September 1955 SCURR: Control of the Blood Pressure and Controlled Hypotension 443

some action, other than that at the neuro-muscularjunction, which is as yet unknown.

BIBLIOGRAPHYBERNARD, CLAUDE (1843), ' Note sur la Curarine et ses effects

physiologiques,' Paris.

GRIFFITH, H. R., and JOHNSON, G. E. (1942), Anaesthesiology3, 4I8.

BENNETT, A. E. (1940), J.A.M.A., 144, 322.GRAY, R. W., et al. (I941), Psych. Quart., 15, 159.WATERTON. C. (x812), 'Wanderings in S. America,' Everyman

Series, Dent, London.BEECHER, H. K., and TODD, D. P. (I954), Ann. Surg., I, 140.

>CONTROL OF THE BLOOD PRESSURE ANDCONTROLLED HYPOTENSIONBy C. F. SCURR, M.V.O., M.B., B.S., D.A., R.C.S., F.F.A.

Consultant Anaesthetist, Westminster Hospital; Honorary Anaesthetist, Hospital of Ss. John and Elizabeth

Control of the Blood Pressure duringAnaesthesia

Blood pressure is the lateral pressure exerted bythe blood on the vessel walls; our considerationsare especially directed to the arterial system. Thedifference between systolic and diastolic pressureis the pulse pressure which depends on the strokevolume of the heart and the volume, elasticity andlength of the arterial tree. In order to studythe various factors influencing the arterial pressure,it is convenient to consider the mean pressurewhich is proportional to the product of the cardiacoutput and the peripheral resistance.'

i. Cardiac OutputThis is the product of the stroke volume and the

heart rate and depends on the force of the heartand the cardiac filling.

(a) The Force of Cardiac Contraction affects theefficiency with which the heart muscles produceemptying. It depends on the initial length of themuscle fibres (Starling's law), so that an increasedvenous return leading to distension of the heartenhances the force of the beat. In a failing heart,however, overdistension occurs and increasingthe venous pressure causes a further fall in output,conversely in such cases venesection may improvethe circulation.The force of the heart is also dependent on its

nutrition and oxygen supply, which are affected bysuch factors as anoxaemia, the state of thecoronary vessels and the arterial blood pressure.Excessive potassium ions cause increasing relaxa-tion of the heart, finally bringing about arrest indiastole; for this reason stored blood is notadvised for aortic transfusion during cardiacsurgery.38 Cardiac contraction is also influencedby body temperature and by nervous effects from

the vagus and sympathetic, it can be improved byhumoral agents (adrenaline) and inotropic drugs,and is readily depressed by certain anaestheticagents which produce dilatation.

(b) Cardiac Filling: This depends on the lengthof diastole and the effective venous pressure.

Venous pressure: The venous system accountsfor 70 per cent. of the total volume of the vascularbed; it is evident that considerable circulatoryadjustment can occur in this region. Surprisinglylittle is known of any venomotor mechanism :,3it is usually stated that there is insufficient musclein the walls of the veins to produce any importanteffect. In the case of the larger veins it is probablethat this thin layer of smooth muscle functions ina manner characteristic of hollow organs havinga relatively thin wall compared with the size of thelumen, the purpose being maintenance of tone inorder to allow considerable variation in capacity orfilling with only slight changes in pressure.4This tone is presumably regulated from thevasomotor centre: anaesthesia will diminishit, digitalis also can reduce venous pressure,noradrenaline can produce constriction of theveins and improve the venous return. A number offactors influence filling of the venous system,notably the blood volume.6 This may be variedin contrary directions by haemorrhage andtransfusion. Closely connected with this is thestate of the arterial bed, which accommodates aproportion of the blood volume and provides athrough pressure to promote the venous return.The state of the body cavities, respiration,muscular activity and especially posture,9 mecha-nically influence the return of blood to the heart.Apart from these effects on venous filling the

venous pressure depends on the efficiency withwhich the heart empties the great veins. For this

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reason attempts to correlate central venouspressure with cardiac output can give inconsistentresults, for increased cardiac output can operate toproduce a fall in venous pressure and.vice versa.This is unfortunate, because the venous pressureis easily measured and would provide valuableinformation if it were a reliable index of cardiacoutput. As a guide to the onset of shock a fallingvenous pressure is an earlier sign than arterialhypotension; the degree of its elevation bytransfusion provides a guide to replacement.5, 6, 7

