MeprcaL Journal
`CLINICAL USE OF THE SPHYGMOMANOMETER.
`1189
`[ Tae Barrise
`DEc, 27, 1924]
`
`THE CLINICAL USE OF THE SPHYGMO-
`MANOMETER.*
`BY
`
`K. DOUGLAS WILKINSON, O.B.E., M.D.,
`M.R.C.P.
`
`the patient is composed before making an
`to wait until
`observation of blood pressure.
`even when considerable in
`Calcification of arteries,
`amount,
`is of little importance as a source of fallacy in
`blood pressure estimations when more than two and a half
`inches of artery are compressed, for such a length of artery
`is never completely calcified. The normal artery offers but
`little if any resistance to compression, but when the artery
`wall
`is contracted to constrict the artery it may offer a
`considerable resistance. The best way to overcome this
`constriction is either to massage the limb for a short time
`or to repeatedly compress and decompress the limb with the
`armlet.
`The first reading of a blood pressure is most likely to be
`fallacious, and if immediately subsequent readings show a
`lower pressure observations should be repeated until a
`constant reading is obtained. The lowest reading is most
`likely to be correct.
`In any case with a frequent heart
`action the readings are likely to be too high, and if
`possible blood pressure should be estimated during a normal
`heart rate.
`
`A.ttHoucH Harvey announced the discovery of the circula-
`tion of the blood in 1628, our knowledge of the circulation
`did not advance materially until Carl Ludwig introduced
`the graphic method of studying the heart’s action two
`centuries later. He fixed a float to a mercury manometer
`and arranged so that the movements of
`the float were
`recorded upon a revolving drum,
`andsince this the evolu-
`tion of instruments and knowledge has been rapid. Each
`instrument invented has added something to our knowledge
`—sphygmographs, polygraphs, electro-cardiographs, etc.—
`and it is an interesting paradox that the use of instruments
`of precision in medicine has a way (largely because of their
`educational value) of diminishing the necessity for their
`use. Thus the sphygmograph taught us many facts about
`A normal child of under 12 years of age should uot have a
`the pulse which could be recognized subsequently without
`systolic pressure of over 100 nor a diastolic pressure of over
`the aid of the instrument.
`The electro-cardiograph was
`75mm. Hg unless it be very obviously in advance of its years in
`size or weight.
`In adults the normal
`systolic pressure varies
`necessary for the detection and explanation of auricular
`between 100 and 160mm, Hg and the normal diastolic pressure
`fibrillation, though we now recognize this condition without
`between 65 and 90 mm. Hg; and while pressure tends to rise with
`its use, and to some extent the sameis true of the sphygmo-
`age there are many old men with quite low pressures. Again,
`manometer,
`pressures vary with physique, big powerful men having higher
`normal pressures than their physical
`inferiors, while in women
`The pulse may be defined as a rhythmic variation of
`the pressures are five or ten points lower than in men, age for
`pressures in an artery. The highest pressure reached—the
`age, and type for type.
`systolic—is the result of the output of blood from theleft
`At each heart beat the left ventricle forces blood into the
`ventricle. The lowest pressure—the diastolic—occurs at the
`aorta and so maintains arterial blood pressure, but
`the
`end of diastole and is the result of three factors:
`(1) the
`height to which this pressure rises depends upon the re-
`rate of blood flow through the arteries and arterioles into
`sistance of the arteries, arterioles, and capillaries, and the
`the capillaries;
`(2)
`the volume of blood in the arterial
`response that the ventricle makes to overcome this resist-
`system; (3) the action of the muscular and elastic coats of
`the arteries on the contained blood.
`ance. With a normal heart the ventricular response varies
`directly with the resistance—that
`is, with the diastolic
`The pulse pressure is the difference between the systolic
`pressure—and this fact is the keynote of physiological and
`and diastolic pressures. The most highly trained finger is
`pathological variations in arterial pressures.
