carotid arteries' below.)

●Acute coronary syndrome – Acute coronary syndrome may occur due to coronary dissection or malperfusion, with consequent onset of myocardial infarction or ventricular failure. Severe preoperative LV dysfunction is a predictor of mortality [12]. Considerations for anesthetic management of patients with myocardial ischemia or heart failure are discussed separately. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Myocardial ischemia' and "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Congestive heart failure'.)

●Acute mesenteric ischemia – Acute mesenteric ischemia may manifest as acute renal failure or abdominal pain with melena. Management of severe renal insufficiency during CPB is discussed separately. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Renal insufficiency or failure'.)

●Acute spinal cord ischemia – Acute spinal cord ischemia may manifest as transient or permanent paraplegia. There is limited clinical experience for managing this condition; decisions are individualized on a case-by-case basis [13].

●Coagulopathy – Acute type A aortic dissection is associated with coagulopathy that worsens during surgery [14], particularly if deep hypothermic techniques are employed. (See 'Deep hypothermia' below.)

Deep hypothermia — If a period of deep hypothermia (eg, temperatures of 16 to 18°C) and use of elective circulatory arrest, SACP, or RCP are planned by the surgeon, specialized monitoring is employed. (See 'Monitoring' below.)

Deep hypothermia causes physiologic changes that may persist during the postbypass and postoperative periods after initial rewarming (table 2) [15-17]. The resultant bleeding diathesis and potential for significant surgical bleeding require adequate central and peripheral venous access, as well as availability of blood products (typically 4 to 6 units of red blood cells [RBCs] and fresh frozen plasma [FFP]). Also, vasoactive infusions are prepared to treat vasoconstriction that typically occurs during cooling and hypothermia and/or vasodilation during rewarming and reperfusion. In addition, an insulin infusion is prepared to control hyperglycemia. (See 'Cardiopulmonary bypass with deep hypothermic circulatory arrest' below.)

MONITORING — Aortic surgery requiring deep hypothermic circulatory arrest (DHCA) with or without selective antegrade cerebral perfusion (SACP) or retrograde cerebral perfusion (RCP) is conducted using standard American Society of Anesthesiologists (ASA) monitors [18], arterial and central venous access, transesophageal echocardiography (TEE), and a bladder catheter to monitor urine output. Also, temperature is measured at multiple sites to monitor cooling to produce deliberate hypothermia and subsequent gradual rewarming to avoid unintentional hyperthermia. In addition, brain monitoring is typically employed (electroencephalography [EEG] and cerebral oximetry), as well as invasive cardiovascular monitoring with a pulmonary artery catheter (PAC).

Intra-arterial catheter — An intra-arterial catheter is typically inserted in an upper extremity prior to induction and is used for continuous monitoring of arterial blood pressure (BP), analysis of respirophasic variations in the arterial pressure waveform, and intermittent blood sampling for intraoperative laboratory tests. Selection of the site for intra-arterial cannulation is affected by the likely accuracy of BP measurements in one or both upper extremities. For example, if the surgical procedure involves reconstruction of the distal aortic arch, the left subclavian artery may be temporarily occluded or interrupted. In such cases, a right radial intra-arterial catheter provides the most accurate monitor of systemic BP. If an aortic dissection extends into an aortic arch branch vessel or involves the subclavian artery (figure 1), malperfusion of one or more extremities may occur. In such cases, BP is more accurately measured in a limb perfused by an artery that is not affected by the dissection. In some instances of limb malperfusion, multiple arterial catheters in different limbs may be necessary for optimal assessment of the central aortic BP during various phases of the operation.

If SACP is planned, it may be useful to place arterial cannulae in both upper extremities. Since the right axillary artery is typically cannulated for both cardiopulmonary bypass (CPB) and delivery of SACP, continuous measurement of arterial BP from the right radial artery will be temporarily interrupted or affected during initial cannulation of the right axillary artery. Ideally, BP measured in the contralateral arm is used to monitor systemic perfusion pressure during this cannulation period. Subsequently, during CPB, the BP measured from the right radial artery (ipsilateral to the cannulated right axillary artery) will overestimate systemic perfusion pressure. However, during SACP delivery via the right axillary artery, the BP measured from the right radial artery provides the best estimate of cerebral perfusion pressure (CPP). Thus, during different stages of the operation, optimal continuous estimates of both central aortic BP and CPP can be obtained only if intra-arterial catheters are present in both upper extremities. (See 'Deep hypothermia with selective antegrade cerebral perfusion' below.)

Pulmonary artery catheter — A large-bore central venous catheter (CVC) is necessary to permit the rapid administration of blood products and provide central vascular access for the infusion of vasoactive agents. Use of an introducer sheath (eg, Cordis) that functions as a large-caliber CVC and as a means to place a pulmonary artery catheter (PAC) is recommended.

A PAC catheter is typically inserted to monitor pulmonary arterial pressure (PAP), central venous pressure (CVP), cardiac output (CO), and mixed venous oxygen saturation (SvO₂) throughout the prebypass and postbypass periods. These values are useful for guiding vasopressor and inotropic administration, as well as for monitoring responses to intraoperative fluid and blood administration. During initiation of CPB or infusion of antegrade cardioplegia, an increase in the PAP may indicate left ventricular (LV) distention due to aortic regurgitation (AR). (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'.)

In the intensive care unit (ICU), continued monitoring of PAC, CVP, and CO values is useful after major thoracic aortic surgery due to a high risk for postoperative bleeding, cardiac tamponade, and cardiovascular instability.

Echocardiography

Transesophageal echocardiography — In addition to the standard intraoperative TEE examination for cardiac surgical patients, TEE is used to confirm and characterize the extent of aortic pathology for ascending aortic and arch surgery [2]. Practice guidelines of the American College of Cardiology/American Heart Association (ACC/AHA) [1] as well as the American Society of Anesthesiologists (ASA) [19] and the Society of Cardiovascular Anesthesiologists (SCA) [1,19] suggest that thoracic aortic surgery is a Class 1 indication (benefit >> risk, "should be performed") for intraoperative TEE.

●Prebypass period – TEE is used to verify the diagnosis and detect complications due to aortic pathology. The aortic valve is examined to determine if there is significant AR and to quantify its severity (movie 2 and image 2 and image 3 and image 4). TEE is also used to assess the structure and function of the other cardiac valves, to evaluate regional and global left and right ventricular (RV) function, and to assess volume status, similar to its use in coronary artery bypass grafting (CABG) and other cardiac surgical procedures. In addition, intraoperative TEE permits rapid diagnosis of the causes of hemodynamic instability. (See "Anesthesia for coronary artery bypass grafting surgery", section on 'Postbypass transesophageal echocardiography'.)

In emergency surgery for aortic dissection, intraoperative TEE examination is necessary to diagnose the extent and classification of the dissection, particularly if hemodynamic instability necessitates initiation of surgery without a definitive preoperative diagnostic study. TEE examination provides information regarding the presence and location of the intimal tear(s), the extent of the dissection flap, presence and quantification of the severity of AR due to dissection involving the aortic valve, detection of cardiac tamponade, and assessment of regional wall motion abnormalities (RWMAs) indicating myocardial ischemia or infarction due to coronary dissection [2,20] (image 5).

