THE LINACRE LECTURE

ON THE

LAW OF THE HEART

GIVEN AT CAMBRIDGE, 1915

f-' 13. JUS. ty 19 S')

V - * *> P1*/
\ f / Vt/

BY

ERNEST H. STARLING
M.D., Sc.D. (Cambridge and Dublin), F.R.C.P., F.R.S.
 THE LINACRE L EC TU R E
ON

THE LAW OF TH E HEART

 THE LIN A C R E LECTURE
ON T H E

LAW OF T H E HEART
G I V E N A T C A M B R ID G E , 1915

BY

E R N E ST H. STARLING
M .D ., Sc.D. ( C a m b r i d g e a n d D u b l i n ) , F.R.C.P., F.R.S.

W IT H D I A G R A M S

LONGMANS, GREEN AND CO.

39 PATERNOSTER ROW, LONDON
F O U R T H A V E N U E & 3 0 t h S T R E E T , N E W YORK

BOMBAY, CALCUTTA, AND MADRAS

1918
 T H E LAW O F T H E H EART.

N o one w h o has attem p ted to in vestigate th e m otion s o f the

heart and to discover th e secret o f th e m anner in w hich it is
ab le to regulate its a ctivity according to the n eed s o f th e b ody
as a w hole, can avoid realizin g th e truth o f th e words w ith w hich
H arvey com m en ces h is im m ortal treatise, On th e M otion o f th e
H eart and B lo o d , W h en I first g a v e m y m ind to v iv isec
tions, as a m eans o f discovering the m o tio n s and uses o f th e
heart, and sou gh t to discover th ese from actu al in spection , and
ivr VlC t QRJA

n o t from th e w ritin gs o f others, I found th e task so tru ly ar

duous, so full o f difficulties, that I w as alm ost tem p ted to think,
w ith F racastorius, that th e m otion o f th e h eart w as o n ly to be
com prehended b y God. F or I cou ld neither rightly perceive at
first w hen th e sy sto le and w hen the d ia sto le to o k place, nor w hen
? and w here d ilation and contraction occurred, b y reason o f th e
| rapidity o f th e m otion w hich in m any anim als is accom plished in
jth e tw in k lin g o f an ey e , com in g and g o in g lik e a flash o f lig h t
en in g ; so that th e sy sto le presented itse lf to m e now from this
point, n ow from t h a t ; th e d iastole th e s a m e ; and then ev ery
th in g w as reversed, the m otion s occurring, as it seem ed , variously
an d con fusedly together. M y m ind w as therefore g rea tly un
settled, nor did I k n ow w hat I should m y se lf conclude, nor w hat
b elieve from oth ers. B u t b y u sin g greater and greater diligence,
h aving frequent recourse to vivisection s, em p lo y in g a v a riety o f
anim als for th e purpose and co lla tin g num erous ob servation s, he
finally attain ed to th e truth and discovered w hat he so m uch d e
sired, both th e m otion and the use o f the heart and arteries.
T h e facts and ex p la n a tio n s adduced b y H a rv ey h ave n ot
had to u nd ergo an y ap preciable m odification during th e three
centu ries w h ich have elap sed sin ce the publication o f his treatise.
2 TH E L I N A C R E L E C T U R E

Indeed th ey have furnished th e groundw ork or sta rtin g p oint for

all subsequent researches. B u t the m ore w e in v estig a te the
actions o f th is organ, th e m ore w e m ust be filled w ith w on d er
and adm iration at the m arvellous w a y in w hich it is fitted b y
nature for th e task w h ich it has to p e r fo r m ; and th e elucida
tion o f th e law s w hich determ ine its pow er o f adaptation, as
su ggestive o f purpose as that o f a sen tien t being, presents an
interest as en thrallin g in th e thousandth ex p erim en t as it w as
in th e first.
N o r has th e significance o f th e circulation o f th e blood
dim inished in an y w ay sin ce its first prom ulgation b y H arvey.
T o a physician or p h ysiologist at th e present d ay-a m ans b od y
is a m achine, or rather a factory full o f m achines, all w orking
harm oniously togeth er for th e g ood o f th e organ ism . E ach
m ach in e is necessary to and d ep en dent on all th e others. A ll
have to be supplied w ith fuel, in th e shape o f food, in order
to perform their functions. M oreover sin ce the en ergy o f the
m achine is derived from th e o x id a tio n o f th e foodstuffs, ju st as
it is in a steam en gin e from the o x id a tio n o f coal, each m ach ine
has to be supplied b y special m eth od s w ith o x y g e n taken in
from th e extern al air. T h e fact th at th ey are im m ersed in th e
b ody fluids renders it necessary that the o x y g e n b e su p p lied in
a state o f solu tion in th ese fluids. W e m ay take th e volu ntary
m uscles as on e ty p e o f such a m achine. T h ese have to obtain
their foodstuffs, in the shape o f carbohydrate, fat or protein, from
th e alim entary canal, and their o x y g e n for th e con su m p tion o f
th e foodstuffs from the lungs. T h eir w a ste products m ust be
rem oved and carried to th e lungs or th e k id n ey s w here th ey are
finally elim inated from th e b ody. A great transport departm ent
is therefore a necessary con d ition for th e proper w orking o f th e
b od y. T h e m edium o f this transport is the blood, w hich circu
lates b y m eans o f fine capillary b lood v essels through all th e
organs o f th e body. T h e circulation is k ep t up b y th e heart,
w hich acts as a pump, p um ping th e b lood from th e v ein s in to
the arteries. From th e arteries th e b lood is distributed eith er to
the lungs to pick up o x y g e n and to g e t rid o f carbonic acid gas,
 T H E L A IV OF T H E H E A R T 3

or to all th e w ork in g tissu es o f th e b od y w hich it su pp lies w ith

o x y g e n and foodstuffs, taking aw a y w aste products in ex ch an ge.
F rom th e tis^ftes or lungs it is returned to the veins and so to
th e heart again.
It is evid en t that th e d em ands on this transport departm ent
m ust be subject to very large variations in accordance w ith the
a ctivity o f th e body. D uring hard m uscular work th e consum p
tion o f o x y g e n and o f foodstuffs m ay be increased eigh t tim es
a b o v e that o f th e b od y at rest. T h is increase is rendered p o s
sib le b y a corresponding augm entation o f th e blood flow through
th e w ork in g tissues. U nder all con d ition s a con sid erable head
o f pressure is m aintained in the b lood on the arterial side o f the
circulation, w hich is raised during a ctive work. It is the function
o f the heart to pum p blood from th e veins into the arteries against
this h ead o f pressures, thus m aintaining it at a nearly co n sta n t
level, w hich o n ly varies according to the m etabolic n eed s o f the
organism . T h e sm all vessels w hich carry th e blood from the
big arteries in to th e tissu es have m uscular w alls w hich can co n
tract or relax, so that the lum en o f the vessels m ay be constricted
alm ost to n oth in g or be w id ely dilated, according as the tissues
supplied b y them have need o f little or much blood. T h e
m uscular w alls o f th e sm all b lood vessels have thus a twofold
function, that o f regulating the local su p p ly o f b lood to the
different tissu es and organs, and that o f m aintaining the total
resistance to th e escape o f blood from th e arterial side at such a
d eg ree that th e general arterial pressure rem ains u naltered even
w h en th e pressure o f b lood through a w orking tissu e is greatly
facilitated b y a w idespread d ilation o f its arterioles. F rom one
p oint o f view therefore w e m ay sa y th at th e function o f th e
h eart is to keep up a head o f pressure in th e arteries w hatever
th e con d ition o f th e arterioles b y w hich th e b lood esca p es in to
th e tissu es. It is esp ecia lly im portant th at no fall o f arterial
pressure sh ould be brought ab out during activity in con sequ en ce
o f th e flushing o f th e w orking tissu es w ith blood, sin ce on th e
gen eral arterial pressure depends th e su p p ly o f blood to th e
m aster tissu es o f th e body, th e brain and spinal cord, any
4 THE U N A C RE L E C TU R E

