Male and female subjects prebreathed air or 100% oxygen through a mask for 3.0 hours while comfortably reclined. Blood pressures, heart rate, and cardiac output were collected before and after the prebreathe. Peripheral vascular resistance (PVR) was calculated from these parameters and increased by 29% during oxygen prebreathing and 15% during air prebreathing. The oxygen contributed substantially to the increase in PVR. Diastolic blood pressure increased by 18% during the oxygen prebreathe while stystolic blood pressure showed no change under either procedure. The increase in PVR during air prebreathing was attributed to procedural stress common to air and oxygen prebreathing

Conkin, J.

Dierlam, J. J.

Horrigan, D. J., Jr.

Riddle, J. R.

Stanford, J., Jr.

Waligora, J. M.

English

NASA Technical Reports Server

/ui_#-y/iz--5_ _ I
NASA Technical Memorandum 58261
NASA-TM-58261 19840022615
Increase in Whole-Body Peripheral
Vascular Resistance During Three
Hours of Air or Oxygen Prebreathing
FoR _EFERENCE
WOT'tO BETAI_SlFROM_ llOOM
August 1984 ..
LIBRARYCSPY
_:,_._1984
LANGLEYRESEARCHCENfER
NationalAeronauticsand UBRAR¥,NASA
Space Administration H,_,MP.TON,VIRGINIA
https://ntrs.nasa.gov/search.jsp?R=19840022615 2020-03-20T22:43:37+00:00Z

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INCREASE IN NHOLE-BODY PERIPHERAL VASCULAR
RESISTANCE DURING THREE HOURS OF AIR OR OXYGEN
PREBREATHING
Johnny Conkin, John J. Dierlam, John Stanford
Jr., and Jeanne R. Riddle.
Technology Incorporated
Houston, Texas 77058
James M. Naligora and David J. Horrigan.
The Lyndon B. Johnson Space Center
Houston, Texas 77058
,¸

