Cardiac Lecture Series:�Aortic Dissection

By Mohamed Ismaeil

Background

Acute type A aortic dissection (ATAAD) is still one of the most challenging diseases that cardiac surgeons and cardiac anesthesiologist encounter.

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Acute aortic dissection is a rare life-threating condition of the aorta and is associated with significant morbidity and mortality.

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The most lethal of dissections involves the ascending aorta and is commonly referred to as acute type A aortic dissection (ATAAD).

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Unless prompt surgical repair is performed, the patients usually die from complications related to the dissection, including rupture of the aorta, pericardial tamponade, aortic regurgitation, end-organ malperfusion, or acute heart failure

Anesthesia for type A aortic dissection

Definition�Disruption of intima of the aortic wall. Blood dissects into media, creating false lumen.

Classification of the aortic dissection

Historical Note�������

First successful outcome of modern treatment of aortic dissection was attributed to Dr. DeBakey in his report, 1955 and later he devised a classification that is widely used today as Debakey classification.

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Technological and technical improvements follow:

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• Cardiopulmonary bypass circuit.
• Synthetic placements.
• Hypothermic circulatory arrest in 1960s to 1975( Barnard , Schrire, Borst and Griepp with colleaques)
• Open distal anastomosis technique by Livesay in 1982.
• Bioglue has been approved by US FDA to strengthen the disrupted layer.

Historical

Note

Anatomy and function of the aorta

anatomy

Anatomy and function

The aorta is the ultimate conduit, carrying, in an average lifetime, almost 200 million liters of blood to the body.

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The aortic wall is composed histologically of three layers:

• Thin inner tunica intima lined by the endothelium.
• Thick tunica media characterized by concentric sheets of elastic and collagen fibers, as well as smooth muscle cells.
• The outer tunica adventitia containing mainly collagen, vasa vasorum, and lymphatics.

Anatomy and function

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Through its elasticity, the aorta has the role of a ‘second pump’ (Windkessel function) during diastole, which is of the utmost importance—not only for coronary perfusion but for the whole-body perfusion.

In addition to the conduit function, the aorta plays an important role in the control of systemic vascular resistance and heart rate, via pressure-responsive receptors located in the ascending aorta and aortic arch.

Mortality and morbidity

Mode of Death

• Most patients who die acutely succumb from false channel rupture with hemopericardium, hemomidiastinum or hemothorax.

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• Death later can result from delayed rupture or organ dysfunction secondary to arterial occlusions.

Pathophysiology

• Aortic dissection is more common in males with a peak incidence at 50–70 years of age.
• Aortic dissection can result either from a tear in the intima and propagation of blood into the media or from intramural hemorrhage and hematoma formation in the media followed by perforation of intima; the former is more common.
• . Blood may re-enter the true lumen at any point, thus making it a communicating dissection.

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More Details

• An intimal tear can occur in the regions of the aorta that are subjected to the greatest stress and pressure fluctuations.
• Because mechanical stress in the aortic wall is proportional to intramural pressure and vessel diameter, hypertension and aortic dilatation are known risk factors for dissections.
• Most aortic dissections occur with an initial transverse tear along the greater curvature of the aorta, usually within 10 cm of the aortic valve.
• Dissection can propagate down/up the aorta through false lumen. May empty back into true lumen of aorta, or rupture through adventitia
• The next most common site is the descending thoracic aorta immediately distal to the origin of the left subclavian artery.

Aortic tear

What are the predisposing factors?

• Predisposing factors include those that increase stress on the arterial wall and those that reduce resistance on the arterial wall. These factors lead to acceleration of degenerative changes of the aortic media and increase the likelihood of a tear.
• Hypertension
• Bicuspid aortic valve
• Aortic coarctation
• Iatrogenic (cardiac surgery and percutaneous catheters)
• Invading atherosclerotic plaque
• Aging
• Connective tissue disorder's (Marfan's syndrome, Ehlers-Danlos syndrome)
• Aortitis (Syphilis, Giant Cell, SLE)

