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Influence of supraglottic airway device placement on cerebral hemodynamics
Article in Minerva anestesiologica · February 2016
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Influence of Supraglottic Airway Device placement on
cerebral hemodynamics
Frank RASULO, Nicola ZUGNI, Simone PIVA, Nazzareno FAGONI, Federico PE,
Arturo TONINELLI, Stefano CALZA, Nicola LATRONICO
Minerva Anestesiol 2016 Feb 09 [Epub ahead of print]
MINERVA ANESTESIOLOGICARivista di Anestesia, Rianimazione, Terapia Antalgica e Terapia Intensiva
pISSN 0375-9393 - eISSN 1827-1596
Article type: Original Paper
The online version of this article is located at http://www.minervamedica.it
1
Influence of supraglottic airway device placement on cerebral hemodynamics
*Frank Rasulo 1, Nicola Zugni 1, Simone Piva 1, Nazzareno Fagoni 1, Federico Pe 1,
Artuto Toninelli 1, Stefano Calza 2, Nicola Latronico 1
1Department of Anesthesiology, Intensive Care & Perioperative Medicine, Spedali Civili Hospital
of Brescia, University of Brescia, Italy; 2Department of Molecular and Translational Medicine, Unit
of Biostatistics and Biomathematics, University of Brescia, Italy
Congresses: None
Conflicts of interest: None
Funding: None
Acknowledgements: None
Corresponding Author:
Dr. Frank Rasulo
Department of Anesthesiology and Critical Care Medicine,
Spedali Civili University affiliated Hospital of Brescia
Piazzale Ospedali Civili, 1
25123 Brescia, Italy
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2 BACKGROUND: Supraglottic airway devices (SGDs) are of current use in anesthesia practice and
in emergency conditions. It has been suggested that cerebral blood flow (CBF) can decrease after
SGD insertion or cuff inflation; however, it is uncertain if this reduction is caused by the SGD or
the anesthetic drugs utilized for the anesthetic procedure. During minor surgery we separated CBF
measurements by an adequate time interval in order to measure the distinctive changes in cerebral
hemodynamics associated with anesthesia induction, SGD insertion and cuff inflation.
METHODS: Patients scheduled for minor surgery requiring general anesthesia and SGD placement
were included. Middle cerebral artery mean flow velocity (FVm-mca) and the pulsatility index (PI)
were measured through use of trans-cranial Doppler (TCD) at baseline, after anesthesia induction,
SGD insertion and cuff inflation, once a steady cardio-circulatory state was reached and end tidal
CO2 (etCO2) was within normal range.
RESULTS: A total of 21 patients were included. Following anesthesia induction, in concomitance
to a reduction in mean arterial pressure (MAP), there was a mean decrease in FVm-mca by 16.60
cm/s, p<0.005 and a mean increase in PI by 0.24, p<0.0015. MAP, FVm-mca and PI did not change
significantly, neither after SGD placement (p>0.05), nor after SGD cuffing (p>0.05).
CONCLUSION: SGD insertion and cuff inflation did not influence cerebral hemodynamics in
anesthetized patients undergoing minor surgery. At normal etCO2 range, the CBF reduction with
transient increase in PI was associated with anesthesia induction and not SGD insertion itself.
Key words: Laryngeal Mask - Carotid Artery - Transcranial Doppler Sonography - Blood Flow
Velocity
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3 Introduction
The Laryngeal Mask Airway device (LMA) was first developed by British Anesthesiologist Dr.
Archie Brain and has been in use since 1981.1 In patients with out-of-hospital cardiac arrest
(OHCA) undergoing cardiopulmonary resuscitation (CPR), although the gold standard for airway
management is represented by endo-tracheal intubation, the SGD has been used as an alternative
due to its rapid placement without the need for CPR interruption.2-6 In fact, pre-hospital
endotracheal intubation requires elevated competency, causes interruption of CPR maneuvers and,
when performed by unskilled practitioners, can produce adverse events.7,8 Yet, there is substantial
evidence showing that outcome of OHCA patients is worse when airway is managed with SGDs
than when intubated.9-11 The actual mechanism by which SGD placement could be correlated to
poor outcome is currently not known with certainty.
