Anesthesia for aortic surgery with hypothermia and elective circulatory arrest in adult patients

INTRODUCTION — Open surgical repair of the ascending aorta or aortic arch requires temporary interruption of cerebral and systemic blood flow [1,2]. Deliberate circulatory arrest is induced with the aid of cardiopulmonary bypass (CPB) to allow surgical replacement of the ascending aorta or aortic arch, and hypothermia helps protect vital organs from ischemia during the period of elective circulatory arrest. This topic discusses anesthetic management and strategies for cerebral protection during proximal aortic surgery with deep hypothermic circulatory arrest (DHCA).

Preparations for, management of, and weaning from CPB are discussed in separate topics:

●(See "Initiation of cardiopulmonary bypass".)

●(See "Management of cardiopulmonary bypass".)

●(See "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 ASSESSMENT AND PLANNING — General considerations for preanesthetic consultation before cardiac surgical procedures are discussed separately. (See "Preoperative evaluation for anesthesia for cardiac surgery".)

Coexisting pathology — Patients with acute or chronic disease of the ascending aorta or arch have coexisting conditions that may affect anesthetic and surgical management, as described below. (See "Overview of open surgical repair of the thoracic aorta", section on 'Preoperative evaluation and preparation'.)

●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 heart failure. Diagnosis with preoperative transthoracic or transesophageal echocardiography (TEE) is confirmed by intraoperative TEE examination during the prebypass period. (See 'Transesophageal echocardiography' below.)

Modifications in cardioplegia delivery technique and/or left ventricular (LV) venting during cardiopulmonary bypass (CPB) may be necessary if significant AR is present, as discussed separately. (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 that increases the risk of cerebral and systemic thromboembolic complications may be present. Also, the presence of significant occlusive cerebrovascular disease may lead to choosing selective antegrade cerebral perfusion (SACP) rather than retrograde cerebral perfusion (RCP), as discussed below. (See 'Selective cerebral perfusion during DHCA' below.)

●Mediastinal mass effect – Some patients have a mediastinal mass effect 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) [3-6]. This may result in hemodynamic or airway compromise during induction. Details are discussed separately. (See "Anesthesia for patients with an anterior mediastinal mass", section on 'Airway management during induction' and "Anesthesia for patients with an anterior mediastinal mass", section on 'Hemodynamic management during induction'.)

Review of the surgical plan — Planned cerebral protection strategies during elective circulatory arrest are reviewed with the surgical team; these are institution- and surgeon-specific [1,7]. Most cases of planned circulatory arrest are performed with either moderately deep hypothermia (in the range of 20 to 28 °C) or deep hypothermia (in the range of 16 to 20°C) [8,9], usually supplemented with SACP or RCP [10-13]. (See 'Selective antegrade cerebral perfusion' below and 'Retrograde cerebral perfusion' below.)

Planned use of moderately deep or deep hypothermia — Surgical replacement of the ascending aorta or aortic arch requires temporary interruption of cerebral and systemic blood flow. Inducing moderately deep or deep hypothermia with the aid of CPB permits surgical reconstruction of the aortic arch without cross clamping a diseased aorta or instrumenting and possibly injuring aortic arch branch vessels. Multiple temperature monitoring sites and specialized brain monitors are used before, during, and after a period of deep hypothermia. (See 'Temperature monitors' below and 'Brain monitors' below.)

Moderately deep or deep hypothermia cause physiologic changes that can persist (table 1) [14-16]. (See 'Considerations for anesthetic management' below and 'Problems in the postbypass period' below.)

Preparations include:

●Since coagulopathy with persistent bleeding is common, adequate venous access is necessary. Typically, four to six units each of red blood cells (RBCs) and fresh frozen plasma (FFP) are crossmatched, as well as four to six pooled whole blood-derived platelet concentrates (or one apheresis unit).

●Vasoconstriction typically occurs during cooling and hypothermia, while vasodilation typically occurs during rewarming and reperfusion. Vasoactive infusions are prepared in advance to treat blood pressure that is either too high or too low (table 2 and table 3). (See 'Control of blood pressure' below.)

●Since nearly all patients undergoing moderately deep or deep hypothermic circulatory arrest (DHCA) develop hyperglycemia requiring control with intravenous (IV) insulin administration, an insulin infusion is prepared.

Planned use of selective cerebral perfusion techniques — DHCA is often combined with SACP or RCP. Plans for selective cerebral perfusion guide selection of site(s) to monitor direct arterial pressure. (See 'Intra-arterial catheter' below.)

Considerations for emergency surgery for acute aortic dissection — Emergency surgical repair is necessary for acute ascending (type A) aortic dissection (movie 1 and image 2 and figure 1). Surgical and preanesthetic evaluation and preparation are expedited so that induction of general anesthesia can proceed without delay [7]. 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.

Factors that increase risk and affect anesthetic and surgical management include [7,17]:

●Acute AR – Acute AR may occur as a consequence of dissection involving the aortic root. 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) is withheld or administered cautiously to prevent cardiogenic shock in a patient with acute AR.

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. Signs of cardiac tamponade on physical examination should be noted. 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 cardiac tamponade is assessed with preoperative transthoracic echocardiography (TTE) but may worsen during preoperative evaluation. Thus, severity is reassessed with intraoperative TEE after induction of general anesthesia. (See "Anesthesia for patients with pericardial disease and/or cardiac tamponade", section on 'Assessing diagnostic tests' and 'Transesophageal echocardiography' below.)

