Laryngoscopy and intubation are highly stimulating procedures, that causes varied degrees of significant sympathetic responses ^1-7. Orotracheal intubation done with direct laryngoscope necessitates elevation of the epiglottis and exposure of the glottis, which is accomplished by forward and upward lifting the laryngoscope blade. During tracheal tube insertion, the trachea experiences deformation stresses⁸. These stressors are transmitted to hemodynamic centers by sensory nerve fibers, which causes sympathetic nervous activation resulting in haemodynamic alterations. Extended laryngoscopy times result in greater and longer-lasting hemodynamic responses. In 1951, King and associates initially reported on these 

automatic circulatory reactions to direct laryngoscopy.  They are in turn linked to elevated intracranial pressure, capillary wedge pressures, pulmonary arterial pressure (PAP), systemic arterial pressure, and heart rate (HR). Elevated blood pressure and tachycardia are concerning, Because of the increased myocardial oxygen demand, reduced oxygen supply, and potential for a cerebrovascular and cardiovascular accident,. In healthy adults, transient hemodynamic alterations caused by laryngoscopy and intubation are not very significant. Nonetheless, those with hypertension⁹, unstable coronary heart disease¹⁰, high intracranial pressure, or cerebral vascular disorders may have negative effects. There are numerous techniques and pharmacological approaches that can be used to lessen the intubation-induced circulatory reaction. There have been several attempts at use of non-laryngoscopic intubation devices, such as the flexible fiberoptic bronchoscope¹¹, Augustine guide, laryngeal mask airway ¹², and others. Success rate of intubation  is  96% of intubations done using the laryngeal mask airway. ^15,16.

Many studies have shown ILMA success even in cases of difficult airway ^17,18. Compared to the simple laryngeal mask airway, this improved version offers better ventilation and is intended to serve as a conduit for tracheal intubation¹⁴. With the intubating laryngeal mask airway design, the glottis can be reached without anatomical deformation of upper airway. I LMA does not require head and neck motions during insertion and may accommodate an endotracheal tube (ETT) with an internal diameter of up to 8.0 mm. The ability to keep the patient's airway open and their oxygen saturation levels stable during the ILMA intubation process is another noteworthy aspect.  The tracheal intubation done via  intubating laryngeal mask airway may therefore be less stimulating than traditional laryngoscopy.  The question of whether the haemodynamic responses to intubation by laryngeal mask airway differ statistically significantly from those of direct laryngoscopy is still up for debate ^{19,20,21,22,23,24}.  According to research by WellMeyer, Mahajan, et al., intubating a patient's laryngeal mask airway reduces their cardiovascular responses to intubation in cases of peripheral vascular and coronary illness. Although intubating the laryngeal mask airway lowers hemodynamic responses, Harvey, Avidan et al. and Kamata, Kotoe, Komatsu et al. found that this effect is not clinically relevant.  According to Kihara et al., hypertensives experience a reduction in hemodynamic responses when their laryngeal mask airway is intubated, but not normotensives. Comparing ILMA to traditional laryngoscopy and intubation, Shuchita Garg and colleagues have demonstrated that ILMA is advantageous in preventing the cardiovascular stress response. Therefore, a study comparing direct laryngoscopy and intubation to the hemodynamic effects of intubation using a laryngeal mask airway was proposed.

 Aims and Objectives

To compare the haemodynamic responses to endotracheal intubation using ILMA (Fastrach ^TM) and using direct laryngoscopy in adult patients with normal airway.

The study included sixty adult patients with normal airways who were ASA grades I and II and were having elective lumbar spine operations under general anaesthesia. Following approval from the institutional ethics committee and the participants' signed informed permission, the study excluded individuals under the age of 15 and above the age of 60, as well as those with cardiovascular illness, cerebrovascular disease, hypertension, difficult airway, and cervical spine instability. Patients who needed more than one attempt at intubation were also eliminated. Following an overnight fast, all patients received a premedication injection of glycopyrrolate 0.2mg intramuscularly half an hour before anaesthesia induction. According to a randomised computer chart, patients were randomly assigned to either group A (Laryngoscopy) or group B (I LMA) (Fastrach™ ). All patients underwent the conventional anaesthetic method, which is as outlined below. On arriving in the operating room, the patients were monitored using a conventional anaesthesia monitor that included an electrocardiogram, automated non-invasive blood pressure, pulse oximeter, and end tidal CO2(ETco2).