It has been suggested that following placement and cuff inflation this device may cause variations
in carotid artery blood flow (CABF), yet very little is known regarding its effects on cerebral
hemodynamics.12 Due to their anatomical location, the carotid arteries may be vulnerable to
increases in pressure applied within the retropharyngeal space, such as that transmitted by SGD
insertion and inflation of cuff.13-16 This in turn would cause a decrease in carotid bulb cross
sectional area, which may potentially lead to a decrease in CABF leading to variations in cerebral
blood flow (CBF).14 A recent animal model of cardiac arrest and CPR demonstrated instantaneous
reductions in CABF following placement of the SGD.17 Nevertheless, evidence regarding the
clinical consequence of the reduction in the carotid bulb cross sectional area is inconclusive, and not
all agree that the insertion of SGD may in fact induce a reduction in carotid artery section.18,19
Induction of anesthesia may cause systemic hypotension leading to variations in CBF, particularly
in patients with altered cerebrovascular autoregulation (CVA), and in the presence of intact CVA,
variations in CBF may not always directly reflect changes in arterial blood pressure (ABP) or
CABF.20,21
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4 Therefore, it is currently not clear if SGD insertion and/or cuff inflation induce significant
variations of cerebral hemodynamics in humans, or if the observed changes in CBF described in
literature are indeed caused by anesthetic drugs or coincidental systemic ventilatory variations.
We took advantage of minor elective surgical operations, where procedural times are not as
stringent as in major or emergency surgery, to separate CBF measurements by an adequate time
interval in order to measure the distinctive changes in cerebral hemodynamics and to evaluate if
these changes are associated with anesthesia induction or SGD insertion and/or cuff inflation.
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5 Materials and Methods
Approval for the study, was obtained from the Local Ethics Committee on the 2nd of July, 2014 (ID-
1625 n.29) and written inform consent was obtained from all participants. The study was conducted
in the Plastic Surgery and Gastro-intestinal Endoscopy operating rooms of the Spedali Civili
university-affiliated hospital of Brescia, from July 2013 to January 2014. Patients were included if
they were 18 years of age or older, were scheduled for elective plastic or reconstructive surgery or
colonic and rectal endoscopy surgery requiring general anesthesia and SGD placement, were
hemodynamically stable with an ASA Physical Status Classification System of 2 or less, and had a
valid cranial acoustic temporal bone window for Doppler insonation. Patients with known carotid
artery disease, dysautonomic conditions that can be associated with altered CVA status either
caused by central nervous system disease (Shy-Drager syndrome, Parkinson’s disease, Lewy-body
dementia, pure autonomic failure) or peripheral nervous system disease (diabetes, amyloidosis,
Sjogren syndrome, autonomic neuropathies) were excluded from the study.22-25 All patients had the
same type of SGD, (Laryngeal Mask Airway Unique, Le Rocher, Victoria, Mahe, Seychelles)
which was placed by the same anesthesiologist . The SGD size and the cuff inflation volumes were
chosen according to those suggested by the manufacturer; size 3 SGDs (adults up to 50kg) were
inflated with 20 ml room air, size 4 (adults 50-70kg) with 30 ml and size 5 (> 70kg) with 40 ml.
The anesthesia technique was standardized using total intravenous anesthesia, and comprised
induction with propofol 1-2 mg kg-1 and fentanyl 1-2 μg kg-1, and maintenance with propofol 3-6
mg kg-1 hr -1 and remifentanyl 0.05-0.1 μg kg1 min-1. No muscle relaxants were used.
Monitoring included non-invasive ABP, heart rate (Infinity®Delta monitor, Dräger, Lübeck,
Germany), arterial oxygen saturation with pulse oximetry and end-tidal CO2 (etCO2). Mechanical
ventilation (Primus®ventilator, Dräger, Lübeck, Germany) settings were standardized so as to
maintain normal ranges in order to avoid any influence of arterial blood gases on cerebral
vasoreactivity and CBF (tidal volume 6-8ml/kg, respiratory rate set in order to maintain a etC02
between 35 - 40 mmHg and fraction of inspired oxygen at 0.35). After SGD insertion and before
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6 cuff inflation, etCO2 was immediately monitored to be sure that its value remained stable. All
patients had a clinically free airway and procedures were carried out uneventfully.
