THE ORIGIN OF THE SENSATIONS OF DYSPNEA? Dyspnea has

THE

ORIGIN

OF

THE

SENSATIONS

OF

DYSPNEA?

BY

GEORGE

W.

WRIGHT,

M.D.,

and

(by

invitation)

BEN

V.

BRANSCOMB,

M.D.*

C

LEVI

lAND,

OHIO

Dyspnea

has

no

general'y

accepted

meaning

in

the

scien-

tific

literature.

Some

use

the

term

to

indicate

hard

or

labored

breathing

as

contrasted

to

eupnea.

Used

thusly,

the

word

has

an

objective

nature

and

does

not

signify

anything

abnormal,

since

vigorous

and

labored

breathing

develops

during

intense

physical

exertion

by

normal

persons.

Others

consider

the

term

always

to

denote

abnormal

or

pathologic

breathing

and

con-

cieve

it

to

embrace

the

subjective

as

well

as

the

objective

aspects

of

breathing.

In

this

paper

the

authors

define

dyspnea

as

"the

awareness

of

respiratory

distress".

Careful

interrogation

of

those

who

are

concerned

or

dis-

tressed

by

being

"breathless"

under

certain

circumstances,

reveals

that

for

many

the

sensation

of

breathlessness

differs

in

no

way

from

the

familiar

normal

response

to

exercise.

The

distress

that

they

associate

with

breathing

resides

primarily

in

the

fact

that

for

them

breathlessness

now

occurs

during

less

intense

exertion

than

formerly

was

the

case.

Recovery

from

breathlessness

may

now

be

unusually

prolonged.

For

these

persons,

dyspnea

is

simply

a

matter

of

the

intensity

of

effort

which

is

required

to

bring

forth

an

otherwise

normal

sensation.

The

sensation

of

breathlessness

that

accompanies

physical

ex-

ercise

by

the

normal

man

is

a

pleasant

one.

Each

deep

breath

relieves

the

intense

desire

to

breathe

and

when

the

steady

state

of

exercise

is

reached,

a

balance

between

respiratory

desire

and

From

the

Dept.

of

Experimental

Medicine,

St.

Luke's

Hospital.

The

authors

wish

to

acknowledge

that

part

of

the

experimental

observation

contained

in

this

paper

was

carried

out

while

they

were

associated

with

the

E.

L.

Trudeau

Foundation.

*National

Institute

of

Health,

Washington,

D.

C.

116

ORIGIN

OF

SENSATIONS

OF

DYSPNEA

its

satisfaction

by

breathing

is

attained.

Even

at

the

highest

sustained

levels

of

exertion

by

healthy

young

men,

the

hyper-

pnea

of

80

to

100

liters

per

minute

is

devoid

of

any

unpleasant

or

distressing

sensations.

Gratification

of

the

respiratory

ap-

petite

is

achieved

even

at

maximum

intensities

of

exercise.

In

some

persons

who

complain

of

dyspnea,

respiratory

satisfaction

may

prevail

at

rest

or

during

low

intensities

of

exercise; but,

as

exertion

becomes

increasingly

severe,

each

breath

no

longer

satisfies

the

intense

desire

for

breathing

and

a

sensation

akin

to

smothering

develops.

It

is

probable

that

all

persons

who

complain

of

dyspnea

would

experience

the

sensation

of

"smothering"

if

they

would

force

themselves

to

a

high

enough

intensity

of

exercise.

The

sensations

of

smother-

ing

occur

under

some

circumstances,

even

when

a

person

is

at

rest.

It

is

pertinent

to

ask

whether

or

not

a

normal

person

ever

experiences

precisely

the

same

sensations

of

which

the

syspneic

person

complains.

A

few

years

ago,

one

of

us

was

the

subject

of

an

experiment

to

induce

dyspnea

by

reducing

the

maximum

breathing

capacity.

In

the

position

of

quiet

expiration

the

entire

thorax

and

abdomen

were

bound

from

suprasternal

notch

to

os

pubis

by

broad

adhesive

tape.

This

procedure

limited

the

excursions

of

the

thorax

sufficiently

to

reduce

the

maximum

breathing

capacity

from

190

liters

per

minute

to

130

liters

per

minute.

