VENTILATORY CONTROL OF HEART RATE DURING INHALATION OF 5% CO1 AND TYPES OF PANIC ATTACKS

Studies

designed

to

evoke

panic-disorder

patients S’%

inhalation

of

challenge)

reveal

heart

While

rate.

and Heninger of

CO1

did not panic,

Roth

increase

of

“panicked”.

subjects

who CO?.

reported from period

but

of about

patients

5.5%

(IY87).

a small

increase

of CO1

l-1 patients

6 b/min who

did

not.

heart

on

one bimin

each.

both

“panicked” And (M

of inhalation

other for

two

which

during and

75.X

of 5.5%

CO1 (M

for

a group

of Iti patients

with

of panic

attacks

during

seven

through = 76.0

of

changes

in

from

the poini

there

with will

I ‘Ji

or

of 5%

of

which

a

arc reported The

purthese

of respiratory

of view

no

that

rccog-

nature

(Lcy,

of

in press).

tiir.cpc.f physiological

increases

without

increase

in ventilation

by the :tddition

of view

prolonged

and .sigrl[fi’crrrlt

rate

in

and reflexive

is

these

the absence

attacks?

to CO,

between

people

creases

of whom

of

of diffcr-

is to address

;I point

responses

heart

no history

a

tight

among

studies

study

ventilatory

for

range

for

panic

present

the volitional

S’%, CO2

a

with

sleep.

of the subjects

experienced the

Although

b/

CO? (A4 =

16 patients

increases

accounts

portion

connection

rate

.SI>

the large

nizcs both

of

(IYYO)

in heart

b/min)

sleep.

contained

in

b/min.

during

what

psychophysiology. of

inhalation

rate

questions

rc-

groups

Barlow

no increase =

hand,

non-significant

of

Craske

essentially

baseline

the

rate

And

have

post

statistically

for

heart

significant to

attacks

incrcasc

of 5.5%

11.8) for

accounts in

studies?

and

=

M = 77.3

“panicked”.

ences

patients

(M

inhalation

SLI

of panic

What

a uniform

for

b/min,

whom

who

baseline

I I .7) through

history

and

absolutely

and

rate from

77.3

patients

reported

patients

in

increase

eight

=

CO2

normals.

Sanderson ported

min)

about

the

a mean

for

“panicked”, heart

Goodman.

inhalation

(IYYO)

in

of increase

for

of I6 bimin

asymptomatic

IO

(bimin) during

(i.e.

Charney,

( 198X) reported

a mean increase

who

air

attacks

of prolonged

range

Woods.

“panicked”

mean

in

a large

25 beats/minute

who

panic

by means

in

of

in heart

rate

panic

disorder,

proportion

beyond CO2

inhalation

that

to room

to

in-

demanded air.

Thus,

R0NAI.I)

104

one explanation

for

sonle.

if

not

aII.

of

the

in heart rate during

inhalation of 5% CO1 may lie in voluntary hypcrncic breathing (overbrcathing) i.e. an increase in ventilation beyond the involuntal-y cupneic level (reflesivc breathing) demanded by the addition of 5% increase

(‘02.

The

following

cicmonstr~rtion

was designed

for the purpose of illustrating how changes in heart rate can be controlled through (a) voluntury changes in breathing during prolonged inhalation of 5?0 CO2 and (h) voluntary changes in breathing during prolonged brea thing of room air. This clcmonstr~ltio~~ was not designed to test :I hypothesis: it is offered hel-c as a first-hand empirical illustration of the 1’sy’ti(‘physioloFic~li process by Lvhich partial control of heart rate can be achievccl through simple voluntary ventilatory mancuvcrs. This case study provides tangential data on the connection between respiration and panic (a) by demonstrating that involuntar! brea ovcrbreathin~ (i.e. thing and voluntary hypcrpnea) during prolonged inhalation of 5% CO2 in air produce respiratory and cardiac changes associated with primary panic attacks and (b) by demonstrating that voluntary hypcrventilatory breathing and involuntary rcspiratory effects immediately following prolonged CO2 in air produce acute inhalation of 5% hyperventilatory

hypocapnea

sudden drop in pC02 increase in heart rate.

and

iI11

marked cqu;dIy

by

:I

sudden

I.1.Y

history of respiratory clisorders. and was not experiencing an\ acute rcspiratorq clistrcss. The subject understood the physiology of t-cspiration and the purpose of the experiment.

