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An analysis of postoperative pyrexia
JOURNAL
OF SURGICAL
RESEARCH
17, 79-84
An Analysis G.
TV.
MOLNAR,
(1974)
of Postoperative PH.D.
AND
The
DURING THE HOURS IMMEDIATELY after major operations, the internal temperature of the body commonly rises to 3P-40%. The concurrent oxygen consumption has been measured by a few workers [7-lo], and various factors have been adduced to account for the pyrexia [l-3]. The trend of the rise in temperature, however, has not been analyzed and as a consequence the factors which delimit the pyrexia cannot bc clearly delineated. The analysis presented herein is an inversion of Newton’s law of cooling [4, 51. The basic idea is that when the rate of heat input suddenly increases and then holds constant, body temperature rises ‘exponentially’ toward a final limiting value at which once again heat input equals heat loss. The resulting curve is shown in Fig. 1. At zero time, when body temperature has an initial value T,, the rate of heat input is suddenly increased from ill, to M, + AM = Mz. This increment, AnI, causes the body to warm toward a final temperature, Tf, at which it is again in a steady state, i.e., heat input again equals heat loss. The rise in temperature, however, proceeds neither as a sudden jump from T, to T,, nor in constant amounts at equal intervals of t,ime, but instead in a const’ant ratio, R, at equal intervals of time. In Fig. 1 these ratios are :
R=
T, - T? Tf - TI T1 Tf - To = T,T, - Ta
= T, - T,'
etc.
READ,
PH.D.,
curve
Equation form :
in
Fig.
M.D.
1 was
drawn
1 can also be expressed
(Tf -
with
T)t = (T, -
in the
T),e@.
(2)
The exponent k is the natural logarithm of R; e is the base of natural logarithms; i.e., Ic = In R. For the curve in Fig. 1, 12 = In 0.5 = 0.69315, and the curve depicts the ‘exponential’ rise of temperature toward the final limiting value, T,. An exponential curve is a model curve, and it is informative to learn whether temperature measurements conform to the model. If they do, then the derived value for 7’f can be used to compute AM without further effort and expense. If the data do not conform, then it is necessary to find the cause of the deviation. The major causes of deviation are changes in heat input and changes in heat loss [S]. Analysis of py,-
(1) 2
3
4
5
6
TIME
Fig. 1. Illustration of a theoretical curve rising CTxponcntinlly towards the limiting value, T,. At TX it is interrupted and held constant thereafter.
79 @ 1974 by Academic Press, Inc. of reproduction in any form reserved.
C.
R = 0.5.
From the Veterans Administration Hospital, Little Rock, Arkansas 72206 Supported by VA Research Project No. 5781X05 Submitted for publication October 19, 1973.
Copyright 811 rights
R.
Pyrexia
80
JOURNAL
OF
SURGICAL
liZSEARCH,
rexia, therefore, is a matter of testing the conformity of temperature measurements to an exponential trend and the determination of causes of deviation, if any, from the trend. In some instances, there may be both sufficient conformity to obtain T,, and also a sudden deviation, which is a manifestation of an intervening factor. This possibility is illustrated in Fig. 1. The exponential rise is interrupted when it reaches T, ; thereafter it continues constantly at this level. Up to this point there is sufficient curvature to permit an extrapolation (dashed segment) for an estimate of Tf. In many of our cases the interruption occurred too early, as say at T, in Fig. 1 up to which the curve is too straight to direct an extrapolation to a limiting Tf. MATERIALS
AND
METHODS
Symbols : T,, = rectal temperature at any time t. T,, = maximum rectal temperature attained by the patient. Trr = final steady-state rectal temperature, obtained by curve fitting and att’ained by only one patient. T, = air temperature. H = Combined coefficient of heat transfer by radiation, conconduction, and vection, evaporation. Subscript 0 = zero time. Rectal and toe temperatures were moniwith male patients tored in 22 thermocouples and a recording potentiomand et,er during open-heart operations subsequently in the intensive care unit (ICU) . The mean age was 49.2 (36-63) yr; mean weight, 77.8 (57-110) kg. The mean time in the operating room, starting with the induction of anesthesia, was about 4.25 (2.4-6.5) hr. Premeditation was fentanyl
VOL.
17,
NO.
