Downloaded From: on 06/09/2014

Principles of Management of Cor Pulmonale*
Peter Harris, J1.D.
'
or pulmonale.' medns different things to different people and so it is necesmry to start with
a definition. Here is the definition given b! \VHOz:
"Hypertrophy of the right ventricle resulting from
diseases affecting the function and/or structure of
the lung, except \\,hen the pulmonan alterations are
the result of diseases that primaril) affect the left
side of the heart or of congenital heart disease."
The \VHO' classificat~ondnides the causes of cor
pulrnonale into three main groups. The first group
consists of diseases primarily affecting air passages,
lungs and alveoli and includes the pulmonary hypertelisio~l of high altitude. The second group
consists of diseases primaril! affecting movements of
the thorac~ccage. .\nd the third group consists of
diseases primarily affecting the pulmonan vasculature. Each of these groups contains a large number
of diseases and it tvould not be possible to discuss
each one in detail. I proposc. therefore. to select a
small number of causes of car pulmonale which
will illustrate the main processes occurring during
the evolution of this disease. These processes are
threefold-mechanic:~I overload of the right ventricle, hypoxia and hypercapnia.
Table 1 sho\vs the diseases which have been
chosen to illustrate the three processes. Overload of
the right ventricle can he acute as in massive
pulmonary embolis~n or chronic as in multiple
diffuse embolization of the pulmonary arterial tree
or as in primary pulmonary hypertension. Chronic
hypoxia in its simplest form occurs in life at high
altitude. It may also be due to diffuse pulmnnar)
fibrosis or granulomata which impair the diffusing
capacity of the lungs. In these latter diseases,
ho\vever. the situation may often be complicated by
involvement of the pulmonary arterial vessels by
organic disease. Finally, there is no example of
pure c.ul)on dioxide retention, but I have chosen the
classic and common disease of chronrc bronchitis in
which there is a combination of carbon dioxide
'Instihit? of C.nrd~olop!, L'nnrrsih
En~.l.md
retention, hyposia and right ventricular overload
\IECHASICAL
OVEHLOAD
OF THE RICM VESTRITLE
llthooah acute masswe pulmonary embolizahon i~ a dramahc and f a d ) common etpenrnce to all of us in horp8tal
prachce, it may not be enhrrly realized how eeteenalre the
~ r c l u i o nnf the polrnonary arteries ha\ to Iw In thu clt\e.~u.
The sudden occln\ion of one main branch of the polmonar)
.arter> hy rnrana of a balloon on the end of a cardlac catheter
leads to an increae m p o l r n o n a ~ arterial prrcsurr of nnl)
\"me 5 rnm HE.?-' T h k bean nut the obser\.ahuns of the
pathologists that maoi\.e pulmonan ernbol~zationto l x fatal
lhas tu tn\.i,l\.r cons~derabl) more than 50 percent of the
pulmonary arterial hrc. Here we are faced w ~ t hthe effects of
a wddm cnrrloadtne of the nght \.enhbcle and thew are
rathrr dlfferrnt from the more well-knoun effects of a gradual incrmqr an lo.ld tvliich ma) lart fur loonthq or for )ran.In
the c z e of maslve pulmonary embol~~?tion
the presmre ~n
the puIm,,n,>q nrtrr? d w r not oruall) nse nearly to th? -me
rttcnt as ~t can do in chronlr dbease. Nr\erthele\s, the r i ~ h t
~ m t n c l rd w s not ha\.r time to de\elop h?pertrophy I" order
t,, cope with the exha load and becomes rapidly and aenonsl)
rinbarraa\ed. It\ uutput falls and the rllnical ptcttlrr is often
ciomlnatrd as much h) the appearance of shwk a
5 it i, b? the
,pcrlfic rffrch of pullni,nan I?? wrtrnston.
