ANTI-G SUIT INFLATION EFFECTS DURING LOW-INTENSITY -/ + GZ MANEUVERS

Michael Nicholas Colapinto

A thesis submitted in conformi ty wi th the requirements for the degree of Master of Science

Gradua te Department of Community Heal th University of Toronto

@ Copyright by Michael Nicholas Colapinto 2000

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Abstract

ANTI-G SUIT INFLATION EFFECTS DURLNG LO W-INTENSITY -/+ GZ MANEUVERS

For the dcgree of Master of Science, 2000 Michxi Nicholas Colapinto Graduate Depart ment of Community H d t h University of Toronto

Purpose: It was hypothesized that early initiation of G-suit inflation with increased

pressure and rate would offer greater protection agaïnst the hypotensive response ("push-

pull effect". PPE) resulting from -/+Gz transitions ("push-pull effect maneuver", PPEM)

venus the existing inflation schedule.

Methods: Using a tilt table, subjects were rapidly tilted from HUTL (15' from vertical;

+l Gz) to HDT (135'; -0.71 Gz for 15 secs) to HUT2(1S0. for45 secs). Physiological

measurements for 1 unprotected and 4 protection schedules were analyzed.

Resulîs: Al1 G-suit schedules maintained b l d pressure suggesting inflation is an

adequate protecti ve measure during low-intensi ty PPEMs. Few statisticall y signi ficant

differences were observed between the protection schedules.

Conclusions: (1) G-suit inflation arneliorated the hypotensive response to the PPEM, (2)

Results were not conclusive as to whether inflations of certain timing or pressure will

further melionte this hypotensive response. An inmased G-envelope and operationally

proper inflation pressures are recomrnended for futun investigations.

Acknowledgements

There are so many people that 1 would Iike to thank for both direct and indirect

involvement in the successful completion of this thesis. Fint and foremost, 1 must thank

my supervisor, Dr. Len Goodman. 1 cm not express how important his guidance was to

me. If you are one of his future students reading this thesis. consider younelf lucky to

have such a kind, helpful, intelligent, and congenial mentor.

1 would also like to thank my fellow students Paul Handley, Carmen Hertzenkg,

Tim Mandzak, and Farheen Rashid, dong with Capt. Helen Wright and 2Lt. Victor Mota,

for king there for a chat, a joke, or even the odd compiiiint; not that 1 was bitter or

anything. (1 apologize to those who do not understand the previous staternent. Along with

the terms "Scowley" and "Sideshow" it is an inside joke).

I must also thank the subjects who partook in this experiment. Without you, this

would not have been possible. Thankî goes to Jim Maloan and Ted h o n for their

invaluable technical expertise as well as Vahid Askan, Bill Fraser, and the entire ALSS

and SAILSS groups for their assistance. 1 would especially like to thank Tom Gee for his

help with the UNM programs (some day I'm going to ask him how the heck he

understands this stuff!) md Macella Maxwell for providing me with wonderful colour

slides for my defence.

My thanks is also extended to Pierre Turgeon for his assistance with the barocuff

(my original project) and for ensuring that 1 was never zapped once by the radio-

frequency sealer. A special thank you to Gary Macpherson for allowing me to use the

garage gyrn and, therefore, enabling me to keep my sanity. 1 must also thank Bill Martel1

for keeping me hydrated and fed and DMig Vaughn for sponing me in the weight m m , 1

iii

would aiso like to thank the people that originally got me involved at DCIEM as a test

subject. Dr. Stephen Cheung, Dr. Tom McLellan. Jan Pope. and Doug Bell. Thank you

for sparking my interest in huma. physiologicd research.

1 would like to thank my fnends David Cherry. Roger Near, Mark Borthwick.

Mark Balaban, Briget Belton. Paul Bailey. and Erin Harris, dong with the entin Centm

Valet stalf including Jeff Ross. Mike Milosh. and Jason Woolmer. Over the past two and

a half years. you have al1 at one point (or more) asked me what exactly 1 was doing.

Thank you for listening to me. nodding your head. and appearing interested even though

you were most likely wishing 1 would just shut up.

1 would also like to thank my Grandmother Katherine Finnerty and Mr. John

O'Halloran. These two people pnyed for me on alrnost a daily basis. 1 am not a religious

man but 1 can not help but think that in some imperceptible way this made an incredible

di fference.

Finaily, 1 would like to thank the most important people in the world to me. To

my sisters Kimberly, Cynthia. and Nicole: 1 do not Say this often enough but 1 love you

and am proud that you nre my siblings. To my parents Dr. Nicholas Colapinto and

Margaret Colapinto: Your interest. support, and caring throughout my life and education

has been incredible. You aiways put me and my interests ahead of youn. You instilled in

me a hard work ethic and the belief that 1 could achieve anything as long as 1 put my

rnind to it. For al1 this and more, you mean so much to me. 1 love you both.

Table of Contents

2 3 The physiologkd effkct of exposure to +Gz o o . o o ~ o ~ o o ~ o u ~ o o o ~ o o o ~ o o o o e o w w e w ~ o o e o o o o e o o o e o o o o o o o o o e o o o o o o o o o o 7 2.2.1 Hydrostatic effect. caused by increased +Gz .............................................................. . . 7 2.2.2 Importance of +Gr-induced HLBP changes ................................................................................ 8 2.2.3 Hydrostiitic effects of -Gz and the effect of -Gr on HLBP ............................................................... 8

2.6 Tilt table test for the push-pull effect ~ o ~ ~ o ~ ~ o o o o ~ o ~ o ~ ~ ~ o o o ~ o e o ~ e o o ~ ~ o o o o o o o o ~ ~ o ~ o o o o ~ o o o u ~ o o u o ~ o o ~ o ~ o o u m m w ~ ~ e o o u o o o o o 13 2.6.1 Advantages of the tilt table simulation of the PPEM .................................................................... 13 2.6.2 Disadvantages of the tilt table simulation of the PPEM ................................................................ 14

2-7 Current countermQamns o~-we*wo.onoe"n.noowotoeeooomooooHo.eomooooo..oooeoooooooooooeoooeooowooeooo*eeooooooeosoeeoooooooH* 15 2.7.1 Extendecl Coverage G-suits ..................................................... , ....................... ........ .... ........-... 16 2.7.2 The control of G-suit inflation by the G-valve: timing and rate of inflation ..............-.. ................. 16 2.7.3 Use of *e anti-G suit for protection against the push-pull effect .................................................. 18 2.7.4 The development of an electronic 'srniut' G-valve for protection ûgninst the push-pull effect ...... 18

. 3 3 Tut table test for the push-pull ePlmt . . . . . . m . . . . . m ~ ~ ~ o ~ ~ m ~ ~ ~ ~ ~ C I ~ ~ m ~ m ~ ~ ~ ~ e ~ . ~ ~ n . ~ ~ ~ . ~ m m 39 ...................................................................................... 3.3.1 Review of tilt table acceleration r e m c h 39

....................................................................... 3.3.2 Why the tilt-table G-reserirch gap of over 30 yem'? 44 ......................................................... 3.3.3 The tilt table as a method for examining the push-pull effect 45

............................................. 3.3.4 Review of the tilt table simulation of the push-pull effect maneuver 35

3 3 AntLG d t ..ee.....n...~~o*~~~~*~eu~*~~~*~~~~.**m*~***~****~o*****~.to.t~n*mw**~~m~n~~*~"~*~~.~***~o*.**e**.~~~.. 46 ........................................................................................................ 35.1 The G-suit inflation during tilt 47

............................. .................................................. 3.5.2 Modem G-suit design developments ... 4 9 3.52 G-suit inflation: timing and rate of inflation ................................................................................. 50

................................. 3.5.3 Use of the Anti-G suit for protection against the push-pull cffect maneuver -52

4.1 Subjects ...t...e.H...~..~....u...~......H.n.....~~....,~..~ee........m...o....m............~..................~...o...~.....nHt.o.tt.....e~... . 54 4.1.1 Recruitment ..................................................................................................................................... 54 4.1.2 Subject Training ............................................................................................................................ 55 4.1.3 Subject restrictions ........................................................................................................................ 55 4.1.4 Subjwt characteristics ..................................................................................................................... 56

4.2 Physiological monitoring and instrumentation .......,....,......e..~......~...~.......e.....,...i..t.....~........e.......... 56 4.2.1 Blood pressure .....~................~......~.................................................................................................. 58

...................................................................................... 4.2.1.1 Systolic and diastolic blood pressure 58 42-22 Mean arterial blood pressure ................................. ,, ................................................................ 59 1.2.2.3 Head-lcvel blood pressure ( WLBP) ........................................................................................ 59

4.22 Hewt rate .................................................................................................................................. ... 60 4.2.3 Impedance cwdiogrriphy ......................................................................................................... 6 1 4.2.4 Venous Occlusion Plethysmogmphy .............................................................................................. 62

4.3 Subjective mepsu~menls,....~.. ...-........*.......................*.................---....-... 64 4.3.1 Visual ligfit loss .......................... ...,,, ............................................................................................ 64

...................................................................................................... 4.3.2 Other subjective measuremtnts 6)

