THE EFFECT OF HIGH INTRACRANIAL VENOUSPRESSURE UPON THE CEREBRALCIRCULATION AND ITS RELATION TOCEREBRAL SYMPTOMS

Eugene B. Ferris Jr.

J Clin Invest. 1939;18(1):19-24. https://doi.org/10.1172/JCI101020.

Research Article

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THEEFFECTOFHIGH INTRACRANIAL VENOUSPRESSUREUPONTHECEREBRALCIRCULATION ANDITS RELATION

TO CEREBRALSYMPTOMS'

By EUGENEB. FERRIS, JR.(From the Departnent of Internal Medicine, Cincinnati General Hospital, and the College of

Medicine, University of Cincinnati, Cincinnati)

(Received for publication August 16, 1938)

The term " increased intracranial pressure " isoften loosely applied to a syndrome consisting ofhigh cerebrospinal fluid pressure, edema of theoptic nerve head, often nausea and vomiting, andsometimes unconsciousness and other manifesta-tions of cerebral anoxia. In this syndrome, thehigh cerebrospinal fluid pressure is generallythought to be an important factor in causingcerebral dysfunction. Our original interest inthis subject arose from the fact that many ob-servers have found an increase in the cerebrospinalfluid pressure in venous hypertension of cardiacorigin (1, 2, 3, 4, 5, 6), and several (2, 7, 8)have postulated that because of the venous stag-nation within the brain, or because of the ac-companying increase in intracranial pressure, cere-bral anoxia results and is responsible for theorthopnea of congestive failure. That such aconclusion may not be warranted is suggested bythe fact that cardiac patients, regardless of theheight of their venous pressure, rarely, if ever,exhibit the subjective or objective manifestationsthat are generally associated with " increased in-tracranial pressure " nor do they have symptomsknown to result from cerebral anoxia, such asfaintness or unconsciousness (9, 10).

To the author's knowledge, studies directlyconcerning the effect of high peripheral venouspressure upon the circulation through the craniumof man have not been carried out. Because thereare many factors, besides venous hypertension,which play a role in producing the syndrome ofcongestive failure, it would seem that a helpfulstudy of this problem could be made on patientswho have a high venous pressure in the upperpart of the body but who are free from heartfailure. Wehave had the opportunity to observe

1 Read by title at the May 1936 meeting of the Ameri-can Society for Clinical Investigation, Atlantic City, NewJersey.

a number of such patients, suffering from superiorvena caval obstruction, of whom few had cardio-respiratory symptoms and none had clinical evi-dence of "increased intracranial pressure" de-spite the presence of venous pressures in the upperpart of the body as high as 55 cm. H20. A de-tailed study of five such patients is herewithpresented as material which may clarify the rela-tionship between high venous pressure and thecerebral circulation and explain the absence ofcerebral manifestations in this type of increasedintracranial pressure.

METHODOF OBSERVATION

The diagnosis of superior vena caval obstruction wasmade from the usual clinical findings and by comparativemeasurement of the pressure in the cubital and femoralveins, a procedure described by Ferris and Wilkins (11).The diagnosis was verified by necropsy in Cases 1 and 3,and by biopsy in Case 5. All studies were made afterthe patients had rested in bed for several hours andwhile they were in a horizontal position and in as near abasal state as was possible under the circumstances.

In order to estimate the degree of stagnation of bloodwithin the brain, blood was drawn under oil from theinternal jugular vein and internal carotid or femoralartery, using the technique of Myerson, Halloran, andHirsch (12), and analysis for carbon dioxide content,oxygen content, and oxygen capacity was begun im-mediately. In one of the cases similar gas studies weremade on blood from the cubital and femoral veins as well.In this patient (Case 5) all venous blood samples wereobtained without stasis or pain within a period of 3 min-utes. By means of lumbar puncture, the cerebrospinalfluid pressure of 3 cases was determined within a fewhours of the other observations. The patients were ex-amined for and questioned about clinical manifestationswhich might be associated with increased intracranialpressure or cerebral anoxia. Venous pressures were ob-tained by the direct method of Moritz and Tabora (13),the final reading being referred to a point 5 cm. belowthe manubrium sterni; blood oxygen content and capacityand carbon dioxide content were determined in duplicateby the manometric method of Van Slyke and Neill asdescribed by Peters and Van Slyke (14).