As noted above for patients with acute AR, beta-blocker therapy is withheld in a patient with cardiac tamponade to prevent cardiogenic shock.

●Malperfusion of extremities – Aortic branch vessels involved in the dissection or perfused from the false lumen of the aorta may result in limb malperfusion that determines which sites are suitable for intra-arterial catheter insertion for continuous monitoring of BP (see 'Intra-arterial catheter' below), as well as for arterial cannulation for CPB. 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.

●Acute stroke – Malperfusion or dissection of the aortic arch vessels may cause an acute stroke [18]. Preoperative or intraoperative surface vascular ultrasound or carotid artery duplex imaging may be used to diagnose extension of the dissection into the common carotid arteries and to assess blood flow in these arteries.

●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 [19]; management is discussed separately. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Left ventricular dysfunction'.)

●Acute mesenteric ischemia – Acute visceral ischemia may manifest as acute renal failure or abdominal pain with melena. Renal risk mitigation during cardiac surgery is discussed separately. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Chronic kidney disease and renal risk mitigation'.)

●Acute spinal cord ischemia – Rarely, aortic intramural hematoma may cause spinal cord ischemia with paraparesis/paraplegia [20].

●Coagulopathy – Acute type A aortic dissection is associated with preoperative coagulopathy that worsens during and after surgery, particularly if deep hypothermia is used [21]. (See 'Control of coagulopathy to achieve hemostasis' below.)

MONITORING — Usual monitoring for cardiac surgery with cardiopulmonary bypass (CPB) is discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring'.)

Monitoring considerations specific to aortic surgery with deep hypothermia and elective circulatory arrest (DHCA) are noted below [2].

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. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation", section on 'Uses'.)

For patients with pathology of the ascending aorta and aortic arch, selection of the intra-arterial cannulation site is affected by the likely accuracy of BP measurements or the presence of malperfusion in each upper extremity. Examples include:

●In most cases, arterial catheters are placed in both upper extremities to optimally estimate central aortic BP and cerebral perfusion pressure (CPP) during various phases of the operation. For example, during delivery of selective antegrade cerebral perfusion (SACP) (see 'Selective antegrade cerebral perfusion' below), BP measured from the right radial artery provides the best estimate of CPP. However, during right axillary artery cannulation for delivery of SACP, continuous measurement of right radial arterial BP will be temporarily interrupted, necessitating BP measurements in the left arm only.

●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 catheter provides the most accurate monitor of systemic BP.

●If an aortic dissection extends into an aortic arch branch vessel or involves the innominate or subclavian arteries (figure 1), malperfusion of one or more extremities may occur. This complication of upper extremity malperfusion manifests as a pulse deficit in one or both arms. In such cases, arterial catheters are placed in both upper extremities to measure the arterial pressure differential to estimate the severity of malperfusion. However, estimates of systemic BP are derived from measurements in the limb with the higher BP. Normalization of the arterial pressures in the upper extremities after surgery indicates a successful repair.

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

We typically use a PAC catheter 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. Also, an increase in the PAP may indicate left ventricular (LV) distention due to aortic regurgitation (AR); this may be noticed during initiation of CPB or infusion of antegrade cardioplegia. (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 remains useful after major thoracic aortic surgery to detect problems such as severe LV dysfunction or cardiac tamponade caused by persistent bleeding. Also, residual lactic acidosis is common following reperfusion after DHCA; measurements of CO and SvO2 obtained via the PAC aid in circulatory management in the postoperative period.

Transesophageal echocardiography — Typical uses of transesophageal echocardiography (TEE) during cardiac surgery are reviewed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Transesophageal echocardiography' and "Anesthesia for cardiac surgery: General principles", section on 'Postbypass transesophageal echocardiography'.)

We agree with practice guidelines regarding use of intraoperative TEE during thoracic aortic surgery published by the American College of Cardiology/American Heart Association (ACC/AHA) [1], the American Society of Anesthesiologists (ASA) [22], and the Society of Cardiovascular Anesthesiologists (SCA) [1,22]. In a matched cohort study of 872,936 patients in the Society of Thoracic Surgeons (STS) database, intraoperative TEE was associated with lower 30-day mortality after proximal aortic surgery compared with not using TEE (3.81 versus 5.27 percent; odds ratio [OR] 0.69, 95% CI 0.67-0.72) [23]. Composite outcomes were also lower (ie, stroke or 30-day mortality; reoperation or 30-day mortality). Specific uses in this setting include:

●Prebypass period – In addition to standard examination, TEE is used to confirm and characterize the extent of aortic pathology [7]. The aortic valve is examined to determine if there is significant AR and to quantify its severity (movie 2 and image 3 and image 4 and image 5).

In emergency surgery for type A aortic dissection, intraoperative TEE examination is used to diagnose the extent and classification of the dissection (movie 1 and image 2), particularly if hemodynamic instability necessitates initiation of surgery without computed tomographic angiography (CTA) images. TEE examination provides information regarding the presence and location of the intimal tear(s) and 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 indicating myocardial ischemia or infarction due to coronary dissection [7,24].

●Aortic cannulation – TEE can be used to guide placement of the aortic and other cannulae for CPB. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

For example, in a patient with aortic dissection, aortic cannulation may be 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 within the true lumen (image 6). 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 CTA images of the aorta are available for viewing in the operating room, comparison of these with the intraoperative TEE images is useful to confirm correct identification of the true and false lumens after aortic dissection [1].