Therapy d i t ~ d e srtsrlf tnto thore measures whlch are taken
d~rectl?on the rrnir,lus and those ohtch are taken to prc\mt
further release of etnholi from their rttc of origin. \V~ththe
.td\ancea ~n cardlac \urger).. dl-t
*t~rgicalattack on the
r l n h l u r h z I m a m e a prachcal propnsihon. But, while the
procrdr~re is logical and there are e\-~dmtlypatients who d ~ e
under !nore conventional regimms u h o might be smed by
ernerEency surgPr), it ,till has to be demonshated that the
overall mortality k irnprov~l.The inhcdochoo of fibrinoly*~
agents has placed the p,,slb~lity of direct attack on d ~ e
embolus in the hands of the physictans.
The pre\rntlon of further emboliahon also has both
surgical and medical prop,nenh. Here there are rather clearly defined trans-Atlanhc differences of opinion, since operations on the lnferior vena c a m are not mrnrnonly perfomled
in Enplnnd where reliance 1s uruall) placed on the unaided
effecb of adrquate anticoapulahon.
~ e s sspectacular hot certainly no less sinister than the
effects of rnasrlre pulmonary thrarnboernholization are the
effects of widespr~adocclvsion of the srualler pulmonary
arterial vessels by thrornboemboli. To affect the pulmonary
artenal precsure rrich embolization ha\ to Ix widespread and
occon o\.rr a penod w h ~ h
may e\tend from a few weeks tn
of Loodon. London,
43
Downloaded From: http://publications.chestnet.org/ on 06/09/2014
PETER HARRIS
Table I - D i e a m Choren t o Illu.rrote Meehon"ms
Leadins t o Cor Pulnuonak.
.I &lerhanieal uvrrload oi t h r~~ g h tventr~rlc
B
C
Arute
thromboemlml~sm
Chronlr recurrat pulmonar)- rmhhzation
Prtmary pulmannry hypertea%iun
Hypoxia
Htgh alt~tude
D i f f w pulmonary fibrosm
Retention of carbon dloxlde
Chrunir I,ronrhitl>
several yean. Under the m~croscope~t is the muscular pulmonary arteries and the small elashc pulmonary artenes
which are affected. Their lumens become m l u d e d by clot
and organlzahon and recanalmation cmor. The pressure in
the pulmonary artery rises sometimes to an extreme degree
and the right ventricle hypertroph~esand ulhmately fails.
The symptoms of the disease are ~nsidious.There is not
usually any history of hemoptysis or pleontic pain. Instead
the patient complains of a gradually increasmg shortness of
breath sometimes with an unproducb\.e cough, w a s ~ o n a l l y
with syncope
from bme to hme with
.
. on effort and wrhaps
.
rpaodxler of une~plaineddyrpnea.
Perhapp the most important contnbotir,n the physician can
bring to the management of this disease IS an awareness of its
frequency, for m its early stages it a a treatable disease while
in iis later stages tt is untreatahle and fatal. Treatment in the
early stager is by anticoagulation which has to be prolonged
and probably should be conhnued indefinitely. Certainly I
can recall on one m a s i o n stopping ~t after three yean only to
have the patient return with a pulmonary infarction a few
weeks later. Probably tt is best to err on the safe s ~ d eas the
risk to the patient's life are serious.
Another condition giving me to chron~coverload of the
right ventricle is the rare dihease of primary pulmonary
hypertenston. It tends to occur most frerluently ~n young
women and is masionally familial. Under the microsmpe the
muscular pulmonary arteries undergo the changes described
by Heath and Edwards3 under the term "hypertensive pulmonary vascular disease." Thew is an increa.e m the rnurculature of the media with intimal proliferation in the early
stages. Latrr in the m u n e of the disease the muscular
polrnonar) arteries become m l u d e d and fibrotic while their
small arteriolar branches debclop the bizarre dilated malformations which are called by Edwards and Heath the "dilatation Ipsions."