Appmtus otltl ptwcdrrt~c~. ‘l‘hc apparatu\ consistcd of ;i flowp;ist system hy which ;I stream of gas wfl;is conducted past the distal Cnd of the mouthpiece through which the \ut3Ject breathctl. I’he t’low t-ate was such that it exceeded the inspiratory flow ralcs ot the subject so that by controlling the composition of the gas stream the cxpcrimcntcl- was able to control the inspired ga4 concentrations ol the sut>,icct. The expired gases were car-rid ;I\\;I\ in the gas stream. Ail- ~;IS drawm 1’1roni the room and pumped at ;I stcadv rate of 75 limin into ;I mi\ing chamber. .lud prior to entering the chamber. put-c (‘(I1 coiIIc1 bc 2ctdecl to tlic ait- stream. A mass spectt-ometcr prcdw Iving in the g;14 stream just distal to lhc mixing chamhe~ allowed the Icvcl of (‘0, IO lx mcasuretl. The experimenter was ;ible to adjust the flop r-ate of the pure CO1 to produce ;I mixed gas concentration of 5’!/,, (‘0, 93”!4, ail-. Ilie flom ot (‘0, could bc turned on or off using a tap thus allowing the gas stream to bc changed from ait onlv (tap closed) to 5% (‘0, in air (tap open). Th&c gas rnixturcs u’ct-c then conductccl through and

subject

of this

to

past the mouthpiece

the

rroom.

A

length

ot

was ad&d on the down-stream 4icle of the mouthpiece to act as ;I dead space so that if peak inspiratory flow rates excet~~cd 73 Vmin inspired gas would still be dl-awn in from the tubing

ml). The

tubing

vented

flow-past system and not the room. The subJect wore a noes clip and breathed through the mouthpiece; this in turn was conncctcti to the flow-pat system \,i;t ;I l”icumot~lchograph (Fleisch #3. ctuaclspacu 1X.i

Method Srrl?jcct.

wide-bore

then

single-case

study

was ;I healthy %-year-old male volunteer recruitcti from the staff of the Charing Cross Hospital and Westminster Medical College staff, who had no history of panic attacks. no

Thi\

allowed

inspir-atory

and

the

mcasurcmcnt

expiratorq’

was recorded and integration a record of inspirccl

flow

prmiuwd (VI

flows.

). Hand

chart

records

analysis allowed

both

ot’ this signal tidal

of these signals inspired

of

Inspirator)i volume

f’rom paper

respiration

rate,

tidal

volume.

and minute

volume

to be calcu-

lated. respiratory

mass

MGA200)

allowing

both

just to

single

was

lead

recorded

CO,

allow

lips

(lead

rate

to

VS)

be

re-

corded.

volume. for

each

Figure fksign.

Respiration

liters

-

per

minute. (beats

breath.

minute

and pCOl

throughout

the

first

sisted

were

six

and

phase,

which

period

were breathed

during

followed

during

which

the

5%

CO,

in air i.e..

effort

to control

no voluntary

no effort

respiration third without

which

interruption. during

which

voluntary fourth

i.e..

effort phase

which

consisted the subject

attempting

to

on room

air),

without

interruption.

period

during

breathed while

room

attempting

each

lowed

which

breath. the

fifth

;I

S-min

breathed

of

room

made

on

5%

followed

which

period

tidal

5% while

volume

of

(hyperventilating the fourth

consisted the

dur-

breathed

the

in

without

of 30 breathdmin phase

no The

CO1

phase

of a 5-min

fifth

The phase

breathing.

third

maximize

The

he

either

second

voluntarily

in air at the rate

each breath.

of

the

made

volume.

his

(overbrcathing followed

interruption, ing which CO1

to control

subject

of

phase

;I

S-min

voluntarily

air at the rate of 30 brenthdmin to maximize The phase

sixth

the tidal phase.

without

rate

of

arc given

the in

data

for

in Figure

2.

the respiration

a pattern

of

standard

measures

breathing

normal Table

respiration I. which

deviations

volume

which interruption.

fol-

-_

Of

I I

I

I

of the

of room contains of

the

I

air)

under

period breathed

subject

heart

without

or &a-case

the

the

phases

tidal

pCOZ)

25) are given

sat

his breathing;

consisted

three

second

phase

the subject

first

baseline

IS-min

the

All

conditions.

con-

the subject

followed

rate.

and end-tidal

one through

(ad libitum

and

The

tidal

phase

means

reflexively

or

Phu.sc~ I. first

relaxed

air)

the all of

experiment.

the subject

;I

to increase

reflexively

air).

subject

frequency

phase,

period

of

while

show

which

the first

consisted

I,

of

(min

continuously

ad libitum.

interruption. (eupnea)

per rate

room

made while

the

in

in liters

of the -

volume

and heart

recorded

(baseline

of a S-min

upright

Hg)

phases

phase

measurements

made

min

(respiration

volume,

each min of all six phases

(respiration

tidal

volume

in mm

per minute)

The

measures

beats per minute,

measures

minute

experiment

frequency

which

reflexively.

