Anesthesia for deep hypothermic circulatory arrest

DR / SAMI SAMIR

Postoperative neurological injury still remains the main cause of mortality and morbidity after aortic arch operation

.Cardiopulmonary bypass (CPB) & hypothermic circulatory arrest & temporary interruption of brain circulation & transient cerebral hypoperfusion, and manipulations on the frequently atheromatic aorta all produce neurological damages.

Effect of temperature on Effect of temperature on cerebral metabolic ratecerebral metabolic rate

Temperature ( c )

CMRDURATION OF SAFE C A (M_)

CMROpMPFR

37100 51.4100

3270) 66- 74( 7.5) 6.5-8(.82242

3056) 52-60( 9) 8-10(.6544

2848) 44-52( 10.5)9.5-11.5(.5134

2537) 33-42(14)12-15(.3624

2024 ) 21-29( 21)17-24(.2014

1817) 20-25( 25)21-30(.1611

1514) 11-18( 31)25-38(.118

Consequences of circulatory arrest in relation TO temperature and duration of cerebral

ischemia ..

The light color safe circulatory arrest. The dark color obligatory harmful circulatory arrest. The transitional area the periods where the risk and extent of brain damage are dependent on the conduct of surgery and pharmacological intervention. The light gray area is reversible deficits, while the dark gray area is irreversible injuries.

DIRECT AND DELAYED ISCHEMIC INJURY

Cerebral protection

Hypothermia & cerebral blood flow & pharmacological

Methods&

glucose control&

Haemodilution & acid–base management and Surgical techniques

Strategies

H C A A C P R C P

Cerebral Protection During Surgery for AcuteCerebral Protection During Surgery for Acute

Aortic Dissection Type AAortic Dissection Type A

Results of the German Registry for Acute Aortic Dissection Type

A (GERAADA)

Tobias Kru¨ger, MD*; Ernst Weigang, MD*; Isabell Hoffmann; Maria Blettner, PhD;

Hermann Aebert, MD; on behalf of the GERAADA Investigators

ConclusionThis study reflects current surgical practice for acute aortic dissection type A in Central Europe. For arrest times less than 30 minutes, hypothermic circulatory arrest and ACP lead to similar results. For longer arrest periods,

ACP with sufficient pressure is advisable. Outcomes with unilateral and bilateral ACP were equivalent. (Circulation.

2011;124:434-443(.

Aim

Hypothermia is the most efficient measure to prevent or reduce

ischemic damage to the central nervous system when blood

circulation is reduced

Cooling and rewarming

The cooling phase should be gradual, long enough to obtain a homogenous allocation

of blood to the various organs.

For a final bladder and esophageal temperature

of 10°–13°C, cooling should last at least 30

min,35) or even more than 50 min.

“Temperature gradient” not exceeding 7°C or 10°C .

After the reinstitution of CPB a short period of 5 min with hypothermic reperfusion at 15°C to attenuate neural injury.The rewarming phase should be gradual not exceeding 10°C gradient to avoid

cerebral vasoconstriction or increase of oxygen demand/supply ratio The final nasopharyngeal temperature not above 36°C, and discontinued when the patient reaches 35°C

depends on the temperature gradient and the blood flow and a tissue-specific coefficient of temperature exchang.

Rapid cooling the affinity of oxygen for hemoglobin rises may create a temporary state of insufficient oxygen availability.

Rewarming which any additional harm to cerebral cells might induce permanent injury or precipitate their death. .

Providing a favorable hematologic environment, hemodynamic conditions, and avoiding cerebral hyperactivity for optimal recovery of the brain.

Cooling and Rewarming

,Restart perfusion slowly after circulatory arrest." washes out accumulated metabolites, buffers free radicals, and provid high-energy molecules before the resumption of cerebral electrical activity.

Glycemia increases intracellular acidosis and can prevent or delay metabolic homeostasis.

During rewarming glucose is derived in part from the less efficient anaerobic pathway, This vulnerable period can last for 6 to 8 hours after initiation of reperfusion

. Hyperthermia exacerbates cerebral activity and disturbs cellular metabolism after circulatory arrest. It should be stressed that nasopharyngeal temperature underestimates by 2 to 3°C the brain temperature during rewarming.

The temperature should not be allowed to exceed 37°C, keeping in mind that a relative hypothermia actually might be beneficial for optimal brain recovery.

Detection of increased cerebral activity should prompt immediate therapeutic action, which includes deep anesthesia, appropriate sedation, and reduction of temperature.

•

.Topical (head) cooling

An experimental study that a recovery of the metabolic function is more than 50% improved in the group with their heads packed in ice in comparison to those that are notSystems of continuous cooling of the head consist of a cooling cap and an incorporated circuit of continuously circulate water at a desirable temperature

The safest arterial cannulation

The sites of cannulation are either the femoral or the axillary (subclavian) artery

The axillary artery’s cannulation improves neurological outcomes .

avoiding peripheral arteriopathy and of being able to use the same cannula later for ACP.

the use of femoral cannulation is safe and apply a lower body, or “thoraco-abdominal” hypothermic perfusion, combined with ACP

MonitoringMonitoring

Essential monitoringEssential monitoringElectrocardiogram

Arterial oxygen saturations

Peripheral and core temperatures

Central venous pressure

Pre- and postarch arterial lines

Transoesophageal echocardiogram

Most anesthetists consider SvO2 the key for safe monitoring of aortic arch surgery.

