EFFECTS OF HIGH SPINAL ANESTHESIAON CEREBRALCIRCULATION ANDMETABOLISMIN MAN1,2

By JEROMEKLEINERMAN, SALVATOREM. SANCETTA, ANDDONALDB. HACKEL

(From the Department of Pathology and Medicine, Western Reserve University School ofMedicine at Cleveland City Hospital, Cleveland, Ohio)

(Submitted for publication August 1, 1957; accepted September 12, 1957)

The effects of high spinal anesthesia on thegeneral (1, 2), hepatic (3), and coronary (4)hemodynamics have been previously reported byour group. Because hypotension produced byhigh spinal anesthesia may be a potential hazardto the circulatory sufficiency of the brain, it wasconsidered important to study the effects of highspinal anesthesia on the cerebral circulation andmetabolism.

Studies by others have been concerned with theeffects of differential spinal block on the cerebralcirculation of hypertensive individuals (5) and theeffect of hypotensive drugs on the cerebral circu-lation of aged persons (6) and hypertensives (7).The majority of patients in this study are normo-tensive, but the effects of high spinal anesthesiaon a small group of hypertensives is included. Theanesthetic level is higher and the amount of spinalanesthetic agent employed is larger than in studiesreported by others, simulating the dosage used inproducing surgical high spinal anesthesia, al-though surgical procedures were not undertakenin these subjects.

MATERIAL AND METHODS

Nineteen patients were selected from the medical wards.Of these, 15 were normotensive and free of cardiopulmo-nary disease, and 4 were hypertensive. Following anovernight fast and morning sedation (pentobarbital so-dium, 0.1 Gm.) the patients were transported to thecardiovascular laboratory, where the ambient temperaturewas maintained between 23 and 24° C. In some instancesa No. 6-8 F Goodale birds-eye catheter was introducedvia a medial arm vein into the jugular bulb and the posi-tion of the tip checked repeatedly by fluoroscopic exami-nation. In other instances direct puncture of the jugular

1 This work was done in part during the tenure of aResearch Fellowship of the American Heart Association(Jerome Kleinerman and Donald B. Hackel).

2Supported in part by Research Grants Nos. H-1382and H-863 from the National Heart Institute of theUnited States Public Health Service.

bulb was employed. Blood samples were then drawn forbasal determination of cerebral blood flow, arterial andjugular venous blood gases, pH, glucose, lactate, and py-ruvate. Following the basal determinations, one groupof 13 patients (age range, 22 to 60; average, 41.6 years)was given a spinal anesthetic of 150 to 200 mg. of pro-caine by barbotage. In all instances the arbitrary criteriapreviously described for high spinal anesthesia (1, 2)were met and confirmed by plethysmographic (8) dem-onstration of increased finger blood flow. Thirty minutesafter the administration of the anesthetic all studies wererepeated. A second group of six patients (age range,44 to 66; average, 56 years) served as "double controls."Thirty minutes after the initial basal study a secondset of determinations was performed without the ad-ministration of the anesthetic. In all instances patientswere maintained in total head-down body tilt of 5 de-grees. Vasopressor drugs were not given at any time.

Blood oxygen contents, carbon dioxide contents andpH determinations were performed in duplicate, andchecks required to 0.2 volume per cent for oxygen andCO2 and to 0.01 pH unit. Jugular venous and brachialarterial oxygen contents and arterial oxygen capacitywere determined spectrophotometrically according to themethod of Hickam and Frayser (9) and frequently spot-checked by simultaneous gasometric analysis. Carbondioxide content of arterial blood was determined by themanometric method of Van Slyke and Neill (10) andarterial blood pH readings were obtained by use of theCambridge glass electrode potentiometer at room tempera-ture, and corrected to body temperature (11). Valuesfor pCO, were obtained from the nomogram of Singerand Hastings (12). Glucose (13), lactate (14), andpyruvate (15) determinations were done in duplicate onarterial and venous blood.