2,
AUGUST
1974
and droperidol (Innovar) . Anesthetic before and after extracorporeal circulation (ECC) was methoxyflurane (Penthrane), nitrous oxide, and succinylcholine; during ECC, thiamylal (Surital) and fentanyl. Isoproterenol (Isuprel) was administered during a few operations. Morphine was used postoperatively. ECC was employed for an average of 96 (21-204) min in the following operations: five mitral valve replacements, one aortic vaIve replacement, two excision of atria1 myxoma (twice on the same patient), coronary artery bypass grafts: two single, six double, four triple, and one quadruple. ECC was not employed in an excision of a mediastinal cyst and in a double mamimplantation artery myocardial mary (Vineberg) operation. Patient care in the ICU was that which medical judgment considered necessary for each patient. Hence, there was some variability with respect to factors which could affect heat loss. The principal one was a heated pad which covered the whole mattress. Four patients were placed on a prewarmed mattress, 11 with heating continued for about an hour (2g-174 min) after placement on the pad. The heating unit was regulated by the rectal temperature of the patient. When the unit was turned off, the alcohol in the channels of the pad cooled slowly. The remaining patients were placed directly on t,he mattress without the pad. A first estimate of T,f was obtained by visual extrapolation on a plot of temperature vs time. The error of this estimate was minimized as follows. Equation 2 in linear form is: In [CT,, - T,&/(T,,,
- T,Jd
= -/ct.
(3)
It yielded a linear trend on a semilogarithmic plot when the right estimate of Trf and measured values for T,, were substituted. When the trend was not linear, other values for T,, were tried until it became linear. The percentage of increment in heat
MOLNAR
input, Al?1c/o, was calculated Eq. 4: AM%
= (n1,/fl1,
AND
READ
: POSTOPERATIVE
PYREXI.
by means of
- 1) X 100
(4) (5)
For M,, T,f = T,, at zero time, i.e., rectal temperature when it started to rise in the ICU, usually soon after entry. Because 11, and HI could not be determined, Eq. 5 could be used only when H, = HI and thus could not hc canceled. Therefore, Alus computed by Eq. 4 for the patients placed on a heating pad, which had H, < H, without the pad. T,f, however, could he estimated for them. RESULTS Figure 2 shows the temperature curves for a representative patient (mitral valve replacement). By means of ECC, TV, was maintained at normothermia in the operating room. After about 18 min in the ICU on a heated pad, T,, started to rke exponentially towards T,f = 40.5OC. This
Fig. 2. Rectal and toe temperatures of patient At in the operating room (OR) and in the intensive care unit (ICU). ECC = cxlracorporeal circulation. T,., = final steady-state temperat,urc toward which the rectal was rising before the intcrruption by peripheral vasodilatation mnnifwtcd by the rise in toe temperature.
0 .I5
1 0
I TIME
I 2
3
IN HOURS
Fig. 3. Example of finding T,, by linearization on the semilogarithmic plot. Upper open circles, trial Z’,, = 40.8”C ; solid circles, 40.4” ; lower open circles, 40.0”. Data of Fig, 2.
value gave the best linear trend in the semilogarithmic plot as seen in Fig. 3. For T,f = 40.8% the points (upper open circles) deviated upward from linearity; for T,rf = 40.0° (bottom open circles) they deviated downward from linearity. The scatter of points can be attributed to random displacements of the covering sheet, to air flow from the nebulizer when used, and to minor changes in heat production as effected by sedatives, tracheal aspiration, etc. As Fig. 2 shows, T,, did not continue to rise until it reached T,.f = 40.4W. Instead it stopped at T,, = 39.4W. This occurred at about the time of peripheral vasodilatation as manifested by the rising toe tcmperature. Results similar to those in Fig. 2 were obtained after 12 operations on 11 patients-with recumbency on an unheated pad after three operations, on a preheated pad aft’er two, and on a heated pad after seven operations. Two extreme deviations from an exponential trend are shown in Fig. 4, both obtained during recumbency on an unheated mattress. For patient blu (dotted curves) the initial trend for T,-, was still esscnti-
82
JOURNAL
OF
SURGICAL
RESEARCH,
Fig. 4. Two extreme courses of rectal temperature with corresponding toe temperatures. Dotted curves, pnlient Mu. Continuous curves, patient RO.
