CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 6, July 2013
AFRICA
229
in standard CPB surgery, the lungs are deflated and pulmonary
blood flow is shunted. After weaning from CPB, pulmonary
reperfusion leads to I/R injury with the release of oxygen free
radicals and the resultant lipid peroxidation and endothelial
damage.
4
As a consequence of I/R injury, pulmonary vascular
endothelial dysfunction results in secondary vasoconstriction
and increased vascular permeability, and finally pulmonary
hypertension, oedema and hypoxia.
15
The alveolar–arterial oxygen gradient is widened and lactate is
released as a result of lung injury. The levels of pulmonary lactate
release correlate well with systemic lactate levels. This lactate
release is increased in procedures employing CPB and correlates
with prolonged respiratory support.
6
Furthermore, deflated/
unventilated lungs during CPB induce atelectasis,
12
which
may further induce pro-inflammatory cytokine production.
17
Atelectasis is also blamed for post-CPB pulmonary injury.
Moreover, the degree of intrapulmonary shunt and atelectasis
was found to be correlated.
Computed tomography studies also showed a correlation
between atelactatic areas and intrapulmonary shunt.
18
Based
on this finding ventilation was suggested to protect lungs from
ischaemic damage.
Gasparovic
et al
.
6
studied pulmonary lactate release and
changes in
∆
A–aO
2
during CPB. They reported that the lungs
were a significant source of lactate release and there was a
correlation between pulmonary lactate release and peripheral
lactate concentrations. The duration of CPB correlated with
increased pulmonary lactate release and widened
∆
A–aO
2
. We
also observed that lactate release was increased with CPB and
∆
A–aO
2
was widened in both groups, but unlike their study,
we studied the effects of continued ventilation on
∆
A–aO
2
and
peripheral lactate levels in order to document its effects on
pulmonary functions.
The lactate levels were significantly lower only immediately
after discontinuation of CPB in the ventilated group; in other
determined time periods there was no difference. In each
group,
∆
A–aO
2
widened with time. When the two groups were
compared,
∆
A–aO
2
was lower in the ventilated group in all time
periods, except for six hours following discontinuation of CPB,
when there was no difference. We also report that
∆
A–aO
2
was
higher following induction of anesthaesia in the non-ventilated
group, and this may be the cause of differences in the following
time periods.
In an experimental porcine study, Imura
et al
.
19
documented
that low-frequency ventilation caused reduction of ischaemic
changes and lower rates of atelectasis. They also observed that
lactate levels were lower in the ventilated group compared to
the control. We also documented similar results with regard to
∆
A–aO
2
, but lactate levels were higher only in the non-ventilated
group immediately after discontinuation of CPB.
Schreiber
et al
.
20
revealed that to date, there have been three
trials that investigated the effects of continued ventilation during
CPB on pulmonary functions. Gagnon
et al
.
4
determined a tidal
volume of 3 ml/kg during CPB and John
et al
.
21
5 ml/kg. Boldt
et
al
.
22
continued normal ventilation during CPB. They all failed to
document a significant difference with regard to
∆
A–aO
2
. Only
John
et al
.
21
reported less extravascular lung fluid accumulation
and a decreased period of ventilation.
In our study, we employed a modified ventilation strategy, the
tidal volume was 5 ml/kg, but frequency was 5/min to avoid an
uncomfortable operating field. Different from these studies, we
documented higher
∆
A–aO
2
in the non-ventilated group, except
for six hours after discontinuation of CPB.
The effects of continued ventilation during CPB on pulmonary
function are still controversial. This controversy is very briefly
summarised by Schreiber
et al
.
20
in a recent systematic review
and meta-analysis comprising 814 participants of 16 randomised
trials. They concluded that continued ventilation was beneficial
when serum levels of inflammatory cytokines were considered.
Moreover, oxygenation parameters were improved and shunt
fraction was decreased. However, all these documented effects
were short-lived, questionable, and did not influence the clinical
course and final outcomes.
A similar review reported by Vohra
et al
.
23
also concluded that
no convincing results of any ventilation strategies were available.
In our study, aside from the cytokine levels and other formula
measurements, the clinical outcomes were not affected by
continuous ventilation during CPB. The intubation time, length
of stay in ICU and hospital, and occurrence of postoperative
adverse events were not different between the groups.
Conclusion
We did not document an objective finding that continuous,
low-frequency ventilation attenuated the inflammatory response
and positively affected postoperative pulmonary functions,
adverse events and outcomes. We believe that further studies with
increased numbers of patients and more detailed investigation of
inflammatory markers should be done to be able to draw any
conclusions.
The IL kits were provided by Sanovel Pharmaceutical Company, Istanbul,
Turkey.
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