|Year : 1979 | Volume
| Issue : 3 | Page : 20-23
Effects of different types of pulmonary ventilation on intra-ocular pressure under general anaesthesia
P Mukherjee1, N Bose2, R Mukherji1
1 Department of Ophthalmology, Calcutta National Medical College & Hospitals, Calcutta, India
2 Department of Anaesthesiology, Calcutta National Medical College & Hospitals, Calcutta, India
Department of Ophthalmology, Calcutta National Medical College & Hospitals, Calcutta
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mukherjee P, Bose N, Mukherji R. Effects of different types of pulmonary ventilation on intra-ocular pressure under general anaesthesia. Indian J Ophthalmol 1979;27:20-3
|How to cite this URL:|
Mukherjee P, Bose N, Mukherji R. Effects of different types of pulmonary ventilation on intra-ocular pressure under general anaesthesia. Indian J Ophthalmol [serial online] 1979 [cited 2016 May 31];27:20-3. Available from: http://www.ijo.in/text.asp?1979/27/3/20/31219
The success of an intra-ocular surgery largely depends on the skill of an anaesthetist and on how best he can keep the patient quiet during and after surgery and can maintain the intraocular pressure sufficiently low during surgery.
One of the major factors during anaesthesia which may lead to significant alteration in the intra-ocular pressure is the type of breathing i.e., spontaneous and controlled ventilation, Duncalf and Weitzner, Utting and Davidson.
Hypoxia and hypercarbia increase the intraocular pressure while pulmonary hyperventilation, high arterial blood oxygen tension and low CO 2 tension lower the intra-ocular pressure, Utting and Davidson, Thornton and Levy.
In the present study it was contemplated to observe the effects of spontaneous and controlled ventilation on intra-ocular pressure under general anaesthesia during surgery which involves minimal trauma and minimal blood loss.
| Material and methods|| |
The cases for this study were selected from the General Surgical Division of the Calcutta National Medical College Hospital. Study was carried out in forty normal male adult patients all of whom were normal except for the surgical ailments. The eyes of all these patients were normal. Patients were premedicated with Injection Pethidine hydrochloride (1 mg/kg body weight), Injection Promethazine 10.5 mg/kg body weight), Injection Atropine sulphate (0.65 mg) intramuscularly 45 minutes prior to the start of anaesthesia.
These patients were divided into two groups according to the type of ventilation adopted during maintenance of anaesthesia.
Group I -Spontaneous/assisted ventilation with Thiopentone, Succinyl choline, N 2 0-0 2 , single intravenous dose of Pethidine hydrochloride (25 mg), intermittent gallamine as and when required.
Group II-Controlled ventilation with Thiopentone, Succinyl choline, N 2 0-0 2 , a single intravenous dose of pethidine hydrochloride (25 mg) and Gallamine as and when required through a C0 2 absorption circuit with an intentional leak.
Sleep was induced with Thiopentone t2.5% solution with an approximate dose of 5 mg/kg of body weight intravenously. Smooth atraumatic endotracheal intubation was facilitated by intravenous injection of succinyl choline with an approximate dose of 1.5 mg/kg body weight. Intubation was done after spraying the larynx with 4% lignocaine hydrochloride and tube was lubricated with lignocaine jelly to avoid bucking or coughing etc. A single dose of pethidine hydrochloride (25 mg) was given intravenously to provide analgesia. Anaesthesia was subsequently maintained with N 2 0-0 2 and intermittent dose of gallamine (initial dose of gallamine was 1.5 mg/kg of body weight). Subsequently gallamine 15 20 mg was given intravenously as and when required.
The proportion of flow of N 2 0 to 0 2 was 6L: 3L. These patients were on spontaneous/assisted ventilation. When there was gross hypoventilation, respiration was assisted for the safety of the patient.
Tidal volume and minute volume were recorded both pre-operatively and also during anaesthesia.
Induction and incubation were same as in group 1. A single dose of pethidine hydrochloride (25 mg) was given intravenously to provide analgesia. Anaesthesia was maintained with N20 and 0 2 4L: 2L and intermittent injection of gallamine (1.75 mg/kg body weight approx.) was given intravenously (1st dose). Gallamine was repeated as and when required in 20 mg intravenous dose. Respiration was controlled through a C02 absorption circuit with an intentional leak. All attempts were made to prevent hypoxia and hypercarbia. Significant change in blood pressure, pulse or other clinical manifestations of shock were not observed in any patient in this series.