●During CPB – Upon initiation of CPB, intraoperative TEE is used to verify blood flow in the true lumen of the dissected aorta. TEE is also used to monitor for AR that will lead to LV distention before aortic crossclamping if ventricular fibrillation or asystole occur and ventricular ejection ceases. LV distention may also occur after application of the cross-clamp if the LV fills due during administration of antegrade cardioplegia to an 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).

●Weaning from CPB – Shortly before weaning from CPB, TEE is used to guide removal of intracardiac air from the left-sided cardiac chambers (ie, left atrium and LV) and 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 severity of residual AR [1]. In some cases, it may be necessary to reinstitute CPB to perform additional aortic repair or to replace the aortic valve. Furthermore, aortic root reconstruction involves reimplantation of the coronary arteries into the prosthetic root graft. TEE can evaluate both LV and right ventricular (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'.)

●Postbypass period – In the postbypass period, TEE is used to note the presence or absence of residual dissection and blood flow patterns in the true and false lumens of the descending thoracic aorta, as well as detect iatrogenic new aortic dissection. TEE can also detect hypovolemia or blood in the pericardial or pleural cavities that may indicate ongoing surgical bleeding or coagulopathy. Furthermore, global LV and RV function may be impaired or recover slowly due to the effects of a long duration of CPB, as well as ischemia and reperfusion injury following the period of circulatory arrest. Frequent reassessment of LV and RV function with TEE facilitates management of inotropic and vasopressor support, as well as fluid administration to achieve optimal LV filling. (See "Anesthesia for cardiac surgery: General principles", section on 'Postbypass transesophageal echocardiography'.)

Brain monitors — Intraoperative neuromonitoring is often used as an aid in managing hypothermia and monitoring for cerebral hypoperfusion [2,7,18].

Electroencephalography

●Endpoint for cerebral effects of cooling – Deliberate hypothermia causes incremental changes in the electroencephalography (EEG) that correlate with the reduction of cerebral metabolic rate associated with hypothermia (figure 2) (see "Neuromonitoring in surgery and anesthesia", section on 'Temperature'). Electrocortical silence on the EEG ensures hypothermia-induced maximum suppression of cerebral metabolic activity before CPB pump flow is discontinued to initiate circulatory arrest [25-27]. EEG activity and electrocortical silence are better predictors of cerebral hypothermia than monitored temperature sites alone because brain and neuronal temperatures cannot be measured directly (figure 3) [25-28].

However, the EEG is also affected by anesthetic agents. Volatile inhalation agents cause a dose-dependent decrease in EEG amplitude and frequency, and high doses of some intravenous (IV) anesthetic agents (eg, propofol) cause burst suppression or electrocortical silence that cannot be distinguished from the effects of hypothermia. For this reason, if EEG guidance of deliberate hypothermia is being used, anesthetic agents should be discontinued as the EEG begins to slow or at the onset of burst suppression to avoid interference with the detection of hypothermia-induced electrocortical silence. If use of propofol or a barbiturate is planned as an adjunct for cerebral protection, administration is delayed until after the EEG endpoint or the target temperature for DHCA has been reached. (See 'Considerations for anesthetic management' below and "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic effects on neuromonitoring'.)

Processed EEG monitors such as the bispectral index (BIS) may be more readily available for emergency surgery (eg, acute ascending aortic dissection) than full neuromonitoring that includes multi-channel raw unprocessed EEG monitoring [7]. The single raw EEG channel of a BIS or similar monitor can be continuously monitored. Although the digital BIS value appears to decrease reliably in response to progressive hypothermia, it is less sensitive than raw EEG for detecting electrocortical silence, only monitors the frontal cortex, and is more vulnerable to artifacts caused by anesthetic agents and neuromuscular blocking agents than the raw unprocessed EEG [29].

●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, particularly if also evident on a cerebral oximetry monitor (see 'Cerebral oximetry' below). Such abrupt changes should be promptly communicated to the surgeon and perfusionist since they may influence decisions regarding further intraoperative management [30].

●Monitoring for awareness – Inadequate anesthetic depth resulting in awareness is possible during CPB, particularly during the rewarming phase after DHCA [29,31]. To avoid inadequate anesthetic depth, administration of a volatile inhalation or IV anesthetic agents is resumed as soon as EEG activity has reappeared during the rewarming phase. (See 'Considerations for anesthetic management' 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 [7,32-36]. NIRS is not affected by anesthetic agents or nonpulsatile perfusion during CPB.

Typically, rSO₂ values increase as deliberate hypothermia is induced, then gradually decrease during either DHCA alone or DHCA with retrograde cerebral perfusion (RCP) once CPB pump flow has been discontinued for circulatory arrest [37-47]. During DHCA with SACP, rSO₂ values increase or remain at baseline [41,44,45]. Recovery of rSO₂ values toward baseline values occurs during reperfusion.

A sudden unilateral decrease in rSO₂ during any stage of the procedure indicates a regional decrease in cerebral perfusion and should be promptly communicated to the surgeon and perfusionist since this may influence decisions regarding further intraoperative management [7,36]. Bilateral sudden decreases in EEG amplitude and frequency indicates likely cerebral ischemia due to malperfusion [7]. Examples include [38,42,48-50]:

●During onset of CPB, unilateral or bilateral decreases in rSO₂ may indicate malperfusion. Bypass is discontinued to evaluate and potentially revise cannulation sites used for CPB.

●During temporary clamping of the common carotid or innominate artery (image 7):

•An ipsilateral decrease in rSO₂ indicates decreased cerebral blood flow in the affected cerebral hemisphere, although this may not necessarily indicate cerebral ischemia or hypoperfusion since it does not provide a measure of neuronal function. Concomitant EEG and NIRS monitoring can determine if unilateral decreases in rSO₂ correlate with EEG evidence of cerebral ischemia or hypoperfusion.