Trans-cranial Doppler measurements
In all patients studied, a 2 MHz Trans-cranial Doppler (TCD) probe (DWL Multidop®, Singen,
Germany) was used in order to measure FVm-mca as an indirect indicator of CBF, and the
pulsatility index (Peak systolic blood flow velocity - End diastolic blood flow velocity / mean
systolic blood flow velocity), as an indirect measurement of intracranial pressure (PI values > 1
were considered indicative of elevated ICP). The temporal acoustic bone window with the strongest
signal was chosen for insonation, and all exams were performed manually without continuous TCD
probe fixation. The variables were measured in four different time frames: a) basal condition, while
in the pre-anesthesia room before induction of anesthesia. Here the patient was positioned supine
and the head tilted and maintained at a 20° angle throughout the measurement in order to improve
vessel alignment; b) immediately following induction of anesthesia before SGD insertion; c) after
SGD insertion and d) after cuff inflation. Between times “c” and “d” CBF measurements were
performed only if a steady-state cardio-circulatory condition was achieved, meaning when ABP and
heart rate remained unchanged for more than 60 seconds. The TCD examiner was blinded to the
vital parameter values. Once all four TCD measurements were performed, the rest of the anesthesia
was conducted based on the judgment of the anesthesiologist.
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7
Statistical analysis
We expressed continuous variables as means and standard deviation (SD) or as medians and range
(absolute range or interquartile range [IQR]), and discrete variables as counts (percentage), unless
otherwise stated. Differences of CBF variables at various time points were analyzed by means of
repeated measurement ANOVA fitted by linear mixed models using subject as random effect.
Assuming a minimum effect size (expected difference between group means/standard deviation) of
0.7 (assumed within group standard deviation = 10) and 0.15 (SD = 0.2) respectively for FVm-mca
and PI, power 0.8 and significant level of 0.05 we estimated a sample size of 21.26 Tests were two
tailed, and p<0.05 was considered as significant. The data were analyzed with STATA 8.0 and R
(version 3.1.1 R Development Core Team, GNU General Public License).
Results
A total of 21 consecutive patients undergoing general anesthesia with SGDs were included and
studied within a time-span of three months. Surgical interventions included 12 patients who
underwent plastic surgery and 9 patients colonic and rectal endoscopy surgery.
Patient demographics, including ASA mean = 2 [range 1-3], BMI mean = 24.6 [range 20-37], age
mean = 45.6 [range 18-75], and etCO2 values post-SGD insertion and post-SGD cuffing and the
difference between the readings during these two time frames (p>0.05), are listed in Table 1. The
etCO2 ranged from 35-40 mmHg (mean 36.6 mmHg [SD 2.7]) during the measurements, and the
average cuff inflation volume was 30.7 ml (range 30-40 ml [SD 5.1]) with an average pressure of
57.4 cmH2O [SD 1.7] (range 54 – 60 cmH2O). Anesthesia induction was performed with propofol
and fentanyl, and maintenance with propofol and remifentanil in all patients.
Following anesthesia induction, there was a statistically significantly decrease in mean arterial
pressure (MAP, Figure 1a) from a baseline value of 93.5 mmHg [SD 13.8] to 66.0 mmHg after
induction [SD 9.8]; (mean decrease 27.5 mmHg [CI95% 20.9-34.2]), (p<0.005). FVm-mca also
decreased significantly from the baseline value (baseline: 54.52 cm/s [SD 16.1]; to 37.90 cm/s [SD
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8 8.3] after induction; (mean decrease 16.62 cm/s [CI95% 11.8-21.4]), (p<0.005). (Figure 1b).
Regarding the PI, however, there was a statistically significant increase following anesthesia
induction from a baseline value of 1.02 [SD 0.28], to 1.26 [SD 0.23] following anesthesia induction,
(mean increase 0.24 [CI95% 0.10-0.39]), (p=0.0015) (Figure 1c).
MAP did not change significantly after SGD placement, 66.2 mmHg [SD 10.4] (p>0.05), nor after
SGD cuffing, 66.0 mmHg [SD 10.7] (p>0.05), compared to the values measured after induction
(Figure 1a).
FVm-mca also did not change significantly after SGD placement, 35.19 cm/s [SD 7.8] (p>0.05), nor
after SGD cuffing, 37.00 cm/s, [SD 8.3] (p>0.05) (Figure 1b).
