INFLUENCE OF HEAD FLEXION AFTER ENDOTRACHEAL INTUBATION ON INTRAOCULAR PRESSURE AND CARDIORESPIRATORY RESPONSE IN PATIENTS UNDERGOING CATARACT SURGERY

Background: During preparation and draping of periorbital area, neck flexion causes displacement of the endotracheal tube tip toward the carina. Stimulation of the tracheal mucosa may cause bucking, increased intraocular pressure (IOP), laryngospasm, bronchospasm, change in end-tidal carbon dioxide pressure (PETCO2) or peripheral arterial haemoglobin oxygen saturation (SpaO2) during light anaesthesia. Objective: To investigate the influence of head and neck flexion after endotracheal intubation on heart rate (HR), systolic and diastolic blood pressure (SAP and DAP), SpaO2, PETCO2 and IOP in patients undergoing cataract surgery during general anesthesia. Method: In this prospective observational study, 106 ASA physical status I and II patients scheduled for elective cataract surgery under general anaesthesia were studied. Anaesthesia was induced with thiopental sodium, lidocaine and fentanyl. Atracurium 0.5 mg/kg was given to facilitate tracheal intubation. HR, SAP, DAP, SpaO2, PETCO2, and IOP were measured at 1, 2, and 5 minutes after head flexion. Results: Mean SAP, DAP, IOP, and HR were significantly increased after head flexion compared with baseline values (P < 0.05). PETCO2 and SpaO2 were significantly decreased at 1 and 2 minutes after head flexion compared with baseline values ( P < 0.001). Conclusion: It is concluded that endotracheal tube movement by changes in head and neck position has significant effects on heart rate, systolic and diastolic blood pressures, laryngeal reflexes, SpaO2, PETCO2, and intraocular pressure in patients undergoing cataract surgery under general anaesthesia.


INTRODUCTION
Cataract is a common cause of visual impairment in older individuals.Cataract extraction is usually performed under regional eye block or general anesthesia. 1 After induction of general anesthesia and endotracheal intubation, the periorbital area is prepared and draped.For this purpose, the patient's head and neck is usually flexed 30 to 45 degrees.6][7][8] Inflation of the endotracheal cuff also induces above signs. 8hanges in depth of anaesthesia can modify the laryngeal and respiratory responses to tracheal irritation. 9ryngoscopy and endotracheal intubation are the anesthesia-related practices most likely to increase intraocular pressure (IOP) significantly, that is, by at least 10 to 20 mm Hg . 102] Laryngeal constriction and all components of the tracheal response caused by tracheal stimulation following endotracheal tube movement may impair end-tidal carbon dioxide pressure (PETCO2) and peripheral arterial haemoglobin oxygen saturation (SpaO2).This study investigated the influence of head and neck flexion after endotracheal intubation on heart rate (HR), systolic and diastolic blood pressure (SAP and DAP), SpaO2, PETCO2, wheezing, coughing, stridor, and IOP in patients undergoing cataract surgery.