•A contralateral decrease in rSO₂ may occur due to vascular steal via a patent circle of Willis 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.

●During unilateral delivery of SACP:

•An acute decrease in rSO₂ on the ipsilateral side may indicate malpositioning of the SACP cannula.

•A severe contralateral decrease in rSO₂ as unilateral SACP is initiated may influence the surgeon to additionally cannulate the contralateral carotid artery so that bilateral SACP is provided [7,33,38-45].

●Either unilateral (or bilateral) cerebral ischemia may also occur due to extension of aortic dissection or thrombosis of an arterial graft.

Similar to other cardiac procedures, bilateral decreases in rSO₂ indicating global cerebral hypoperfusion may be observed during routine CPB. This may be due to hypoxemia, hypocarbia, anemia, venous hypertension, or inadequate anesthetic depth [7,36]. Management of decreased rSO₂ during routine CPB is described separately (algorithm 1). (See "Management of cardiopulmonary bypass", section on 'Neuromonitoring modalities'.)

Temperature monitors — Temperature is continuously monitored during initiation of CPB, cooling, the period of DHCA, rewarming, and throughout the postbypass period. Multiple temperature monitoring sites are used (eg, nasopharyngeal, blood [via the thermistor in the PAC], bladder [via a thermistor in the urinary catheter], tympanic membrane [via a thermistor in the ear canal]). Blood temperature is also monitored in the extracorporeal bypass circuit in both the arterial outlet blood temperature perfusing the patient and the venous blood inlet temperature re-entering the CPB circuit. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

For temperature measurements using a nasopharyngeal probe, it is important to position the tip of the probe within the nasopharynx and not the esophagus. Esophageal temperatures are affected by ice or cardioplegic solution in the pericardial sac and may not accurately reflect brain temperature.

Laboratory testing — Intraoperative point-of-care 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 viscoelastic tests of hemostasis (eg, thromboelastography [TEG] or rotational thromboelastometry [ROTEM]) if available, are used to guide administration of blood products in a bleeding patient [51]. (See "Clinical use of coagulation tests" and "Intraoperative transfusion and administration of clotting factors", section on 'Point-of-care tests'.)

THE PREBYPASS PERIOD

Anesthetic management — Typical anesthetic management during the prebypass period for cardiac surgical procedures requiring cardiopulmonary bypass (CPB) is addressed in a separate topic. (See "Anesthesia for cardiac surgery: General principles".)

Additional considerations for patients undergoing aortic surgery with deep hypothermia and elective circulatory arrest (DHCA) may include:

●Use of acute normovolemic hemodilution – Since blood loss is typically higher in complex procedures requiring a prolonged duration of CPB with a period of DHCA, acute normovolemic hemodilution may be used to reduce the need for intraoperative transfusion of red blood cells (RBCs) and other blood products in the postbypass period [52]. (See 'Control of coagulopathy to achieve hemostasis' below and "Surgical blood conservation: Acute normovolemic hemodilution".)

●Modifications in anesthetic agent selection and dosing – If electroencephalography (EEG) monitoring is being performed in anticipation of a period of DHCA, the dose of a volatile inhalation anesthetic is maintained at a fixed end-tidal concentration before cooling and discontinued at the onset of EEG burst suppression to minimize confounding anesthetic-induced EEG changes. Also, bolus doses of intravenous (IV) anesthetic agents are avoided if possible since these may produce acute transient changes in the EEG independent of temperature-induced changes. (See 'Electroencephalography' above.)

●Hemodynamic management – Most 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 for patients undergoing coronary artery bypass grafting (CABG) surgery. (See "Anesthesia for coronary artery bypass grafting surgery", section on 'Avoidance and treatment of ischemia'.)

For patients with acute aortic syndromes (eg, aortic dissection), key hemodynamic considerations in the prebypass period also include fastidious control of systolic blood pressure (BP) and heart rate (HR) to minimize the likelihood of aortic rupture, progression of aortic dissection, or worsening aortic regurgitation (AR) and heart failure [1]. Beta blockers (eg, esmolol) are administered in small incremental doses to achieve a HR of 60 to 80 beats per minute and systolic BP <120 mmHg. However, in patients with cardiogenic shock due to acute AR or cardiac tamponade, beta blockers are avoided. Details are discussed in a separate topic. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Anti-impulse therapy'.)

●Use of transesophageal echocardiography – Transesophageal echocardiography (TEE) is used to detect treatable causes of cardiogenic shock including cardiac tamponade, acute AR, hypotension due to hypovolemia, low systemic vascular resistance (SVR), or severe ventricular dysfunction. (See 'Transesophageal echocardiography' above.)

Preparations for cardiopulmonary bypass — Standard preparations for initiation of CPB, including anticoagulation and antifibrinolytic administration, are discussed in separate topics (table 4). (See "Blood management and anticoagulation for cardiopulmonary bypass" and "Initiation of cardiopulmonary bypass".)

Additional considerations for patients undergoing procedures on the ascending aorta or aortic arch include selection of the site for arterial cannulation for CPB. This is most commonly an axillary artery site, but may be the aorta, or the innominate or femoral artery [8]. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

In patients with aortic dissection, TEE can be used to confirm wire placement in the true lumen of the vessel during arterial cannulation of the selected arterial site (image 6). (See 'Transesophageal echocardiography' above.)