In this disease the pulmonary artery pressure rises to
rinkter proportions, the right venbicle hypertrophies and the
patient dies ultimately with a failing nght renhicle. There is
unfom~nnhlylittle enough one can do for patients with this
disease which is invariably fatal. Drugs which might wssibly
have a vasodilating action on the pulmonary c~rculationh a w
been hied without success. Pulmonary s)mpathectomy has
also been found to have no affect and anticoagulant drugs are
of no value Cardiac catheterizahon and especially angiographg carry sn increased nsk In t h s mndition.
Although there s no eRective keatment for pnmary pulmonary hypertension. the last few years have brought new
information which might possibly lead to a greater understanding of tts etiology and thus greater hope for ,is prevention. R ~ e n t l yGurtner" has d r a m attention to an epidemic
of primary pulmonary hypertenston ~ ~ r in nS w i~~ e r lga n d .
Among 65 patients, 50 had taken an anorectic drug, Amino~
rex ( 2 amino-5 phenyl4 oramline) Similar epidenlin h a \ e
been noted in Austria and Gern~anywhere the dnlg was also
marketed, the geagraph~cdlitrrbution of the zp~delnicas
well ar the date of its appearance rn~ncidedwlth the availablllty of thr dnrg.
Although the epidemiologic evidence is strong, no effects
of Aminore\ m\en by mouth have so far k n reported in
animah. Lest. however, it be doubted whether a rutstance
given by month can cause a specific prtlrnonar?. h>pertens~nn,
we have the example of the effects of Crotabno rpectabilis ~n
the rat.' \\%en the seeds of t h a plant are added to the dirt of
weanling rats they develop severe pulnlonary hypertension
which causes right ventrinllar hypertrophy and failure fmm
which they die In about four weeks.
Conmand and his c a l l e a ~ \ l e r6~n t sho\ved the increare in
polmunary arterial pressure whlch ackompanies acute hypoxla in man. People h l m g at high alhhide are subjected to
chrontc h>poiva and also shou, an Increase in the pressure in
the pulmonary artery. In the Prnnian Andes there ir an
mdigenous population li\ing at an altihlde in the region of
1 5 , W feet above sea Iwel where studies of the pulmonary
circulation ha\" been earned out by Peaalow and his colleagues."'o Table 2 shows data taken from PeBalnza 'I' In
the normal wptllahon the pohlonary arterial pressure ha\ a
mean value of borne 33 to 30 mm Hc. Such a mild elevatnon
~n pressure doer not seem to affect the funchon of the heart to
any practical extent. People l i \ ~ n gunder such condibnns are
capable of se\.err physical rxerclsr and the effects of h > p > r i a
do not seem to limit the length of their life. \\hen they are
taken to sea level the polmonar) arterial presborr falls to
nonnal. Although their ptdmonary arteridl and muscular
pulmonary artenrs show some increase in medial muscle"
the severe changes described by Heath and Edwards in
extreme hypertenalve pulrnonar) vascular d~sease do not
IICCIIT.