Walking

on

a

motor-driven

treadmill

at

a

rate

of

work

such

that

the

respiratory

minute

volume

was

48

liters

per

minute

was

tolerated

with

complete

comfort

when

the

thorax

and

abdomen

were

free

to

move,

but

the

same

stint

of

exercise

induced

intense

respiratory

discomfort

when

the

thorax

and

abdomen

were

bound

by

adhesive

tape

in

the

man-

ner

just

described.

It

had

been

anticipated

that

a

recogniz-

able

and

more

severe

breathlessness

would

develop

when

the

respiratory

apparatus

was

restricted

than

when

it

was

free

to

move,

but

the

intensity

of

breathlessness

induced

by

the

re-

striction

of

breathing

was,

in

actual

fact,

far

greater

than

expected.

A

note

was

made

at

the

time

that

the

sensations

of

"air

hunger"

were

greater

than

the

subject

felt

when

respiring

double

this

volume

of

air

per

minute

during

maximal

exercise

11l7

1

18

GEORGE

W.

WRIGHT

AND

BEN

V.

BRANSCOMB

with

the

thorax

and

abdomen

free

of

any

encumbrance.

This

experience

led

us

to

suspect

that

the

breathlessness

of

the

respiratory

and

cardiac

cripple

and

perhaps

even

of

the

neu-

rasthenic

may

be

something

that

the

normal

person

never

experiences

in

its

entirity.

It

is

this

aspect

of

dyspnea,

namely

the

sensation

of

smothering

or

intolerable

breathlessness,

that

we

wish

to

discuss

further.

Subsequent

to

the

above

experience,

the

same

sensation

of

intolerable

air

hunger

was

induced

during

experiments

designed

to

study

the

effect

of

low

oxygen

tension

of

ambient

air

on

oxygen

uptake

by

the

body.

For

this

purpose,

one

of

us

constructed

a

mechanism

designed

to

impose

any

desired

rate

and

depth

of

breathing

upon

the

subject

under

study.

For

reasons

that

soon

became

apparent,

this

apparatus

came

to

be

known

as

the

smothering

machine

or

the

'SMO".

It

was

found

that

when

a

subject

initially

began

to

respire

with

a

pattern

dictated

by

the

apparatus,

intense

air

hunger

would

develop

if

the

permitted

depth

of

breath

was

too

shallow.

Also,

a

rate

and

depth

of

breathing

found

to

be

entirely

com-

fortable

for

long

periods

while

respiring

room

air,

on

occasions

would

rapidly

lead

to

intolerable

air

hunger

when

maintained

at

the

same

values

after

switching

the

subject

to a

low

oxygen

mixture.

It

was

discovered

accidentally

that

the

feeling

of

air

hunger

could

be

abolished

entirely

or

in

part

by

holding

several

successive

inhalations

in

the

lungs,

thus

permitting

the

thorax

to

expand

by

multiples

of

a

single

tidal

volume.

We

also

noted

that

whenever

the

rate

and

depth

of

breathing

were

such

as

to

induce

air

hunger,

the

act

of

expiration

was

always

de-

layed

until

just

before

the

next

inspiration

was

permitted

by

the

apparatus.

The

pattern

was

that

of

inspiratory

rather

than

expiratory

pause

between

each

breath.

The

sensations

produced

in

these

experiments

were

similar

to

those

that

ac-

company

breath

holding,

except

for

the

fact

that

there

was

an

intermittent

partial

relief

induced

by

each

inspiratory

effort.

To

use

the

word

"smothering"

is

probably

inaccurate

in

de-

scribing

the

sensation

induced

by

these

experiments

because

the

subject

could

terminate

the

experience

immediately

and

voluntarily

by

simply

removing

the

mouthpiece.

If

these

sensations

were

to

develop

under

circumstances

beyond

one's

ORIGIN

OF

SENSATIONS

OF

DYSPNEA

control,

they

would

be

terrifying

in

the

extreme

sense.

In

such

terms

the

panic

of

unrelieved

dyspnea

is

understandable.

Can

one

learn

something

regarding

the

origin

of

these

sen-

sations?

Where

do

they

arise

and

why?