Changes in the thorax may have importanteffects on the blood pressure. The lungs duringfull inspiration hold 120 cc. more blood thanduring expiration; it follows that with the smallervascular bed available during expiration there isincreased resistance to blood flow. The calibreof the vessels may also vary reflexly, but littleinformation is available on pulmonary vasomotorphenomena. Reflexes initiated by deep inspira-tion or inflation produce generalized cutaneousvasoconstriction. Apart from these vasomotoreffects, inspiration by reducing intrathoracicpressure and by the descent of the diaphragmimproves the venous return-the respiratorypump effect. In expiration the converse is true:expiration against resistance (Valsalva manoeuvre)impedes the venous return and the cardiac outputand blood pressure (especially pulse pressure)fall.8 During expiration some blood is expelledfrom the lung vessels and the outflow into thearteries is thereby increased; there is also a directtransmission of changes of thoracic pressure to thearterial system. In view of the lag of two or threebeats for venous return changes to be manifest asarterial pressure fluctuations, it is not surprisingthat mixed effects upon the blood pressure arereported.10 These phasic variations can bedetected by means of direct electromanometry,and during average respirations are minimal.As most examples of protest to surgical stimuliduring inadequate anaesthesia take the form of anincrease in expiratory tone with decrease in size ofthe thorax, it is evident that relaxants by preventingsuch voluntary muscular activity will obviateblood pressure fluctuations of this type. Passiveventilation reverses the normal pressure phasesin the chest. During inflation the venous return isimpeded, especially if there is active muscularresistance due to inadequate anaesthesia, and so thearterial pressure will tend to fall. With the chestopen such changes are less striking. Recentinvestigation indicates that cardiac output isgreatest with a rapid build-up of inflation pressurefollowed by a total release of pressure in expiration,the duration of the expiratory phase being longerthan inspiration. If these conditions are notfulfilled cardiac output may be reduced, especially

if the circulation is already impaired (e.g. haemor-rhagic shock, constrictive pericarditis). 11 Aspassive ventilation is now undertaken duringmany anaesthetics, these facts merit seriousconsideration.

2. The Peripheral Resistance.Peripheral vascular resistance depends upon

two factors: (i) the viscosity of the blood, and(2) the total cross-sectional area of the availableexit vessels, which varies according to (a) theanatomical state of the vessels, (b) nervous controland (c) peripheral chemical and humoral effectson the'vessels.

Nervous Control: The most important part ofthis mechanism is the medullary vasomotorcentre, the function of which is to adapt thevolume of the vascular bed to the volume of bloodavailable; this it does by regulating the calibre ofthe vessels, notably the arterioles which constitutethe most important part of the peripheral re-sistance. Nervous contrbl has also been demon-strated in the larger arteries and on the venousside of the circulation. All these changes incalibre are mediated through constrictor anddilator nerves of various types. Numerousfactors act on the vasomotor centre to producethese effects, including the hypothalamus andhigher centres. Raised carbon dioxide tensionand oxygen lack exert a pressor effect. Afferentimpulses from the lungs, muscles and abdominalorgans produce varied results. Experimentallydemonstrable reflexes involving the centre may bepressor or depressor according to the strength andfrequency of the stimulus and the type of nervefibre excited; for example, ' C' fibre stimulationcharacteristically produces a fall of blood pressure.Under anaesthesia many of these effects areabolished, but presumably reflex changes inpressure resulting from traumatic stimuli are oftenobserved during light anaesthesia.The most important impulses acting on the

vasomotor centre emanate from baroceptors inthe carotid sinus, aortic arch and certain otherareas. The higher the arterial pressure thegreater is the rate of discharge of these special endorgans. The resulting impulses have a depressoraction on the vasomotor centre: by thismechanism it has been said ' the blood pressureregulates the blood pressure.' Pressure on thecarotid sinus may stimulate these nerve endingsand lead to a depressor effect associated withvasodilatation and cardiac inhibition.12 Anaes-thesia has been said to depress this sinoaorticapparatus; this will not, however, serve as anexplanation for hypotension because depressionof the carotid sinus will reduce inhibition of thevasomotor centre and so should lead to a rise in

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blood pressure. Creyssel has blocked the sinusnerves with procaine in shocked patients anddescribed clinical improvement with a rise in thearterial pressure.13A fall in blood pressure can result from block

of vasoconstrictor reflexes at any level: chlorpro-mazine affects the hypothalamus, the vasomotorcentre may be depressed by anaesthetic agents, thesympathetic nerves may be blocked (e.g. by spinalor epidural anaesthesia) or the block may be atganglionic level (T E A B, hexamethonium, etc.).

Local Chemical Influences can act directly onblood vessels: CO2, histamine and metabolitesgenerally produce vasodilatation, noradrenalineand numerous pressor drugs are vasoconstrictors.

Hypertension During AnaesthesiaThe Effects of Carbon DioxideAnoxia and carbon dioxide retention may both

produce hypertension. In so far as these factorsare due to maladministration of the anaesthetic,such changes in pressure are avoidable. Increasein carbon dioxide tension affects the blood pressurein two directions: acting on the vasomotor centreit causes vasoconstriction, peripherally dilatationis produced by a direct action on the vessels. Inthe anaesthetized patient carbon dioxide accumu-lation, due for instance to soda lime exhaustion,frequently leads to a rise in pressure. In patientsunder extensive spinal anaesthesia this pressoreffect is annulled due to the sympathetic block, andin these patients the peripheral dilator effect pre-dominates leading to hypotension. Similar con-siderations may apply after ganglioplegics orduring deep anaesthesia. Under cyclopropane,carbon dioxide retention, due to hypoventilation,may maintain the blood pressure at a relativelyhigh level despite major surgical trauma. (YandellHenderson's carbon dioxide therapy of shock willbe recalled.) When the anaesthetic is discontinuedthe carbon dioxide level falls with resultinghypotension-' cyclopropane shock.'l4 It isobvious that any anaesthetic technique which maycause hypoventilation (e.g. the relaxants) canproduce a similar effect. When such methods areemployed assisted or passive ventilation must beundertaken, ensuring an adequate minute volume,to avoid carbon dioxide retention. There is anurgent need at present for the development ofsome indicator to place ' controlled respiration'on a basis other than empirical. Carbon dioxidebalance is far more difficult to assure than adequateoxygenation. The post-operative hypotensionfollowing such hypercapnia may be of longduration; its severity appears to be directly relatedto the degree of hypercapnia but not to the durationof the hypercapnic state.15 In so far as ganglio-plegics (e.g. pentamethonium) prevent the pressor

