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POSTURAL STRESS TESTS FOR THE CLINICO-PHYSIOLOGICAL EVALUATION OF CARDIOVASCULAR REFLEXES M. B. DIKSHIT* Nottingham, U. K. Summary: Postural stress tests are useful in the assessment of cardiovascular reflex response of normal subjects who may be involved in specialised occupations such as flying; in order to stuoy the effects of physiological stresses such as heat stress, hyopoxia, simulation of weightlessness; physiological evaluation of cosmonaut candidates, in patients who may have autonomic neuropathy. Most commonly quiet standing is used but head-up tilt table test and the application of lower body suction may provide a better method of evaluation. These three tests for assessing reflex cardiovascular function are discussed. Key words blood pressure head-up tilt heart rate postural hypotension The maintenance of normal blood pressure and the limitation of the peripheral blood pooling (which occurs because of a shift of blood in to the legs) during postural stress is a function of cardiovascular reflexes. In certain work situations for. example in aviation (during the application of exaggerated postural stress produced by radial acceler- ations) inadequacy of these reflexes can cause hypotension which may be severe enough to produce episodic unconsciousness. Other physiological stresses such as hypoxia (12, 24), exercise (30), space flight (31) and heat exposure (32) may alter tolerance to postural stress and may need investigation. In clinical situations an abnormality of cardiovascular reflex response during postural stress may indicate the presence of neurological disorder (4) or adverse effects of a drug. It may therefore become necess- ary to eva!uate the integrity of the cardiovascular reflexes in apparently healthy indivi- duals (such as aircrew) who may present with a clinical history suggestive of intolerance to postural stress (15), for assessing a subject's cardiovascular function during various physiological stresses, or in the clinical evalution of patients with neurological disorders (4). Such an assessment can be done using postural stress tests in the field, by the bedside. or in the laboratory. Present address: Department of Physiology, Armed Forces Medical College. Pune-411 001. India.

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Page 1: POSTURAL STRESS TESTS FOR THE CLINICO … archives/1987_31_1/1-11.pdf · POSTURAL STRESS TESTS FOR THE CLINICO-PHYSIOLOGICAL EVALUATION OF CARDIOVASCULAR REFLEXES M. B. DIKSHIT* Nottingham,

POSTURAL STRESS TESTS FOR THE CLINICO-PHYSIOLOGICALEVALUATION OF CARDIOVASCULAR REFLEXES

M. B. DIKSHIT*

Nottingham, U. K.

Summary: Postural stress tests are useful in the assessment of cardiovascular reflex

response of normal subjects who may be involved in specialised occupations suchas flying; in order to stuoy the effects of physiological stresses such as heat stress, hyopoxia,simulation of weightlessness; physiological evaluation of cosmonaut candidates, in patientswho may have autonomic neuropathy. Most commonly quiet standing is used but head-uptilt table test and the application of lower body suction may provide a better method ofevaluation. These three tests for assessing reflex cardiovascular function are discussed.

Key words blood pressure head-up tilt heart rate postural hypotension

The maintenance of normal blood pressure and the limitation of the peripheralblood pooling (which occurs because of a shift of blood in to the legs) during postural

stress is a function of cardiovascular reflexes. In certain work situations for. example inaviation (during the application of exaggerated postural stress produced by radial acceler­ations) inadequacy of these reflexes can cause hypotension which may be severe enoughto produce episodic unconsciousness. Other physiological stresses such as hypoxia(12, 24), exercise (30), space flight (31) and heat exposure (32) may alter tolerance topostural stress and may need investigation. In clinical situations an abnormality ofcardiovascular reflex response during postural stress may indicate the presence of

neurological disorder (4) or adverse effects of a drug. It may therefore become necess­ary to eva!uate the integrity of the cardiovascular reflexes in apparently healthy indivi­duals (such as aircrew) who may present with a clinical history suggestive of intoleranceto postural stress (15), for assessing a subject's cardiovascular function during variousphysiological stresses, or in the clinical evalution of patients with neurological disorders(4). Such an assessment can be done using postural stress tests in the field, by thebedside. or in the laboratory.

