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.