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Page 4 of 15 Troncone et al. Vessel Plus 2023;7:14 https://dx.doi.org/10.20517/2574-1209.2023.08

typically quoted at the most conservative to be around 30-35 min in the absence of adjunctive cerebral
[18]
perfusion .
Technique
DHCA requires cannulation to facilitate cardiopulmonary bypass, including adequate venous drainage and
arterial return. Cannulation is thus most often extra-mediastinal including femoral and/or jugular access for
venous drainage and femoral, axillary, or distal aortic cannulation for arterial inflow, depending on
aneurysmal extent. As CPB demands a high degree of systemic anticoagulation, most surgical dissection to
facilitate repair is completed prior to cannulation to avoid unnecessary blood loss. Once surgical exposure is
obtained or the limit to which dissection can be safely performed without cardiovascular support, heparin is
systemically administered, and the patient is cannulated; when placing venous cannulas from the femoral
vein, transesophageal echocardiography is often helpful in confirming adequate right atrial placement to
[19]
provide maximum drainage . Additional strategies to maximize venous drainage include concomitant
jugular vein cannulation with a Y-connection, as well as utilization of vacuum-assisted venous drainage.
Adequate venous output to the pump is a crucial consideration for aneurysm repair with CPB and DHCA,
as inadequate drainage will yield suboptimal pump flows, leading to slower, incomplete systemic blood
cooling, and once cardiac fibrillation occurs, inadequate cardiac drainage may precipitate distention as the
heart can no longer eject.

A technical point worth further discussion is the specific conduct of peripheral CPB during the period of
2
cooling and subsequent circulatory arrest. Flows equal or greater than 2 to 2.2 L/min/m are minimally
sufficient to facilitate efficient cooling and subsequent rewarming . Once CPB is established, cooling is
[20]
[21]
initiated and generally requires at least 30 min . During this period of cooling, the patient is fully
heparinized and on cardiopulmonary bypass; the heart is emptied as much as possible by the venous
cannula. During cooling and re-warming, the temperature gradient of blood coming from and returning to
the patient during cooling is limited to 10 degrees Celsius to prevent generation of gaseous emboli. The
duration of cooling should be at least thirty minutes or longer to minimize the effect of temperature
alterations of tissue function [22,23] .

Myocardial protection for DTA and TAAA repair is an issue present only with the use of deep hypothermia.
As other perfusion strategies for DTA/TAAA repair utilize either LHB or partial CPB, both of which
maintain spontaneous cardiac activity, there is no period of cardiac ischemia and thus no need for
myocardial protection. In the process of achieving deep hypothermia for cerebral, spinal, and visceral
protection, the heart will fibrillate, and coronary perfusion will become impaired, necessitating strategies for
myocardial protection. The combination of hypothermia with induced cardiac arrest is a commonplace
practice amongst contemporary cardiac surgeons. The greatest reduction in myocardial O2 consumption in
the arrested heart occurs between 37 °C and 25 °C, with a relatively small decrease in energy requirements
achieved thereafter . Hypothermic fibrillatory arrest (HFA) will spontaneously occur, usually beyond
[24]
temperatures of 28 to 30 degrees Celsius resulting in a reduced metabolic demand of the myocardium .
[25]
Major disadvantages of hypothermic fibrillatory arrest are the compromised subendocardial perfusion,
particularly in patients with LV hypertrophy or LV distension particularly in patients in significant aortic
regurgitation [24,26] . Ischemia, despite CPB-provided coronary perfusion, occurs due to the strength of the
fibrillating myocardium exerting forces on subendocardial vasculature, as well as any potential intracavitary
distention also exerting transmural pressure on these vessels. Both these situations are gravely exacerbated
in the patient with left ventricular hypertrophy, in addition to their baseline elevated myocardial oxygen
demand, placing this myocardium at elevated risk of ischemic complications . Thus, patients with left
[26]
ventricular hypertrophy are at higher risk of myocardial injury during the period of HFA because of
subendocardial ischemia, despite ongoing continuous coronary perfusion provided by the pump. Cardiac