Finally, there was no significant change in PI following SGD placement (PI after anesthesia
induction 1.26 [SD 0.23], after SGD placement 1.29 [SD 0.33], or cuff inflation, 1.23 [SD 0.23]
(Figure1c). There were no significant variations in etCO2 measured immediately after SGD
placement and after cuffing (p>0.05) (Table 1).
Linear regression analysis demonstrated significant correlations between LogMFV and MAP, and
between PI and MAP, ( CI95% is represented [p<0.05]) (Figures 2a, 2b).
Discussion
We found that SGD placement and cuffing did not influence cerebral hemodynamics in patients
undergoing general anesthesia for minor elective surgery. Conversely, ABP and FVm-mca
decreased and PI increased significantly after the induction of anesthesia. Both FVm-mca and PI
correlated to the decrease in ABP. Our results suggest that the hypotension following anesthesia
induction was the true determinant of cerebral hemodynamic changes, not SGD placement or cuff
inflation itself. The induction agent used was Propofol, which causes dose dependent reduction in
systolic and diastolic ABP, cardiac output, cardiac index and systemic vascular resistance, and,
despite its ability in preserving CVA, can reduce the CBF in a substantial proportion of patients.27-30
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9 Another finding of this study was that PI increased concomitantly with the decrease in FVm-mca
and CBF. Several studies support the interpretation of PI as a reflection of the distal cerebro-
vascular resistance, attributing greater PI to higher cerebro-vascular resistance. However, PI may
also increase as a consequence of reduced cerebral perfusion pressure in animals with intact CVA,
such as during hypercapnia31. In order to exclude the influence of CO2 on PI, etCO2 was monitored
immediately following SGD placement and for the rest of the procedure. The difference in etCO2
values immediately post-SGD placement and post-SGD cuffing were not statistically significant
(Table 1). Consequently, the increase in PI was most likely caused by cerebral vasodilation
secondary to ABP reduction with secondary transient increase in cerebral blood volume and
intracranial pressure. These changes, which are transient and likely to be clinically irrelevant in
patients with good general condition and normal brain compliance, support the paradigm of
anesthetic-induced systemic hypotension with secondary cerebro-vascular modification.
In order to exclude the influence of SGD cuff pressure on FV and PI, we maintained cuff pressure
constant throughout the whole procedure at pressures suggested by the manufacturers. The
importance of SGD cuff pressure on the incidence of pharyngo-laryngeal adverse effects has been
recently underlined in a study which confronted the incidence of “pharyngo-laryngeal discomfort”
between a tight control of pressure maintained at 60 cmH2O with a second control group in whom
there were no corrections in cuff pressure but only measurements. Compared to the control group,
there was a reduction in adverse events in the group in whom the cuff pressure was maintained
constant at 60 cmH2O, although the influence on cerebral hemodynamics was not evaluated.32
Some differences compared to a few papers published previously in literature should be pointed out;
our results contradict those of Colbert SA and colleagues who showed that SGD cuff inflation
caused a reduction in the cross sectional area of the carotid artery leading to a reduction in CABF.14
In their study the time intervals used between CABF measurements were not specified, and hence,
it is not certain to what extent the reduction of CABF was due to the reduced cross section area of
the carotid artery or the hypotensive effect of the anesthetic drugs. Furthermore, it is not clear why
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10 cuff deflation lead to a significant increase of carotid cross-sectional area without any significant
variations in blood flow velocity. Compared to the study by Segal N and colleagues, who based
their study on a swine model during CCA, our study was performed in humans, and within a
general anesthesia setting.17 Another difference between the two models may be anatomical; in fact,
the human carotid arteries are found more lateral and further away from the trachea, and the
digestive tract is covered by the deep cervical fascia which may inhibit further changes in the
carotid cross section, rendering the carotid artery less vulnerable to effects caused by SGD insertion
compared to pigs.18
Limitations of the study
First, only a limited number of surgical patients in a hemodynamically stable condition were
studied; therefore, generalizing the results to other patient populations with more severe clinical
conditions such as those with cardiac arrest undergoing cardio-pulmonary resuscitation, is not
warranted. Second, cerebral blood flow velocity is not a direct measurement of CBF and depends
greatly on the radius of the middle cerebral artery that should remain constant for the measurement
to be accurate. Third, we did not test CVA before induction of anesthesia, although we carefully
excluded patients with autonomic dysfunction who are at increased risk of altered CVA alteration.