Therr is, however, a small group of people Intng permanently at high altitude who develop what has become Lmoum
as c h m n s mountain sichess or \longr's disease. These
patientt become dyrpnelc. To look at, they are ckarly polycythernlc and they dexelop a high hematowit and hemoglobin
(Table 2 1. The pulmonary arterial pressure is no\+ dstinctly
elevated and may lead to rlght vcntrlcular failure. It s
usually consider~dthat the condition arises becanw of a lack
of response of the rsplrator) center tn the hyporic stimulus,
and Table 2 shows that the arterial oxygen saturation tends to
k lower in thts group of patients than it a in normal people
at the same altitude. Another poss~bilityis that these patients
hale some degree of emphysema, for the disease appean to
Table 2--Loboratory Findin68 in Chronic Mountain
Sickness m 4,300 meter. (Data from PeMlolo. 1969)
Arterlnl oxygen snturntlon (51
Hematorrit ( % )
\lean ~,nlmonaryarterial
prssnre imm H R I
Cardtar output ( I ~ t r r srmn m21
Chronic
llo~mtaln
Slrknew
IlOCa.%
Sormal
Kesldents
(IPCa-sl
70
79
8I
59
47
4.0
23
3.8
CHEST, VOL. 58, SUPPLEMENT NO. 2, OCTOBER 1970
Downloaded From: http://publications.chestnet.org/ on 06/09/2014
MANAGEMENT OF COR PULMONALE
be more common in men of middle age. .4t this altitude the
oxygen saturation of the arterial blmd is poised an the elbow
of the oxygen dissociation curve. Thus a small decrease in the
parfial pressure of oxygen due to alveolar hypoventilation can
h a w a very much greater effect on the oxygen saturation of
the arterial blood than it would at sea level. Whatever the
p m w nature of the patholog~cprocess the only advice one
can give to such pahenb is that they should remove
themselves to sea level w k r e their disability rapidly dirap
-.I@
How the myocardium responds to the stimulus of chronic
hypoxia might well be an impartant factor in the natural
history of many diseases associated with hypoternla. h great
deal of knowledge has been accumulated concerning the
metabolic response of the myocardium to acute hypoxia. The
respiratory physician, however, would be more interested in
how the myocardium responds to chronic hypoxia, and here
one is more m n c e d with changes in the activity of
enzymes than ~n the immediate changes in substrate concenbations which arc so obvious in acute hypoxia. Knowledge of
the effech of chronic hypoxia on the myocardium a, hawever, scanty. R e n t studies m the Peruvian Andes have
shorn a sltbstantial increase in the activity of m)ocardial
succinic dehydmgenase in high altitude animak while lactic
dehydrogena~eactivity remains unaffected. Thus the shmulus
of chronic hypoxia appears to stimulate activity or ryothesis
of a mitochondria1 enzyme linked to the respiratory cham and
playing an important role in oxidative catabokm.'? There is
great need for further knowledge concerning the metabolic
adaptations of the heart to chronic hypoxia.
There are also important changes in the functional capacity of the heart during adaptation to high altitude.13 Soon
after arrival at high a l h h ~ d ethe cardiac output is abnormally
high during exercise. Within two to three week, however.
the reslxlnsr of the cardiac output to exercw return to
normal. I believe ~t IS importaot to bear in mind these
adaptation5 of the heart to chronic hypoxja just as ~t is
Important to di\tinpu\h Iwhveen the e f f f f h of an acute and
c h m n ~ cmechantcal overload on the right ventricle.
The nert group of patienb with chronic h m x i a are those
with diffuse fibmru or granulomatmis of tbe lungs in whom
there is a prominent deficiency of the diffusing capactty. In
these patients the pulmonary hypertensinn tends to be more
severe because to the effects of h y p ~ x i a are added the
mechanical effecb of disease in relation to thr small pulmonary arteries. Thus the right ventricle tends to be more
seriously overloaded and ruffen at the same time fmm the
disabil~tyof a shortage of artenal o\ygen. The Pro1 tends to
be low k n a r e of the hyperventilation which so often accompanies such diseases and because there is no impediment
to the parrage of carbon dioxide across the alveolar-apillary
nwmhnne. For these patienb the giving of oxygen is the
logical t r e ~ t m e n tand some of them indeed can only exist
under these circumstance. Occasionally one might hope that
the giving uf oxygen might allow the patient to sunive until
same other means of therapy ( p e r h a p steroids) can alleviate
the pathr,!ogic p r m s in the lungs themselves. Slore often,
however, the outlook for these patients is very limited.
Nevertheless. the giving of oxygen a important in order to
keep them comfortable during the last days of their hves.
In this everyday d i s e ~ s e~ , have
e
to deal not only with the
effecb crf h y p x i a hut also with the effects of hypercapnia.