Results Respiration

heart

during

air

and O7

be recorded. electrocardiogram

to

period

room

from

to the subject’s

and expired

breathed

(Centro-

gas continuously

distal

inspired

concentrations A

spectrometer

sampled

the mouthpiece

air

of a S-min

subject

A nits

consisted

I

the

respir-

ation measures and heart rates for each ot‘ the six phases, provides ;I statistical profile. During Phase I, hasclinc mcasurcs show ;I respiration rate of IO brcathsimin. tidal volume of .X0 I/breath, minute volume of 7.83 liniin. pC@ of 38.22 mm Hg. and heart rate of 69.2 Mnin (a rate consistent with the subject’s personal record of heart rate during relaxed

wnkefulncss

taken

over

;I

period

of several

years).

I’IIUSf’ 2. nc cffccts of adding 5% c01 to room air can be seen in min 0 through 20 of Figure 2 and in the data of the second Phae of Table I. All respiration measures showed a sharp increase (incan respiration rate rose

from 10 to 17.27 breathdmin. mean tidal volume rose from .X0 to 1.25 I/breath, mean minute volume rose from 7.84 to 23.23 Vmin. and mean pC0, rose from 3X.22 to 47.41 mm Hg) while mean heart rate remained virtually constant from Phase 1 (6Y.2 b/mill) to Phase 2 (6Y.Y b/min). P/~rr.sc~3. The termination of 5% CO? at the end of the second Phase (20th min) and the resumption of reflexive ad lib. breathing of room air in Phase 3 (min 21 through 25) resulted in a reduction in the respiration measures. However. comparisons with the baseline mcasurcs indicate that the reduction in respiration to a mean of 14 breaths/min was still significantly greater than the mean of IO breathdmin during Phase 1. evidence of the “afterdischarge” or “flywheel” phenomenon (Folgering, lYX8). Mean tidal volume (.72 I/ breath) and mean pCOl (35.02 mm Hg) were slightly lower than corresponding mean baseline measures of Phase I. Minute volume. a correlate of respiration rate and the variable underlying pCOI, also showed evidence of the flywheel phenomenon i.e., the mean volume of Y.Y6 I/min was L greater than the mean baseline of 7.84 limin. Although heart rate rose from 6Y.Y b/min during Phase 2 to 70.X b/min during Phase 3. the singular datum of this phase was the level of pCOl during the first min following terminatier: of 5% CO? (30.1 mm Hg). Compared with the level of pCOz of the last min of Phase 2 (47.4 mm Hg), this sudden decrement (47.430.1 = 17.3) represents a 36% drop in pC02. Pl~nse 4. Respiration measures for the last min of Phase 3 (25th min) and for each min of the last three phases of the experiment (min 26 through 40) are given in Figure 3. The effects of voluntary forced overbreathing (30 breaths/ min plus voluntary effort to maximize tidal volume of each breath) of 5% CO? in air can be seen in the second panel of Figure 3. where all four respiratory measures show a sharp rise from the 25th min (the last min of Phase 4).

Evidence that voluntary forced overbreathing increased ventilation beyond that produced by eupneic breathing of 5% CO, in air can be seen in a comparison of the respiratory data of Phase 4 with those of Phase 2. Table 1 shows that mean tidal volume during Phase 4 (1.63 I/ breath) was greater than mean tidal volume during Phase 2 (1.25 I/breath); mean minute volume during Phase 4 (4Y. IY Vmin) was more than twice mean minute volume during Phase 2 (23.23 I/min); while pCOl was about the same (46.86 mm Hg during Phase 4 vs 47.41 mm Hg during Phase 2). For the purposes of the present paper. the most significant datum was the sharp increase in heart rate (set Figure 2 and Table 1) from ;I mean of 6Y.Y bimin during Phase 2 (eupneic breathing of 5% CO1 in air) to 81.2 b/min during Phase 4 (overbreathing 5% CO1 in air.

li0NAl.l)

I ‘JS

I’/IN.Y~ lation

5. The

effects

(maintaining

hreathsimin) ing

when

in

Phase

of

the

sharp

5 in

tidal

and minute

tory

drive.