Classification of the aortic dissection

Consequences of dissection

Consequences of Dissection

• Aortic regurgitation, myocardial ischemia or infarction, and tamponade which eventually will lead to heart failure and cardiogenic shock
• Aortic regurgitation may accompany 40–75% of patients with type A aortic dissection.
• Myocardial ischemia or infarction may be present in 10–15% of patients with type A aortic dissection secondary to compression or obliteration of the coronary arterial ostium.
• Neurological symptoms may occur with dissection of the carotid or vertebral arteries. The frequency of neurological symptoms in type A aortic dissection ranges from 10 to 40%, and in half of affected patients, symptoms are transient
• Mesenteric ischemia occurs in < 5% of patients with both type A and B aortic dissection
• Fewer than half of all patients with rupture arrive at the hospital alive; mortality may be as high as 54% at 6 h and 76% at 24 h after the initial event

Diagnosis

Classical presentation of aortic dissection

• Symptoms and clinical findings often depend on the extent and involvement of dissection.
• Abrupt and severe retrosternal or inter scapular chest pain is sometimes felt as a tear, with subsequent migration down the back occurs in 90% of patients.
• Classically, the pain is of maximal intensity at onset,.
• Complications of the dissection can produce additional signs and symptoms such as acute aortic insufficiency and pericardial effusion.

• Dissection can compress or occlude a branch of the aorta and produce acute ischemia.
• Ischemia occurs in the arms or legs in 20%, in the kidney in 15%, myocardium in 10%, brain in 5%, and mesentery or spinal cord in 3%.
• The patient will sometimes complain of exacerbation of the pain with each heartbeat.
• If the aortic arch is involved, patients may also feel pain in the jaw, neck, or teeth.
• In rare cases, patients may also be asymptomatic.

Classical presentation of aortic dissection

What is the common physical evidence for dissection?

• The loss of any pulse can occur with compromise to any major artery arising from the aorta.
• Aortic regurgitation can occur with disruption of the supporting structures of the aortic valve.
• Neurologic symptoms can occur with compromise of the head and neck vessels.
• Horner's syndrome with compression of the superior cervical ganglion.
• Vocal cord paralysis and hoarseness with pressure against the recurrent laryngeal nerve.
• Superior vena cava syndrome.
• Dyspnea secondary to tracheal or bronchial compression
• Hemorrhagic pleural effusion.
• Myocardial infarction as the hematoma dissects retrograde across the coronary ostium.

Goals of diagnostic tools in Type A aortic dissection

Imaging procedures available for diagnosis of aortic dissection

For many years, the gold standard in diagnostic studies has been aortography(Invasive).

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Current techniques available for evaluation include:

• CT angiogram
• Transthoracic echocardiography (TTE)
• Transesophageal echocardiography (TEE)
• MRI
• Aortography
• CXR

Procedure Sequence/Diagnostic Algorithm

CT, MRI, and TEE are all effective imaging techniques for aortic dissection.

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Most patients end up having multiple imaging studies.

• The initial imaging study was
• CT - 61%,
• TEE - 33%
• aortography - 4%.

CT Scan

CT Scan

CT Scan

TTE

(A), short-axis view (B), and suprasternal notch view (C), demonstrating a dissection flap (white arrows) in the ascending aorta at the level of the sinuses of Valsalva. In the apical five-chamber view (D), Doppler color flow of the aortic valve showed severe aortic regurgitation

TEE

Aortography

Chest X-Ray

On chest X-ray (CXR):

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Aortic knuckle changes may be observed, with intimal calcification.

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A widened mediastinum, cardiomegaly (pericardial effusion).

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Loss of costophrenic angle secondary to the presence of a hemothorax may also be noted.

Preoperative assessment

Preoperative assessment

Preoperative management

The patient should be initiated on antihypertensive and chronotropic therapy.

β-Adrenergic blockers are typically first-line therapy for the control of hypertension.

Vasodilator therapy or calcium channel blockade can be added to optimize control before operative intervention.

Although nicardipine, sodium nitroprusside, and nitroglycerin can all be used as antihypertensives, current evidence suggests that nicardipine may be more effective in controlling blood pressure in patients undergoing cardiac surgery.

Preoperative management

Some patients with TAAD may present with signs of systemic hypoperfusion. In these patients, the suspected etiology of their shock should guide therapy before surgical intervention.

Hypovolemia or pericardial tamponade (heart rate) require volume expansion and vasopressors to maintain end-organ perfusion.

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If there is evidence of coronary artery occlusion and myocardial dysfunction, inotropic therapy may be required.

