CONGESTIVE
HEART
FAILURE
IN INFANCY
I.
Abnormalities
in Blood
Gases
and
Acid-Base
Equilibrium
Norman S. Talner, M.D., S. K. Sanyal, M.B.B.S., Katherine H. Halloran, M.D.,
Thomas H. Gardner, M.D., and Nelson K. Ordway, M.D.
Department of Pediatrics, Yale Unicersity School of Medicine
and the Grace-New haven Community Hospital
(Submitted Max’ 18; revision accepted for publication Juls’ 6, 1964.)
Presented in part at the section on Cardiology Meetings, American Academy of Pediatrics, October,
1963.
Supported h a Grant (11-239-64) from the National Institutes of Health.
l)r. Talner hc)lds a Career Development Award from the National Institutes of Health.
l)r. Sanyal holds an Abel Holbrook Fellowship from the New Haven Heart Association.
ADDRESS: (N.S.T.) 333 Cedar Street, New Haven, Connecticut.
20
PEDIATRICs, January 1965
LTIIOUGII the clinical picture of congestive
heart failure in infancy has been the
subject of several reviews in the pediatric
literature”2’3’4 there has been scant
j)hysio-logic documentation of alterations in cardiac and pulmonary function. The need for de-fining altered physiology has been I)Ointed
out by Blumenthal,5 who suggested using
hemodynamic techniques and pulmonary
function studies similar to those carried out in adult patients in congestive failure. This paper reports values for blood gas tensions and acid-base equilibrium in infants in con-gestive heart failure and will serve as an initial exploration of cardiac and respiratory function in this group. Evaluation of respira-tory function in infants in cardiac failure is of paramount importance since pulmonary symptoms dominate the clinical picture of cardiac decompensation in infancy. The lungs by virtue of their position in the cir-culatory stream may serve as a sensitive in-(licator of left heart performance in infancy.
MATERIALS AND METHODS
Twenty infants varying in age from 2 weeks to 8 months have been included in the
study. Their diagnoses were established by
cardiac catheterization and/or angiocardiog-raphy and are presented in Table I. In 5 patients the diagnosis was confirmed by
postmortem examination. All defects in the series are characterized by increased pul-monary blood flow and/or pulmonary venous
hypertension . The calculated net
right-to-left shunts ranged from 15-56% of systemic
flow and Wollld thus exert minimal influence
on Pcos values.6
The presence of cardiac failure was estab-lished on clinical grounds by two
cardiolo-gists incorporating the features seen in Table II. All infants had the cardinal signs of
cardiac decompensation including
tachy-cardia (rate over 150 per minute),
cardio-megaly and tachypnea (respiratory rate greater than 60 per minute). Wheezing was
noted in the majority of infants while bubbling rales suggesting pulmonary edema were noted infrequently. Hepatomegaly
(liver edge> 3 cm below the costal margin)
was present in 16 infants while peripheral
edema was observed only rarely. Blood, nose, and throat cultures were obtained on all pa-tients and no pathogens were isolated. Isola-tions of common respiratory tract viruses were attempted in 10 patients and no
signifi-cant results were obtained.
As soon as the presence of cardiac decom-pensation was established and prior to treat-ment, arterial blood samples were obtained for the study of blood gases and serum elec-trolytes. The samples were obtained
TABLE I
CLINICAL DATA
Patient .4 ge Sex Diagno.sis
TABLE IL
SIGNS AND SYMPTOMS: CONGESTIVE hEART FAILuRE
Tachycardia Cardiomegaly
Tachypnea QO
Wheezing 13
hlepatomegaly 16
Peripheral edema
1)11.
T.C.
‘J.P.
K.L.
ILY.
E.A.
All.
N.H.
T.S.
I).B.
1).P.
N.H.
E.F.
L.M.
G.J.
V.McG.
B.St.J.
AS.
It.”.
Lrsl.