Arterial blood pressure was measured (HP 1290C-J06, Quartz pressure transducer, Andover, USA) using an arterial cannula implanted in the radial artery under local anaesthetic before inducing general anaesthesia. Fentanyl (2 micrograms/kg), thiopental (5mg/kg), and xylocard 1.5mg/kg were used to induce anaesthesia. Vecuronium Bromide 0.20mg/kg body weight was administered intravenously to promote muscle relaxation. Patients were ventilated with a facemask containing isoflurane (1%), nitrous oxide (67%), and oxygen (33%). After 3 minutes, intubation was attempted with a regular laryngoscope equipped with a McIntosh blade or an appropriate-sized ILMA(Fastrach™). Direct laryngoscopy was performed using appropriate-sized tracheal tubes (Portex Tracheal Tube, SIMS Portex Limited, Kent, UK). A well-lubricated adequate size internal diameter silicone flexometallic tracheal tube was employed to intubate the laryngeal mask airway group. During intubation, the patient in the laryngoscopy group was positioned in the sniffing position (flexion at the neck and extension at the atlanto-occipital joint), whereas the patient in the laryngeal mask airway group was placed in the neutral or slightly extended position. Intubation by ILMA is a two-step process that involves LMA 

insertion and validating its position with a pair of check breaths.  Chest wall movement and capnography (to maintain ETCO2 within normal range) were used to assess successful ILMA installation and ventilatory capacity during gentle manually assisted ventilation. The tracheal tube was then passed through an intubating laryngeal mask airway (FIGS 1, 2, 3).

The ETT cuff was inflated until there was no leak observed. The time taken for each attempt, from the moment the device was inserted into the oropharynx to till when the endotracheal tube (ETT) is connected to the ventilator and the patient takes their first breath following intubation was recorded as intubation time. Failure to intubate was defined as the failure to insert a tracheal tube or visualize cords during laryngoscopy on the first try. In both groups, the procedure was performed by senior staff with extensive experience in either type of intubation. Anaesthesia was maintained using 0.6% isoflurane and 67% nitrous oxide in 33% oxygen. In both groups, patients were ventilated with a tidal volume of 6- 8 ml/kg body weight and a respiratory rate of 10-12 breaths per minute to maintain end tidal carbon dioxide tension (ETCO2) at 25-35 mm of Hg. Systolic, diastolic, and mean blood pressures (SBP, DBP, and MBP) and heart rate (HR) were measured before induction, after induction, every minute for three minutes after induction, and during laryngoscopy and intubation. In all groups, observations were made before induction, post-induction, every minute for three minutes after induction, at ILMA insertion, after intubation, and then every 10 seconds for the next two minutes and then every minute for the next three minutes. For analysis purposes, the pre-intubation value will be used as a baseline.  'The highest value' of SBP, DBP, MBP, and HR is defined as the average of all individual maximum values measured after intubation compared to the baseline value. 'The maximum increase' in SBP, DBP, MBP, and HR is defined as the mean difference between pre-intubation values (baseline value) and maximum values after intubation.' Hypertensive response'^6,7 was defined as a 20% increase in blood pressure over the baseline. 'Tachycardia'^6,7 is defined as a 20% increase in heart rate following intubation compared to the baseline. ILMA was kept in the pharynx until cardiovascular data for the study was acquired, and then removed after the study using the stabilizer rod.

Statistical Methods

Statistical methods Chi-square and Fisher exact test was used to test the significance of homogeneity of sex distribution. Student t test (two tailed) has been used to find the significance of mean difference of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), intubation time and also to test the homogeneity of samples on age, height and weight. Changes in the haemodynamic variables (SBP, DBP, MBP and HR) within each group were analysed with multiple paired t- tests. The maximum values and maximum increase in arterial blood pressure and heart rate observed following intubation were analysed using student t-test. The incidence of “Hypertensive response” and “tachycardia” were analysed using chi- square test. A P value ≤ 0.05 is considered statistically significant. Values are presented as mean ± standard deviation.

Statistical software: The Statistical software namely SPSS 11.0 and Systat 8.0 were used for the analysis of the data and Microsoft word and Excel have been used to generate graphs, tables etc.

There was no statistically significant difference between the two groups with respect to age, weight, height and gender (Table no 1).