●Aortic cannulation – TEE is used to guide placement of the aortic and other cannulae for CPB. For example, if aortic cannulation is performed using a Seldinger technique with a guidewire, TEE guidance can be used to identify the true and false lumens of the aorta and verify guidewire placement and cannula positioning in the true lumen of the dissected vessel (image 6). (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

Although there are no definitive TEE criteria to distinguish the true from the false lumen in aortic dissection, typical features of the true lumen include:

•Smaller than the false lumen

•Continuity with the aortic valve

•Expansion during systole

•Rounded borders

•Blood flow through intimal fenestrations, with direction of flow from the true lumen into the false lumen

Typical features of the false lumen include:

•Larger than the true lumen

•A crescent shape

•A sharp edge where the intimal flap joins the adventitia

•Presence of spontaneous echocardiographic contrast or thrombus due to a low flow state

If computed tomographic angiography (CTA) images of the aorta are available for viewing in the operating room, comparison of these with the intraoperative TEE images may be useful in confirming correct identification of the true and false lumens after aortic dissection [1].

●During CPB – Upon initiation of CPB, intraoperative TEE can be used to verify blood flow in the true lumen of the dissected aorta. TEE is used also to monitor for AR or LV distention that may occur during initiation of CPB before application of the aortic crossclamp due to ventricular fibrillation or asystole with absent ventricular ejections. LV distention may also occur after application of the cross-clamp due to administration of antegrade cardioplegia that flows back across the incompetent aortic valve [1]. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'.)

TEE monitoring is subsequently necessary to detect LV distention after the aortic crossclamp is removed (during the rewarming phase of CPB), which may occur if LV contraction is absent (ie, asystole) or infrequent (ie, bradycardia) because the LV chamber is not emptied.

●Weaning from CPB – Shortly before weaning from CPB, TEE is employed to guide removal of intracardiac air within the left-sided cardiac chambers (ie, left atrium and LV) and the aorta. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Arterial air embolization'.)

If a valve-sparing procedure was performed (eg, aortic valve repair or resuspension), TEE can characterize aortic valve and aortic root structure and detect or quantify the severity of residual AR [1]. In some cases, it may be necessary to reinstitute CPB to perform additional aortic repair or to replace the valve. Furthermore, aortic root reconstruction involves reimplantation of the coronary arteries into the prosthetic root graft. Thus, TEE is used to evaluate LV and RV function to verify that coronary blood flow has been properly restored. (See "Overview of open surgical repair of the thoracic aorta", section on 'Involvement of the aortic root'.)

TEE can also be used to detect iatrogenic aortic dissection and to assess for evidence of hypovolemia or other causes of hypotension during the weaning process. (See "Weaning from cardiopulmonary bypass".)

●Postbypass period – In the postbypass period, global LV and RV function may not immediately recover from the effects of CPB, cardioplegia, and elective circulatory arrest. Frequent reassessment facilitates management of inotropic and vasopressor support, as well as fluid administration to achieve optimal LV filling while avoiding hypo- or hypervolemia. TEE can also be used to detect blood in the pericardial or pleural cavities that may indicate ongoing surgical bleeding. For patients undergoing surgery for aortic dissection (figure 1), the postbypass TEE examination should also note the presence or absence of residual dissection and the blood flow patterns in the true and false lumens of the descending thoracic aorta.

Surface vascular ultrasound of the carotid arteries — Intraoperative surface vascular ultrasound or carotid artery Duplex imaging is used in many patients undergoing ascending aortic or arch surgery. Blood flow is assessed in the common carotid arteries during each stage of the operation, particularly if there is suspected extension of an aortic dissection into these vessels. Typically, carotid dissection appears as a thin intimal flap within the lumen of the carotid artery, with reduced or absent blood flow in the true lumen during systole (image 7).

Subsequently, after initiation of CPB, color-flow Doppler imaging can be used to confirm blood flow in the common carotid arteries. This technique may also detect cerebral malperfusion caused by cannulation of the false lumen, cannula malposition, occlusion of the aortic arch branch vessels by the intimal flap, or extension of the aortic dissection into the branch vessels of the aortic arch.

Brain monitors — Intraoperative neuromonitoring is typically used to manage hypothermia and monitor for cerebral hypoperfusion [11].

Electroencephalography — EEG monitoring is employed to establish a neurophysiologic endpoint for the cerebral effects of cooling (electrocortical silence) in patients undergoing DHCA, as well as to detect cerebral hypoperfusion and monitor anesthetic depth [2].

Endpoint for cerebral effects of cooling — Deliberate hypothermia causes incremental changes in the EEG that correlate with the reduction of cerebral metabolic rate associated with hypothermia (figure 2). Electrocortical silence on the EEG can be used to ensure hypothermia-induced maximum suppression of cerebral metabolic activity before CPB pump flow is discontinued to initiate circulatory arrest [21-23]. EEG activity and electrocortical silence are better predictors of cerebral hypothermia than temperature measurements alone because brain and neuronal temperatures cannot be measured directly (figure 3) [21-24].

However, the EEG is also affected by anesthetic agents independent of temperature, cerebral metabolic rate, or cerebral perfusion. Volatile inhalation agents cause a dose-dependent decrease in EEG amplitude and frequency, and certain intravenous (IV) anesthetic agents (eg, propofol or barbiturates) administered at higher doses may cause burst suppression or electrocortical silence that cannot be distinguished from effects of hypothermia. Thus, anesthetic agents should be discontinued during deliberate hypothermia as the EEG begins to slow or at the onset of burst suppression to avoid interference with detection of hypothermia-induced electrocortical silence. If use of propofol or a barbiturate is planned as an adjunct for cerebral protection (see 'Pharmacologic agents' below), administration is delayed until after the EEG endpoint or the target temperature for DHCA has been reached. (See 'Anesthetic requirements' below and "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic effects on neuromonitoring'.)

Furthermore, rather than full EEG monitoring with a neuromonitoring technician, processed EEG monitors such as the bispectral index (BIS) are more commonly available in the operating room setting and may be the only readily available brain monitor for urgent aortic surgery cases such as acute ascending aortic dissection [2]. Although the BIS value appears to decrease reliably with progressive hypothermia, it only monitors the frontal cortex and is more vulnerable to artifacts caused by anesthetic agents, neuromuscular blocking agents, and other intraoperative factors than the raw unprocessed EEG [25]. Therefore, it may be less sensitive than a full montage EEG for detection of electrocortical silence.

The average nasopharyngeal temperature for electrocortical silence is 18°C, although 50 percent of patients do not exhibit electrocortical silence at 18°C [21,23]. Thus, in the absence of EEG monitoring, a nasopharyngeal temperature of approximately 12°C is necessary to ensure that electrocortical silence has been achieved in nearly all patients [22,23]. (See "Neuromonitoring in surgery and anesthesia", section on 'Temperature'.)

