Controlled Hypotension 443 Some Other Than That at the Neuro-Muscular GRIFFITH, H
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Postgrad Med J: first published as 10.1136/pgmj.31.359.443 on 1 September 1955. Downloaded from September 1955 SCURR: Control of the Blood Pressure and Controlled Hypotension 443 some other than that at the neuro-muscular GRIFFITH, H. R., and JOHNSON, G. E. (1942), Anaesthesiology action, 3, 4I8. junction, which is as yet unknown. BENNETT, A. E. (1940), J.A.M.A., 144, 322. GRAY, R. W., et al. (I941), Psych. Quart., 15, 159. BIBLIOGRAPHY WATERTON. C. (x812), 'Wanderings in S. America,' Everyman BERNARD, CLAUDE (1843), ' Note sur la Curarine et ses effects Series, Dent, London. physiologiques,' Paris. BEECHER, H. K., and TODD, D. P. (I954), Ann. Surg., I, 140. >CONTROL OF THE BLOOD PRESSURE AND CONTROLLED HYPOTENSION By 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 during the vagus and sympathetic, it can be improved by Anaesthesia humoral agents (adrenaline) and inotropic drugs, Blood pressure is the lateral pressure exerted by and is readily depressed by certain anaesthetic the blood on the vessel walls; our considerations agents which produce dilatation. Protected by copyright. are especially directed to the arterial system. The (b) Cardiac Filling: This depends on the length difference between systolic and diastolic pressure of diastole and the effective venous pressure. is the pulse pressure which depends on the stroke Venous pressure: The venous system accounts volume of the heart and the volume, elasticity and for 70 per cent. of the total volume of the vascular length of the arterial tree. In order to study bed; it is evident that considerable circulatory the various factors influencing the arterial pressure, adjustment can occur in this region. Surprisingly it is convenient to consider the mean pressure little is known of any venomotor mechanism :,3 which is proportional to the product of the cardiac it is usually stated that there is insufficient muscle output and the peripheral resistance.' in the walls of the veins to produce any important effect. In the case of the larger veins it is probable i. Cardiac Output that this thin layer of smooth muscle functions in This is the product of the stroke volume and the a manner characteristic of hollow organs having heart rate and depends on the force of the heart a relatively thin wall compared with the size of the and the cardiac the maintenance of tone in filling. lumen, purpose being http://pmj.bmj.com/ (a) The Force of Cardiac Contraction affects the order to allow considerable variation in capacity or efficiency with which the heart muscles produce filling with only slight changes in pressure.4 emptying. It depends on the initial length of the This tone is presumably regulated from the muscle fibres (Starling's law), so that an increased vasomotor centre: anaesthesia will diminish venous return leading to distension of the heart it, digitalis also can reduce venous pressure, enhances the force of the beat. In a failing heart, noradrenaline can produce constriction of the however, overdistension occurs and increasing veins and improve the venous return. A number of the venous pressure causes a further fall in output, factors influence filling of the venous system, on September 24, 2021 by guest. conversely in such cases venesection may improve notably the blood volume.6 This may be varied the circulation. in contrary directions by haemorrhage and The force of the heart is also dependent on its transfusion. Closely connected with this is the nutrition and oxygen supply, which are affected by state of the arterial bed, which accommodates a such factors as anoxaemia, the state of the proportion of the blood volume and provides a coronary vessels and the arterial blood pressure. through pressure to promote the venous return. Excessive potassium ions cause increasing relaxa- The state of the body cavities, respiration, tion of the heart, finally bringing about arrest in muscular activity and especially posture,9 mecha- diastole; for this reason stored blood is not nically influence the return of blood to the heart. advised for aortic transfusion during cardiac Apart from these effects on venous filling the surgery.38 Cardiac contraction is also influenced venous pressure depends on the efficiency with by body temperature and by nervous effects from which the heart empties the great veins. For this Postgrad Med J: first published as 10.1136/pgmj.31.359.443 on 1 September 1955. Downloaded from 444 POSTGRADUATE MEDICAL JOURNAL September I955 reason attempts to correlate central venous if the circulation is already impaired (e.g. haemor- pressure with cardiac output can give inconsistent rhagic shock, constrictive pericarditis). 