Present address: Department of Physiology, Armed Forces Medical College. Pune-411 001. India.

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2 Dikshit January- March 1987Ind. J. Physio!. Pharmac.

Postural stress reduces the intra-thoracic blood volume and shifts it in to the legswhere it forms a pool, thereby producing a fall in blood pressure and a reduction in the

circulating blood volume (40). Compensation to this is brought about by (i) a reflextachycardia and (ii) arteriolar constriction which are aimed at maintenance of the arterialblood pressure and. (iii) venoconstriction which helps to limit the expansion of tho blood

pool in the legs. keeps up the pre-load. and is helped by the increased activity of theabdomino-thoracic respiratory pump, the pumping action of the leg muscles and thevenous valves (40). The details of the physiological mechanisms involved in bringing

about the cardiovascular effects are not in the perview of this paper and can be foundelsewhere (1,4,22).

Heart rate and arterial blood pressure are the variables commonly measured toassess the reflex integrity (13, 15), and if facilities permit peripheral vascular resistancemay be measured.

Various methods can be employed to give the postural. stress and can involvequiet standing, head-up tilting (both of which produce a change in posture from thesupince to the erect) and the application of lower-body subatmospheric pressure (LBSP).

Quiet standing: By far the simplest test for eliciting cardiovascular response to

postural stress is Quiet standing for 5-20 minutes after the heart rate and blood pressurehave stabilised while supine. The change of posture displaces about 600 mlof blood from

the thorax in to the legs (44), deactivates arterial baroreceptors to produce a reflex

tachycardia (2) which is mediated mostly by vagal tone withdrawal (20), produces aslight fall in the systolic blood pressure, and a slight increase in the diastolic bloodpressure.

The immediate heart rate increase on sti:nding in healthy young subjects is seenby about the 15th beat (20), and this 13tar settles down to a steady state valuewhich is about 10-15 beats min-1 higher than the supine value. In the elderly (65years and above) (10) and in patients with autonomic neuropathy (4) the tachycardiaresponse is markedly attenuated and may be accompanied by postural hypotension.

The immediate cardiovascular changes are difficult to demonstrate unless continuousinstant heart rate and intra-arterial blood pressure monitoring are available. The blood

pressure can be measured by an independent observer using a spygmomanometer whileit is best to monitor ECG for heart rate. Instant heart rate measurement by a rate-meteris the method of choice if the equipment is available but in the absence of any recording

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Volume 31Number 1

Orthostatic Stress Tests 3

~acilities, counting of the apex beat by an independent observer using a stethoscope maybe resorted to. Palpating a peripheral artery may be confusing. If available, a random-zerospygmomanometer which eliminates observer bias (39) should be used for blood pressuremeasurements which can be made comfortably at 1 minute intervals. The spygmomano­meter cuff is inflated above the resting systolic blood pressure level before the subjectstands up so as to enable the observer to make the earliest possible measurement after thestress is given in order to reduce the disadvantage of not having an on-line bloodpressure record from an indwelling arterial cathetp.r.

The passive standing test recommended by Hyatt et al. (26) may also be used. In

this the subject on rising from the supine position. leans his back against a wall withhis heels 6 inches in front of the wall, and relaxes in this position for the duration ofthe test.

One of the criticisms of the standing test is that calf muscles are activated whilestanding and aid venous return, and that this may modify the cardiovascular response (36),but this drawback is offset by the simplicity of the test which can be given in the field,by the patient's bedside and in the laboratory with equal ease and with minimum

equipment.

Head-Up tilt test: The head-up tilt (HUT) is used extensively as a postural stresstest in physiological (12,13,14,15,48), and in clinical investigations (4, 11,27,28)

where reflex cardiovascular response may be affected.