The use of a retrograde jugular bulb cannula to monitor brain temperature and transcranial oxygen saturation

SvO2 measurement It should exceed the level of 95% since continuous oxygen extraction is an index cerebral metabolic activity.

Transcranial Doppler is used to measure cerebral blood flow velocity in the basal cerebral arteries and to detect microemboli

.Using paired optical sensors placed on thescalp, NIRS measures the oxygen saturation of blood in all vessels to a depth of 20–40 mm. Ease of use and limited potential for harm have prompted the increasing use of NIRS monitoring

Pharmaceutical manipulations

,Until today there has been no pharmacologicalmedication to reliably protect the ischemic brain.

)a (thiopental (protection of neural membrane,neurocognitive improvement) 5 mg/kg, 5 minutes before induction of arrest,

)b (lidocaine (protection of neural membrane,neurocognitive improvement) 200 mg, just before thearrest’s application,

)c (magnesium sulphate (protection of neural membrane) 2 g simultaneously with lidocaine infusion

)d (mannitol (reducing oedema), 25 g into the prime,and 12.5 g given intravenously after the termination ofcirculatory arrest,

)e (aprotinin (anti-inflammatory, reducing the modulationof embolic load, reducing bleeding), 2–4 × 106 beforeCPB,

)f (steroids membrane stabilization, but neurohyperglycemia and increased neural ischemia

30 mg/kg before CPB,)g (b-blockers (improving neurocognitive deficit)

)h (acadesine (reducing stroke rate).

CEREBRAL BLOOD FLOW

Low-Flow and Intermittent Perfusion

to maintain intracellular stores of high-energy substrates, prevent anaerobic

glycolysis and intracellular acidosis . , in animals at 15°C was 10 mL/kg per minute

in humans 11 mL/kg per minute at 18ºC

should not be used without monitoring of the jugular venous saturation or cerebral

oxygenated statePulsatile Flow

is able to maintain the microcirculation open with a lower mean perfusion

pressure and. ,overcomes this critical reopening pressure of the capillaries more quickly. results in a swifter and more homogeneous

restitution of brain perfusion. .

pH Strategy

alpha stat   A pH of 7.4 and a PaCO2 is only normal for 37o blood¸ If cool a sample of blood:

i) CO2 becomes more solubleii) PaCO2 decreases to maintain a constant CO2 contentiii) pH rises

• preserves brain autoregulation and enzyme activity.

• the curve of oxyhemoglobin dissociation is shifted toward the right, At deep temperature, oxygen diluted in blood represents the major source of oxygen to tissues.

The pH-stat strategy

  ,pH is maintained constant over varying temperatures as blood is cooled :

•     CO2 must be added •   extracellular & intracellular ratio of H+ to

OH is changed• total CO2 stores are elevated

• Autoregulation of brain perfusion is lost,

• Hypercapnia shifts the oxyhemoglobin dissociation curve to the left ·   

 

•Haemodilution .Haematocrit of 20%, is thought to improve

flow in the microcirculation.

.Normovoaemic haemodilution is often achieved byremoving heparinized blood via the arterial cannula immediatelybefore commencement of CPB

MEASURES TO PREVENT ISCHEMIC NEUROLOGIC DAMAGE

•Perfusion techniques to reduce ischemic injury to the brain. Bilateral antegrade cerebral perfusion obtained

by selective cannulation of the innominate and left common carotid arteries. (Inset, top right) Retrograde cerebral perfusion via the superior vena cava. (Inset, bottom right) Regional cerebral perfusion (unilateral

antegrade perfusion) via cannulation of the right

subclavian artery

Bilateral antegrade cerebral perfusion obtained by selective cannulation of the innominate and left common carotid arteries.

Retrograde cerebral perfusion via the superior vena cava.

unilateral antegrade perfusion via cannulation of the right subclavian artery

Antegrade Cerebral Perfusion

Antegrade perfusion of the brain tprovide temperature at 18°C and flow between 10 and 20 mL/kg per minute or a pressure of between 40 and 50 mm Hg in the right radial artery.

The drawbacks are The presence of additional cannulas in the operating field and can result in dissection of the wall and embolism of plaque or air.

Retrograde Cerebral Perfusion

The blood delivered in the superior vena cava flows in inferior vena cava via the azygos system, the perivertebral venous plexus, and the thoracic wall veins.

The drawbacks are steal of blood to the inferior venous territory .

Cerebral edema and when the perfusion pressure above 25 mm Hg.

the jugular system may contain competent valves .

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