ally linear when its rise was halted by peripheral dilatation manifested by the sudden rise in toe temperature. Hence, it was impossible to fit a unique exponential curve. A similar difficulty was encountered with 10 patients (four on unheated pads, two on preheated and four on heated pads), although the linear rise was halted sooner, and, therefore, shorter, than in Fig. 3. Finally, patient Ro in Fig. 3 (continuous curves) was unique in that his T,, rose slowly from 37.4% to 38.4OC over a period of 7.5 hr, at which time the rise was halted by peripheral vasodilatation as manifested by the sudden rise in toe temperature. Table 1. Summary Number of patients All Heated pad No pad Heated pad No pad
Ini Gal T,O 23 1.5 8 9 3
37.0 + 0.13 36.9 i 0.12 37.2 + 0.28 36.8 * 0.14 37.1 + 0.19
17,
VOL.
NO.
2,
AUGUST
All patients except one started with pcriphcral vasoconstriction in the ICU. The exception was patient Ro in Fig. 4, where he shows an initially warm toe that cooled off after 1 hr in the ICU. Mean rcct’al temperatures are summarized in Table 1. The rise in T,, stopped at an average maximum, T,m = 38.7”C, with and without the heating pad. In most patients this halt occurred when peripheral vasodilatation occurred, as evidenced by warming of the toe. In three cases there was sweating instead of toe warming. In one patient there was neither. Table 1 also shows the estimated final steady-state temperature, T,f, toward which T,, was rising before the intervention of thermoregulatory reactions. It was 40.0% with the heating pad, 38.9O without the pad. For the t,hree cases for which it could be calculated by Eq. 4, A&f = +13% (12%.15%). Even for those patients resting on a heating pad, the increment was always only from internal generation, as T,, was always higher than back skin temperature, which in turn was higher than pad temperature. The pad exerted its effect by reducing the loss from the back to the mattress. DISCUSSION The increment in rate of heat input, $1370, based on Eq. 4 is the same as the mean basal metabolic rate of +12.5% obtained from oxygen consumption by Sturridge et al. [lo] on the first postoperative day of 70 cardiovascular patients. Roe et
of Rectal Temperatztres,
Means and Standard
Errors,
Maximum T ?rn 38.7 * 0.12 38.8 * 0.14 38.4 f 0.19 39.1 k 0.17 38.1 + 0.21
* P for difference between heated pad and no pad. **P for difference between T,, and T,f.
1974
“C
Estimated P*
T 71
final P*
p**
0.1 <.Ol
40.0 + 0.16 38.9 + 0.17
<.Ol
<.Ol < .0?5
MOLNAR
AND
READ:
POSTOPERATIVE
nl. [91 reported an average postoperatiw increment of 8% iu oxygen uptake by two patients with abdominal surgery administered the same anesthetic as ours. They found halothane to cause shivering and to increase oxygen uptake by 126%. Only two of our patients exhibited shivering and that only momentarily early after the operation. Raison et al. [7] made their measurements of oxygen uptake on patients with openheart surgery while they were still rewarming from hypothermia, and who, therefore, were not in a thermal state comparable to that of our patients. The fact that, when thermoregulation did not intervene too early, it was possible to fit T,, to an exponential trend implies that there was a constant increment to the rate of heat input. This increment would have caused a warming to T,.f had thermoregulation not int’ervened. The temperature correlate of the increment in heat, therefore, in the state of peripheral vasoconstriction and no sweating, was not any transient T,,; it was T,J, which, however, could be ascertained only by curve fitting (except for the one case which attained T,) . In the state of thermoregulation however, i.e., with peripheral vasodilatation and/or sweating, the correlate was T,,. The fact that in the lattcr state T,, did not return to the initial value (at midnight mean T,, = 38.2%) implies that the heat increment was due to internal generation and not to storage during peripheral vasoconstriction. Thus, when properly analyzed and interpreted, temperature measurements yield much information about t’he thermal dynamics of the body. They arc not merely a “static measurement” providing little information about heat loss and gain, as has been contended [S]. Since, in routine patient care, it is usually impractical to measure oxygen uptake, patient management rnust continue to be based on temperature measurements. But these are more informative if made frequently, at least on the toe and in the rectum, and if analyzed and interpreted as outlined herein.