im pairm ent o f w h ose action w ould b e fatal to th e efficiency o f th e

organism as a w hole. Thus, if m ost o f th e arterioles are dilated,
as w ould happen w hen all th e m uscles o f th e b o d y are actin g
strongly, th e blood w ill escap e from th e arteries very easily, and
the heart m ust pum p m uch m ore blood in to the arteries in order
to m aintain th e head o f pressure con stant. A s a m atter o f fact
w e find that under th ese con d itions th e efficien cy o f th e h eart is
such that th e arterial pressure actu a lly rises h igher than norm al
in sp ite o f th e free escape o f b lood from th e arteries in to the
veins, and the rapidity o f th e circulation through heart and
tissu es is therefore largely increased.
D uring th e last fifty years th e application o f th e ex p erim en ta l
m ethod has throw n m uch lig h t on th e m anner in w hich th e
heart is able to carry out its functions. W e h a v e been a b le to
learn m uch as to th e n atu re o f the au tom atic a ctiv ity o f th e
heart. W e k now th e startin g p oin t o f th e ex c ita to r y process
w hich is resp onsible for each beat, and w e can trace th e cou rse
o f this process in the form o f a w ave through out th e different
parts o f th e heart. W e can stu d y m in u tely th e course o f th e
pressure ch an ges in th e various cavities at each p hase o f th e
heart's cycle. W e k n ow th e action o f th e valves and th e e x a c t
m om ent at w hich their closure is effected. W e h a v e learnt that
th e heart is subject to the control o f th e central nervous sy stem
b y m eans o f its inhibitor and au gm en tor nerves, and that on the
other hand it m ay send up m essages to th e nervou s sy stem
which w ill affect th e con d ition o f th e b lood v essels in other parts
o f the body.
B u t to m any p h ysiologists th e m ost rem arkable, because th e
m ost essen tially vital, o f the characteristics o f th e heart is its
power o f adaptation, o f alterin g its activity, i.e. th e am ou n t o f work
it performs at each beat, according to th e requirem ents o f the
b ody as a whole. T h e m echanical work d one b y th e heart can
be estim ated if w e k now the arterial pressure w hich is overco m e
by each heart beat and the am oun t o f b lood sen t o u t ' b y the
heart at each beat or during a m inute. It is p o ssib le to d eter
mine both th ese quantities either in m an or in anim als. K ro g h
 TH E L A W OF T H E H E A R T 5

h a s sh o w n th a t in th e n o rm a l in d iv id u al a t re s t th e left v e n tric le
p u m p s o u t a b o u t 3 litre s o f b lo o d p e r m in u te. D u rin g m o d e ra te
m u sc u la r ex e rc ise th is q u a n tity m a y rise to 12 litres, o r in an
a th le tic in d iv id u a l u n d e r ta k in g v e ry h a rd w o rk to as m u c h as
21 litre s p e r m in u te. T h is la st figure m e a n s th a t th e h e a rt can
p u m p th e to ta l b lo o d c o n ta in e d in th e b o d y ro u n d th e w h o le
c irc u la to ry sy ste m six o r seven tim e s in th e co u rse o f a m in u te ,
a n d th is in sp ite o f th e fact th a t d u rin g m u sc u la r e x e rc ise th e
a rte ria l p re ssu re a g a in st w hich th e h e a rt h as to w o rk is c o n s id e r
a b ly h ig h e r th a n in c o n d itio n s o f rest, b e in g e q u iv a le n t in th e
la tte r ca se to a b o u t n o m m . H g . a n d in th e fo rm er to 150
to 160 m m . H g .
A sim ila r p o w er o f a d a p ta tio n is sh o w n in cases o f d ise ase .
W e can im ita te th e d ise a se d c o n d itio n e x p e r im e n ta lly b y d e
s tro y in g a n a o rtic valve, so th a t th e a n im a l su ffers from a o rtic
re g u rg ita tio n , o r b y d im in ish in g th e lu m en o f th e a o rta b y m e an s
o f a lig a tu re , so a s to p ro d u c e artificial a o rtic ste n o sis. T h e
a v e ra g e a rte ria l p re ssu re u n d e rg o e s n o a lte ra tio n as a re s u lt of
e ith e r o f th e se p ro c e d u re s, a lth o u g h th e le ft v e n tric le h a s to p e r
form tw o o r th re e tim e s as m u c h w o rk as it d id b efo re in o rd e r
to m a in ta in th e b lo o d p re ssu re a t its p rev io u s level. T h e circu
la tio n o f b lo o d th ro u g h th e b o d y re m a in s th e re fo re unaffected.
T h is a d a p ta tio n o f th e h e a r t to v a ria tio n s in th e d e m a n d m a d e
u p o n it o ccu rs e q u a lly w ell a fte r to ta l d e s tru c tio n o f th e n erv e s
c o n n e c tin g th e h e a r t w ith the' c e n tra l n e rv o u s sy stem . So we
m u s t c o n c lu d e th a t th e g o v e rn o r m e ch a n ism , in v irtu e o f w h ic h
th e h e a rt is a b le to d o m o re o r less w o rk , a c c o rd in g to th e
a m o u n t o f b lo o d w hich h a s to be s e n t on a n d th e re sis ta n c e to
th e flow p re s e n te d b y th e a rte ria l p ressu re, m u s t b e s itu a te d in
th e w alls o f th e h e a r t its e lf an d p re su m a b ly in th e m u sc le fib res
o f w h ich th e s e a re com p o sed . I t is th e n a tu re o f th is m e c h a n ism
w h ich I w ish to d iscu ss w ith y o u to-d ay .
I n o rd e r to ' in v e stig a te it w e m u s t b e a b le in th e iso la te d
h e a r t to c o n tro l e x a c tly all th e m e c h a n ic a l c o n d itio n s o f th e
h e a r t, e.g. volu m e, p ressu re, a n d te m p e ra tu re o f e n te rin g b lo o d ,
a n d th e re sis ta n c e to th e outflow offered b y th e a rte ria l re sist
6 TH E L IN A C R E L E C T U R E

ance. A t th e sam e tim e w e m u st d ev ise m e an s to m e a su re

a c c u ra te ly th e o u tp u t o f th e h e a rt, th e p ressu res in its v ario u s
cavities, an d th e v o lu m e o f th e h e a rt a t d iffe ren t p h ases in th e
card iac cycle. T h e vo lu m e o f th e h e a rt serv es as a re la tiv e
m e asu re o f th e le n g th o f its m uscle fibres. S u c h a c o n tro lle d

F ig . . D iagram o f arrangement o f the heart-lung preparation (the parts are

i
not drawn to scale).
P.A., pulmonary artery (the lungs are not shown). L .A ., left auricle. I.V .C ., in
ferior vena cava. Az., azygos vein ligatured at its entrance into superior vena
cava, S.V.C. Ao., aorta. C.A., cannula in innominate artery. V., X tube
opening into B, a vessel filled w ith air to serve as a resilient cushion and to
take the place o f the elastic arterial wall, and into the artificial resistance R.
T., glass tube surrounding artificial resistance, and communicating by W . w ith
a syringe for injecting air, and so raising the a rtificial resistance. X., side
tube for drawing off blood and determining output.
M lt M2, M3, M 4, manometers attached to different parts o f the system.

s tu d y o f th e m e ch an ical c o n d itio n s o f th e h e a r ts ac tio n is

re n d e re d possible b y th e use o f w h a t I h a v e ca lle d th e h e a r t
lu n g p re p a ra tio n
T o m a k e th is p re p a ra tio n (fig. I), all th e a rte rie s c o m in g off
 T H E L A W OF TH E H E A R T 7

fro m th e m a in a rte ry , th e a o rta , a re tie d e x c e p t o n e, th e in n o m in