Haemodynamic variables

Systolic blood pressure (SBP)

SBP increased in both groups after intubation compared to preintubation readings. There were substantial variations between the two groups in terms of SBP fluctuations at various time points following intubation. The maximal SBP following intubation in the Laryngoscopy group was 135 ± 20 mm Hg, while in the ILMA(Fastrach™) group it was 117 ± 18 mm Hg. There was a significant difference in maximum SBP values after intubation between the two groups (P < 0.001) (see Table 2). In the Laryngoscopy group, the mean maximum increase in SBP from baseline to intubation was 33 ± 18 mm Hg, while in the ILMA(Fastrach™)  group, it was 16 ± 16 mm Hg. Between the two groups, there was a statistically significant difference in the greatest increase in SBP following intubation from baseline (P < 0.001). The Laryngoscopy group experienced a maximum increase in SBP of 24 ± 14 seconds after intubation, while the Fastrach™ group experienced a maximum increase of 22 ± 17 seconds (P = 0.57). Twenty percent increase in baseline blood pressure was considered a "hypertensive response." In the Laryngoscopy group, hypertensive response in SBP was observed in 24 patients (80%) and in the ILMA(Fastrach™) group in 15 patients (50%) (P <0.001).(Table no 3)

Mean blood pressure (MBP)

Following intubation, MBP rose in both groups compared to preintubation levels. Regarding variations in MBP at different times after intubation, there were notable differences between the two groups. Following intubation, the maximal mean blood pressure (MBP) in the Laryngoscopy group was 104 ± 17 mm Hg, while in the group ILMA(Fastrach™) it was 91 ± 15 mm Hg (see table no 4). The maximal MBP values following intubation varied significantly amongst the groups (P= 0.002). In the Laryngoscopy group, the maximum increase in mean blood pressure from baseline was 33 ± 18 mm Hg, while in the ILMA(Fastrach™) group, it was 20 ± 16 mm Hg (P <0.001). The Laryngoscopy group experienced a maximum increase in MBP of 25 ± 17 seconds after intubation, while the ILMA(Fastrach™)  group experienced a maximum increase of 22 ± 18 seconds (P = 0.51). 26 (87%) patients in the Laryngoscopy group and 17 (57%) patients in the ILMA(Fastrach™) group experienced a hypertensive response in MBP (P < 0.001) (see table 5).

Heart rate (HR) 

HR increased in both the groups after induction till 1^st minute and decreased over next two minutes. It again increased in both the groups after intubation from the preintubation values. There was significant difference between the two groups with respect to changes in HR, at various points of time after intubation. The maximum value of HR after intubation in the Laryngoscopy group was 107 ± 14 mm of Hg and in the Fastrach™ group it was 101 ± 16 mm Hg (see table ) . There was no statistically significant difference in the maximum values of HR after intubation between the groups (P= 0.11). The Maximum increase in HR from baseline in the Laryngoscopy group was 19 ± 14 mm Hg and in the Fastrach™ group it was 14 ± 11 mm Hg. Time at which the maximum increase in HR occurred after intubation was 41 ± 23 seconds in the Laryngoscopy group and 19 ± 19 seconds in the Fastrach™ group. There was significant delay in maximum response in laryngoscopy group (P<0.001). Tachycardia occurred in 14(47 %) patients in Laryngoscopy group and 13 (43 %) patients in Fastrach^TM group (P = 0.79)(see table 7). 

Intubation Time (Mask – ETT insertion)

Intubation  time is measured from when the mask is removed and device inserted  to till the endotracheal tube(ETT) is connected to the ventilator and the patient takes their first breath following intubation. The mean intubation  time in the Laryngoscopy group was 24 ± 6 seconds. This includes the time required for laryngoscopy and intubation. The ILMA(Fastrach™)  group averaged 68 ± 21 seconds. Intubation  time was considerably higher in the ILMA(Fastrach™)  group (P<0.001) (see table 8). This is  attributed to procedure of inserting the ILMA, which includes doing a few check breaths via ILMA after its placement, then placing the endotracheal tube through the device.