To carry out the test, the subject is strapped supine on to a tilt table which canbe rapidly tilted to the required head-up position mechanically or manually. Physiolo­gical measurements are made while the subject is supine, immediately on tilting, andthereafter at suitable intervals up to 20 minutes. The heart rate however should be moni­tored continuously using a cardiac monitor as far as possible in order to detect adversereactions at an early stage. Otherwise the method can be the same as that used in thestanding test. The test is normally performed in a thermally controlled laboratory at about25°C, and at fixed time of the day to avoid circadian variations (3, 29). The subject isnormally supported by a torso harness and by a soft saddle in the tilted positon. These

device are comfortable (15). The presence of a foot'board during tilt is likely to activate themuscles because of weight bearing, and in turn promote muscle pumping which may affectthe cardiovascular response because of an increase in the venous return but others suggestthat the foot board does not affect the results (36) It is our practice to avoid the foot

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4 Dikshit January-March 1987Ind. J. Physiol. Pharmac.

support. After the subject's blood pressure and heart rate stabilize. he is tilted rapidly« 5 sec) head-up. Various degrees of tilt ranging from 30° to 90° have been used(15, 21, 35, 47). but 70° head-up has been most common as the cardiovascular effectsproduced using this angle are simi! ar to those produced with 90° HUT (sine angle 70° =0.94 and sin 90°=1; (21,35», but without the attendent discomfort. The rate of tilt isimportant as it affects the reflex response of the cardiovascular system (36).

The normal cardiovascular response to HUT is a reflex increase in heart rate, anincrease in the diastolic blood pressure, little or no change in the systolic blood pressure(Fig. 1) and an increase in the mean arterial pressure (15). The tachycardia seen during

+ + +

I? 16

Fig. 1: Mean and SE values for the diastolic (DB?), me~n arterial (MAP) and systolic (S8P) bloodpressure (mmHg). and heart rate beats/min (H R) while supine (S). immediately on 70°head-up tilt (0 min) and at 3 min intervals during the 20 min of HUT (lung strippled area)and during 4 min of post-tilt recovery in the supine posture (short strippled area) in 20normal young males. Time peliods from supine to 0 min HUT to 0 min recovery are notto scale.

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Volume 31Number 1

Orthostatic Strees Tests 5

HUT differs slightly from that seen with standing because the relative vagotonia afterabout the initial 30 beats seen with the latter is not observed with the former. The

cardiac and stroke volume indices calculated from the left ventricular ejection time (23)reduced by about 17% and 35% respectively (16), and the myocardial contractilitymeasured from the systolic time intervals (49) is significantly compromised even in normalsubjects (17).

Head-up tilt table test. though a good technique for assessing cardiovascular res­ponse to postural stress, is not always found comfortable by all the subjects. Vestibularstimulation may occur during the rapid change in body position (1). In case of a syncope,reverting to the supine posture can take time. Its main advantage over the standing testis that to an extent the central blood volume content can be depleted in a graded mannerby giving the subject increasing degree of HUT. However in both these tests the physiolo­gical effects produced by the low-pressure cardio-pulmonary receptor and the arterialbaroreceptors can not be separately studied.

Lower-body subatmospheric pressure.' The application of lower-body subatmos­pheric pressure (LBSP or lower body suction) at the level of the iliac crests produces acentral hypovolaemia without a change in posture (9) because the blood is shifted fromthe chest in to the lower limbs by the pressure gradient created by the suction betweenthe upper and lower regions of the body (51).

Lower-body suction is applied using a domestic vacuum cleaner connected to thesuction box via an adjustable leak. A foot plate prevents a downward shift of the subjectduring suction. A seal must be applied around the waist in order to prevent a loss of thedesired suction pressure. Various methods of doing this have been advocated (51). One

of the simpler ones get the subject to wear a plastic "skirt" tightly around the ""aist andthen mount its free end over the box edges (5, 18). A pressure transducer, or more simply,a mercury or water manometer is used to monitor the degree of suction. Electrical con­trols should include an on/off switch for instantaneous termination of the suction and a

rheostat control to regulate the rate o(application.