Monitoring for cerebral hypoperfusion — EEG monitoring may detect cerebral hypoperfusion manifesting as a decrease in EEG amplitude and frequency. Sudden decreases in amplitude and frequency or onset of seizure activity indicate an acute decrease in cerebral perfusion. Such abrupt EEG changes should be promptly communicated to the surgeon and perfusionist since they may influence decisions regarding further intraoperative management [26]. (See 'Cerebral protection' below.)

Monitoring for awareness — Inadequate anesthetic depth resulting in awareness is possible during CPB, particularly during the rewarming phase [25,27]. To avoid inadequate anesthetic depth, administration of a volatile inhalation agent and/or other anesthetics is resumed as soon as EEG activity has reappeared during rewarming. (See 'Anesthetic requirements' below and "Accidental awareness during general anesthesia", section on 'Brain monitoring'.)

Cerebral oximetry — Near-infrared spectroscopy (NIRS) cerebral oximetry is used in many centers to continuously monitor cerebral regional oxygen saturation (rSO₂) in the frontal cortex in patients undergoing major thoracic aortic operations with CPB and DHCA [2,28-32]. NIRS is not affected by anesthetic agents and does not require pulsatile perfusion.

Use of cerebral oximetry to monitor for adequate cerebral perfusion has been employed during DHCA alone, DHCA with retrograde RCP, or DHCA with SACP [33-43]. Typically, rSO₂ values increase as deliberate hypothermia is induced, then gradually decrease during either DHCA alone or DHCA with RCP once CPB pump flow has been discontinued for circulatory arrest [33,40,42,43]. Subsequent recovery of rSO₂ values occurs during reperfusion. During DHCA with SACP, rSO₂ values either increase or remain at baseline [37,40,41]. (See 'Cerebral protection' below.)

A sudden unilateral decrease in rSO₂ indicates regional decrease in cerebral perfusion [2,32]. An abrupt change should be promptly communicated to the surgeon and perfusionist since this may influence decisions regarding further intraoperative management. For example, this may occur during temporary clamping of the common carotid or innominate artery (image 8). If a severe contralateral decrease in rSO₂ occurs when unilateral SACP is initiated, the surgeon may decide to additionally cannulate the contralateral carotid artery so that bilateral SACP is provided. Sometimes, the unilateral decrease in rSO₂ is caused by vascular steal through the contralateral carotid artery that is open to the aortic arch. In this situation, clamping the contralateral carotid artery during SACP may improve cerebral perfusion to the contralateral hemisphere. Other causes of unilateral cerebral ischemia include acute extension of aortic dissection, Circle of Willis insufficiency, arterial cannula malposition, or thrombosis of an arterial graft; such events may also cause bilateral decrease in rSO₂ [34,38,44-46].

Bilateral decreases in rSO₂ may indicate global cerebral hypoperfusion due to hypoxemia, hypocarbia, anemia, venous hypertension, or inadequate anesthetic depth, or may occur during initiation of CPB or application of the aortic crossclamp [2,28-32]. Concurrent EEG monitoring may be useful in determining if the decrease in rSO₂ is associated with cerebral ischemia. (See "Management of cardiopulmonary bypass", section on 'Neuromonitoring modalities'.)

Cerebral flow index — A commercially available device, the c-FLOW monitor, noninvasively measures the cerebral flow index (ie, relative changes in brain cortical blood flow) using monochromatic laser and pulsed ultrasound. A case report demonstrated that CFI monitoring detected cerebral hypoperfusion due to malpositioning of an innominate artery cannula during selective antegrade cerebral perfusion [47]. In this case, decreases in CFI caused by cerebral hypoperfusion were observed earlier than the corresponding changes in regional cerebral oxygen saturation (rSO₂) measured by NIRS.

Temperature monitors — Temperature is continuously monitored for deliberate hypothermia during initiation of CPB, cooling, the period of DHCA, rewarming, and the postbypass period. Multiple temperature monitoring sites are employed. Monitoring sites in the body typically include the nasopharynx, blood (via the thermistor in the PAC), bladder (via a thermistor in the urinary catheter), and ear canal (tympanic membrane). Blood temperature is also monitored in the extracorporeal bypass circuit in both the arterial outlet blood temperature perfusing the patient and venous blood inlet temperature reentering the CPB circuit. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

Standard monitors — (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring'.)

●Noninvasive monitors – Standard noninvasive monitors are similar to those used for patients undergoing CABG surgery. A peripheral nerve stimulator may be employed to monitor degree of neuromuscular blockade. Defibrillator/pacing pads may be placed on the patient so that cardioversion, defibrillation, or pacing can be rapidly accomplished if necessary (figure 4).

●Bladder catheter – A bladder catheter with a temperature probe is inserted after induction for intermittent measurement of urine output approximately every 30 minutes and to provide one of several temperature monitors. (See "Management of cardiopulmonary bypass", section on 'Urine output' and "Management of cardiopulmonary bypass", section on 'Temperature'.)

●Intraoperative laboratory testing – The acute care laboratory or point-of-care testing facility is used to diagnose and manage rapid and unpredictable changes in physiologic conditions during major thoracic aortic operations with DHCA. Testing includes arterial blood gas (ABG) measurements with pH and base deficit, hemoglobin, electrolytes, calcium, glucose, lactate, and activated whole blood clotting time (ACT).

Results obtained from standard laboratory tests of hemostasis (eg, prothrombin time [PT], activated thromboplastin time [aPTT], and platelet count), as well as point-of-care tests (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) if available, are used to guide administration of blood products in a bleeding patient [48]. (See "Clinical use of coagulation tests" and "Intraoperative transfusion of blood products in adults", section on 'Point-of-care tests'.)

THE PREBYPASS PERIOD

Preoperative briefing — A focused preoperative briefing that includes the surgeon, anesthesiologist, perfusionist, and operating room nurse is critical for understanding and managing the proposed procedure and alternative techniques that may become necessary. General details regarding a preoperative surgeon-led briefing and specific details regarding surgical procedures and techniques that may be necessary to accomplish open aortic surgical repair are available in other topics:

●(See "Safety in the operating room", section on 'Briefings'.)

●(See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

●(See "Overview of open surgical repair of the thoracic aorta", section on 'Aortic arch'.)

Anesthetic management — Agents and techniques to induce general anesthesia are similar to those used for patients undergoing coronary artery bypass grafting (CABG) surgery. Administration of antimicrobial therapy should be initiated within 60 minutes of surgical incision. (See "Anesthesia for cardiac surgery: General principles", section on 'Induction of general anesthesia' and "Anesthesia for cardiac surgery: General principles", section on 'Antibiotic prophylaxis'.)

We prefer a volatile inhalation anesthetic (eg, sevoflurane, isoflurane, or desflurane) as the primary agent to maintain general anesthesia [49], typically administered together with a benzodiazepine, sedative-hypnotic agent (eg, propofol, etomidate), opioid (eg, fentanyl), and neuromuscular blocking agent (NMBA) to ensure prevention of hypertensive responses to noxious surgical stimuli or movement. In a 2016 systematic review of 45 trials that included 4890 cardiac surgical patients, volatile anesthetic agents were associated with reduced mortality (odds ratio [OR] 0.55, 95% CI 0.35-0.85) and a lower incidence of pulmonary complications (OR 0.71, 95% CI 0.52-0.98) and other complications (eg, overall cardiac events, myocardial infarction, renal failure, hepatic failure; OR 0.74. 95% CI 0.58-0.95) compared with total intravenous anesthesia (TIVA) [49]. Most patients in this review were undergoing CABG rather than aortic or other cardiac surgery. A TIVA technique may be a reasonable alternative [50-53]. (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance of general anesthesia'.)