The

experimental

study

of

the

sensation

is

beset

by

many

problems,

not

the

least

of

which

is

the

impossibility

of

recording

either

the

quality

or

the

quantity

of

the

sensation.

Moreover,

incentive

and

judge-

ment

are

constantly

at

play

in

any

experiment

wherein

sen-

sation

is

the

object

of

study.

We

present

the

following

obser-

vations

while

fully

cognizant

of

the

limitations

of

the

methods

used.

With

a

subject

at

rest

and

the

tidal

volume

limited

to

350

cc.

at

a

respiratory

rate

of

10

per

minute,

intolerable

breath-

lessness

with

a

generalized

sensation

of

tension

and

uncontrol-

able

twitching

of

the

abdominal

muscles

and

diaphragm

can

be

expected

to

develop

in

about

three

to

four

minutes.

At

that

time

an

alveolar

sample

may

be

found

to

have

a

carbon

dioxide

concentration

of

6.2

volumes

per

cent,

and

an

oxygen

concentration

of

10.8

volumes

per

cent.

If

at

the

moment

of

most

intense

discomfort

one

is

permitted

to

inhale

as

deeply

as

possible

a

gas

mixture

made

up

of

virtually

pure

nitrogen,

the

sensation

of

intolerable

breathlessness

will

completely

and

immediately

disappear.

As

a

matter

of

fact,

by

the

time

that

the

deep

inhalation

of

nitrogen

is

finished

there

is

no

longer

any

sensation

of

an

irresistable

desire

to

breathe.

If

a

mixture

of

gases

containing

7.4

volumes

per

cent

of

carbon

dioxide

is

substituted

for

pure

nitrogen,

the

same

immediate,

complete

relief

of

the

sensation

of

smothering

is

obtained.

Immediately

following

the

exhalation

of

the

single,

deep

inhalation

of

either

gas

mixture,

one

can

return

to

breathing

at

the

limited

depth

and

rate

imposed

by

the

'

SMO"

which

was

previously

intoler-

able.

The

breathing

pattern

which

had

become

intolerable

is

now

tolerable

for

a

period

of

30

to

120

additional

seconds.

It

was

noted

that

the

tolerated

period

was

always

less

following

inhalation

of

the

carbon

dioxide

mixture

than

following

the

inhalation

of

pure

nitrogen.

Another

experiment

bearing

on

the

problem

is

as

follows.

If

one

inhales

room

air

as

deeply

as

possible,

then

holds

the

119

120

GEORGE

W.

WRIGHT

AND

BEN

V.

BRANSCOMB

breath

until

the

desire

to

take

another

breath

can

no

longer

be

withstood,

and

then

exhales

into

a

previously

empty

bag

and

immediately

reinhales

the

gas

that

has

just

been

exhaled

from

the

lungs

to

a

point

of

full

inspiration,

it

will

be

observed

that

the

breath

can

again

be

held

for

an

appreciable

period

of

time.

This

maneuver

can

be

carried

out

through

three

or

four

suc-

cessive

exhalations

and

inhalations

of

the

same

gas

and

on

each

occasion

the

breath

can

be

held

for

a

brief

additional

period;

each

additional

period

becoming

shorter

than

the

pre-

ceeding

one.

A

variation

of

the

above

experiment

is

to

hold

the

breath

at

the

position

of

ordinary

expiration

until

the

desire

to

inhale

is

intolerable

and

then

following

a

deep

in-

halation

of

room

air

one

finds

it

easy

to

hold

the

breath

for

an

additional

period.

The

sum

of

the

time

that

the

breath

is

held

in

quiet

expiration

and

in

full

inspiration

always

exceeds

the

duration

of

breath

holding

with

the

lung

held

initially

in

a

full

inspiratory

position.

If

one

repeats

this

experiment

by

holding

the

breath

initially

in

a

position

of

quiet

expiration

and

then,

when

compelled

to,

inhales

to

a

position

of

full

in-

spiration

taking

in

a

mixture

of

gas

high

in

carbon

dioxide

and

low

in

oxygen,

it

will

be

noted

that

the

breath

still

can

be

held

in

the

inspiratory

position

for

an

additional

period

of

time.