At suction pressures below 30 mmHg, there is no change in heart rate or bloodpressure despite a reducation in the central venous pressure, but the forearm blood flowdecreases because of a sympathetic vasoconstriction mediated by the low-pressure cardio­vascular receptors (1, 22). At higher suction pressures the heart rate increases the systolicblood pressure falls and the diastolic BP increases slightly (18, 37), but there is no further

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6 Dikshit January-March 1987Ind. J. Physio!. Pharmac.

significant change in the forearm vasoconstriction (Fig. 2). The mean arteria! pressure isnot affected until a suction of 60 mmHg and above is aptllied (37). When applied in a gra­ded manner, LBSP produces incremental central hypovolaemia and progressive increasein the heart rate (37). Normal subjects may suffer a vaso-depressor syncope at a LBSP

60

FVR 1.0MM HG/ML100MljMIN

20

+ +

Ol------L--....I.-----'I.----'

I.

Mean and Se.'values for the mean arterial pressure'(MAP mmHg). heart rate (HR; beats!min). forearm blood flow (FBF ml!100 ml!min) and forearm vascular resistance (FVRmmHg/ml/100 ml/min) when 0, 30. 40 and 50 mmHg Lower bcdy subatmosphericpressure (LBSP) is applied continuously for 5 mm each in healthy young males (N=9) inthe supine posture in an incremental manner.

+50

+1.0

MM HG

o 30

lBSP

+- +

HR70--I

MIN

SO

100MAP

MM HG 80

FBFML/100ML/MIN2

o!'""'"---""__...a..-_----'__...J

90

Fig. 2:

of 50-60 mmHg applied for 10 min while at even higher degree of suction, the syncopemay occur sooner (37). The cardiovascular effects of standing and LBSP of 40 mmHgare equivalent because an equal volume of blood (about 600 m/) is displaced peripherallyin both the conditions (38, 44).

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Volume 31Number 1

Orthostatic Stress Tests 7

Lower-body suction can be applied in a controlled manner to selectively deactivatelow-pressure cardiovascular receptors (at pressures between 10-30 mmHg), and then todeactivate the arterial baroceptors at suction pressures above 30 mmHg (2). In thismanner the reflex effects mediated by the low-pressure and the high pressure barore­ceptors can be separately investigated. The procedure can be safely used to inducepostural hypotension in a controlled manner (37). Further this method of simulating pos­tural stress eliminates some inherent disadvantages of head-up tilt, the interruption whichoccurs while making physiolog ical measuresments in the process of tilting, and also thesetting-up of gravity induced hydrostatic pressure gradients in the cardiovascular system,making it an excellent technique for assessment of cardiovascular reflexes in human sub­jects in health and disease.

Variabilty of cardiovascular response to postural stress tests: Inter individual vari­abilty of the response of the cardiovascular variables to postural stress is high for tilt heartrate and di .stolic blood pressure, but comparatively low for systolic blood pressure (43.46). In a large series of 166 head-up tilt tests in normal young males. the coefficient ofvariation of the systolic blood pressure. diastolic blood pressure. the mean arterial pressureand the heart rate was 6.8%,9%,7.5% and 14% respectively (15). Similar pattern of

variabilty was observed during LBSP (50). Smith et al. (46) concluded that the heartrate WiiS the most sensitive index of postural stress as it correlated well with the reductionin the intra-thoracic blood volume, but was the least reliable because of its high vari­ability while the systolic blood pressure was the most reliable as it showed the leastvariability.

The overall intra-individual variability for the cardiovascular variables on the otherhand is comparatively less (46. 50). Nevertheless some subjects may sh~w greater consi­stency than others during postural stress, and it is suggested that while interpreting anindividual response during the stress. an average of about 2-3 values for each variable

during the test is taken in to consideration. Averaging more data has no' added advant­age as it has no further effect on variability (52). It has been our practice to base theassessment of patients with a past history of syncope/pre-syncope on at least 3 stresstests(15).

Abnormal response to postural stress tests: A systolic hypotension (20 mmHg or

more) with or without an episodic loss of consciousness constitutes the main abnormalresponse to postural stress. This has been reported in apparently normal healthy youngadults (25,30), and in patients with autonomic neuropathy (4) who are subjected topostural stress. We however did not find any incidence of postural hypotension in a

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8 Dikshit January- March 1987Ind. J. Physio!. Pharmac.

large series of tilt tests in normal military personnel (15). This difference in findingcould be attributed the difference in the methods used in applying the postural stress; tothe better tolerance of heat adapted subjects to the stress; or to ethnic differences.

