33
Članek prispel / Received
22. 5. 2018
Članek sprejet / Accepted
14. 3. 2021
Abstract
Purpose: The induction of anesthesia 
with direct laryngoscopy and orotracheal 
intubation are two interventions, which 
can influence oxygen delivery. Rapid ad-
justments of treatment to restore oxygen 
delivery are crucial to improving the out-
comes for patients.
The aim of this study was to compare the 
effects of induction of anesthesia with 
propofol and sevoflurane on oxygen deli-
very in elderly patients undergoing colo-
rectal surgery.
Methods: We studied forty patients 
with physical status II or III, according to 
the American Society of Anesthesiology, 
who were older than 65 years and un-
dergoing elective surgery for resection of 
colorectal carcinoma. The patients were 
randomly divided into the propofol group 
(P-group) and sevoflurane group (S-gro-
up), according to the anesthetic received 
Izvleček
Namen: Uvod v splošno anestezijo z 
direktno laringoskopijo in vstavitvijo di-
halne cevke je postopek, ki lahko močno 
vpliva na prenos kisika. Hitra in pravil-
na izbira učinkovin ter njihovih odmer-
kov za vzdrževanje prenosa kisika pripo-
more k izboljšanju izida zdravljenja.
Namen raziskave je bil primerjati vpliv 
propofola in sevoflurana v uvodu v ane-
stezijo na prenos kisika pri starostnikih, 
anesteziranih zaradi operacije debelega 
črevesja. 
Metode: V raziskavo smo vključili 40 
bolnikov, starejših od 65 let, uvrščenih 
po ASA v 2. in 3. skupino, ki so bili 
programsko operirani na debelem čreves-
ju. Glede na anestetik so bili bolniki na-
ključno razdeljeni v propofolsko skupino 
(skupina P) ali sevofluransko skupino 
(skupina S) 
Rezultati: Po uvodu v anestezijo so 
Ključne besede: 
Propofol, sevofluran, uvod v 
anestezijo, prenos kisika, starostnik.
Key words: 
Propofol, sevoflurane, induction of 
anesthesia, oxygen delivery, elderly.
Vpliv intravenskega ali inhalacijskega uvoda 
v anestezijo na prenos kisika pri starostnikih, 
operiranih zaradi kolorektalnega raka
Effects of intravenous and inhalation induction of 
anesthesia on oxygen delivery in elderly patients 
undergoing colorectal surgery
Avtor / Author Dušan Mekiš1, 2, Vesna Sok1
Ustanova / Institute 1Univerzitetni klinični center Maribor, Oddelek za anesteziologijo, intenzivno terapijo in 
terapijo bolečin, Maribor, Slovenija; 2Univerza v Mariboru, Katedra za anesteziologijo in 
reanimatologijo, Maribor, Slovenija;
1University Medical Centre Maribor, Department of Anesthesiology, Intensive Care 
and Pain Management, Maribor, Slovenia; 2University of Maribor, Faculty of Medicine, 
Department of Anesthesiology and Reanimation, Maribor, Slovenia;
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
Naslov za dopisovanje /  
Correspondence
Izr. prof. dr.  Dušan Mekiš, dr. med., 
Univerzitetni klinični center Maribor, 
Oddelek za anesteziologijo, intenzivno 
terapijo in terapijo bolečin, Ljubljanska 
5, 2000 Maribor, Slovenija
Telefon +386 23211568
Fax +386 23312393
E-pošta: dusan.mekis@ukc-mb.si
34
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
INTRODUCTION
Oxygen delivery (DO
2
) is an important parameter that 
represents the amount of oxygen delivered to the tissues 
per minute and is determined by oxygen saturation of 
arterial blood, hemoglobin, and cardiac output (CO). 
The oxygen delivery index (DIO
2
) is DO
2
 standardized 
to the patient’s body surface area (BSA).