ABSTRACTR
Male and female subjects prebreathed air
or 100% oxygen through a mask for 3.0 hours while
comfortably reclined. Blood pressures, heart rate,
and cardiac output were collected before and after
the prebreathe. Peripheral vascular resistance
(PVR) was calculated from these parameters and
increased by 29% during oxygen prebreathing and
15% during air prebreathing. The oxygen
contributed substantially to the increase in PVR.
Diastolic blood pressure (DBP) increased by 18%
during the oxygen prebreathe while systolic blood
pressure (SBP) showed no change under either
procedure. The increase in PVR during air
prebreathing was attributed to procedural stress
common to air and oxygen prebreathing.
I NTRODUCT I ON m
Prebrsathlng I00_ oxygen while comfortably
seated at sea level for several hours has been the
traditional approach for aviators to remove
nitrogen prior to high altitude exposure. The
removal of nitrogen decreases the probability of
subsequent decompression sickness. However, oxygen
at one atmospheric pressure has a vasoconstrictive
affect on the vasculature (refs. 1_2,3). Sitting
quietly for hours could also reduce heart rate,
blood pressure, and cardiac output which may
decrease a nitrogen washout. Studies on nitrogen
washout indicate that cardiac output is directly
related to the efficiency of the washout (refs.
4,5,6)•
Increasing the resistance to blood flow
through a tissue may retard the removal of
nitrogen from that region. This study attempts to
quantify the change in whole body (PVR) in males
and females prebreathing oxygen at sea level for
3.0 hours. It attempts to distinguish what
fraction of the PVR change is attributed to 100%
oxygen prebreathing and what fraction is
attributed to other procedural factors.
METHODm
Three males and two females prebreathed dry
aviators oxygen at 21"C for 3.0 hours for a total
of 9 tests. The same 5 individuals also
prebreathed dry compressed air on one occasion for
the same duration. Table I shows the physical
characteristics and total number of oxygen
exposures for each subject.
The oxygen or air was delivered through a
pressure demand full face diving mask_ Subjects
were reclined with legs parallel to the floor for
3.0 hours in a comfortable rec!iner during the air
or oxygen prebreathe. They were allowed to stand
and stretch after the first and second hour and
#mrs required to stand during the transition from
the sitting to the supine position after the third
hour.
Peripheral vascular resistance was calculated
prior to and following the 3.0 hour tests. A
simple relationship exists to discribe PVR (ref.
7).
mean arterial pressure (mmHg)
EQ (1) PVR =
cardiac output (liters/min)
Mean arterial pressure (MAP) being calculated
as (ref. B):
SBP + 2(DBP)
EQ (2) MAP =
3
Blood pressures were obtained by standard
TABLEI
SUBJECT PHYSICAL CHARACTERISTICS
i iiii ii i ii r
SUBJECT NUMBERTEsTSOF AGE WEIGHT(KG,) HEIGHT(cM,) BOD_ _AT SEX
1 2 28 88,6 185,4 18 M
2 3 35 68,0 180,3 12 M
3 1 24 68,0 170,1 13 M
4 1 28 58,9 167,6 24 F
5 2 34 58.0 165,1 22 F
sphygmomanometry with the cuff over the brachial
artery. Cardiac output was calculated from data
supplied during noninvasive 2D and M-Mode
echocardiography=(refs. 9,10) by a trained nurse.
After stabilizing the subjects in a supine
position for 5.0 minutes the cardiac output was
determined. Three quality estimates were collected
in 5.0 minutes and an average of the 3 was our
baseline value. 8till in the supine position_ 3
measures of 8BP, DBP, and heart rate were taken
and averaged. This same procedure was repeated
after 3.0 hours of oxygen or air prebreathlng.
Blood pressure and heart rate were collected at
30, 60, 120, 150, and 180 minutes during the
tests. The first oxygen prebreath test was done
without the PVR estimate for each subject. This
was done to lessen any "anxiety" effect caused by
naive subjects prior to a PVR estimate.
RESULTS --
The collected data was analysed by two
methods. A nondirectional paired t-test was
applied to all pre- and postoxygen or air
prebreathe data. Probability values less than 5.0%
were considered significant. This analysis
determines significant changes within each
procedure. Since changes occurred under oxygen and
air prebreathing an analysis of the absolute
difference between measured parameters using air
or oxygen was also performed. This was possible by
applying the same t-test and analyzing the mean
differences between oxygen and air data. This
would determine significant changes between both
procedures.
During 9 oxygen prebreathes for 3.0 hours in
males and females PVR increased on an average by