Progressive acidosis and shock due to organ malperfusion should be managed with pressors, inotropes and other supportive measures.

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Hemodynamic support should be provided until flow can be reestablished to the occluded vessel via surgical repair.

Hypotensive patients

Preoperative Initial management

• Oxygen (ABC as indicated)
• Detailed medical history and complete physical examination (whenever possible)
• HR, BP, and SpO2 monitoring
• A line, Central line, IVs
• Lab (Cross match, CK, Troponin, Myoglobin, D-dimer, LDH)
• 12-lead ECG: documentation of ischemia

Preoperative Initial management

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• Pain relief (be very cautious)
• Careful i.v. fluid infusion
• BP titration to about 110–120 mm Hg systolic with i.v. esmolol, metoprolol, or labetalol first.
• Imaging studies at the earliest opportunity
• Transfer to theatre, intensive care unit as appropriate

Preoperative Planning and considerations

Arterial Line considerations

• Arterial pressure monitoring should proceed with consideration of the pathophysiology of the aortic dissection and the surgical plan in mind

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• If antegrade cerebral perfusion (ACP) with hypothermic circulatory arrest is planned, arterial pressure monitoring in both the right upper extremity and either left upper extremity or femoral artery is necessary to allow for pressure monitoring during ACP and systemic CPB, respectively.

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• The right radial artery may provide falsely elevated readings during CPB if right axillary or innominate cannulation is used.

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• If retrograde cerebral perfusion (RCP) is planned, placement of an internal jugular or subclavian central venous catheter is necessary to allow for pressure monitoring during RCP.

Neuromonitoring

Jugular venous oxygen saturation

• Jugular venous oxygen saturation is a measure of global cerebral oxygen supply and demand, but it requires additional invasive catheter placement and has not been reliably shown to predict outcome after aortic surgery.

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• The jugular bulb is the dilated portion of the jugular vein just below the base of the skull that contains blood with little extracerebral contamination.

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• Analysis may be performed by intermittent blood sampling via standard intravascular catheters or Continuous oxyhemoglobin saturation monitoring via fiberoptic oximetry catheters.

Disadvantages

• CVL insertion complications
• Only gives information of global cerebral metabolism not regional
• If both cerebral blood flow and O2 consumption decrease, then SjO2 may be unchanged
• venous thrombosis -> infarction

Jugular venous oxygen saturation

EEG Monitor

• EEG is sometimes used to evaluate for electrocerebral silence before the initiation of hypothermic circulatory arrest.

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• EEG can also detect abnormal recovery or seizure activity after circulatory arrest and during rewarming, which can be associated with adverse neurological outcomes.

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• The use of full EEG monitoring during a TAAD repair is uncommon, owing to the complexity of monitor application in the setting of an emergent surgical procedure and the need for additional training to reliably interpret EEG.

BIS monitor

• Processed EEG monitors such as the bi-spectral index (BIS) are used to assess depth of anesthesia and the presence of electrocerebral silence in patients undergoing TAAD repair.

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• Although the BIS value appears to decrease reliably with progressive hypothermia, it only monitors the frontal cortex and is vulnerable to a number of artifacts common in patients undergoing cardiac surgery.

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• These artifacts include high-dose opioids, the use of N-methyl-D-aspartate (NMDA) receptor antagonists, neuromuscular blocking agents, and even forced-air warming devices
• The value of BIS or EEG-guided electrocerebral silence in improving neurocognitive outcome remains unclear.

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Near Infra Red Spectroscopy (NIRS)

Near Infra Red Spectroscopy (NIRS)

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• NIRS allows for the non-invasive evaluation of regional cerebral oxygen saturation and is commonly used for neuromonitoring in aortic surgery.
• The average baseline value is between 60% and 70% and should be measured on room air in the absence of sedatives or opioids, if possible.
• Although NIRS typically allows for reliable monitoring of cerebral oxygen saturation, it does have a few limitations.
• NIRS monitoring is limited to the frontal cortex, and measurements may be affected by extracerebral tissues and changes in the ratio of cerebral venous to arterial blood volume.
• It can also be affected by patient-specific derangements, including haemodilution, elevated bilirubin, and pathological alterations in cerebral autoregulation.