The intra-ocular pressure was measured in all the cases with a Schiotz Tonometer pre-operatively on the day before operation using 5.5 gm and 10 gm weights. Second reading was recorded after administering premedication. Third reading was recorded after intubating the patient. Fourth reading was taken when the action of succinyl choline wear off. Subsequent readings were taken at an interval of fifteen minutes during operation. In all the cases, the mean pressure was noted from the table for paired reading (Friedenwald).
Tidal volume, minute volume were recorded with Wright's respirometer both pre-operatively and during anaesthesia at different period of observation. Arterial blood 0 2 tension (Pa0 2 ) arterial blood CO 2 tension (PaC0 2 ) were done in some unselected cases for both groups pre-operatively and also during anaesthesia (15 minutes after intubation).
| Results|| |
[Table - 1] shows that changes in intra-ocular pressure after premedication in both groups were lower than those of control values. After the action of succinyl choline wear off, the mean values of both the groups were same with the values after pre-medication.
It also shows that mean value of intra-ocular pressure in group I was significantly higher than that of group II. The `t' values between the two groups were highly significant.
[Table - 2] shows that tidal volume, minute volume after premedication were slightly lower than control value, and the mean values of tidal volume and minute volume 15 minutes after intubation and 30 minutes after intubation were much lowered than those of control values while the intra-ocular pressure raised significantly during that period.
Sample studies of blood gas analysis revealed that hypoxia and hypercarbia occurred in group I during anaesthesia. In group II neither hypoxia nor hypercarbia occurred during the period of anaesthesia, rather there was increased arterial oxygen tension and lowered arterial carbon-dioxide tension.
| Discussion|| |
The type of ventilation during anaesthesia can play a significant role in alteration of intraocular pressure. Therefore, technique of anaesthesia is an important factor for the successful outcome of operation in ophthalmic surgery, Duncalf and Weitzner, Utting and Davidson.
In this study the group of patients who were on spontaneous/assisted ventilation, there was hypoventilation as indicated clinically (Wright's respirometer) by a low tidal volume and a low minute volume. Thus hypoventilation might be responsible for rise in intra-ocular pressure in this group of patients.
The tension of CO 2 in the arterial blood is a very important factor in controlling the intraocular pressure. A rise in arterial CO., tension increases the intra-ocular pressure in group I patients. On the contrary, in the group of patients on controlled ventilation the blood gas analysis shows a low arterial CO 2 tension and a high arterial oxygen tension which may be the cause of lowering the intra-ocular pressure in this group of patients as stated by Duncalf and Weitzner.
This hypoxia and hypercarbia might be increasing the cerebral blood flow by cerebral vasodilatation which ultimately increases the intracranial blood volume thus increasing the volume of blood in the eye and as there was no time for a compensatory decrease in the volume of aqueous, a rise in intra-ocular pressure resulted (Utting and Davidson).
| Summary|| |
On comparing the results of intra-ocular pressure of the two groups it was noted that the difference between the average values of intraocular pressure after premeditation and also after intubation was statistically insignificant. When the action of succinylcholine wears off, the difference between the values of intra-ocular pressure was also statistically insignificant but the difference between the average values of intra-ocular pressure was statistically significant 15 minutes after intubation, 30 minutes after intubation and 45 minutes after intubation.
It may be concluded from these observations, that the rise in intra-ocular pressure (Group 1) was significantly higher than that of Group II both clinically and statistically. This is in conformity with Duncalf and Weitzner and Utting and Davidson.
| Acknowledgement|| |
We are grateful to Prof. S.M. Lahiri, Head of the Department of Surgery, Calcutta National Medical College & Hospital for allowing us to carry out the work in his department and to Dr. H.N. Ghosh, Principal-Superintendent, Calcutta National Medical College & Hospital for his kind permission to publish this.
| References|| |
Duke Elder, 1968, The physiology of the eye and of vision, Vol. IV, Henry Kimpton, London.
Duncalf, A. and Weitzner, S.W., 1963, Anaesth. & Analg., 42,
Goldsmith Eric, 1967, Anaesth. & Analg. Cur. Res., 46, 557
Thornton, J.A. and Levy. C.J. 1974, Techniques of Anaesthesia. 263, Chapman and Hall, London.
Utting and Davidson, 1974, Quoted from Cecil Gray, T. and Nunn, J.F. 1971, General Anaesthesia. Vol 2, 3rd Ed., p. 448. Butterworth & Co.
[Table - 1], [Table - 2], [Table - 3], [Table - 4]