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EUGENEB. FERRIS, JR.

RESULTS

The more important observations which mightbe related to a high venous pressure in the upper

part of the body are tabulated in Table I. Thedegree of superior vena caval obstruction is in-dicated by the venous pressure obtained from thecubital vein. The values ranged from 22 to 50cm. saline, being above 45 cm. in 2 cases. In eachcase the venous pressure was equal in both arms,

and the veins of the head and neck were distendedproportionately, indicating that the pressure in all

veins draining into the superior cava was equallyhigh. That the cubital venous pressure closelyrepresents the intracranial venous pressure inthese cases is shown by the work of Weed andHughson (15). Their experiments on cats re-

vealed a close correlation between the pressure inthe brachial vein and saggital venous sinus. Thefemoral venous pressure was normal in all butCase 4, where, in addition to superior caval ob-struction, there appeared to be some obstructionto the inferior cava as well. The history, andabsence of a perceptible superficial venous col-

lateral circulation, suggest that the superior cavalobstruction had developed rapidly and was ofshort duration in Cases 1 and 4. It appeared tohave developed gradually over a period of monthsin the others.

Subjective symptoms. The patients experi-enced very few symptoms which could be relatedspecifically to vena caval obstruction and resultinghigh venous pressure. Patients 1, 4, and 5 com-

plained of fullness in the head and swelling ofthe face and neck, while Cases 2 and 3 had no

symptoms referable to caval obstruction. All fivepatients were conscious, completely rational, anddenied having headache, visual disturbances, or

nausea, and vomiting.Objective symptoms. All five patients lay flat

in bed without discomfort and without orthopneaof necessity or choice. At the time of observa-tion the rate and character of respirations were

normal in Cases 1, 2, 3, and 5. In Case 4, therespiratory rate was increased because of pul-monary infection. Case 1 had been free of re-

spiratory symptoms for 36 hours following the

TABLE I

Clinical observations and blood gas studies on 5 patients sufering from superior vena caval obstruction(All studies were carried out with the patients resting in a horizontal position.)

a3 Venous Arterial blood Intermal jugular311~~~~~@ 1i5lSe+Mmiii-atc miiru mm. spinolvolumes per cen c" volumes per Cent

1 164955 |Aortic |22 |Normal5 0 |4 2 |45 1 |80|160/30 19.7 33.7 22.11 891 10.51 40.1 9.2

2 166778 |Aoerticm 18 |Normal |0 |2 1 |32 8 90l 130/85 |33.4| 17.8 |42.8 18.3| 97| 10.2| 50.2 |7.6

3 |68317 |Aortic |30 |Shallow |0 |1 0 |24 5 110| 76/48| 113.5 |44.8 14.4| 94| 7.3 49.9 |6.2

4 |68959 Hodgin'ase 20 |Normal 0 2 4 |50 20O 90l 140/80 |49.0| 16.6 |48.4 20.01 83| 11.8| 53.2 |4.85 l Fibrou 18 |Normal 0 1 1 22 12I 72|120/96| 18.0 21. 44.3| 22.9| 95 18.1| 3.8

* Respirations were normal at the time of these observations; however, the patient had suffered from a severe attackof hyperpnea a few minutes before.

t Thiis patient was observed in the Holmes Hospital through the courtesy of Drs. Russell Speckman and JohnsonMcGuire.

i: (i.c.) indicates internal carotid artery.§ (f.) indicates femoral artery.

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HIGH INTRACRANIAL VENOUSPRESSURE

onset of the obstruction, but began having briefbut severe attacks of hyperpnea a few hoursbefore death, one of which occurred shortly be-fore blood samples were obtained.