4.4 Equipment ..u.w...n........ ~ ~ ~ o H e ~ e ~ e " ~ ~ ~ ~ ~ n ~ ~ e M ~ ~ H ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ " o ~ ~ ~ ~ ~ ~ ~ ~ H . ~ ~ ~ m ~ ~ ~ H ~ ~ ~ H ~ ~ ~ " ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ o ~ ~ H ~ ~ ~ e ~ ~ ~ ~ m w ~ ~ ~ ~ ~ e o ~ 65 4.4.1 Tilt table .......................................................................................................................................... 65 4.4.2 Anti-G suit and pressure delivery system .................................................................................. 6 5

4.6 Ihlb A W y m . . e . . . . . . . . n . . ~ ~ . ~ ~ . ~ n ~ . u ~ m m r n - ~ ~ ~ * m t . ~ ~ ~ ~ ~ * w ~ w . . ~ ~ ~ ~ . * ~ ~ e ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ * ~ ~ ~ m ~ ~ w ~ ~ w . r t e n ~ n . . e m ~ * ~ m ~ ~ ~ ~ ~ ~ o."o"rn 70 4.6.1 dp and dt for Systolic Blood Pressure (SBP) ................................................................... .............. 70 4.6.2 SBP. MAP. HLBP. HR. Zo. SI. CI. TPRi. FBF. ruid FVR ......................................... .... 7 1 4.6.3 Re-anrilysis ................... ,... ................... .. .................................... ,,,, .............., 72

5.2 Sysîok B l d Pressure ..........-..... ............---...... 75 53.1 Deamse in SBP (dp) .., ..... ....-. .... ....-..... ........... . . - ........... .. ................. , ............ . . 75 533 T i e of SBP recovery (dt) ............,,.....~.~...,~~..~~~~...~.~........,...................................... 76

5.2.3 Repeated mesures ANOVA for percent change in SBP .......... . ............................................... 7 8

6 3 Insight into the cardiovascular respoiise to the PP EhZ.~.m..,...,-.mm~m~~~m~~~~ n " ~ O H O O m U H O H . . O O O O . H ~ ~ . m 99 6.3.1 Cardiovascular efftcts of HDT for the unprotected schcduie ............-.... ,... ....................... . . . 100 6.3.2 The cardiovsiscular effects of subsequent HUT during unprotecteâ runs ........................... . ......... 104

6.4 The e t l i t oTG-suit inflation upon the physiologie mponses to tbe PPEM, ,.,,, ...mm,. 110 6.4.1 The acute effects of G-suit inflation .................... .... .......................................................... 1 10 6.4.2 The tffect of Ci-suit inflation ovcr time ...................... ... .... CC.CC.C~CC ...... C.~C..C...CCC...C .........+.... . . . . 115 6.4.3 The efiect of vwying the timing and pressure of G-suit inflation ........................................... 117

6.5 C ~ ~ ~ ~ I ~ ~ m - n w u o o - ~ m - o m ~ - m m . r + t . r - ~ m m o m m ~ o m o m o m o m m o o o - o o m ~ o ~ m m m - ~ m o m o o m m m ~ ~ m ~ - m m t - m ~ m o ~ n m u ~ m ~ - - 121 6.5.1 tmplications for operations. future rcsearch, and the dcvelopment of an optimd protection systern md schedule versus the PPE., ..... , ...... ... ......... . ..............................e...................... . .... ,...... .... ........ . . . . 121 6.5.2 Conclusions brrsed upon nul1 hypotheses ......- ,.....,....,..............,,,........... ... ....... . ...................... 122

vii

List of Tables

TABLE 2-1 EXPLANATION OF G-SUIT INFLATION SCHEDULES ................................................... 22 TABLE 4-1 SUMMARY OF PHYSIOLOGICAL MEASUREMENTS. TECHNIQüES . AND

...................................................................................................................... INSTRüMENTATION 57 ................. ..................... TABLE 4-2 TILT TABLE PROFILE AND EXPERIMENTAL SCHEDULES ,., 69

..................................................................... TABLE 5-1 SUBJECT CHARACTERISTICS -74

List of Figures

FI4 FI4 FI( FlI FII FI(

GURF, 2-1 ANGULAR VELOCITY DURING FLIGHT .................................................................... 5 CURE 2-2 TERMINOLOGY FOR ACCELERA'TION FORCES ON THE BODY ............................ .... 6

......... GURE 2-3 REFLEX MECHANISMS FOR COPING WITH P O S m AND NEGATIVE GZ 10 ... CURE 2 4 (A) G-TIME TOLERANCE CURVE (B) EFFECT OF G-ONSET ON G TOLERANCE 12

GURE 2-5 TILT TABLE PROFILE WTH EXPERIMENTAL SCHEDULES ..................................... 22 GURE 3-1 SCHEMATIC OF SYSTOUC BLOOD PRESSURE IN 'ME SUPiNE AND ERECT

POSIIION AT +1 GZ ............................................................................................................ 25 GU= $2 THE PUSH-PUU EFFECT .................................................................................................. 31 GURE 4-1 DATA COLLECTION .......................................................................................................... 57

........................... .*..............................................--........... CURE 5-1 DECREASE IN SBP (DP) ......... 7 6 SURE 5-2 TCME OF SBP RECOVERY (Dm ....................................................................................... -77

........................................................................................... SURE 5-3 PERCENT CHANGE IN SBP 7 9 SU RI.. 5-48 PERCENT W G E IN M A P ............................................................................................. 81 SURE 5-5 PERCENT CHANGE N HLBP ............................................................................................ 83 CURE S 4 PERCENT CHANGE IN HR ................................................................................................ 85 SURE 5-7 PERCENT CHANGE IN 20 ................................................................................................. 87

.................................................................................................. SURE 5-8 PERCENT CHANGE IN SI 89 SURE 5-9 PERCENT CHANGE IN CI .................................................................................................. 91

........................................................................................... SURE 5-10 PERCENT CHANGE IN TPRI 93 SURE 5-11 PERCENT CHANGE iN FBF ........................................................................................ 9 5

....................................................................................... SURE 5-12 PERCENT CHANGE IN FVR 9 7

List of Appendices

.......................................................................... APPENDIX A S AMPLE RECORDiNGS 133 ................................................................................ APPENDIX B ANOV A RESULTS -139 .................................................................................. APPENDIX C MEANS TABLES.. 172

................................................................................... APPENDIX O CONSENT FORM 184 .................................................................. APPENDIX E FBF SAMPLE MEASUR 187

APPENDCX F G-SUIT APPARATUS/EXPERMENTAL SETUP ............................................. 189 APPENDIX G INTER-SUBJECT COMPAlUSION OF ABSOLUTE CHANGES IN

SBP. HLBP. AND HR ........................................................................................... 191

1.0 Introduction

Recent studies have shown that if a pilot experiences a period of -Gz directly

preceding a +Gz maneuver, G-tolerance may be impaired [LI. This phenornenon h a been

tenned the 'push-pull' effect 12).

In 1998. studies conducted by the Canadian and United States Air Forces

concluded that the push-pull effect (PPE) has ken a contributing factor in numerous

mi litiuy ainraft accidents [3-51. These studies implicated push-pull mediated impairnent

of G-tolennce as a major nsk to pilot performance that could ultimately lead to aircrew

injury andor death. Thus, it is important to leam more about -Gz to +Gz maneuvea

(known as the push-pull effect maneuver or PPEM) and develop methods to protect

pilots rgainst the PPE that these maneuvers induce.

Although the basic physiological responses that occur during the PPEM have been

described, a detailed mechanistic understanding is still incomplete since opparatus used to

study the physiological effects of push-pull make complex measurements difficult. Most

centrifuges. a common investigative tml in acceleration nserirch, cannot perform the -Gz

accelerations necessary to mirnic the PPEM. ln-flight measurements are also limited by

practical constraints, since only certain monitoring equipment is feasible in the cockpit

environment,

The tilt table is the most recent experimental tool used to study the PPE. The tilt

table has been used in orthostatic hypotension msearch for numemus years and has been

successfully implemented in numemus cwdiovascular and acceleration studies. 16-12].

The tilt table is a rotating bed that cm be tilted at various angles around its centre

point. A subject. secured to the table in a supine or seated position. cm be tilted at

specific angles. B y subjecting a person to a head-up tiit (HUT) to head-down tilt (HDT)

to HUT sequence. the tilt table cm reproduce a low-intensity PPEM and its

corresponding physiological nsponse with the added advantage of pater control over

the testing environment. Monitoring equipment that cannot be used for in-flight studies

due to size and feasibility constnints can be readily applied in the tilt table lab [SI.

In addition to mimicking the physiological changes caused by the PPEM. the tilt

table also provides an opportunity for testing countemeasure equipment, such as the anti-

G suit. Although G-suit inflation in high +Gz situations has been studied thoroughly. very

little is known about the effect of the G-suit upon the PPE. G-suit inflation is a known

method for maintaining blood pressure at head-level and increasing G-tolerance.

however, the initiation of inflation, the onset rate and the pressure at which the G-suit

should be inflated dunng the PPEM to counteract the PPE is still unknown. This

investigation will attempt to elucidate these concems by using the low-intensity tilt table

PPEM while exposing human volunteers to various G-suit inflation scheduks. G-suit

inflation will be initiated at different times dunng the tilt maneuver to detennine if the

onset of inflation and/or the maximum inflation pressure has an effect on protection

against the PPE.