29%. This was a statistically significant increase
(p<O.01) from the baseline value (15.2 _ 3.4 yrs.
21.3 ± 5.b mmHg/lit/mln). During 5 air prebreathe
tests a significant increase (p<O.05) of 15% in
PVR was also evident (15.5 ± 3.a yrs. 18.3 _ 3.5
4
mmHgllit/min).
During quiet prebreathing using air, changes
occurred in DBP, heart rate, and cardiac output
that were in the same direction as changes noted
under oxygen prebreathing. However, the magnitude
of the changes using oxygen were always greater
and statistically significant whiZe the changes
under air prebreathing were not statistically
significant except for the PVR which is a derived
parameter based on data that did show trends but
never achieved statistical significance.
Figure 1 shows the percent change from
baseline of the measured and derived data. The
shaded areas indicate that portion of the change
caused by oxygen that was above the contribution
of sitting quietly in a reclined position with the
breathing system.
Table II shows the average data for each
eubject during the oxygen prebreathing. Applying a
paired t-test to the pre- and pomtsupine data
reveals that DBP, heart rate_ and cardiac output
were statistically different at least at the
p<O.05 level. Since MAP and PVR were derived from
the above, data they also showed significant
differences.
Heart rate decreased by 15%, cardiac output
decreased by 18%, and DBP increased by 18% over
the course of the oxygen prebreathe. Mean arterial
pressure increased by 12% which reflected the
increased DBP.
Table III shows the data for each subject
during the air prebreathe. Heart rate decreased by
12%_ cardiac output decreased by 14_p DBP
increased by 7%_ and MAP increased by 4% over the
3.0 hours. These were not statistically
significant changes from pretest data.
To establish which parameters were
substantially affected by oxygen prebreathing a
paired comparison of the differences in the air
and oxygen data was performed. This analysis
B
° iIIndicatesdata collected during oxygen prebreathe
i I Indicates data collected during air prebreathe
o i Ie_ ** I
L._._ /
v
,,, I|
.... ! I
u-_ . ! |
F- I I
,,, I
DIASTOLIC SYSTOLIC HEART CARDIAC MEAN ARTERIAL PERIPHERAL VASCULAR
o_ BP BP RATE OUTPUT PRESSURE RESISTANCE
c)
0-_ M_ • *
_ uJ
0
0
Figure 1. Changes induced in various parameters by oxygen and other procedural factors. Shaded
areas indicate changes above those observed foe the same procedure using air. * indicates
significantdifferences(p(O.05) from pre and post data in air or oxygen. ** indicates
the oxygen induced change that was significantlydifferent (p(O.05) from the changes
induced by procedural factors.
TABLEII
STATISTICAL ANALYSIS OF PRE AND POSTPREBREATHE PROCEDURES(oXYGEN)
i i , im
SUBJECT NUMBER OF SYSTOLIC DIASTOLIC HEART MEAN ARTERIAL CARDIAC PERIPHERAL
# TESTS BP BP RATE PRESSURE OUTPUT VASCULAR RESISTANCE
(OXYGEN) MMHG MMHG MMHG LIT/MIN MMHG/LIT/MIN
m il • i i
PRE 123 69 71 87 7.81 11.11
1 2
POST 128 79 63 95 6,56 14,65
PRE 141 84 74 103 5.53 18,97
2 J
-_ POST 152 111 52 125 4,61 27,19
PRE 115 60 55 79 6,26 12.56
3 i
POST i15 84 51 95 5.83 16.20
ii i i
PRE 115 67 78 83 5.53 15,04
4 1
POST 116 75 68 89 3.52 25.17
i lll|u |irai| iii
PRE 120 80 71 93 5,43 18,29
5 2
POST 123 88 63 100 4.45 23.50
• ii. im im ii
MEAN (_) PRE 123 + 11 72 + 10 70 + 9 89 + 9 6.11 + 1.00 15.19 + 3.4
MEAN (_) POST N=5 127 ± 15 87 ± 14 59 ± 7 101 _ 14 4.99 ± 1.20 21.34 _ 5.6
n
TABLEIII
STATISTICALANALYSIS OF PRE AND POST PREBREATHEPROCEDURES(AIR)
SUBJECT NUMBER OF SYSTOLIC DIASTOLIC HEART MEAN ARTERIAL CARDIAC PERIPHERAL
TESTS BP BP RATE PRESSURE OUTPUT VASCULAR RESISTANCE
# (AIR) MMHG MMHG MMHG LIT/MIN MMHG/LIT/MIN
PRE 126 69 73 88 7,38 11.92
I i
POST 130 76 66 94 6.70 14,02
PRE 133 77 76 96 6.80 11.32
2 1
POST 136 93; 60 107 5.07 15.38
oo
PRE 116 58 49 77 5.50 17.45
3 1
POST 112 61 53 78 5.05 21,18
PRE 111 68 81 82 4.17 19.66
4 1
POST 108 74 72 85 4.47 19.01
I I
PRE 126 84 82 96 5,63 17.125 1
POST 118 79 65 92 4.18 22,00
MEAN (7) PRE 122 + 9 71 + 10 72 + 13 88 + 8 5.89 + 1.24 15.49 + 3.7
MEAN ('_)POST N=5 121 + 12 77 + 11 63 + 7 91 + 11 5.09 + 0.97 18.31 + 3.5
showed that the increase displayed in figure 1 for
DBP above the level for the air prebreathe (shaded
area) was statistically significant. This was also
true for MAP, but not for cardiac output, heart
rate, and PVR. There was no statistically
significant change in heart ratep cardiac output,
or PVR on oxygen when compared to the changes
observed in the air prebreathe, however the trends
are evident with the magnitude of the differences