Edema was present in the face, neck, and armsin most instances and the amount was roughlyproportional to the height of the cubital venouspressure. None of the patients had edema ofthe lower part of the body. The degree of facialcyanosis evident in the various patients was moremarked in those with the higher venous pressures(Table I). It was difficult to estimate in Case 4because the patient was colored. Examination ofthe ocular fundi revealed no evidence of edemaof the optic disk or retina in any case. The retinalveins, however, were moderately distended in allcases.

Cerebrospinal fluid dynamics. The cerebro-spinal fluid pressure was roughly the same as thecubital venous pressure in 3 cases studied. InCase 2, bilateral jugular compression caused arise in pressure from 33.4 to 35.4 cm., or only2.0 cm., and abdominal compression a rise to 39.4or 6.0 cm.; the pressure was 17.0 cm. after re-moval of 15 cc. of cerebrospinal fluid. In Case4, bilateral jugular compression did not affectthe cerebrospinal fluid pressure, while maximalabdominal compression raised it from 49.0 to 56.0or 7.0 cm.; the pressure was 45.0 cm. after re-moval of 15 cc. In Case 5 the pressure was 18.0cm. Both Cases 2 and 4 developed severe head-ache subsequent to lumbar puncture, while inCase 5, from which no fluid was removed, thissymptom did not develop.

Blood gas studies. The results of determina-tions of the oxygen and carbon dioxide contentand oxygen capacity of arterial and internal jugu-lar venous blood are tabulated in Table I.

Except for Case 4, the oxygen saturation ofarterial blood was relatively normal. The ar-teriovenous oxygen difference of internal jugularblood ranged from 3.8 volumes per cent in Case5, to 9.2 volumes per cent in Case 1. A com-parison of these figures with those obtained byLennox and his associates (16, 17) 2 on patients

2The average arteriovenous oxygen difference obtainedby Lennox and his associates in 120 cases was 6.16 vol-umes per cent. In 50 cases which they tabulated in-dividually the mean arteriovenous oxygen difference was

with normal vascular systems indicates no ap-preciable difference except possibly in Case 1,where the value is at the upper limit of the normalrange. This can be explained on the basis of anattack of severe hyperpnea which the patient suf-fered just before the time of blood sampling andwhich was probably responsible for the low carbondioxide values obtained from both arterial andvenous blood. Lennox and Gibbs (17) haveshown that a fall in the carbon dioxide tensionof the blood produced by hyperventilation willcause a marked increase in the arteriovenousoxygen difference.

In Case 5 the oxygen content of internal jugu-lar blood was 1.5 volumes per cent greater thanthat of antecubital blood and was roughly equalto the oxygen content of blood from the un-obstructed femoral vein (Table II).

The carbon dioxide content of the arterial bloodwas relatively normal except in Case 1. Arterio-venous carbon dioxide differences roughly paral-leled the arteriovenous oxygen differences in allinstances.

TABLE II

Blood gas studies of samples obtained almost simultaneously(Case 5)

Oxygen Carbon A-VSource of blood content dioxide oxygen

content difference

wolumes per centFemoral artery ............. 21.9 44.3Internal jugular vein ....... 18.1 3.8Antecubital vein ........... 16.5 51.2 5.4Femoral vein ..... . 18.2 48.0 3.7

DISCUSSION

The similarity of the cerebrospinal fluid andvenous pressures in 3 of these cases corroboratesthe findings of Becht (18), Myerson and Loman(19) and others (20), that there is a close rela-tionship between intracranial venous and cere-brospinal fluid pressure.86.65 ± 0.23 volumes per cent with a standard deviation of2.45 0.16.

8 In connection with the effect of venous upon cerebro-spinal fluid pressure, it is of interest that a patient withinferior vena caval obstruction had a normal cerebro-spinal fluid pressure and normal responses to bilateraljugular and abdominal compression. The obstruction wasproved to be between the right renal and hepatic veins.The venous pressures were: antecubital 2.0 cm. H,O,

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EUGENEB. FERRIS, JR.