This research will provide insight into the cdovascular regulatory pmcesses

involved in the PPE and will contribute to the development of an effective PPEM

protection schedule. This schedule could then be further evaluated in a high-G PPEM

environment before becoming operational. Hopefully, this schedule will be used in the

future to better pmtect pilots against the PPE, ultimately saving aircrew h m potential

injury andor loss of life.

2.0 Background

2.1 Physics involved in military tactical aviation

Newton's Second Law of Motion States that the magnitude of an object's

accelention is directly pmportional to the magnitude of the net force and inversely

proportional to the object's mas:

Equation 2-1

Where F is force in Newtons (N), m is the mass of the object in kilograms (kg), and a i s

the accelention in metres per second per second (ms-2) [13]. Since m a s is a constant,

only changes in acceleration c m alter the magnitude of the force exerted on an object.

Equation 2-1 can be modified for centripetal accelerations, accelerations that are

conunonly expenenced during military tactical aviation. Centripetal acceleration is equd

to the square of the angular velocity multiplied by the radius of the object to the centre of

rotation. Thus:

Equation 2-1 b

Where u2 is the square of the angular velocity and r is the radius of the object to the

centre of rotation. The angular velocity during flight is illustrated in Figure 2-1:

Figure 2-1

Angular velwity during flight

w O O 1 velocdy

O O

H

-pdh

(w) .. circunferwRid vebcdy (v)

1

adapted from [14]

In acceleration research, the magnitude of an applied accelention is often

expressed in tenns of the Earth's standard acceleration due to gravity, 9.8 mr2. if this

value is used as a denominatot, the acceleration applied to an object can be expressed

relative to the stanâmi acceleration of gravity in units of O:

Equation 2-2

applied acceleration in ms-' G =

std. accelention of gravity (9.8 ms-')

Since it is a vector quantity. acceleration not only has magnitude but direction as

well. Using Newton's Third Law of Motion that every action has an equal and opposite

reaction, standard acceleration nomenclature defines +Gz as a gravito-inertial reaction in

the direction of the feet in opposition to a headward acceleration. Using the same

methodology, -Gz is defined as a gravito-inenial reaction in the direction of the head as a

result of a footward acceleration. Figure 2-2 illustrates standard acceleration

nomenclature across 3 axes:

Figure 2 3

T e ~ o l o g y for accelemtion forces on the body adapted h m 1151

2 2 The physiological effeet of e x p u r e to +Gz

Most heaithy individuals cm cope with the effects of +L Gz without difficulty.

However. symptoms of cardiovascular insufficiency arise in situations such as milit*

tactical aviation when pilots perfom banked tums, dives. and pull-outs which result in

varied centripetal accelerations and gravito-inertial forces. Forces other than +l Gz cause

relative changes in the hydrostatic foms within al1 vessels in the circulatory system.

These changes can have many deletenous effects ranging from Mnor visual distuhances

to the possibility of loss of consciousness [L4].

I f 1 Hydrostatic effkts caused by inc@ +Gz

Gravito-inenid forces act not only on the body but the blood in the vasculature as

well, +Gz causes blood to shift in the footwd direction. Due to the elastic nature of the

venous circulation, this results in passive dilation of the lower vasculature and an inmeose

in blood volume, blood flow, and blood pressure in the lower limbs. Since there is an

increase in blood volume below heart level, there is less blood in the vasculature above

hem level. This results in the decreased diameter of upper vasculature and, therefore,

decreased b l d flow and blood pressure above the heart. Ultimately. this leaàs to a

decrease in head-level blood pressure (HLBP).

2.23 Importance of +Gz-induced HLBP changes

Changes in HLBP caused by f f i z are of great interest and importance. Decreased

HLBP effects the perfusion of the eyes and the brain, two vital organs during flight. Any

loss of vision or decrease in cognitive ability could drastically effect pilot cornpetence

and put aircrew at risk for injury andor death. Therefore. in an effort to dirninish this

risk, numerous studies have been perfomed to leam more about the effects of +Gz and its

effect on HLBP.

At +l Gz, HLBP is approximately 98 mmHg. This is more than enough pressure

for adequate visual and cognitive function. However, as gravito-inertial force increases

beyond +L Gz, blood flow to the head is compromised. This results in a decrease in

HLBP at a rate of approximately 22 mmHg per G. Therefore, at +4 Gz, HLBP decreases

to approximately 32 mmHg effecting retinai blood flow. This resulis in a loss of

peripheral vision (greyoui). At +5 Gz, HLBP is approximately 10 mm Hg which leads to

i complete lack of ocular perfusion. The result is a complete loss of vision (blackout). At

+5.5 Gz, HLBP is approximately O rnmHg. Since there is no blood pressure at head-level.

the brain is no longer perfused. This ultimately leads to in gnvity induced loss of

consciousness (G-LOC).

22.3 Hydmtaüc effeets of -Gz and the effet of -Gz on HLBP

-Gz pmduces a blood shifi in the headward direction. This inmase in blood flow

above heart-level causes HLBP to inmase at rate of approximately 22 mmHg per G.

Therefore, at -3 Gz. HLBP is approximately 186 mmHg, at -4 Gz, 208 mmHg, and so on.

This translocation of fluid to the head is very unpleasant experience since it results in

extensive facial edema. breathing difficulties, and possible disorientation.

It may be postulated that a -3 to -4 Gz increase would result in cerebral vesse1

rupture and brain hemorrhaging. However, this does not occur. During -Gz. the increase

in vascular pressure in the brin is bdsuiced by similar incnlses in cerebrospinal fluid

pressure. Therefore. the nsk of rupture is minimal. Nonetheiess. -Gz remains an

uncornfortable experience.

2.3 Reflex mechanisms for coping with positive and negative Gz

The deleterious effects caused by +Gz and -Gz exposun described in the previous

two sections are the result of the inability of the cardiovascular system to cope with

increased hydrostatic forces and, therefore, maintain HLBP [16].

When arterial pressure fluctuates, the cardiovascular reflexes are invoked in an

attempt to sustain HLBP. The carotid baroreceptors. dong with the cardio-pulmonuy

baroreceptors of the aortic arch and other less undentwd sensors throughout the

cardiovûscular system, are al1 part of this neurological reflex mechanism. The carotid

bmreceptoa indirectly monitor HLBP by sensing changes in cacotid artery diameter due

to alterations in blood flow to the head.

If a pilot is exposed to +Oz, HLBP begins to decrease. The carotid baroreceptors

sense this change and act to increase arterial blood pressure in an attempt to maintain

HLBP (known as the baroreflex). This reflex triggers an increase in hem rate (ER) and

vasoconstriction. This is done in an effort to protect against the visual disturbances and

G-LOC associated with increased +Gz.

If exposed to -Gz and HLBP beings to increûse. the baroreflex causes a decrease

in HR and vasodilation in an attempt to decrease HLBP back towards normal levels.

Under -Gz, the bamreflex mainly acts to limit the amount of uncomfortiible fidcicial edema,

breathing difficulties, and symptoms of disorientation associated with the translocation of

blood to the head and chest.

Figure 2-3 sumrnarizes the rrfiex mechanisms for coping with both positive and

negative Gz:

Figure 2.3

ARTERIAL PRESSURE

Artarial Barorocoptor

Meduila Cardiavarculai

Nuclai 1

He8n Rata C (aiow. 5-15 sacs) Cardkc Output Vascuiar Rosistanca

Reflex mechanisms for caping with positive and negative Gz

aâapted h m [17]

2.4 The effeet of +&-onset rate and duration at higb +Gz

G-onset rate and G-duntion also have an effect upon G-tolerance. As illustrated in

Figure Ma, the cardiovascular reflexes are best able to defend against short durations of

ffiz. If the length of G-exposure is minimal. the body is protected by a 5 second oxygen

reserve in the brain. Therefore, there is littie risk of G-LOC even if cerebral perfusion and

XLBP are significantly diminished. If G-exposure is sustained. the carotid barorenex will

attempt to countenct the decrease in HLBP but. after a pend of time, will eventually

Fil. The body is simply not able to defend itself against such a severe. sustained, low

HLBP situation.

As illustrated in Figure W b . the body is also effective in defending itself against

graduai-onset Gz exposure. A graduai-onset rate gives the cardiovascular reflexes time to

react to the exposure to G. Thus. up to n point (usually +4 to 5.5 Gz) the body has an

opportunity to counteract the effects of the increased Gz conditions. The barorefiex reacts

tw slowly to defend itself against rapid-onset G. Rapid-onset causes HLBP and cerebral

perfusion to be diminished quickly, taxing the brin's oxygen reserve. The subject is then

at nsk for G-LOC [18].

1 \ G-LOC

(a) G-time Tolerance Cuwe

Human tolerance to +Gz

(b) ElIcrt of G-onset on G Tokrance

Muman tolerance to various G-onset rates

adapted from [ la]

2.5 - to + Gz transitions

The effects of acceleration becorne more complicated when a -Gz maneuver is

performed before a +Gz maneuver. When a pilot experiences a p e n d of -Gz directly

preceding ffiz, G-tolerance is diminished [19]. This demase in +Gz tolerance caused by

negative to positive Gz transitions has k e n lrbeled the "push-puli" effect (PPE) [2].