Oxygen supply and demand are imbalanced in several 
acute pathophysiological changes that may lead to 
increase mortality due to the switch to anaerobic 
metabolism and tissue hypoxia (1-7). Numerous 
studies have shown that maintaining proper DO
2 
reduces mortality and complications both in critically 
ill patients and in patients who require major surgery 
(1-8). Measuring DO
2
 allows appropriate selection of 
medications and their doses, and rapid adjustment of 
therapy according to patient requirements (1, 2, 7, 8).
The induction of anesthesia with direct laryngoscopy 
and orotracheal intubation (OTI) are two interventions 
that can influence DO
2
 in two opposite ways. OTI is a 
very painful procedure, which can trigger the release of 
stress hormones and activate the sympathetic nervous 
system, leading to an increase in systemic vascular 
resistance (SVR), mean arterial pressure (MAP), heart 
rate (HR) and the emergence of arrhythmias (17, 38).
Intravenous or inhaled anesthetics used for induction 
of anesthesia, cause depression of the central nervous 
system, which is different between the anesthetics, 
because their actions on different parts of the central 
nervous system vary.  Depression of the sympathetic 
nervous system can influence the cardiovascular 
system. They also have a direct vasodilator effect, 
depress the myocardium and inhibit the baroreceptor 
reflex, and decrease SVR and MAP. When MAP and 
SVR are reduced, the baroreceptor reflex compensates 
by increasing HR; therefore, CO is only minimally 
reduced (8, 11, 18-21). 
Studies comparing propofol and sevoflurane have 
demonstrated a small decrease in MAP and HR before 
OTI and a small increase in MAP and HR during 
and immediately after OTI  following induction with 
sevoflurane (15, 16, 22-31). 
Elderly patients with anatomical and physiological 
changes are a particularly vulnerable group and can 
develop hemodynamic instability during the induction 
of anesthesia. A decrease in the DIO
2
 can rapidly lead 
to tissue hypoxia, including hypoxia of the central 
nervous system and myocardium (8-17).
The aim of the present prospective single-blind study 
se srčna frekvenca, srednji arterijski pritisk, minutni volumen 
srca in indeks prenosa kisika statistično značilno zmanjšali v 
obeh skupinah v primerjavi z izhodiščno vrednostjo. Po uvodu 
v anestezijo se je srčna frekvenca statistično značilno hitreje 
zmanjšala v skupini P. Takoj po vstavitvi dihalne cevke so 
se srčna frekvenca, srednji arterijski pritisk, minutni volumen 
srca in indeks prenosa kisika statistično značilno povečali v 
skupini S, vendar že naslednjo minuto ta razlika med skupi-
nama ni bila več statistično značilna. 
Po vstavitvi dihalne cevke so bili srčna frekvenca, srednji arte-
rijski pritisk, minutni volumen srca in indeks prenosa kisika 
statistično značilno znižani v obeh skupinah v primerjavi z 
izhodiščno vrednostjo.
Zaklju~ek: V uvodu v anestezijo pri starostniku imata propofol 
in sevofluran klinično primerljiv učinek na prenos kisika.
for the induction of anesthesia.
Results: After induction of anesthesia, heart rate, mean ar-
terial pressure, cardiac output and the oxygen delivery index 
significantly decreased in both groups compared to the baseline 
values. Following induction of anesthesia, the decrease in heart 
rate was significantly more rapid in the P-group. 
Immediately after orotracheal intubation, heart rate, mean 
arterial pressure, cardiac output and the oxygen delivery index 
significantly increased in the S-group, but one minute later these 
diferences were not statistically significant. Heart rate, mean 
arterial pressure, cardiac output and the oxygen delivery index 
were significantly lower after orotracheal intubation in both gro-
ups, compared to baseline.
Conclusion: Propofol and sevoflurane are clinically compara-
ble in the induction of anesthesia in elderly patients according 
to the effect on oxygen delivery.
35
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
was to compare the effect of propofol and sevoflurane 
on the DIO
2
 during the induction of anesthesia in 
elderly patients undergoing major surgery. The goal 
of the study was to determine what type of induction 
anesthesia allows more stable functioning of the 
circulatory system in the elderly.