`incapable of estimating systolic blood pressure accurately,
`When (under experimental conditions) the inflow into the
`and cannot give any certain information about diastolic
`heart is kept constant the output of the left ventricle is
`pressure ; indeed, the routine use of the sphygmomanometer
`unaltered by changes in the heart rate or arterial resist-
`will quickly convince anyone that it is useless to expect
`ance; but when the inflow varies the heart automatically
`any exact information about blood pressures from digital
`alters its output to equal the inflow,
`so that in a given
`examination of the pulse,
`since the size of
`the vessel,
`time the amount of blood entering the aorta equals that
`the condition of
`its wall, and the force of
`the pulse
`entering the right auricle. With a heart rate of 60 per
`may easily lead the finger
`to form quite an incorrect
`minute the duration of ventricular systole is about three-
`conclusion as to the pressures in the artery.
`eighths of a second, so that the heart works three-eighths
`The best: method of obtaining the blood pressures is by
`of the day (nine hours) and rests five-eighths of the day
`auscultation over the brachial artery, but palpation may
`(fifteen hours). @. N. Stewart calculates the daily work
`also be used to determine the systolic pressure.
`of the heart (ventricles only) at about 150,000 foot-pounds,
`After reassuring the patient as to the painlessness of the pro-
`and this is the work of a heart maintaining a systolic
`cedure (this is important because fear is a frequent cause of a
`blood pressure of 120 mm. Hg.
`Prolonged increase in
`raised ‘blood pressure) put
`the patient as flat as
`possible and
`apply the armlet to the upper arm well above the
`bend of the
`arterial resistance acts as a stimulus to the heart, increases
`elbow..See that both the patient and the arm are comfortable
`ventricular volume, and, by giving the heart more work,
`and relaxed. Apply a stethoscope to the inner side of the bend of
`causes hypertrophy.
`the elbow over the lower end of the brachial artery, and while
`The pulse pressure and the systolic pressure are raised by :
`listening pump up the armlet. At first there is no sound, but as
`the pressure rises a sound appears which is dull and indistinct at
`1. Excitement, nervousness, exercise.
`first, but later becomes loud
`and clear, and then as the pressure
`2. Tonic contraction of the arterial wall such as occurs in asthma,
`is raised further the sound gets softer and finally disappears
`migraine, etc.
`.
`entirely. Now let
`the pressure fall by just opening the valve
`3. Nephritis, acute and chronic.
`.
`;
`on the apparatus;
`the point at which the sound first reappears
`4. Aortic regurgitation (patent ductus arteriosus, and arterio-
`is the systolic pressure; allow ‘the pressure to fall further, and the
`point at which the loud clear sound becomessoft and dull is the
`venous aneurysm).
`.
`.
`.
`5. Organic diseases of
`the artery, senile fibrosis, and arterio-
`diastolic pressure. The finger on the radial pulse first detects
`sclerosis, although a raised blood pressure does not necessarily
`the pulse beat at a point just below systolic pressure as read by
`accompany arterial disease.
`.
`.
`the ear, but the finger cannot estimate
`diastolic pressure. Often the
`6. Hyperpiesis—the condition described by Sir Clifford Allbutt
`patient can tell the diastolic pressure, for as the pressure in the
`in which there is a primary rise of blood pressure.
`bag is raised there is a point at which a sensation of throbbing
`in the arm becomes very evident, and this is at or very near
`The pulse pressure and the systolic pressure are lowered
`diastolic pressure.
`by:
`to realize that an instrument only
`It
`is
`important
`resistance from relaxation of arterioles,
`1. Loss of peripheral
`becomes really helpful when it has been used so often that
`such as occurs
`in all atrophic and wasting diseases—phthisis,
`its use is easy andits fallacies are obvious. In no individual
`cancer, acute fevers, especially pneumonia and SypHaidke
`Anaemia from any cause,
`loss of blood (haemorrhage from
`does systolic or diastolic pressure remain constant: changes
`of position, exercise,
`food, or drugs produce changes of
`lungs, etc.).
`.
`Ly as
`.
`3. Gardiac asthenia in Addison’s disease and starvation.
`pressure which are more or less temporary. Excitement,
`4, Vagus overaction in fainting attacks, collapse, and shock.
`with its accompanying cardiac frequency, always causes a
`But apart from the detection of abnormally high or low
`considerable rise of pressure, so that it may be necessary
`pressures
`the sphygmomanometer gives us
`information
`* Read before the Coventry Division of the British Medical Association,
`December 4th, 1923.