Since a reduced G-tolerance increûses a pilot's risk of visual disturbance andor Ci-

LOC at a lower f f i z threshold, the PPE remains a hazard for aircrew dunng flight. This

problem has been expecienced by military tactical pilots [3-51 and avilian aembatic

aviators [15, 201 for many years. However, for nasons stated in section 1.0. very little is

knom about the complex cardiovascular reflexes occuning during the PPEM due to

expnmental limitations and even less is known about the effect of current G-protection

countermeasures against the PPE. Countemieasures such as the anti-G suit, positive

pressure breathing (PPB), and the anti-G stnining maneuver (AGSM) must be tested

dunng PPEM simulations to discover their usefulness in counteracting the PPE.

ültimately, a protection schedule must dso be developed to better defend pilots against

the effects of negative-to-positive G-transitions.

2.6 TM table test for the push-pull effect

As stated previously, the tilt table has recently ken used to study push-pull

physiology [2 11. B y subjecting a person to a HUT-HDT-HUT sequence, the tilt table can

reproduce the +Gz to -Gz to +Gz transition of the PPEM. This allows for the examination

of the physiological response to the PPEM, the push-pull effect (PPE).

2.6.1 Advantap of the tilt tabh simulation of the PPEM

The tilt table is a good lab-based approach for push-pull testing which has several

advmtages over other experimental methods. Tilting a subject at various angles for

certain durations cm rnirnic maneuven experienced during tactical flight with the added

advantage OF greater control over the testing environment. Although the amount -Gz and

+Gz experienced by the subject are not of the same magnitude as in-flight or centrifuge

situations, the tilt table can produce sirnilar patterns of physiological change. Monitoring

equipment that cm not be used in in-flight studies due to size and feasibility constraints

can be readily utilized in the tilt table Iab [21]. With the tilt table, investigatocs also have

instant access to the measurement apparatus. Equipment problems that would nonnally

force an in-flight experiment to be aborted can be quickly addressed and corrected.

Environmental concems such as dangerous winds, high temperatures. or bad weather that

could compromise in-flight studies rue easily controlled for or of no concern in the tilt

table lab.

2.6.2 Disadvantagcs of the tilt table simuiation of the PPEM

The tilt table is limited as a labontory tool since it can not precisely mimic the in-

flight experience. Subjects cm only by exposed to a maximum of -0.71 Gz (135' HDT,

referenced from vertical) and +1 Gz ( 1 5 O HUT, referenced from vertical) on the tilt table,

far less than the -4 Gz to over +9 Gz experienced by tacticd aircrew when perfoming in-

flight maneuvers. The tilt table ha the further problem of not king similar to the cockpit

of a iacticai aircraft. Different seating position, and the Iack of a control panel. control

stick and foot pedals could al1 effect the experience of the subject and alter results.

2.7 Current countermeasures

There is a point at which the cardiovascular mechanisms for coping with G begin

to fail. As explained in section 2.2.2, as the magnitude of +Gz increases, the result is a

gradua1 loss of vision followed by G-LOC. To avoid these problems and their associated

risks, countermeasures have been developed in an attempt to increase Ci-tolerance. The

oldest yet still most common protection method is the anti-G suit.

Anti-G suits have been used since World War iI to counteract the effects of high

+Gz accelerations [16]. These suits, wom around the legs and abdomen. contain air

bladders which are inflated when gravito-inertid forces are above +2 Gz. This inflation

causes pressure to be placed directly upon the lower extremities and splanchnic region.

This results in increased periphenl vascular nsistance through increased lower body

tissue pressure. a decrease in the venous pooling capacity of the lower limbs, increased

venous retum, and elevation of the heart. All of these factors act to maintain HLBP under

high +Gz and afford the wearer of the G-suit a 1-1.5 Gz increase in G-tolerance 1221.

Since its inception over 50 years ago, the G-suit has undergone few alterations,

most of which have had only minor effects on G-protection. Since modem tactical aircraft

are capable of achieving greater than +9 Gz, improved G-suits and gRater G protection

for pilots has become a necessity. Recent military aviation accidents have highlighted this

shortcorning in G-protection. To combat this problem, acceleration physiologists began to

develop new methods of G-protection including improved G-suits and new G-valves with

innovative inflation schedules.

2.7.1 Extendcd Covecage G-suits

Military establishments including the Royd Air Force (RAF), the United States

Air Force (US@, the United States Navy (USN), and the Canadian Air Force (CAF)

have made attempts to irnprove their G-protection with the development of a new

genention of G-suits; respectively the FAGT, ATAGS, EAGLE, and STING. These G-

suits follow the concept of extended bladder coverage over the lower extremities for

increased G-protection. The extended coverage provided by these suits work on the

principle that increased bladder coverage will cause a larger increase in lower body tissue

pressure venus older style, cut-away G-suits. It is believed that this will allow for better

maintenance of HLBP under high +Gz and. therefore, increased G-tolerance.

Studies have ken inconclusive on whether these extended coverage G-sui ts

actually increase maximum G-tolerance. However, extended coverage G-suits have been

shown to reduce pilot fatigue and increase G-tolennce time venus older style G-sui&

[23.24]. Also. ment centrifuge and in-flight tests of STING have provided definitive

evidence that extended coverage G-suits offer a significant increase in protection over

standard G-sui ts w hen used with PPB as part of a G-protection ensemble (25-281.

2.73 The control of Csuit hflation by the Evalve: timing and rate of inflation

The anti-G suit inflates when a pilot is exposed to increased gravito-inertial

forces. This inflation is conmlled by a volve which is sensitive to G-intensity. When a

pilot experiences increased +Gz the valve opens and. using air bled from the jet engine.

the G-sui t is inflated.

Current, standard O-valves are mec hanical and their design is viriuall y unc hanged

from those used since the 1940s. When gravito-inertial forces are above +2 Gz, the valve

passively opens causing the G-suit to inflate at a rate of approximately 1.5 psi per G to a

maximum of 10 psi [Ml. This +Z Gz dehy is necessaiy to prevent the G-suit from

inflating under circumstances in which it is not meded such as aircnft buffeting and low

G-level moderate tums. In these situations, G-suit inflation cm be uncornfortable and

distracting to the pilot 1291.

There has been considerable debate in the field of aviation over when and how

npidly the G-suit should inflate. It seems logicai that, since HLBP begins to decrease

irnmediately with the onset of Gz and that the G-suit provides hypertension upon inflation

to countenct this decrease, the G-valve should provide pressures which coincide with the

G-profile. However, studies on this subject have been inconclusive.

Scientific conclusions on optimal G-suit inflation rates have nnged from

immediate, very rapid G-suit inflation as a necessity for increased O-tolerance to those

studies that show slower-onset inflation or even a slight delay in the onset of inflation has

no il1 effect on G-protection [30]. The overriding problem is the Iack of direct evidence to

support any conclusion.

27.3 Use of the anti-G suit for protection against the push-pull effoet

Since few studies have been conducted on G-protection during the PPEM, very

little is known about the protection afforded by the anti-G suit against the PPE. In-flight

push-pull protection studies have found that although the initial decrease in blood

pressure caused by negative-to-positive G-transition was unaided by G-suit inflation, the

G-suit did speed the rate of blwd pressure recovery compared to unprotected mns [ l , 3 11.

Thus. the G-suit appears to pmvide some protection against the PPE. However. the

optimal tirne for G-suit inflation dunng the PPEM for maximum protection benefits has

yet to be examined.

2.7.4 The development of an electronic

2,s Problem

The physiological effects of f f i z the countenneasures developed to counteract

these effects. and the protection afforded by this equipment has been studied thomughly

since World War ï I [22]. However, very linle of this research has been focused on the

push-pull effect. As stated previously, knowledge of the PPE is incomplete since complex

measurements are difficult to perform using current appmtus and protocols. Because of

these limitations, not only is very little known about the physiologic effects of the PPEM,

even less is known about how to protect tactical pilots from its effect. Investigation is

therefore warranted.

23 Purpose of this study

The purpose of this study is to use the low-intensity tilt table mode1 of the PPEM

while intervening with various G-suit schedules to determine which schedule is the most

effective against the PPE. It is hoped that this will:

(1 ) Provide insight into the cardiovascular response to the PPEM.

(2) ïmprove the understanding of the effect of various G-suit inflation timing and

pressure schedules on protection against the PPEM.

(3) Aïd in the discovery of a protection system with an electronic 'smart' G-valve that

could deliver this G-suit timing and pressure schedule for optimal protection against the

PPEM.

(1) G-suit inflation will have no effect on the blood pressure response to the PPEM.

(2) Varying the timing of G-suit inflation will have no effect on the blood pressure

nsponse to the PPEM.

(3) Varying the pressure of G-suit inflation will have no effect on the blood pressure

response to the PPEM.

2.11 Expectations

Based on the known Rsponse to the HUT-HDT-HUT tilt table simulation of the

PPEM [8] and the hemodynamic effects of G-suit inflation [22,32] certain results are

expected. It is known that G-suit inflation during HUT causes increased vascular

resistance in the lower extremities and, therefore, demased translocation of central blood

volume toward the lower vasculature. Thus, it is expected that G-suit inflation during

transition to and upon reacbing subsequent HUT will act to help maintain HLBP and,

therefore, ameliorate the PPE. Increased inflation pressure is expected to further aid in the

maintenance of HLBP upon reaching subsequent HUT and therefore, offer even greater

assistance in arneliorating the PPE.