Cerebral blood flow (CBF) was determined by themanometric technique of Kety and Schmidt (16) and ex-pressed as ml. per 100 Gm. of brain tissue per minute.Cerebral oxygen consumption (CMR 02) was calculatedas the product of CBF and the arterial-jugular venous(A-VO,) oxygen difference. This is expressed in termsof ml. per 100 Gm. of brain tissue per minute. Cerebralglucose consumption (CMR gl) was similarly calculatedby using the arterial-jugular venous glucose (A-Vgl) dif-ference and is expressed as mg. per 100 Gm. per minute.

The brachial arterial pressure was measured througha No. 19 indwelling arterial needle, transduced via Sta-tham strain gauges, amplified by a Brush D.C. amplifier,

285

JEROMEKLEINERMAN, SALVATOREM. SANCETTA, AND DONALDB. HACKEL

and recorded on the Brush multi-channel oscillograph.Mean arterial blood pressures (MABP) were obtainedby planimetric integration of the contours recorded dur-ing two successive respiratory cycles.

Cerebrovascular resistance (CVR) was calculated bythe formula

CVR= mean arterial blood pressureCBF per 100 Gm. per minute'

and expressed as mm. Hg per ml. per 100 Gm. per minute.In calculating the mean arterial blood pressure, the read-ings taken prior to and immediately after the flows were

averaged.

RESULTS

The data are presented in Tables I through III.The data have been treated statistically, althoughin the case of the hypertensives the small numberof observations precluded such analysis.

Mean arterial blood pressure

The MABP in the normotensive group fellfrom 93 to 63 mm. Hg during high spinal anes-

thesia. The decrease in mean blood pressure forthe four hypertensives was from 158 to 79 mm.

Hg. In the double control group the change was

from 100 to 106 mm. Hg. The marked decreasein the normotensive spinal anesthesia group ishighly significant when compared to the variationin the double controls.

The cerebral blood flowThe mean CBF in the normotensive group did

not change significantly during high spinal anes-

thesia. The prespinal value was 45 ml. per 100

TABLE I

Cerebral hemodynamics and blood gases in high spinal anesthesia*

Normotensives

Patient F. D. J. R. B. M. C. T. M. L. S. K. M. B.

Diagnosis Chronic Pneumonia, Pneumonia, Chronic Pyelo- General L Barbituratealcoholism recovered recovered alcoholism nephritis, paresis. intoxication.

recovered treated recovered

Sex M M M M F M F

Age 22 38 26 60 26 42 51

Spinal level T2-Ts Ts Ts(R)-TW(L) Tr-Ts Ti T2 T2

C E C E C E C E C E C E C E

Art. 02, 9.6 10.6 18.5 18.4 18.9 19.4 10.6 10.5 13.1 12.4 17.2 16.2 16.0 16.0vol. %

Jug. Ven. Os, 3.1 4.0 12.7 12.6 13.7 12.5 4.9 3.8 6.8 6.9 8.4 8.3 10.2 10.3vol. %

A-V Os, 6.5 6.6 5.8 5.8 5.2 6.9 5.7 6.7 6.3 5.5 8.8 7.9 5.8 5.7vol. %

02 Cap., 10.6 11.6 20.2 19.4 19.8 19.7 11.8 11.6 13.9 13.3 18.2 17.6 17.6_J 17.3vol. %

Art. Sat., 91 91 92 95 96 99 90 90 94 93 95 93 91 91

Art. C02, 39.4 41.9 47.0 46.4 46.3 48.0 45.5 45.3 40.1 40.2 39.0 39.7 44.0 42.4vol. %

Art. pH 7.41 7.35 7.41 7.40 7.34 7.35 7.38 7.42 7.40 7.40 7.41 7.42 7.42 7.40

Art. pCO2, 31 37 40 40 46 46 38 35 33 33 33 32 35 35mm. Hg

Pulse 75 60 83 86 91 94 81 73 70 68 79 68

MABP, 92 62 92 66 100 66 99 59 69 55 98 61 86 72mm. Hg

CBF, 37 41 58 60 55 49 31 29 50 59 46 49 41 49ml./100 Gm./min.