effect of anoxia or hypercapnia,16 their administra-tion may obviate hypotension following carbondioxide retention: such an action may be partlyresponsible for the improved post-operative stateobserved when these drugs have been given.

Reflex Hypertension: Reflex rises in bloodpressure due to stimuli from the field of operationare occasionally seen; the type of stimulus anddepth of anaesthesia especially conducive to thisreaction are uncertain.17 Distension of thebladder, and injection of solutions into the capsuleof the prostate often lead to a transitory hyper-tension. In paraplegics the response to suchstimuli can be very dramatic: hypertensive crisesresult from the operation of a mass autonomicreflex; this complication can be controlled by theadministration of a ganglioplegic drug.18,19 Ofespecial interest to anaesthetists is the hypertensionreflexly produced by laryngoscopy and intubationduring light anaesthesia.20, 21

Adrenaline and Pressor Drugs: Handling theadrenal gland during adrenalectomy (even whenthe gland is normal) commonly produces a briefhypertension. This response can be preventedby the anti-adrenaline drug, chlorpromazine(I2.5 mg. to 25 mg. intravenously). When aphaeochromocytoma is present such hypertensivecrises may be very severe, even fatal,22 and mustbe controlled during extirpation of the tumour bythe intravenous injection of adrenolytic drugs,23e.g. Benzodioxane 15 mg., Regitine 3 mg., orchlorpromazine 25 mg.; these doses may needto be repeated. Hypotension following removalof the tumour may need to be counteracted by1 noradrenaline given in a drip (4 mg. 1 noradren-aline to I litre of normal saline).24

1 noradrenaline is -the most powerful overallvasoconstrictor available (being the physiologicalagent).25 Adrenaline produces a marked increasein cardiac output while acting as an overallvasodilator.26 Chlorpromazine reverses the pressoreffect of adrenaline and if this drug be givenbeforehand infiltration of io cc. of I:Io,oooadrenaline can be used during the fenestrationoperation to produce local ischaemia combinedwith hypotension.Many other drugs (with varying activity on

cardiac output and peripheral resistance) can begiven to raise the blood pressure: most of these areallied chemically to adrenaline and many producedangerous types of tachycardia during anaesthesia.Evidently beneficial results from these agents canbe expected when hypotension is associated withvasodilatation (e.g. during spinal or hypotensiveanaesthesia): during oligaemic shock when theblood pressure is falling despite intense vaso-constriction such drugs are not indicated, but inshock when massive blood replacement fails to

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restore the pressure (vascular paralysis) theseagents have a place.27 It is important to note thatrestoration of arterial pressure by these agents,e.g. after hexamethonium, is the result of genera-lized vasoconstriction. The capacity of the bodyfor physiological redistribution of blood byvasomotor reflexes is not restored. Furthermore,the effect of the pressor drug, especially whengiven intravenously, may wane before the ganglio-plegic and hypotension will then recur. Prolongedindiscriminate vasoconstriction maintained fordays, e.g. by 1 noradrenaline drip, leads to tissueanoxia and liver necrosis has been described as aresult of such therapy. Examples of usefulpressor drugs are: ephedrine (50 to Ido mg.),Phenylephrine (5 to Io mg.) and methyl-amphe-tamine or methedrine (IO to 30 mg.)-the lastagent has a marked analeptic effect, and may causepost-operative restlessness and insomnia.

Arterial HypotensionFrom physiological considerations it follows

that a fall in arterial pressure may be due to areduced cardiac output, to reduced peripheralresistance or to a combination of these. Thesedisturbances may be classified:

I. Reduction in vasomotor tone.2. Reduction of cardiac output

(a) Reduced venous return(b) Reduced force of contraction(c) Changes in heart rate.

Under normal conditions a reduction in cardiacoutput or peripheral resistance will be compensatedreflexly and so long as this is adequate no markedchange in blood pressure will be observed. Themost important compensatory mechanisms againsthypotension are increasing the heart rate andvasoconstriction. Inglis28 has suggested that thepulse rate is the key to the treatment of hypo-tension occurring during anaesthesia. Hypotensionassociated with tachycardia is usually due toreduction of the cardiac output from a fall in thevenous return: treatment is to increase the venousreturn by posture or transfusion. Cardiac outputmay also fall owing to reduced force of cardiaccontraction, which may be due to anaestheticoverdosage: treatment should be directed tomaintaining perfect oxygenation and promotingelimination of the anaesthetic-it has been sug-gested that cardiac and medullary stimulants maybe given.