S3
PYREXIA
SUMlLL4RY
AND
CONCLUSIONS
The rise in rectal temperature during the initial hours after open-heart surgery in 22 patients (23. operations) was tested for an exponential trend. It was discernible in 12 cases and for them a final limiting steadystate value for rectal temperature, Tc,, could be calculated. In only one case, however, did the rectal temperature, T,,, actually rise to T,f. In all of the other casts, including those for which T,, could not be determined, the rise in T,, was interrupted by a thermoregulatory reaction. In most cases this was peripheral vasodilatation as evidenced by the sudden rise in tot temperature, which was initially near room air temperature. In a few cases sweating was apparent. The increment in heat input which caused the warming could be calculated by means of Trf in three cases. It averaged +13%, which agreed favorably with published values obtained from oxygen consumption. This increment caused T,, to rise toward an average T,, = 38.9% for these three patients who had not been placed on a heating pad, to 40.0% for nine who had been placed on a heating pad. Thcrmoregulation interrupted when T,., = 38.1° for the former, 39.1° for the latter. For all 23 operations, the interruption occurred at an average T,., = 38.7”C = T,., (maximum attained). Because an increment in rate of heat input causes T,, to approach T,.[ without thermoregulation, and T,, with thcrmoregulation, the heat increment can be corrclated, not with any transient T,,> hut only with T,f or T,,, depending on whether thermoregulation is in operation. This can be resolved satisfactorily only by detection of sweating and of peripheral vasodilatation (hy measurement of t,oe t,cmperature) .
REFERENCES 1. Allison, F. Postoperative fever. IPI J. D. Hardy (Ed.). Criticnl Sz~rgicnl Illrress, Saunders, Philadelphia, 1971.
pp.
75-82.
84
JOURNAL
OF
SURGICAL
RESEARCH,
2. Lunn, H. F. Observations on hrat gain and loss in surgery. Guys Hosl). ISep. 118:117-127, 1969. 3. Modell, J. H. Septicemia as a cause of immediate postoperative hyperthermia. Anesthesiology 27:32%330, 1966. 4. Molnar, G. W., Hurley, H. J., Jr., and Ford, R. Application of Newton’s law to body cooling. PfEuegers Arch. 311:X-24, 1969. 5. Molnar, G. W. The determination of the parameters of cooling. Znt. J. Biometeorol. 14:267-274, 1970. 6. Molnnr, G. W. Factors which cause deviation from Newton’s law of cooling. 3. Assoc. Adv. Med. Instrum. 4:89-93, 1970.
VOL.
17,
NO.
2,
AUGUST
1974
7. Raison, J. C. A., Osborn, J. J., Beaumont, J. O., and Gerhode, F. Oxygen consumption: after open heart surgery measured by a digital computer system. .4n~. Surg. 171:471-484, 1970. 8. Roe, C. F., and Kinney, J. M. The caloric equivalent of fel-cr: II. Influence of major trauma. Ann. Swg. 161:140-147, 1965. 9. Rot, C. F., Goldberg, M. J., Blair, C. S., and Kinney, J. M. The influence of body tempernturc on early postoperative oxygen consumption. Surgery 60:85-92, 1966. 10. Sturridge, M. F., Theye, R. A., Fowler, W. S., and Kirklin, J. W. Basal metabolic rate after cardovascular surgery. J. Thorac. Curtliovasc. Surg. 47:298-307, 1964.
OF SURGICAL
RESEARCH
17, 79-84
An Analysis G.
TV.
MOLNAR,
(1974)
of Postoperative PH.D.
AND
The
DURING THE HOURS IMMEDIATELY after major operations, the internal temperature of the body commonly rises to 3P-40%. The concurrent oxygen consumption has been measured by a few workers [7-lo], and various factors have been adduced to account for the pyrexia [l-3]. The trend of the rise in temperature, however, has not been analyzed and as a consequence the factors which delimit the pyrexia cannot bc clearly delineated. The analysis presented herein is an inversion of Newton’s law of cooling [4, 51. The basic idea is that when the rate of heat input suddenly increases and then holds constant, body temperature rises ‘exponentially’ toward a final limiting value at which once again heat input equals heat loss. The resulting curve is shown in Fig. 1. At zero time, when body temperature has an initial value T,, the rate of heat input is suddenly increased from ill, to M, + AM = Mz. This increment, AnI, causes the body to warm toward a final temperature, Tf, at which it is again in a steady state, i.e., heat input again equals heat loss. The rise in temperature, however, proceeds neither as a sudden jump from T, to T,, nor in constant amounts at equal intervals of t,ime, but instead in a const’ant ratio, R, at equal intervals of time. In Fig. 1 these ratios are :
R=
T, - T? Tf - TI T1 Tf - To = T,T, - Ta
= T, - T,'
etc.