METHODS 
We studied forty patients with physical status II or III, 
according to the American Society of Anesthesiologists 
physical status classification system, who were older 
than 65 years and undergoing elective surgery for 
the resection of colorectal carcinoma. The study was 
approved by the National Medical Ethics Committee. 
All the patients were informed of the aims of the study 
and its protocols, and provided written consent to 
participate in the study.
Patients with an allergy or sensitivity to volatile 
anesthetics or to propofol, with known or suspected 
genetic susceptibility to malignant hyperthermia, 
chronic abusers of illicit substances or alcohol and 
patients with aortic insufficiency, intraaortic balloon 
pump, arrhythmias and vasoconstriction of peripheral 
veins due to poor reliability of LidcoRapid monitoring 
were excluded from the study.
The patients were randomly divided into two groups 
by a person not involved in the study by choosing a 
sealed envelope. The propofol group (P-group) received 
propofol and the sevoflurane group (S-group) received 
sevoflurane for the induction of anesthesia.
Patients were orally premedicated with midazolam 7.5 
mg 60 minutes before the induction of anesthesia. 
A blood sample was collected for the measurement 
of serum hemoglobin (Hb) before the induction of 
anesthesia. An epidural catheter at level Th 10-11 and 
an arterial catheter were inserted in all patients, which 
allowed invasive continuous monitoring of DIO
2
 
values with the LidcoRapid device, which included 
the patented and clinically verified algorithm PulseCo. 
MAP, DIO
2
, HR, SVR and cardiac index (CI) were 
obtained by constant analysis of the pulse wave from 
beat to beat.
For patients in the S-group, a circle CO
2
 absorber 
circuit with a 3-L reservoir bag was used. The circuit was 
primed with sevoflurane 8% in a 2:1 ratio of nitrous 
oxide to oxygen at a fresh gas flow rate of 6 l/min for 
1 minute. 
During the induction of anesthesia, patients in both 
groups received the analgesic fentanyl 2 μg/kg. One 
minute later, the face mask was placed over the mouth 
and nose of the patients in the S-group and they started 
breathing the mixture of 100% oxygen and sevoflurane 
8 vol %. When 4.5% end tidal concentration of 
sevoflurane was reached, the concentration of 
sevoflurane was reduced to 4%. 
One minute after fentanyl application, patients in the 
P-group received a total of 2 mg/kg propofol.
Following the loss of eyelash reflexes, patients in 
both groups received 0.6 mg/kg rocuronium. One 
minute after the application of rocuronium, OTI was 
performed and mechanical ventilation with a tidal 
volume of 6-8 ml/kg was started to maintain end tidal 
CO
2
 concentration between 4 and 4.5 kPa. In both 
groups, anesthesia was maintained with sevoflurane at 
the concentration of 1 MAC at a 40:60 ratio of nitrous 
oxide to oxygen at a fresh gas flow rate of 2 l/min.
The bispectral index (BIS), MAP, HR, CI, SVR, and 
Hb saturation (SpO
2
) were continuously measured and 
the DIO
2
 was calculated two minutes before and fifteen 
minutes after orotracheal intubation according to the 
formula:
DIO
2
 = (CO × SpO
2
 × Hb) / BSA
During the period of measurements, we registered the 
number of cardiovascular side effects necessitating 
rescue treatment and the dose of rescue medication. 
Hypertension was defined as a MAP greater than 85 
mmHg. Hypotension was defined as a MAP lower than 
65 mmHg. Tachycardia was defined as a heart rate higher 
than 90 beats/min and bradycardia as a heart rate lower 
than 40 beats/min. Rescue medication was started 
when the duration of cardiovascular events exceeded 
1 minute. Hypertonic events and/or tachycardia were 
treated with increments of fentanyl 2 μg/kg. Hypotonic 
events were treated with increments of phenylephrine 
25 μg to maintain MAP above 65 mmHg.  Rescue 
medication for bradycardia was increments of atropine 
at 0.5 mg until HR increased. 
The obtained data were processed using the IBM 
36
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
SPSS program and the use of relevant statistical tests. 
Demographic data and baseline values  were compared 
using the t-test for independent samples. The ANOVA 
test was used to process repeated measurements of the 
variables, thus comparing the values  of the variables 
between and within groups. P values <0.05 were 
considered statistically significant.