MATERIALS AND METHODS
After obtaining approval from the our institutional ethics committee and written informed consent, in a prospective observational study, 100 ASA physical status I and II patients, aged 40-80 years, were scheduled for elective cataract surgery under general anaesthesia with duration between 40 and 70 minutes.Patients with anticipated difficult tracheal intubation, direct laryngoscopy lasted more than 15 seconds, respiratory disease or recent respiratory tract infection, cardiovascular disease, IOP more than 20 mmHg, and cigarette smokers were excluded from the study.Patients with more than 15 seconds laryngoscopy were excluded because prolonged duration of direct laryngoscopy may affect the magnitude of circulatory stimulation associated with tracheal intubation. 13ter establishing intravenous access and routine monitors, patients were ventilated with 100% oxygen.Anaesthesia was induced with thiopental sodium 5 mg/kg, lidocaine 1.5mg/kg and fentanyl 1.5 µg/kg.Atracurium 0.5 mg/kg was given to facilitate tracheal intubation.Approximately 2 minutes after drug administration, direct laryngoscopy was performed and trachea was intubated within 15 seconds by using an un-lubricated 7.5-8.5 mm internal diameter high volume/low pressure tracheal tube (PVC, SUPA, Tehran, Iran) and cuff was inflated with a volume of air to a maximum pressure of 25 cm H2O.After tracheal intubation, periorbital area was prepared and draped.During this period, head was elevated and the degree of head flexion was estimated by goniometry and recorded.The lungs were mechanically ventilated using a tidal volume of 8-10 mL/kg and the respiratory rate was adjusted to maintain normocarbia.Anaesthesia was maintained using isoflurane oxygen and 50% nitrous oxide.Neuromuscular blockade was maintained using increments of atracurium 0.15 mg/kg as required.Three-electrode electrocardiogram (ECG) monitoring system was used for the detection of arrhythmias during anaesthesia.HR, SAP, DAP, SpaO2, PETCO2, and IOP were measured at 1, 2, and 5 minutes after head flexion.If patients had arrhythmias after head and neck flexion, it was recorded and patient closely monitored for 5 minutes.Ineffective coughing movements (bucking) and wheezing were also noted after head flexion.Before induction of general anaesthesia, intraocular pressure was measured using a Schiotz Tonometry in both eyes in supine position.
After completion of surgery, residual neuromuscular block was reversed using neostigmine 0.04 mg/kg and atropine 0.02 mg/kg.A blinded observer noted the presence or absence of cough and stridor during emergence of anaesthesia.Presence or absence of cough was recorded as either "yes" or "no."If cough was present, it was graded using a three-category scale (Table 1). 15ta are expressed as mean ± standard deviation (SD) of the mean.Results were analyzed using one-sample T-test, paired sample T-test, the Chi squared test and repeated measure analysis of variance.A p value of <0.05 was considered to represent statistical significance.Statistical analyses were performed using the SPSS 11.0 for Windows software application.

RESULTS
The patients' demographic data, duration of surgery and total opioid administration were summarized in Table 2. Mean (SD) degree of head flexion was 36.4 ± 4.4.Mean SAP, DAP, IOP, and HR was increased significantly after head flexion compared with baseline values and returned to normal at 5 minutes (Table 3, Fig 1).PETCO2 and SpaO2 were decreased significantly at 1 and 2 minutes after head flexion compared with baseline values and returned to normal at 5 minutes (Table 3).Incidence of arrhythmias, bucking and wheezing after head flexion were summarized in Table 4.The incidence of coughing and stridor observed in patients emerging from general anaesthesia was 5% and 2% respectively.

