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Page 6 of 14 Monaco et al. Vessel Plus 2023;7:23 https://dx.doi.org/10.20517/2574-1209.2023.113

[20]
Aspern et al. have employed collateral network near-infrared spectroscopy (cnNIRS) . By monitoring the
perfusion of the paraspinal muscles at both thoracic and lumbar levels, cnNIRS can serve as an indirect
[22]
measure of the perfusion of the spinal cord collateral network by assessing its oxygenation patterns .
Nevertheless, NIRS still lacks clinical validation in this setting and its routine utilization is not yet
recommended [23,24] .

ANESTHESIOLOGIC STRATEGIES
The main objective of anesthesia management is to avoid abrupt hemodynamic changes that can critically
reduce spinal cord perfusion. The main factors that alter hemodynamics in patients undergoing TAAA are:
cardiac function, the level of aortic clamping, hemoglobin levels, distal aortic perfusion with partial left
heart bypass (PLHB) circulatory assistance, patient’s body temperature, intrathecal administration of
medications and cerebrospinal fluid (CSF) pressure. Hence, by acting on the above-mentioned factors, a
goal-directed hemodynamic strategy is mandatory for the anesthesiologist to achieve adequate spinal cord
oxygenation and perfusion.

It is logical to think that mean arterial pressure (MAP) serves as the driving pressure, and higher values of
systemic pressure lead to a lower risk of paraplegia. However, it is not the MAP as an “absolute value” that
reduces the risk of paraplegia but the difference compared to its preoperative baseline value . For instance,
[5]
patients with a preoperative history of hypertension require significantly higher MAP during the
perioperative period compared with normotensive patients. Within this pathophysiological approach to
spinal cord perfusion, central venous pressure (CVP) also plays a quintessential role . Indeed, the outflow
[5]
from the spinal cord relies on the systemic venous pressure and therefore the CVP. Since the vertebral
venous plexus is functionally a large single plexus with high-capacity vessels that extend along the entire
spinal cord, an increase in CVP is associated with increased pressure in the vertebral venous plexus. As the
spinal canal is a non-expandable space, increased pressure in the vertebral plexus directly causes an
elevation of cerebrospinal fluid pressure (CSFP). The effect of elevated CVP is irrelevant when
vascularization is intact but is crucial in cases of extensive sacrifice of intercostal arteries. In their experience
with monitoring of MEP and SSEP during repair of TAA/A in 100 consecutive patients in whom spinal
cord artery reattachment was (with 1 exception) not carried out, Etz et al. reported that spinal cord
perfusion proved to be profoundly unstable under the above-mentioned conditions, with spinal cord
perfusion pressure (SCPP), defined by the difference between mean arterial pressure distal to clamp
(MAPd) and CSFP, being around 20 mmHg in the hours and days following surgery . With such a low
[25]
driving pressure value, elevated CVP can significantly increase CSFP and reduce spinal cord outflow,
leading to SCI. Because spinal arteries cross the vertebral venous plexus, congestion of this plexus,
secondary to high cardiac preload, exhibits a compressive effect on the segmental arteries that nourish the
spinal cord.

Cardiac function
Cardiac function is the main determinant of MAP and CVP, which in turn are modulated by the right (RV)
and left ventricle (LV). Transesophageal echocardiography allows for early identification of right and left
heart dysfunction and its determinants (preload, contractility, or afterload).

Right ventricular dysfunction
Right ventricular (RV) dysfunction is one of the causes of CVP elevation; hence, cardiac function must be
constantly monitored and supported in the event of a decline in performance. Echocardiographic criteria of
RV dysfunction are summarized in Table 2.