Neural damage during CPB

A) Embolism

1) Microembolism

i) Gas

ii) Fat

iii) Cellular aggregates

vi) CPB circuit material

2) Macroembolism

i) Air

ii) Particulate matter

a) Atheroma

b) Calcific debris

c) Thrombus

B) Cerebral Hypoperfusion

1) Systemic hypoperfusion

2) Low pump flow

3) Nonpulsatile flow

4) Incorrect cannula placement

· Cardiac surgical patients develop more frequent, more severe brain injury than patients with comparable preoperative risk factors undergoing noncardiac surgery

• Frank neurological disturbances such as stroke may reflect a mechanism such as macroembolization

• Subtle changes detected by neuropsychological testing may be due to microembolization or anaesthetic effects

• There is continuing debate about whether the fate of the brain is predominantly determined by blood flow & pressure or by embolization; and if perfusion methods do have an effect, is this due to the effect on global cerebral perfusion or on total embolic load delivered to brain

Etiology of CNS Damage during CPB

A.Focal ischaemia

· Most often due to isolated cerebral arteriolar obstruction by a particulate or gaseous embolus

· Emboli vary in size, natue (gaseous versus particular), and origin (patient versus equipment)

· Open-chamber procedures entail a greater risk of embolic debris than do closed-chamber procedures

Sources of emboli:

1. Patient related:

· Aortic atheroma: 2° aortic clamping & cannulation; dislodgement of atheroma due to jetting from arterial cannula

· Intraventricular thrombi: recent mural thrombi

· Valvular calcifications: embolisation of intracavitary valve debris

2. Procedure related:

· Open chambered procedures; entrainment of air via vents

· Aortic cannulation & clamping

· Long durations of CPB

3. Equipment related

· Filters on arterial line & cardiotomy reservoir

· Membrane versus bubble oxygenators

· Use of NO₂

B. Global Ischaemia

Watershed areas

• Boundary areas or watershed zone infarcts in the brain are situated between the territories of major cerebral or cerebellar arteries

Cerebral perfusion pressure

• 28-30°C & alpha stat: autoregulation preserved over CPP range from 20 - 100 mmHg
• 15-20°C: hypothermia-induced vasoparesis —> loss of autoregulation
• Diabetic patient may have impaired autoregulation at moderate hypothermia
• Raised CVP: decrease CPP

Circulatory Arrest

• 16-18°C (Profound circulatory arrest) used to decrease CMRO2 and increase tolerance for ischaemia