It

will

be

noted

that

the

additional

period

of

breath

holding

in

the

full

inspiratory

position

when

the

high

carbon

dioxide

mix-

ture

is

used

will

be

shorter

than

when

this

experiment

is

done

when

room

air

is

inhaled.

A

striking

similarity

will

be

noted

between

these

experi-

ments

concerning

the

sensation

of

breathlessness

and

those

carried

out

many

years

ago

by

Hering

and

Breuer

and

later

by

Head

concerning

the

influences

of

the

various

stages

of

in-

flation

of

the

lung

on

breathing

patterns.

These

investigators

showed

that

whenever

the

lung

was

placed

upon

stretch,

show-

ers

of

impulses

were

transmitted

from

the

lung

via

the

vagus

nerve

to

the

brain

stem

which

influenced

the

respiratory

center

in

such

a

way

that

the

inspiratory

discharge

was

interrupted.

They

and

subsequent

workers

also

reported

that

collapse

of

lung

tissue

would

tend

to

initiate

an

inspiratory

act

and

also

that

these

afferent

impulses

in

some

way

would

influence

the

rate

of

discharge

of

the

inspiratory

center

and

the

rate

of

ORIGIN

OF

SENSATIONS

OF

DYSPNEA

breathing.

That

the

influence

of

the

act

of

inspiration

on

the

sensation"

of

breathlessness

is

not

humoral

but

neurogenic

in

mechanism

is

demonstrated

by

the

great

speed

with

which

the

event

occurs

and

also

by

the

fact

that

relief

is

immediately

obtained

in

spite

of

inhaling

pure

nitrogen

or a

high

concen-

tration

of

carbon

dioxide.

That

the

sensations

of

breathlessness

to

some

degree

must

reflect

the

state

of

activity

of

the

respiratory

center

seems

a

logical

conception.

On

this

basis

one

might

speculate

that

whenever

the

a

fferent

impulses

arising

from

the

stretch

re-

ceptors

in

the

lung

during

inhalation

are

of

sufficient

strength

to

neutralize

the

activity

of

the

inspiratory

cells

in

the

res-

piratory

center,

the

sensations

of

breathing

are

devoid

of

discomfort

such

as

that

felt

when

one

is

breathless.

When,

however,

the

activity

of

the

inspiratory

cells

in

the

respiratory

center

is

so

strong

that

it

cannot

be

neutralized

by

the

afferent

stretch

impulses

of

normal

intensity

arising

within

the

lung,

then

the

inspiratory

cells

may

continue

to

discharge

through-

out

the

entire

respiratory

cycle

and

a

feeling

of

breathlessness

ensue.

Likewise,

abnormally

weak

impulses

arising

from

the

stretch

receptors

within

the

lung

may

fail

to

neutralize

inspi-

ratory

impulses

of

a

normal

intensity

and

thus

lead

to

a

per-

sistance

of

inspiratory

discharge

throughout

the

respiratory

cycle

and

the

sensations

of

breathlessness.

In

short,

breath-

lessness

might

be

considered

to

be

caused

by

undue

prolonga-

tion

of

inspiratory

cell

discharge

in

the

respiratory

center,

arising

either

because

of

abnormally

weak

neutralizing

im-

pulses

from

the

stretch

receptors

in

the

lung

or

from

abnor-

mally

strong

activity

of

the

inspiratory

cells

of

the

respiratory

center.

That

the

act

of

taking

a

deep

breath

dissipates

sen-

sations

of

breathlessness

is

certainly

not

a

new

observation,

but

that

this

relief

comes

about

because

of

stretch

of

the

lung

rather

than

a

drop

in

the

CO2

or

a

rise

of

02

concentration

in

the

lung

gas

is

perhaps

not

universally

appreciated.

The

role

of

the

Hering-Breuer

or

pulmonary

stretch

reflex

in

termi-

nating

the

act

of

inspiration

during

normal

breathing

is

gene-

rally

accepted;

we

would

like

to

emphasize

its

role

in

the

sen-

sation

of

breathlessness.

121

122

GEORGE

W.

WRIGHT

AND

BEN

V.