RESULTS 
In this study, 40 patients were randomly allocated 
into the sevoflurane group (S-group) or propofol 
group (P-group, Figure 1). There were no statistically 
significant differences between the groups in terms of 
age, gender, weight, height, Hb, MAP, HR, CO, and 
DIO
2
 (Table 1).
Time to loss of palpebral reflex (T
LPR
) and time 
to orotracheal intubation (T
OTI
) were statistically 
significantly longer in the S-group (Table 2). Statistically 
significantly higher BIS values at the loss of palpebral 
reflex (BIS
LPR
) and before OTI (BIS
OTI
) were observed 
in the S-group (Table 2).
Before and during the induction of anesthesia 
until insertion of the breathing tube, there were no 
statistically significant differences between the groups 
in terms  of SpO2, MAP, CO and DIO
2 
values. 
HR, MAP, CO and DIO
2 
significantly decreased after 
the induction of anesthesia in both groups compared 
to baseline values (Table 3). Following the induction 
of anesthesia, the decrease in HR was significantly 
more rapid in the P-group (Table 3). Immediately 
after OTI, the HR, MAP, CO and DIO
2
 significantly 
increased in the S-group compared to the P-group, but 
after one minute these differences were not statistically 
significant (Table 3). 
The DIO
2
 was significantly lower after OTI compared 
to baseline (Table 3, Figure 2). After anesthesia 
induction, the DIO2 increased in both groups, but was 
significantly higher in the S-group than in the P-group 
(Table 3, Figure 2).
SpO
2
 values ranged between 98% and 100% over the 
measured time period.
We observed hypotension, which required rescue 
medication in 12 patients in the S-group and in 10 
patients in the P-group, but the difference was not 
Figure 1. Study flow diagram 
Table 1. Demographic data and baseline values  of the 
hemodinamic parameters.
P-group
(n = 20)
S-group
(n = 20) P
Age (years) 71.2±6.2 71.5±6.5 0.88
Gender (Female/Male) 
(n) 8/12 8/12 0.48
Weight (kg) 72.3±15.9 73.6±13.9 0.78
Height(cm) 167.1±7.3 169.4±9.2 0.39
Hb before induction 
(mmol/l) 122.4±15.9 122.9±17.4 0.92
MAP before induction 
(mmHg) 99.6±12.8 101.2±11.9 0.69
HR before inductio 
(min-1) 69.8±9.3 70.9±11.1 0.72
CO before induction 
(ml/min) 3.1±0.9 3.4±1.0 0.28
DIO2 before 
induction(ml/min/m²) 497.5±167.6 550.5±182.1 0.34
Legend: Data is the mean value ± standard deviation; n = absolute number; 
*  P < 0,05 compared between groups; HR = heart rate; CO = cardiac out-
put; Hb = serum hemoglobin concentration; DIO
2
 = oxygene delivery index; 
MAP = mean arterial pressure
37
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
statistically significant, and the cumulative dose of 
phenylephrine was not significantly different between 
the groups (Table 4). We observed bradycardia, which 
required rescue medication in 2 patients in the P-group 
and in 7 patients in the S-group, which was significantly 
different, and the cumulative dose of atropine was 
also significantly different between the groups (Table 
4). None of the patients developed hypertension or 
tachycardia during the study period.
DISCUSSION 
The aim of this study was to compare the effects of 
propofol and sevoflurane on the DIO
2
 in elderly patients 
during induction of anesthesia and for 15 minutes 
after OTI, and to determine which anesthetic provided 
greater stability of the circulatory system. A number of 
Table 2. Time to loss of palpebral reflex (TLPR), time to 
orotracheal intubation (TOTI)), BIS at loss of palpebral 
reflex (BISLPR) and BIS before orotracheal intubation 
(BISOTI).
