Severe Acidosis and Hyperpotassemia Treated
with Sodium Bicarbonate Infusion
By
KUNO
C. SCHwARZ, M.D., BURTON D).
CohEN,
AL).,
r,
RBIN,
M.D.
AND ALBENRT
GLENN
I). LUBASI, MI.)._
Four uremic patients with severe acidosis, hvperpotasseli'm, anid electrocardiographic
signs of toxicity were treated with intravenous sodium bicarbonate. Serial determination,,;
showed a fall in plasma potassium, a rise in blood pH, .anid regression of the electrocardiogram toward normal. The iiiechmanisass responsible for tliese changes ar1e dis(usse(l.
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and Schales, as modified by Summiierson. Venous
blood pH was determined on a Camiibridge Research
pH metem. with use of a constant-temperature water
bath to niainitain at 37 C. Plasma volumiie was
measured by the dve-dilution techlnic with T 1824.
H YPERPOTASSEMIA is a serious and
often fatal complication of advaniced
reiial insufficiency. Its principal lethal action
is its depressant effect on the myo(.ardiuin.1 2
In uremia, hyperpotassemia is frequently
accompanied by acidosis, hyponatreniia, hypoealeemia, alterations in body water, and
changes in cellular imetabolism.3 Correction
of these associated electrolyte abn orinalities
is often accompanied by improvement in the
electroeardiographie manifestations of hyperpotassemia. In the correction of hyperpotas-
CASE REPORTS
Case 1. B. R., a 46-year-old woman with polycy'stic kidney disease, was admitted to amnother
hospital with symptomns of uremiiia. On admission,
physical examination revealed mimasses in both
flanks. The blood urea nitrogen was 90 mll. per
cent. The plasma sodium ws< 134 mnEq./L, plasma
potassium 4.8 mEq. 1/., acnd plasma chloride 108
inEq /L. Carbon dioxide combining power was
not determnimied. An electrocardiogramn was within
normal limiiits. Five dlays after admission the patient became disoriented, acnd deep respiration.s
weere noted. She was transferred to Bellevue llospital for possible dialysis with the artificial kidney.
Plasma electrolyte vallies on admission welme
potassiumii 5.9 mEq.JL., chloride 89 inEq./L., carbon dioxide combining, loweL 1 .3 mM/L, and blood
pH 7.18. Tile blood urnea nitrogen was 100 mug-.
per cent. Plastma volue was markedly reduced.
The electro(.ardiog,.rami revealed peaked T waves
(fig. 1, 10 :05) p.m.). Because of the severe symnptomnatie acidosis, aim intravenous infusion of 5 per
cent sodium bicarbonate was begmun. After adiiimiistration of 408 miiM (34 Gmll.) of sodium bicarbonate in 4 hours, the platient's respirations became
mmorm'mal and her se!ns;orium cleared. An electrocardiogramn at this time had changed amnd now sug-
seinia and acidosis with alkali salts, therapeutic success has been achieved with both sodium
bicarbonate and sodium lactate. Recently,
the latter agent has been the more popular.
This report outlines our experience with 4
uremic patients with severe acidosis, hyperpotassemia, and electrocardiographic evidence of
advanced cardiac effects. Treatment consisted
of the rapid infusion of 5 per cent sodium
bicarbonate and, in each case, correction of
the acidosis was accompanied by lowering of
plasma potassium and reversal of the electrocardiographic signs.
METHODS
Plasma sodium and potassium were deterimined
on a Perkin-Elmer, AModel 52-A flame photometer,
gested hypol)potassemiiia. The duration of the QRS
complex was now miormual (fig. 1, 2 :00 .). The
plasmna ele(trolyte values wvere sodium 144 inEq./L.,
plotassiumml 3.0 iiEq. ,'L., chloride (89 mEq./L,..and
carbon dioxide coimibining power 6.2) moML. The
blood 1)11 was 7.29. During this interval urinary
output was 200 niil, with electrolyte concentrations
of sodiumi 87.0 imiE(q.,/L., potassium 31 .0 imiEq./L.,
and chloride 38.0 mEq./L.
Subsequently the patient was niaintained oml 5
to 10 Gm. of sodium bicarbonate a day during
with use of a lithium internal standard. Plasma
chlorides were determined by the method of Sehales
From the Cardio-Renal Laboratory of the Seconid
(Cornell) Medical Divisioni, Bellevue Hospital, and
the Department of Medicine, Cornell University Medical College, New York, N.Y.
This work wvas supported in part by grants from
the New York Heart Association and the U.S. Public
Health Service (H-2054C).
215
Circulation, Volume XIX, February 1959
2S161CWARZ COHEN, Ii BASI1L RUBIN
'M1216
LEAD V4
LEAD V2
B.R.