`about the regularity of pulse pressure, and is therefore of
`
`1
`
`APPLE 1019
`
`1
`
`APPLE 1019
`
`

`

`THe Barrise
`Mepica JouBNAL
`1190 Dec. 27, 1924] CLINICAL USE OF THE SPHYGMOMANOMETER.
`
`
`|
`
`the greatest assistance in the diagnosis of cardiac irregu-
`larities, and indeed it often renders the electro-cardio-
`graphic or polygraphic examination of the patient needless,
`as it enables us to make an exact diagnosis.
`so
`is
`In auricular
`fibrillation—important because it
`common, because it often implies grave myocardial disease,
`and because in certain cases the condition is now curable
`by means of quinidine—the pulse is irregular in force as
`well as in time, and in the cases with unusually slowly
`acting hearts the irregularity may not be easily felt by the
`finger. But when the sphygmomanometer is applied the
`irregularity is at once obvious by the variation in the
`sound heard over the artery—a variation which makes it
`difficult
`to determine exactly either the systolic or
`the
`diastolic pressure, for as the pressure in the bag is raised
`the more feeble beats are cut out and the heart appears
`to be less frequent, until at a certain pressure only an
`occasional beat can be heard. There are several facts which
`may enable us to diagnose the condition without the use
`of any instrument at all: a markedly irregular heart in
`which the heart rate as counted at the apex is greater than
`that at the wrist, because the weakersystoles fail to open
`the aortic valves; or
`the association of marked pulse
`irregularity with the disappearance
`of
`a_
`presystolic
`murmur; or the marked slowing of the pulse which usually
`follows the use of digitalis, and the fact
`that neither
`exercise nor atropine as a rule produces either a greater
`regularity or a marked increase in heart rate.
`In the form of irregularity known as pulsus alternans
`the sphygmomanometer may enable us to detect the irregu-
`larity before it is obvious to the finger. Here the pulse
`is regular in time but the beats are alternately strong and
`weak. Occasionally there is a slight alteration in time
`also, and where this is present the longer pause follows
`the stronger beat.
`In some cases extra-systoles follow
`every normal beat,
`so that the pulse waves are felt as
`alternately strong and weak, but
`there is always a well
`marked irregularity in time, and the longer pause always
`follows the weaker beat; or, to put it in another way, the
`pulse is felt as two beats,
`the second of which is the
`weaker, and a pause. Except
`in the alarm that
`they
`occasion in the patient these extra-systoles are of no im-
`portance. The true alternating pulse is always indicative
`of a very serious condition; it is found in advanced cases
`of myocardial disease,
`in renal disease, and in advanced
`arterio-sclerosis;
`it
`is
`sometimes discovered
`in
`acute
`diseases such as pneumonia, typhoid, or influenza; and may
`be the only discoverable physical sign in patients with
`angina.
`In my experience this form of pulse irregularity
`always implies an early fatal termination of the condition
`in which it appears.
`The pulsus paradoxus is the pulse irregularity which is
`commonly associated with pericardial effusions.
`In this
`irregularity there is a failure of pulse volume during
`inspiration, so that at each inspiration the pulse either
`disappears entirely or becomes reduced in size. A slight -
`degree of
`this irregularity is produced by quite small ,
`effusions into the pericardium, but suchslight irregularity
`may be quite imperceptible unless it
`is sought
`for by
`means of
`the sphygmomanometer. Although the pulse
`pressure appears to be quite regular to the finger in such a
`condition, when the armlet is applied and the pressure in
`it is raised to near the systolic pressure the sound will
`be heard to vary markedly in intensity, being louder in
`expiration and softer or absent entirely during inspiration.
`Pericardial effusion may be particularly difficult to detect,
`and this sign is often of assistance in doubtful cases. Con-
`ditions which interfere with the inspiratory negative
`pressure in the thorax can also produce this pulse irregu-
`larity. A large pleural effusion, whether of gas or fluid,
`may lead to the paradoxical pulse, and in the war this
`irregularity was fairly commonly found in men with wounds
`of the chest, especially those in whom there was a large
`wound which allowed free ingress and egress of air to the
`pleural cavity at each respiration. Some children also
`show a slight degree of this irregularity of pulse volume
`in association with the juvenile type of
`irregularity in
`which the heart rate quickens during inspiration and slows
`during expiration.