READ,
PH.D.,
curve
Equation form :
in
Fig.
M.D.
1 was
drawn
1 can also be expressed
(Tf -
with
T)t = (T, -
in the
T),e@.
(2)
The exponent k is the natural logarithm of R; e is the base of natural logarithms; i.e., Ic = In R. For the curve in Fig. 1, 12 = In 0.5 = 0.69315, and the curve depicts the ‘exponential’ rise of temperature toward the final limiting value, T,. An exponential curve is a model curve, and it is informative to learn whether temperature measurements conform to the model. If they do, then the derived value for 7’f can be used to compute AM without further effort and expense. If the data do not conform, then it is necessary to find the cause of the deviation. The major causes of deviation are changes in heat input and changes in heat loss [S]. Analysis of py,-
(1) 2
3
4
5
6
TIME
Fig. 1. Illustration of a theoretical curve rising CTxponcntinlly towards the limiting value, T,. At TX it is interrupted and held constant thereafter.
79 @ 1974 by Academic Press, Inc. of reproduction in any form reserved.
C.
R = 0.5.
From the Veterans Administration Hospital, Little Rock, Arkansas 72206 Supported by VA Research Project No. 5781X05 Submitted for publication October 19, 1973.
Copyright 811 rights
R.
Pyrexia
80
JOURNAL
OF
SURGICAL
liZSEARCH,
rexia, therefore, is a matter of testing the conformity of temperature measurements to an exponential trend and the determination of causes of deviation, if any, from the trend. In some instances, there may be both sufficient conformity to obtain T,, and also a sudden deviation, which is a manifestation of an intervening factor. This possibility is illustrated in Fig. 1. The exponential rise is interrupted when it reaches T, ; thereafter it continues constantly at this level. Up to this point there is sufficient curvature to permit an extrapolation (dashed segment) for an estimate of Tf. In many of our cases the interruption occurred too early, as say at T, in Fig. 1 up to which the curve is too straight to direct an extrapolation to a limiting Tf. MATERIALS
AND
METHODS
Symbols : T,, = rectal temperature at any time t. T,, = maximum rectal temperature attained by the patient. Trr = final steady-state rectal temperature, obtained by curve fitting and att’ained by only one patient. T, = air temperature. H = Combined coefficient of heat transfer by radiation, conconduction, and vection, evaporation. Subscript 0 = zero time. Rectal and toe temperatures were moniwith male patients tored in 22 thermocouples and a recording potentiomand et,er during open-heart operations subsequently in the intensive care unit (ICU) . The mean age was 49.2 (36-63) yr; mean weight, 77.8 (57-110) kg. The mean time in the operating room, starting with the induction of anesthesia, was about 4.25 (2.4-6.5) hr. Premeditation was fentanyl
VOL.
17,
NO.
2,
AUGUST
1974
and droperidol (Innovar) . Anesthetic before and after extracorporeal circulation (ECC) was methoxyflurane (Penthrane), nitrous oxide, and succinylcholine; during ECC, thiamylal (Surital) and fentanyl. Isoproterenol (Isuprel) was administered during a few operations. Morphine was used postoperatively. ECC was employed for an average of 96 (21-204) min in the following operations: five mitral valve replacements, one aortic vaIve replacement, two excision of atria1 myxoma (twice on the same patient), coronary artery bypass grafts: two single, six double, four triple, and one quadruple. ECC was not employed in an excision of a mediastinal cyst and in a double mamimplantation artery myocardial mary (Vineberg) operation. Patient care in the ICU was that which medical judgment considered necessary for each patient. Hence, there was some variability with respect to factors which could affect heat loss. The principal one was a heated pad which covered the whole mattress. Four patients were placed on a prewarmed mattress, 11 with heating continued for about an hour (2g-174 min) after placement on the pad. The heating unit was regulated by the rectal temperature of the patient. When the unit was turned off, the alcohol in the channels of the pad cooled slowly. The remaining patients were placed directly on t,he mattress without the pad. A first estimate of T,f was obtained by visual extrapolation on a plot of temperature vs time. The error of this estimate was minimized as follows. Equation 2 in linear form is: In [CT,, - T,&/(T,,,
- T,Jd
= -/ct.
