Download Respiration and Circulation in Patients with Portal Cirrhosis

CLINICAL PROGRESS
Respiration and Circulation in Patients with Portal
Cirrhosis of the Liver
By H.
0.
HEINEMANN, M.D.
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this metabolite is frequently elevated in patients with liver disease." Poor correlation between the ammonia content of arterial blood
and the minute ventilation casts some doubt
on the significance of ammonia as a respiratory stimulus and leaves this problem open for
further investigation.9 Another stimulus that
must be considered to explain the hyperventilation is the low oxygen tension of arterial
blood, not infrequently observed in patients
with cirrhosis of the liver. Determination of
the partial pressure of oxygen in arterial blood
reveals tensions, however, which are not of
the order of magnitude commonly assumed to
be necessary to increase ventilation,9' 12 and
the mechanism maintaining hyperventilation
in the absence of adequate physiologic stimuli
(pCO2, pH, and P02) remains, at present
unsatisfactorily explained.
The above-mentioned low arterial oxygen
tension, observed in some patients with cirrhosis of the liver, leads to an increased
gradient in the partial pressure of oxygen
between the blood and alveolar air.13 This
gradient is further accentuated by the high
alveolar oxygen tension caused by hyperventilation. The low arterial oxygen tension in
cirrhosis of the liver might be due to hypoventilation of well-perfused lung tissue, because
of elevation of the diaphragm secondary to
ascites, or these patients may have intrinsic
lung disease with reduced diffusing capacity
for oxygen. Pulmonary function remains
within normal limits and unsaturation of
arterial blood persists, however, irrespective
of the presence or absence of ascites,9 and
paracentesis has no apparent effect on ventila-
IT IS generally known that cirrhosis of the
liver may be accompanied by marked
changes in the hepatic and splanchnic vasculature, which in turn lead to reduced hepatic
blood flow, increased portal venous pressure,
and the development of collateral vessels permitting bypass of the diseased liver.'-7 Less
well known is the fact that cirrhosis of the
liver may also be associated with changes in
the respiratory pattern, the pulmonary vasculature, and the systemic circulation.8-10
Information on this subject is at present incomplete. It may even seem questionable that
impairment of the function of a single organ
can lead to such a varied pathologic pattern.
This review attempts to fulfill a dual purpose:
first, to draw attention to the above-mentioned,
less well known complications of cirrhosis of
the liver, and, secondly, to present a more
unified concept of the respiration and circulation in patients with this disease.
Patients with cirrhosis of the liver may
hyperventilate at rest in the absence of reduced hemoglobin content of the blood and
without apparent increase in oxygen consumption. This leads to the development of mild
respiratory alkalosis.10 To explain the hyperventilation in the face of reduced carbon dioxide tension and normal, or slightly elevated,
pH of the arterial blood, the assumption is
often made that the respiratory center is stimulated by ammonia, because the blood level of
From the Department of Medicine, Francis Delafield Hospital, and the College of Physicians and
Surgeons, Columbia University, New York, N.Y.
Supported in part by Grant C-2332 from the National Cancer Institute, U.S. Public Health Service.