In the common variety of the abnormal response which may be seen in apparentlynormal individuals, the sequence of events which culminates in to postural hypotensionconsists of tachycardia, fall in systolic blood pressure, a narrowing of the pulse pressurefollowed abruptly by a precipitous fall in the systolic BP and a bradycardia. This sequenceof events has been described as the sympathicotonic response (41) and is often accom­panied by restlessness, sighing respirations, sweating, nausea and a feeling of Iight­headedness. The reaction usually interrupts a normal reflex response and may occurwhen the compensatory activity which is aimed at maintaining arterial blood pressure annlimit the peripheral blood pool formation is inadequate. This may happen because ofprolongation of the stress, dilatation of skin blood vessels during heat exposure, and asympathetic cholinergic vasodilatation of the muscle resistance vessels brought about byemotional distress, fear, anxiety, pain and discomfort (7,42), or by standing in thehyperlordotic posture (as on parade) (8). A pre-existing reduction in circulating fluid

volume because of dehydration (as in heat exposure) and haemorrhage can furtheraggravate the situation. The hyper-excitation of the sympathetic nervous system thatensues is accompanied by pre-syncopal symptoms, and signs which include markedtachycardia. falling systolic blood pressure, sweating and pallor. Th profound brady­cardia and the precipitous fall in systolic and diastolic blood pressure that may followhave been attributed to a va so-depressor reflex activated by the stimulation of ventricularwall pressure receptors (42, 45). There is evidence that the sympathe-tic venoconstrictionis unaffected during the syncopal reaction (19). The subject recovers rapidly on cessa­tion of the postural stress when the tempornrily sequestred circulating blood volume israpidly restored to normal.

In the more serious variety of postural hypotension [the asympathicotonic rec;ction ;(41)] there is a progressive fall in the arterial blood pressure without a change in the heartrate. It is usually found in patients with neurological disorders such as diahetic autono­mic neuropathy, Shy- Drager's syndrome. and tabes dorsalis (4, 6, 33) but may also beseen in normal elderly individuals (> 65-70 years of age) as a result of structuralchanges in the vascular tree or autonomic dysfunction (10,34).

In conclusion, cardiovascular reflex effects can be assessed using various posturalstress tests effectively for physiological and clinical investigations in the field, by thepatient's bed side. or in the laboratory using more elaborate equipment. Physiologists,clinicians and medical students can make use of these tests to assess or understand cardio­vascular reflex response in man in health or disease.

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Volume 31Number 1

REFERENCES

Orthostatic Stress Tests 9

1. Abboud, F.M., D. D. Heistad, A. L. Mark and P. G. Schmid. Reflex control of the peripheral cir­culation. Plog. Caldiovasc. Dis., 18 : 371-403. 1976.

2. Abboud. F.M .• D.L. Eckberg. U.J. Johannsen and A.L. Mark. Carotid and l>aroreceptor control ofsplanchnic and forearm vascular resistance during venous pooling in man. J. Physiol. (London),286 : 173·184, 1979.

3. Aschoff, J. and J. Aschoff. Diurnal rhythms of orthostatic cardiovascular response. Pflug. Alch.,306 : 146-152, 1969.

4. Bannister. R. Testing autonomic reflexes in Autonomic Fai/ule; edited by R. Bannister; Oxford Medi­cal Publications Oxford; p 52-63, 1983.

5. Bennett, T., D. J. Hoskins and J. R. Hampton. Cardiovascular responses to lower body negativepressure in normal subjects and in patients with diabetes mellitus. Caldiovasc. Res., 13 : 31-38.1979.

6. Bennett. T. Physiological investigation of diabetic autonomic failure in Autonomic Fai/ule; edited byR. Bannister; Oxford Medical Publications Oxford. p 406-436. 1983.