The results indicate that in all cases the dif-ference between the oxygen content of arterialand internal jugular venous blood is within nor-mal limits. Calhoun, Cullen, Harrison, Wilkins,and Tims (21) also obtained normal arteriovenousoxygen differences from arterial and internal jug-ular venous blood in 3 of 4 patients sufferingfrom orthopnea of cardiac origin, but made nonote of the venous pressures in their cases. Theirfourth case had a value of 10.53 volumes percent, but like Case 1 of this series the patienthad a low carbon dioxide tension in his bloodas the result of hyperventilation. Since there isno reason to suspect that the patients herein re-ported had an abnormally low tissue metabolism,the arteriovenous oxygen differences obtainedclearly indicate that the blood flow through thecranium was relatively normal in spite of thevenous hypertension. There is also considerableclinical evidence which suggests that the bloodflow through the cranium was normal; namely,no symptoms indicative of cerebral anoxia, suchas weakness, dizziness or faintness, were present.The normal blood flow is in marked contrast tothe venous stasis which appeared to be present inthe superficial veins, as evidenced by facial cyano-sis and edema. The fact that in Case 5 the oxy-gen content of cubital venous blood was 1.5 vol-umes per cent less than that in the femoral andinternal jugular veins, is further indication forthe existence of more marked stasis in the upperextremity than in the head. This latter observa-tion seems significant because Lennox (16, 22)has shown that normally the oxygen content ofblood from the internal jugular vein is less thanthat of blood obtained simultaneously from pe-ripheral veins.

The compensatory mechanism responsible forthe normal cerebral blood flow is not clarified bythis study. Among others, Cushing (23) andBecht (18) have shown that great increases incerebrospinal fluid pressure are accompanied byan increase in arterial pressure, but it is thoughtthat this mechanism is not brought into actionuntil the intracranial pressure approaches that ofarterial blood. However, Becht's data show thatelevations of cerebrospinal pressure within the

femoral 22 cm. Cerebrospinal fluid pressures were:initial, 12 cm. spinal fluid; during jugular compression,18 cm.; during abdominal compression, 22 cm.

limits encountered in the cases herein reportedmay often produce a definite increase in systemicarterial pressure. In recent unpublished experi-ments, Williams and Lennox (24) have shownthat the cerebral blood flow is normal in patientshaving increased intracranial pressure. Theysuggest that the compensatory mechanism mayresult from the vasodilating action of CO2 onthe cerebral vessels. Conclusive proof as to theimportance of either of these mechanisms is lack-ing because the blood pressure change necessaryto compensate for the increased cerebrospinalfluid and venous pressures would be so small thatthe recorded arterial pressures would not be al-tered significantly.

It is of considerable interest that patients mayhave venous and cerebrospinal fluid pressures ashigh as 500 mm. H20 and not only maintain anormal rate of blood flow through the brain, butalso be free of any clinical manifestations gen-erally associated with increased intracranial pres-sure. Friedfeld and Fishberg (3) have alsonoted the lack of cerebral symptoms in a patientwith congestive failure whose cerebrospinal fluidpressure was 450 mm. spinal fluid, and Weigeldt(1) has commented on the absence of papilledemain a case of superior caval obstruction. The lackof abnormal cerebral manifestations and the ab-sence of any edema of the optic disc suggeststhat, in contrast to the superficial tissues, thereis no significant alteration in fluid exchange be-tween the blood and tissue of the brain in thesecases.