`
`
`
`In heart disease severe heart failure may takeplace
`without any noticeable change in blood pressure, for the
`heart will maintain the blood pressures at or near the
`normal even when its output per beat
`is insufficient
`to
`ensure anefficient circulation. As Sir T. Clifford Allbutt
`says,
`‘‘ the heart dies sword in hand.’’ But sometimes we
`can recognize
`impending heart
`failure in changes
`in
`blood pressure.
`In cases of hyperpiesis, renal disease, cr
`arterio-sclerosis in which there has been a high pressure
`for years, a fall in the systolic pressure without any change
`in the diastolic pressure is significant, and whether it be
`associated with an increase in distress, or with dyspnoea,
`or appear alone,
`such a change in pressures is
`to be
`regarded with apprehension.
`It has recently been shown
`that the higher the diastolic pressure the greater must be
`the pulse pressure for the same diastolic output per beat;
`so when a patient with a high diastolic pressure shows
`a fall
`in systolic pressure without any corresponding fall
`jin diastolic pressure the output of his heart per beat
`is
`less, and, except there be a corresponding increase in pulse
`rate, his circulation is already beginning to fail. This
`fact shows the importance of reading the diastolic pressure
`as well as the systolic.
`One of the well known signs of aortic regurgitation is
`the collapsing pulse, which was described by Corrigan
`ninety-two years ago—its peculiar character being due to
`the combination of a raised systolic pressure and a lowered
`diastolic pressure.
`In adults with aortic incompetence the
`systolic pressure is always above 120mm. Hg, and the
`diastolic pressure is usually below 65mm. Hg. Often it is
`very difficult to ascertain the exact diastolic pressure, as the
`pulse sound is loud even when the pressure in the armlet
`is at zero. Sometimes the sound heard overthe arteryis so
`loud that it resembles a pistol shot.
`There is another curiosity in the arterial pressures in
`aortic disease which was first described by Professor Leonard
`Hill.
`In a normal
`individual standing up the arterial
`pressure in the leg at the knee is higher than the pressure
`in the arm at the elbow by the weight of a column of blood
`equal in height to the distance from the knee to the elbow;
`but when the normal man lies down, the pressures in arm
`and leg soon become approximately equal. On the other
`hand, in the great majority of cases of aortic regurgitation,
`when the patient is lying flat the pressure in the leg is con-
`siderably higher
`than that in the arm. The suggested
`explanation is that,
`in order to maintain a good supply
`of blood to the brain when the patient
`is erect, those
`arteries in which blood flow is retarded by gravity (those
`above the level of the heart) are completely relaxed, while
`those arteries in which the blood flow is assisted by gravity
`are in a state of tonic constriction, and that this spasm
`persists even when the patient is lying flat.
`In observing
`the leg pressures the armlet (or leglet) should be applied
`just above or just below the knee, and the stethoscope is
`applied either over the popliteal or posterior tibial artery.
`It is important to have a bag of sufficient width, as too
`narrow a bag gives high readings. The width of the bag
`should be about a quarter the circumference of the limb.
`While this peculiarity is not invariably present in aortic
`regurgitation there is usually a difference of 30mm. Hg
`between the systolic pressure in the arm and leg. The
`severity of
`the valvular
`lesion may be gauged by the
`pulse pressure—the higher the pulse pressure the worse the
`lesion; but if the diastolic pressure is 70 or more it is
`certain that the amountof the aortic regurgitation cannot
`be serious,
`In hemiplegia from a cerebral haemorrhage the pulse
`pressure is always high, while in a thrombosis the pulse
`pressure is less than the normal for the diastolic pressure.
`Jf the hemiplegic is found to have a high and rising pulse
`pressure heis sure to die of his haemorrhage, orif the pulse
`pressure is low andfalling he will die of his thrombosis.
`As an example of this statement I will quote a case, a man
`of 57, who had extensive arterial disease and a large heart.
`His blood pressure was 200/140.
`(Note that the normal
`pulse pressure for a diastolic pressure of 140 should be
`about 120mm. Hg, while here it
`is only 60mm. Hg,
`so
`that
`the systolic output of
`the heart must have been
`considerably: reduced.) The patient had several cerebral
`
`2
`
`

`

`CHRONIO INTESTINAL STASIS AND EPILEPSY.