a t e a rte ry . T h e a o rta its e lf is tie d ju s t b e y o n d th is a rte ry . In
th is is p la ce d a g lass tu b e w h ich h a s tw o b r a n c h e s ; o n e b ra n c h
is in c o n n e c tio n w ith a m erc u rial m a n o m e te r to m e a su re th e
p re s s u re in th e ao rta , th e o th e r tu b e le ad s to w h a t w e m a y term
t h e artificial resistan c e. T h is co n sists o f a tu b e o f th in ru b b e r
( R ) p la ce d w ith in a w id er g la ss tube. B y m ean s o f a sy rin g e a ir
c a n b e p u m p e d in to th e g lass tu b e, th e p re ssu re o f th e a ir b ein g
m e a su re d b y a m erc u rial m a n o m e te r, M 2, a tta c h e d to th is tu b e . I t
is e v id e n t th a t if th e p re ssu re o u tsid e is g re a te r th a n th e p re ssu re
in sid e th e th in ru b b e r tu b e , th is m u st collapse, a n d if a n y fluid
is to flow th ro u g h th e ru b b e r tu b e th e p re ssu re o f th e fluid m u s t
b e g re a te r th a n th e p re ssu re o f th e air o u tsid e. W e can th u s ,
b y p u m p in g in air, a d ju s t th e re sis ta n c e to th e flow o f fluid
^ th r o u g h th e tu b e a t a n y h e ig h t w e desire. F ro m th e o th e r en d
<rof th e re sista n c e an o rd in a ry r u b b e r tu b e p a sse s in to th e g la ss
j s p ira l from w h ich a n o th e r tu b e le ad s in to th e v e n o u s reservoir.
' T h e g la ss sp ira l is im m e rse d in w arm w a te r a n d is m a in ta in e d a t
- th e te m p e r a tu re o f th e b o d y . F ro m th e b o tto m o f th e ven o u s
^ re se rv o ir a w id e tu b e p ro v id e d w ith a screw clip lead s d o w n in to
"a-large vein, th e su p e rio r cava, S .V .C ., a n d p a sse s in to th e r ig h t
^auricle. T h e o th e r la rg e v e in e n te rin g th e r ig h t h e a rt, viz. th e
in fe rio r v e n a ca v a, is lig a tu re d . W e ca n m e a su re th e p re ssu re in
''th e r ig h t a u ric le b y c o n n e c tin g a m a n o m e te r, M s, w ith its in te rio r
b y m e a n s o f a tu b e p a sse d u p th e in ferio r v en a cava. T h e h e a rt
a n d lu n g s in th is p re p a ra tio n a re e n tire ly c u t off from th e re st o f
th e b o d y a n d m ay , if d e s ire d , b e c u t a w a y from th e c a rcase o f
th e a n im a l. T h e b lo o d from th e le ft v en tricle p asses th ro u g h
th e artificial re sista n c e , th e p re ssu re b ein g m a in ta in e d a t a n y d e
s ire d h e ig h t, sa y IO O m m . H g . I t th e n passes b a c k th r o u g h th e
v e n o u s re se rv o ir in to th e r ig h t auricle. F ro m h e re it p asses in to
th e r ig h t v e n tric le , th e n th ro u g h th e p u lm o n a ry a r te ry a n d lu n g s
in to th e left au ric le, a n d so a g a in in to th e left v en tricle . The
lu n g s a r e b lo w n u p r h y th m ic a lly w ith a ir so th a t th e b lo o d in
p a s sin g th ro u g h th e m b ec o m e s fu lly o x y g e n a te d .
A h e a r t p re p a re d in th is w ay m a y go o n b e a tin g fo r a w h o le
 TH E L IN A C R E L E C T U R E

d ay , an d m ay b e re g a rd e d as p ra c tic a lly n o rm al for th re e o r fo u r

hours. I t w ill be seen th a t w e h a v e all th e m e ch a n ica l c o n d itio n s
o f its a c tiv ity u n d e r co n tro l. B y p u m p in g a ir in to th e a n n u la r
space s u rro u n d in g th e artificial re sista n c e w e can ra ise th e a rte ria l
p ressu re a n d th e re sista n c e w h ich th e h e a rt h a s to o v erc o m e to
a n y d esire d e x te n t. B y u n sc re w in g o r sc re w in g u p th e c lip o n
th e tu b e fro m th e v en o u s re se rv o ir w e c a n m o d ify w ith in w id e
lim its th e inflow o f b lo o d in to th e b ig v e in s a n d so in to th e
h e a rt. W e c a n k e e p th e b lo o d a t a n y te m p e r a tu re a n d so a lte r
th e te m p e ra tu re a t w h ic h th e h e a r t m u scle acts.
L e t u s n o w see h o w th e h e a r t in su ch a p re p a ra tio n re a c ts to
v aria tio n s in th e d e m a n d s m a d e upon it. T h e m e a s u re m e n t o f
th e w o rk o f th e h e a r t u n d e r th e s e c o n d itio n s is v e ry easy. A ll
we h av e to d o is to c o n n e c t th e a rte ria l tu b e w ith a m e rc u ria l
m an o m eter, M j, so as to re g iste r th e a v e ra g e p re ssu re in th e ao rta .
T o m easure th e o u tp u t w e allo w th e b lo o d to flow th ro u g h th e
tu b e m a rk e d X in to a g ra d u a te d cy lin d er, a n d b y m e a n s o f a
sto p w a tch d e te rm in e th e n u m b e r o f se co n d s ta k e n to co llect
io o c.c. o f blood. T h is gives us th e o u tp u t o f th e h e a r t p e r
b e a t o r p e r m in u te. T h e o u tp u t d e te rm in e d in th is w ay le av e s
o u t o f a c c o u n t th e b lo o d w h ich p asses o u t from th e first p a r t
o f th e a o rta th r o u g h th e c o ro n a ry a rte rie s to s u p p ly th e h e a r t
m uscle, w h en c e it is re tu rn e d d ire c tly in to th e r ig h t auricle.
T h is fractio n o f th e to ta l o u tp u t can b e m e asu red b y ta p p in g
th e c o ro n a ry sinus, i.e. th e vein o f th e h e a r t in to w h ich m o st o f
th e b lo o d vessels s u p p ly in g th e h e a r t m u sc le p o u r th e ir c o n te n ts.
S pecial e x p e rim e n ts h a v e sh o w n th a t ^ o f th e b lo o d flow ing
th ro u g h th e m u sc u la r w alls o f th e h e a r t p a ss th r o u g h th e
c o ro n a ry sinus. T o find o u t th e to ta l a m o u n t o f b lo o d esc a p in g
from th e a o rta th ro u g h th e c o ro n a ry arte ries, th e fig u res o b ta in e d
b y ta p p in g th e c o ro n a ry sin u s m u s t b e th e re fo re m u ltip lie d b y

th e factor T h e follow ing figures w ere o b ta in e d fro m o n e

e x p e rim e n t in w h ich th e a rte ria l p re ssu re w as a lte re d b y v a ry

in g th e a ir p ressu re o n th e a rte ria l resistan c e, w h ile th e inflow
o f b lo o d in to th e h e a r t w as m a in ta in e d c o n s t a n t :
 T H E L A W OF T H E H E A R T 9

A rterial Systemic T otal T otal Venous

P ressure O utput Coronary O utput P ressure
mm. H g. c.c. per O utput of Left cm. H 2O.
m in. (calculated). H eart.

84 8 11 40*80 8 5 1*8 0 g *6 12*4

10 8 79 0 50*30 840*30 8*8 - 12*0
14 0 77 0 7075 8 4 0 -75 8*0 - 11 * 2
170 75 0 117*4 0 8 67*4 0 8 *o - 10*8
208 600 2 6 0 *3 ^ 860*30 12 *0 22*0
104 76 0 80-30 8 4 0 *0 0 ' 8*4 - 10*4
104 75 0 8 0-30 830*00 8*0 - 10*0
44 790 3 '4 820*00 7*6 io * o

T w o im p o rta n t fac ts a re re n d e re d e v id e n t b y th e s e resu lts.

I n th e first place, p ro v id e d th e inflow re m a in s c o n sta n t, it seem s
to b e im m a te ria l to th e h e a rt w h e th e r it h as to c o n tra c t a g a in st
a re sis ta n c e o f 4 4 m m . H g , o r 2 08 m m . H g . I n ea c h c a se it
p u ts o u t a s m u c h b lo o d as it receives, so th a t th e to ta l o u tflo w
re m a in s c o n s ta n t w h a te v e r th e a rte ria l pressure. O f c o u rse th e re
is a lim it w h ic h m u st n o t be ex c ee d ed . I f th e p re ssu re is p laced
to o h ig h , sa y a t 2 0 0 to 2 2 0 m m . H g , th e h e a r t m a y fail a n d b e
c o m e d is te n d e d w ith b lo o d w h ich it is u n a b le to e x p e l. W ith in
p h y sio lo g ic a l lim its, how ever, w e m a y sa y th a t th e o u tp u t o f th e
h e a r t is in d e p e n d e n t o f th e a rte ria l resistan ce, so th a t w h a te v e r
w o rk is g iv e n th e h e a r t to d o , it c a n d o it w ith o u t fail. T h e
se c o n d fact w h ich re su lts from th is e x p e rim e n t is th a t th e frac
tio n o f th e to ta l o u tp u t o f b lo o d w h ich p asses th r o u g h th e
c o r o n a ry v essels rises ste a d ily w ith th e h e ig h t o f th e a rte ria l
p ressu re. T h is m e an s th a t th e m o re w o rk th e h e a rt h a s to do,
th e b e tte r it is su p p lie d w ith b lood, i.e. w ith th e o x y g e n a n d
n u tr im e n t n ec essary to fu rn ish it w ith en erg y .
A lth o u g h a lte rin g th e a rte ria l p re ssu re h a s n o in flu en ce on
th e o u tp u t o f th e h e a rt, a g r e a t effect is a t o n ce p ro d u c e d b y
a lte rin g th e v e n o u s inflow. T h e v en o u s inflow m a y b e in c re a se d
fro m o n e o f 100 c.c. p e r m in u te to o n e o f 3 0 0 0 c.c. p e r m in u te
sim p ly b y u n sc re w in g th e clip o n th e v en o u s s u p p ly tu b e. The
a rte ria l re sis ta n c e m a y b e m a in ta in e d c o n s ta n t b y a d ju s tin g th e
p re s s u re o f a ir a r o u n d th e th in ru b b e r tu b e. W e th e n find th a t
a s w e in c re a se th e inflow, th e outflow is p a r i passu in c re ase d , so
 10 TH E L INACRE LECTURE