7, Blair D. A .• W. E. Glover, A. D. M. Greenfield and I. C. Roddie. Excitation of cholinergic vasodi­lator nerves to human skeletal muscles during emotional stress. J. Physiol. (Land.). 148 : 633-647,1959.

8. Bridgen. W.. S. Horvath and E. P. Sharpey-Schaefer. Postural blood flow of normal subjects withobservations on vasovagal fainting reactions as a result of tilting. lordotic posture. pregnancy andspinal anaesthesia. Clin. Sci., 9 : 79-91. 1950.

9. Brown. E.. J. S. GoeL A. D. M. Grennfield and G. C. Plassaras. Circulatory responses to simulatedgravitational shifts of blood in man induced by exposure to the body below the iliac crests to sub­atmospheric pressure. J. Physiol. (London), 183 : 607-627, 1966.

10, Collins, K.J .• A.N. Exton-Smith, M.H. James and D.J. Oliver. Functional changes in the autonomicnervous responses with aging. Age and Aging, 9 : 17·24, 1980.

11. Cryer, P. Disorders of the sympathetic neural function in human diabetes mellitus: hypoadrenergicand hypoadrene/gic postural hypotension. Metabolism. 29 : 1186-1189. 1980.

12. Dikshit. M.B. and P.C. Chatterjee. Changes in orth cstatic tolerance duri ng short duration mi Id hypoxiaAviat. Med., 20 : 9-14. 1976.

13. Dikshit. M.B. Comparative cardiovascular responses to 70° head-up tilt in pilots and non·pilots. Aviat.Med.. 27: 36-42. 1983.

14. Dikshit. M.B., P.K. Bannerjee, J.S. Kulkarni. E.M. Iyer and M.M. Singh. Medical evaluation of cosmo­nauts: phy~iological stress testing. Aviat, Med., 28 : 107-115, 1984.

15. Dikshit, M.B., P.K. Bannerjee and P. L.N. Rao. Orthostatic tolerance of normal Indians and those withsuspected abnormal cardi ovascular reflex status. Aviat. Space end Envilon. Med.. 57 : 168-173.1986.

16 Dikshil. M.B., P.K. Bannerjee. P.L.N. Rao and E.M. Iyer. Left ventricular ejection time based cardiacoutput changes in pilots and non-pilots during orthostatic stress. Indicn J. Med. Res .. 83 : 301-303.1986.

17. Dikshit. M.B., P.K. Bannerjee, P.L.N. Rao and E.M. Iyer. Systolic time intervals in pilots and non­pilots during 70e head up tilt. Aviat. Space and Envilon. Med., 57 : 332-335. 1986.

18. Dikshit, M.B. and J.M. Patrick. Forced expiratory flow-volume curves during the application of lower­body negative pressure. Submitted to EUlop. Bull. Physiopath. Respilat. Clinical Respilat. Physio/..1986.

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10 Dikshit January-March 1987Ind. J. Physiol. Pharmac.

19. Epstein, S.E., M. Stampfer and G,D. Beiser. Role of capacitance and residence vessels in vasovagalsyncope. Circulation, 37 : 524-533, 1968.

20. Ewing, D.J., L. Hume. I.W. Campbell, A. Murray, J.M.M. Nielson and B,F. Clarke. Autonomicmechanisms in the control of initial heart rate response to standing. J. Appl. Physiol., 49 : 809·814,1980.

21. Gauer, D.H. and H.L. Thron. Postural changes in circulation. Handbook of Physiology. Section 2.Circulation III. Washington D.C., Amer. Physiol. Soc.. 2409p·2439p, 1966.

22. Grassi, G., C. Gavazi. A. Cessura, G.B. Picotti and G. Mancia. Changes in plasma catecholaminesIn responses to reflex modulation of sympathetic vasoconstrictor tone by cardiopulmonary receptors.Clin, Sci.. 68 : 503-510, 1985.

23. Harley, A., C.F. Starmer and J.C. Greenfield, Pressure flow studies in man. An evaluation of theduration of the phases of systole. J. Clin. Invest., 48 : 895·905, 1969.