Hypotension with an unchanged pulse rate isprobably due to reduction in peripheral resistance:vasomotor tone may be increased by pressor drugsgiven intravenously, e.g. noradrenaline 4 mg. perlitre given as a drip, methylamphetamine io to30 mg., or phenylephrine io mg. Hypotensionwith bradycardia may be due to vagal reflex action:

treatment consists in removing the precipitatingcause and blocking the vagal efferents withatropine gr. 1/100 to 1/50 intravenously. Duringanaesthesia many variable factors are implicated,29so that it will not always be possible to determinethe cause of any blood pressure change accordingto these simple rules; therefore, further discussionseems merited.

Induction of Anaesthesia is usually accompaniedby depression of the vasomotor apparatus bothcentrally and peripherally. This is evidenced bythe usual signs of vasodilatation (loss of tempera-ture gradient in the limbs, dilatation of the super-ficial veins and increase in limb blood flow).30Some authorities hold that consciousness of itselfhas a pressor influence.31 Many agents, notablythe barbiturates and chloroform also depress themyocardium and lead to cardiac dilatation; thesefactors reduce the circulatory reserve, but hypo-tension does not invariably occur in young people.In the elderly, compensation is less effective andone report suggests combining methylamphe-tamine with thiopentone to avoid hypotension insuch patients.32 Ability to compensate againsthypotension resulting from changes in postureis lost at a very light level of anaesthesia: in oneinvestigation 60 per cent. of men over forty yearsof age who had previously received morphinegr. i had hypotension and fainted when they wereabruptly tilted into the head-up position. Bursteinsuggests that such falls in pressure can be avoidedby inducing anaesthesia in the position desired foroperation. Vasoconstriction is still possible duringlight anaesthesia and blood loss may be wellcompensated thereby. Pallor of the ears whichdevelops during major operations is evidence ofthis. On rubbing with the hand, the ear becomesred due to vasodilatation as long as any circulatoryreserve remains and to this it provides a guide.Blood oxygenation can be assessed by this test andthe rapidity and intensity with which the pallorrecurs is a guide to the state of the circulation.

Blood and Fluid Loss associated with theoperation lead to decreased venous return and afall in cardiac output. Compensatory widespreadvasoconstriction may mask blood pressure changesbut after brisk or severe haemorrhage there isusually marked hypotension, the systolic pressurefalling by a greater degree than the diastolic.More gradual loss of an even larger volume mayoften be effectively masked in respect of bloodpressure changes, but anaesthetics impair thehomeostatic mechanisms in varying degrees.33It is certain that modern balanced anaesthesia,employing nitrous oxide-oxygen supplemented byanalgesics such as pethidine and relaxants asindicated, allows these circulatory mechanisms toact to a greater extent than during ether anaes-

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thesia.35 It is not clear that these influences areentirely beneficial, vasoconstriction by reducingblood flow leads to tissue anoxia-a stage insurgical shock. It is possible that ganglioplegics(and also chlorpromazine), by blocking thesechanges, may prevent shock during severe surgicaloperations, provided that any blood loss ispromptly replaced by transfusion. Observationshave been made of the amount of blood lost duringvarious surgical procedures and it has been notedthat the measured loss is the minimal amount thatmust be replaced because additional blood is lostinto traumatized areas by post-operative oozing,etc.34 When the arterial pressure has fallen dueto haemorrhage mere restoration of this pressureto normal by transfusion is not the index of ade-quate therapy, for persisting vasoconstrictionplays a part in this rise. Transfusion cannot beconsidered adequate until the tone of the vessels isrestored to normal and good peripheral circulationis re-established. Examples of increase in thearterial pressure above normal due to excessivetransfusion are rare, the usual sign being a rise inthe venous pressure as evidenced by distensionof superficial veins. Recent investigation of thearterial route for transfusing blood shows that indesperate cases (e.g. patients in moribund condi-tion following profound blood loss) this methodmay produce dramatic resuscitative effects. Livesmay be saved which would be beyond the reach ofintravenous transfusion.36 The aortic route maybe the most rapid and effective in such emer-gencies;37 the coronary flow is improvedimmediately the transfusion into the arterialsystem is begun and improvement in the arterialpressure is more rapid than that produced byintravenous transfusion.