Near Infra Red Spectroscopy (NIRS)

• Previous studies have shown broad variation in the threshold values for absolute and relative cerebral desaturation, which are associated with postoperative neurocognitive deficits, but it appears that both the degree and duration of desaturation are important in predicting adverse outcomes.

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• In aortic surgery, a decrease in the regional cerebral oxygen saturation to ≤55% or 76%–86% of baseline has been associated with an increase in postoperative neurological events.

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• Importantly, the use of NIRS may allow for early identification of technical issues, such as cannula malposition, that may cause catastrophic neurological injury if left uncorrected.

NIRS desaturation differential diagnosis

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The management of regional cerebral oxygen desaturation includes:

• Optimization of cannula and head position
• Augmentation of mean arterial pressure and oxygen saturation
• Avoiding hypocarbia
• Increasing systemic oxygen delivery through transfusion and increasing cardiac output

Near Infra Red Spectroscopy (NIRS)

Intraoperative �TEE

• TEE is critical to the management of patients presenting to the operating room with TAAD.

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• After the induction of anesthesia, TEE examination should be undertaken to confirm the presence of the aortic dissection before proceeding with central venous access and surgery.

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• The echocardiographer should be aware of possible TEE artifacts that may be confused for a dissection.

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• A true TAAD is characterized by random dissection flap movement, consistent echo intensity, and a clear change in color-flow Doppler signal around the dissection flap.

TEE

Location of the dissection flab

M mode imaging through the aorta in a patient with an ascending aortic dissection demonstrating systolic expansion of the true lumen

TEE diagnosis of the aortic dissection complications

TEE evaluation in a patient with TAAD should focus on assessing for complications that may alter surgical management.

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The presence of left ventricular regional wall motion abnormalities suggests coronary ostia obstruction or dissection and may indicate the need for revascularization.

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Proximal extension of the dissection into the aortic annulus may also result in acute AI, and rupture of the dissection into the pericardium may cause pericardial tamponade.

Similarly, TEE may be used to assess for pleural effusion, which can suggest leaking of blood from the dissected aorta

Aortic regurgitation

Aortic regurgitation

Pericardial effusion

TEE for surgical repair

Measurement of the dimensions of the aortic annulus, sinuses of Valsalva, and the sino-tubular junction can help guide whether surgical repair includes the ascending aorta alone or also includes the aortic root and/or the aortic valve.

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If present, the mechanism and severity of AI should be defined to help guide whether surgical repair includes aortic valve repair or replacement.

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TEE can also be used to assess the extent of the entry tear.

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Unfortunately, the location of the aortic arch in relation to the trachea can make it difficult to obtain satisfactory images of the arch vessels, and assessment of the branches of the descending thoracic aorta is typically nondiagnostic.

TEE for surgical repair

Multiple mechanisms may be responsible for AI in TAAD, including

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(1) annular dilation from a preexisting thoracic aortic aneurysm

(2) aortic valve leaflet disruption from proximal extension of the dissection into the aortic root

(3) prolapse of the dissection flap through an anatomically normal aortic valve

(4) preexisting aortic valve pathology

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TEE: True Vs false lumen

Differentiation of the true from the false lumen should be made echocardiographically.

The true lumen is characterized by systolic expansion, whereas the false lumen typically expands in diastole.

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The false lumen may also demonstrate either spontaneous echocardiographic contrast or hematoma, further assisting in differentiation.

Identification of the true lumen is important to assist in guiding aortic cannulation via the Seldinger technique, via either retrograde or anterograde passage of a wire into the true lumen with subsequent placement of the arterial cannula.

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If elevated line pressure is noted on the initiation of CPB, immediate reevaluation should be performed to ensure that the previously identified true lumen is receiving blood flow from the CPB circuit because pressurization of the false lumen with the initiation of CPB may result in rapid propagation of the dissection and aortic rupture.

TEE for evaluation of surgery repair

After surgical repair, the aorta should be reexamined to ensure that the entry tear and false lumen have been excluded and that flow has been restored to the true lumen.

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The aortic valve should be interrogated to confirm that no significant AI persists after repair or replacement.

New left ventricular regional wall motion abnormalities may indicate the need for further coronary intervention, either via coronary artery bypass grafting or percutaneous coronary intervention.

