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Year : 1967  |  Volume : 15  |  Issue : 6  |  Page : 203-212

Physiological considerations from ocular changes in hypothermia during cardiac surgery

Postgraduate Institute of Medical Education and Research Chandigarh, India

Date of Web Publication22-Jan-2008

Correspondence Address:
I S Jain
Postgraduate Institute of Medical Education and Research Chandigarh
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Source of Support: None, Conflict of Interest: None

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How to cite this article:
Jain I S, Agarwal D C, Singh K, Chitambar I A. Physiological considerations from ocular changes in hypothermia during cardiac surgery. Indian J Ophthalmol 1967;15:203-12

How to cite this URL:
Jain I S, Agarwal D C, Singh K, Chitambar I A. Physiological considerations from ocular changes in hypothermia during cardiac surgery. Indian J Ophthalmol [serial online] 1967 [cited 2023 Dec 3];15:203-12. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1967/15/6/203/38811

Table 2

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Table 2

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Table 1

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Table 1

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It is because of hypothermia that open heart surgery has been made pos­sible. With hypothermia one is able to occlude circulation for a good length of time without causing any permanent damage to the central ner­vous system. The main methods to achieve this end are:

1. Surface cooling, and

2. Extra corporeal circulation.

In the first method the body tem­perature is lowered from 37° C to 30°C or a bit lower. At this temperature because oxygen requirements are re­duced, it is possible to occlude the cir­culation for 6 to 7 minutes.

In the extra corporeal technique, the heart and lungs are by-passed com­pletely by a pump oxygenator. The additional advantage of cooling the blood directly is also achieved. Where­as in the former method a long time is required to cool the body and also to warm it subsequently, in the latter method both these can be quickly achieved. DREW and ANDERSON (1959) used deep hypothermia, where temperature of body fell to 15°C. The method was modified by SIMPSON, GIBSON and BLOOMFIED (1960) who achieved a profound hypothermia for open heart surgery. LAMB (1961) was the first to study the ocular res­ponses to such low temperature of the body achieved by this method of SIMPSON et al. At different places, the methods employed for cardiac surgery are likely to vary because of the limitation of availability of a particu­lar type of appliance. Because of these differences, the observations are likely to vary accordingly. It was with this view in mind that we have tried to make our own observations and compare them with those of Lamb.

  Material and Methods Top

The study was conducted on 12 cases operated for various cardiac defects in the Institute of Postgraduate Medi­cal Education and Research, Chandi­garh. Three cases were operated under surface hypothermia only, while 9 were operated under extra-corporeal circu­lation with cooling. In the latter tech­nique following steps were followed:­

i) Premedication with Pethidine and Phenergan

ii) Induction of anxsthesia with Pentothal sodium and relaxant.

iii) Anaesthesia with ether, nitrous oxide and oxygen.

During anaesthesia, the cannulations were done in the external jugular vein and radial and femoral arteries. The chest was opened, venous and arterial cannulae were placed and the patient was made ready for circulatory by­pass.

iv) By-pass-cooling: When the cir­cuit was complete, the mechani­cal pump was turned on which circulated the blood through oxygenator and cooling device.

In LAMB's series, following cool­ing, the circulation was occluded for some time, but in our study this occlu­sion was not resorted to.

v) By-pass rewarming: When sur­gery was complete, rewarming of the blood was started.

During both these procedures when cooling was started intraocular ten­sion, pupil size and fundus changes were noted down at regular intervals.

  Observations Top


In surface cooling there were 3 cases as shown in [Table - 1].

Intraocular Tension

The table clearly indicates that by lowering of temperature on surface cooling, the intraocular tension re­mains almost unchanged; if at all there is a small fall.

Pupil size

As can be seen from graphs I and II, the pupil shows a definite dilata­tion on cooling the body. In graph I of the first case, the pupil began to dilate as the temperature dropped to 35.5° C and the change became more abrupt when the temperature fell from 33.8° to 33.0°C. After this maximum dilata­tion, the pupil began to lose its dilata­tion on further lowering of the tem­perature, the drop being more abrupt at first. On removing the hypothermia the pupil continued to contract and not go through a reverse phase, as the previous levels began to be reached from 30° back to 34°C.

In graph II of the second case a similar change was observed in pupil size, the dilatation curve first gradual, then abrupt began to flatten out to 32.5°C to reach the maximum dilata­tion (7mm) between 31° and 30.6°C. With further cooling the pupil began to contract (or lose dilatation). At 30°C when the aortic clamp was applied the pupil became further dilated to 8mm after which the pattern of the drop followed that in graph I.

It may thus be noted that dilata­tion of the pupil which accompanied hypothermia was not achieved propor­tionately with it. There was a maxi­mum which was achieved between 32.4°C and 32.0°C in one case and at 30.6°C in the other two cases, after which the pupil began to contract, or lose dilatation. Aorticclamping caused a reflex dilatation of the pupil which was independent of hypothermia.