`[wieder 1191
`DEO. 27, 1924]
`
`
`
`post-mortem exam-
`accidents, and finally succumbed. The
`thrombosis.
`ination showed a very extensive cerebral
`In enteric fever there are two accidents which it is often
`difficult to differentiate—perforation and haemorrhage.
`In
`the former a rise of blood pressure occurs after the primary
`shock, but in the latter the fall of blood pressure is always
`very marked andprolonged.
`.
`In pneumonia a rise of blood pressure before the crisis is
`often the first sign of some complication, while a fall may
`indicate impending heart failure.
`Finally, blood pressure observation may be of considerable
`assistance in cases of albuminuria, a high blood pressure
`indicating renal disease—either a nephritis or that type of
`renal damage which results from hyperpiesis or arterio-
`sclerosis.
`In pregnancy the sphygmomanometer may be
`especially helpful, for it is often difficult to decide how much
`importance should be attached to a small amount of albumin
`in the urine of a pregnant woman. The normal systolic
`pressure of a woman of about 30 of average physique is
`abcut 112 mm. Hg. A pressure of over 130 would suggest
`the need for careful and frequent examination, and a
`pressure of over 150 would probably indicate the onset of
`eclampsia.
`I do not think that a blood pressure of over 160 systolic or
`90 diastolic is ever normal, although there are casesin which
`the diastolic pressure remains about 100 for a time without
`anyascertainable cause, and then returns to normallimits.
`Excitement may cause such considerable rises of pressure
`that it is well to bear in mind the rule that a high pressure
`is of greatersignificance when accompanied bya slowpulse.
`BIBLIOGRAPHY.
`Corrigan: Edin. Med. and Surg. Journ., April, 1832.
`Stokes: Diseases of the Heart and Aorta, 1854.
`Oliver, T. : Studies in Blood Pressure.
`Hill, Leonard: Further Advances in Physiology, 1910.
`MacWilliam and Melvin: Heart, v, 1914.
`Bramwell, and Hill, A. V.: Proc. Roy. Soc., xciii, B, 192
`Bramwell, Hill, A.
`V., and McSwiney : Heart, x, 3, 1923.
`Lewis, Sir T.:; Heart, x, 4, 1923.
`
`
`CHRONIC INTESTINAL STASIS AND EPILEPSY.*
`BY
`
`A. WHITE ROBERTSON, L.R.C.P. anv S.Epry.,
`LONDON.
`
`Ix the study of epilepsy it seems clear that whatever the
`actual exciting element the vascular system is the main
`source of the epileptic phenomena, either alone or as a
`carrier of toxic agents, and the work that has been done
`experimentally by the advocates of both views has been very
`considerable in the last twenty years. Cells cut off from
`theircirculation, even momentarily, show a reaction towards
`acidity, and this acidity factor must not be lost sight of in
`the interpretation of the experimental results recorded by
`the mechanical and vascular theorists. Faradization, and
`epinephrin will also blanch pial vessels and produce epilepti-
`form convulsions. The proteoses of Cuneo, to be presently
`described, have the same effect when painted on the cortex.
`Lastly,
`lactic acid given intravenously will also produce
`convulsive seizures. Acidosis, therefore, whether produced
`locally or remotely, would appearto play a considerable role
`in the production of the epileptic convulsion, and the work
`of Cuneo! during the last nine years at Genoa goes perhaps
`further than that of any other investigator to establish
`its importance.
`in the blood of persons
`Cunco established the presence,
`who had just had an epileptic seizure, of a substance which
`he identified with the proteoses, and this substance intro-
`duced intravenously into animals faithfully reproduced the
`epileptic phenomena. At the same time he showed that the
`urine of these persons contained an extraordinarily high
`percentage of organic acids. Other features were a reten-
`tion of total nitrogen, an increase in the nitrogen content,
`and continuous acidity of
`the faeces. Comparative tests
`in epileptic groups with a protein-rich and with a carbo-
`hydrate-pure diet next gave unexpected results, the acidosis
`
`in the former group being reduced, with a corresponding
`* An address to the Tunbridge Wells Division of
`the British Medical
`Association, February 27th, 192
`
`improvement in the severity and numberof thefits, whilst
`there was a percental
`increase in acidity in the second
`group, and the fits increased in number andseverity.