If retrograde cerebral perfusion (RCP) is planned as an adjunct to DHCA, rather than using a single right atrial cannula for venous drainage, separate cannulae are inserted into both the superior vena cava (SVC) and inferior vena cava (IVC) in order to separately perfuse the SVC (figure 4 and figure 5). (See "Initiation of cardiopulmonary bypass", section on 'Venous cannulation'.)

CARDIOPULMONARY BYPASS WITH DHCA — Management of routine aspects of cardiopulmonary bypass (CPB) is addressed separately. (See "Management of cardiopulmonary bypass".)

Additional considerations for patients undergoing deeper levels of hypothermia are addressed below.

Deep hypothermia — Many procedures involving the ascending aorta or aortic arch require temporary interruption of cerebral and systemic blood flow. During this period of elective circulatory arrest, the brain, spinal cord, and vital organs (kidneys, liver, and gastrointestinal tract) are protected by inducing deliberate hypothermia [2]. Although the optimal temperature and safe duration for deep hypothermic circulatory arrest (DHCA) are unknown, experimental and clinical data support the effectiveness of DHCA lasting approximately 20 minutes, and up to 60 minutes in some cases (figure 6).

Cooling strategies — Active systemic cooling is accomplished after CPB has been established using the heat exchanger in the CPB circuit. All external patient warming devices are discontinued. 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). After reaching the target temperature and/or confirming electrocortical silence on the electroencephalogram (EEG) (figure 2 and figure 3) (see 'Electroencephalography' above), exsanguination into the CPB circuit and discontinuation of CPB pump flow establishes elective circulatory arrest [8].

Target temperature during DHCA — The average nasopharyngeal temperature for electrocortical silence is 18°C; however, 50 percent of patients do not exhibit electrocortical silence at 18°C [25,27].

●Selection of a target temperature – The selected target temperature before initiating circulatory arrest for part of a specific surgical procedure varies and depends on the following considerations:

•If EEG monitoring is available, it is used to ensure an endpoint of electrocortical silence indicating that hypothermia-induced maximum suppression of cerebral metabolic rate has been achieved before discontinuing CPB pump flow to initiate circulatory arrest (figure 2) [25-27]. 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 can be used as a neurophysiologic surrogate to monitor for adequacy of brain hypothermia (figure 3) [25-28]. (See 'Electroencephalography' above.)

•If EEG monitoring is not available, nasopharyngeal and oxygenator arterial outlet temperature sites are used as the primary surrogate for brain temperature during cooling. Although a temperature of approximately 12.5°C would ensure that electrocortical silence has been achieved in >99 percent of patients, a temperature of 16 to 18°C produces EEG electrocortical silence in most patients [12,26,27]. A warmer temperature target in the range of 28°C may be selected if selective cerebral perfusion is provided during circulatory arrest, particularly if cold selective antegrade cerebral perfusion (SACP) is selected [10,11]. (See 'Selective cerebral perfusion during DHCA' below.)

•If the duration of DHCA is anticipated to be longer than 30 to 40 minutes, a target temperature closer to 12.5°C may be justified [25-28]. If the anticipated duration of DHCA is brief (<20 minutes), moderately deep hypothermia with a target temperature in the range of 20 to 28°C may be acceptable for brain protection. Mild hypothermia in the range of 28 to 34 °C is believed to provide <10 minutes of safe circulatory arrest [8].

•Other factors that influence target cooling temperatures include surgeon preference, institutional practice patterns, and established perfusion protocols.

●Circuit temperature monitoring – Thermistors in the CPB circuit continuously monitor blood temperature. These thermistors are located at the arterial outlet of the oxygenator just before entry into the patient, as well as at the entry into the venous reservoir to sample venous blood re-entering the CPB circuit. The temperature gradient between the venous inflow from the patient and arterial outlet on the oxygenator for outflow to the patient 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 and maintenance of hypothermia [53,54]. A nasopharyngeal or tympanic membrane temperature probe provides an additional estimate. (See 'Electroencephalography' above.)

●Topical cooling – In some institutions, the patient's head is packed in ice bags to augment or maintain cerebral cooling. However, there is limited evidence to support the effectiveness of currently available techniques and devices, and topical cooling is not a substitute for systemic hypothermia delivered via CPB [55].

Duration of DHCA — After target temperature is achieved, a duration of DHCA of 30 to 45 minutes is generally considered to be safe [8]. Under normothermic conditions, irreversible ischemic neuronal injury is detected within four to five minutes after cerebral blood flow is interrupted. However, cerebral metabolic rate of oxygen consumption (CMRO₂) decreases by a factor of 2.3 for every 10°C decrease in body temperature (figure 6) [56,57]. 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 [57]. 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 [13,58-60]. Experimental evidence in rats also demonstrates functional and histologic deficits after 30 to 60 minutes of DHCA [61].

Selective cerebral perfusion during DHCA — DHCA is often combined with SACP or retrograde cerebral perfusion (RCP) [2]. Experimental and clinical data support use of these techniques to supplement the cerebral protection provided by deep hypothermia. There are no randomized trials comparing these techniques. (See 'Review of the surgical plan' above.)

Selective antegrade cerebral perfusion — SACP is used by many surgeons to reduce the period of cerebral ischemia during DHCA [7,62-64]. Oxygenated blood at temperatures as low as 10 to 12°C is delivered via the CPB circuit into a directly cannulated axillary or innominate artery; the open ends of the aortic arch branch vessels; through a vascular graft sewn onto the axillary or subclavian artery; or a combination of these techniques (figure 7). (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

During SACP, decreases in unilateral or bilateral cerebral oximetry regional oxygen saturation (rSO₂) values may indicate cerebral hypoperfusion [7]. (See 'Cerebral oximetry' above.)