In all the cases there was no change in the fundus. In one case where aor­tic clamp was applied, there was im­mediate pallor of the disc and the colour returned to normal, as soon as the clamp was relieved.


In this group there were 9 cases, as analysed in [Table - 2] and in these cases, by-pass cooling technique was em­ployed.

There were five males and four females with ages ranging from 3 to 35 years. The changes in pupil size and intraocular tension are shown in four illustrative cases in graphs III, IV, V and VI.

Pupil Size

i) It is observed from these that pu­pillary dilatation set in 5-10 minutes after the cooling started.

ii) The maximum pupillary dilata­tion observed was 7 mm.

iii) As is seen in graphs V and VI, when aortic clamping was needed and applied then pupil dilated to 8.0 mm, while in graph IV, it can be seen that when cardiac arrest occurred, the pupil dilatated to 8.0 mm.

iv) On rewarming after 10-15 minutes the pupil size got smaller and then remained constant.

Intraocular Tension

Intraocular tension showed a fall during anaesthesia in all cases but no further drop occurred during cooling. In one case there was a fall by 1.5 mm. whereas in another there was a rise by 1.5 after the initial fall. [Table - 2]. However during cardiac arrest as seen in graphs IV and VI it became unrecorded.

Fundus Changes

There were no changes in the fundus picture in any of these cases. However, in the cases where cardiac arrest oc­curred, there was generalised fungus pallor, with absence of pulsation and fullness of veins. The picture returned to normal on restoration of circulation.

  Dicussion Top

Intraocular Tension

Intraocular tension in surface cool­ing as well as in by-pass cooling show­ed a fall. In the first group there was a negligible fall of 0.5 to 1.0 mm in two cases, while in one case it re­mained unchanged. In group II of by­pass cooling there was an average fall of 2.5 mm Hg. during anaesthesia and later during cooling it remained at the same level, except in one case where during the cooling procedure tension fell by 1.5 mm Hg. and in one it rose by 1.5 mm. LAMB also noted a fall of about 2 mm Hg. during anesthesia, and also noticed a fall during occlu­sion. In our series because no circula­tory arrest was attained, no fall was ob­served. However, in two cases where aortic clamp was applied, and in the other two cases where cardiac arrest occurred, it became unrecordable but soon returned to the original level. In one case only, we observed a slight fall in tension during cooling and in one a rise, while in LAMB'S series the tension during cooling was fairly con­stant showing only a slight fall.

On rewarming no change was notic­ed in the tension, however in one case where it had fallen from 16 to 14.5 mm. Hg. it returned to 16 mm. when rewarming started in 15 minutes time. By and large it indicates that cooling has no effect on the intraocular aque­ous circulation and cilliary body func­tion remains normal as long as circula­tion is maintained.


Generalising from these studies, it can be stated that on surface cooling the pupil becomes dilated, but the dila­tion does not keep pace with the pro­gressive body cooling. It is gradual at first, becoming abrupt as cooling pro­gresses till a maximum dilatation of 7 mm is reached at an average tempe­rature of about 31°C. With further cooling the pupil ceases to dilate and begins to contract. In extra-corporeal cooling, because of the very rapid cooling and rewarming the pupils show more precise correlation with the tem­peratures. If during this contraction stage any vascular catastrophe is in­troduced, like clamping of the aorta or cardiac arrest, a reflex dilatation of the pupil occurs which is greater (8 mm) than the maximum obtained during cooling. It is interesting to ob­serve that in case 9 where there was cardiac arrest before cooling started the pupil became abruptly dilated from 5 to 8 mm and then a fall to 5 mm on recovery. Then cooling was started on recovery and the pupil dila­tation continued.

Comparing Graphs I and III of the two different forms of cooling which are not vitiated by any vascular cata­strophe we find that although there is a basic resemblance in the patterns, there appears to be a slight difference.

Whereas in Graph III the rise and fall are abrupt and uniform because of rapid cooling and rewarming, the curve in Graph I, because of its slow rise and fall becomes available for more effective study. In Graph I there is first a slow rise then an abrupt one reaching a maximum of 7 mm between 33° and 32°C, then it drops to 6 mm at 31°C and remains steady till 29° C, after which it tends to fall. Just after 28°C is reached, rewarming begins and there follows a continuous drop, slow at the beginning, gaining in speed as normalcy is reached.

In the hypothalamus there are thermo-regulators which control body temperatures and which operate through the sympathetic and para­sympathetic tones. In the neighbouring thalamus (mid-brain) there are pupil regulating centres which operate simi­larly through the two autonomic ner­vous systems. Impulses directed to the thermo-regulators may therefore easily affect the pupillary centres or over­flow into them.