If electroencephalography (EEG) monitoring is being performed in anticipation of a period of deep hypothermic circulatory arrest (DHCA), the dose of a volatile inhalation anesthetic is maintained at a fixed end-tidal concentration before and during cooling in order to minimize anesthetic-induced EEG changes. Also, bolus doses of intravenous (IV) anesthetic agents are avoided if possible, and are noted on the neurophysiologic monitoring record since these may produce acute transient changes in the EEG independent of temperature-induced changes. (See 'Electroencephalography' above.)

Other aspects of anesthetic management during positioning, incision, and sternotomy are similar to those for the prebypass period in patients undergoing CABG surgery. (See "Anesthesia for coronary artery bypass grafting surgery", section on 'Prebypass period' and "Anesthesia for cardiac surgery: General principles".)

Hemodynamic management — Hemodynamic management during the prebypass period is similar to that for patients undergoing CABG surgery, including performance of a complete transesophageal echocardiography (TEE) examination, fluid management, and control of hemodynamics during incision and sternotomy (table 3). (See "Anesthesia for coronary artery bypass grafting surgery", section on 'Prebypass period'.)

Many patients undergoing repair of the ascending aorta or arch have generalized cerebrovascular and ischemic heart disease. Avoidance and/or treatment of myocardial ischemia is similar to the approach taken in patients undergoing CABG. (See "Anesthesia for coronary artery bypass grafting surgery", section on 'Avoidance and treatment of ischemia'.)

In hemodynamically stable patients, acute normovolemic hemodilution may reduce the need for intraoperative transfusion of red blood cells (RBCs) and other blood products in the post-bypass period [54]. (See "Surgical blood conservation: Acute normovolemic hemodilution" and "Reversing anticoagulation and achieving hemostasis after cardiopulmonary bypass", section on 'Achieving hemostasis and management of bleeding'.)

In patients with acute aortic dissection, key hemodynamic issues in the prebypass period include:

●Arterial blood pressure (BP) should be precisely controlled to prevent hypertension that may cause extension of an aortic dissection, aneurysm rupture, or heart failure in a patient with aortic regurgitation (AR). In such cases, treatment is targeted to maintain systolic BP <120 mmHg [1]. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Anti-impulse therapy'.)

●In patients with cardiac tamponade, intravascular volume is maintained, while anesthetic or other agents that cause vasodilation or myocardial depression are avoided. (See "Anesthesia for thoracic trauma in adults", section on 'Cardiac tamponade' and "Anesthesia for thoracic trauma in adults", section on 'Anesthetic considerations for specific procedures'.)

●Administration of beta-blockers should be cautious (ie, small incremental doses) or avoided in patients with cardiac tamponade or acute AR due to aortic dissection because beta-blockers can worsen heart failure or precipitate cardiogenic shock in these conditions [1]. (See "Acute aortic regurgitation in adults", section on 'Treatment'.)

●Patients with cardiogenic shock or evidence of malperfusion of extremities due to aortic dissection are especially vulnerable to hypotension because of poor organ perfusion in the prebypass period and high risk of postoperative end-organ injury. Treatable causes are immediately addressed, including cardiac tamponade, hypovolemia, low systemic vascular resistance (SVR), severe ventricular dysfunction, or severe valvular dysfunction (eg, severe AR). These causes may be diagnosed with TEE. (See "Anesthesia for cardiac surgery: General principles", section on 'Transesophageal echocardiography'.)

Preparations for cardiopulmonary bypass — Standard preparations for initiation of cardiopulmonary bypass (CPB), including anticoagulation and antifibrinolytic administration, are discussed separately (table 3). (See "Initiation of cardiopulmonary bypass".)

Arterial cannulation for CPB can be performed centrally via the aorta, or at the axillary, innominate, or femoral arterial sites. This critical aspect of the surgical plan and alternative techniques should be discussed with the operating room team (surgeon, anesthesiologist, perfusionist, operating room nurse) during the preoperative briefing (see 'Preoperative briefing' above). If the proposed plan changes because of intraoperative findings, the necessary equipment, monitors, and perfusion techniques must be available. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta' and "Overview of open surgical repair of the thoracic aorta", section on 'Aortic arch'.)

Transesophageal echocardiography (TEE) is useful for confirming wire placement in the true lumen of the vessel during arterial cannulation of the selected arterial site. (See 'Transesophageal echocardiography' above.)

If retrograde cerebral perfusion (RCP) is planned as an adjunct to DHCA, venous cannulation is accomplished using separate cannulae in both the superior vena cava (SVC) and inferior vena cava (IVC) in order to separately perfuse the SVC, rather than using a single right atrial cannula (figure 5 and figure 6). (See "Initiation of cardiopulmonary bypass", section on 'Venous cannulation'.)

CARDIOPULMONARY BYPASS WITH DEEP HYPOTHERMIC CIRCULATORY ARREST

General principles — Cardiopulmonary bypass (CPB) is necessary to accomplish surgical repairs of the upper thoracic aorta. Management of routine aspects of CPB is addressed separately. (See "Management of cardiopulmonary bypass".)

Surgical anastomoses performed on portions of the ascending aorta or aortic arch require temporary interruption of cerebral and systemic blood flow. The brain, spinal cord, and vital organs (kidneys, liver, and gastrointestinal tract) are protected by inducing deliberate deep hypothermia during this period of elective circulatory arrest. This is accomplished by systemically cooling the patient using the heat exchanger in the CPB circuit. Once the target temperature is reached, the patient is partially exsanguinated into the circuit, then CPB pump flow is discontinued [55].

Although the optimal temperature and safe duration for deep hypothermic circulatory arrest (DHCA) are unknown, experimental and clinical data support the effectiveness of deep hypothermia to provide organ protection during circulatory arrest lasting approximately 20 minutes, and as long as 60 minutes in some cases (figure 7). Experimental and clinical data support use of selective antegrade cerebral perfusion (SACP) or retrograde cerebral perfusion (RCP) to supplement cerebral protection provided by deep hypothermia, although there are no randomized trials comparing these techniques. (See 'Cerebral protection' below and "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta' and "Overview of open surgical repair of the thoracic aorta", section on 'Aortic arch'.)

Cerebral protection — Selection of a cerebral protection strategy during elective circulatory arrest is institution- and surgeon-specific [1,2]. Most cases are performed with deep hypothermia supplemented with SACP or RCP [56-59]. (See 'Deep hypothermia with selective antegrade cerebral perfusion' below and 'Deep hypothermia with retrograde cerebral perfusion' below.)