Time P-group S-group p
TLPR(s) 111.6±9.5* 144.8±21.7* < 0.05
TOTI(s) 172.1±9.9* 205.4±22.7* < 0.05
BISLPR (s) 64.9±8.7* 80.0±8.1* < 0.05
BISOTI(s) 31.8±6.6* 54.3±10.7* < 0.05
Legend: Data is the mean value ± standard deviation; * P < 0.05 com-
pared between groups
Table 3. Hemodynamic parameters before the induction of anesthesia, 1 and 2 minutes after the start of induction, before 
and immediately after orotracheal intubation  and 2, 4, 6, 8, 10 and 15 minutes after orotracheal intubation.
Time MAP(mmHg)
HR
(beat/min)
CO
(ml/min)
DIO
2
(ml/min/m2)
P-group S-group P-group S-group P-group S-group P-group S-group
baseline value 100±13 101±12 70±9 71±11 3.1±1.8 3.4±1.1 497±167 550±182
1 min after 
induction 97±12 98±13* 67±9*‡ 71,±12‡ 3.0±0.8 3.4±1 493±167 545±187
2 min after 
induction 81±13* 82±16* 66±10* 67±12* 2.5±0.8* 2.7±1.0* 424±163* 440±179*
before OTI 70±17* 71±12* 62±10* 64±12* 1.7±0.7* 2.1±0.8* 279±110* 338±127*
after OTI 74±15*‡# 86±17*‡# 70±13‡# 81±17‡# 1.9±0.5*‡# 2.7±1.0*‡# 319±102*‡# 454±190*‡#
2 min after OTI 70±15* 76±15* 65±14* 67±13 1.9±0.7* 2.2±0.7* 315±122* 366±126*
4 min after OTI 69±12* 70±11* 64±12* 60±10* 1.7±0.7* 1.9±0.7* 288±118* 318±117*
6 min after OTI 67±12* 64±8* 61±10* 58±8* 1.7±0.6* 1.8±0.6* 273±101* 290±98*
8 min after OTI 64±12* 62±7* 60±10* 56±8* 1.6±0.5* 1.7±0.6* 264±92* 271±87*
10 min after OTI 66±9* 63±9* 57±9* 57±9* 1.5±0.5* 1.7±0.5* 250±88* 274±88*
15 min after OTI 64±8* 61±8* 56±8* 57±8* 1.5±0.4* 1.6+0.5* 241±79* 263±79*
Legend: Data is the mean value ± standard deviation; n = absolute number; *  P < 0.05 compared to baseline value; ‡  p < 0.05 between group compari-
son; #  p < 0.05 compared to value before OTI; HR = heart rate; CO = cardiac output; MAP = mean arterial pressure; DIO
2
 = oxygene delivery index; 
OTI = orotracheal intubation
38
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
Figure 2. Changes in oxygene delivery index (DIO2) before the induction of anesthesia, 1 
and 2 minutes after the start of induction, before and immediately after 
orotracheal intubation and 2, 4, 6, 8, 10 and 15 minutes after orotracheal 
intubation . 
 
Legend: 
DIO2 = oxygene delivery index 
Data = (the mean value / the baseline mean value)  100%  
OTI = orotracheal intubation  
ind = induction 
*  P < 0,05 compared to baseline value 
‡  p < 0.05 between group comparison 
♯  p < 0.05 compared to value before OTI 
 
  
‡ ♯
0
20
40
60
80
100
120
% DIO2  P
% DIO2  S
Figure 2. Changes in oxygene delivery index (DIO2) before the induction of anesthesia, 1 and 2 minutes after 
the start of induction, before and immediately after orotracheal intubation and 2, 4, 6, 8, 10 and 15 minutes after 
orotracheal intubation .
Legend:
DIO
2
 = oxygene delivery index
Data = (the mean value / the baseline  
mean value) x 100%  
OTI = orotracheal intubation 
ind = induction
*  P < 0,05 compared to baseline value
‡  p < 0.05 between group comparison
#  p < 0.05 compared to value before OTI
Table 4. Commulative dose of the rescue medications.