The pullnonary hypertension in such patients tends to be
CHEST. VOL. 58, SUPPLEMENT NO. 2, OCTOBER
Downloaded From: http://publications.chestnet.org/ on 06/09/2014
labile, increasing dramatically when an acute respiratory
infection occun. Under there circumstance there is a sharp
decrease in the arterial oxygen saturation which is probably
the main cause of the pulmonary hypertension. There is
endeoce, however, that the ~ n c r e a datrways resistance may
lbelf contribute mechanically to the raised pulmonary vascular resistanm.14
The retention of carbon dioxide which accompanies the
hypoxia adds a risk to oxygen therapy which is not present in
the other condrtions we have been dirursing. Thus it has
been known for many years that the administration of h ~ g b
conceobahons of oxygen to these patienb may caw a
dangerous fall ~n ventilatian.l5 This is a problem which has
been considered ekewhere in the symposium. What s unequivocal, however. is the need to unprove overall alveolar
vinhlation-by hronchdilators, antibioticr, respiratory stimulants. mehanical vendahon or hacheostomv. The details of
such therapy do not come strictly wlthin the terms of reference of the present communication. It may, nevertheless, be
helpful to emphasize here that probably the most important
therapy to the heart ibelf in this condition u the establ>shlnent of an increased exchange of respiratory gases in the
lungs.
This is the fint princ~pletn the management of the cor
p u h o n a l e of chron~cbronchihs. The semnd principle is
almost a corollary to the first-the reduction of the need to
exchange respiratory gases in the lungs by a reduchon in the
metabolic requirement\ of the body. Some of the measwe have already mns~deredudl have this effect, for instance,
a reduction in the work of breathing or in the body. tempera.
h~re.Within this principle also one should consider the
o-ity
for bodily rest.
The third principle ir to improve the function of the
myocardium, but this is not such a simple problem as in other
forms of heart disease. Thew patienb have an elevated
qrtemlc venous pressure and edema-the classic phyrical
signs of congestive cardiac failure. Nevertheless, in contract
to patienb with valvar disease of the heart it doer not appear
that this situation is ammpanred by a decrease in the
cardiac output.16 It might, therefore, be debated whether
one is strictly dealing with a mndltion of cardiac failure. The
combination of a normal resting cardiac output with an
increased filling pressure might suggest that the right ventricle is not behaving normally. On the other hand, cyclical
changes in inhathoracic pressure may, by themselves, cause
the mean hydrostahc pressure in the cardiac chambers to
increase without the need to invoke ventricular failure.'?
Oplnions have varied concerning the e5cacy of digitalis ~n
this condihon. The careful hemodynamic studies of Dr.
Ferrer and her c o l l e a g u e s , ~ ~ o w e v e rhave
,
s h o w that the
gi\ing of digitalis is a-mparued
by an increase in the
cardiac output and a fall in the end diastolic pressure in the
right ventricle although there is some increase tn the pulmonary arterial pressure. On hemdynamic grounds, therefore.
there would seem to be an indtcatioo for the giving of thls
drug, although rt has to be admitted that its clinical effecb
are not so oh\ious in this dkeare as they are in patienb with
chronic valvar disease associated with atrial fibrillation.
These patienb also show a greater tendency than others to
develop ectopic rhythms following treaiment with digitalis.
The cause of this increase in senriti\ity has not been properly
elucidated. It may possibly be due directly to the presence of
hrpaxia or it may be associated with the depletion of potassium which is so common in this conditian.'a,20
Venesection either in the acute or chronic phase of hronchitic cor pulmonale has its advocates, although 1 am not
PETER HARRIS
numbered among them. The studies of Srgel and Bishop"
on the rffects of repeated venesection lo patients with chronic
bronchatis who were suffering from a chronic p o l ~ c ~ t l ~ e m i a
ga\.e ven lnttle evidencr of benefit.