11 As results, for increased cardiac output can operate to passive ventilation is now undertaken during produce a fall in venous pressure and.vice versa. many anaesthetics, these facts merit serious This is unfortunate, because the venous pressure consideration. is easily measured and would provide valuable information if it were a reliable index of cardiac 2. The Peripheral Resistance. output. As a guide to the onset of shock a falling Peripheral vascular resistance depends upon venous pressure is an earlier sign than arterial two factors: (i) the viscosity of the blood, and hypotension; the degree of its elevation by (2) the total cross-sectional area of the available transfusion provides a guide to replacement.5, 6, 7 exit vessels, which varies according to (a) the Changes in the thorax may have important anatomical state of the vessels, (b) nervous control effects on the blood pressure. The lungs during and (c) peripheral chemical and humoral effects full inspiration hold 120 cc. more blood than on the'vessels. during expiration; it follows that with the smaller Nervous Control: The most important part of vascular bed available during expiration there is this mechanism is the medullary vasomotor increased resistance to blood flow. The calibre centre, the function of which is to adapt the of the vessels may also vary reflexly, but little volume of the vascular bed to the volume of blood information is available on pulmonary vasomotor available; this it does by regulating the calibre of phenomena. Reflexes initiated by deep inspira- the vessels, notably the arterioles which constitute tion or inflation produce generalized cutaneous the most important part of the peripheral re- vasoconstriction. Apart from these vasomotor sistance. Nervous contrbl has also been demon- effects, inspiration by reducing intrathoracic strated in the larger arteries and on the venous pressure and by the descent of the diaphragm side of the circulation. All these changes Protected by copyright. in improves the venous return-the respiratory calibre are mediated through constrictor and pump effect. In expiration the converse is true: dilator nerves of various types. Numerous expiration against resistance (Valsalva manoeuvre) factors act on the vasomotor centre to produce impedes the venous return and the cardiac output these effects, including the hypothalamus and and blood pressure (especially pulse pressure) higher centres. Raised carbon dioxide tension fall.8 During expiration some blood is expelled and oxygen lack exert a pressor effect. Afferent from the lung vessels and the outflow into the impulses from the lungs, muscles and abdominal arteries is thereby increased; there is also a direct organs produce varied results. Experimentally transmission of changes of thoracic pressure to the demonstrable reflexes involving the centre may be arterial system. In view of the lag of two or three pressor or depressor according to the strength and beats for venous return changes to be manifest as frequency of the stimulus and the type of nerve arterial pressure fluctuations, it is not surprising fibre excited; for example, ' C' fibre stimulation that mixed effects upon the blood pressure are characteristically produces a fall of blood pressure. of these effects are reported.10 These phasic variations can be Under anaesthesia many http://pmj.bmj.com/ detected by means of direct electromanometry, abolished, but presumably reflex changes in and during average respirations are minimal. pressure resulting from traumatic stimuli are often As most examples of protest to surgical stimuli observed during light anaesthesia. during inadequate anaesthesia take the form of an The most important impulses acting on the increase in expiratory tone with decrease in size of vasomotor centre emanate from baroceptors in the thorax, it is evident that relaxants by preventing the carotid sinus, aortic arch and certain other such voluntary muscular activity will obviate areas. The higher the arterial pressure the blood pressure fluctuations of this type. Passive greater is the rate of discharge of these special end on September 24, 2021 by guest. ventilation reverses the normal pressure phases organs. The resulting impulses have a depressor in the chest. During inflation the venous return is action on the vasomotor centre: by this impeded, especially if there is active muscular mechanism it has been said ' the blood pressure resistance due to inadequate anaesthesia, and so the regulates the blood pressure.' Pressure on the arterial pressure will tend to fall. With the chest carotid sinus may stimulate these nerve endings open such changes are less striking. Recent and lead to a depressor effect associated with investigation indicates that cardiac output is vasodilatation and cardiac inhibition.12 Anaes- greatest with a rapid build-up of inflation pressure thesia has been said to depress this sinoaortic followed by a total release of pressure in expiration, apparatus; this will not, however, serve as an the duration of the expiratory phase being longer explanation for hypotension because depression than inspiration. If these conditions are not of the carotid sinus will reduce inhibition of the fulfilled cardiac output may be reduced, especially vasomotor centre and so should lead to a rise in Postgrad Med J: first published as 10.1136/pgmj.31.359.443 on 1 September 1955.