CMR02, 2.4 2.7 3.2 3.3 2.9 3.4 1.8 1.9 3.1 3.2 4.1 3.9 2.4] 2.8ml./100 Gm./min.

CVR 2.4 1.7 1.7 1.0 1.8 1.3 2.9 2.0 1.4 0.9 2.1 1.4 2.1 1.5

CMRgI.. . 6.3 4.1 3.3 3.4 1.6 2.9 2.5 2.0 3.0 5.9 4.1 2.9 5.6 0.6mg./100 Gm./min.

* Abbreviations: MABP- mean arterial blood pressure; CBF-cerebral arterial blood pressure; CMR02 - cerebral oxygen consumption;CVR - cerebral vascular resistance expressed as mm. Hg/ml./100 Gm./min.; CMRgl - cerebral glucose consumption.

t Signifies a statistically significant difference when compared with the double control group (p = <0.01).

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CEREBRALHEMODYNAMICSIN HIGH SPINAL ANESTHESIA

TABLE i-Continued

Cerebral hemodynamics and blood gases in high spinal anesthesia

Normotensives-continued Hypertensives

M. S. A. G. Mean M. B. E. T. J. H. F. E. Mean

Pneumonia, Chronic Essential Essential Essential Essentialrecovered pancreatitis hypertension hypertension hypertension hypertension

M F 6 male F F M F 1 male3 female 3 female

35 54 39.3 39 36 52 60 46.8

Ts Ts Ti Ti Ts T2-T4

C E C E C E C E C E C E C E C E

20.1 19.2 19.2 18.4 15.9 15.7 16.4 14.6 15.4 13.6 20.2 19.0 18.1 17.1 17.5 16.1

12.5 10.0 12.3 10.3 9.4 8.7 9.1 6.0 9.5 6.8 11.0 5.1 11.7 9.8 10.3 6.9

7.6 9.2 6.9 8.1 6.5 6.9 7.4 8.6 5.9 6.8 9.2 13.9 6.4 7.3 7.2 9.2

21.2 20.4 20.5 19.7 17.1 16.8 17.6 16.0 16.4 14.6 19.2 18.5 17.7 16.4

9S 94 94 93 93 93 94 91 94 93 94 93 94 92

48.4 42.7 45.2 44.1 43.9 43.4 38.3 36.3 43.0 34.9 49.4 48.0 43.6 39.7

7.41 7.43 7.40 7.40 7.40 7.39 7.43 7.41 7.41 7.54 7.42 7.41 7.41 7.44

41 35 37 37 33 31 37 23 41 40 37 31

79 79 68 62 78 74 89 79 81 58 84 68 98 102 88 77

91 69 106 61 92.5 63.4t 124 59 157 110 151 48 199 98 158 79

37 38 46 41 44.6 46.1 42 34 46 44 60 32 38 40 46.5 37.5

2.8 3.5 3.2 3.3 2.9 3.1 3.1 2.9 2.7 3.0 5.5 4.3 2.4 2.9 3.4 3.3

2.5 1.8 2.3 1.5 2.1 1.St 3.0 1.7 3.4 2.5 2.5 1.5 5.2 2.5 3.5 2.1

5.7 S.5 6.0 3.3 4.2 3.2 2.1 3.4 2.4 4.5

Gm. per minute as compared to 46 ml. during unchanged during the double control studies.high spinal study. Three of the four hypertensive When the variation in mean CMR02 valuespatients showed a decrease in CBF during spinal from prespinal to high spinal was compared toanesthesia. The double control studies showed a those noted in the double control groups, therevariation in mean values from 45 ml. to 43 ml. was no significant difference.per 100 Gm. per minute. When the variation inthe mean CBF in the normotensive high spinal The cerebral vascular resistancegroup is compared to the double control variations, There was a marked and statistically significantthe change is not statistically significant. decrease in the mean CVRin the normotensive Da-