154
4 C irculation, Volume XXII, JulI 1960
CIRCULATION IN CIRRHOSIS
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tion.14 It is also conceivable that changes in
the hemoglobin molecule, leading to a shift in
the oxygen dissociation curve, may be responsible for the hypoxemia in liver disease.15' 16
Such a mechanism can similarly be excluded,
however, because blood of hypoxemic patients
becomes fully saturated by equilibration in
vitro with gas mixtures containing oxygen at
tensions similar to the ones observed in vivo.9
These considerations leave shunting of
venous blood into the systemic circulation as
a third possibility to explain the hypoxemia
of liver disease. The presence of such venousto-arterial shunts is made likely by the fact
that administration of 100 per cent oxygen
does not abolish either the increased gradient
for oxygen tension between alveolar air and
arterial blood, nor the hypoxemia in patients
with marked unsaturation.8' 17 In adults with
portal cirrhosis, in contrast to patients with
so-called juvenile cirrhosis,* these shunts are
apparently not located between the pulmonary
arteries and pulmonary veins.'8' 19 Abnormal
vascular channels, which could account for
extrapulmonary shunting of venous blood into
the systemic circulation, have been documented by Calabresi and Abelman,20 who
demonstrated communications between the
portal vascular bed and the pulmonary veins
via periesophageal and mediastinal veins. The
volume of portal venous blood entering the
systemic circulation per unit of time must
depend on the available pressure gradient between the portal and pulmonary veins and
may, therefore, vary considerably during the
respiratory cycle because of the unusual location across the diaphragm.t
Unpublished observations indicate that cirrhosis of the liver may in some instances be
associated with changes in the pulmonary
arteries (vasculitis?) and an elevated pulmonary artery pressure. The underlying
*Rydell and Hoffbauer'8 observed arteriovenous
anastomoses between the pulmonary artery and the
pulmonary vein in a patient with juvenile cirrhosis.
tThe so-called shunt equation cannot be applied to
calculate the volume of blood flowing through these
vascular communications because the oxygen content
of portal blood is not readily measurable.n
Circulation, Volume XXII, July
1960
1 5a
mechanism is at present not understood. But
the question arises whether there is a relationship between the pulmonary hypertension and
the fact that metabolites, originating from the
gastrointestinal tract, have direct access to the
pulmonary arteries via acquired or surgically
induced anastomoses of portal vein to vena
eava. It is tempting to compare this situation
with the pulmonary hypertension in patients
with the carcinoid syndrome, where serotonin
escapes hepatic inactivation because of overproduction or metastases beyond the liver and
then affects the pulmonary vessels. At present,
however, there is no evidence to suggest that
the changes in the pulmonary arteries, occasionally observed in patients with cirrhosis
of the liver, are due to a specific metabolite
such as serotonin.-*
Patients with cirrhosis of the liver may
have unexplained cardiac hypertrophy. Lunseth, Olmstead, and Abboud23 reported such
cardiomegaly in 12 out of 108 autopsies on
patients with portal cirrhosis, an incidence of
11 per cent. Coronary artery disease and hypertension are generally considered to be less
common in these patients.24 To account for this
abnormality, one has therefore to consider
other mechanisms. One possibility would be
that portal cirrhosis is associated with a
specific type of myocardial disease. Such a
mechanism is not unlikely because microscopic
examination of the myocardium in the patients
studied by Lunseth, Olmstead, and Abboud23
and others25 revealed an unusual type of
diffuse fibrosis, often only in portions of a
single muscle fiber.
Predominant right ventricular hypertrophy
is another characteristic feature of the cardiomegaly in patients with cirrhosis of the liver.
This may be due to the occasionally observed
increased pulmonary artery pressure. It is
also known that patients with cirrhosis of the
liver may have a high cardiac output at rest,
irrespective of the presence or absence of collateral circulation, portocaval shunt, anemia,
*The serotonin content in blood of patients with
cirrhosis of the liver is reported to be lower than in
normal subjects.9
156
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or nutritional deficiencies.8 26-28 Such persistent elevation of the cardiac output could
account for cardiac hypertrophy. The increase
in cardiac output is not associated with increased oxygen consumption and is therefore
different from the circulatory pattern observed in the so-called hypermetabolic state.
The rise in cardiac output is similar to the
change noted in patients with arteriovenous
fistulae29' 30 and thiamine deficieney.31 All
these syndromes have in common a reduction
of the peripheral resistance.
It is conceivable that cardiomegaly, perhaps
in combination with degenerative changes in
the myocardium, may lead to cardiac failure.