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Global assessment of right and left ventricular function is important to evaluate for the need for more aggressive inotropic support to prevent postoperative low cardiac output syndrome, which is associated with an increase in mortality after TAAD repair.65

Induction and maintenance

Surgical approach for aortic dissection

The surgical approach

• Classically, the thoracic aorta, from the aortic root to the very proximal descending aorta, may be approached through a sternotomy.

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• This is the easiest, safest and least painful and troublesome approach.

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• It provides an excellent view on the whole anterior aorta (ascending and transverse arch) as well as the origin and the first segments of the supra-aortic vessels.

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• It allow preservation of both internal thoracic arteries for either an immediate or future use if needed

Cardiopulmonary bypass

Cannulation options and cardiopulmonary bypass

• Cardiopulmonary bypass (CPB) is established using various cannulation sites depending on the anatomy and urgency.
• Arterial cannulation for antegrade perfusion is accomplished either via the distal aortic arch if not involved, right subclavian artery, innominate artery, or true lumen of the dissected ascending aorta.
• An alternative cannulation site for antegrade perfusion is through the left ventricular apex and aortic valve.
• Cannulation of either femoral artery will provide retrograde aortic perfusion with potential extension of the dissection area.
• Venous cannulation is most often through the right atrium using a two-stage venous cannula. Femoral or bicaval venous cannulation are other options.

Femoral vessels cannulation

The right axillary artery cannulation

The innominate artery cannulation

Cannulation options and cardiopulmonary bypass

• If the aortic valve is incompetent, a left-ventricular vent is necessary to prevent left-ventricular distension and subsequent subendocardial ischemia.

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• TOE is very useful in guiding various cannulation maneuvers.

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• The procedure may require partial CPB or deep hypothermic circulatory arrest (18–20°C) while performing the distal aortic anastomosis.

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• CPB time and aortic cross-clamp times may be prolonged because of the complexity of surgery. Circulation is re-established through the true lumen after surgical repair and then the patient is weaned off CPB appropriately.

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Aortic reconstruction Surgery

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• The type of surgical repair depends on several important principles:

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• (1) involvement of the aortic root
• (2) status of the aortic valve and associated AI
• (3) involvement of the aortic arch.

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• The main objective of surgical repair is the resection of the dissection tear in the ascending aorta or arch, obliterating the false lumen and redirecting flow into the true lumen.
• Patients undergoing surgical repair must have a thorough evaluation of the aortic valve via TEE and by visual inspection once the aorta is opened.

Surgical procedure for ascending aortic dissection without any aortic root or valve pathology

Surgical procedure for ascending aortic dissection with aortic root or valve pathology

David procedure 1

David procedure 2

David procedure 3

David procedure 4

Ycoub procedure

Bentall procedure

Bentall procedure

Aortic Arch Reconstruction

The aortic arch surgery techniques

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• Techniques of replacement of the aortic arch are variable and numerous.

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• However, they all start by a complete dissection and control of the transverse arch and the first centimetres of the supra-aortic vessels and ends a few centimetres beyond the origin of the left subclavian artery.

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The elephant trunk technique

• In some patients with dilated or jeopardized descending aorta or with connective tissue disease and a significant probability of aneurismal evolution requiring further re-operations, the technique of “Elephant trunk” may be quite useful.
• it consists of folding asymmetrically, a long-enough prosthesis with the longer part inverted into the shorter one. The prosthesis is then placed in the descending aorta and sutured on the trans-section of the descending aorta at the site of the fold.
• This has the advantage of allowing one single suture and of performing a safer and tighter suture thanks to the double layer prosthetic part. The longer part of the prosthesis is then retrieved and used for the transverse arch replacement.

The “Elephant Trunk” technique

Hybrid techniques for repair of the aoric arch

The “Frozen Elephant Trunk” technique

• After the development of the graft-stenting of the descending aorta, the idea that such a technique could be used antegrade during the replacement of the transverse arch came out and rapidly gained interest.
• This procedure combines the concepts of the elephant trunk principle and endovascular stenting of descending aortic aneurysms.
• It associates the use of a stented Dacron graft to the conventional technique of transverse arch replacement; we do not consider this method as a “Hybrid procedure” of aortic arch replacement.
• The endo-prosthesis has indeed no role in the repair of the transverse aortic arch itself, except for the distal anastomosis.

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Hybrid aortic arch repair, types I, II, and III.