7 mo :i Endocardial cushion defect Patent ductus arteriosus
i wk F Coarctation
Patent ductus arteriosus
3 1110 F Atrial septal defect Ventricular septal defect
7 1110 F Patent ductus arteriosus
1III() M Ilypoplastic left heart
syn-drome
7 1110 i\l Total anomalous pulmonary
venous returll. Pulmonary
venous obstruction*
4 mo F Anomalous origin left
coro-nary artery*
3 wk F Ventricular septal defect
‘ mo F Ilypoplastic left heart syri-drome*
3 mo F Patent ductus arteriosus
.5 mo F Endocardial cushion defect
.5 mo F Patent ductus arteriosus
2 mo M Hypoplastic left heart
syn-drome*
1 mo F Transposition of great vessels Large ventricular septal
de-fect
6 mo F Venticular septal defect
8 nmo F Transposition of great vessels Patent ductus arteriosus
Atrial septal defect
1 mo M Transposition of great vessels Ventricular septal defect
lnio M Ilypoplastic left heart syn-drome*
I mo M Ventricular septal defect
3mo F Ventricular septal defect
* Postmortem confirmation of diagnosis.
No. P/s.
following determinations were carried out
immediately following sample withdrawal:
PH, Po2, Pc02, and sodium, potassium, and
chloride. All chemical determinations were
carried out in a research laboratory with plI
checks within 0.01 p11 units, Pco2 within 1 mm Hg and P02 within 1 mm Hg under
con-ditions of room-air breathing. The pH
meas-urements were I)erformued with a Radiometer p11 Meter. A modified Clark electrode7 was
utilized for P02 estimation while the Sever-inghaus electrode was utilized in determin-ing Po2.7 The analyses for blood gases were
performed at 37#{176}C (with suitable corrections
included for infants’ body temperature at the
time of sample withdrawal). Oxygen satura-tions were derived from the P02 values using
the Severinghaus nomogram incorporating
temperature and pH correction factors.
Serum sodium and potassium were deter-mined by flame photometry while the chlo-ride determinations were carried out using a Cotlove Titrometer. Bicarbonate levels were estimated from the Henderson-Hasselbach
equation using the measured pH and Pco2
values, a pK’ of 6.1 and solving for bicar-bonate (HCO3j.
For control purposes additional blood gas studies were carried out in 8 infants varying
in age from 3 to 18 months with left-to-right shunts but not in congestive failure.
RESULTS
p/f (7.38-7.41) Pco, (39-4!) mn’n Hg P02 (85-100) mm Fig
Percentage 02 Sat. (>95%) Patient 1).!!. T.C. .J.p. K.L. R.Y. E.A. All. KR. ,IS. l).B. l).p. Kit. E.F. L.M. (;.J. V. Mc(;. B. St..J. AS. RI!. LM. 7.30 7.33 7.37 7.35 7.34 7.’29 7. 7.36 7.31 7.34 7.38 7.36 7. 7.33 7.35 7.36 7.!7 7.41 7. 7.35 Mean: (7.33) Range: (7.0-7.41) 53 49 36 3-2 47 56 48 42 53 56 47 48 55 48 53 48 75 53 64 65 (51.4) (3l-75) 62 59 73 6-2 46 68 8’2 37 5! 76 8 33 26 48 40 ‘25 68 64 (55.7) (‘25-8’2) 87.7 88.3 93.4 88.9 76 90.7 95 65.5 83.5 94.5 93 54.5 45.5 81 73 40 87 6 89.9 (79.4) (40-95)
Infant Control Group
.‘son-Congestire Ifearl Failure
40 36 37 36 35 33 33 36 38 (36) (33-40) 90 88 87 91 93 80 7’2 66 (84.3) (66-93) 96.4 96.3 95.4 95.9 96.5 96.8 95.3 94.’2 91.4 (95.3) (91.4-96.8) iI.II. 7.41 K.l. 7.38 K.(;. 7.33 A.M. 7.39 P.S. 7.41 ItS. 7.4’2 .1.11 7.41 T.C. 7.41 ,J.L. 7.38 Mean: (7.393) Range: (7.33-7.4’2)
heart failure most P0, values were above
the normal PC02 40 isopleth with a mean
value of 51 mm Hg. The mean pH value is in the acidotic range (7.33). These data indicate
the !resence of respiratory acidosis and add
the element of respiratory failure to cardiac decompensation. By way of contrast it can
be seen in Table I and Figure 1 that the PCO,
values obtained from the 8 patietits with
left-to-right shunts who were not in failure
center around the P0. 40 isopleth or slightly
below it, indicating either normal values or
hyperventilation and mild respiratory
alka-losis. The arterial P0. values in the presence of congestive failure were lower than might have been predicted by the nature of the in-fant’s cardiac defect. This was best demon-strated by observing the arterial P02 values in 6 infants obtained while they were in con-gestive failure and then following control of
decompensation (Fig. 2). During failure, as
might be expected, the P0. values were lower
than the values obtained when their failure was controlled. In terms of changes in oxygen TABLE III
CHF
C0MP.