(3)
It yielded a linear trend on a semilogarithmic plot when the right estimate of Trf and measured values for T,, were substituted. When the trend was not linear, other values for T,, were tried until it became linear. The percentage of increment in heat
MOLNAR
input, Al?1c/o, was calculated Eq. 4: AM%
= (n1,/fl1,
AND
READ
: POSTOPERATIVE
PYREXI.
by means of
- 1) X 100
(4) (5)
For M,, T,f = T,, at zero time, i.e., rectal temperature when it started to rise in the ICU, usually soon after entry. Because 11, and HI could not be determined, Eq. 5 could be used only when H, = HI and thus could not hc canceled. Therefore, Alus computed by Eq. 4 for the patients placed on a heating pad, which had H, < H, without the pad. T,f, however, could he estimated for them. RESULTS Figure 2 shows the temperature curves for a representative patient (mitral valve replacement). By means of ECC, TV, was maintained at normothermia in the operating room. After about 18 min in the ICU on a heated pad, T,, started to rke exponentially towards T,f = 40.5OC. This
Fig. 2. Rectal and toe temperatures of patient At in the operating room (OR) and in the intensive care unit (ICU). ECC = cxlracorporeal circulation. T,., = final steady-state temperat,urc toward which the rectal was rising before the intcrruption by peripheral vasodilatation mnnifwtcd by the rise in toe temperature.
0 .I5
1 0
I TIME
I 2
3
IN HOURS
Fig. 3. Example of finding T,, by linearization on the semilogarithmic plot. Upper open circles, trial Z’,, = 40.8”C ; solid circles, 40.4” ; lower open circles, 40.0”. Data of Fig, 2.
value gave the best linear trend in the semilogarithmic plot as seen in Fig. 3. For T,f = 40.8% the points (upper open circles) deviated upward from linearity; for T,rf = 40.0° (bottom open circles) they deviated downward from linearity. The scatter of points can be attributed to random displacements of the covering sheet, to air flow from the nebulizer when used, and to minor changes in heat production as effected by sedatives, tracheal aspiration, etc. As Fig. 2 shows, T,, did not continue to rise until it reached T,.f = 40.4W. Instead it stopped at T,, = 39.4W. This occurred at about the time of peripheral vasodilatation as manifested by the rising toe tcmperature. Results similar to those in Fig. 2 were obtained after 12 operations on 11 patients-with recumbency on an unheated pad after three operations, on a preheated pad aft’er two, and on a heated pad after seven operations. Two extreme deviations from an exponential trend are shown in Fig. 4, both obtained during recumbency on an unheated mattress. For patient blu (dotted curves) the initial trend for T,-, was still esscnti-
82
JOURNAL
OF
SURGICAL
RESEARCH,
Fig. 4. Two extreme courses of rectal temperature with corresponding toe temperatures. Dotted curves, pnlient Mu. Continuous curves, patient RO.
ally linear when its rise was halted by peripheral dilatation manifested by the sudden rise in toe temperature. Hence, it was impossible to fit a unique exponential curve. A similar difficulty was encountered with 10 patients (four on unheated pads, two on preheated and four on heated pads), although the linear rise was halted sooner, and, therefore, shorter, than in Fig. 3. Finally, patient Ro in Fig. 3 (continuous curves) was unique in that his T,, rose slowly from 37.4% to 38.4OC over a period of 7.5 hr, at which time the rise was halted by peripheral vasodilatation as manifested by the sudden rise in toe temperature. Table 1. Summary Number of patients All Heated pad No pad Heated pad No pad
Ini Gal T,O 23 1.5 8 9 3
37.0 + 0.13 36.9 i 0.12 37.2 + 0.28 36.8 * 0.14 37.1 + 0.19
17,
VOL.
NO.
