Introduction
Aortic dissection results when intimal disruption leads to entry of
blood into a cleavage plane in the diseased media, creating a false
lumen within this disrupted aortic layer. This false lumen is separated
from the true lumen by an intimal-medial flap. Further propagation of
the dissection depends on the balance of the hydrodynamic gradient
between the two lumens 1. The hydrostatic pressure
within the false lumen may give rise to additional intimal tears as exit
points, most commonly at aortic branch origins, which may establish
significant re-entry sites into the true lumen 2.
The further expansion of the false lumen may lead to an increased risk
of aortic rupture, and/or collapse of the true lumen which may possibly
lead to hypo-perfusion of the involved vascular bed, often referred as
“malperfusion”. Aortic rupture/tamponade is the commonest cause of
mortality after type-A aortic dissection, followed by visceral ischemia
from malperfusion 3. End-organ malperfusion has been
reported in 16% to 34% of type-A aortic dissections, and may involve
any of the major arterial branches resulting in myocardial, cerebral,
spinal cord, visceral and/or limb ischemia4,
5 6 . The counterbalance of forces between the two
lumens can also lead to a state of dynamic obstruction as evident by the
waxing and waning of peripheral pulses. This is due to the mobility of
the intimal-medial flap with dynamic prolapse of the false lumen
membrane into the branch vessel ostium. A greater circumferential extent
of dissection, higher blood pressure, increased heart rate and lower
peripheral resistance to true lumen outflow may exacerbate this process.7
When cardiopulmonary bypass is initiated to perform repair of an acute
Type-A dissection, it is critically important that arterial cannulation
achieves adequate/preferential true lumen perfusion. This should prevent
false lumen expansion that may lead to progression of dissection,
rupture, and malperfusion.