`It
`was next established that the fault in the starch metabolism
`occurred in thefirst stage of conversion to the disaccharides,
`maltose, lactose, cane sugar, etc. Normally this takes place
`through the action of the amylolytic ferments,
`the sub-
`sequent conversion of maltose being effected by maltase
`ferment through hydration into glucose. The failure in the
`first stage resulted, in the absence of sufficient amylolytic
`ferment, in the production of a more or less intense concen-
`tration of organic acids—acetic, butyric, lactic, tartaric,etc.
`—and these, which should normally have been united with
`alkaline bases in the small intestine, passed in the epileptic
`into the blood stream and urine unchanged.
`Thealkaline
`salts in normal
`individuals are oxidized—if ammoniacal
`through ammonium carbonate into urea,
`if sodium into
`sodium carbonate, and this is the vitally necessarysalt for
`maintaining the alkalinity of the blood and tissues. Cuneo
`concludes from his work that this transformation of organic
`salts into sodium carbonate begins in the mucosa of the small
`intestine and is completed in the liver, whence the sodium
`carbonate is returned to the gut with the bile. Lack of
`bases favours the production of acidosis, while a sufficiency
`of sodium tartrate favours the activity of the liver ferments
`and the preduction of sodium carbonate.
`If sodium acetate
`or tartrate is introduced directly into the circulation it
`causes typical epileptic convulsions, and Cuneo was able to
`remove from the carotid artery of
`the animals used a
`substance which proved to be a proteose.
`The source of these proteoses Cuneo found in the reduc-
`tion of that fundamental constituent of all cellular nuclei,
`nucleo-histone, and in the case of the serum and leucocytes
`of the blood also this reduction takes place under conditions
`of acidosis due to the concentration of organic acids.
`In
`an acid medium hewas able to demonstrate the reduction of
`nucleo-histone from both these sources into an innocuous
`acid and a toxic base having the chemical and biological
`properties of nucleinic acid and of proteose.
`Introduced
`intravenously in dogs the latter not only produced typical
`epileptic convulsions, but the gost-mortem appearances in
`dogs dying in status epilepticus so induced were identical
`with those found in the viscera and the brain and its cover-
`ings in persons dying of proteosaemia (albumosaemia), and
`as described by Tanzi and Lugaro in their findings in
`patients who died in typical status epilepticus.
`He believes that albumosaemia exists in epilepsy and that
`this is caused by an insufficiency of the alkali-forming func-
`tion in the liver and the small intestine, so that the acid
`organic salts, which are transformable into sodium car-
`bonate, do not undergo this metabolic change, but enter the
`circulation and cause a division undercertain conditions of
`the nucleo-bistone element and the nucleo-proteins into
`nucleinic acid and proteoses. These latter remain free and
`exhibit their convulsive action.
`;
`Localized acidosis in derangements of
`the circulation
`mayalso set free albumoses, or it may be other toxins,
`as in Jacksonian seizures; and in the convulsions associated
`with cranio-cerebral
`injury with scar adhesions, brain
`abscesses, circumscribed areas of encephalitis, brain tumour,
`cysts, general paralysis,
`cerebral arterio-sclerosis,
`the
`acidosis produced by interference with the vascular supply
`may, as suggested by Professor Osnato,? determine the
`release of proteoses locally in cells cut off
`from their
`circulation, and so excite the convulsions associated with
`these conditions.
`In general paralysis and arterio-sclerosis,
`and probably also in encephalitis, the vascular disturbances
`and the local cellular destruction processes in the brain
`elements are ideally combined to produce generalized
`convulsive seizures.
`A little over two years ago it was my privilege to address
`you on the possibility of proving a close connexion between
`epilepsy and chronic intestinal stasis. More recently I
`have published a preliminary report? on a small group of
`epileptics treated on lines directed exclusively to the relief
`of the gastro-intestinal conditions found associated in these
`patients with the epileptic phenomena. To-day, thanks to
`Cuneo’s researches, I find myself in a stronger position to
`press the importance of chronic intestinal stasis as @
`
`3
`
`3
`
`