The fourth pnncnple of management is the restoration of
electrolyte imbalnnm. The effects of a retention of carbon
dioxide on electrolyte metaboli5m ar? probably dictated more
by ewhangrr between the tissue cells and the e\tracellular
fluid than they are by altrrahons in renal function.223
There i* a lms of sodium and potassium from the eel$ in
exchangr for hydrogen iona and a specific exchange of
chloride for hicarbunate by the red e l l s . The reabsorption of
bicarbonate by the kidney wr lncrraced and thew s an
increased orinar) loss of potasir~m.
In pntirnts in an edmmatous state, however, these even&
are complicat~l by specific changer in renal h1nction.24
There is a reduction tn renal b l d Bow and a smaller
rerluction ~n glolnemlar filtration rate with a renal rptention
of sndiurn similar to that found in patients with edema doe to
valvar d i s e a ~
Whatever duuhts one might ha\e concerning the cllniral
efficacy of d ~ g i t a l ein this condition the value of d~ureticc
must be undicputed. Both mercurial and nonrnercunal dlureti n am effective although mndern practice tends to favor the
latter especially now that such drugs are available for inhavenous rl*r. The rmponsp is often dramahc and in some
mysterious wny the giving of diumtin appears to tmpn,\.e
respirator). gas etchange bringing the arterial levek towards
One mold lmagine that this action e due to the
the norn~al.s%
removal of Auld retamed in the lung hrsor spaces. The u,ork
of Tunno and his colleagnessu suggests that the \olnme of
exhava*c~tlarr a t r r in the lungs a h~gherin ernphyse~nntou\
patients with edema than in t h w without. In the giving of
thiaz~drdjurrtin one has to be particolarlj careful to prevent
a Ims of patassiom s i n e so many of these patients have a
depletion of bod) potaqrium before the Iwginmng of treatment.
SUXI~IMY
Three main processes underlie the pathogenesis
of cur pulmonale-mechanical overload of the right
ventricle, hypoxia and hypercapnia. A number of
causes of cur pulmonale has been selected to
illustrate the varying role of these three processes
and the way in which an understanding of their
nature prolldes principles on which therapy can be
based.
REFERES~
1 Bull \VHO: Tech RepSer So. 213, 1961
2 Snderholm B: The h a e m o d p a m i n of the lesser circulation in pulmonary hikrcttlmis. Scand J Clin Lab Invest 9
( rupp126 ), 1957
3 Widimsky J, Fa*altcky J . Cardiovascular adaptation to
acute pulmonary hyperternion. \led Tharac 21.339-382,
1964
4 H a m s P. Segel S . Bishop 111: The relation between
presaore and Row in the polmonar). circulation m normal
subjects and in p a t i w b with chronic bronchitis and mitral
stenoris. Canliovas Rrs 2373-83. 1968
5 Heath D, Edwards J E : The patholog). of hypertensive
pulmonary vascular <lnea\r. Circulation 18533-547, 1958
6 Gurtner HP. Pulmonary hypertension produced by ingestion of substances. Bull Phyaio-path Resp 5:435-441, 1969
7 Kay J\I. Hamr P. Hrath D: Rtlmonary hypertenston
prwloced in rats by ingeshon of Crotnloria spectabilis
seeds. Thora, L2.:176-179, IS67
8 Jlatlr, HL, Cournand A, \Verko L, r t al: The influence
of short periods of induced hrpoxia upon pulmonary
artrr! prt,ssore, ~n man. .4n,er J Physiol 150:315320,
194i
9 Pedaloza D, Slme F, Banchero S , c t al: Pulmonary
hypcrtmrion ~n healthy men born and living at high
altihldca, hmrr J Cardiol 11:130-157, 1963
10 Pedaloza D. Corazon pulmanar chronico par desadaptacron a la alhlra. Tesi, doctoral, Unirrrsidad Peruana
Cayetano Heredla. Lima, Peru, 1969
I I Ariac-Strlla J, Snldan., \ I : The tcrndnal portion of the
pulmonary arterial tree in
nahve to hrgh altitudm.