Cooling and deep hypothermia — Active systemic cooling is initiated only after CPB has been established, and the rate of cooling can be increased after application of the aortic cross clamp at the calculated full pump flow rate approximating normal cardiac index (typically 2.2 to 2.4 L/minute/m² in normothermic patients). If there is evidence of cerebral malperfusion during onset of CPB (see 'Brain monitors' above), bypass is discontinued to evaluate and potentially revise the cannulation sites. When effective CPB has been confirmed, cooling is continued until the target temperature for circulatory arrest has been reached and/or electrocortical silence has been achieved on the electroencephalogram (EEG) (figure 2 and figure 3) (see 'Electroencephalography' above). Because it is not possible to deliver any medication during circulatory arrest, any anesthetics, neuromuscular blocking agents, antibiotics, or other drugs that might be necessary should be administered before initiation of DHCA. All intravenous (IV) drug infusions and delivery of volatile anesthetic agents should be discontinued during the period of DHCA.

●Temperature during DHCA – For a circulatory arrest period of 30 to 40 minutes, a temperature of 16 to 18°C will produce electrocortical silence on the EEG in many patients, but cooling for 50 minutes or a nasopharyngeal temperature of 12.5°C is necessary to generate electrocortical silence in 99.5 percent of all patients [23,58]. If the duration of DHCA is anticipated to be greater than 30 to 40 minutes, a target temperature closer to 12.5°C may be justified [21-24]. If cerebral perfusion is provided by SACP during circulatory arrest, warmer temperatures in the range of 28°C are often used [56,57] (see 'Deep hypothermia with selective antegrade cerebral perfusion' below and 'Deep hypothermia with retrograde cerebral perfusion' below). Some surgeons and anesthesiologists also like to pack the patient's head in ice bags to augment or maintain cerebral cooling, but this technique is not a substitute for deliberate hypothermia delivered by CPB. In specialized centers, topical cooling has been used successfully to achieve deliberate hypothermia for DHCA but there is limited evidence to support the effectiveness of topical cooling using the techniques and devices presently available [60].

The chosen target temperature for DHCA for an individual patient in a specific clinical setting is variable and depends on many factors, including whether SACP or RCP is used, whether intraoperative neurophysiologic monitoring is available, and the type and planned duration of the operation. Other factors include surgeon preference, institutional practice patterns, and established perfusion protocols.

During cooling and hypothermia, thermistors in the CPB circuit continuously monitor blood temperature at the arterial outlet of the oxygenator just before entering the patient, as well as the venous blood reentering the CPB circuit into the venous reservoir. The temperature gradient between the venous inflow and arterial outlet on the oxygenator is maintained at <10°C. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

The oxygenator arterial outlet temperature is used as the primary surrogate for the cerebral temperature target during cooling [61,62]; a nasopharyngeal or tympanic membrane temperature probe provides an additional estimate. Despite monitoring temperature at multiple sites, there is no direct way to measure actual brain temperature during CPB and DHCA. Thus, the presence of burst suppression or electrocortical silence on the EEG is frequently used as a neurophysiologic surrogate to monitor for adequacy of brain hypothermia [21-23]. (See 'Electroencephalography' above.)

●Duration of DHCA – After target temperature is achieved, a duration of DHCA of 30 to 45 minutes is generally safe. Under normothermic conditions, irreversible ischemic neuronal injury is detected within four to five minutes after cerebral blood flow is interrupted. However, cerebral oxygen consumption (CMRO₂) decreases by a factor of 2.3 for every 10°C decrease in body temperature (figure 7) [63,64]. Thus, if the brain's tolerance to ischemia is correlated solely with its metabolic rate, a five-minute tolerance for circulatory arrest at 37°C would increase to 25 to 38 minutes at temperatures of 13 to 20°C [64]. Also, it is likely that hypothermia has protective actions independent of its effect on cerebral metabolism. Experimental studies suggest that hypothermia attenuates the release of excitatory neurotransmitters and inflammatory mediators, maintains the integrity of the blood–brain barrier, and helps to prevent neuronal apoptosis in response to ischemic injury.

Clinical evidence suggests that the incidence of postoperative neurologic complications such as stroke, transient neurologic deficit, neurocognitive dysfunction, and seizures correlates with duration of DHCA, and is significantly associated with DHCA duration >45 minutes [59,65-67]. Direct measurement of cerebral metabolites and electrophysiologic activity in humans has demonstrated evidence of cerebral ischemia within 30 minutes of DHCA with RCP. (figure 8) [68]. Experimental evidence in rats also demonstrates functional and histologic deficits after 30 to 60 minutes of DHCA [69].

Deep hypothermia with selective antegrade cerebral perfusion — Many surgeons employ SACP to reduce the period of cerebral ischemia during DHCA [2,70,71]. (See "Surgical and endovascular management of acute type A aortic dissection", section on 'Antegrade cerebral perfusion'.)

SACP with oxygenated blood at temperatures as low as 10 to 12°C can be delivered by direct cannulation of the open ends of the aortic arch vessels during reconstruction of the aortic arch, selective cannulation of the innominate artery, perfusion through a vascular graft sewn onto the axillary or subclavian artery, or a combination of these techniques (figure 9) [72-74]. Flow rates for SACP are typically 5 to 7 mL/kg/minute at a pressure of 60 to 70 mmHg measured in the ipsilateral radial artery. (See 'Intra-arterial catheter' above.)

The anesthesiologist can assess adequacy of cerebral perfusion during SACP by employing both continuous EEG (while EEG activity is still present at warmer temperatures) and cerebral oximetry (see 'Electroencephalography' above and 'Cerebral oximetry' above) [2]. During SACP under isothermic conditions, cerebral hypoperfusion may be diagnosed by noting acute slowing or decreased amplitude of the EEG waveforms or acute decreases in unilateral or bilateral cerebral oximetry regional oxygen saturation (rSO₂) values. If SACP is delivered unilaterally, an acute decrease in rSO₂ on the ipsilateral side may indicate malpositioning of the SACP cannula, while an acute decrease in rSO₂ on the contralateral side may indicate a need for greater perfusion pressure on that side or institution of bilateral SACP [2,29,34-41]. Bilateral sudden decreases in EEG amplitude and frequency indicates likely cerebral ischemia due to malperfusion [2].

Although the effectiveness of hypothermia for brain protection in aortic operations is well proven, the optimal temperature with optimal delivery of SACP has not been established. Performing the operation with deliberate hypothermia at a higher target systemic temperature may have the advantage of decreasing CPB duration because it takes less time to cool and rewarm in addition to decreasing the risk of hyperthermia during rewarming. A 2014 meta-analysis of retrospective studies that included 5100 patients noted no differences in mortality or postoperative neurologic deficits when unilateral SACP was employed compared with bilateral SACP, even though some patients may have an incomplete circle of Willis [75]. In that meta-analysis, a longer duration of DHCA or higher temperature during DHCA was associated with higher mortality and postoperative neurologic deficits. However, a 2018 meta-analysis that included 1215 patients in the "cold," cohort with mean temperature 20.3°C and 1417 patients in the "warm," cohort with mean temperature 26.5°C noted that temporary neurologic deficit, postoperative dialysis, duration of controlled ventilation, and intensive care unit stays were reduced in the "warm," cohort group [76]. However, mortality between the groups did not differ.  