The cerebral oxygen consumptionThere was no significant change in the mean

CMR02 in the normotensive patients during highspinal anesthesia as compared to the prespinalvalue. The small group of hypertensives similarlyshowed no change in mean CMR02 during highspinal anesthesia. The mean CMR 02 was also

tients during high spinal anesthesia. The hyper-tensive patients showed a similar change. Indouble control studies there was a slight increasefrom 2.1 to 2.4 units; this change was not signifi-cant. The marked decrease in mean CVR in thenormotensive patients during high spinal anes-thesia was significant when compared to the varia-tion in the double control group.

287

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The cerebral glucose consumption

The mean CMRgl showed no significant changein the normotensive high spinal group, varyingfrom 4.2 mg. per 100 Gm. per minute in the pre-

spinal study to 3.2 mg. per 100 Gm. per minutein the spinal period. In the double control group

the mean values decreased from 4.4 mg. per 100Gm. per minute in the first study to 3.9 mg. per

100 Gm. per minute in the second, again a changewhich was not significant. The values in the hy-pertensive patients during high spinal anesthesiashowed no consistent change. The mean changein CMRgl in the normotensives during high spinalanesthesia was not significantly different from themean change observed in double control studies.

Blood gases

In normotensive patients the mean changes inarterial oxygen content, jugular vein oxygen con-

tent, arterial-jugular venous oxygen difference,oxygen capacity and arterial oxygen saturationduring high spinal anesthesia were not of statisti-cal significance when compared to the prespinalvalues. This was also true for the mean changesin arterial CO2 content, arterial pH and arterialpCO2 in the normotensives. The small changesin oxygen and carbon dioxide concentration and inarterial pH likewise were not significant whencompared to the variations observed in the doublecontrol group. In the hypertensive group therewere more distinct and consistent decreases in themean arterial oxygen content, jugular vein oxygen

content, and oxygen capacity, and a notable in-crease in the arterial-jugular vein oxygen differ-ence. It is of interest that the decrease in mean

oxygen capacity in the hypertensives during highspinal anesthesia paralleled that of the mean arterialoxygen content so that no change in mean arterialoxygen saturation occurred. The mean arterialCO2 content and arterial pCO2 showed small butconsistent decreases during high spinal anesthesiaas compared to prespinal values. Although thesmall number of hypertensives studied precluded a

statistical analysis, there was a suggestive differ-ence between the normotensive and hypertensivegroups in the response of oxygen values and car-

bon dioxide contents and pressures to spinalanesthesia.

Carbohydrate metabolitesThe mean arterial glucose and venous glucose

levels showed slight increases during high spinalanesthesia and similar but smaller increases dur-ing the double control studies. The mean arterial-jugular vein glucose difference showed a slightdecrease in the normotensive spinal group and asimilar but smaller decrease in the double controlgroup. The hypertensives behaved similarly inthis. regard. These changes in the spinal groupwhen analyzed against the double control changeswere not statistically significant.

In a small series of five determinations there ap-peared to be a slight increase in the mean arteriallactate level during high spinal anesthesia. Thiswas not seen in two double control studies. Aslight increase was also consistently present in themean arterial pyruvate level in six high spinalstudies, but was seen in only one of two arterialpyruvate studies done in the control series. Therewere no consistent changes in the mean arterial-jugular vein lactate and pyruvate differences ofthe high spinal and the double control groups.However, the mean arterial-jugular venous lac-tate difference, although negative, was less nega-tive in four of five observations during high spinalanesthesia. These results are summarized inTable III.