Time / rescue 
medication P-group S-group p
Phenylephrine 
(mcg) 45.0±66.7 67.5±74.8 0.322
Atropine (mg) 0.05±0.1‡ 0.2±0.3‡ < 0.05
Legend: Data is the mean value ± standard deviation
‡ P < 0.05 compared between groups
studies which investigated the influence of anesthetic 
drugs during induction of anesthesia on the function 
of the circulatory system, both in adults and exclusively 
in the elderly, were limited to the study of MAP and 
HR changes during the induction of anesthesia (15, 16, 
22-31). Only a few studies have compared the effect of 
propofol and sevoflurane on CO or DO
2 
(32-35).
Studies that compared intravenous induction of 
anesthesia with propofol and sevoflurane demonstrated 
greater stability of the circulatory system following 
induction with sevoflurane; a lower decrease in MAP 
and HR before OTI and a lower increase in MAP and 
HR between and immediately after OTI were observed. 
Following the induction of anesthesia with sevoflurane 
or propofol, we observed significant decreases in MAP, 
HR, and CO, which caused a statistically significant 
decrease in the DIO
2
, without statistically significant 
differences between the S-group and P-group.
Husedzinovic et al. compared the effect of sevoflurane 
and propofol on the contractility of the heart muscle in 
adult patients using transesophageal echocardiography, 
and reported statistically significant higher values of 
the stroke volume after the induction of anesthesia in 
the group receiving sevoflurane (32). Nishikawa K et 
al. proved that propofol compared to sevoflurane has 
a greater negative inotropic effect on the heart in the 
elderly (33). 
Based on our results we cannot confirm that sevoflurane 
allows more stable MAP and DIO
2
 during the induction 
and after OTI.
We observed a significantly more rapid decrease in HR 
after induction of anesthesia in the P-group in the first 
minute, but after that and up to OTI no statistically 
significant differences in HR were noted between the 
groups.  However, patients in the S-group showed 
significantly more bradycardia events, requiring more 
rescue doses of atropine (Table 3 and 4). This was 
attributed to the inhibitory effect of high concentrations 
of sevoflurane on the baroreceptor reflex (34). On 
the other hand, propofol should inhibit cardiac 
parasympathetic nerves depending on the dose (35).
Despite the satisfactory depth of anesthesia, according 
to the BIS values, statistically significant increases in 
HR, MAP, and CO were observed after OTI in the 
S-group compared to the P-group, but these diferences 
were subsequently not statistically significant (Table 3).
Based on the present results we cannot confirm the 
results by Dwivedi et al. and Bharti et al., who reported 
39
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
greater stability of the circulatory system during and 
after OTI with sevoflurane induction; however, only 
MAP and HR were compared in these studies (36, 37).
Nevertheless, despite the increase in DIO
2
 in the 
S-group after OTI, the average DIO
2
 value remained 
just below the lower limit of the desired value of 520 
– 600 ml/min/m2 (1). The DIO
2
 in the P-group was 
even lower and achieved only 60% of the baseline 
value. According to the present results, we suggest 
using a lower dose of propofol during induction, as 
propofol decreases the DIO
2
 significantly more than 
sevoflurane. We agree with studies recommending 
titration of the propofol dose according to the BIS 
to achieve greater hemodynamic stability (39). We 
cannot support the use of a continuous infusion of 
phenylephrine or noradrenaline to increase MAP and 
improve hemodynamic stability during induction, as 
these drugs may further decrease the DIO
2
.
The time to loss of palpebral reflex and the OTI was 
statistically significantly longer in the S-group, but still 
within a clinically acceptable time frame. Similar results 
were also observed by other researchers (22-25).
In conclusion, propofol and sevoflurane are clinically 
comparable in the induction of anesthesia in elderly 
patients according to the effect on oxygen delivery. 
Inhalation induction with sevoflurane offers no 
advantage over intravenous induction with propofol, 
with respect to hemodynamic stability and oxygen 
delivery in elderly patients undergoing major surgery.
CONFLICT OF INTEREST STATEMENT 
The authors have no conflicts of interest to declare.
REFERENCES
1. Mansjoer A, George WHY. Pathophysiology of 
Critical Ill Patients:Focus on Critical Oxygen De-
livery. Acta Med Indones-Indones J Intern Med 
2008; 40: 161-70.