The explanation of the intracranial dynamicsin venous hypertension of this type probably de-pends upon the fact that the craniovertebral con-tents are enclosed in a container which is almostrigid, with the exception of the emerging vasculartree (25). Except for the venous and capillarysystems, the craniovertebral cavity is filled withcerebrospinal fluid and tissue, both of which arenon-compressible, and with arterial blood whichwill decrease in volume only under relatively highexternal pressure or with marked diminution inarterial pressure. The fact that, in man, bilateraljugular compression and release results in aprompt rise and return to normal of the cere-brospinal fluid pressure, suggests that the highpressure in these cases is not owing to an in-crease in fluid volume; and the work of Becht

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(18) and of Bedford (20) on animals supportsthis belief. Increased pressure distributed uni-formly throughout the intracranial veins and cap-illaries should therefore be transmitted completelyto other intracranial systems, because, owing tothe inability of the surrounding contents to changein volume, the vessel walls cannot distend suffi-ciently to absorb a significant amount of pressure.The close similarity of the cerebrospinal fluid andperipheral venous pressures in the three observedcases is consistent with this concept. Experi-ments in animals, adequately reviewed by Bedford,indicate that in general when the veins are oc-cluded, the cerebrospinal fluid pressure does notquite reach the venous pressure; and observationsin man of the cerebrospinal fluid pressure invenous hypertension of cardiac origin show con-siderable discrepancy between the two pressures.Such observations are not necessarily inconsistentwith the above explanation because in the animalstudies occlusion of all veins draining the craniumwas not effected as it was in these cases, and inman, marked alteration in cerebrospinal fluid pres-sure will result from the respiratory abnormalities(26, 27) which occur so regularly in cardiac fail-ure. If one accepts the hypothesis that meningealtension, caused either by edema, displacement, orvenous dilatation, will produce headache (28, 29),limitation of volume changes within the craniumby the factors described above would account forthe absence of this symptom and its appearanceafter removal of cerebrospinal fluid.

The absence of orthopnea in these cases indi-cates that high venous pressure alone cannot causeorthopnea. Blumgart and his associates (7, 8)suggest that venous hypertension results in venousstasis within the brain and that the resultingstagnation anoxemia, which would be moremarked in the horizontal position, accounts forthe orthopnea of congestive heart failure. Har-rison (2), too, explains orthopnea on the basisof anoxia but postulates another mechanism,namely, that the increased cerebrospinal fluidpressure which results from the venous hyper-tension, so obstructs the cerebral blood vesselsthat anoxia ensues. Since it appears from thestudies herein reported that venous hypertensionof extreme degree does not necessarily result invenous stagnation within the cranium, or in dim-inution of the rate of cerebral blood flow, such

hypotheses require further proof of the existenceof cerebral anoxia in orthopneic cardiac patients.The studies of Calhoun et al. (21), showed thatin orthopneic patients the oxygen difference be-tween arterial and internal jugular blood wasnormal and did not vary significantly with changesin position. Robb and Weiss (30) also foundthat many patients with orthopnea of cardiac ori-gin had normal venous pressures. These obser-vations throw additional doubt upon the impor-tance of venous hypertension as a cause for car-diac orthopnea.

SUMMARYAND CONCLUSIONS

1. Observations on 5 patients with superiorvena caval obstruction are presented.

2. In 3 patients tested, the elevation in venouspressure was accompanied by a similar increasein the cerebrospinal fluid pressure.

3. In spite of high venous pressure in the up-per part of the body, and evidence of venousstasis in the face and arms, the rate of bloodflow through the cranium was normal. This wasevidenced by: (a) normal arteriovenous oxygendifferences between arterial and internal jugularvenous blood; and (b) the absence of any mani-festations suggesting cerebral anoxia.

4. In contrast to the presence of edema in theface and arrns, there was no clinical evidence ofcerebral edema.

5. It is suggested that in the presence of highintracranial venous pressure the rigid coveringof the craniovertebral cavity is the importantfactor in preventing sufficient venous distentionand alteration in fluid exchange between the bloodand tissues of the brain to cause symptoms.

6. These observations do not support the hy-pothesis that venous hypertension, through itseffect on the cerebral blood flow, is an importantcause for orthopnea.

The author is indebted to Miss Rose Shore for tech-nical assistance.

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EUGENEB. FERRIS, JR.

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