(‘(I7

decrcasc volume

which

addition

room

5%

IO

indicate

of

5”/;,

the

C‘O,

tlowevcr,

to to

the

to to

cotiipat-iaon

during

hc

the

mm

3O.S-l).

cstcnt

contrihutcs

I .13)

can

Phax

limin

30

follow-

air.

I .h3 l/breath

(4X.

4 to

close to those of the baselines of Phase I. It should he noted. however. that while minute volume slows down quickly to baseline levels during Phase I. pc‘O1 does not. Although pc’0, shows ;I steady rise from 3.4 mm Hg

at

air

in t’t-om

(

volume

reductions the

hypcrvcnfirate

breathing

overhreathing

seen

of voluntary respiration

I.LJ\r’

Hg

first

during

min

of

the

fifth

the

final and

phase finai

of minute

short of 07% of resting pC’02 prior \,entilation. thi5 condition indicates

23.7.3 limin).

h5l”t-\,‘“til~rtioti.

during

I’h;isc

Tidal cotiipirccl

ingfully qucnq

bxs

with

5

minute

volumes Ixx~ruse

t-cstrictecl

cannot be nieantrc9piration (I-C2 coti4tant of 30 it w;15 pct-tiiit-

10

hreathdmin

dur-iny

ted

frcclv during I’haw 2. significant rcspit-ation datum of the dramatic cleclinc in pC’O1 from during the last min of I’Ii;~sc 4 to

to vat-> I‘he most I’hasc 5 M’;IS 47.5 tiini t1g

35.5

mm

I’hasc

tlg during

decline csccc& mm fig

5 while

the

i’ir4t

min

of

I’Ii;iw

5.

;I

of -IO?,, ’ I‘hi4 drop of 22 mm kig the 17.3 111111liy drop from the -17.1 of the last miti 01‘ I’hax 2 (cupncic

breathing of 5”‘c1 C’O1 in air) to 30. I nini 1 l,c ot the first miti of I%:Iw 3 (ad lit>. tlreathing ot room ail-). The theorelical \ignificancc of thee

ant1 dramatic

sudden acute the

onset

of

termination

cspcciallb in

of

if one

dir.

rate

In

the 90 himin

of

ot

the

room

by air

the

Ihc

in

air.

3”%

sui-gc

C‘O,

in hear1

Pliasc -I to of I’hasc 5 Icncls

last

min

miti lhc

in the follows

(‘(IT

during of

hvpocapnic

volitntarv

when

in

to

lies that

5%)

fourth

support

producccI CO,

breathing

o\,ct-hr’cathc\

S3 tdmiti

additional

in p(‘02 alkatosis

conncctic~n.

this

from

drops

rcspir;ttorv

II\

ot

o\et-ht-edthing

normal

and

.5?,

ait-.

forced

h. In this

lib.

breathing

and

l‘ahle and

sutu

of

final room

phase ait-).

the

data

of

Figure

I treveat heart

recocery

pet-iod

oral

an

fixation

of

following

Since

report

panic during

Harclonk

that

if after

three

min

the

subject

coiilcl

Ixcathecl the

not

be

espcri-

obtained

trial w;14 tcrniinated. the end of Phiisc 0. the he felt no ansictv during pha4ck and expct-icticcd of the DSILI-IIIK cl:t\\iattacl\s pha~

esccpt 5. the

for lightpcrioci ot

for-cccl

voluntary h~l~~rv~~itil~ttion ot room ait-. mild dysptlc;i during Phase 7. eupncic inhalation of 5% (‘(IT in air. Esccpt for sonic clisconitort in the jam m~iscles and ;I dr\ mouth. conditions cotiltiio~i to prc~loiipd hr-eathins \,ia 3 nioitthpiecc. the onlv itnpleas;rnt sensalion espcricticed L\;IS the sense of loss of volittitat-v control of tlreathing dut-ing the I--niin pet-iod of inhalation ot .TJ”~, and

CO2

in air (l’hasc

2). The suhjcct repot-tccl that an Ltncontrollahtc and for-cccl increase in frquenc\ and depth of ventilation was unplcos;ant and might ha\ e tx~n ;I stimulus i’or fear if hc had not knc~n what to anticipate sensation

of

t7re~tthing

.S”,,,

(‘0,

in

air.