Retrograde cerebral perfusion — RCP is a technique that provides partial perfusion to the brain and potentially prolongs the safe duration of circulatory arrest during DHCA when antegrade cerebral perfusion is interrupted [7]. The superior vena cava (SVC) cannula is ensnared between the right atrium and the azygous vein, and cold oxygenated blood is perfused retrograde at a rate of 150 to 250 mL/minute into the SVC cannula (figure 4). During RCP, the patient is maintained in a 10-degree Trendelenburg position to decrease the risk of cerebral air embolism. Using the side-port of an introducer sheath in the internal jugular vein, the anesthesiologist continuously monitors SVC pressure and guides RCP flow rates to maintain a pressure <25 mmHg to prevent cerebral edema. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

Compared with SACP, there a greater risk of air embolism with RCP if any air remains in the venous CPB circuit catheter before initiating RCP. Furthermore, during DHCA, the metabolic demands of the brain are not fulfilled by RCP (figure 8) [65]. Similar to DHCA without RCP, a gradual decline in rSO₂ is typically observed with cerebral oximetry monitoring [37,44,46,47] (see 'Brain monitors' above). However, the RCP technique does provide some degree of cerebral blood flow and serves to maintain brain hypothermia during DHCA, as well as possibly decreasing the risk of antegrade arterial air embolism or particulate thromboembolism when normal antegrade cerebral perfusion is resumed [2].

Considerations for anesthetic management — Deep hypothermia during CPB requires additional strategies for anesthetic administration and for management of hyperglycemia, anticoagulation, hemodilution, and acid-base status [2]. Furthermore, residual effects of deep hypothermia on coagulation and the cardiovascular system influence postbypass management (table 1). (See 'The postbypass period' below.)

●Anesthetic requirements – Since 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.

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) [66]. (See 'Electroencephalography' above and 'Rewarming strategies' below.)

●Management of hyperglycemia – Nearly all patients develop hyperglycemia after DHCA. This requires control with IV insulin administered by infusion during the remainder of CPB and throughout the postbypass period. As recommended in published guidelines, blood glucose concentration should be maintained <180 mg/dL (10 mmol/L). However, it is important to monitor blood glucose frequently to prevent unintentional hypoglycemia. Details are discussed separately. (See "Management of cardiopulmonary bypass", section on 'Glucose'.)

●Anticoagulation – The duration of 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 at least every 30 minutes during CPB in operations that require deep hypothermia. If available, plasma heparin concentrations are monitored using a point-of care (POC) heparin-protamine titration assay, as discussed in other topics. (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Heparin administration and monitoring' and "Management of cardiopulmonary bypass", section on 'Maintenance of anticoagulation'.)

After weaning from CPB, optimal neutralization of systemic anticoagulation with protamine is based on stoichiometric measurements of currently circulating heparin levels, using a POC heparin-protamine titration assay, as discussed separately. (See "Protamine: Administration and management of adverse reactions during cardiovascular procedures", section on 'Protamine administration after cardiopulmonary bypass'.)

●Acid-base management

•Blood gas management – Similar to routine CPB without deep hypothermia in adult patients [67,68], we use alpha-stat blood gas management during cooling for DHCA and during rewarming. Evidence suggests that alpha-stat management (ie, temperature-uncorrected blood gas measurements) preserves cerebral blood flow autoregulation, as well as decreases risk of cerebral thromboembolism, cerebral edema, reperfusion injury, and unintended cerebral hyperthermia during rewarming [69,70]. (See "Management of cardiopulmonary bypass", section on 'Oxygenation, ventilation, and arterial blood gases'.)

•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 [71]. 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 [71]. Although mild hyperventilation is commonly used to attenuate the severity of metabolic acidosis, excessive hyperventilation may have undesirable effects on cerebral blood flow. Pre-emptive management to minimize other causes of metabolic acidosis such as the use of buffered crystalloid solutions to prevent hyperchloremic acidosis may be helpful to decrease the overall severity of metabolic acidosis during reperfusion. Small doses of sodium bicarbonate 8.4 percent (50 mEq/50 mL) may be titrated to treat metabolic acidosis if base deficit is <–7 mEq/L or pH is <7.20. However, we avoid excessive administration of sodium bicarbonate to prevent postoperative hypernatremia [72].

●Hemodilution and anemia – As with patients undergoing CPB without a period of DHCA, we treat hemoglobin values <7.5 g/dL with hemoconcentration, and transfusion if necessary. Hyperviscosity with potentially adverse effects on microcirculatory flow at deep hypothermic temperatures is a risk if hemoglobin levels are high (eg, >10 g/dL) [73]. (See "Management of cardiopulmonary bypass", section on 'Hemoglobin/hematocrit'.)

●Control of blood pressure – Mean arterial pressure (MAP) is maintained at 50 to 70 mmHg during the period after elective circulatory arrest. It is often necessary to treat higher MAP values with pharmacologic agents (table 2).

Pharmacologic agents for cerebral protection — Although pharmacologic adjuncts are commonly administered for cerebral protection, efficacy remains unproven [1,2,74].