PV
10:05 pm
1
>_
4l
;
Na 132, K 79, CO2 49 mEq/L
LEAD V4
LEAD V2
Na 34, K 49, C024.0 mEq /L
8:00pm
2:00am
Na l31, K8.6, C02 1.3mEq/L,
pH 7.10
fj
AFTER 180 mEq (15 gm) NaHCO3 I.V
AFTER 408 mEq (34gm) NaHCO3 I.V.
V4
;ll
4:00pm
LEAD V4
LEAD V2
K 3.0 mEq/L, C02 6.2 mM/L, pH 729
HM
LEAD V4
LEAD V2
K 5.9 mEq/L, C02 1.3 mM/L, pH 718
G.C.
LEAD V3
Na 134, K 6.6, C02 73 mEq/L, pH 718
LEAD V2
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r. I|
5:00pm
400 pm
....... ......
.5.c.
V4
72..
...
|.
I.T
LEAD V3
LEAD V2
Na 143, K4.3, C02 77 mEq/L, pH 7 38
Na 136, K 6.5, C02 4.0 mEq/L, pH 7.32
7:15pm
..
7:30pm
After 144 mEq (12gm) NaHCO03 I.V
AFTER 150 mEq (12.5gm) NaHCO3 IV.
FIG. 1 Top left. Electiocad(liogr.am11 b)efore and after the administration of sod(ilullhicarlmolatC.
Note the ailterations suggestive of libylpopotassenijia. at 2:00 a.mn.
kFIG. -2 Bottom left. Electrocardiogalim before aind after the at(ldminiistr.tioii of sodiumi icarbonate showing regression of coniductioni disturibances anlil return of siuontrial acetivity.
FIG. 3 Top righlt. Electrocardiogaim before and .after the adminiistration of sodliulm bicarlbollate sloioiiig regression of conduction distiiriaeiice, lowvering of the T wae-s aild return of
sinoatrial activsity.
FIG. 4 Bottoo riylh t. Electrocardiogram before and11( :after the adumimnistration of sodiummi hi(ealrollate suggesting lowering of peaked T wvaves.
hospitalization. This amouit of sodiumt bi(cia11)o01ate was found necessary to iiiaiiita.iin the carbon
dioxide combining power between l15 and 20 AI/uL.
She was accordil dischaged On maintenance
bicarbonate therapy.
Case 2. II. M., a 28-year-old white woman, was
admitted to a local hospital with acute reiial failure
associated with a Bacillas llel(.lii infection following, an induced abortion. She was oliguric for 8
days and was transferred to Bellevue Hospital for
dialysis with the artificial kidney. On admission
the blood pressure was 90/60 and the respirations
were deep. Chvostek and Trousseau signs were
present. The electrocardiog.rlan showed prolongaarrest (fig. 2,
tion of the QRS complex and atrirl
5 :00 p.111.). Plasma electrolyte values were solium 131 inEq.,L., potassium S.6 miEq.,/L., chloride.
91) mnEq./L., carbon dioxide (coimibining, lowelr 1.3
muM /L., and calcium 55.4 ing. per cent. Blood pH
\vls t.10 nld urea initro-eni was 210 lug. per cent.
Plasinn volumme was within noirual limits.
While l)repalrations for dialysis were being- imade,
144 niM (12 Gni.) of sodium bicarbonate and(l 2
Gmi. of calcium gluconate were administered intravenously- ini 2 hours and 15 mnillutes amld, at the
start of dialysis, the electrocardiogram revealed
inorniail5su1s rhli-t1lii with normllal intraventriculaum
conduction (fig. , 7 :15 p.imi.). At this time,
plasmiia sodiumo was 136 inEq./L., potassiuum 6.5
inEq./r., carbon dioxide combining. l)ower 4.0
ni
,/L, tlei blood pH was 7.32. Urilnary output
wvas negligible. The patient did not improve and
(lied 24 hours after dialysis.
Case.e. P. V., an1 89-yetar-old white womuan, w'a1S
a(Imliitted( to the urologic service because of 2 weeks
of (lvsuria. Two days prior to admuissiomi she (dveloped hemuaturia, suprlapubic pain, andl nmhuse.
On admuissiom she appeared cachectic and dehyi-
12li17
SEVERE ACIDOSIS AND HYPERIPOTASSEMAIA
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drated. Blood pressure was 170/60 and respirationls were deep and regular at a rate of 24 pec
iinute.