Neurogenic Hypotension: It is widely acceptedthat hypotension can occur as the result ofneurogenic or reflex activity. Conclusive proofof this mechanism is lacking. Presumably nervousimpulses due to trauma travel up afferent nerves toproduce inhibition of the vasomotor centre. Itwas commonly believed that anaesthesia of ade-quate depth could prevent this type of fall. It isdoubtful if this view can be sustained since reflexhypotension rarely occurs during light generalanaesthesia accompanied by relaxants. Directrecordings of arterial pressure show that tractionon mesentery can produce an immediate fall inpressure with instant recovery on the release oftraction:10 these reactions are prevented by nerveblock. The conclusion that such changes are dueto a reflex seems inescapable. One disturbance ofthis type is of great interest and has been referredto as the coeliac plexus reflex;12 it may be en-countered during various upper abdominalprocedures.71 When operative stimulation in the

coeliac region is maximal the pressure suddenlybecomes unassessable by auscultation. The pulseremains palpable, however, and is not materiallychanged in rate. With careful auscultation,allowing the cuff pressure to fall slowly, a readingcan be obtained in the region of the previousdiastolic level: the pulse pressure is greatlydiminished, e.g. the reading may be 90/85. Directmanometry has confirmed that such bizarrereadings are not due to artefact associated withthe Riva-Rocci method. Such fantastically lowpulse pressure can only be caused by a greatreduction in cardiac output. It is not known howthis is produced reflexly; one report suggests thatthe phenomenon is due to vagal cardiac inhibitionand advises treatment with intravenous atropine.39In confirmation of this view high right auricularand venous pressures have been observed duringthe operation of this reflex.4' 7 This disturbanceis unlikely to occur when adequate dosage ofrelaxant has been given. An alternative explana-tion is a fall in the venous return due to pressureby the surgeon on the great veins (by packs or-retractors). Extension of the spine (e.g. by arest or bridge) or the lateral jack-knife posturemay produce similar effects to stimulation in thecoeliac region.10 Should such posturing lead toserious hypotension, a prompt return to a morenormal position is indicated: elevation of the legsand head-down. tilt may further improve thevenous return.

Spinal Anaesthesia: Arteriolar dilatation re-sulting from vasoconstrictor paralysis in theanaesthetized part of the body is the principalcause of hypotension during spinal anaesthesia.The ratio between the area of vasodilatation andthat of compensatory vasoconstriction in the restof the body determines the degree of bloodpressure fall. When sympathetic block is com-plete such compensation cannot occur. It isprobable that some reduction in cardiac outputresults from the increased circulatory bed duringwidespread vasodilatation.41 The above con-siderations apply equally to epidural block.Gillies40 has advocated total spinal block anaes-thesia leading to a hypotension of 40 mm. to70 mm. systolic, to reduce haemorrhage andfacilitate surgery during lumbodorsal sympathec-tomy. He pointed out that the pressure at thearterial end of the capillaries is normally 40 mm.and stated that in cases thus anaesthetized themajor site of resistance is removed by dilatationof the arterioles so that the arteriolar capillarypressure approximates the existing arterial pressureof 40 mm. to 70 mm. With the patient in thehead-down posture and breathing plentiful oxygen,tissue blood flow and oxygenation in importantorgans is adequate. Coronary blood flow being

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dependent on the diastolic pressure may suffer,but this effect is mitigated by the reduced cardiacwork lowering oxygen need. Other methods ofproducing controlled hypotension include the useof ganglioplegics such as pentamethonium andarterial bleeding. The ganglioplegics act in asimilar fashion to spinal anaesthesia, producing,however, not only a sympathetic block but also ablock of parasympathetic ganglia. When arterialbleeding is used to produce hypotension, vaso-constriction occurs which is likely to produceharmful tissue anoxia (haemorrhagic shock).On the other hand, a dry field is likely to beobtained at a relatively higher blood pressure level,furthermore the patient's own blood can bereinfused promptly to produce restoration ofpressure immediately if it is indicated. Thistechnique and the apparatus required are fairlycomplicated and reference should be made to theoriginal articles.42'43 44 The excellence of theresults obtainable with ganglioplegics even inneurosurgery have caused arteriotomy to fall intodesuetude.

Controlled HypotensionThe aim of this technique is to provide the

surgeon with an ischaemic operating field and toprotect the patient against shock. Indications forcontrolled hypotension have not been rigidlydefined and differ in various centres. Justificationmust be a product of the risk, the pathology andthe possible advantage to be gained.45Three main methods are available as indicated:i. Arteriotomy.2. Spinal or epidural block. These methods

carry the advantage that not only the bloodlessfield but analgesia and muscular relaxation areprovided by the same manoeuvre. For furtherdetails reference should be made to publishedwork on these applications of spinal block.31, 46\ 3. Ganglionic blockade in which the hypo-tension is produced by intravenous agents, e.g.pentamethonium iodide.47' 48 Reduction in peri-pheral vascular resistance, gravitational pooling ofblood in the veins of dependent parts and somereduction in cardiac output may all play a part.41When the subject has been deprived of the nervouscontrol of his circulation, changes in posture havea profound effect. When the body is tiltedgravity induces a gradient of arterial pressure(30 mm. Hg. for every 15 in. vertical height fromheart level).49 This fact, combined with thehypotension, enables the anaesthetist to providea remarkably dry operative field. For adequatecontrol of surgical haemorrhage it may be necessaryto reduce the blood pressure at the site of operationto 35 to 45 mm. A pressure of at least 60 mm.must always be maintained at heart level. The