2. Mekiš D. Merjenje minutnega volumna srca pri 
bolniku med operativnim posegom in v enoti in-
tenzivne terapije. Medicinski mesečnik 2005; 6, 
7: 8-25.
3. Marino PL. The ICU book. 3rd ed. New York: Lip-
pincott  Williams & Wilkins; 2007. 
4. Darovic GO. Monitoring oxygenation. In: Darovic 
GO. Hemodynamic monitoring: Invasive and non-
invasive clinical application 3rd ed. Philadelphia: 
Saunders; 2002: 263-9. 
5. Treacher DF, Leach RM. ABC of oxygen: Oxygen 
transport – 1 basic principles. Brit Med J 1998; 
317:1302-6. 
6. Treacher DF, Leach RM. ABC of oxygen: Oxygen 
transport – 2 tissue hypoxia. Brit Med J 1998; 
317: 1370-3. 
7. Hameed SM, Aird WC, Cohn SM. Oxygen deliv-
ery. Crit Care Med 2003; 31: 658-67. 
8. Morgan GE Jr., Mikhail MS, Murray MJ. Clinical 
Anesthesiology. Fourth edition. USA: McGraw-
Hill Companies; 2006.
9. Gibson JR, Mendenhal  MK, Axel NJ. Geriatric an-
esthesia: minimizing the risk. Clinics in geriatric 
medicine 1985; Vol. 1 Issue 2.
10. Sophie S. Anaesthesia for the elderly patient. J 
Pak Med Assoc 2007; 57: 196-201.
11. Tonner PH, Kampen J, Scholz J. Pathophysiologi-
cal changes in the elderly. Best Pract Res Clin 
Anaesthesiol 2003; 17: 163-77.
12. Priebe HJ. The aged cardiovascular risk patient. 
Br J Anaesth 2000; 85: 763-78.
13. Chan VW, Chung FF. Propofol infusion for induc-
tion and maintenance of anesthesia in elderly pa-
tients: recovery and hemodynamic profiles. J Clin 
Anesth 1996; 8: 317-23.
14. Walpole R, Logan M. Effect of sevoflurane con-
centration on inhalation induction of anaesthesia 
in the elderly.  Br J Anaesth 1999; 82: 20-4.
15. Kirkbride DA, Parker J, Williams GD, Buggy 
DJ.Induction of anesthesia in the elderly ambula-
tory patient: A double-blinded comparison of pro-
40
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
pofol and sevoflurane. Anesth Analg 2001; 93: 
1185-87.
16. Yamaguchi S, Ikeda T, Wake K, Okuda Y. A sevo-
flurane induction of anesthesia with gradual re-
duction of concentracion is well tolerated in el-
derly patients. Can J Anesth 2003; 50: 26-31.
17. Mekiš D, Kamenik M. Primerjava učinkov remifen-
tanila in fentanila na obtočila med anestezijo za 
premostitev zožitev venčnih arterij. Zdrav Vestn 
2003; 72: 417–21.
18. Campagna J, .Miller KW, Forman SA, Mecha-
nisms of Actions of Inhaled Anesthetics. N Engl J 
Med 2003; 349: 2110-24.
19. Grasshoffa C, Rudolphb U, Antkowiaka B. Mo-
lecular and systemic mechanisms of general 
anaesthesia:the 'multi-site and multiple mecha-
nisms' concept. Current Opinion in Anaesthesiol-
ogy 2005; 18: 386-91.
20. Longnecker DE, Murphy FL. Introduction to an-
esthesia. 8th ed. Philadelphia: W.B. Saunders 
Company; 1992.
21. Rang HP, Dale MM, Ritter JM, Moore PK. Phar-
macology. 5th ed. Edinburgh: Churchill Livings-
ton; 2003.
22. Ti LK, Chow MYH, Lee TL. Comparison of sevo-
flurane with propofol for laryngeal mask airway 
insertion in adults. Anesth Analg 1999; 88: 908
23. Kati I, Demirel CB, Huseyinoglu UA. Comparison 
of propofol and sevoflurane for laryngeal mask 
airway insertion. Tohoku Journal Of Experimental 
Medicine 2003;  200:111-18.