Clrculstinn 2 8 . 9 1 5 - 9 5 , 1963
12 Hams P, Cashllo 1,Gibson I;, et al: Succinic m d lachc
dehydrogrnae achkity in myocardial homogmates from
animals at high and low altitude. J \lolec Cell Carrltul.
1.189-195, 1970
13 \i,grl ]A, Hanccn JE. Harris O V : Cardlovascular respmw in man during e\haush\p work a t sea level and
high alhh~de.J Appl Physiol L3.3-531-539,1969
I4 Hsni* P. Segrl S . Green I, et al: The idtnrnce of the
airways rmistanm and alveolar pressure on the pulmonary
\-awular rrslstancr I" clrronnc bronchlhs. Cardio\.asc Hes
5:84-92. IS68
1.5 Rlch.trd5 D\V Jr, Barach A L : Prolonged residence in hirh
o\sarn ahaospherer. Effects on normal indiv~dualsand on
patlent, r l t h chronic rardlac and pulmunar) insclfficiency
Quart J \Ird 3:137-466, 1934
16 Harm P, Heath D: The human pulmonap circulation.
Edtnh~trgh,E, and S. Li\.ing\tone, 1962
17 Harris P. Helatic,n of always resistance and polmonary
va\cnkr rfiistance. Bull Physlo-path Resp 4:65-73, IW8
18 Ferrer 111, Hanuy R\I, C;~thcartRT, et al: Same effects
of dlgo\in ttjn~nthc heart and circulation tn man. Digonn
tn chronic ror pulnlr,nale. Circulatmn 1:161-186, 1950
19 Baun,, CL. Dick \I\!, Blum A, et al: Factom involved in
dlgltalis ,ensth\.lt). in chronic polmonar) mrufficiency.
Amer Hrart J .57:460-464, 1959
20 Bawn CL, D ~ c k \!\I, Blum A, ct dl. Total bod) erchang~ahlrjn,ta*sirtm and sodium and r\tracellular fluid
in chronic pulmonar) ~nsufficiency.Amer Heart J 58:5358, 1959
21 Segal S. Bshop ]\I: The circulation ~n patients with
chronic brnnch*h* and cmph!\rrna at rest and during
e ~ e m i ~with
,
\pecial rpferencr to the inEuencp of
c h a n g r ~ ~n hlmd vlrcosih and hlmd vr>htrnt. on the
poltnonaq clrculahon J Clin In\,rst 15:1558154%, 1966
22 Giehsch G , b r g r r L, Pitb RF: The rrtra-renal response
to acute acid-base dishlrbances of respiratory origin. J
Clin Invest 31-231-245. 1955
23 Cartrr S \ Y , Seldln D\V. Teng HC: Tissue and renal
respome to uhnjns rpcplratnr). acidoris. J Clin Invest
38.949-960, 19.59
24 A b r (311, Baylry TJ, Blrhop 111: Intrrrelationshlp betwwn renal and cardlac funchon and resptratory gas
exchange in nbstmct~vcalways d ~ s e a ~Cltn
e . SCI 25:159170, 1963
25 Nnhle 11111. Trcnchard D, Cuz A: T h r \.slue of diureti n in respiratory failure. Lancet. 23257-260, 1966
26 Turino (;\I, Edelman S H , Senior R\I, et al: Erbavascular
lung water in cor pulrnonale. Entrehem Phgs~o-Path
Resp 7 : 259-277, 1967
Reprint requests: Dr. Harris, Institute of Cardiology, 35
W i m p l e Street, London \\'i\l SEX, England
CHEST, VOL. 58, SUPPLEMENT NO. 2, OCTOBER 1970
Downloaded From: http://publications.chestnet.org/ on 06/09/2014
`