As would be natural the sympathe­tic, being the alarm system resists the unnatural and sudden chilling and the resistance increases progressively as the chilling progresses. The resistance becomes more pronounced as a tem­perature of about 35°C is reached. The limit of resistance is reached at about 31°C after which the sympathe­tic tone is overcome by the slower para-sympathetic. The pupil ceases to dilate, the para-sympathetic counter resistance asserts itself and after a slight drop a balance is reached. The pupil dilatation is maintained at about 7 mm till rewarming begins.

On rewarming, since the process is towards normalization there is no at­tempt on the part of the sympathetic to offer resistance. On the contrary it gives up its resistance which is again reflected in the pupil which continues to contract or lose dilatation. In Graph IV, however, a momentary reflex dila­tation on commencing rewarming can be observed.

That the sympathetic is not knocked out of action but only offers resistance can be gathered from the fact, that another kind of reflex, a vascular cata­strophe like shock is still capable of producing a pupil dilatation. We have two instances of those in our series of observations. One was when an aortic clamp was applied during the phase when the pupil was contracting, when the pupil showed a brisk dilatation even greater than the maximum ob­tained at 31°C and another when there was cardiac arrest during the same phase, when again the pupil dilated similarly. Case 9 was an instance of pupil dilatation due to cardiac arrest before cooling was started where again the pupil dilatation was upto 8 mm.

One can conclude therefore that surface hypothermia first stimulates and later inhibits the sympathetic control of the thermo-regulators in the hypo­thalamus but the sympathetic is still ready to go into action to face a cata­strophe of another kind. In vascular shock when the blood-pressure drops, the sympathetic reacts by trying to compensate the drop in pressure. How­ever, the demands on the body struc­ture being minimum in a hypothermia state, the vascular balance is soon achieved as can be seen reflected in return of the pupil size to that pre­sent on preapplication of clamp or after cardiac arrest.

Intraocular Pressure

The negligible effect on the intra­ocular pressure in hypothermia sug­gests an absence of any sympathetic control mechanism to the secretory part of the ciliary body and the ciliary vessels just as the cerebral and coro­nary vessels are supposed to have no sympathetic control mechanism in order to keep all vital circulation mov­ing at an even pace under all condi­tions of stress. This may appear strange because the ciliary vessels are known to become congested under emotional stress and cause increased I.O.P. However in hypothermia there is no stimulation of an emotional nature, but the capillaries all over the body must contract in order to resist reduction in body temperature. The cilliary capillaries must contract along with the other capillaries and conse­quently the effect on the I.O.P. will be its reduction if at all. Our observa­tions show that on an average there was no drop in IOP further than that obtained during general anesthesia pre­ceding the hypothermia although the pupil dilated with hypothermia, thus maintaining the IOP at a vital level.

However when circulation through the ciliary body is excluded by aortic clamping or by cardiac arrest, the ten­sion drops to zero although the pupil dilates maximally indicating a high degree of sympathetic alarm reaction. Arguing on these lines it seems very probable that there is very little or no sympthetic control for the ciliary ves­sels bringing them under the same category of vital vessels as the cere­bral and the coronary.

Retinal Circulation

The same applies for retinal vessels for no changes in the retinal vessels were noticed during hypothermia but during cardiac arrest there was blanch­ing of the fundus vessels.

Some retinal damage has been en­countered by LAMB (1961) during total occlusion and as a result this technique has been changed to low flow by-pass system. We have not en­countered any change in fundus pro­duced by cooling per se, however in some cases where cardiac arrest oc­curred, the immediate fundus changes were the same as reported by LAMB (1961).

  Summary Top

Observations on pupil size, intra­ocular pressure and fundus of the eyes of 12 cases in which hypothermia was produced are recorded. Pupils became dilatated to a maximum of 7 mm at which level or at a little lower the dilatation was maintained. Further di­latation to 8 mm was reached during vascular catastrophies like aortic clam­ping or cardiac arrest. The intraocular tension remained constant during hy­pothermia after the usual drop during induction of anesthesia. Retinal cir­culation also showed no change during hypothermia.

These observations are used to argue that although there is a sympathetic alarm mechanism in the case of the pupils, this mechanism is not present in the case of ciliary and retinal cir­culations which latter have to be main­tained under all conditions of stress.[3]

  References Top

DREW C. E. and ANDERSON I. M (1959) Lancet 1, 748.  Back to cited text no. 1
LAMB, A., Ocular changes occurring during cardiac survey under profound hypothermia and occlusion: Brit. Jour. Ophthal. (11)61) 45. 490.  Back to cited text no. 2
SIMPSON. .J. A.. GIBSON, P. and BLOOMFIFLD, D. A. (1960), Med. J. Australia 1. 647.  Back to cited text no. 3


  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6]

  [Table - 1], [Table - 2]


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