th a t th e re is n o d a m m in g u p o f th e b lo o d o n th e v en o u s sid e
n o r failure o f th e h e a rt to send th e b lo o d o n from th e v en o u s to
th e a rte ria l side. In th is case also th e r e m a y b e so m e in c re a se
o f c o ro n a ry flow, w h ich is n o t h o w ev e r so m a rk e d as w h en
w e th ro w m o re w o rk o n th e h e a r t b y in c re asin g th e a rte ria l
resistan ce.
D o e s th is a u to m a tic a d a p ta tio n o f th e w o rk o f th e h e a r t to
th e d e m a n d s m a d e u p o n th is o rg a n m e a n th a t a g r e a te r p ro p o r
tio n o f th e chem ical en e rg y o f th e c o n tra c tin g m u scle is tr a n s
form ed in to m ech an ical en e rg y , o r d o es th e h e a r t m u sc le a c tu a lly
se t free m o re e n e rg y w h en its w o rk is in c re a se d ? T h is q u e stio n
h as b een an sw e re d b y L o v a tt E v an s. J u s t as th e r e s p ira to ry e x
c h a n g e s o f th e w hole b ody, viz. th e in ta k e o f o x y g e n a n d th e
o u tp u t o f ca rb o n ic acid, m a y b e u se d as a m e a su re o f th e ch em ical
ch an g es, a n d o f th e to ta l e n e rg y se t free in th e b o d y , so th e re
s p ira to ry e x c h a n g e s o f th e h e a r t m a y be u tilize d for d e te rm in in g
th e to ta l e n e rg y se t free in th is o rgan. In th e h e a rt-lu n g p re p a ra
tio n th e re s p ira to ry m e ta b o lism o f th e h e a rt c a n b e in v e stig a te d b y
m e a su rin g th e o x y g e n ta k e n u p from th e lungs, a n d th e c a rb o n ic
acid g iv e n o u t b y th e lu n g s. W h e n w e d o th is w e find th a t a n y
in c re ase in th e w o rk o f th e h e a rt, h o w ev e r cau sed , w h e th e r b y a
rise in th e a rte ria l p re ssu re o r b y a m o re ra p id v en o u s inflow, is
a tte n d e d b y a c o rre sp o n d in g a u g m e n ta tio n o f th e to ta l ch em ical
changes. T h is is sh o w n in th e follow ing ta b le s :
EXP. I . A R T E R IA L R E S IS T A N C E V A R IE D . IN F L O W C O N S T A N T .

H eart, 57 gm s.

O utput A.P. 0.2 W ork

per hour mm. H g. Efficiency.* per hour kgm. *
litres. c.c.

31 42 4 per cent 234 20

130 8 371 60

* I have recently found that in these experiments both the work done and the
mechanical efficiency were underestimated. In exp. 2 (p. 11) the mechanical effi
ciency w ith an inflow of 62 litres per hour was probably about 25 per cent, and the
other figures must be increased in proportion.
 T H E L A W O F TH E H E A R T 11

EXP. 2. A R T E R IA L R E S IS T A N C E C O N S T A N T . V E N O U S IN F L O W
V A R IE D . , .

H e a rt, 53 g m .

In flo w o2 H eart V.P. W ork

per hour per hour E ffic ie n c y .*
V o lu m e . m m . H vO k gm .*
litre s. c.c.

13 115 0 5 per cent 5 12

62 331 + 86 9 70 60

In these tables the oxygen consumption serves as an index o f the total chemical
changes and o f the chemical energy set free. T his may be measured in calories,
and compared w ith the total work done by the heart in the same time, the result
being the mechanical efficiency o f the heart as a machine.
The work o f the heart in kilogrammetres was determined by m ultiplying the
output per hour by the average arterial pressure (in metres o f blood).
In the first experiment the work o f the heart was varied by altering the arterial
resistance, in the second by altering the venous inflow.
A.P. = arterial pressure. V.P. = venous pressure.
The heart volume is measured from an arbitrary base line, viz. the volume at
the beginning o f the experiment. Note the marked enlargement o f the heart which
attends increase in venous inflow.

W e th u s find th a t th e h e a r t h a s a m a rv e llo u s p o w e r o f a d
ju s tin g n o t o n ly its o u tp u t o f m e ch a n ica l e n e rg y b u t also its to ta l
e n e rg y c h a n g e s to th e w o rk w h ich is im p o sed u p o n it b y th e
m e ch a n ica l c o n d itio n s o f th e c irc u la tio n . In m u sc u la r ex e rc ise
fo r in sta n c e , w h en th e inflow o f b lo o d in to th e la rg e v ein s is
in c re a se d b y th e p u m p in g a c tio n o f th e m uscles a n d th e a rte ria l
p re ssu re is raise d b y th e c o n tra c tio n o f th e sm all a rte rie s g o in g to
th e a lim e n ta ry ca n al, th e h e a rt picks u p all th e b lo o d w hich co m es
to it a n d se n d s it o n w ith in c re a se d force in to th e a rte ria l sy stem ,
w h en c e it ca n be d is trib u te d in ric h m e a su re to th e c o n tra c tin g
m u sc le s ; so th a t, as K ro g h has show n, its o u tp u t p e r m in u te m a y
rise from 3 litre s to th e e n o rm o u s fig u re o f 21 litres. W e m ay
form so m e id e a o f th e p ro cesses in v o lv ed in th is a d a p ta tio n b y
c o m p a rin g th e h e a r t to a m o to r cycle. H e r e also th e e n e rg y is
d e riv e d from th e o x id a tio n o f c e rta in co m b u stib le su b stan ce s, in
th is case p e tro l sp irit. W h e n o n ce a d ju ste d th e m o to r cy c le w ill
12 TH E L IN A C R E L E C T U R E

tra v e l re g u la rly w ith o u t fu rth e r in te rfe re n c e o n a flat surface.

A s soon h o w ev e r a s th e ro ad b e g in s to m o u n t, th e e n g in e b eg in s
to slow do w n a n d m a y sto p a lto g e th e r. T o av o id th is o cc u rrin g
th e rid e r le ts in m o re m ix tu re o f p e tro l a n d a ir, th e ch e m ic al
en e rg y av a ila b le for th e e x p lo sio n is th u s increased , a n d th e cy cle
m o u n ts th e h ill a tith e sam e p a c e as it h a d b efo re on th e level. In
th e h e a r t w e h av e so m e a u to m a tic a r r a n g e m e n t b y w h ich , so to
speak, m o re m ix tu re is le t in as so o n as m o re w o rk is th ro w n
u p o n it. W h a t is th e n a tu re o f th is a u to m a tic a rra n g e m e n t ?
T h is w as th e q u e s tio n th a t c o n fro n te d us as so o n as w e h a d seen
h o w in d e p e n d e n t th e o u tp u t o f th e h e a rt w as o f a rte ria l p ressu re,
a n d h o w p erfectly th e h e a rt w as a b le to re a c t to a n in c re ase d
v en o u s inflow b y th ro w in g o u t m o re b lo o d in to th e a rte rie s.
T h e clue to th e so lu tio n o f th e q u e s tio n w as g iv e n b y a s tu d y
o f th e c h a n g es
(a) In v o lu m e o f th e v en tricle s,1
( b) I n th e p re ssu re in sid e th e v e n tric le s o f th e h e a rt,
w hich a c c o m p a n y its a d a p ta tio n to rise o f a rte ria l p re ssu re o r
in crease o f v en o u s inflow. L e t us ta k e first th e re a c tio n o f th e
h e a rt to c h a n g e s in a rte ria l resistan c e. W h e n w e p u t u p th e
a rte ria l p re ssu re su d d e n ly fro m 8 0 to 140 m m . H g , w e find, as
m ig h t b e e x p e c te d , th a t th e re is a c o rre sp o n d in g rise in th e
m a x im u m p re ssu re w h ich o b ta in s in th e v e n tric le s a t each b ea t.
T h is is o b v io u sly n e c e ssa ry in o rd e r to o v e rc o m e th e in c re ase d
resistan c e o f th e a rte rie s. B u t th e p ressu re d o es n o t a tta in its
m a x im u m a t once, a n d in fact m a y in c re a se ste a d ily fo r th re e to
te n beats. I f d u rin g th e sa m e tim e w e record th e v o lu m e o f th e
v entricles, w e find th a t for th e first th re e to te n b e a ts th e a v e ra g e
v o lu m e also ste a d ily increases. T h is is sh o w n in th e d ia g ra m
(fig. 2), w h ich re p re se n ts th e v o lu m e c h a n g e s in th e v e n tric le s as
m easu red b y a c a rd io m e te r. I t w ill b e seen th a t d ire c tly a fte r
1 The volume o f the ventricles is measured by enclosing them in a glass globe
(cardiometer) from which a side tube leads to a piston recorder w ritin g on the
blackened surface o f a drum. Any increase in the volume o f the ventricles forces
air into the piston recorder and causes a rise o f the lever. In the experiments from
which the figures 2 and 3 are taken the piston recorder was inverted, so that a
descent o f the lever signifies increased volume o f the ventricles.
 T H E L A W OF T H E H E A R T 13