Endovascular techniques for repair of the aoric arch

Endovascualr repair I

Endovascular repair II

Endovascular repair III

Cerebral protection

• Effective cerebral protection remains the principal concern during aortic arch surgery.
• Hypothermic circulatory arrest (HCA) is entrenched as the primary neuroprotection mechanism since the 70s, as it slows injury-inducing pathways by limiting cerebral metabolism.
• However, increases in HCA duration has been associated with poorer neurological outcomes, necessitating the adjunctive use of antegrade (ACP) and retrograde cerebral perfusion (RCP).

• ACP has superseded RCP as the preferred perfusion strategy as it most closely mimic physiological perfusion.
• There is a lot of uncertainty regarding several technical details, such as unilateral versus bilateral perfusion, flow rate and temperature, perfusion site, undue trauma to head vessels, and risks of embolization.
• Because of convenience, simplicity and effectiveness of straight DHCA justifies its use in most elective and emergency cases.

Cerebral protection

The physiology of hypothermia

• The central nervous system is vulnerable to ischemia and has a huge metabolic demand with limited energy stores; mean cerebral blood flow, which is autoregulated at 750 mL/min at 37 °C, is 16% of total cardiac output.

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• Hypothermia provides neuroprotection by substantially decreasing the global cerebral metabolism of glucose and oxygen.

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• Hypothermia also substantially reduces the temperature-dependent release and extracellular levels of glutamate and other excitatory neurotransmitters, inhibits proapoptotic activity, and lowers levels of free radicals and inflammatory cytokines.

The basic Requirements of achieving DHCA

• Ensure adequate anticoagulation prior to The start of DHCA

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• Eliminate glucose from all intravenous solutions to reduce the risk of hyperglycemia

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• Administer anesthetics and neuromuscular blocking drugs to decrease oxygen consumption and ensure paralysis

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• Deep levels of anesthesia may decrease the harmful physiologic stress responses to DHCA

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Clinical techniques of DHCA

• After initiation of CPB through the appropriate arterial and venous access, the temperature will be reduced to 15-22 degree.
• The cooling process should occur slowly (over 30–60 minutes) to ensure homogenous hypothermia.
• Maintain full flow CPB for at least 30 minutes to ensure adequate cerebral cooling
• Verify cerebral electrical silence on electroencephalography or bispectrality index
• Establish circulatory arrest by discontinuing CPB flow.

Clinical techniques of DHCA

• At normothermia, brain injury occurs after around four minutes of circulatory arrest. But the duration of DHCA that is considered safe is controversial.
• After 40 minutes of circulatory arrest, the stroke rate increases. After 65 minutes, overall mortality increases.
• When feasible, maintaining a low level of pulsatile CPB flow (“trickle”) improves microcirculatory flow and the balance between myocardial oxygen supply and demand.
• The optimal hematocrit during DHCA is unknown. Hemodilution improves the microcirculation but may lead to cerebral hypoxia

Clinical techniques of DHCA

• Rewarming the patient from DHCA is not without risk. Initial reperfusion with cold blood for at least 10 minutes prior to rewarming enables removal of metabolic waste and free radicals.
• By increasing cerebral blood flow, excessively rapid rewarming increases the risk of cerebral edema, embolization, and hyperthermic cerebral injury.
• Rewarming should be gradual (about 60 minutes) and cease at 37°C (nasopharyngeal), 36°C (esophageal), or 34°C (bladder). The gradient between core and peripheral temperature should be 5–8°C.
• Total arch replacement can also be performed within 20-40 minutes for the distal anastomosis and 20 minutes for the arch anastomoses.

�Physiological effects of deep hypothermia�

Bleeding diathesis

• Decreased platelet count
• Splanchnic sequestration of platelets
• Partial activation of circulating platelets causing aggregation and adhesion
• Slowing of enzymatic reactions in the coagulation cascade
• Enhanced fibrinolysis as a consequence of vascular injury
• Impairment of tissue factor activity
• Inflammatory responses to CPB
• Ischemia-reperfusion injury that further exacerbates coagulopathy
• Disseminated intravascular coagulation may occur

Physiological effects of deep hypothermia

Cardiovascular effects

Prolongation of PR interval and QRS complex on the ECG

Decreased heart rate

Decreased cardiac output

Vasoconstriction during cooling and hypothermia

Vasodilation during rewarming and reperfusion

Hyperglycemia due to:

Stress response

Glucocorticoid administration

Catecholamine administration

Physiological effects of deep hypothermia

Changes in metabolic rate

Decreased metabolic rate and oxygen consumption during hypothermia

Increased metabolic rate during rewarming, particularly with shivering (mitigated by administration of neuromuscular blocking agents)

Decreased metabolism of drugs

Decreased anesthetic requirements

Leftward shift of the oxygen-hemoglobin dissociation curve, with increased binding affinity of hemoglobin to oxygen

Cerebral perfusion

Surgery involving the aortic arch frequently requires interruption of systemic circulation with or without selective perfusion of the cerebral vasculature.

With the advent of ACP and RCP, there has been a shift in aortic surgery from deep hypothermic circulatory arrest (14°C–20°C) to more modest degrees of systemic cooling, with equivalent or improved neurological outcomes.

Selective Antegrade Cerebral Perfusion

Retrograde cerebral perfusion

Cerebral perfusion

Selective cerebral perfusion is commonly used in aortic cases requiring hypothermic circulatory arrest to maintain cerebral blood flow and attempt to minimize neurological injury.

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The two most common strategies include ACP and RCP.

In ACP, blood is directed from the axillary or innominate artery in an antegrade direction up the right common carotid artery to provide perfusion to the brain after clamping of the innominate artery and discontinuation of systemic blood flow

While ACP is advantageous because it maintains continuous circulation through the arterial system, it can result in embolization or vascular injury during manipulation of the arch vessels and risks nonuniform perfusion of the brain if only unilateral ACP is used.

Cerebral perfusion and monitoring

If NIRS is used for intraoperative neuromonitoring, it can help detect cannula malposition, if present, and guide the decision to use bilateral ACP.

A small patient series used a decrease in the left regional cerebral oxygen saturation to <55% and/or a decrease of 15%–20% below baseline as a threshold to initiate bilateral ACP.

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This process was associated with a significant increase in left-sided cerebral oxygen saturation after initiation of bilateral ACP and no postoperative neurological deficits.

Retrograde cerebral perfusion

In RCP, blood is directed in a retrograde direction through the internal jugular veins and cerebral venous sinuses to provide flow of oxygenated blood through the brain during circulatory arrest.78 This technique consistently provides bilateral perfusion through the cerebral venous sinuses and can promote flushing of embolic material from the cerebral vasculature, but its use is limited by concerns about cerebral edema and inadequate neuroprotection due to decreased overall cerebral blood flow.

Retrograde cerebral perfusion

Technically, RCP is typically accomplished utilizing a bicaval cannulation technique. When RCP is initiated, the superior vena cava cannula is snared, the arterial cannula is clamped, and oxygenated blood is given retrograde through the superior vena cava into the cerebral venous system.

RCP pressure can be assessed using the central venous pressure reading from an internal jugular or subclavian central venous catheter and typically ranges from 15 to 25 mm Hg, with a maximum pressure of approximately 40 mm Hg.

While ACP remains the most common method of cerebral perfusion during aortic surgery, the clinical benefit of ACP over RCP remains a topic of continued debate.

The use of combined ACP and RCP during circulatory arrest has been proposed, but this approach has yet to be rigorously evaluated.

Side effects of DHA

Neuroprotective strategies during hypothermic circulatory arrest

Numerous drugs have been used to attempt to provide protection to the brain and spinal cord during aortic surgery, and broad institutional variation exists regarding which specific drugs are used for neuroprotection.

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Steroids, barbiturates, propofol, and mannitol are most used for neuroprotection in aortic surgery.

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In a recent, large, retrospective analysis of patients with a TAAD, corticosteroid use was associated with a decreased risk of new permanent postoperative neurological dysfunction, although the specific dose, timing of administration, and corticosteroid type were not defined.

Neuroprotective strategies during hypothermic circulatory arrest

Mannitol and barbiturates were not found to be neuroprotective.

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Propofol may also be used to decrease cerebral metabolic oxygen consumption and induce burst suppression on EEG.

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However, no studies to date have focused specifically on propofol in hypothermic circulatory arrest, and propofol-induced burst suppression has not been shown to improve neurological outcomes in previous studies of patients undergoing cardiac surgery.