Deep hypothermia with retrograde cerebral perfusion — RCP is a technique employed by some surgeons to prolong the safe duration of circulatory arrest during DHCA [2]. This technique uses a standard CPB circuit without need for cannulation or instrumentation of the aortic arch vessels. During delivery of RCP, the superior vena cava (SVC) cannula is ensnared between the right atrium and the azygous vein (figure 5). After the cannula is ensnared, cold oxygenated blood at a rate of 150 to 250 mL/minute is perfused retrograde into the SVC cannula. (See "Surgical and endovascular management of acute type A aortic dissection", section on 'Retrograde cerebral perfusion'.)

During RCP, the patient is maintained in a 10-degree Trendelenburg position to decrease the risk of cerebral air embolism. The anesthesiologist continuously monitors SVC pressure during RCP, which should be maintained <25 mmHg to prevent cerebral edema. The theoretical risk of cerebral edema as a consequence of RCP may be greater in patients with significant cerebrovascular disease. SVC pressure is typically monitored via the side-port of an introducer sheath in an internal jugular vein.

RCP does not fulfill the metabolic demands of the brain even with concomitant deep hypothermia. A gradual decline in rSO₂ is typically observed with cerebral oximetry monitoring during DHCA with or without RCP [33,40,42,43] (see 'Brain monitors' above). Also, direct measurements of cerebral metabolites and electrophysiologic activity in humans undergoing DHCA with RCP have demonstrated evidence of cerebral ischemia within 30 minutes of DHCA (figure 8) [68].

Although RCP does not prevent neuronal ischemia, the technique does provide low cerebral blood flow (which may be better than absent flow) and serves to maintain brain hypothermia during DHCA. Also, the retrograde perfusion decreases the risk of antegrade arterial air embolism or particulate thromboembolism when normal antegrade cerebral perfusion is resumed. (See "Overview of open surgical repair of the thoracic aorta", section on 'Aortic arch'.)

Rewarming strategies — After completion of the portion of the surgical repair requiring circulatory arrest with deep hypothermia, CPB is reinstituted with initial reperfusion of the brain at the original cold target temperature for approximately 10 minutes before beginning the rewarming process. During rewarming while the arterial blood outlet temperature is <30°C, a temperature gradient no greater than 10°C is maintained between the venous inflow to the oxygenator and the arterial outlet. Once arterial outlet temperature has reached 30°C, this arterial-to-venous temperature gradient should be no greater than 4°C. At all times, the arterial blood outlet temperature should remain no higher than 36.5°C. In general, rewarming should be accomplished slowly, with a rewarming rate limited to ≤0.5°C/minute. The time required to achieve such gradual rewarming after deep hypothermia to ≤16°C may be ≥90 minutes. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

During rewarming, the oxygenator arterial outlet temperature is again used as the primary surrogate for cerebral temperature, although nasopharyngeal and/or tympanic membrane temperatures are also continuously monitored [61,62]. Clinical data have demonstrated that each of the temperature monitoring sites within the body (see 'Temperature monitors' above) underestimates temperature monitored with a jugular venous catheter positioned with its tip in the jugular bulb, considered to be the optimal site for monitoring cerebral temperature [62,77]. Since monitoring jugular bulb temperature is not usually feasible, the best alternative for avoiding cerebral hyperthermia is to ensure that no temperature site ever exceeds 37°C, particularly the arterial outlet temperature, even if this prolongs the rewarming process. During rewarming, temperature of the venous blood returning into the venous reservoir of the CPB circuit estimates systemic temperature, while the bladder temperature provides an estimate of "core" temperature (ie, the body temperature at thermal equilibrium in the periphery). (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

These recommendations for rewarming are similar to consensus statements in guidelines published by several professional societies [1,61]. It is important to avoid cerebral hyperthermia because of its deleterious effects on the brain [1,61,78-80]. Injury is particularly likely after a period of DHCA due to potential exacerbation of neurologic injury due to ischemia-reperfusion injury. Hyperthermia may also exacerbate neurologic injury that occurs as a consequence of cerebral thromboembolic events during open aortic or open cardiotomy surgery. Thromboembolism of air or particulate debris is most likely to occur when cerebral perfusion resumes or after removal of the aortic crossclamp when ventricular ejection resumes.

Pharmacologic agents — Although pharmacologic adjuncts (eg, antiinflammatory agents, barbiturates, or propofol) are commonly administered for cerebral protection, efficacy has not been proven [1]. If intraoperative neurophysiologic monitoring is being used to guide adequacy of cerebral hypothermia, administration of barbiturates, propofol, or volatile anesthetic agents may lead to electrocortical silence on the EEG unrelated to brain temperature, metabolic activity, or hypothermic cerebral protection. (See 'Electroencephalography' above.)

Otherwise, administration of pharmacologic adjuncts such as glucocorticoids, anesthetic agents, magnesium, mannitol, furosemide, or lidocaine involves minimal risk. Clinicians cite this low risk as justification for administering such pharmacologic adjuncts as well as theoretical physiologic and biochemical rationales for possible cerebral protection based on small clinical and experimental investigations and individual clinical experiences.

Effects of deep hypothermia — Use of deep hypothermia during CPB requires additional strategies for anesthetic administration and management of hyperglycemia, anticoagulation, hemodilution, and arterial blood gases (ABGs). Residual effects of deep hypothermia on coagulation and the cardiovascular system also influence postbypass management (table 2). (See 'The postbypass period' below.)

Anesthetic requirements — Anesthetic requirements are reduced during deliberate deep hypothermia, and general anesthesia is not needed after the onset of EEG burst suppression and throughout the period of electrocortical silence. However, anesthetic administration should be resumed during rewarming to ensure an anesthetized state when nasopharyngeal temperature has reached approximately 30°C or when consistent EEG activity has returned (typically approximately 30 minutes after initiating rewarming) [81]. (See 'Electroencephalography' above.)

Hyperglycemia — After DHCA, nearly all patients develop hyperglycemia requiring control with IV insulin administration. As recommended in published guidelines, blood glucose concentration should be maintained <180 mg/dL (10 mmol/L), but it is important to monitor blood glucose frequently to prevent unintentional hypoglycemia [5,82]. Insulin infusion therapy to treat hyperglycemia may exacerbate hypokalemia in the postbypass period. (See "Management of cardiopulmonary bypass", section on 'Electrolytes and lactate'.)

Anticoagulation — Anticoagulation is somewhat prolonged during hypothermia due to delayed metabolism and excretion of heparin. During rewarming, heparin concentrations decrease as heparin is metabolized. Activated whole blood clotting time (ACT) is checked every 30 minutes during CPB in operations that require deep hypothermia.

Acid–base management

●Blood gas management – Targets for blood gas management during deep hypothermia may be guided by two different strategies, one termed alpha-stat and the other pH-stat. The fundamental difference between these two approaches is that at any given patient temperature, alpha-stat management results in lower ABG partial pressure of carbon dioxide (pCO₂) values and higher pH values compared with the alternative pH-stat management approach [83].