t h e a rte ria l p ressu re is raised, th e v e n tric le d o e s n o t c o n tra c t a n d

th e re fo r e d o es n o t e m p ty its e lf to th e sa m e e x te n t as before.
A t th e co n c lu sio n o f sy sto le th e re fo re , th e h e a r t c o n ta in s m o re
b lo o d th a n it co n ta in e d a t th e en d o f th e p re v io u s b ea t. I t is
re c e iv in g a c o n s ta n t inflow fro m th e venous rese rv o ir, so th a t
during th e follow ing d ia sto le it is d iste n d e d to a g r e a te r e x te n t
t h a n before. A t th e seco n d c o n tra c tio n it still fails to se n d o u t
a s m u c h b lo o d as before, i.e. as it receives ; b u t th e a m o u n t o f
b lo o d s e n t o u t a t each b e a t ste a d ily in creases u n til, w h e n th e
d ila ta tio n o f th e h e a r t h a s re a c h e d a c e rta in p itch , th e o u tp u t o f
t h e h e a r t a t ea ch b e a t a n d p e r m in u te is th e sa m e as it w as w h en
t h e a rte ria l p ressu re w as 8 0 m m . H g .
T h e c o u rse o f e v e n ts m a y be re n d e re d c le a re r if w e ta k e a
n u m e ric a l ex a m p le .
3 W e s ta r t w ith a h e a r t in w h ic h th e le ft v e n tric le is fo rc in g
i o u t 6 0 0 c.c. o f b lo o d p e r m in u te a g a in s t a m e a n a rte ria l p ressu re
* o f 8 0 m m . H g . T h is m ean s th a t th e p re ssu re in th e a rte ria l
s y s te m w ith ea ch p u lse p ro d u c e d b y th e h e a rt b e a t w ill v a ry
PUUuiC LiuHARY u

fro m 65 m m . H g to 100 m m . H g . T h e first d ro p s o f b lo o d

le av e th e h e a r t a t a p re ssu re ju s t o v er 65 m m . H g , b u t a t th e en d
o f ea c h sy sto le th e h e a r t h a s to e x e r t a p re ssu re o f 100 m m . H g ,
t o d riv e th e la st p o rtio n s o f b lo o d in to th e a o rta .
W e now in c re ase th e artificial re sista n c e so as to p u t u p th e
-m ean a rte ria l p re ssu re to 100 m m . H g . A fte r a few b e a ts th e
t o t a l o u tp u t is fo u n d to b e 6 0 0 c.c. as before. T h e h e a r t c o n
tin u e s to p u t o u t as m u c h b lo o d as it rec eiv e s, th o u g h , as sh o w n
a b o v e (E vans), a t a g re a te r e x p e n d itu r e o f chem ical en e rg y . L e t
u s tra c e o u t th e e v e n ts o c c u rrin g a t ea c h b ea t. A t 8 0 m m . H g
p re s s u re th e h e a r t a t each sy sto le is d e v e lo p in g ju s t e n o u g h
energy to p u t o u t s a y 8 c.c. o f b lo o d a g a in s t a re s is ta n c e w h ich
m a y v a ry from 65 m m . H g a t th e b e g in n in g o f th e o u tflo w to
1 00 m m . H g to w a rd s th e en d . T h e a rte ria l re s is ta n c e is th e n
suddenly in creased , so th a t it n ee d s a p re ssu re o f I i o mm. H g
t o fo rce a n y b lo o d th ro u g h it a n d a m ean p re ssu re o f 140 m m .
H g in th e a o r ta to k e e p u p a flow th r o u g h it a t th e r a te o f 6 0 0
c.c. p e r m in u te. T h e n e x t h e a r t b e a t g e ts u p e n o u g h p re ssu re
14 THE L INACRE LECTU RE

F ig . 2. E ffects o f rise o f a rte ria l re s is ta n c e o n th e v o lu m e o f th e h e a r t. (C u rv e s t o

be re a d from le ft to rig h t.)
C, cardiometer tra c in g ; B.P., arterial pressure; V .P ., venous pressure. The:
data o f the experiment are as follows :
Rate O .P.
T. A.R. B.P. V .P. in 10" in 10"
35 C . 40 68 65 22 74 C.C.
35 103 128 90 22
35 42 75 55 22

In this, and in the protocol attached to fig. 3,

T. = temperature o f blood flowing into the heart.
A.R. = the artificial resistance, as measured by the pressure in the air space
surrounding the thin rubber tube, in mm. Hg.
B.P. = the arterial blood-pressure as measured by a mercurial manometer con
nected with the side branch of the cannula in the innominate artery, in mm. H g .
V.P. = the pressure in the inferior \ena cava close to the heart, measured irt>.
mm. H aO.
Rate = number of beats in 10 seconds.
O.P. = output in c.c. per 10 seconds, as measured on the peripheral side o f th e
artificial resistance.
 T H E L A IV OF T H E H E A R T 15

to force so m e b lood in to th e a o rta a n d d iste n d it u p to 100 m m .

H g le t us sa y 3 c.c. H e re th e outflow sto p s. A t th e b e g in
n in g o f th e n e x t sy sto le th e re a re th e re fo re 5 c.c. o f b lo o d m o re
in th e le ft v e n tric le th a n a t th e b e g in n in g o f a n y p re c e d in g d ia
sto le. B u t th e 'v en o u s inflow is still p ro ce ed in g s te a d ily a t 6 0 0
c.c, p e r m in u te o r 8 c.c. p e r beat. A t th e b eg in n in g o f th e n e x t
sy sto le th e h e a r t th e re fo re c o n ta in s its o rig in a l resid u a l b lo o d ,
p lu s 5 c.c. resid u a l b lo o d from th e la st c o n tra c tio n , p lu s 8 c.c.
w h ic h h a v e e n te re d it d u rin g d ia sto le.
T h e h e a rt th u s s ta rts its n e x t sy sto le in a d ila te d co n d itio n .
B u t w h e n th is sy sto le occu rs w e find th a t it is m o re forcible th a n
th e prev io u s ones, so th a t th e te n sio n e x e r te d b y th e c o n tra c tin g
m u sc u la r w alls, a n d th e p re ssu re p ro d u c e d w ith in th e v e n tric le
a re also g re a te r. W e m a y a s s u m e th a t th e m u scu lar w alls g e t
u p e n o u g h te n sio n to d riv e o u t b lo o d a g a in s t a p re ssu re o f 13 0
m m . H g. T h e o utflow o f b lo o d in to th e a o r ta th ro u g h th e re
sistan c e g o e s o n u n til th e p ressu re rises to 130 m m . H g a n d th e n
ceases. L e t us a s su m e th a t 6 c.c. o f b lo o d a re d riv en o u t. A t
th e b e g in n in g o f th e n e x t sy sto le th e h e a r t th e re fo re c o n ta in s
re sid u a l b lood, 5 c . c . + 2 c .c .+ 8 c.c. I t is still m o re d iste n d e d
th a n before, a n d a g a in m o re e n e rg y is se t free o n c o n tra c tio n .
T h is m a y b e e n o u g h to d riv e o u t th e w h o le 8 c.c., w h ich are
e n te r in g it ste a d ily d u rin g d ia sto le , a g a in s t a m e an a rte ria l p re s
su re o f 140 m m . H g . I f n o t, th e pro cess o f in c re a sin g d ila ta tio n
g o es o n u n til th e e n e rg y o f th e c o n tra c tin g fibres is j u s t sufficient.
T h e h e a rt th e n c o n tin u e s to b e a t a t th is in c re ase d v o lu m e a n d to
m a in ta in th e o rig in a l outflow a g a in s t th e g re a tly raised a rte ria l
p ressure.
T h e d ia g ra m in fig. 2 sh o w s th e v o lu m e o f th e h e a r t in
s y sto le a n d d ia sto le (a) w h en it is forcing o u t a c e rta in a m o u n t
o f b lo o d a g a in s t a n a v e ra g e p re ssu re o f 6 8 m m . H g , ( b) w h en it
is fo rcin g o u t th e sa m e a m o u n t o f b lo o d a g a in st a p re ssu re o f
128 m m . H g ., ( c) w hen it is e x p e llin g th e sa m e a m o u n t a g a in s t
a p re ssu re o f 75 m m . H g .
I f w e a lte r th e w o rk o f th e h e a r t b y in c re a sin g th e v e n o u s
inflow , so m e w h a t sim ila r c h a n g es a re p ro d u ce d . T h e r e is a rise
i6 TH E L I N A C R E L E C T U R E