No adequate information, however, is available
on the incidence of such a complication in
patients with cirrhosis of the liver. Dyspnea
and cough, frequently noted in these patients,
is usually ascribed to the elevated diaphragm
because of ascites and the higher susceptibility
to respiratory infections.32 Peripheral edema
is as frequent as ascites in these patients and
may occur irrespective of the presence or
absence of fluid in the abdomen.32 Hvdrothorax may develop, most commonly in association with ascites. Pulmonary infections or
leakage of ascitic fluid into the pleural cavity
is usually implicated as a cause. If heart failure, indeed, complicates cirrhosis of the liver,
it may be difficult to detect because most synmptoms can also be ascribed to the underlying
disease. Measurement of venous pressure and
the response to a cardiotonic regimen may be
helpful in differentiating the cause of fluid
retention. Furthermore coincidence of cirrhosis of the liver and heart failure does not
imply a causal relationship, because both conditions have a high incidence in the same age
group. However, 2 well-documented cases of
high output failure have been reported in the
literature.8' 18 Emphasis, therefore, on high
output failure as a potential complication of
cirrhosis of the liver seems justified and may
lead to more frequent recognition.
The increased cardiac output in patients
with cirrhosis of the liver is presumably due
to decreased peripheral resistance and the resulting increased peripheral blood flow. These
HEINEMANN
changes in the hemodynamic pattern are
clinically discernible by the increased pulse
pressure,33 flushed palms, and capillary pulsationS.8' 34' 35 The mechanism responsible for the
reduction in peripheral resistance is unknown.
It has been postulated that either increased
production or diminished inactivation of vasoactive substances is involved. Such a substance,
originating from the area drained by the
splanchnic vessels and normally inactivated
by the liver, could escape hepatic inactivation
and gain access to the systemic circulation via
collateral vessels. Increased levels of circulating estrogen35 have also been implicated as a
cause for both the development of palmar
erythema (peripheral vasodilatation) and the
appearance of arterial spiders.
Cirrhosis of the liver is occasionally
accompanied by hypertrophic osteoarthropathy,Y' 34, 36 The cause of clubbing remains unknown, but it has been postulated that this
abnormality is related to increased peripheral
blood flow, increased cardiac output,37 or
shunting of venous blood into the systemic circulation, changes also observed in patients
with portal cirrhosis of the liver. But hypertrophic osteoarthropathy is apparently more
often observed in patients with biliary cirrhosis,8 where such a hemodynamic pattern
seems not to occur.
.Patients with cirrhosis of the liver have
frequently an enlarged total blood volume.38 41
This is mainly due to an increase in the plasma
fraction, the red cell mass being within normal limits. This leads to lowering of the hematocrit level, a fact that should be taken into
consideration if the anemia of liver disease is
to be evaluated. A normal hematocrit value
in patients with cirrhosis of the liver, in the
face of an elevated blood volume, represents
a rise in red cell mass. It is conceivable that
hypoxemia, if present, may stimulate red cell
production and induce a relative or absolute
polycythemia. Two such patients with cirrhosis of the liver and secondary polycythemia
have been reported in the literature.8' 18 The
mechanism causing the rise in plasma volume
is unknown. But a similar hypervolemia is
observed in other conditions associated with
Circulation, Volume XXII, July 1960
CIRCULATION IN CIRRHOSIS
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decreased peripheral resistance, such as arteriovenous fistulas,42 thiamine deficiency,31' 43
and pregnancy.44 Reduction of the peripheral
resistance, due to whatever mechanism, nmay
conceivably initiate a cycle of events that ultimately leads to an increased plasma volume. 45' 46
From the foregoing review, one can conclude that cirrhosis of the liver may be accompanied by marked changes in the respiratory
pattern, pulmonary vasculature, and systemic
circulation. Information about the incidence
of these changes and their relationship to the
stages of the disease and the type of cirrhosis
is at present not available. Most observers have
limited their studies to individual phenomena,
such as the cardiac output, in selected
patients. Rydell and Hoffbauer,15 on the other
hand, performed a careful study in a single
patient with so-called juvenile cirrhosis and
were able to define a disease entity characterized by hypoxemia, secondary polycythemia, high cardiac output, heart failure, and,
apparently in contrast to adults with portal
cirrhosis, multiple intrapulmonary arteriovenous fistulas. Comparable studies are not
available in adults with cirrhosis of the liver.