DISCUSSION
Our study showed that in patients undergoing cataract surgery during general anesthesia, endotracheal tube movement by changes in head and neck position had significant effect on heart rate, systolic and diastolic blood pressures, laryngeal reflexes, SpaO2, PETCO2, and intraocular pressure.
SAP, DAP, and HR increased after head flexion compared with baseline values.Incidence of arrhythmias after head flexion was 2-5 %.These changes could be due to stimulation caused by laryngoscopy, endotracheal intubatin and/or head flexion.Laryngoscopy and intubation are associated with tachycardia and a rise in blood pressure. 16These changes have been observed to be associated with rise in plasma noradrenaline levels, confirming a predominantly sympathetic response to it. 17ad flexion causes displacement of the endotracheal tube tip toward the carina. 2In one study, neck flexion caused 5.5 m inward movement of the endotracheal tube. 2 In another study, the mean extent of endotracheal tube displacement was 3.1 mm with neck flexion in low birth weight neonates. 3Displacement of the endotracheal tube caused by flexion of the neck was also investigated in 10 small children between the ages of 16 and 19 months by means of a fiberoptic bronchoscope.The endotracheal tube tip moved a mean distance of 0.9 cm toward the carina with flexion of the neck. 4imulation of the tracheal mucosa by endotracheal tube displacement induces bradycardia, arrhythmias and hypotension.Bradycardia and arrhythmias are independent responses that occur rapidly and are not related to developing hypoxia or dependent on the respiratory responses. 5In our study, head flexion stimulated the tracheal mucosa and caused bradycardia and arrhythmias at 1 and 2 minutes after it.
Predominant response after laryngoscopy and intubation is sympathetic. 16In contrast, parasympathetic response is dominant following stimulation of tracheal mucosa by endotracheal tube movement. 5As fig 1 shows, increase in HR was more sustained than the increase in SAP.Increase in DAP was almost slight.So, it is hypothesized that head flexion after intubation probably causes biphasic cardiac response.At the first phase, direct laryngoscopy caused increased sympathetic response so that HR, SAP and DAP were increased above the baseline.At the second phase, head flexion caused parasympathetic stimulation and apposed sympathetic response following direct laryngoscopy.
In a recent trial by Kihara et al 18 , both systolic and diastolic pressure increased after intubation for 2 minutes with highest values in the hypertensive group . 19In our study, head flexion was done about 6 min after endotracheal intubation.At this time, it is probable that sympathetic response to laryngoscopy has been attenuated.So, it seems that increase in SAP and DAP after head flexion was more due to stimulation of tracheal mucosa by endotracheal tube movement.Therefore, it is concluded that head flexion after intubation have both sympathomimetic and parasympathomimetic effect.
] SpaO2 also decreased significantly at 1 and 2 minutes after head flexion compared with baseline values.Wheezing and bucking after head flexion was presumably due to stimulation of the tracheal mucosa. 8,22 nchospasm is triggered by mechanical stimulation, especially of the laryngotracheal area.Laryngeal and glottic stimulation may not only evoke varying degrees of laryngospasm, but if the stimulus is of sufficient intensity, bronchospasm may be induced as well . 23ronchospasm and laryngospasm after stimulation of the tracheal mucosa by neck flexion caused decreased SpaO2.
The incidence of coughing and stridor observed in patients emerging from general anaesthesia was 5% and 2% respectively. .The cough reflex is initiated chiefly by stimuli applied to the mucosa of the tracheobronchial tree.Endotracheal intubation is a common cause in anesthetic practice for inciting cough or bucking. 24s patients emerge from general anaesthesia, the stimulating effect of positive pressure ventilation on the mechanosensitive receptors of the trachea and larger bronchi may provoke coughing. 25The occurrence of coughing and stridor on emergence from anesthesia could probably be due to stimuli applied to the mucosa of the tracheaobronchial tree by tracheal tube or cuff after head flexion.Inoue and colleagues 6 showed that endotracheal tube movement after head flexion causes significant increase in intracuff pressure (> 25 cm H2O) in some patients.In another study done by Rao et al 7 , over-inflating the sealing cuff had caused a significant prolongation of the expiratory time during the first challenged breath in dogs. 7e increased IOP after head flexion might be due to stimulation of tracheal mucosa by head flexion.The mechanism is not clear, but it probably relates to sympathetic cardiovascular responses to head flexion 11 or blockage of aqueous outflow by acute venous congestion. 12Any straining, bucking, breath holding or obstructed airway during the induction, maintenance, or emergence from general anesthesia will increase venous congestion in the ophthalmic veins and therefore raise IOP. 12

CONCLUSION
Our study showed that endotracheal tube movement by changes in head and neck position has significant effects on heart rate, systolic and diastolic blood pressures, laryngeal reflexes, SpaO2, PETCO2, and intraocular pressure in patients undergoing cataract sur-gery during general anaesthesia.So, head flexion after endotracheal intubation can be hazardous in patients with coronary artery disease, glaucoma and perforating eye injuries where minimal changes in hemodynamic and intraocular pressure are detrimental.

Figure 1
Figure 1 The cardiovascular changes during intubation period and after head flexion in study patients.Data are expressed as mean ± SD.SAP= systolic arterial pressure; DAP=diastolic arterial pressure; HR=heart rate; EI= endotracheal intubation.AHF = after head flexion. P <0.05 vs. baseline.

Table 1 :
Three-Category Scale for Scoring Cough on Emergence

Table 2 :
Characteristic of patients, duration of surgery and intraoperative fentanyl administration

Table 3 :
Cardiovascular, respiratory, and intraocular pressure changes after endotracheal intubation and head flexion.

Table 4 :
Incidence of arrhythmias, bucking, and wheezing at 1, 2 and 5 minutes after head flexion