Discussion

4

iiic;i-

to

levels

ot

falls to hyxrchronic

pC‘02

throughout

until the cxperiniental Initiiccliatel~ I’ollowing sithicxt t-cported that any part of the 4i\ none of the scnsationk llc~~dedticss

by

maintain

h~l”t-\‘entilation.

.Ylrl~jc~.l‘.s ~por’f. through ii mouthpiccc 111ent,

specified

who

of ad

(t-esumpfion

that the respiration rate show ;I return

of recovery

( 1979).

voluntary

when /‘/zK\c

range

Beunicr

a 5-min

the

eft’ccb

hV}‘ct-v”itilation

prcccded

36.6 pCO1

falls ,just short of the lowest measure during Phase I, namely. 36.5 mm 1lg. This relativeI>, sIow rccovcry is. howe\,er. well within the

which vcntila-

\~oIum~~ during I’hasc ? (rei’lcsivc breathing of 5”L C‘O, in air) makes it clear that voluntary hypcr\,cntilation of room air result5 in ;I significantI) greatctventilation (tiw3;it1 = 3h.M limiti) than reflexive breathing ot 5’!4, (‘0, in air (tiic;iti = volume

to

tnin

The

results

of

the

clcmonstratior~

present4

here illustrate the psychophysiological process by which voluntary overbreathing during prolonged inhalation of 5% CO1 in air can lead to a significant increase in heart rate. The results of this demonstration also indicate that voluminous voluntary hyperventilatory breathing can produce an even greater increase in heart rote. The implications of these results bear directly on the differences in heart rate reported in studies that have employed the 5% CO, and thus provide the basis for the challenge, hypothesis that some of the variance in heart rate data may be attributable to variability in volitional overbreathing among the subjects tested. If this is the cast. then the magnitude of increases in heart rate during the 5% CO? challenge could be attributed to differences in excessive ventilation that reflect the degree of ventilatory anxiety induced by differences in experimental procedures. While differences in experimental procedures may be a potent source of variability in heart rate during inhalation of 5% CO?, another factor that may contribute to heart rate variability lies in individual differences in the nature and severity of the presenting complaint i.e.. panic disorder appears not to be a unitary phenomenon (Ley. lYX7: Wolpe & Rowan. IYXX). This hypothesis will be discussed in the following answer to the cluestion: *‘What accounts for the absence of heart rate changes in studies in which a significant portion of the subjects are reported to have experienced panic attacks?” Panic Attacks

Heart

Without

Increases

in Heart Rate

palpitations are the most common symptom of the DSM-IIIR list of symptoms of panic attacks (Barlow, Vermilyea, Blanchard, Vermilyea. DiNardo, & Cerny. IYXS; Margraf. Taylor, Ehlers. Roth, & Agras. lYX7). In terms of intensity. Barlow et al. (lY85) reported that palpitations topped the list of I2 symptoms. while Ley (lY8Sb) found

them to be second from the top discounting fear. The intensity ratings of these two independent studies. which correlated highly (I = .77), are consistent with the findings of adventitious panic attacks that occurred during physiological assessments of panic-disorder patients. La&r and Mathews (lY70) reported three cases of adventitious attacks in which heart rate rose from a resting level of X4 b/min to ;I panic peak of 120.7 (i.e. mean increase = 45.7 bimin); and Cohen. Barlow. and Blanchard ( 1085) reported two cases of adventitious panic in which the mean increase in heart rate rose from ;I relaxation level of 64.5 b/min to II panic peak of 108.S b/min (mean increase = 44.S himin). Other studies which describe panic attacks during the course of laboratory experimentation also report large and sudden increases in heart rate. Murgraf. Ehlers, and Roth (lYX7) reported ;I sudden large increase in heart rate of about 5 I b/min following false feedback that heart rate had increased; and Sander-son. Rapee. and Barlow (IYXX) reported ;I smaller but similar sharp increase in heart rate from X6 to IO5 b/min in a patient who believed that she was inhaling a panic-inducing gas. In view of (a) the plethora of retrospective reports of the high frequency of intense heart palpitations during panic attacks, (b) the objectively recorded tachycardia during adventitious panic attacks. and (c) the relatively high frequency of increases in heart rate during panic attacks induced by laboratory challenges, what accounts for the negligible increase in heart rate during attacks reported by Sanderson (lYX7) and the absence of any increase in heart rate reported by Craske and Barlow (lYYO)? An answer may lie in a refinement in the definition

of “panic”.