●Barbiturates of propofol – The most used agents are barbiturates or propofol to further suppress cerebral electrocortical activity and the 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 [75,76]. Also, administration of barbiturates, propofol, or volatile anesthetic agents interferes with the interpretation of temperature-dependent changes in intraoperative neurophysiologic monitoring and may cause premature onset of electrocortical silence on the EEG unrelated to brain temperature, metabolic activity, or hypothermic cerebral protection. For this reason, administration of these agents is delayed until after the EEG endpoint or the target temperature for DHCA has been reached. (See 'Target temperature during DHCA' above and "Neuromonitoring in surgery and anesthesia", section on 'Anesthetic effects on neuromonitoring'.)

If a barbiturate or propofol is used to further suppress cerebral metabolic activity beyond the effects of hypothermia, dosing should be guided by the goal of achieving electrocortical silence during DHCA rather than using a fixed dose. 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 [77,78].

●Mannitol – Another agent is mannitol, which is often a component of the CPB pump prime solution because of its diuretic effects and theoretical free radical scavenging properties. However, there is insufficient evidence supporting its use for cerebral (or renal) protection [79].

●Other agents – Other agents used in some institutions include anti-inflammatory or anticonvulsant agents, lidocaine, magnesium, or a calcium channel blocker [1,2,80]. Clinicians cite minimal 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 or institutional practices.

Evidence does not support the use of glucocorticoids for cerebral protection (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 [78,81-83].

Rewarming strategies — We agree with professional society recommendations for rewarming guidelines that avoid cerebral hyperthermia [1,53]. It is important to avoid cerebral hyperthermia because of its deleterious effects on the brain with potential exacerbation of ischemia-reperfusion injury following a period of elective circulatory arrest [1,53,84-86]. Also, hyperthermia may exacerbate neurologic injury due to cerebral thromboembolic events that may occur during open aortic or open cardiotomy surgery. Thromboembolism of air or particulate debris is most likely at the time that cerebral perfusion resumes or after removal of the aortic crossclamp when ventricular ejection resumes.

●Rate and duration of rewarming – 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 thermistor located at the venous inflow to the oxygenator and the thermistor located at the arterial outlet before entry into the patient. Once the arterial outlet temperature has reached 30°C, this venous-to-arterial temperature gradient should be no greater than 4°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. At all times, we ensure that the arterial blood outlet temperature is no higher than 36.5°C. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

●Temperature monitoring during rewarming – We also ensure that the temperature at all monitoring sites is ≤37°C. During rewarming, the oxygenator arterial outlet temperature is used as the primary surrogate for cerebral temperature, although nasopharyngeal and/or tympanic membrane temperatures are also continuously monitored [53,54]. The 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). 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 [54,87]. Since monitoring jugular bulb temperature is not usually feasible, the best alternative for avoiding cerebral hyperthermia is to ensure that temperature at all monitored sites remains ≤37°C, even if this prolongs the rewarming process. (See "Management of cardiopulmonary bypass", section on 'Temperature'.)

●Discontinuation of CPB – Many institutions discontinue CPB when the bladder temperature has reached 34.5 to 35.5 °C, thereby permitting mild hypothermia in the early postbypass period to provide some ongoing degree of cerebral protection. However, these potential cerebral protective effects are balanced against potential deleterious effects of hypothermia on coagulation and bleeding risk (see 'Control of coagulopathy to achieve hemostasis' below). Hence, there are wide institutional variations in the temperature target for discontinuing rewarming and weaning from CPB.

THE POSTBYPASS PERIOD — The process of weaning from cardiopulmonary bypass (CPB) is discussed in a separate topic. (See "Weaning from cardiopulmonary bypass".)

Problems in the postbypass period — Postbypass problems after weaning from CPB are discussed separately. (See "Intraoperative problems after cardiopulmonary bypass".)

The following problems are particularly challenging after CPB with deep hypothermia and circulatory arrest (DHCA) to achieve surgical repair or replacement of the ascending aorta or aortic arch.

Control of coagulopathy to achieve hemostasis — Surgical bleeding is exacerbated by coagulopathy due to (table 1) [7,14,15]:

●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

●Underlying aortic vascular pathology and nature and extent of the surgical repair

Intermittent measurements (approximately every 30 minutes) of hemoglobin (Hgb) are obtained to guide packed red blood cell (RBC) transfusion and avoid excessive hemodilution from crystalloid or colloid administration. Hemodilution and transfusion have both been associated with the risk of acute kidney injury after thoracic aortic surgery [88-90].

Management of persistent bleeding, anemia, massive transfusion, thrombocytopenia, and coagulopathy after CPB is addressed separately. (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass".)

In addition to bleeding and transfusion, dynamic intravascular fluid shifts occur after major thoracic aortic operations because of vasodilation during reperfusion. Intravascular volume status is assessed and monitored using transesophageal echocardiography (TEE) examinations and pulmonary artery catheter (PAC) measurements (eg, cardiac output [CO], mixed venous oxygen 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'.)

In rare cases, sternal closure must be delayed because of persistent bleeding, hemodynamic compromise during sternal approximation that compresses 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'.)

Control of blood pressure — Episodes of hypertension and hypotension are common after aortic surgery with DHCA and should be promptly treated.

●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 2). 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 CO. Vasoconstrictor or inotropic agents may be necessary (table 3).

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

In the ICU, patients typically remain sedated and tracheally intubated with controlled mechanical ventilation 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. Coagulopathy and persistent bleeding and/or cardiac tamponade may require mediastinal re-exploration [7].

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

●Preanesthetic assessment and planning – Routine aspects of the preanesthetic consultation for cardiac surgery are discussed separately. (See 'Preanesthetic assessment and planning' above.)