2.12 G-suit infiation schedules

Various G-suit inflation schedules will be used to detemiine if these expectations

are indeed correct. G-suit schedules were selected which varied by initial time of inflation

(inflation dunng transition to subsequent HUT venus inflation upon reac hing subsequent

HUT), inflation onset m e (normal versus slow), and maximum inflation pressure (normal

versus high). The profiles of these schedules are illustrated in Figure 2-5 and explained in

Table 2-1 (see next page).

2.13 Significance of this Expriment

As stated previously, recent studies have shown that the PPE has been a

contnbuting factor in numerous military aircraft accidents [3-51. These studies have

concluded that an impaireci G-tolerance caused by the PPEM is a major nsk to pilot

performance and could possibly cause injury andor death. Thus, it is important to l em

more about the PPEM and discover methods to protect pilots against its effect.

This research wi II provide insight into the neurological and cardiovascular

processes involved in the PPE. It will also lead to a pa te r understanding of the

protection schedules necessary to counteract the effects -Gz to +Gz transitions.

Hopefully, this information will contribute to the creation of a new electmnic G-valve

algorithm and, therefore. improved G-suit inflation schedules that will better protect

pilots during al1 aspects of high performance flight. Ultimately, this will Save aircrew

from potentiaî injury andior loss of life.

Figure 2-5

Tilt table profile with experimentai schedules

135O HDT

15 O Hm

nit Angk

2 psi

\ "npmtcmed (no inflation)

Table 2-1 Explmation of G-suit inilation schedules

Run Description of G-suit scbeduie

Unpmtected

RDTr

PsüTr

No G-suit inflation

Pressure aormzil, inflaiion During Triinsition to Hm- I

Pressure n o d , slow inflation During T ~ u o n to HUE

3.0 Review of Literature

3.1 The physiological effeet of expusure to G

As stated in section 2.2. most healthy individuais can cope with the effects of +L

Gz without difficulty. However, problems arise in situations such as military tactical

aviation w here pilots experience gravi to-inertial forces beyond + 1 Gz. Increased +Gz

causes a dative increase in the hydrostatic forces within d l vessels in the circulatory

system. This often results in inadequüte blood pressure above hem level and decreased

perfusion of the brain. This decreased perfusion leads to visual disturbances and the

possibility of gravity induced loss of consciousness (G-LOC) [ 14 1.

3.1.1 Hydmstatic effkcts

Blomqvist and Stone presented a thomugh, mathematical explanation of the

hydrostatic changes caused by +GE [13]. They simplify hydrostatic forces under high

+Gz conditions by assurning b l d in the vasculature is analogous to a column of tluid in

a ngid container. This assumption allows physicd pnnciples that govem a fluid-filied

column to be applied to the cardiovascular system.

The hydrostatic pressure at the bottom of a column of fluid in a rigid container is

a product of the density of the fluid. the applied gravito-inertiai force. and the height of

the column.

Equation 3-1

Where P is the pressure, p is equal to the density of the fluid, G is the gravito-inertial

force. and h is the height of the column.

If the density of the blood in an individual is assumed to be constant and. as

assumed by Blomqvist and Stone. the blood in an individual in an upright position is an

unalterrd rigid column. Equation 3-2 can be used to estimate changes in blood pressure

caused by gravito-inenial forces.

Equation 3-2

Where Pm is the calculated systolic blood pressure (SBP) at a certain distance and

P, is the reference point SBP (heart-level SBP, in most cases).

For instance, to calculate the effect of +1 Gz on b l d pressure at head level, the

values for density of blood (1/13.1), gravito-inenial force (+1 Gz = 9.8 m d ) , and the

column height (for example, heart-to-eye distance = 30 cm) can be substituted into Equation 3-2:

As illustrated in Figure 3-1, Equation 3-2 c m be used to determine systolic blood

pressure ai any distance from the hem. in the footward or headward direction.

Figure 3-1

Schemtic of systolic b k à prrswur in the supine and emt position at +1 Ga

adapted h m 1181

The density of blood and the height of the column will remain nearly constant

under most acceleration forces. Thus, according to Equation 3-2, changes in the gravito-

inertial force itself is thc only variable that altea hydrostatic column pressure. For

instance, if the blood pressure at hem level is 120 mmHg, at +3 Gz the blwd pressure at

head level will be:

P, =P,+pGh

=120 mmHg + (11 l3.l)(9.8 x 3)(-30)

=120 - 66

=54 mmHg

Thus. head-level blood pressure (HLBP) under increased accelention can be calculated

using Equation 3-2, decreasing at approximately 22 mmHg per unit of Gz.

In a system comprised of ngid tubes of unvarying diameter, blood flow would not

be impeded by these differences in pressure. However, the humon cardiovascular system

is not a set of tigid tubes as assumed in the equations above. The cardiovascular system

consists of multi-branched, elastic vasculature of varying dimeter containing blood of

unique composition and propenies. Nonetheless, physical pnnciples cm still be applied

to this varying system.

One of the principles, Poiseuille's Law, relates the fiow of fiuid in a cylinàrical

tube as directly proportional to the pressure difference across the tube, directly

proportional to the fourth power of the radius of the tube, inversely proportional the

length of the tube. and inversely proportional the viscosity of the fluid These

relationships are illustrated in Equation 3-3:

Equation 3-3

Where Q is the blood flow. (P, - P,,) is the pressure difference, r is the radius of the tube, q

is the viscosity of the fluid (blood), C is the length of the tube, and R/8 is the

proportionali ty constant [33].

Since resistance (R) is pressure divided by flow, Equation 3-3 cm be rearranged

to give the resistance to flow.

Equation 3-4

Resistance is, therefore, proportional to the viscosity of the fluid and the dimensions of

the tube. In the cardiovascular system, the length of the circulation and the viscosity of

blood is nearly constant. Therefore. changes in resistance to flow are main1 y due to

changes in the radius of the vessels. Since the radius is to the fourth power and is

inversely proportional to R. smdl changes in radius can cause a tremendous change in

resistance and flow. These changes in radius can be initiated by many environmentai

factors inc luding gravito-inertial forces.

Gnvito-inertial forces act not only on the body but the blood in the vessels as

weli. ffiz causes biood to be shifted in the footward direction- Due to the elastic nature of

the venous circulation, this shift results in passive dilation of the lower vasculature and a

pooling of blood in the lower limbs. This increase in blood volume in the lower

extremities creates a problem. Since blood is pooled in the legs, there is less blood in the

vasculature above heart level. This results in the decteased diameter of vessels above

hem level and, therefore, decreased blood flow above the hem-

Gravito-inertial forces also make maintenance of blood flow more difficult. Under

increased gravito-inertial force, the heart must perfom, more forceful contractions in

order to overcome increased hydrostatic effects and maintain b l d flow above hem-

level. Therefore, it is more difficult for the heart to maintain blood flow to the head.

Ultimately, increased gravito-inertial forces result in decreased b l d flow and

decreased blood pressure above hem-level. This results in a reduction in head-ievel blood

pressure (HLBP) which leads to decreased perfusion of the eyes and brain. This lack of

perfusion is a significant problem caused by inmased magnitudes of +Gz.

3J.2 Importance of HLBP changes

Changes in HLBP caused by +Gz are of great interest and importance. Decreased

HLBP effects the eyes and the brain, two vital organs dunng flight. Any loss of vision or

decrease in cognitive ability could drastically effect pilot cornpetence and put aircrew at

risk for injury andor death. Therefore. in an effort to diminish this risk. numerous studies

have been performed to learn more about the effects of +Gz and its effect on HLBP.

One of the pioneen of G-research was Earl Wood. Before Wood conducted his

studies on the effect of accelention on humans in the L94ûs, it had long been believed

that the visual disturbances and unconsciousness associated with increased +Gz was due

to a decrease in venous retum (VR). However, Wood found that these disturbances were

a result of a decrease in HLBP, not a decreased VR [34]. Wood subjected healthy adult

volunteers to npid-onset +Gz of various magnitudes using the human centrifuge at the

Mayo research facility 1161. He discovered that as gravito-inertial forces increased above

+4 Gz. blood flow to the head was compromised. This lack of perfusion resulted in a loss

of peripheral vision (greyout), followed by complete loss of vision (blackout), and

ul ti matel y resulted in gravi ty induced loss of consciousness (G-LOC). Wood concluded

that the loss of vision and loss of consciousness caused by high +Gz was a result of the

inability of the body's reflex mechanisms to cope with these increased hydrostatic forces

and maintain HLBP 1161.

3.1.3 Reflex mechanism for HLBP maintenance

The carotid baroreceptors, along with the cardio-pulmonary baroreceptors of the

aoitic arch and other less understood sensoa throughout the cardiovaxular system, are

part of n neurological mechanism which controls HLBP transient fluctuations. Located in

the camtid sinus, the carotid baroreceptors are specialized stretch receptots which rapidly

estimate changes in blood pressure in the head by sensing changes in the diameter of the

camtid orteries. The carotid baroreceptors attempt to maintain appropriate HLBP by

sending an afferent signal to the cardiovûscular control centre of the medulla whenever

the diameter of the carotids change.