Such observations are necessary, however, before a similar disease entity can be confidently
described for portal cirrhosis. As a working
hypothesis for future studies, one can separate
the changes observed in adults with portal cirrhosis into 3 different groups.
First, communications between the portal
vascular bed and either the pulmonary veins
or the venae eavae may (a) permit venous
blood to enter the systemic circulation and
cause hypoxemia or (b) may allow intestinal
metabolites to escape hepatic inactivation and
gain direct access to the systemie circulation.
Secondly, metabolites escaping hepatic inactivation may be responsible for the changes
in the pulmonary vessels, pulmonary hypertension, reduced peripheral resistance, and
hyperventilation.
Finally, reduction of the peripheral resistance leads to a rise in cardiac output and perhaps also the plasma volume. The increased
cardiac output may eventually cause cardiac
Circulation, Volume XXII, July 1960
157
hypertrophy and heart failure, a complication
difficult to recognize in older patients in whom
heart disease may occur independently and
fluid retenition and dyspnea can be attributed
to the underlying disease.
Acknowledgment
The author wishes to express his appreciation to
Dr. A. P. Fishman for his suggestions and helpful
criticism.
Addendum
Sinlce this paper was subnmitted for publication,
another well-documented example of arterial hypoxemia in cirrhosis of the liver has been described by
Rodman and associates.47
Summario in Interlingua
Es generalmente cognoscite que cirrhosis del hepate
pote esser accompaniate de mareate alterationes in le
vasculatura hepatic e splanchnic e que isto, de su
parte, resulta in un reduction del fluxo hepatic de
sanguine, in un augmento del tension venose portal,
e in le disveloppamento de vasos collateral que permitte le circuition del hepate morbide. Es minus ben
cognoscite que cirrhosis del hepate pote etiam esser
associate con alterationes del respiration, del vasculatura pulmonar, e del circulation major. Le presente
articulo ha le duple objectivo de (1) signalar le
supra-mentionate, minus ben cognoscite complicationes
de cirrhosis del hepate e (2) presentar un plus unlificate conception del respiration e del circulation iti
patientes con ille disordine.
In summation de su argumento e como base pro
futur studios, le autor presenta le hypothese que le
alterationes observate in patientes adulte con cirrhosis
portal pote esser separate in tres differente gruppos.
1. Communicationes inter le vasculatura portal e, cle
un latere, le venas pulmonar o, del altere latere, le
venas cave pote resultar in (a) le entrata de sanguine
'venose in le circulation major con le effecto de hypoxemia o (b) le non-inactivation de metabolitos intestinal per le hepate e le consequente transition directe
de ille metabolitos a in le circulation major.
2. Metabolitos que escappa al inactivation per le
hepate pote devenir respoaisabile pro alterationes i
le vasos pulmonar, pro hypertension pulmonar, pro
le reduction del resistentia peripheric, e pro hyperventilation.
3. Le reduction del resistentia peripheric resulta in
un augmento del rendimento cardiac e forsan etiam
del volumine de plasma. Le augmentate rendimento
cardiac pote, in le curso del tempore, devenir le causa
de hypertrophia cardiac e disfallimento del cordeun complication que es difficile a identificar in patientes de etates plus avantiate, proque in tales le
HEINEMANN
1.58
disveloppamento de morbo cardiac pote esser un occurrentia independente e le retention de liquido e
le presentia de dyspnea pote esser interpretate como
attribuibile al morbo subjacente.
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,
I
Medical Eponyms
By ROBERT
W.
BUCK., M.D.
The true worth of an experimiienter consists in his pursuing not onlv wvhat he seeks in
his experimuent, but also what be did not seek.-CLAUDE BERNARTD. (Subm11itted by H. M1.
Alarvin, M.D.)
Circulation, Volume XXII, July 1960
Respiration and Circulation in Patients with Portal Cirrhosis of the Liver
H. O. HEINEMANN
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Circulation. 1960;22:154-159
doi: 10.1161/01.CIR.22.1.154
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