2,
AUGUST
All patients except one started with pcriphcral vasoconstriction in the ICU. The exception was patient Ro in Fig. 4, where he shows an initially warm toe that cooled off after 1 hr in the ICU. Mean rcct’al temperatures are summarized in Table 1. The rise in T,, stopped at an average maximum, T,m = 38.7”C, with and without the heating pad. In most patients this halt occurred when peripheral vasodilatation occurred, as evidenced by warming of the toe. In three cases there was sweating instead of toe warming. In one patient there was neither. Table 1 also shows the estimated final steady-state temperature, T,f, toward which T,, was rising before the intervention of thermoregulatory reactions. It was 40.0% with the heating pad, 38.9O without the pad. For the t,hree cases for which it could be calculated by Eq. 4, A&f = +13% (12%.15%). Even for those patients resting on a heating pad, the increment was always only from internal generation, as T,, was always higher than back skin temperature, which in turn was higher than pad temperature. The pad exerted its effect by reducing the loss from the back to the mattress. DISCUSSION The increment in rate of heat input, $1370, based on Eq. 4 is the same as the mean basal metabolic rate of +12.5% obtained from oxygen consumption by Sturridge et al. [lo] on the first postoperative day of 70 cardiovascular patients. Roe et
of Rectal Temperatztres,
Means and Standard
Errors,
Maximum T ?rn 38.7 * 0.12 38.8 * 0.14 38.4 f 0.19 39.1 k 0.17 38.1 + 0.21
* P for difference between heated pad and no pad. **P for difference between T,, and T,f.
1974
“C
Estimated P*
T 71
final P*
p**
0.1 <.Ol
40.0 + 0.16 38.9 + 0.17
<.Ol
<.Ol < .0?5
MOLNAR
AND
READ:
POSTOPERATIVE
nl. [91 reported an average postoperatiw increment of 8% iu oxygen uptake by two patients with abdominal surgery administered the same anesthetic as ours. They found halothane to cause shivering and to increase oxygen uptake by 126%. Only two of our patients exhibited shivering and that only momentarily early after the operation. Raison et al. [7] made their measurements of oxygen uptake on patients with openheart surgery while they were still rewarming from hypothermia, and who, therefore, were not in a thermal state comparable to that of our patients. The fact that, when thermoregulation did not intervene too early, it was possible to fit T,, to an exponential trend implies that there was a constant increment to the rate of heat input. This increment would have caused a warming to T,.f had thermoregulation not int’ervened. The temperature correlate of the increment in heat, therefore, in the state of peripheral vasoconstriction and no sweating, was not any transient T,,; it was T,J, which, however, could be ascertained only by curve fitting (except for the one case which attained T,) . In the state of thermoregulation however, i.e., with peripheral vasodilatation and/or sweating, the correlate was T,,. The fact that in the lattcr state T,, did not return to the initial value (at midnight mean T,, = 38.2%) implies that the heat increment was due to internal generation and not to storage during peripheral vasoconstriction. Thus, when properly analyzed and interpreted, temperature measurements yield much information about t’he thermal dynamics of the body. They arc not merely a “static measurement” providing little information about heat loss and gain, as has been contended [S]. Since, in routine patient care, it is usually impractical to measure oxygen uptake, patient management rnust continue to be based on temperature measurements. But these are more informative if made frequently, at least on the toe and in the rectum, and if analyzed and interpreted as outlined herein.
S3
PYREXIA
SUMlLL4RY
AND
CONCLUSIONS
The rise in rectal temperature during the initial hours after open-heart surgery in 22 patients (23. operations) was tested for an exponential trend. It was discernible in 12 cases and for them a final limiting steadystate value for rectal temperature, Tc,, could be calculated. In only one case, however, did the rectal temperature, T,,, actually rise to T,f. In all of the other casts, including those for which T,, could not be determined, the rise in T,, was interrupted by a thermoregulatory reaction. In most cases this was peripheral vasodilatation as evidenced by the sudden rise in tot temperature, which was initially near room air temperature. In a few cases sweating was apparent. The increment in heat input which caused the warming could be calculated by means of Trf in three cases. It averaged +13%, which agreed favorably with published values obtained from oxygen consumption. This increment caused T,, to rise toward an average T,, = 38.9% for these three patients who had not been placed on a heating pad, to 40.0% for nine who had been placed on a heating pad. Thcrmoregulation interrupted when T,., = 38.1° for the former, 39.1° for the latter. For all 23 operations, the interruption occurred at an average T,., = 38.7”C = T,., (maximum attained). Because an increment in rate of heat input causes T,, to approach T,.[ without thermoregulation, and T,, with thcrmoregulation, the heat increment can be corrclated, not with any transient T,,> hut only with T,f or T,,, depending on whether thermoregulation is in operation. This can be resolved satisfactorily only by detection of sweating and of peripheral vasodilatation (hy measurement of t,oe t,cmperature) .
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