If the afferent message from the carotid baroreceptors indicates that there is an

inmase in the dimeter of the carotid arteries. the medulla interprets this as an increase in

HLBP. The medulla sen& an efferent message to the end organs by stimulating the vagus

nerve and decreasing sympathetic nervous system activity. This results in a reflex

decrease in HR. a decreased stroke volume (SV) and. through periphed vasodilation. a

decreased total peripheral resistance ("PR). This reflex acts to maintain HLBP and keep

the brain perfused under varying hydrostatic forces.

If the carotid buoreceptors sense decreased stretch in the carotid meries an

opposite reflex reaction occurs. The medulla recognizes decreased carotid stretch as a

decrease in HLBP and sends an efferent message inhibiting the vagus nerve, thus

increasing HR. The message also stimulates sympathetic nervous system activity

cesulting in an increased SV and increased TPR. This translates into an elevation of heart

level BP in an attempt to maintain HLBP.

The cardiovascular reflexes are invoked when carotid arterial stretch is increased

or decreased occur during -Gz and +Gz. This is illustrated in Figure 2-3.

3.2 The push-pull effect

Another dimension of complexity is added to the cardiovascular effects of

aviation when a pilot performs a -Gz maneuver before a +Gz maneuver. Although tactical

pilots do not routinely experience sustained -Gz, they sometimes push' -Gz after a +Gz

tum in order to gain enough aerodynamic energy to 'pull' into another +Gz tum. This is

olten referred to as 'unloading' the aircnft since it is used to increase acceleration in the

subsequent f f i z tum. Pilots also experience -Gz acceleration dunng air combat when

navigating their plane into a nose down position white attempting to get a better view of a

target. In these situations. pilots sometimes 'push' -Gz before they 'pull' +Gz [Il. This

maneuver is illustrated in Figure 3-2.

Figure 3- 2

adapted fmm [35]

It has been found that when a pilot experiences G z directly before +Gz. G-

tolerance is diminished [19]. This nduction in G-tolemnce can be attributed to

cardiovascular reflexes. When exposed to -Gz. the body's reflexes react by decreasing

HR, cardiac contractility, and TPR in order to defend agsiinst high HLBP. Yet, under

4 2 . HR. cvdiac contnctility, and TPR must be incieased in order to maintain iidequate

perfusion of the brain and avoid G-LOC. Therefore, by expenencing -Gz directly before a

+Gz maneuver, the body is ill-prepared to cope with +Gz [36]. The resulting decreased

G-tolerance phenornenon has ken termed the "push-pull effect" (21.

Since a reduced +Gz tolerance increases the nsk of pilot visuai disturbance andior

G-LOC nt a lower f f i z threshold the push-pull effect remains a hazard for ircrew during

flight. This hazard is believed to have resulted in several aircraft accidents.

Brush examined the prevalence of the push-pull effect in recent Canadian Forces

(CF) accidents and incidents [3]. He reviewed 284 CF jet and miner accidents that

occurred from 1976-1995. 18 of these accidents were selected for ""detailed review". Of

these accidents, the push-pull effect was a probable or possible factor in iit lest 5

accidents and 2 incidents. Due to the "hazards and insidious nature" of the push-pull

effect. Bmsh stressed the need for continued push-pull research and inc~ased aircrew

education of i ts potential hazards.

A similar study was conducted by Michaud and Lyons for United States Air Force

(USAF) [SI. They reviewed USAF reports of the 24 accidents from 19824990

detennined to be caused by G-LOC. They focused on the maneuvers prior to the

accidents such as extension. diving, acceleration, and unloading that could cause the

push-pull effect. They concluded that in 7 of the 24 accidents (298) the push-pull effect

was either probable or highly probable. Michaud and Lyons therefore concluded that

push-pull is an operatïonally significant source of risk for accidents in USAF high-

performance aircnft. They suggest inmased pilot education and aitered protection

training as a means of increasing awareness of the push-pull effect in the USAF and the

flying community.

Michaud and Lyons also examined the frequency of the push-pull effect in the

USAF by reviewing 48 head-up display videotapes containing over 240 USAF air combat

training missions [4]. For each mission they noted the presence of push-pull effect

maneuvers (PPEMs). PPEMs were determined by Gz profiles of a pend of less than

4 . 8 Gz lasting for moE than 1 second followed by a pend of p a t e r than +3 Gz k i n g

for more than 4 seconds. Using this criteria, the authors found that almost one-third of the

engagements they reviewed contained PPEMs. They therefore concluded that push-pull

effect is present in USAF fighter missions and considered it a significant source of risk

for aircraft accidents.

Even though the problem of the push-pull effect has been experienced and

documented by military tactical pilots [3-51 and civilian aerobatic aviators [15,20] for

many years, very little physiology of this effect is hown apart from basic BP and HR

measurements,

As stated previously. physiological measuns during the push-pull maneuver are

difficult to collect since most centrifuges, a common investigative tool in acceleration

research. are incapable of ~producing -GE to +Gz acceierations. In-flight experiments are

dso difficult to perform because the constraints of the cockpit environment limit the type

and amount of data that can be collected. In-flight experiments are also lirnited by the

pilots ability to follow flight paths with the precision and repetition neeâed for proper

scientific research. Despite these limitations. there is still a smail base of literature on

push-pull.

The rwts of push-pull research have been traced to an in-fIight study performed

by Von Beckh in the late 1950's 1351. Von Beckh hiid pilots in jet propelled intercepior

aircraft follow various flight paths in an attempt to study human reactions to acceleration.

One of the flight paths. "post-weightlessness acceleration" consisted of a penod of

b'weightlessness" (less than O Gz) followed by a d.5-6 Gz spiral. When examining the

results of this experiment, Von Beckh noted that in these pst-weightlessness trials,

pilots' G-tolerance was greatly diminished when compaxed to other flight paths

performed in the study. Although Von Beckh did not give a through explanation for these

findings, his nseûrch can be regarded as a prelude to the push-pull experiments of the

future,

Studies of civilian aerobatic pi lots also foreshadowed modem push-pull research.

Mohler examined the effects of G on pilots by studying the gravito-inertial forces

experienced during aerobatics [15]. He studied various aerobatic maneuvers including

"loops", "rolls", and "pull-outs". Mohler noted that during one maneuver termed the

"vertical 8 , where the aerobatic pilot would experience -Gz before ffiz, there was a

delay in the cardiovascular refiex response to +Gz. Even though Mohler stated that no

physiological h m would come from this iGz transition, he mentioned that the -Gz to

+Gz maneuver did increase the Iikelihood of blackout.

Bloodwell also studied civilian aerobatic competitive flying [20]. He measured

HR, G exposure, and maneuvenng time for 15 pilots involved in aerobatic cornpetitions

in Fredncksburg. Virginia and Fond du Lac, Wisconsin in L98 1. Bloodwell observed that

the mean minimal HR occurred during -Gz exposures and the mean maximal HR

occurred during +Gz exposures. He also noted that the maneuver most difficult for

efficient cardiovascular compensation involved cyclic variations of negative and positive

G. Although it was not yet labeled as such, this +G transition mimicked what would later

be termed the push-pull maneuver.

In 1990, Diednchs studied the effects of negative to positive G transitions by

examining flight profile statistics compiled from USAF training missions [37]. Using

data collected by the US AF Sdety and Inspection Center of California, Diednchs found

that the highest incidence of G-LOC occurred when a pilot perfonmd a "sp1it-S"

followed by either r "spin prevent or spin recovery and loop". Diednchs noted that this

sequence of maneuvers subjected the pilot to negative or zero G just prior to high +Gz.

He believed that the disproportionate amount of G-LOC episodes accompanying this

maneuver sequence were caused by this G-transition. Diednchs hypothesized that r

pend of -Gz immediately pnor to a +Gz maneuver resulted in a demased O-tolerance

and therefore G-LOC at a lower G-level. The author stated that this hypothesis had been

supported by the testimonials of over 3 0 trainer and fighter pilots who were questioned

in a non-threatening environment during physiological training at Williams Air Force

Base. Texas. He concluded that there was a need for increased military research and pilot

education with respect to the adverse effccts of -Gz to +Gz transitions.

Lehr, Prior, and colleagues were the fint to study the effects of -Gz exposure on

G-tolerance [19]. Using a multi-axled. gimballing human centrifuge, Lehr and Prior

exposed subjects to either - 1 .O, -1.4, or -1.8 Gz for 2, 16, or 30 seconds. Subjects were

then immediately exposed to f f i z increasing at 1 G per second until they reached their

reiaxed G-tolerance (determined as 60% loss of periphenl vision). The results showed a

significant reduciion in relaxed G-toierance when -Gz occurred pnor to +Gz. The

influence of the magnitude of -Gz was found to be relatively small, however. longer

durations of -Gz exposure were found to cause a greater reduction in G-tolerance. Lehr

and Prior found th* even -Gz exposures of only 2 seconds were enough to cause a

significant reduction in nomal G-tolerance.

In 1994. an in-flight study by Banks and Gray examined the effect of -Gz

exposure on HR [38]. 2 Canadian Forces pilots were studied while passengers in CF4 14

Tutor jet aircrafts. The flight profile included a 15 second, - 1 Gz maneuver which was

preceded and followed by 5 minutes of straight, level flight at +1 Gz. HR was monitored

and ncorded using and ECG. Both pilois were observed to have irnmediate and profound

bradycardia dunng -Gz exposure. The investigators attributed this decrease in HR to

increased ponsympathetic activi ty as a result of carotid barorecepior stimulation. Banks

and Gray noted that in addition to bradycardia, this increased parasympathetic activity

would also cause periphetal vasodilation and decreased cardiac contractility. They

believed that the parasympathetic activity during G z could adversely affect Ci-tolerance

since the bady requires increased caniiac output and vasoconstriction during +Gz stress.