always being greater for oxygen prebreathing. A
statistically significant difference may have been
obtained for PVR with a larger subject population.
CONI::LUS ][ON m
It was possible to measure a true whole
body increase in PVR during oxygen prebreathing
with the techniques described. An effective
increase in PVR of 29% occurred on oxygen with 15%
of the increase being attributed to other
procedural factors.
Diastolic blood pressure and therefore MAP
consistantly increased while breathing air or
oxygen over the course of 3.0 hours. They
increased to a greater degree on oxygen which
indicates general vascular constriction. 9ystolic
blood pressure remained constant under all test
conditions while heart rate and cardiac output
decreased in both procedures. Only during the
oxygen prebreathe were these decreases
statistically significant.
Past data (ref. 3) indicates that specific
organs, especially brain structures and viscera,
increase vascular resistance in response to 100%
oxygen. This technique does not allow a detailed
analysis of specific organ systems. Instead, a
whole- body response to o×ygen was determined.
This has operational implications since the
technique reproduces the general procedures used
by aviators to remove tissue nitrogen prior to
altitude exposure.
9
JOxygen can be considered aS a drug that has
dose-response characteristics. Individuals could
respond to oxygen differently. This may explain
some of the variability in individual
susceptibility to decompression sickness.
Sitting quietly for 3.0 hours breathing air
did increase PVR to a degree (15%). This proved to
be a counterproductive situation in this
procedure. It is desirable to keep PVR as low as
possible so the total magnitude of the oxygen
contribution and the contribution due to specific
prebreathe procedures will not be excessive. The
amount of nitrogen removed from the body may be
improved if PVR can be reduced.
The results from this study show that oxygen
as well as general sedentary conditions increased
PVR over extended periods. It is suggested that
aviators perform moderate physical activity during
the course of lengthy oxygen prebreaths. This will
increase cardiac output which may offset the
increase in PVR since carbon dioxide in active
tissue will regulate vascular beds. It is not
certain that vascular structures near the knees,
ankles, and elbows respond to 100% oxygen as do
more sensitive neural structures. Moderate
exercise may not have a beneficial effect in these
"bends" susceptible areas but any increase in
cardiac output has the potential of improving a
nitrogen washout.
The results presented in this study were obtained
from a pre- and postmeasurement period. The
measurements were separated by 3.0 hours. The
oxygen and procedural effects were cummulative in
nature and a detailed study of the changes during
the 3.0 hours would be beneficial.
lO
REFERENCES
1. Bird, A.O., and A.B.M. Telfer. The effect of
increased oxygen tension on peripheral blood flow.
In: Hyperbaric Oxygenation: Proceedings of the
Second International Congress. McA. I. Ledingham.
Edinburgh; Livingstone, pp. 424. !9a5.
2. Norman, 3.H., T.T. Zrvin, and S. Smith. The
effect of inspired oxygen tension on renal blood
flow. In: Blood Flow Through Organs and Tissues.
W.H. Bain and A.M. Harper. Edinburgh; Livingstone,
pp. 449. 1968.
3. Plewes, 3.L., and L.E. Farhi. Peripheral
circulatory responses to acute hyperoxia. Undersea
Biomed. Res. 10(2): 123-129, 1983.
4.Theis, C.F., 3.D. Adams, and K.W. Stevens.
Nitrogen washout in the supine position.
Proceedings of the 1979 Aerospace Medical
Association Meeting. May 14-17, pp. 262-263. 1979.
5. Sroom, A.C., S.H. Song, Y. Ohta, and L.E.
Farhi. Effects of anesthesia on rate of nitrogen
washout from body stores. 3. of Appl. Phys. 37(2):
219-223. 1974.
6. Balldin, U.I. Effects of ambient temperature
and body position on tissue nitrogen elimination
in man. Aerospace Med. 44(4): 365-370, 1973.
7. Kelman, S.R. Applied Cardiovascular Physiology.
Second Edition. Butterworths Inc., Mass. pp. 18.
1977.
8. Burton, A.C. Physics of the Circulation. Year
Book Medical Publishers Inc., Chicago. pp. 86.
1968.
9. EC-200 Operators Manual, Digisonics, Inc.,
Houston, Tx. Ssp. 29, 1983.
w
10. Lust, R.M. 3., L.O. Lutherer, and M.W. Vooper.
Applicability of echocardiography in volume
determinations in experimental animals. 3. Appl.
Physiol.: Respirat. Environ. Exercise Physiol.
56(6): 1670-1674, 1984.
II
FOOTNOTES
J
1. Intertechnique Type 409716 Oxygen Breathing
Mask. 78 Plaisir, France.
2. ATLIADR Model 4000S/LC Ultrasound. Tempe,
Arizona.
NASA-JSC
12