24. Heist<ld, D.O. and RC. Wheeler. Effect of acute hypoxia on vascular responsiveness in man. J. Clin.Invest. 49: 1252-1265, 1970.

25. Hickler, R.B., R.G. Hoskins and J.T. Hanilin. The clinical evaluation of faulty orthostatic mechanisms.Med. Clin. N, Am., 44 : 1237 -1250, 1960.

26. Hyatt, K.H., L.B. Jacobson and V.S. Schneider. Comparison of 700 tilt, lBNP, and passive standin9as measures of orthostatic tolerance. Aviat. Space and Environ. Med., 46 : 801-808, 1975.

27. Ibrahim, M.M. locolization of lesion in patients with idiopathic orthostatic hypotension. Br. Heart J ..37 : 868-872, 1975.

28. Jeffrey, F.. K. Fareeduddin and W.H. Abelman. Increased tolerance of patients with circulatory con­gestion to orthostatic stress. Am. J, Med. Sci.. 259 : 323-332, 1970.

29. Klein, K.E.. H.M. Wegmann and H. Brunner. Circadian rhythm in human performance, physical fitnessand stress resistance. Aerospace Med., 39 : 512-518, 1968.

30. Klein, K.E., H. Brunner, D. Jovy, L. Vogt and H.M. Wegmann. Influence of stature and physicalfitness on tilt and acceleration tolerance. Aerospace Med., 40 : 293-297, 1969.

31. Klein, K.E., H.M. Wegmann and P. Kuklinski. Atheletic endurance training-Advantage for spaceflight?: the significance of physical fitness for selection and training 01 Spacelab crews. Aviat Space­and Environ. Med., 48 : 215·222, 1977.

32. lind, A. R., C. S. leithead and G. W. McNicol. Cardiovascular changes during syncope inducedby tilting men in the heat. J. Appl. Physio/" 25 : 268-276, 1968.

33. low, P. A., J. C, Walsh, C. Y. Huang and J. G. Macleod. The sympathetic nervous system Indiabetic neuropathy. Brain, 98 : 341 -356, 1975.

34. Maclennan, W. J., M. R. P. Hall and J. I. Timothy. Postural hypotension in old age: is it adisorder of the nervous system or of blood vessels? Age and Ageing, 9 ; 25-32, 1980.

35. Matalon, S. V. and L. E. Farhi. Cardiopulmonary readjustments in passive tilt. J, Appl. Physiol.Respirat. Environ, and Exercise Physioi.. 47 : 503-507, 1979.

36. Murray, R. H., J. A. Bowers and W. H. Abelman. Comp rison of foot board and saddle supports fororthostatic tests on a til t table. J. Appl. Physiol.. 21 : 1409-1411, 1966.

37. Murray, R. H. L. J. Thomson, J. A. Bowers and C. D. Albright. Hemodynamic effects of gradedhypovolemia and vasodepressor syncope induced by lower body negative pressure on the cardiovascularsystem. Am. Heart J., 76 : 799-811, 1968.

38. Musgrave, F. S., F. W. Zechman and R. C. Mains. Comparison of 70 0 tilt and several levels otlower-body negative pressure on heart rate and blood pressure in man. Aerospace Med.. 42 :1065·1069,1971.

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Orthostatic Stress Tests 11

39. Raftery, E. B. The methodology of blood pressure recording. Sr. J. Clin. Pharmacol., 6 : 193·202,1977.

40. Rushmer, R. F. Cardiovascular Dynamics; 4th edition; W. B. Saunders Co.• Toronto, 1976.

41. Schneider, P. B. Orthostatic hypotension. Arch. Int, Med.. 110 : 240-248, 1962.

42 Sharpey·Schaefer. E. P., C. J. Hayter and E. D. Barlow, Mechanisms of acute hypotension fromfear or nausea. Srit. Med. J .. ii : 878·880, 1958.

43. Shvartz, E. Reliability of quantitative tilt table data. Aerospace Med.. 39 : 1094-1097 1968.

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