Banks and Gray concluded that future operational research should focus on the potential

hazards and implications of -Gz exposure on G-tolemce.

Banks continued this research using the Coriolis Acceleration Platform (CAP) [2].

The CAP is a circular, horimntally rotating platfom with a movable cab on a track along

its radius. Banks placed his subjects in a supine, seated position in this moveable cab. By

spinning the plaâorm at certain speeds and moving the subject along the track. Banks

could alter the magnitude of -Gz and f f i z experienced by the subject by changing the

distance of the subject's head or feet fmm the edge of the platform [2].

Banks found that exposing subjects to -Gz More +Gz resulted in decreased BP

and decreased G- tolerance in the subsequent +Gz exposure. Since this negative to

positive Gz exposure rnimics the anaiogous to a pilot 'push9-ing forward then 'pull'-ing

back on an aircnfts yoke. Banks labeled the decreased G-tolerance caused by IGz

transition the "push-pull effect".

In his studies with the CAP. Banks also examined the effect of magnitude and

duration at -Gz on G-tolerûnce during a subsequent +Gz. By altering these variables.

Banks determined that both magnitude and duration of the -Gz exposure immediately

preceding f f i z acted to decrease G-tolemce. The greater the magnitude and the longer

duration at -Gz, the greater the âecrease in G-tolerance [2,39].

G-transitions can cause large changes in cvotid arterial pressure and, therefore,

carotid baroreceptor activity. Understanding that this could possibly effect the control of

vascular sist tance and ultimately G-tolerance, D œ et al. examined the effect of changes

in cmtid sinus pressure on the magnitude and time course of bmreceptor mediated

vascular nsponses [40]. Using anesthetized dogs, Doe constnicted a perfusion circuit

which allowed independent perhision pressure and flow control of the aorta and the

carotid sinuses (which. as stated in section 3.13, are the two main baroreceptor areas). By

keeping subdiaphramatic perfusion pressure constant and altering carotid perfusion

pressure. Doe was able to determine the effect of a l t e~d carotid bmreceptor pressure on

vascular resistance. Doe found that the time tdcen to reach 75% of the maximum dilator

response was significantly shorter than that for the corresponding constrictor response.

Doe concluded that, since carotid baroreceptor mediated vasodilation occurs more npidly

than vasoconstriction, maneuvers such as -Gz accelemtions that cause mpid changes in

carotid baroreceptor pressures may reduce vascular resistance. Thus. when -Gz precedes

+Gz. Doe predicted larger demases in artenal BP and a decreased G-tolennce dunng the

subsequent +Gz exposure.

In 1999, Wright and Buick published an in-flight study of the push-pull effect in

an attempt to validate the centrifuge as a ground-based simulator of the push-pull

maneuver [4 11. Using CF4 8 aircraft, Wright and Buick exposed 16 relaxed and

unpmtected subjects to 2 G/sec onset rate, 15 second duration G-profiles, in increments

of 0.5 G over the subject's G-tolerance. These different Gtxposures were preceded by 5

seconds of +1.4 to -2 Gz. Head and heart-level BP were measured as well as ear opacity.

The investigators found that the push-pull scenarios (-Gz to +Gz transitions)

caused a significant reduction in G-tolerance. G-tolerance was decreased by up to 1.3 Gz

when f f iz was preceded by -0.5 to -2.0 Gz. This reduction was found to be similar to

previously reported centrifuge data, therefore validating the multi-axled, gimballing

centrifuge as a useful twl in push-pull nsearch.

3.3 Tilt table test for the push-pull effect

The experimental tool used most recently to study the push-pull effect is the tilt

table. As stated in section 1.4, the tilt table is a rotating bed that cm be tilted amund its

centre point. A subject can be secured to the table in a supine or seated position and can

be tilted at various angles to observe physiologicd changes. A rapid HUT to HDT to

HUT sequence cm be used to mimic the push-pull effect maneuver 181.

3.3.1 Review of tilt table acceleration research

The tilt table has ken used in acceleration research for many years but has also

been successfully implemented in many other cardiovascular investigative applications

including syncope research [9-111. Since this is an acceleration study, the focus of this

review will be upon reports involving tilt table expenments for G research.

In 1941, Graybiel and McFarland investigated the use of n tilt table for aviation

medicine 1421. Using a custom made tilt table, they subjected 91 healthy individuals (the

majonty of which were pilots) to HUT 65" h m horizontal in order to place gravitational

stress on the subjects' cardiovascular system. Subjects were left in this position for up to

30 minutes unless collapse occurred During the experiment pulse rate and b l d pressure

measurements were made at 1 to 3 minute intervals. AIthough 69 of the subjects tolerated

HUT quite well. 9 of the 9 L subjects collapsed and 13 subjects responded p r l y to HUT.

The investigators noted that collapse usually occuned within the frst few minutes of the

test after a rapid increase in pulse rate, a decrease in pulse pressure. and a large decrease

in sy stolic BP. The subject was often observed to penpire and develop pallor of the face

and hands just pnor to fainting.

Graybiel and McFarland concluded chat this tilt table test was a good test of

physical fimess and believed that it could be used as a physiological aptitude test for

aviators' G-iolerançe. However, this daim was Iater contradicted by Estes who found

only weak correlations between tilt table response and G-tolerance [43].

Green and his colleagues studied the effect of tilt on BP and HR [44]. Of the over

200 subjects tested, 15 were detailed in Green's report. Subjects were tilted ai a moderate

rate of speed from the 20" HUT position to the 4S0 HDT position wheni they remained

for at least 15 seconds. Subjects were then retumed to 20' HUT. Thmughout the

experiment, BP was recorded from either the radial or brachial artery and HR was

recorded using an ECG.

Green found that during HDT, BP increased for a period of 8 to 18 seconds then

pmceeded to fa11 towards initial levels. HR was found to slow abruptly upon the inmase

of BP in the majority of subjects. Upon re tm to HüT, BP was found to decrease for 8 to

18 seconds then begin to recover towards normal. HR was found to increase suddenly

upon the decrease of BP. Green postulated that the relation between body position. BP,

and KR suggested that the change in HR was one of the reflex mechanisms that was

responsible for the regulation of BP.

In 1950, Wilkins et al. studied the cardiovascuIar effects of -Ch using a tilt table

[7]. Wilkins subjected 42 individuals to 7S0 HDT h m horizontal (considered a 1 Gz

shift) and 75" HOT from 75" HUT (considered a 2 Gz shift). The HDT phase was

maintained for between 2-30 minutes depending on the necessary measurements and

subject tolerance. Artenal BP. venous pressure. and subjective comments were recorded.

Most subjects experiencing HDT complained of a w m , flushed and congested

face. Subjects also noted cranial swelling, breathing difficulties. and watering eyes.

Objectively, HDT was found to cause numerous cordiovascular effects. Wilkins found the

head-down position caused a siowing of the HR which was often accompanied by ka t

imgularities. Stroke volume and CO was found to increase during HDT. Arterial BP

decreased slightly upon HDT and then decreased even further after a 3 or 4 pulse beats.

Wilkins noted that when a subject was tilted head-down from the HUT position that the

acute changes in arterial BP and HFt were "qualitatively sirnilar to but quantitatively

greater than" when an individual is subjected to HDT from horizontal. Wilkins believed

that this phenomenon could be attributed to the "opposite effects" of experiencing HUT

before HDT,

Wilkins findings were supported by Ryan and his colleagues [6]. Ryan's protocol

involved subjects experiencing a sequence of horizontal to 60" HDT followed by three

successive 60" HUT to 60° HDT tilts then a period of rest at horizontal. ECG and subject

perceptions were recorded. Dunng HDT, subjects had complainu similar to Wilkins'

group. These included increased pressure in the head. headache, fullness of the face, eye-

bulging, and respiratory difficulties.

Ryan observed that HR decreased when subjects were tilted from the horizontal to

HDT position. This decrease was more pronounced for the HUT to HDT tilts. Ryan

calculated that 93% of this HR change o c c m d in the first 3 seconds after naching HDT.

HR decreased for 15 seconds after HDT was reached then slowly recovered towards

resting values. The possibility of arrythmias was also noted.

Ryan found the opposite results For HDT io HUT transitions. When a subject went

from HDT to HUT. HR increased and 928 of this change occurred within the first 3

seconds of HUT. After 15 seconds, HR began to retum towards resting levels. Ryan

believed that the 15 second delay before retum iowards resting values w u due to the

carotid sinus reflex mechanism.

In 1960, Fletcher and Girling also used a tilt table to investigate the effect of tilt

angle on HR [45]. Their experiment involved subjects in tilt positions in multiples 45' to

the horizontal, rnaintained for 30 seconds each. HR was recorded using chest electrodes

and a cardiotachometer. A systemûtic relationship was found between HR and tilt angle

for al1 subjects. HR was highest in the vertical HUT position and lowest in the vertical

HDT position. The difference in HR between vertical HUT and vertical HDT was quite

large ranging from 22-62 bpm with an average difference of 40 bpm. Fietcher and Girling

also noted that cardiac deceleration was a faster pmcess thm cardiac rceleration.