•Coexisting pathology – The presence of aortic or carotid arterial atherosclerosis; chronic or acute aortic regurgitation (AR) (movie 2 and image 3 and image 4 and image 5); cerebral, coronary, or limb malperfusion; or a mediastinal mass effect will influence anesthetic and surgical management. (See 'Coexisting pathology' above.)

•Review of the surgical plan – Specialized monitoring is used if the surgeon plans a period of moderately deep hypothermia (in the range of 20 to 28 °C) or deep hypothermia (in the range of 16 to 20°C) with elective circulatory arrest (DHCA) or with selective antegrade cerebral perfusion (SACP) or retrograde cerebral perfusion (RCP). (See 'Review of the surgical plan' above.)

•Considerations for acute aortic dissection – Emergency surgical repair is necessary for acute type A aortic dissection (movie 1 and image 2 and figure 1). Factors that increase risk and affect anesthetic and surgical management may include acute AR, cardiac tamponade, acute coronary syndrome, stroke, visceral ischemia, malperfusion of extremities, and coagulopathy that worsens after DHCA.

●Monitoring – Usual monitoring for cardiac surgery with cardiopulmonary bypass (CPB) is discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring'.)

Considerations specific for aortic surgery with DHCA include:

•Cardiovascular monitors

-Intra-arterial catheter – Selection of the cannulation site is affected by aortic pathology and the likely accuracy of blood pressure (BP) measurements in each upper extremity. (See 'Intra-arterial catheter' above and 'Pulmonary artery catheter' above.)

-Echocardiography – Transesophageal echocardiography (TEE) can confirm the extent of aortic pathology and diagnosis and quantify severity of AR (movie 2 and image 3 and image 4 and image 5). TEE is also used to guide placement of cannulae for CPB, detect ventricular distention during CPB, and guide removal of intracardiac air during weaning from CPB. In emergency surgery for type A aortic dissection, intraoperative TEE examination is used to diagnose the extent of the dissection (movie 1 and image 2). (See 'Transesophageal echocardiography' above.)

•Brain monitors – Processed or raw electroencephalography (EEG) may be used to confirm electrocortical silence due to hypothermia before establishing elective circulatory arrest, to potentially detect cerebral hypoperfusion and assess anesthetic depth. Cerebral oximetry with near-infrared spectroscopy may be used to detect and treat unilateral or bilateral cerebral hypoperfusion (image 7 and algorithm 1). (See 'Brain monitors' above.)

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

•Laboratory testing – Laboratory values are measured before, during, and after CPB. These include arterial blood gases (ABG), pH and base deficit, hemoglobin (Hgb), electrolytes, calcium, glucose, lactate, activated whole blood clotting time (ACT), and standard and viscoelastic tests of hemostasis. (See 'Laboratory testing' above.)

●Prebypass management – Key prebypass considerations for patients with acute aortic syndromes include:

•Systolic BP and heart rate (HR) are carefully controlled to achieve a HR of 60 to 80 beats per minute and systolic BP <120 mmHg. Details are discussed in a separate topic. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Anti-impulse therapy'.)

•TEE is used to detect treatable causes of cardiogenic shock including cardiac tamponade, acute AR, or hypotension due to hypovolemia or severe ventricular dysfunction. (See 'Transesophageal echocardiography' above.)

●Use of deep hypothermia – Deliberate hypothermia is induced using CPB to provide protection of the brain and vital organs (figure 6). (See 'Deep hypothermia' above.)

•Cooling – The oxygenator arterial outlet temperature is used as the primary surrogate for brain temperature during cooling. The average nasopharyngeal temperature is 18°C when CPB pump flow is discontinued for a period of elective circulatory arrest with or without selective cerebral perfusion techniques. In some centers, a hypothermic temperature that produces electrocortical silence is targeted, rather than using temperature monitors alone (figure 2 and figure 3). (See 'Cooling strategies' above and 'Target temperature during DHCA' above and 'Electroencephalography' above.)

•Duration of DHCA – A duration of DHCA of 30 to 45 minutes is generally safe. (See 'Duration of DHCA' above.)

●Use of selective cerebral perfusion – Cerebral protection during moderately deep or deep hypothermia is often supplemented with SACP (figure 7), or RCP (figure 4), as discussed in a separate topic. (See "Overview of open surgical repair of the thoracic aorta", section on 'Ascending aorta'.)

●Rewarming strategies – After a period of DHCA, CPB is reinstituted with gradual rewarming at a rate of ≤0.5°C/minute, which may require ≥90 minutes after deep hypothermia ≤16°C. To avoid cerebral hyperthermia that may exacerbate neurologic injury due to ischemia-reperfusion injury, the arterial blood outlet and nasopharyngeal temperatures are not allowed to exceed 36.5°C. (See 'Rewarming strategies' above.)

●Considerations for anesthetic management

•Anesthetic requirements – These are reduced during deep hypothermia, and anesthesia is unnecessary during the period of electrocortical silence. However, anesthetic administration should be resumed during rewarming and when EEG activity has returned to ensure absence of awareness. (See 'Considerations for anesthetic management' above.)

•Physiologic changes – Strategies to manage hyperglycemia, anticoagulation, acid-base status, hemodilution and anemia are discussed above (table 1). (See 'Considerations for anesthetic management' above.)

●Postbypass period – 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, underlying aortic vascular pathology, and the nature and extent of the surgical repair. Episodes of both hypertension and hypotension are common and should be promptly treated. (See 'Problems in the postbypass period' above.)