BRANSCOMB

The

dypsnea

that

is

associated

with

disease

has

generally

been

explained

on

the

basis

of

an

abnormally

powerful

drive

or

stimulation

of

the

respiratory

center

by

hypoxia

or

hypercapnia

or

in

a

vague

way

with

the

statement

that

the

Hering-Breuer

reflex

is

unusually

"sensitive."

It

is

true

that

abnormalities

such

as

a

high

CO2

or

low

02

tension

of

the

blood,

both

of

which

are

known

to

stimulate

the

respiratory

center

in

such

a

manner

as

to

cause

an

increase

in

the

inspiratory

discharge,

have

been

observed

in

diseases

characterized

by

dyspnea

on

exertion.

Must

one

accept

the

idea

that

these

abnormalities

are

the

sole

cause

of

dyspnea?

Is

it

not

possible

that

inadequate

stretch

of

the

lung

or

some

abnormality

of

the

pressoreceptors

or

of

the

tissue

in

which

they

reside

may

be

equally

important

because

of

a

consequent

failure

to

develop

strong

enough

im-

pulses

to

neutralize

a

normal

or

abnormally

strong

respiratory

drive

?

Dyspnea

is

a

characteristic

of

severe

di

ffuse

obstructive

emphysema.

In

this

disease

a

high

pCO2

and

low

pO2

of

ar-

terial

blood

does

occur

but

sensations

of

intolerable

breath-

lessness

during

exercise

may

develop

in

such

patients

when

the

blood

gas

abnormalities

are

relatively

mild.

It

is

of

interest

that

in

this

disease

the

lungs

are

held

in

an

increased

or

ab-

normally

high

state

of

distention,

the

functional

residual

volume

being

increased

in

all

such

cases.

Although

the

stretch

reflex

sends

out

impulses

for

a

long

period

of

time

at

any

degree

of

inflation,

it

is

capable

of

being

fatigued

and

it

may

be

that

in

this

chronic

state

of

over-distention

abnormally

weak

im-

pulses

are

being

generated

in

the

pressoreceptors

of

the

hyper-

inflated

lung.

Furthermore,

it

is

known

that

the

emphysema-

tous

lung

resists

distention,

and

that

the

minute

ventilation

is

increased

during

exercise,

chiefly

by

an

increase

in

rate

rather

than

by

any

increase

in

depth

of

breathing.

It

seems

to

us

possible

that

the

dyspnea

of

which

the

patient

with

diffuse

obstructive

emphysema

complains

may,

in

part,

be

explained

by

inadequate

strength

of

the

inspiratory

inhibitory

impulses

arising

from

pressoreceptors

in

the

lung

during

cyclic

inflation.

A

combination

of

an

increased

basic

stimulation

of

the

respi-

ratory

center

by

abnormal

blood

gases

with

an

abnormally

low

neutralization

of

this

stimulus

because

of

inadequate

stretch

of

ORIGIN

OF

SENSATIONS

OF

DYSPNEA

the

lungs,

seems

a

more

complete

explanation

of

the

degree

of

breathlessness

observed

in

emphysema.

It

has

been

our

experience

that

the

improvement

in

terms

of

lessened

breathlessness

during

exertion

which

follows

decor-

tication

of

the

lung

has

sometimes

been

out

of

proportion

to

the

degree

of

increase

in

maximum

breathing

capacity.

Perhaps

this

is

another

example

of

greater

freedom

of

lung

motion

lead-

ing

to

more

powerful

stretch

impulses

bringing

about

a

better

neutralization

of

the

inspiratory

discharge

in

the

respiratory

center.

It

has

been

our

experience

that

restitution

of

normal

arte-

rial

oxygen

tension

by

breathing

pure

oxygen

during

exercise

in

cases

of

pulmonary

granulomatosis

of

berrylium

workers

has

at

times

failed

to

completely

relieve

the

sensations

of

dysp-

nea

and

to

return

the

ventilation

equivalent

to

normal.

It

is

conceivable

that

in

this

disease,

changes

in

lung

compliance

prevent

large

areas

of

lung

from

being

properly

distended

and

thus

interferes

with

the

development

of

an

adequate

stretch

reflex

discharge.