o f p ressu re in th e v en tricle s sin ce a g re a te r a m o u n t o f b lo o d h as

to be se n t o u t in a given tim e a g a in s t th e sa m e a rte ria l r e
sistance. T h e re is also an in c re ase d v o lu m e o f th e h e a rt d u e n o t
so m u c h to th e in c re ase d resistan c e to th e outflow o f b lo o d as to

Fm. 3. Effect o f alteration in venous supply on volume o f heart. (Read from left
to right.)
Dog, 5*15 kilos; heart, 67 gms.
O .P. per
O .P. per beat
A.R. B.P. V .P. Rate. O .P . beat calc. observed.
A. 100 124 95 22 86 3'9 57
B. 100 130 145 22 140 6-4 8-0
C. 100 122 55 22 33 1-5 2-5

th e increased inflow d u rin g each d ia sto le . T h e effect o f in

creasin g th e v en o u s inflow o n th e v o lu m e o f th e h e a rt is show n
in th e d ia g ra m (fig. 3). I t w ill be n o tic e d th a t in fig. 2,
 T H E L A IV O F T H E H E A R T 17

a lth o u g h th e v o lu m e o f th e h e a r t b o th in sy sto le a n d d ia sto le

is in c re ase d , th e e x c u rsio n a t e a c h b e a t re m a in s th e sam e. In
fig. 3, on th e o th e r h a n d , th e in d iv id u al e x c u rsio n s a lte r w ith
in c re a se d inflow , since th e o u tp u t o f b lood a t each b e a t is in
creased .

F i g . 4 . Arrangemento f apparatus for recording isometric contractions o f tortoise

ventricle under varying degrees o f fillin g . The frog or tortoise ventricle V is
tied on to the perfusion cannula. W e can record spontaneous contractions, or,
if these are not present, can excite single contractions by means of an induction
shock. By turning A, the heart empties itself by C. A is then turned so as to
put the cavity o f the heart in connection w ith the rubber manometer T. By
means o f the tap B any required amount o f fluid can be allowed to flow from
the burette M into the heart. No change in heart volume occurs as it contracts
since all the tubes are rigid, and the excursion o f the manometer membrane is
negligible in comparison w ith the size o f the heart. The heart thus contracts
isometrically. (See note on p. 18.)

N ow h e re a re tw o co n d itio n s in w hich th e w o rk o f th e h e a rt
is increased a n d in w h ich th is o rg a n a d a p ts its e lf b y in c re a sin g
th e chem ical c h a n g e s in its m u scle a t ea c h c o n tra c tio n to th e in
cre ase d d e m a n d s m a d e u p o n it. I t is e v id e n t th a t th e re is o n e
fa c to r w hich is co m m o n to b o th cases, a n d th a t is th e in c re ase d
 i8 TH E L IN A C R E L E C T U R E

v o lu m e o f th e h e a rt w hen it b eg in s to c o n tra c t. S o th a t w e m a y
m ak e th e follow ing g e n e ra l sta te m e n t. W it h in p h y s io lo g ic a l
lim its th e la r g e r th e v o lu m e o f th e h ea rt, th e g r e a t e r a re th e
e n e r g y o f it s co n tr a c tio n an d t h e a m o u n t o f c h e m ic a l c h a n g e
a t ea c h co n tra c tio n .

o '5 i 'o i '5 2-o 2*5 3 'o 4-0

F ig . 5 . Isometric contractions of tortoise ventricle (from a large tortoise) w ith
varying fillin g . The figures below each curve refer to the volume o f fluid
in c.c. contained by the ventricle.

T h e sam e s to ry is to ld w hen w e stu d y th e b e h a v io u r o f th e

h e a rt o f th e co ld -b lo o d ed anim al, such as th e fro g o r to rto ise .
S u ch a h e a r t p re se n ts th e a d v a n ta g e th a t it c a n b e m a d e to
c o n tra c t is o m e tr ic a lly 1 w ith o u t b e in g d a m a g e d , w h erea s th e
1 An iso m e tric contraction is one that occurs w ithout change o f length o f the
muscle, the whole energy o f the contractile process being spent on setting up a
state o f tension in the muscle. To measure this tension in an ordinary muscle, the
muscle is allowed to contract against a strong spring, the movements o f which are
magnified by means of a very long lever. Thus the shortening o f the muscle is
almost entirely prevented, but the increase in its tension causes a m inute but pro
portionate movement o f the spring which is recorded in a magnified form by the
lever.
A similar method may be applied to the heart o f the frog or tortoise. A double
tube ( perfusion cannula ) is tied into the ventricle. One tube connects the cavity
o f the ventricle w ith a reservoir of fluid by which the heart may be filled to any
desired extent, the other tube passes to a tambour covered w ith a th ick elastic
membrane (membrane manometer). When the heart contracts it cannot expel any
appreciable amount o f its contents: it simply raises the pressure in its interior ;
thus causing a slight excursion o f the membrane on the manometer. This excur
sion is recorded, and much magnified, by means o f a lever on a smoked surface, and
 TH E LA W OF THE H E A R T '9

sm am m alian h e a rt u n d e r sim ila r c o n d itio n s w o u ld so o n sh o w

h ae m o rrh a g es a n d o th e r sig n s o f d isin te g ra tio n o f its m u scle fibres.
T h e a d v a n ta g e o f th e iso m etric m e th o d o f re c o rd in g th e c o n tra c
tio n s lies in th e p o ssib ility o f m e a su rin g in th is w a y th e to ta l
m e c h a n ic a l e n e rg y se t free as te n sio n a t ea c h co n tra ctio n . In
t h e a c c o m p a n y in g d ia g ra m (fig. 6) is sh o w n th e re la tio n b etw een
t h e v o lu m e o f th e to rto is e v en tricle a n d th e p re ss u re in its c a v ity
during d ia s to le a n d th a t d e v e lo p e d d u rin g sy sto le, th e p re ssu re
i n each case se rv in g as a m e a su re o f th e te n sio n e x e rte d b y th e
m u s c le fibres. I t will b e o b se rv e d th a t as th e v o lu m e o f th e
5

40

05 1-0 I '5 2-0 2 '5 3 -0 3 -5 4 '0

F i g . 6. Diagram showing relation between fillin g , in itia l tension, and final tension
in a heart contracting isom etrically (abscissa = volume o f heart contents,
[T"_ ordinates = intracardiac pressure in mm. Hg).

h e a r t is in c re a se d th e re is a c o rre sp o n d in g rise in th e h e ig h t
of th e p ressu re d e v e lo p e d d u rin g c o n tra c tio n . I t w as fo rm e rly
t h o u g h t o n th e b asis o f F r a n k s e x p e rim e n ts th a t th e e sse n tia l
fa c to r d e te rm in in g th e s tre n g th o f c o n tra c tio n o f th e card iac m u scle
-was th e te n sio n it w as u n d e r a t th e b e g in n in g o f th e c o n tra c tio n .
I t w ill be o b se rv e d , how ever, from th is d ia g ra m th a t th e rise o f
diastolic te n sio n is a t first n eg lig ib le a n d th a t as soon as th e
p re s s u re w ith in th e v e n tric le d u rin g d ia sto le b e g in s to in c re a se
thus serves to measure the amount o f tension produced in the heart muscle at each
contraction. The arrangement o f the experiment is shown in the diagram (fig. 4)
a nd the actual record o f a series o f contractions w ith different fillin g is given in fig. 5.
20 THE L INACRE LECTU RE

a p p re c ia b ly , so as to ca u se a passiv e s tre tc h in g o f th e m u s c le
fibres, th e a b s o lu te te n sio n d e v e lo p e d d u rin g c o n tra c tio n rise s
v ery little m o re o r m a y even fall. T h e r e ca n b e n o q u e s tio n
th erefo re th a t it is th e v o lu m e o f th e v e n tric le s a t th e b e g in n in g
o f co n tra c tio n ra th e r th a n th e p re ssu re w ith in th e ir c a v itie s,
w hich d e te rm in e s th e a m o u n t o f e n e rg y se t free d u rin g th e c o n
tractio n . T h is free en e rg y d isp la y s its e lf as c o n tra c tile stress*
a n d causes a rise o f p ressu re w ith in th e c a v ity o f th e v en tricle.