sonzotic

Ley (IYYO. in press) has proposed that there are three distinct types of panic attacks, all of which meet the criteria of the DSM-IIIR classification of panic. but each of which differs

IION/‘.l.l~

‘700

the others

from

physiological sic)

panic

on five

psychological

variables. attack

is

While the

and five

the Tyl~

I (clas-

blown”

attack

“full

marked by dyspncic-fear (Lcy. 1%-49) and a sharp increase in heart rate (high probability) (c.g. the adventitious panic attacks reported by Cohen ct al.. IW5: La&r M Mathews. 1970: Margraf. Ehlers. CC Roth. 1987). the Type II (anticipatory) panic attack is marked by fear, but no dyspnca. and less intense heart palpita tions (moderate probability) (e.g.. C’02induced panic attacks reported by Woods et al., I9XX). and the Type III (cognitive) panic attack is the pcvit ~YK~~~~L~ attack marked by anxiety, but neither dyspneic-featnor anticipatory fear. and the absence of palpitations (low probability) (e.g. sc‘c symptoms of SubJect 9. Lcy,

I.l‘L

expected

to show

those

fewer

Type

reported

II

et al..

by Woods

those rcportcd

by Sanderson

attacks

than

hut more

than

( IYX7).

In addition to such rcasscssments. ;I conparison of the details of the experimental procedures employed in thcsc studies ncucls to bc

with

made

those

aspects

might

be

special

expected

excessive

to

ventilation

ing of 5%

CO,.

would

based

be

attention

focused

of the experimental elicit

during

The

overhrcathing

(i.e.

ing inhalation

of 5%

that

differcnccs

in

prolongec!

crucial

on

breath-

comparison

minute

here

volume.

hypcrncic

on

methods

Since

ventilation)

dul-an incrcasc in heart rate, differences in the Increase\ in mean minute volume would predict differences in mean increases in heart rate. C~ produces

lOX5a).

in the classification of panic. the negligible increase in heart rate reported by Sanderson ( 1X37) and the conpletc absence of an increase in heart rate Based on this refinement

reported by C’raskc and Barlow ( 1990) might be explained on the basis of differenccs in the types of panic attacks presented bv their respective patients. That is. sine prolonged inhalation of 5% CO2 prevents the full blown symptoms of h~pcrventilatory hypcaipnca. panic attacks during such inhalations are limited to Types II and 111. Since increases in heart

rate are less typical

II attacks.

it follows

the panic attacks

may most.

the

alI.

it’ not

and Barlow

that some

reported

been

have

of

reported

by the patients answer

theoretical

issues

A similar whom their

the

important

raised

et al.

study

would

preponcierancc

of

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cmderate

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type

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vidual to

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in

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to account

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of prolonged

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patients

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in thcsc

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of panic

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in heart

rate

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to experimental

ventilatory

and

severity

may each contribute

factors Type

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of .5”:,

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in cxperirncntal

dyspneic-fear sensitive

induce

helps

rate during

experienced

of severe

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which

excessive

differences

panic attacks

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rate,

studies

empirical

of the patients

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studies

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the

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CO,

attacks

studies

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variability

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(19Xx)

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111 cognitive panic

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reasscasment

Woods

the patients

of the

asymptomatic. this.

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panic-disorder

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by Cl-aske

reported

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of

( 10X7)

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those

A

to

large portion

healthy.

can

Iargc

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by Sanderson

Type

attacks. help

of Type

The data presented hcrc illustrate how ;I relatively large range of heart rates (i.e.. 69-c)O b/min) can be achieved in ;I single subject bq means of voluntary breathing maneuvers ciuring inhalation of 3% CO2 and room ail-. If ;I

to

procedures (e.g.

uncom

trollable

breathing

inducing

gas through

of

patients

without

Differences

in research positions

may

be resolved

research yield the

that

complex

findings

precision problem

for

such

attention

of

is paid

to

Certainly

investigation

panic

in

findings

such differences

in the

than

1 attacks.

and conflicts

on

of panic attacks.

controls

panicmask)

of Type

based

if cloacr

in types

greater

purport4

:I history

theoretical differences

a

an inhalation

disorder.

will of

Ventilatory control of heart rate during inhalation of 5% CO2 and types of panic attacks.

Differences in the magnitude of increases in heart rate during prolonged inhalation of 5% CO2 range from a mean of 25 b/min for a group of eight panic...
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