question obviously arises as to whether suchhypotension can be tolerated or whether it en-dangers the life of the patient. The work ofGillies40 appears to show that adequate tissueoxygenation can be maintained provided the bloodis well oxygenated and that vasodilatation isensured. The low blood pressure associated withvasodilatation is not, of course, of the same serioussignificance as a similar fall in pressure due tohaemorrhage with which is associated extremevasoconstriction, low tissue circulation, anoxia andcapillary damage. In a 30 to 35° head-up tilt thecerebral blood pressure has been calculated to be35 to 40 mm. when the heart pressure is 60 mm.Hg. but other vital organs are at a pressure higherthan heart level. Studies during hexamethonium-induced hypotension have shown an increase inthe cerebral arteriovenous oxygen differencewhich implied a decrease in cerebral bloodflow.16' 50 There is, however, a decrease incerebral oxygen need during anaesthesia and theincreased oxygen utilization which the aboveresearches demonstrated appeared to be adequate;other reports have suggested that cerebral bloodflow may not, in fact, be reduced because there isa fall in cerebrovascular resistance.51 (Cerebraloxygen needs may be further reduced by hypo-thermia, which has been proposed as an adjunctto increase the margin of safety.) Electroence-phalograms have shown that virtually all corticalactivity ceased when the pressure was reduced to55 mm. systolic.6' 52,53 Some alteration incerebral function has also been shown by theflicker fusion test of Berg.54

Renal blood flow may not be greatly de-creased;55,56,57 naked eye changes in the liverhave been observed during laparotomy but theirsignificance may have been misinterpreted.58

Technique:47, 59, 60 A well-adjusted blood pres-sure apparatus (auscultatory or oscillometric)must be fitted from the start and the bloodpressure must be checked frequently. Access toa vein must be ensured by means of a diaphragmneedle or an intravenous drip. Respiratoryobstruction must be avoided and a high level ofoxygenation must be maintained; therefore someauthorities suggest that endotracheal intubationshould be the rule. It does not greatly matterwhich agents are used, but since most generalanaesthetics produce a tendency to posturalhypotension very deep planes of anaesthesiashould be avoided. The combination usuallyemployed has been thiopentone, nitrous oxidewith abundant oxygen and a relaxant or supple-ment as necessary. Apnoea, though not to befeared provided oxygenation is maintained, isperhaps better avoided, firstly because spontaneousrespiration provides a valuable continuous indica-

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tion of the patient's condition, and secondlybecause controlled respiration may cause a furtherlowering of the pressure. It must be noted,however, that controlled respiration is at all timesmandatory in preference to inadequate spontaneousventilation.The patient is placed in the appropriate posture

as soon as possible after the induction of anaes-thesia, in order to assess the lability of the bloodpressure and to give as long a time as possible forblood to drain away from the operation site. Thefirst dose of ganglioplegic is then given intra-venously; the aim is to obtain a systolic pressureof 60 mm. Hg. because the best results are obtainedat this level. A lower pressure is physiologicallyundesirable and renders observation of the leveldifficult. Should excessive hypotension occurminute doses of a pressor agent are given to raisethe pressure to 60 mm. Hg. or, in the case ofArfonad, the drip is temporarily stopped and theadverse tilt reduced.

Several factors are available as guides inassessing the dosage of hypotensive agent:

I. The body weight.2. The metabolic rate. When this is high, as

in thyrotoxicosis, very large doses may be neededfor successful results.

3. The initial blood pressure.4. The lability of the circulation as assessed by

the hypotension resulting from induction ofanaesthesia plus posturing. When this fall isprofound (as is commonly observed in hyper-tensive subjects) small doses of ganglioplegicsuffice.

5. Age. This is the most valuable guide.Young patients require much larger doses than theaged. The young commonly develop tachycardiawhich tends to prevent the fall in blood pressure.

Bearing these factors in mind one may use thefollowing initial doses.Average robust young adults:

Pentamethonium Iodide .. 50 to 200 mg.Hexamethonium Bromide .. 20 to 60 mg.Pentapyrrolidinium Bistartrate I0 to 20 mg.Arfonad: drip solution I mg. per I mil-

60 drops per minute.60Older patients:

Pentamethonium Iodide .. Io to 50 mg.Hexamethonium Bromide .. 10 to 30 mg.Pentapyrrolidinium Bistartrate 5 to 20 mg.Arfonad: I mg. per I mil--o to 30 drops

per minute.Subsequent doses are given as indicated by the

blood pressure readings, aiming to keep thesystolic pressure in the 60 to 70 mm. Hg. range.