L.M. RH. AM. IA. DR. V.McG.
1 60 N
0
0.
-j
4 40
w
4
Q0 4,0
PLASMA
Co2
CONTENT
(mM/L )
.0 Roflo.Rosp.s,,] Cuo] Ob.t
(rnmHg)
____ _____
/
___
[uolnI$1
L::::
]-I
Puln. Roso,uo l,f.uIu,R.yAdo
7.0 7.2 7.4 7.6
WHOLE BLOOD pH
Fic. 1. Acid-base equilibrium at 37#{176}C. saturation the presence of cardiac failure did
cause some depression, although the Po2 changes were more striking due to the fact that many of the tensions fell on the flatter
I)ortiotl of the oxygen-hemoglobin-dissocia-tion curve.
The alterations in serum electrolytes are shown in Table IV. Serum sodium and chlo-ride values were either normal or low while
the potassium values ranged toward the higher side of normal. In 5 patients serum sodium values were below 130 mEq/l while
in 10 patients the chloride values were below 100 mEq/l.
COMMENT
The finding of respiratory acidosis in in-fants in cardiac failure is similar to the ob-servation of respiratory acidosis in severely ill infants with transposition of the great
vessels and pulmonary hyperemia reported previously from this laboratory.8 These ob-servations contrast with studies carried out
in adult patients in congestive heart failure. Studies in adults have in most instances failed to demonstrate elevations in arterial
Pco2 in association with congestive failure, and have revealed either a normal blood gas
composition or a mild respiratory alkalosis.
When bronchial obstruction was present in
the adult groups as reported by Cosby and associates9 minimal arterial oxygen desatura-tion and carbon dioxide retention in associa-tion with obstructive ventilatory insuffi-ciency was found. These patients all had
hy-pertensive heart disease, left ventricular failure and cardiac asthma. It is of interest that all thirteen patients with wheezing
//
7
7
4C
15
///
/// /
/ //
_// 70=
/ /
/ 7
#{176}
0/CHF// ,
‘:i.
//
::i_
VSD VSD Anon,. Anom. PDA TRANS.
LI. Co.. Puim. Von. Rot.
Fmc. 2. Arterial oxygen tension studies.
respirations in our series had significant ele-vations of arterial 1(02 and it is our
ilupres-sion that wheezing constitutes an important
sign of left heart failure in infancy. Squires
et a!.’#{176}have also reported a few adult patients in congestive failure with respiratory acidosis
although most patients in their series showed
respiratory or metabolic alkalosis.
The pathophysiologic mechanisms that
may be responsible for the production of
respiratory insufficiency associated with car-diac decompensation in infancy are sum-marized in Figure 3. Pulmonary congestion arising either from pulmonary vascular
en-gorgement and/or pulmonary venous
hy-pertension in these patients appears as the
hemodynamic common denominator and can
[sPulno.o,n Blood Floo PWnonoyVo,ouo Hyp
Fic. 3. Possible pathophvsiologic mechanisms lead-ing to respiratory insufficiency in infants in
HEART FAILURE IN INFANCY
TABLE IV
SEuUM ELEFROLYTE \ALU ES IN INFANTS IN CONGESTIVE IIEA1IT PA! LEJIS E
Pota.s.s’iu iii (.3JJ-.5..’) iiiEq/l Chloride (102-112) iiiEq/l 4.9 11cm. 4.4 4.5 5.6 Item. 4.1 Item. 5.8 5.0 5.1 4.6 .JP. I Ileill. 5.4 5.3 Item. 5.3 4.2 5.3 (5.0) (4.1-5.8) 101 100 110 105 94 96 98 104 87 99 105 103 98 106 92 102 94 94 100 99 (99.3) (87-110) Sm/in in Patient (l3;-14(;) inEq/i 1)11. 13L T.C. 130 .I.i. 139 NI. 128 R.V. 127 E.A. 127 Alt. 133 Kit. 129 T.S. 121 1)11. 138 1)1’. 135 KR. 134 E.F. 140 L\l. i38 (;..J. 13()
\. MeG. 137
B.St.J. 139 AS. 131) lt.iI. 137 LM. 137 Mean: (133.1) Range: (121-140) I?iearbo nate imiEq/l ‘27.5 ‘28 18.5 27.5 28 27 24.5 27.5 31 ‘29 28.5 ‘25 ‘28.5 31 ‘29.5 35 27 37 (28.4) (18.5-37)
result in certain predictable alterations of
pulmonary function.” The presence of pul-monary congestion will cause stimulation of receptors at various respiratory and cardiac
sites including pulmonary parenchyma, air-way, blood vessels, and the heart’2 and
would, in the absence of obstructive ventila-tory insufficiency, result in hyperventilation and the respiratory alkalosis or normal blood gas values observed in adults with a large
pulmonary reserve’3 and in the infants in our series with left-to-right shunts not in failure.