Deceleration took 2-3 seconds whereas acceleration needed up to 20 seconds for

completion. It was suggested that this difference was due to the different mechanisms

involved in cardio-acceleration and deceleration.

In 1%3, refemng to the importance of body position to systemic BP and cerebrai

blood flow during gravity-induced flight. Abel examined baroreceptor influence on

postural changes in BP and carotid blood flow [46]. Abel monitored the HR. mean

systemic pressure, and carotid b l d flow of sixteen anesthetized dogs positioned for 10

minutes at horizontal, 30" HDT, and 30" HUT. The dogs were then partially or totally

denervated to block the effect of the baroreceptor reflex arc and the measurements were

repeated. Abel found that the animals' ability to compensate to HDT and HUT were

greatly impaired by denervation. During the HUT denervation nins, HR remained nearly

unaltered while both BP and carotid blood flow dropped precipitously with little

compensation. During the denervated HDT mns, HR remained unchanged while both BP

and blood flow increased slightly. These findings suggest the importance of baroreceptor

nflexes as part of the body's compensating mechanisms for gravity transitions.

In 1966. Tuckman and Shillingford investigated the effect of different degrees of

tilt on cardiac output (CO), HR and BP [47]. A tilt table was used to tilt 33 subjects From

a horizontai, supine position to either LOO, 20'. 30°, 40°. 55'. or 60' HUT position for 20

minutes. Subjects were then retumed to horizontai. HR. systolic blood pressure (SBP).

and diabolic blood pressure @BP) were recorded throughout the expriment. Mean

artenal blood pressure (MAP) and pulse pressure (PP) were calculated from SBP and

DBP values. Stroke volume (SV) and CO was measured using a dye indicator injection.

TPR was then calculated using MAP and CO measurements.

Tuckrnan found HR remained relatively unchanged at 10' md 20" HUT and

increased significantly at tilt angles 2 30' W. SBP. MAP, and PP were found to not

alter significantly at any of the tilt position. DBP increased at dl angles of tilt, however.

these changes were not significant until tilt mgle was 2 30'. SV and CO were found to

decrease gradually but significantly for each successive angle of HüT. TPR increased

significantiy at ail angles of HUT. Upon ntum to horizontal. a delay of at least 11-25

minutes occurred before CO was observed at the level recorded before tilt.

In 1998, Newman et ai. used the tilt table to in an attempt to gather evidence of

baroreflex adaptation to repetitive +Gz in fighter pilots [12]. Newman studied the

cardiovascular responses of 8 pilots and 12 non-pilots to t h e rapid-onset tilts to the +7S0

HUT position. Each HUT was held for 2 minutes before return to supine. SBP, DBP.

MAP. PP. and HR were recorded throughout the procedure for al1 subjects. Newman

found that the cardiovascular response to HUT was fundmentaily different between the

pilot and non-pilot groups. When exposed to HUT. pilots experienced a sigificant

increase in systolic. diastolic. and mean artenal pressure. PP was virtually unchanged. In

the non-pilot group. while the change in SBP, DBP and MAP was minimal w hile PP was

found to decrease significantly. HR was found to increase significantly for both groups.

Newman believed that this difference in cardiovascular response was evidence that the

baromflex mechanisms of fighter pilots had adapted to ffiz as a result of fiequent G

exposures.

33.2 Why the tilt-table G-rtsearch gap of over JO years?

A very conspicuous gap in tilt table G-nsearch of over 30 years (1966-1998) may

have been noticed above. The lack of acceletation investigations using the tilt table can

be expiained.

Even though the jet aircraft was invented dunng World War II, most planes of

that era were stiil powered by propellets and. therefore, had a lirnited G-envelope.

Consequently, human G-research only needed to probe within this envelope. Therefore.

the tilt table, even with its low G-threshold, was a prominent tool in G-research.

Over time. as jet aircraft became the military standard, the G-envelope became

larger and more pilots experienced the negative effects of high-Gz. G-LOC was

recognized as a main contributor many tactical aviation incidents and acceleration

physiologists realized thüt more high-Gz reseiirch was necessary. However, due to its

limited Genvelope. the tilt table could not simulate these high-Gz conditions. Therefon.

the investigative focus shifted to methods that could administer large magnitude

accelentions, namely the centrifuge and in-flight research.

33.3 The tilt table as a method for examining the push-pull effect

With the ment acknowledgment of the push-pull effect as a cause of numemus

military aviation accidents [3-51 the tilt table has seen a resurgence in the field of G

research. By subjecting a penon to a HUT to HDT to HUT sequence, the tilt table cm

ceproduce the hypotensive response to the push-pull maneuver [21]. This technique has

both advantages and disadvantages which were outlined in section 2.6.

3.34 Review of the tilt tabk simulation of the push-puU effkct maneuver

Goodman and LeSage [21] recently used the tilt table to study the push-pull

effect. 9 subjects were exposed to a senes HUT-HDT-HUT sequences that varied in HDT

angle (supine. 15O. or 45' HD) and HDT duration (7 or 15 seconds). MAP. HR, and

impedance cardiography data was collected from each subject. These values were used to

cdcdate SV and TPR.

The investigaton found that the tilt table could reproduce cardiovascular

responses seen with the push-pull effect maneuver. They reported that the HUT-EDT-

HUT produced a decreased HR. inçreased SV, and decreased heiut-ievel MAP in the

subsequent HUT maneuver for al1 tilt angles and durations. Tilting to the head-down

position also caused a shift in blood to the torso as measured by a decrease in impedance

(20). The HUT-HDT-HUT sequence resulted in incomplete recovery of HR. TPR and

MAP which Goodman and LeSage concluded was caused by a delay in sympathetic

drive. These results are sirnilar to the physiological responses to the push-pull maneuver

previously observed in the centrifuge, in the aircraft. and on the CAP [l, 2, 19.3 1,381.

3.5 Anti-G suit

There is a point at which the cardiovascular mechanisms for coping with G begin

to fail. As explaincd in section 22.2. as the magnitude of +Gz inmases, the result is a

gradua1 loss of vision followed by G-LOC. To avoid these problems and their associated

risks, countenneasures such as the anti-G suit have been developed in an attempt to

increase G-tolerance.

AntiG suits (also known simply as G-suits) have been used since WorId War lI to

counteraft the effects of high +Gz accelerations [16]. These suits, wom around the legs

and abdomen, contain ait bladders which are inflated w hen gravito-inertial forces are

above +2 Gz. This results in increased peripheral vascular resistance through increased

lower body tissue pressure, a decrease in the venous pooling capacity of the lower limbs,

increased venous retum, and elevation of the hem. Al1 of these factors act to maintain

HLBP under high f f i z and afford the wearer of the G-suit a 1-1.5 Gz increase in G-

tolerance [22].

3.5.1 The G-suit inflation during tilt

Numerous studies have exarnined the effect of G-suit inflation while in-flight or

in the centrifuge. However, very few stwlies have been conducted using both the tilt table

and the G-suit.

In a prelude to tilt/G-suit experiments, the effect of G-suit inflation in a 1 G

environment was investigated by MacKenzie et al. in 1945 [48]. Interested in the effects

of the G-suit on hem rate, the investigators recorded the hem rate of 1 1 seated subjects

using a cardiotachometer from 20-30 seconds before inflation to 20-30 seconds after the

release of pressure. Heart rate was found to slow for al1 11 subjects dunng G-suit

inflation. Moreover, the investigators observed a similar pattern for al1 subjects upon

inflation of the G-suit. The HR did not change for 3 4 seconds after inflation then HR

decreased by 1025% for approximately 5 seconds. HR then attempted to recover towards

pre-inflation values. HR recovered fuUy within 1 to 2 seconds after the nlease of

pressure.

In 1969, Gray and colleagues studied the effect of G-suit inflation on

cardiovascular dynamics [49]. For 5 of their 18 subjects. G-suit inflated with the subjects

in the 60° HUT position. Hem rate was recorded using an ECG and mean arterial

pressure was mcorded directiy from the btachial artery by use of a catheter. Cardiac

output was measured using a dye-dilution technique. Central blood volume (CBV) was

calculated from the data. Measurements wen taken upon inflation of the G-suit, 45

seconds into inflation, and 5 minutes into inflation.

Gray found that during G-suit inflation at 60' HüT, systolic, diastolic, and mean

meriai blood pressure increased 1 8.3 and 1 1 % respective1 y. These value returned to

control values after 5 minutes. CBV was found to increase 42% upon inflation of the G-

suit. This also retumed to normal after 5 minutes. CO inmased 53% dunng G-suit

inflation and HR dec~ased 10 beau per minute. These values penisted after 5 minutes.

In 1985, Seawonh et al. also studied the effect of G-suit inflation in a 1 G

envimnment [32]. Seaworth subjected 10 healthy men to G-suit inflation profiles of 2.4,

and 6 psi in using both the supine and upright position. Ventricular volumes were

~corded using two-dimensional echocardiography. Cardiac output, smke volume, and

end-diastolic volume (EDV) were calculated h m this measurement. Blwd pressure was

recorded by cuff sphygmornanometry to give both SBP and DBP from which MAP was

calculated. Penpherai vascular resistance was calcu