i1. ReportNo. J 2. GovernmentAccessionNo. 3. Recipient'sCatalogNo.
NA_A-TH=_(_ " I
4. Title and Subtitle 5. Report Date
Increasein whole-bodyperipheralvascularresistanceduring Auqust 1984
three hours of air or oxygen prebreathing 6. PerformingOrganizationCode
i • i
7.Author(s) James M. Waligoraand David J. Horrigan JSC 8. Performir_Organizatio_1R INk}.
Johnny Conkin,John J. Dierlam,JohnStanford and
Jeanne R. RiddleTechnologyIncorporated S-537
j_. 10. Work Unit No.
O, Performing Organization Name and Address 199-99-00-00-72
NASA LyndonB. JohnsonSpace Center 11.ContractorGrantNo.
H0uston,TX 77058
NAS9-17200
13. Type of Report end Period Covered
12. Sponsoring Agency Name and Address
NationalAeronautics& Space Administration TechnicalMemorandum
Washington,D.C. 20546 14._w:w)n_w_ri_AgencyCode
15. Supplementary Notes
16. Abstract
Male and female subjectsprebreathedair or i00_ oxygen througha mask for 3.0 hours
while comfortablyreclined. Blood pressures,heart rate, and cardiacoutput were collected
beforeand after the prebreathe. Peripheralvascularresistance(PVR) was calculatedfrom
these parametersand increasedby 29% during oxygen prebreathingand 15% during air pre-
breathing. The oxygen contributedsubstantiallyto the increasein PVR. Diastolicblood
pressure increasedby 18% during the oxygen prebreathewhile systolicblood pressureshowed
no change under either procedure. The increasein PVR during air prebreathingwas attributed
to proceduralstress commonto air and oxygen prebreathing.
17. Key Words (Suggast_ by Authm(s)) 18. Distribution Statement
Aerospacemedicine Physiologicalfactors Unclassified-unlimited
Peripheralcirculation Subjectcategory: 52
Vascoconstriction
Decompressionsickness
Nitrogen
19._ur,tyam,if.(ofthisrefers)Unclassified {:O._c.JritvClas$if._ofthis_)Unclassified 121N°°_Pa_sJ22'mi¢e'14
"For _le by _e National T_hni_l Information _ice, Springfield, Virginia 22161
JSC Form 1424 (R_ Nov 75) NASA -- _C

4I


Increase in whole-body peripheral vascular resistance during three hours of air or oxygen prebreathing

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