Alpha-stat blood gas management (ie, temperature-uncorrected blood gas measurements) is typically used during cooling for DHCA and during rewarming. Arguments for using alpha-stat management include preservation of cerebral blood flow autoregulation, as well as decreased risk of cerebral thromboembolism, cerebral edema, reperfusion injury, and inadvertent cerebral hyperthermia during rewarming [84,85]. In most centers, alpha-stat ABG management is also employed for adult patients undergoing routine CPB without deep hypothermia [4,5]. (See "Management of cardiopulmonary bypass", section on 'Oxygenation, ventilation, and arterial blood gases'.)

Because increased arterial carbon dioxide (CO₂) concentration causes cerebral vasodilation, pH-stat ABG management (ie, blood gas measurements corrected to the patient's actual temperature) results in greater cerebral blood flow than alpha-stat blood gas management. Arguments for using pH-stat management include increased cerebral blood flow to decrease the duration of cooling as hypothermia is induced and to potentially decrease the duration of rewarming [86]. However, cerebrovascular disease may decrease vascular reactivity in response to arterial CO₂ concentration leading to impaired cooling of brain regions supplied by diseased vessels if pH-stat management is used.

●Metabolic acidosis – Lactic acidosis commonly occurs during reperfusion after DHCA and may be associated with hyperkalemia. Blood lactate concentrations increase gradually after the onset of reperfusion and peak at an average concentration of 7.8 mmol/L approximately six hours after DHCA, with return to normal over 18 to 20 hours [87]. Associated metabolic acidosis at an average pH nadir of 7.27 is present in approximately 80 percent of patients after DHCA, with return to normal over 12 to 14 hours [87]. Although sodium bicarbonate 8.4 percent (50 mEq/50 mL) is typically titrated to treat metabolic acidosis if base deficit is <-7 mEq/L or pH is <7.20, clinical efficacy of this treatment is controversial, and excessive administration of sodium bicarbonate should be avoided to prevent postoperative hypernatremia [88]. Although hyperventilation is commonly used to attenuate the severity of metabolic acidosis, it may have undesirable effects on cerebral blood flow.

Hemodilution management — There is insufficient evidence to target a specific hemoglobin (Hgb) concentration to optimize oxygen delivery during DHCA. Hgb values ≥7.5 g/dL (hematocrit [HCT] ≥22 percent) are suggested during routine CPB with mild to moderate hypothermia, and this is the typical target for CPB with a period of DHCA as well. (See "Management of cardiopulmonary bypass", section on 'Hemoglobin/hematocrit'.)

Arguments in favor of maintaining a lower Hgb <7.5 g/dL during deep hypothermia (≤18°C) include mitigation of increased blood viscosity and the leftward shift in the oxygen-hemoglobin dissociation curve. The Hgb level and oxygen delivery are less critical during deep hypothermia due to the profound reduction in metabolic rate. Arguments in favor of transfusion of red blood cells (RBCs) if Hgb is <7.5 g/dL when hemoconcentration is not possible or is ineffective include the beneficial effects of increased oxygen carrying capacity of blood under low flow conditions such as SACP or RCP, which may outweigh the theoretical adverse effects of increased viscosity on microcirculatory flow. Also, a higher Hgb level facilitates avoidance of severe anemia during the postbypass period when surgical bleeding is common.

There is no benefit when higher Hgb levels (eg, 8 to 10 g/dL) are maintained in patients undergoing aortic surgery with DHCA [89].

THE POSTBYPASS PERIOD

●Weaning from cardiopulmonary bypass (CPB) – The process of weaning from CPB and management of problems during weaning are reviewed in a separate topic. (See "Weaning from cardiopulmonary bypass" and "Intraoperative problems after cardiopulmonary bypass".)

●Problems in the postbypass period – Postbypass problems after open aortic surgery requiring deep hypothermia typically include:

•Blood pressure (BP) control

-Postbypass control of hypertension with intravenous (IV) boluses or infusion of antihypertensive agents is critical to decreasing the risk of bleeding from fresh aortic anastomotic sites (table 4). Vasoconstriction due to residual hypothermia may cause or contribute to hypertension. Continuous infusion of antihypertensive agents is often necessary.

-Postbypass hypotension may occur due to vasodilation as rewarming and reperfusion continue, or as a consequence of low cardiac output (CO) (determined by measurements on pulmonary artery catheter [PAC] and/or by noting ventricular dysfunction on transesophageal echocardiography [TEE]). Vasoconstrictor or inotropic agents may be necessary to treat significant hypotension (table 5), and high doses of anesthetic agents (eg, a potent volatile inhalation anesthetic or IV agents) are avoided.

•Controlling coagulopathy and achieving hemostasis – Establishing hemostasis is challenging after aortic surgery with deep hypothermic circulatory arrest (DHCA) (see 'Deep hypothermia' above). Surgical bleeding is exacerbated by coagulopathy due to the anti-hemostatic effects of deep hypothermia (table 2), ischemia and reperfusion injury due to elective circulatory arrest, fibrinolysis and platelet activation due to prolonged duration of CPB, and underlying aortic vascular pathology [2,15,16].

Intermittent measurements (approximately every 30 minutes) of hemoglobin (Hgb) or hematocrit (HCT) are obtained to guide packed red blood cell (RBC) transfusion and to avoid excessive hemodilution due to bleeding in the postbypass period. Hemodilution and transfusion have both been associated with the risk of acute kidney injury after thoracic aortic surgery [90-92].

Management of persistent bleeding, anemia, massive transfusion, thrombocytopenia, and coagulopathy after CPB is addressed separately. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Bleeding and coagulopathy' and "Clinical use of coagulation tests", section on 'Point-of-care testing'.)

In rare cases, sternal closure must be delayed because of persistent bleeding, hemodynamic compromise caused by compression of the right atrium and right ventricle (RV) within the mediastinum, or other technical problems. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Inability to close the sternum'.)

•Fluid management – Dynamic intravascular fluid shifts are common after major thoracic aortic operations because of vasodilation during reperfusion, as well as bleeding and transfusion. Intravascular volume status is assessed and monitored using TEE, as well as data supplied by PAC measurements (eg, CO, mixed venous hemoglobin saturation [SvO₂], pulmonary artery pressure [PAP], and central venous pressure [CVP]). (See "Anesthesia for cardiac surgery: General principles", section on 'Postbypass management of fluids and blood products' and "Anesthesia for cardiac surgery: General principles", section on 'Postbypass transesophageal echocardiography'.)

●Transport to the intensive care unit (ICU) – Hemostasis and hemodynamic stability must be achieved prior to transport to the ICU. (See "Anesthesia for cardiac surgery: General principles", section on 'Transport and handoff in the intensive care unit'.)

Patients typically remain sedated and tracheally intubated with controlled mechanical ventilation in the ICU until thorough rewarming and hemodynamic stability are achieved; metabolic acidosis, bleeding, and coagulopathy have been corrected; and neurologic and pulmonary function are adequate for extubation.