Neuroprotective strategies during hypothermic circulatory arrest

The use of topical cerebral cooling during circulatory arrest is controversial, and evidence is limited for its efficacy.

Most evidence is limited to animal studies of deep hypothermic circulatory arrest, with data suggesting better cerebral cooling and neurobehavioral outcomes in animals who had topical ice application.

Human evidence in deep hypothermic circulatory arrest is limited.

Although topical cooling is a low-risk intervention, it may also interfere with other monitors of cerebral perfusion and has the potential to cause ocular or tissue injury. With the frequent utilization of selective cerebral perfusion, there is likely minimal benefit to the routine use of topical cooling in TAAD surgery.

Controversy

Even less is known about the optimal management during cases with prolonged periods of CA. DHCA without an adjunct has been shown to be safe for less than 30 minutes and up to less than 40 minutes in more contemporary series.

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Beyond 50 minutes, the rates of neurologic dysfunction increase significantly, with stroke rates up to 16.7%.

RCP and ACP can both extend the maximal safe CA time.

However, data on either RCP or ACP specifically for prolonged CA times exceeding 50 minutes are severely lacking in the literature.

Management of coagulopathy

Perioperative bleeding and the need for blood product transfusion are common in aortic surgery.

The pathophysiology of bleeding in TAAD is complex, but recent literature suggests that the dissection activates the hemostatic system, leading to intense fibrinolysis, platelet activation, and clotting factor consumption.

Tissue factor exposure in the false lumen causes excess thrombin generation that is amplified by exposure to CPB.

Studies using thromboelastography to characterize the nature of coagulopathy in TAAD suggest that this preexisting coagulopathy coupled with surgery and hypothermia leads to a progressive reduction in clotting factors, platelet function, and fibrinolysis, resulting in a coagulopathic derangement like disseminated intravascular coagulation.

Little clinical data exist to drive decision making in patients with significant surgical bleeding after TAAD repair.

The optimal approach to the management of coagulopathy after aortic surgery consists of

• Use of point-of-care laboratory studies ( thromboelastometry) to drive decision-making
• Aggressive goal-directed replacement of fibrinogen, platelet, and factor deficiencies
• Use of antifibrinolytic agents to decrease blood component requirements
• Consideration for the use of factor concentrates to help prevent transfusion-related complications.

Management of coagulopathy

• The use of rotational to direct blood component replacement is likely beneficial in patients undergoing aortic surgery.
• The use of thromboelastometry to provide decision support for replacement of factor and fibrinogen deficiency in both thoracoabdominal aortic aneurysm repair and ascending aortic surgery has been shown to decrease intraoperative transfusion requirements as compared to either empiric transfusion or transfusion strategies based on standard laboratory tests.
• Furthermore, thromboelastometry-guided protocols in acute aortic dissection have been shown to reduce rates of surgical re-exploration, massive transfusion, and the cost of transfusion.

Management of coagulopathy

Antifibrinolytic agents in cardiac surgery have been shown to decrease perioperative transfusion requirements and are recommended for routine use in current guidelines.

The most used antifibrinolytic agents in cardiac surgery are the lysine analogues ε-aminocaproic acid (EACA) and tranexamic acid (TXA).

Although some retrospective data indicate that TXA is more effective in reducing blood loss compared to EACA, a recent prospective trial in patients undergoing thoracic aortic surgery found no difference in cumulative blood loss, total packed red blood cells, and total blood product requirements.

However, EACA was associated with a higher incidence of postoperative renal failure, while patients receiving TXA had a higher incidence of postoperative seizure.

This finding was consistent with a larger retrospective review that examined TXA and EACA in patients undergoing cardiac surgery.

Management of coagulopathy

The off-label use of plasma-derived complex concentrates for the correction of coagulopathy after cardiac surgery has been an area of intense recent investigation.

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Prothrombin complex concentrates (PCCs) have been used to correct postoperative coagulopathy after cardiac surgery is associated with a decrease in postoperative bleeding, massive transfusion, and surgical re-exploration.

Management of coagulopathy

A recent, large, retrospective study showed that first-line therapy with coagulation factor concentrates combined with point-of-care testing decreased transfusion requirements and thrombotic complications, with near elimination of the need for fresh frozen plasma transfusion, although this protocol was also associated with an increase in platelet and fibrinogen concentrate utilization

Management of coagulopathy