It seems probable that the danger of overdosageis not great, the theoretical aim being completesympathetic block such limit is unlikely to be

exceeded. In some patients such blockade pro-duces excessive hypotension, in others a' pressurefloor' at a level higher than 60 mm. Hg. may beobserved. Increased and additional doses ofganglioplegic produce no further fall in theseresistant patients and only serve to prolongexcessively such hypotension as is attained. Thephenomenon of tachyphylaxis is frequentlyobserved with these drugs, being least markedwith Arfonad.60, 61 In resistant patients deepen-ing the anaesthetic, increasing the adverse tilt,and administration of procaine amide62 may allhelp to secure satisfactory hypotension. In onecentre a negative pressure is applied to the legs aspart of the hypotensive technique.51, 63

Surgical Technique: Infiltration with adrenalinesolutions is unnecessary and (unless preceded bychlorpromazine) will produce a pressor effectleading to failure of the method. Haemostasismust be meticulous, even the smallest pointsbeing secured. Severe haemorrhage (e.g. damageto a major vessel) promptly leads to a further fallin blood pressure, the patient having been de-prived of his compensatory mechanism. It isessential if much blood is lost, that promptequivalent replacement be made; the bloodpressure then returns rapidly to its former level.59As buffering reflexes are not active, such restora-tion of pressure is an accurate guide to transfusion.At the end of the operation the pressure should berising and preferably should be in the 80 too00 mm. region. Any acute rise is undesirableand may provoke haemorrhage. Frequent post-operative checks on the pressure should be madefor the first 24 hours. Should the hypotensionpersist unduly long cautious antagonism withpressor drugs is indicated.

Operative Shock: The method has been used incertain operations usually regarded as liable tolead to operative shock, e.g. abdominoperinealresection, pelvic evisceration, etc., but providedadequate blood transfusion was undertaken shockdid not occur. To what extent this phenomenonis due to prevention of blood loss or to the obtunda-tion of circulatory reflexes is uncertain.64 Thisobservation has been corroborated65 and is inaccordance with physiological studies. Wiggers66states that recent studies favour the concept thatthe net effect of compensatory vasoconstriction isharmful and that the transition from impendingto irreversible shock can be retarded or preventedby abrogation of sympathogenic vasoconstriction.

Contraindications to Hypotensive Techniqueare:

i. Inexperienced anaesthetist.2. Unsettled anaesthetic conditions. When

smooth anaesthesia cannot be secured or when an

September 1955 449

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450 POSTGRADUATE MEDICAL JOURNAL September 1955

anoxic episode has marred the induction hypo-tensive methods are contraindicated.

3. Established shock.4. Recent coronary infarction or other severe

cardiac disease.5. Severe renal damage: elimination of the

drugs may be retarded.6. Respiratory inefficiency, severe anaemia or

anoxia from any cause.7. Severe diabetes.67Dangers of the Method: Obvious dangers

include acute circulatory failure during thethe induction of hypotension; this has beenreported but fortunately appears to be rare in theabsence of cardiac disease or anoxic incidentduring anaesthesia. In deaths of this type thehypotensive technique seems directly implicated.

Deaths due to thrombosis, reactionary haemor-rhage, renal failure, etc., were by no means un-known prior to the introduction of hypotensivemethods: in one series the incidence of suchcomplications was approximately equal in similarcases anaesthetised with or without hypotension.68Deaths due to anoxia of vital organs due to thehypotension have not been proven as a compli-cation of the method. Opponents of this techniquehave suggested various complications, arguingfrom hypothesis and hearsay but unsubstantiatedby case reports.

In one report69 based on questionable evidencea death rate of i in 450 is suggested, but examina-tion of the various causes of death reveals thatmany were not directly due to the hypotension,other complications were well known beforehypotensive methods were introduced and theattributability of others is doubtful. Anothervaluable and interesting series of fatal case reports70reveals in almost every instance the danger ofanaesthetic ' incidents ' when hypotensive methodsare used. It appears certain that the reserve ormargin of safety is greatly lessened in the hypo-tensive state, any mismanagement of theanaesthetic or infringement of the rules willbe paid for at the highest price-the life of thepatient. For this reason induced hypotensionis only permissible when there are direct andpositive indications, when the anticipated benefitto the patient outweighs the risk and when first-class anaesthetic conditions are assured.

REFERENCESI. WRIGHT, S., Applied Physiology, London, 1953.2. PRIMROSE, W. B. (I954), Brit. J. Anaesth., 26, Ioo.3. EDITORIAL (I954), Ibid., 26, II8.4. SCURR, C. F. (I95I), Curr. Res. Anesth. & Analg., 30, 2II.5. PIERCE, V. K., BOYAN, P., and MASTERSON, J. G.

(I953), S.G.O., 96, 3IO-3I4.6. ANDERSON, M. E., and LUNDY, J. S. (x949), Anesthesiology,

10, I45.7. BISHOP, H. F., CILIBERTI, B. J., and BARENDRICK,

E. H. (I952), Ibid., 13, 297.8. HOWARD, P., LEATHART, G. L., DORNHORST, A. C.,

and SHARPEY-SCHAFER, E. P. (1951), Brit. med. .7.,2, 382.