EARLY POSTOPERATIVE COMPLICATIONS — Major complications in the early postoperative period after ascending aortic or arch surgery requiring a period of deep hypothermia include coagulopathy, bleeding and/or cardiac tamponade requiring mediastinal reexploration [2], stroke or encephalopathy, malperfusion of extremities, renal insufficiency, respiratory insufficiency, or death. These complications are addressed separately. (See "Overview of open surgical repair of the thoracic aorta", section on 'Complications'.)

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: Management of cardiopulmonary bypass" and "Society guideline links: Aortic and other peripheral aneurysms" and "Society guideline links: Aortic dissection and other acute aortic syndromes".)

SUMMARY AND RECOMMENDATIONS

●Routine aspects of the preanesthetic consultation for patients undergoing open surgical repairs of the ascending aorta or aortic arch are similar to other cardiac surgical cases. (See 'Preanesthetic consultation and planning' above.)

•The presence of aortic or carotid arterial atherosclerosis; chronic or acute aortic regurgitation (AR); cardiac tamponade; cerebral, coronary, or limb malperfusion; or a mediastinal mass effect will influence anesthetic and surgical management. (See 'Comorbidities due to ascending aortic or arch disease' above.)

•If a period of deep hypothermia (eg, temperatures of 16 to 18°C) with elective circulatory arrest, selective antegrade cerebral perfusion (SACP), or retrograde cerebral perfusion (RCP) is planned by the surgeon, specialized monitoring is employed. (See 'Deep hypothermia' above.)

●Monitoring during cardiac surgery with cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) includes:

•Cardiovascular monitors – Invasive cardiovascular monitoring includes systemic arterial and pulmonary arterial or central venous catheters. (See 'Intra-arterial catheter' above and 'Pulmonary artery catheter' above.)

•Echocardiography – Transesophageal echocardiography (TEE) is routinely employed to guide placement of the aortic and other cannulae for CPB, to detect AR and/or ventricular distention during CPB, and to guide removal of intracardiac air before weaning from CPB during open aortic surgery. For acute aortic dissection requiring emergency surgical repair, intraoperative TEE is used to verify the diagnosis and detect complications such as cardiac tamponade, acute AR, or global or regional ventricular dysfunction indicating ischemia. Similar to other cardiac surgical procedures, TEE is also used to assess the causes of acute life-threatening hemodynamic instability. (See 'Transesophageal echocardiography' above.)

•Brain monitors – Electroencephalography (EEG) is useful for confirming electrocortical silence due to hypothermia before establishing elective circulatory arrest, as well as for detecting cerebral hypoperfusion and assessing anesthetic depth. Cerebral oximetry with near-infrared spectroscopy (NIRS) is employed, if available, to detect unilateral or bilateral cerebral hypoperfusion. (See 'Brain monitors' above.)

•Temperature monitors – Temperature is monitored at multiple body and oxygenator sites. (See 'Temperature monitors' above.)

•Standard monitors – Standard noninvasive monitors are employed, and urine output is measured intermittently. Laboratory values are measured before, during, and after CPB (eg, arterial blood gas [ABG], pH and base deficit, hemoglobin [Hgb], electrolytes, calcium, glucose, lactate, activated whole blood clotting time [ACT], and tests of hemostasis). (See 'Standard monitors' above.)

●We prefer a volatile inhalation anesthetic as the primary agent to maintain general anesthesia, typically coadministered with intravenous (IV) agents (eg, sedative-hypnotic, opioid, benzodiazepine, and neuromuscular blocking agents [NMBAs]). If EEG monitoring is being performed in anticipation of a period of DHCA, the volatile anesthetic dose is maintained at a fixed end-tidal concentration, and bolus doses of IV anesthetic agents are avoided before and during cooling to minimize anesthetic-induced EEG changes. (See 'Anesthetic management' above.)

●Preparations for initiation of CPB, including anticoagulation and antifibrinolytic administration, are similar to those for other cardiac surgical procedures (table 3). (See 'The prebypass period' above and 'Electroencephalography' above.)

●Surgery on portions of the ascending aorta or arch requires temporary interruption of cerebral and systemic blood flow; deliberate deep hypothermia is induced using CPB to provide protection of the brain and vital organs. Once the target temperature is reached, the patient is partially exsanguinated into the CPB circuit, and pump flow is discontinued. (See 'General principles' above.)

●Use of DHCA for cerebral protection includes the following considerations during CPB (see 'Cerebral protection' above):

•The oxygenator arterial outlet temperature is used as the primary surrogate for brain temperature target during cooling; nasopharyngeal or tympanic membrane temperature probes provide an additional estimate. (See 'Cooling and deep hypothermia' above.)

•A temperature of 16 to 18°C produces electrocortical silence on the EEG for many patients, but 12.5°C is necessary to achieve electrocortical silence in 99.5 percent of patients. If duration of DHCA is anticipated to be >30 to 40 minutes without use of SACP or RCP, such lower target temperatures may be selected. The presence of burst suppression or electrocortical silence on the EEG is frequently used as a neurophysiologic surrogate to monitor for adequacy of brain hypothermia. (See 'Electroencephalography' above and 'Cooling and deep hypothermia' above.)

•Cerebral protection with deep hypothermia is often supplemented with SACP or RCP, allowing use of a warmer temperature (approximately 28°C) during interruption of normal cerebral blood flow. (See 'Deep hypothermia with selective antegrade cerebral perfusion' above and 'Deep hypothermia with retrograde cerebral perfusion' above.)

•After a period of DHCA, CPB is reinstituted with initial reperfusion of the brain at the original cold target temperature for approximately 10 minutes, then rewarming with a temperature gradient ≤10°C between the venous inflow and the arterial outlet of the oxygenator. When the arterial outlet temperature reaches 30°C, this gradient can be ≤4°C. At all times, the arterial blood outlet temperature should remain ≤36.5°C. Cerebral hyperthermia may exacerbate ischemia-reperfusion neurologic injury after DHCA. In general, rewarming should be accomplished slowly at a rate of ≤0.5°C/minute, which may require ≥90 minutes after deep hypothermia ≤16°C. (See 'Rewarming strategies' above.)

•Anesthetic requirements are reduced during deep hypothermia, and general anesthesia is not needed after the onset of EEG burst suppression and throughout the period of electrocortical silence. However, anesthetic administration should be resumed during rewarming to ensure an anesthetized state when nasopharyngeal temperature has reached approximately 30°C or when consistent EEG activity has returned. (See 'Anesthetic requirements' above.)

•Altered strategies are necessary for management of hyperglycemia, anticoagulation, hemodilution, and ABGs (table 2). (See 'Effects of deep hypothermia' above.)

●Residual effects of DHCA in the postbypass period may cause hyper- or hypotension and interfere with hemostasis (table 2). Surgical bleeding is exacerbated by coagulopathy due to the anti-hemostatic effects of deep hypothermia, ischemia and reperfusion injury due to elective circulatory arrest, fibrinolysis and platelet activation due to prolonged duration of CPB, and underlying aortic vascular pathology. Control of blood pressure (BP) and surgical hemostasis must be achieved prior to patient transport to the intensive care unit. (See 'The postbypass period' above.)