DISCUSSION

These studies indicate the cerebral vessels innormotensive persons can dilate sufficiently tomaintain an entirely adequate cerebral circulationdespite the pronounced decrease in mean arterialblood pressure caused by high spinal anesthesia.On the basis of our limited studies in hyperten-sives, these persons do not appear to have the same

capacity for cerebral vascular compensation as dothe normotensives. This is in agreement with theresults obtained by Kety, King, Horvath, Jeffers,and Hafkenschiel (5) in hypertensives.

The MABPin the normotensive group fell ap-proximately 32 per cent from the control valuewhile the hypertensives decreased to 50 per cent ofthe control value during the spinal anesthetic stud-ies. During differential spinal block the meanblood pressure drop was 26 per cent in Kety'sstudy. This difference undoubtedly is a reflectionof the higher anesthetic level and greater anesthetic

290

CEREBRALHEMODYNAMICSIN HIGH SPINAL ANESTHESIA

dosage in the present study (above T4 with evi-dence of vascular dilatation in the upper extremi-ties). The greatest absolute drop in MABPwasobtained in the four hypertensive patients, but theabsolute level of the MABPduring spinal anes-thesia in these hypertensives was no different thanthe arterial pressure level in the normotensivesduring spinal anesthesia. The greater decreasein arterial pressure in the four hypertensives ascompared to the normotensives is consonant withthe known greater reactivity of these patients tospinal anesthesia. Kety and his co-workerspointed to the correlation between the change inmean arterial blood pressure and the change ininternal jugular oxygen content as evidence of in-adequate cerebral circulatory homeostasis at thegreater blood pressure drops. Our limited datain hypertensives corroborate this observation andsuggest an inability of the hypertensive patientsto obtain complete cerebral circulatory compensa-tion during the severe hypotensive episodes. Thearterial-jugular venous oxygen content in the hy-pertensives showed a consistent increase duringthe high spinal study, a finding which would be inkeeping with a decreased cerebral blood flow ifcerebral oxygen consumption is to be maintained.

It is of interest that the arterial lactate and ar-terial pyruvate levels showed a consistent increaseduring spinal anesthesia as compared to the pre-spinal values. Because our observations were nu-merically inadequate to evaluate these findings,we have combined the present data with thosepreviously reported by our group in another facetof this study (4). This compilation of material isreasonable since all determinations were performedby the same laboratory, using the same techniqueand methods. Table III indicates that there was aconstant and statistically significant increase inthe arterial lactate and pyruvate levels during highspinal anesthesia, when compared to the changesobserved in the double control group. The arterialglucose and cerebral arteriovenous differences ofglucose, lactate, and pyruvate showed no suchconsistent change.

The mechanism of this increase in arterial lac-tate and pyruvate is not clear. It seems possiblethat anoxia of one or several organ systems may beresponsible for the lactate and pyruvate changes.Of the systems studied, the heart (4), the splanch-nic bed (3), and the kidneys (17) suffer a de-

creased blood flow incident to the hypotension ofhigh spinal anesthesia. Evidence has been pre-sented that the hepatosplanchnic oxygen consump-tion remains unaltered despite a decreased bloodflow. The splanchnic bed appears to compensatefor the decreased flow by an increased arterio-venous oxygen extraction. The heart, in spite ofa decreased oxygen consumption, has a markedlydecreased work load and the myocardial oxygenextraction coefficient is not increased. This doesnot preclude the possible development of an un-recognized oxygen debt. The effects of spinalanesthesia on the renal circulation are more diffi-cult to assess. Recent studies (17) of the effectsof high spinal anesthesia in pregnant women pointto a decrease in renal plasma flow and an associ-ated increase in renal vascular resistance. Nostudies of renal oxygen consumption were made.However, earlier studies of spinal anesthesia (18,19), in which the anesthetic level was lower,showed no consistent change in renal blood flow.The critical difference between these results ap-pear to be the effect of the spinal anesthetic onthe blood pressure. In the former study, hypo-tension was produced, whereas the blood pressurelevel in the latter studies was not affected. It isreasonable to assume that when spinal anesthesiais associated with hypotension, as was the case inour studies, a decrease in renal blood flow canoccur, and renal anoxemia may occur. This or-gan may conceivably be the source of the increasedlactate and pyruvate levels during the high spinalstudies. It is, of course, possible that temporaryischemia of the liver and splanchnic bed, not dis-cernible by short term physiologic studies, mayalso contribute.