FIG 4- possible pathways for haemodynamic reponse to direct Laryngoscopy

Airway manipulation during laryngoscopy and tracheal intubation alters haemodynamics due to variable degrees of sympathetic activation. Pressure at the base of the tongue, elevation of the epiglottis during laryngoscopy, and placement of the endotracheal tube into the trachea may all result in a sympathetic reflex (somato-visceral reflex), causing strong circulatory responses.²⁵   Afferent stimuli originate in numerous receptors located throughout the larynx and trachea²⁶ and they are transferred through vagus nerve and subsequently through tractus solitarius to vasomotor center positioned in reticular activating system ^27,28.(see Fig4) The stimulation of the epipharynx (i.e., vallecula) produces the most afferent impulses, followed by the nose, nasopharynx, and tracheobronchial trees²⁹. Aside from receiving projections from the vagus and tractus solitarius, the vasomotor center is modulated by higher centers in the brain such as the cortex, anterior temporal lobe, orbital area of frontal cortex, anterior part of cingulate gyrus, amygdala, septum, and hippocampus (FIG-4). For example, pain sensations from unmyelinated C fibers in the larynx and trachea are transferred over the trigeminothalamic tract to cerebral cortex, which in turn modulates the vasomotor center through the hypothalamus^30,31.  The vasomotor center converts the different stimuli received from peripheral receptors as well as impulses from higher regulating areas into efferent signals. These efferent responses travel from the vasomotor center through the reticulospinal tract and terminate bilaterally in sympathetic preganglionic neurons in the thoracic spinal cord. It travels through the sympathetic nervous system to the heart, blood vessels, and adrenal glands, as well as other regions of the body, causing a reflex increase in blood pressure and heart rate.  Haemodynamic reaction to laryngoscopy is mostly caused by pressure applied to the base of the tongue, as well as by endotracheal intubation. Previous research has shown that the haemodynamic response to laryngoscopy is primarily caused by supraglottic stimulation, and endotracheal insertion does not appear to add significantly to the stimulus responsible for the observed haemodynamic response ³². However, additional research revealed that haemodynamic response is caused by both supraglottic stimulation during laryngoscopy and the introduction of the endotracheal tube within the trachea.

Intubation using a laryngeal mask airway may cause haemodynamic responses due to stimulation of supraglottic tissues, epipharynx, and trachea during endotracheal tube installation with the ILMA  device. Tomori et al. found that mechanical stimulation of several parts of the respiratory tract, such as the nose, epipharynx, laryngopharynx, and tracheobronchial tree, resulted in a reflex cardiovascular response and enhanced neuronal activity in cervical sympathetic efferent fibers. A thin nylon fiber with a diameter of 0.5mm was used to apply stimulus. LMA insertion may result in a lower level of cardiovascular reactions, reflecting a lower level of overall afferent stimulation. Hickey and colleagues also discovered that the hemodynamic response induced by LMA insertion was identical to that produced by the insertion of the Guidel airway ³³. ILMA's similarity to normal LMA may result in a comparable response.  Also, passing the endotracheal tube into the trachea using ILMA can result in haemodynamic reaction, similar to passing the endotracheal tube into the trachea during direct laryngoscopic intubation.

In our study, there were statistically significant variations in the haemodynamic response to intubation between the FastrachTM and laryngoscopy groups at different times following intubation. Following intubation, SBP, DBP, MBP, and HR considerably increased from the baseline in the ILMA(Fastrach™)  and laryngoscopy groups. Comparing the laryngoscopy group to the ILMA(Fastrach™)  group, the following hemodynamic measures showed a longer period of significant elevation from baseline: SBP: 4 minutes vs. 2 minutes, DBP: 4 minutes vs. 3 minutes, MBP: 4 minutes vs. 2 minutes, etc. The maximal elevation in blood pressure happened nearly simultaneously in both groups: in the ILMA(Fastrach™)  and laryngoscopy groups, it was 22 ± 17 sec vs. 24 ± 14 sec, 20 ± 17 sec vs. 22 ± 14 sec, and 22 ± 18 sec vs. 25 ± 17 sec, respectively.

HR peaked late in the laryngoscopy group at 41 ± 23 sec, compared to 19 ± 19 sec in the FastrachTM group. The maximum values and maximum rise (difference between maximum value and preintubation value) in SBP, DBP, MBP, and HR from baseline were investigated. The maximal values and increases in SBP, DBP, and MBP were considerably greater in the laryngoscopy group. This significance was not observed with HR (see tables 6,7). 

Also, in our study, we noticed that ILMA insertion itself generated haemodynamic alterations, with an increase in both blood pressure and heart rate relative to baseline; nevertheless, despite this stimulation, reactions due to intubation with ETT in this group were much lower than the laryngoscopy group.

Also, the ILMA group took longer than the laryngoscopy group. This was mostly due to the fact that ILMA intubation is a two-step operation that requires ILMA placement  followed by intubation through the device after a few check breaths. Despite the longer time, haemodynamic responses were significantly lower than those obtained via laryngoscopy and intubation.

We expected that ILMA(Fastrach™)  intubation would induce less haemodynamic response than tracheal intubation because it does not need traction on supraglottic structures like the laryngoscope blade or direct view of the glottic aperture ILMA’s soft tracheal tube reduces distortion stress compared to ordinary portex tubes. ILMA(Fastrach™)  intubation resulted in significantly lower hemodynamic responses compared to laryngoscopic intubation, supporting our hypothesis.