In

summary:

It

is

not

our

contention

that

all

of

the

sensa-

tions

associated

with

breathlessness

or

dyspnea

arise

from

an

inadequate

intensity

of

the

pulmonary

stretch

reflex

or

from

an

abnormally

great

stimulation

of

the

inspiratory

cells

of

the

respiratory

center.

Unusual

sensations

in

terms

of

resistance

to

air

flow,

employment

of

rarely

used

muscles

or

of

an

extra-

ordinarily

great

muscular

effort

in

breathing,

of

claustrophobia

and

of

other

manifestations

of

cortical

sensitivity

all

play

a

role.

The

concept

that

an

inadequate

or

weak

volley

of

impulses

from

the

stretch

receptors

in

the

lung

may

fail

to

properly

neutralize

the

discharge

of

the

inspiratory

cells

of

the

respira-

tory

center

appears

to

us

a

useful

one

in

explaining

some

of

the

facts

of

dyspnea

that

are

otherwise

difficult

to

understand.

DISCUSSION

DR.

C.

SIDNEY

BURWELL

(Boston):

We

have

just

heard

a

very

exciting

paper

and

I

would

like

to

say

that

there

is

more

that

is

new

about

it

than

Dr.

Wright's

modesty

has

led

him

to

suggest.

123

GEORGE

W.

WRIGHT

AND

BEN

V.

BRANSCOMB

I

would

like

to

ask

him

to

comment

on

the

possible

effect

of

chronic

underinflation

of

the

lung

on

the

sensation

of

dyspnea.

I

am

thinking

specifically

of

the

situation

that

exists

in

pregnant

women

in

whom

the

lung

is

characteristically

in

an

expiratory

position.

Pregnant

women

often

suffer

from

dyspnea,

although

they

have

at

the

same

time

a

relatively

low

PCO2

and

a

thoroughly

adequate

supply

of

oxygen.

DR.

FRANCIS

D.

W.

LUKENS

(Philadelphia):

In

connection

with

Dr.

Burwell's

question,

has

the

young

person

with

a

fairly

elastic

chest

who

develops

spontaneous

pneumothorax,

been

used

to

differentiate

the

effects

upon

the

chest

wall

and

the

lung

from

effects

mediated

by

the

respiratory

center?

DR.

ALEXANDER

J.

SCHAFFER

(Baltimore):

I

would

like

very

much

to

have

Dr.

Wright

comment

upon

a

topic

which

will

interest

me

more

than

the

rest

of

you,

and

that

is

the

relationship

of

his

findings

to

the

onset

of

extrauterine

respiration.

DR.

STEWART

WOLF

(Oklahoma

City):

I

would

also

like

to

congratulate

Dr.

Wright

on

a

most

ingenious

experiment.

We

have

made

observations

earlier

on

the

"I

can't

get

a

full

breath"

type

of

dyspnea

that

often

occurs

in

neurotic

individuals.

Its

mechanism

depends

on

the

failure

of

the

upward

excursion

of

the

diaphragm

to

equal

the

lower

excursion,

so

that

the

lung

gets

progressively

inflated

and

the

diaphragm

tighter

and

tighter

until

finally

the

individual

can't

get

a

deep

breath

because

his

lungs

are

already

almost

full.

We

have

often

wondered

why

these

patients

have

troublesome

dyspnea

without

appearing

cyanotic.

Dr.

Wright's

study

explains

that

beautifully

on

the

basis

of

a

lack

of

new

stretching

impulses.

DR.

FRANCIS

C.

WOOD

(Philadelphia):

I

just

wanted

to

say

that

this

to

me

is

a

very

illuminating

presentation,

because

it

explains

to

me

something

I

never

could

quite

understand

before.

I

had

a

patient

some

years

ago,

who,

after

an

injection

of

tetanus

anitoxin,

got

paralysis

of

his

intercostal

muscles

and

most

of

his

diaphragm.

The

first

time

he

ever

noticed

any

trouble

was

when

he

walked

into

a

swimming

pool.

When

the

water

came

up

to

his

umbilicus

he

was

all

right,

but

when

he

got

in

up

to

his

neck

he

experienced

marked

dyspnea

and

had

to

leave

the

pool

at

once.