In the presence of expiratory obstruction as exists in the majority of infants in congestive failure and in adults with cardiac asthma, the drive to hyperventilate is inadequate to
maintain a normal gas exchange, and respira-tory acidosis results. This will also be
re-flected in the lowered arterial oxygen ten-sions observed in the congestive failure group. Obstruction of air flow riiay involve
bronchoconstriction as well as edema of
bronchial mucosa and transudation of fluid into the tracheobronchial tree. Studies of
air-way resistance are obviously needed to allow
more complete evaluation of this important aspect of congestive failure in the young in-fant. From the anatomical and physiological standpoint the presence of pulmonary con-gestion will also result in diminished lung distensibility’4 and possibly alterations in surface tension forces. Studies carried out in adult patients with mitral stenosis and hy-pertensive cardiac disease have demonstrated diminished lung compliance with increase in
the work of breathing and oxygen require-ments for breathing.’5”6 In addition, a direct
relationship between the work of breathing and the respiratory pattern has been noted. The presence of significant cardiomegaly
may further compromise pulmonary reserve
by encroaching on space ordinarily occupied by pulmonary parenchyma, and would thus add to the factors directly associated with pulmonary congestion. Similarly the presence of pulmonary infection may impair lung
result of the operation of these several
fac-tors is respiratory insufficiency causing the
alterations in blood gases and pH that we
have noted.
The observation of lowered serum sodium
and chloride values in some infants in severe
failure prior to the onset of the use of decon-gestive measures is also of interest in terms of the mechanisms involved and the influence
that these alterations may have Ofl the re-sponse to therapy. The decrease in sodium probably reflects to some extent an increased blood volume’7 and water retention in excess of sodium, while the lowered chloride values and the elevated bicarbonate represent the
result of partial renal compensation for the
presence of respiratory acidosis. Hypona-tremia has been noted in adult patients in
congestive failure even when total body
sodium was abnormally 0 .I S,19
When water-loading studies were performed,
these patients failed to excrete the load normally.2#{176} Overproduction or diminished inactivation of antidiuretic hormone was
postulated as the mechanism leading to hy-ponatremia.21’22 Recent studies by Bell et a!.23
suggest that exaggerated proximal renal tubular reabsorption of glornerular filtrate, rather than antidiuretic hormone, may limit formation of free water in some patients in congestive failure. Additional studies carried out in infants in failure including blood volume, renal function, body fluid distribu-tion as well as assessment of antidiuretic hormone activity, angiotensin levels, and aldosterone values are needed to clarify these observations. The electrolyte abnor-malities, particularly the hypochloremia, may limit response to mercurial diuretics.24
In addition, there is experimental evidence that acidosis may increase tolerance to digi-talis preparations as reported by Schafer.25 The finding of elevation of serum potassium values in some infants in congestive heart failure who are acidotic may also increase tolerance to digitalis glycosides.
SUMMARY
Studies of arterial blood gases and acid-base equilibrium in twenty infants in con-gestive heart failure have revealed the
fol-lowing alterations : (1) elevation of arterial
PC09, (2) diminution of arterial P02, (3)
lowered pH. These findings demonstrate the presence of respiratory insufficiency in
in-fants with pulmonary congestion and cardiac decompensation. Studies of serum
electro-lytes have shown in some infants a
hypona-tremnia and hypochloremia present prior to the use of therapeutic agents and these
al-terations may influence response to digitalis and diuretic agents.
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60:388, 1960.Acknowledgment
The authors wish to acknowledge the competent
technical assistance of Miss Dorothy Nixon, Mrs.
Alyce T. Rawlins, and Mrs. Katherine Anlyan,