Pressure
30 60 90 120 150 180 210 240 270 ^ , H # .
* ------------- ------------ '--------------------------- 0

<
o 30-
c
3n>

F i g . 7 . See
text. The abscissae represent pressure in m m . Hg, and the ordinates
measured from above the capacity of the ventricles. The left-hand curve re
presents the condition of the heart during diastole. The right-hand curve
that during systole.

In fig. 7, I h av e a tte m p te d to re p re se n t d ia g ra m m a tic a lly

th e rela tio n b etw e en th e s ta te o f filling o f th e h e a rt, th e h e a r t
volum e, a n d th e ten sio n o r p re ssu re e x e r te d b y its w alls d u rin g
d ia sto le a n d d u rin g systole. T h e n u m b e rs re p re s e n t a p p r o x i
m a tely th e values w hich w ould b e o b ta in e d in a h e a lth y d o g s
h e a rt w eig h in g a b o u t 7 0 g ra m s, if th e c o n tra c tio n s co u ld b e r e
co rd ed iso m etrically . I t will b e seen th a t th e te n sio n d e v e lo p e d
increases a t first ra p id ly a n d th e n m o re slo w ly as th e filling o f th e
v en tricle s is c h a n g e d from o to 30 c.c. T h is w o u ld re p re s e n t t h e
o p tim u m filling, so far as re g a rd s th e a u g m e n to r effect o f in -
 T H E L A W OF TH E H E A R T 21

-crease o f v o lu m e o n s tre n g th o f c o n tra c tio n . A fte r p a s sin g th is

p o in t th e h e a r t r a p id ly fails, in sp ite o f th e ra p id rise in th e
d ia sto lic p re ssu re w ith in th e h e a rt.
I t m u s t b e re m e m b e re d th a t th e in c re ase d v o lu m e o f th e
h e a r t im p lies th a t each o f th e m u scle fibres o r m u scle cells w h ich
m a k e u p its w all is le n g th e n e d . Is th is le n g th e n in g o f a m u scle
fib re o f a n y im p o rta n c e for its r e a c tio n t o s tim u la tio n a n d for
t h e to ta l e n e rg y o f its c o n tra c tio n w h en s tim u la te d ? T h is

i
fO
o
>

u.
0

T
>-
1ca
3
o
3
Ci
a.

F ig .
8. Curve showing the relation o f tension, in itia l length, and energy evolved
in an isometric tw itch. (Note the resemblance o f this curve to that o f the
heart in fig. 6.)
A , Condition o f maximum shortening.
B, Condition o f maximum extension of muscle in its normal relationships in the body.

p ro b le m w as in v e stig a te d m a n y y e a rs ag o b y B lix , a S w e d ish

p h y sio lo g ist, w ho m e asu red th e m a x im u m e n e rg y se t free b y a
c o n tr a c tin g m uscle a t d ifferen t le n g th s b y th e iso m etric m eth o d .
T h e resu lts o f o n e o f h is e x p e rim e n ts a re g iv e n g ra p h ic a lly in
fig. 8. In th is figure th e ab scissa re p re se n ts th e in itial le n g th o f
th e m u sc le (i.e. w h e th e r a t re s t o r in ac tiv ity , its fu rth e r s h o rte n in g
b e in g p re v e n te d b y its a tta c h m e n t to th e s tr o n g s p rin g o f th e
is o m e tric lever). T h e o rd in a te s re p re se n t th e te n sio n e x e r te d
b y th e m uscle, th e low er lin e g iv in g th e te n sio n in th e u n e x c ite d
22 TH E L IN A C R E LEC TU R E

c o n d itio n , th e u p p e r curve, th e te n sio n e x e r te d b y th e e x c ite d

m uscle. I t will b e seen th a t th e te n sio n d ev e lo p e d d u rin g c o n
tra c tio n in c re ase s w ith in c re ase in th e le n g th o f th e m uscle, u p
to th e d e g re e o f m a x im a l e x te n s io n possible in th e b o d y w ith t h e
m uscle in its n a tu ra l relations.
T o stre tc h th e m u sc le b e y o n d th is p o in t re q u ire d a n e v e r-
in c reasin g in itial te n sio n . T h e c o n tra c tile stress s e t u p on p a s s
in g to th e e x c ite d s ta te in c re ase d for a tim e w ith in c re a sin g
te n sio n a n d th e n d im in ish e d , ju s t as w e h a v e seen to b e th e case
in th e to rto ise h e a r t (cp. fig. 6). D u rin g th e la s t few y e a rs a
series o f a d m ira b le e x p e rim e n ts h a v e b ee n c a rrie d o u t b y A . V .
H ill o n th e influence o f c h a n g e s in le n g th o n th e to ta l e n e rg y ,
m e asu red as h e a t, se t free b y a c o n tra c tin g m uscle. W ith E v a n s
h e has in v e stig a te d th e in flu en ce o f in itia l le n g th o f a sk e letal
m uscle o n th e a m o u n t o f m e ch a n ica l e n e rg y a n d to ta l e n e rg y in
th e form o f h e a t se t free a t ea c h c o n tra c tio n . T h e y find th a t fo r
m o d e ra te in c re m e n ts o f le n g th b o th te n sio n a n d h e a t in c re a s e
p ro p o rtio n a te ly w ith th e le n g th , a n d w e m a y th e re fo re c o n c lu d e
th a t in c re ase d le n g th o f m u sc le fibre, w h e th e r h e a rt m u sc le o r
sk e letal m uscle, cau se s c o rre sp o n d in g in c reases b o th in th e
c h e m ic al c h a n g e s a n d in th e m ech an ical e n e rg y d e v e lo p e d in th e
m uscle a t its co n tra c tio n . T h e law o f th e h e a rt is th u s th e s a m e
a s th e law o f m u sc u la r tissu e g en e rally , th a t the energy o f contrac
tion, however measured, is a function o f the length o f the muscle fibre.
D o es th is law c a r ry us a n y f u rth e r? C a n w e form a n y
clearer c o n c e p tio n o f th e p ro ce sses o p e ra tiv e in th e h e a rt a n d
m u sc u la r tissu e g e n e ra lly b y su c h a su m m a rise d s ta te m e n t o f t h e
b e h a v io u r o f th e s e tissu e s ? I n th e first p la ce th e re la tio n b e
tw een le n g th a n d e n e rg y e x p re s s e d in th e g e n e ra l s ta te m e n t
g ives us a clue to th e n a tu re o f th e m u sc u la r m ach in e. W hen
a sk eletal m u sc le p asses from a re s tin g to an a c tiv e co n d itio n ,,
th e c h a n g e o f s ta te o cc u rs in less th a n n y ^ th o f a seco n d . I t
m a y th e n p ass off a lm o st as ra p id ly so th a t th e m u sc le m a y
c o n tra c t a n d r e la x te n to tw e n ty tim es a secon d . I n in se c ts t h e
co n tra c tio n s m a y b e re p e a te d tw o o r th re e h u n d re d tim e s in a
second. M o reo v er A . V. H ill h a s sh o w n th a t th e e n e rg y o f
 T H E L A W OF T H E H E A R T 23