He

also

noticed

marked

dypsnea

when

he

lay

down,

probably

due

to

his

diaphragm

being

pushed

up

by

the

intra-abdominal

hydrostatic

pressure,

in

the

recumbent

position.

DR.

GEORGE

D.

GAMMON

(Philadelphia):

I

would

like

to

ask

Dr.

Wright

if

these

studies

provide

an

explanation

for

the

subjective

sensation

of

dyspnea

that

occurs

in

hyperventilation

of

tetany

where

in

the

early

stages

the

people

continue

to

breathe,

feeling

short

of

breath.

Is

there

a

restriction

of

the

chest

wall

by

contraction

of

the

muscles

as

the

result

of

the

tetany?

DR.

WRIGHT

(Closing):

I

am

sure

that,

as

Dr.

Wood

has

so

nicely

pointed

out

concerning

the

man

who

went

swimming,

there

are

many

similar

fascinat-

ing

experiments

that

are

taking

place

before

our

eyes

every

day

regarding

124

ORIGIN

OF

SENSATIONS

OF

DYSPNEA

some

of

the

commonplace

phenomena

of

respiration.

Actually,

that

was

the

way

much

of

this

study

originated.

Restriction

of

lung

distention

could

conceivably

set

this

chain

of

balances

out

of

kilter.

I

am

very

anxious,

however,

that

you

not

get

the

impression

that

we

think

this

is

the

entire

mechanism

of

the

sensation

of

dyspnea.

This

is

only

one

facet

of

it.

The

under-ventilated

or

hypoventilated

lung

of

pregnancy

is

somewhat

similar

to

the

sensation

that

Dr.

Wolf

touched

on,

and

similar

to

what

I

think

is

the

sensation

that

all

of

us

have

had

when

we

sit

reading

or

concentrating

very

strongly.

Slowly

our

respirations

get

shallower

and

shallower,

and

then

suddenly

we

sigh.

I

was

very

struck

with

Dr.

Wolf's

slides

showing

the

fact

that

the

stomach

must

contract

periodically

or

you

get

nauseated.

Perhaps

there

is

a

center

controling

gastric

contraction

that

slowly

builds

up

and

if

you

don't

have

gastric

contractions

that

center

begins

to

radiate

its

excitation

and

leads

to

a

feeling

of

nausea.

In

the

same

way,

I

have

pictured

that

our

respiratory

center

is

constantly

undergoing

changes

in

irritability,

and

that

periodically

it

must

be

more

fully

discharged.

In

pregnancy,

of

course,

the

lung

gets

set

at

a

progressively

smaller

and

smaller

volume,

and

I

would

think

that

the

intensity

of

impulses

arising

from

stretching

might

conceivably

be

less,

but

I

have

no

evidence

that

that

is

true

because

we

haven't

studied

it.

As

a

matter

of

fact,

I

don't

know

how

to

study

this

sensation

directly.

For

a

good

many

years

we

have

been

thinking

about

these

things,

but

how

would

you

record

the

potentials

of

the

respiratory

center

in

an

unanesthetized

man?

The

only

way

in

which

I

could

get

at

it

is

through

this

inaccurate

method

of

studying

sensations.

About

hyperventilation

in

tetany,

Dr.

Gammon,

I

don't

know,

because

I

have

never

seen

one.

I

would

presume

that

it

is

quite

similar

to

one

case

of

Thompson's

disease

that

I

did

get

to

study.

He

had

great

respiratory

difficulties

because

of

inability

to

relax

the

respiratory

muscles.

This

would

not

be

an

abnormality

inside

the

lung

itself.

I

certainly

don't

want

to

give

the

impression

that

the

lung

pressure

receptors

are

the

only

mechanism

involved.

There

are

undoubtedly

impulses

that

come

from

other

parts

of

the

body

that

play

on

the

respiratory

center.

We

have

plenty

of

information

concerning

that,

qualitatively;

quantitatively,

very

little

information.

I

presume

that

motion

of

the

joints

and

torsion

of

the

cartilage

and

stretching

of

the

intercostal

fascia

should

be

just

as

much

involved

as

these

pressure

receptor

impulses.

1

25