The mechanism of the decreased cerebrovascu-lar resistance during high spinal anesthesia re-mains obscure. It is unlikely that there was adirect effect on the cerebral vessels, since the anes-thetic level was never above T1 and previous stud-ies (20) have shown that bilateral block of thestellate ganglion does not produce a decreasedcerebrovascular resistance in normotensive or hy-pertensive patients. Another mechanism whichmight decrease the cerebrovascular resistance dur-ing high spinal anesthesia is a decrease in thepCO2 or pH of the cerebral tissues. The jugular-venous blood reflects these changes in the cerebraltissues. Wehave not gathered sufficient data on

291

JEROMEKLEINERMAN, SALVATOREM. SANCETTA, AND DONALDB. UIACKEL

jugular-venous pH and pCO2 to implicate thismechanism, but it seems unlikely that metaboliclocal changes in the cerebral tissues of sufficientdegree to alter pH or pCO2 could occur in theabsence of any change in cerebral oxygen uptake,cerebral blood flow, or jugular venous oxygencontent. It is possible that local baroreceptors(21) in the carotid arteries and sinus may producea reflex vasodilation of the cerebral vessels in re-sponse to hypotension.

While these results indicate that there is com-plete circulatory compensation in the brain duringthe hypotension of high spinal anesthesia in nor-motensive persons, it must be emphasized that thisresponse is dependent upon local ability to vaso-dilate and decrease vascular resistance. Foci withvascular sclerosis or other disease may not be ableto compensate completely, and may therefore beliable to ischemia. Since the technique employedgives values only for total cerebral circulation andmetabolism, small foci of brain receiving a dimin-ished blood flow may not be detected.

CONCLUSIONS

1. The effects of the hypotension induced byhigh spinal anesthesia on the cerebral circulationand metabolism of 13 subjects have been studied.Nine of these were normotensive and four werehypertensive. A series of six double control stud-ies served for comparison. In the normotensivegroup given high spinal anesthesia the MABPfell from a prespinal level of 93 to 63 mm. Hg, butthe CBF did not decrease significantly, and theCMR02 was unchanged. The CVR decreasedsignificantly and was responsible for the mainte-nance of the cerebral blood flow in the face of the32 per cent decrease in MABP.

In a small group of hypertensive patients, theMABPfell to 50 per cent of the prespinal valueduring high spinal anesthesia. Suggestive de-creases were found in CBF and CVR but theCMR02 did not appear to change in this group.

2. There were no significant changes in theblood gases and pH in the normotensive groupduring high spinal anesthesia. The arterial oxy-gen content, jugular venous oxygen content andoxygen capacity appeared to decrease and the ar-terial jugular vein oxygen difference to increase inhypertensives during high spinal anesthesia. The

arterial pCO2 and arterial CO2 contents showedconsistent decreases during spinal anesthesia inthe hypertensive patients.

3. The arterial blood lactate and pyruvate weresignificantly elevated during high spinal anesthesiaassociated with hypotension. It is suggested thatrenal or splanchnic ischemia may be responsiblefor these effects.

ACKNOWLEDGMENT

The authors wish to express their thanks to MissGladys Heckman, Miss Hanna Janouskavec, Mr. ErnestShiwanov, and Miss Eileen Mikat for technical assistance.

The encouragement and suggestions of Drs. ThomasD. Kinney, F. A. Simeone and R. W. Scott areacknowledged.

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