9. GORDH, T. (I945), Acta Chir. Scand., 92, Supp. 102.I0. EATHER, K. F., PETERSON, L. H., and DRIPPS, R. D.

(1949), Anesthesiology, Io, 125.II. HUBAY, C. A., et al. (1954), Ibid., 15, 445.12. BURSTEIN, C. L. (1949), Fundamental Considerations in

Anaesthesia, New York.13. CREYSSEL, J., et al. (1947), Lyon. Chir., 42, 23.14. DRIPPS, R. D. (1947), Anesthesiology, 8, 15.15. BUCKLEY, J. J., et al. (1953), Ibid., 14, 226.16. VAN BERGEN, et al. (1954), Ibid., 15, 507.17. HOWLAND, W. S., and PAPPER, E. M. (1952), Ibid., 13, 343.18. RISKIN, A. M., et al. (1954), Ibid., IS, 262.19. CILIBERTI, B. J., et al. (1954), Ibid., 15, 273.20. KING, B. D., et al. (1951), Ibid., 12, 556.21. KING, B. D., et al. (1954), Ibid., Is, 231.22. HARRISON, B. L., and SEWARD, E. H. (1954), Brit. med.. .,

I, 1077.23. COBB, C. C., HALL, J., and HALL, R. A. (1953), Lancet,

1, 973.24. THOMPSON, J. E., and ARROWOOD, J. G. (1954), Anes-

thesiology, 5I, 658.25. CHURCHILL-DAVIDSON, H. C. (1951), Brit. med. J.,

2, 1551.26. SWANN, H. J. C. (1952), Ibid.,'3, 1003.27. ECKENHOFF, J. E., and DRIPPS, R. D. (1954), Anes-

thesiology, 15, 681.28. INGLIS, J. M. (1952), Lancet, 2, 362.29. STEPHEN, C. R., NOWILL, W. K., and MARTIN, R.

(1953), Anesthesiology, 14, x8o.30. LYNN, R. B., and SHACKMAN, R. (195I), Brit. med. J.,

2, 333.31. BROMAGE, P. R. (1954), Spinal Epidural Analgesia, London.32. LOCKETT, J. (1951), Anaesthesia, 6, 83.33. HERSHEY, S. G., ZWEIFACH, B. W., and ROVENSTINE,

E. A. (I953), Ibid., 14, 245.34. BONICA, J. J., and LYTER, C. S. (1951), Ibid., 12, 90.35. STEPHEN, C. R. (1952), Ibid., 13, 540.36. BROWN, A. S. (1953), Lancet, 2, 745.37. HAXTON, H. A. (1953), Ibid., x, 622.38. MELROSE D. G., and WILSON, A. D. (1953), Ibid.,

1, 1266.39. SMITH, B. H. (1953), Ibid., 2, 223.40. GILLIES, J., and GRIFFITHS, H. W. C. (1948), Anaesthesia,

3, I34.4I. SHACKMAN, R., et al. (1952), Ibid., 7, 2I7.42. BILSLAND, W. L. (1951), Ibid., 6, 20.43. MORTIMER, P. L. F. (1951), Ibid., 6, 25.44. JACKSON, I. (1954), Jbid., 9, 13.45. EDRIDGE, A. W. (1954), Broadway Clin. Supp., 1, 7.46. LEARMONTH, J. (1953), Brit. med. J., 1, 743.47. SCURR, C. F. (1951), Acta Anaesthesiologica, 2, 243.48. ENDERBY, G. E. H. (I951), Proc. Roy. Soc. Med., 44, 82g.49. ENDERBY, G. E. H. (1954), Lancet, I, I85.50. HUGHES, G. (1954), Ibid., I, 311.51. JAMES, A., COULTER, R. L., and SAUNDERS, J. W.

(1953), Ibid., I, 412.52. BROMAGE P. R. (1953), Proc. Roy. Soc. Med., 46, 919.53. SCHALLEK, W., and WALZ, D. (1954), Anesthesiology, I5,.

673.54. NILSSON, E. (1953), Brit. J. Anaes'h., 25, 24.55. MILES, B. E., et al. (I952), Clin. Sci., II, 73.56. DE WARDENER, H. E. (1955), Anaesthesia, I0, 18.57. EVANS, B., and ENDERBY, G. E. H (1952), Lancet,, 1045.58. BROMAGE, P. R. (1952), Ibid., 2, I0.59. ENDERBY, G. E. H. (1953), Trans. Med. Soc. Lond., 68, 68.60. SCURR, C. F., and WYMAN J. B (1954), Lancet, 1, 338.61. HAMPTON L. J., et al. (1954), Surgery, 35, 857.62. MASON A. A., and PELMORE, J. F. (1953), Brit. med. J.,.

I, 250.63. SAUNDERS, J. W. (1952), Lancet, x, 1286.64. SCURR, C. F. (1951), Ibid., i, 1020.65. BOYAN, P. (1953), Brit. med. J., I, 728.66. WIGGERS, C. J. (1950). Physiology of Shock, p. 243.67. GRIFFITHS, J. A. (1953), Quart. J. Med., 22,. 405.68. WYMAN, J. B. (1953), Proc. Roy. Soc. Med., 46, 605.69. HAMPTON, L. J., and LITTLE, D. M. (1953), Lancet, I,.

1299.70 . (I953), Anaesthesia, 8, 263..71. SCURR, C. F. (1950), Ibid., 5, 67.

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HypotensionPressure and Controlled Control of the Blood

C. F. Scurr

doi: 10.1136/pgmj.31.359.4431955 31: 443-450 Postgrad Med J 

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