Our findings are consistent with those of several previous research.³⁵. The current study's findings are consistent with those of Shuchita Garg and colleagues in 2003, who discovered that intubation with ILMA produced a much lower cardiovascular stress response than standard laryngoscopy and intubation. They employed propofol as an induction drug, NIBP for blood pressure monitoring, and parameters were measured every minute. Also, they withdrew ILMA shortly after confirmation of endotracheal intubation. In our trial, we employed thiopentone as an induction agent coupled with fentanyl and lignocaine, and invasive arterial monitoring and parameters were recorded every 10 seconds for the first 2 minutes. We also kept ILMA in place throughout the investigation and removed it using a stabilizer rod 5 minutes after intubation. The present study also correlates with the study done by Well Meyer, Mahajan et al done in 2003.

They discovered that the ILMA resulted in much more stable hemodynamics during and after tracheal intubation than direct laryngoscopy. However, their sample size was only 15 patients per group. They also used non-invasive blood pressure monitoring, recording values every minute after intubation. The study included participants with coronary artery disease and peripheral vascular disease.

Our findings are similarly consistent with a previous study by Kahl et al, who examined the stress response to tracheal intubation in patients having coronary artery surgery utilizing direct laryngoscopy versus an intubating laryngeal mask airway. They found that endotracheal intubation via the intubating laryngeal mask reduced cardiovascular and endocrine stress responses when compared with direct laryngoscopy and intubation They also examined ST segments and assessed catecholamine concentrations. Haemodynamics were recorded via invasive continuous arterial pressure monitoring.

Kihara et al. evaluated haemodynamic responses across three tracheal intubation devices (Macintosh laryngoscope, Trachlight^TM , and intubating laryngeal mask airway-ILMA) in normotensive and hypertensive individuals. They discovered that SBP and DBP in the laryngoscope group were significantly higher than the ILMA and TrachlightTM groups for 2 minutes after intubation, although there were no variations in HR across the devices. However, this was only observed in hypertension patients, not normotensive people. They used noninvasive blood pressure monitoring, with values obtained at one-minute intervals alone. In contrast to this study, we discovered a significant reduction in haemodynamic reactions in our study group, which included exclusively normotensive patients. Another difference is that their sample included up to three intubation attempts, whereas we omitted instances requiring more than one effort.

Kamata et al discovered that intubation with an ILMA considerably reduced hemodynamic reactions to intubation as compared to laryngoscopic intubation. In their investigation, laryngoscopic intubation resulted in a substantial rise in SBP and DBP compared to ILMA intubation for up to 4 minutes after intubation. However, there was no substantial change in HR responses. However, they concluded that the differences between the two approaches were of limited clinical value, although being statistically significant. In this investigation, blood pressure was recorded only once per minute with a noninvasive device.

In our study both fentanyl and lignocaine were used during induction of anaesthesia. Both lignocaine and fentanyl are known to suppress the pressor stress response to laryngoscopy. Also, we used thiopentone as induction agent whereas most other studies have used propofol as induction agent. However, since both groups received thiopentone, lidocaine and fentanyl, the two groups should be comparable. 

In our study, ‘tachycardia’ is defined as 20% increase in heart rate after intubation from the baseline.  There are no studies in the literature to which our incidence of tachycardia (HR: 43 % vs. 47%) could be compared. Incidence of tachycardia was similar in both the groups. 

In our study, ‘hypertensive response’ was defined as a 20 % increase in blood pressures from the base line. There is no study in the literature to which our incidence of hypertensive response could be compared. Incidence of hypertension was higher in laryngoscopy group - SBP: 80 % vs. 50 % in ILMA (P< 0.001), DBP: 93 % vs. 63 % in ILMA (P < 0.001), and MBP: 87 % vs. 57% in ILMA (P < 0.001). 

The time required for ILMA(Fastrach™) intubation was longer than that in laryngoscopy group( see table 8) : (68 ± 21 s vs. 24 ± 6 s; P < 0.001) in our study. Similar findings were seen with other studies. In a study by Kamata et al it was 72 ±54 sec vs. 36 ±25 sec. In another study it was 41± 16 vs. 26 ± 6 sec.

Intubation through ILMA(Fastrach™)  is associated with significantly lower cardiovascular responses compared to direct laryngoscopy and intubation. There was a significant increase in blood pressure and heart rate from baseline in both the groups. The maximum increase was above or equal to preinduction values with laryngoscopy and intubation. But maximum values in ILMA(Fastrach™)  group were never beyond preinduction values with respect to changes in blood pressure. The maximum increase in blood pressure and heart rate from base line were similar between the two groups. This occurred in spite of longer time required for intubation in ILMA(Fastrach™)  group in comparison with laryngoscopy group. Hence, we conclude that intubation through ILMA(Fastrach™) attenuated the haemodynamic response associated intubation in normotensive patients with normal airway.

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