Future animal studies should replicate our model with steady-state CBF measurements rather than
CABF measurements during attempted resuscitation following cardiac arrest. If the proposed
hypothesis of anesthetic-induced systemic hypotension with induced cerebro-vascular changes
holds true, patients with intact or altered CVA should demonstrate different PI time-trends.
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11 Conclusions
SGD placement and cuffing did not influence cerebral hemodynamics in patients undergoing
general anesthesia for minor elective extracranial surgery. FVm-mca decreased and PI increased as
a consequence of the reduction in ABP following anesthesia induction. The proposed model of CBF
measurement in steady-state condition using TCD or other invasive methods should be replicated in
experimental animal settings of unstable circulatory conditions to separate the differential effects of
multiple explanatory variables of CBF reduction.
Core Messages
1) SGD placement and cuffing do not cause per se variations in cerebral hemodynamics in patients
with intact cerebrovascular autoregulation, and therefore can be safely used for airway
management during general anesthesia for extracranial surgery;
2) Drugs used for general anesthesia induction, such as propofol and remifentanil, cause a drop in
cerebral blood flow and blood flow velocity, most likely due to anesthetic-induced hypotension
and flow/metabolism coupling;
3) Anesthetic induced hypotension may cause an increase in PI in patients with intact CVA;
4) These findings warrant further investigation in patients with brain injury, at risk of having altered
cerebrovascular autoregulation, undergoing general anesthesia.
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12
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32
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16 TITLE OF TABLE
Table 1. Patients ASA (American Society of Anesthesiology physical status classification
system), BMI (body mass index), age, etCO2 (end tidal carbon dioxide in mmHg)
values post-SGD insertion and post-SGD cuffing (p > 0.05). The last column showing
the differential values between the two etCO2 time frame measurements.
TITLES OF FIGURES
Figure 1a,1b,1c. Box-Plot representation of the variations in *MAP, **MFV and***PI, before and
after anesthesia induction of (1a-1b), after †SGD insertion (c) and after SGD cuff inflation. The
only statistically significant variation in these parameters took place following anesthesia induction
(p<0.05). The boxes display the 1st and 3rd quartiles, while the whiskers correspond to the
maximum and minimum value of each parameter during the four time frames. The median is
represented by the horizontal line inside the box. *MAP (mean arterial pressure), **MFV (mean flow velocity), ***PI (pulstality index), †SGD (Supraglottic airway device) .
Figure 2a, 2b. Linear regression analysis showing the correlations between LogMFV and MAP (a),
and between PI and MAP (b), (CI95% is represented). (p<0.05).
Authors’ contributions
FR was involved in all aspects of the study from conception and design, to data collection
and analysis, to preparation of the manuscript. NZ, AT, FP, SP, NF were involved during
data collection, SC SP and NF were involved in data analysis. NL was also involved in all
aspects of the study as senior author from conception and design, to data collection and
analysis, to preparation of the manuscript.
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Patient Number
ASA BMI (Kg/m2)
AGE etCO2 (mmHg) Differential etCO2
(mmHg) Post-SGD insertion
Post-SGD cuffing
1 2 23 18 36 37 1
2 1 22 38 36 36 0
3 2 31 46 37 36 -1
4 1 25 18 38 40 2
5 2 24 38 40 40 0
6 2 23 18 40 39 -1
7 2 22 52 38 38 0
8 2 20 37 35 36 1
9 2 24 52 38 39 1
10 2 37 60 36 35 -1
11 2 30 63 34 32 -2
12 2 25 68 36 34 -2
13 2 26 65 32 33 1
14 2 24 65 40 38 -2
15 2 23 42 38 38 0
16 1 20 43 32 33 1
17 2 26 41 40 39 -1
18 2 21 47 36 36 0
19 2 22 75 35 34 -1
20 2 24 50 37 37 0
21 2 25 22 38 36 -2
Table 1. Patients ASA (American Society of Anesthesiology physical
status classification system), BMI (body mass index), age, etCO2 (end
tidal carbon dioxide in mmHg) values post-SGD insertion and post-SGD
cuffing (p > 0.05). The last column showing the differential values between
the two etCO2 time frame measurements.
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This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies (either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.
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