24. Joo HS, Perks WJ. Sevoflurane Versus Propofol 
for Anesthetic Induction: A Meta-Analysis. Anesth 
Analg 2000; 91: 213-19.
25. Reich DL, Hossain S, Krol M, Baez B, Patel P, 
Bernstein A et al. Predictors of hypotension af-
ter induction of general anesthesia. Anesth Analg 
2005; 101: 622-8.
26. Siddik-Sayyid SM, Aouad MT, Taha SK, Dima 
G. Daaboul DG, Deeb PG et al. A Comparison 
of Sevoflurane-Propofol Versus Sevoflurane or 
Propofol for Laryngeal Mask Airway Insertion in 
Adults. Anesth Analg 2005; 100: 1204-9.
27. Smith ET, Elliott G. Routine Inhaled Induction 
in Adults: A Safe Practice? Anesth Analg 2006; 
102: 646-7. 
28. De Hert SG, Cromheecke S, Ten Broecke PW, 
Mertens E, De Blier IG, Stockman BA, et al. Ef-
fects of propofol, desflurane, and sevoflurane on 
recovery of myocardial function after coronary 
surgery in elderly high-risk patients. Anesthesiol-
ogy 2003; 99: 314-23. 
29. Van den Berg AA, Chitty DA, Jones RD, Sohel 
MS, Shahen A. Intravenous or Inhaled Induction 
of Anesthesia in Adults? An Audit of Preoperative 
Patient. Anesth Analg2005; 100: 1422-4.
30. Walpole R, Logan M. Effect of sevoflurane con-
centration on inhalation induction of anaesthesia 
in the elderly.  Br J Anaesth 1999; 82:20-4.
31. Beger FA, Schultz B, Grouven U. Epileptiform dis-
charges during sevoflurane anesthesia, postoper-
ative mood, and cognitive recovery: a comparison 
with propofol. Anesthesiology 2003; 99: 306. 
32. Husedžinović I, Tonković D, Barišin S, Bradić 
N, Gašparović S. Hemodynamic Differences in 
Sevoflurane Versus Propofol  Anesthesia Coll 
Antropol 2003; 27: 205-12. 
33. Nishikawa K, Kanaya N, Kawamata M, Namiki A. 
Left ventricular mechanical performance in elder-
ly patients after induction of anaesthesia. A com-
parison of inhalational induction with sevoflurane 
and intravenous induction with fentanyl and pro-
pofol. Anaesthesia 2004; 59: 948-53.
34. Nagasaki G, Tanaka M, Nishikawa T. The recov-
ery profile of baroreflex control of heart rate after 
isoflurane or sevoflurane anesthesia in humans. 
Anesthesia and Analgesia 2001; 93: 1127-31.
35. Kanaya N, Hirata N, Kurosawa S, Nakayama M, 
Namiki A. Differential effects of propofol and 
sevoflurane on heart rate variability. Anesthesiol-
ogy 2002; 98: 34-40.
36. Dwivedi R, Dwivedi S, Chourasia HK. A compara-
tive study of sevoflurane and propofol for larynge-
al mask airway insertion in adults. Int J Sci Study 
2015; 3: 67-71.
37. Bharti N, Chari P, Kumar P. Effect of sevoflurane 
versus propofol-based anesthesia on the hemo-
dynamic response and recovery characteristics 
in patients undergoing microlaryngeal surgery. 
Saudi J Anaesth 2012; 6: 380-4.
38. Desborough JP. Thestressresponse to trau-
maandsurgery. Br J Anaesth 2000; 85: 109–17.
41
Klinična študija / Clinical study
ACTA MEDICO-BIOTECHNICA
2021; 14 (1): 25–37
39. Möller Petrun A, Kamenik M. Bispectral index-guid-
ed induction of general anaesthesia in patients un-
dergoing major abdominal surgery using propofol 
or etomidate: a double-blind, randomized, clinical 
trial. Br J Anaesth 2013; 110: 388-96.