contraction may be measured either as heat or as mechanical

tension, and these are found to be approximately equal, so that
the initial change in muscular contraction may have a mechanical
efficiency of 100 per cent. Such a rapid and complete conver
sion of chemical energy into mechanical energy implies that the
change must take place within molecular dimensions and the
molecular alteration must at once be interpreted into change of
tension. The microscopic study of muscle, as of other cells,
shows us the existence of multitudinous surfaces, separating
dissimilar fluids or phases of a fluid. Muscle differs from other
cells, however, in the regularity of arrangement of its constituent
elements in longitudinal lines or fibrils. When a muscle is e x
cited, there is an instantaneous electrical change which points to
a charging of some surface or surfaces at the excited part, i.e.
to a chemical change occurring at a surface. Many lines of
argument converge similarly in the direction of the view that
the chemical changes, occurring in a muscle as a result of ex
citation, affect surfaces arranged longitudinally in the muscle.
Now the effect of lengthening the muscle will be to increase the
extent of active surface, so that we may restate our general pro
position in the following way. A n y increase in the extent of
active surface increases the energy of change.
The chief manifestation of surface energy is in the form
which we know as surface tension. When a particle of mercury
is dropped from a height on to the table, it flattens out under
the influence o f gravity, then pulls itself together again into the
form of a spherical globule. The force which opposes the
tendency of gravity to flatten out the globule is the tension in
the superficial layer of the mercury, so that we may consider the
mercury as it were enclosed in a stretched elastic membrane
which by its tension keeps the mercury in a globular form.
Just as a twisted bit of elastic may be made to do w'ork, as for
instance in the toy aeroplane, so surface tension of a fluid may
be made to do work under appropriate conditions. Thus in one
familiar lecture experiment, a balanced float is held by the sur
face tension of the water so that the disc of perforated metal is
24 TH E L INACRE LECTU RE

just at the surface. If a little ether be dropped on the surface

of the water its surface tension is at once diminished to such an
extent that it is no longer able to hold the float down, and the
disc jumps up quickly into the air. Another experiment show
ing the result of change of surface tension is the following. A
number of pieces of cork are dropped on to a surface of water.
The surface tension is pulling equally on them in all directions
so that they are evenly distributed as they fall. If now the
surface tension in the middle of the surface be suddenly dim
inished by allowing a single drop o f alcohol or oil to fall on the
surface, the skin of water at the circumference which is now
under a stronger tension than the skin in the middle o f the
surface, retracts rapidly, drawing with it the floating pieces of
cork. These changes occur with extreme rapidity. In such
experiments as these, only an infinitesimal fraction of the fluid is
used, namely, that layer one molecule thick which lies on the
immediate surface. If we could split up the water into a vast
number o f surfaces, we should enormously increase the power of
getting work out of the system. This is the condition which
exists in muscle, which we may therefore regard as a surface
tension machine, i.e. a machine in which chemical energy is
transformed into surface energy. The change o f surface energy
induces a condition of tension in the muscle which may be utilized
entirely for the production of work or may be degraded into the
form of heat. It will perhaps facilitate our conception of the
machine if we consider the muscle fibril as made up o f a series
of globules elongated in the direction of the muscle fibre by the
tension applied to the muscle. During rest the surface tension
of these globules is very slight, so that they offer no resistance
to extension, and in the normal resting position their form will
be elliptical. On excitation a sudden chemical change occurs at
the surface of each globule, which not only gives it an electrical
charge but also increases its surface tension. The globule
therefore strives to recover its spherical form, thus setting
up a state of tension in the whole muscle. This illustration
must not be taken too literally. W e do not yet know enough
 T H E L A W OF T H E H E A R T 25
about the ultimate structure of muscle to decide what are the
surfaces at which the changes in energy occur. But there is no
other explanation which will account for all the changes
chemical, electrical, thermal and mechanical which occur in a
muscle on excitation, so well as this theory of a change in sur
face energy along surfaces disposed longitudinally. We are
enabled by this conception to understand in some measure the
reason for the influence of lengthening of a muscle or of dilata
tion of the heart on the strength and energy of contraction.
But the demonstration of the connection between dilatation
of the heart and energy of contraction does more than merely
bring the behaviour of this organ into line with that of voluntary
muscle. It enables us to form a picture of what is occurring in
the heart in all the vicissitudes and changes in stress to which it
is exposed in the course of a mans life. Thus, if a man starts
to run, his muscular movements pump more blood into the heart,
so increasing the venous filling, while the central nervous system,
by contracting the arteries of the abdomen, increases the peri
pheral resistance, raises the arterial pressure and forces all the
available blood through the active muscles. As a result the heart
is overfilled during diastole, and is impeded from emptying itself
in systole: its volume both in systole and diastole enlarges
progressively until by the lengthening of the muscle fibres
so much more active surfaces are brought into play within the
fibres that the energy of the contraction becomes sufficient to
drive on into the aorta during each systole the largely increased
volume of blood entering the heart from the veins during the
diastole.
In these circumstances therefore the heart is dilated. But in
a healthy individual this condition is only temporary. A rise of
arterial pressure produces a more abundant flow of blood through
the vessels supplying the wall o f the heart, and this increased
supply of oxygen and foodstuffs improves the physiological con
dition of each muscle fibre, so that at each contraction it is able
to concentrate a larger number of active molecules on each unit
o f active surface than it could previously. The physiological
26 T H E L IN A C R E L E C T U R E

condition, or what we are accustomed to speak of as the tone 1

of the heart, is thereby improved and the heart gradually returns
to its normal volume even though it is doing increased work.
It is only when the heart is fatigued or diseased that this
secondary improvement fails to appear. Then we find that the
heart remains dilated over the whole period o f increased work,
and if the work is prolonged this dilatation may become perma
nent. In a failing heart the concentration o f active molecules
per unit surface becomes less and less, so that this surface has
to be continually increased by dilatation of the heart. If this
goes on sufficiently long the dilatation may pass the optimum
length of muscle fibre and the muscle then has to contract at
such a mechanical disadvantage that the heart fails altogether.
With the failure of the prime mover, all the other mechanisms
of the body stop work, and the animal is dead.
The connection which I have shown in this lecture to
exist between the energy of the hearts contraction and the
length of its muscle fibres, enables us to understand not only the
marvellous power o f adaptation of the heart to the varying
strains of everyday life, but also the condition of this organ in
disease, when from overstrain or morbid alterations in its muscles
or its valves it fails to carry on its functions with efficiency.
For years the muscle-nerve physiologist was reproached
1The word tone has been often used in connection with the heart, though a
clear conception of its significance has generally been lacking. When, on opening
the chest, the heart is found to be dilated, it is often said to be lacking in tone ;
on the other hand, if the heart is found small and evidently emptying itself com
pletely during systole and dilating only slightly during diastole, its tone is said to
be increased. But the state of dilatation of the heart may be merely a question of
the amount of blood entering it from the veins. A contracted heart may be in a
bad condition and a dilated heart may be in a good condition. It is clear now that
the word tone is properly employed as synonymous with physiological condition or
fitness of the muscle fibre, and its measure is the energy set free per unit length of
muscle fibre at each contraction of the heart. A heart in good condition, i.e. one
with a good tone, will carry on a large circulation against a high arterial pressure
and nearly empty itself at each contraction, while a heart with a defective tone, as
is the case when it is tired, can carry on the same circulation but only when its
fibres at the beginning of contraction are much longer, i.e. when the heart is dilated.
In the latter case the output of blood will be the same as in the former, but both the
systolic and the diastolic volumes of the heart will be increased.
 T H E L A W OF T H E H E A R T 27

by the so-called practical man with spending his time and at

tention on things which can have little importance in medicine,
for the maintenance of health or the cure of disease. And yet
it is in the researches on a subject, considered even by some
physiologists as wearisome or trivial, that we have found the
clue to the behaviour of the heart under all manner of conditions,
and the explanation of phenomena which have long been a
puzzle to the student of the healthy or diseased organism. But
however plodding the mode of attack may have appeared, there
was nothing trivial in the goal to which Blixs researches were
directed, since this was nothing less than the essential nature
o f the contractile process: they were to bring within the scope
o f known categories of phenomena the mysterious vis insita of
muscle, which to the older physiologists, and indeed to ourselves,
is a type or a part of life itself. In physiology, as in all other
sciences, no discovery is useless, no curiosity misplaced or too
ambitious, and we may be certain that every advance achieved
in the quest of pure knowledge will sooner or later play its part
in the service of man.

PUGUC UERAKY OF VICTOR!/;.

P R IN T E D IN GR EAT B R IT A IN BY T H E U N IV E R S IT Y P R E S S , A B ER D EEN .