Initially the patient was oliguric, with a urinary
output of less than 10 nil. per hour, and urinalysis
revealed a specific gravity of 1.020, 2 plus albumin,
a trace of acetone, and many red blood cells. The
heniatocrit level was 27 per ceiit. The plasma
electrolyte values were sodium 137 mEq./L., potassium 8.3 inEq./L., chloride 112 iiiEq./L., and carbon dioxide combining power 6.3 mMi/L. The
blood urea nitrogen was 164 iug. per cent.
Because of the dehydration and oliguria she was
given 3,000 itil. of 5 per cent dextrose in water in
the first 12 hours, during which time she reniaiiied
oliguric. Her neck veins became distended and a
venous pressure was 180 lini. of saline, at which
time she was seen by a medical consultant. Plasma
volume was expanded by approximately one liter
over the mean predicted value. The red cell mass
was decreased, and the hematocrit level was 18
per cent. Electrocardiogram showed peaking of
the T waves, prolongation of the QRS complex,
and atrial arrest (fig. 3, 4:00 p.m.). The plasma
electrolyte values were sodium 132 miEq./L., potassium 7.9 mEq./L., and carbon dioxide combining
power 4.9 mnM L. At this time the blood pressure
became unobtainable.
In view of the abnormal electrocardiogram, the
appearance of shock, and the persistent, severe,
symptomatic acidosis, an intravenous infusion of
5 per cent sodiumn bicarbonate was begun. After
admiministration of 180 miM (15 Gm.) of sodium
bicarbonate in 4 hours followed by 1 unit of whole
blood, the electrocardiogramii revealed normal sinus
rhythm, lowering of the T waves, and normnal
intraventricular conduction (fig. 3, 8 :00 p.m.).
The plasma electrolytes were sodium 134 mnEq./L.,
potassium 4.9 mnEq./L., chloride 111 mnEq.,/L., and
carbon dioxide combining power 4.0 millM L. During this interval, respirations becanme normal, the
arm venous pressure fell to 110 mmi. saline and the
blood pressure rose to 110/70. Throughout the
succeeding 24 hours she received an additional 150
mEq. (12.5 Gm.) of sodium bicarbonate and the
plasma carbon dioxide combining power rose to
10.8 iimM /L. Oliguria persisted, and cystoscopy
revealed severe, generalized, pseudomembranous
cystitis obscuring both ureteral orifices. Culture
of the urine showed Bacillus 1proteufs, and the patient was treated with tetracycline. During this
period urinary volumes increased to 1,000 ml. daily.
Subsequently, the patient developed high, spiking
fever and hypotension and died on the eighth hospital day. Postmortem examination revealed
chronic pyelonephritis with contracted kidney,
severe hemorrhagic cystitis, partial ureteral obstruction bilaterally, and hydronephrosis.
Case 4. G. C., a 19-year-old white girl with chronic
glonlmerulonephritis, was admitted to the hospital
because of oliguria. She was comatose and respirations were deep and labored. Electrocardiogramii revealed normal sinus rhythm and suggested
peaking of the T waves (fig. 4, 4 :00 p.m.). Plasma
electrolyte values were sodium 134 mnEq./L., potassium 6.6 iiEq. L., chloride 109 niEq./L., carbon
dioxide combiniing power 7.3 mMAI/L.; the blood
p11 was 7.18. The blood urea nitrogen was 1 02
imig. per cent. Plasmiia volume was normal.
.An intravenous infusion of 5 per cent sodium
bicarbonate was begun. After 150 aiMl (12.5 Gni.)
had been administered in 31/2 hours, the electrocardiogramn showed slight decrease in the height of
the T waves (fig. 4, 7 :30 p.imm.). Plasma electrolyte
values were sodium 143 nmEq./L., potassium 4.3
mEq. /L., chloride 105 inmEq., L., carbon dioxide
comiibining power 7.7 mMil/L., and blood pH 7.38.
Respirationis becanie normal but there was no other
change in clinical status. The following day, after
an additional 108 miM (9.0 Gin.) of sodium bicarbonate intravenously, the plasma carbon dioxide
comibining power rose to 11.2 iiM/L. Subsequently,
urinary volumiies increased to between 700 and 1,000
nil. daily, and the patient improved markedly oven
a 2-week period.
DISCUSSION
The serial electrocardiographic changes in
potassium intoxication are well known.4 The
relatively poor correlation of these changes
with the plasma level of potassium5' 6 probably reflects the role of ions other than potassium as well as the complex shifts in intracellular-extracellular ion concentrations that
occur in the presence of altered states of
hydration, acid-base balance, and cellular
metabolism.7
In uremia only a few of the factors contributing to potassium metabolism and cardiac
toxicity can be defined. These include metabolic acidosis, hyponatremia, hypocalcemia,
dehydration, and increased catabolism.
Animal experiments have shown an inverse
relationship between blood pH and plasma
potassium concentration.5 It has been demonstrated in dogs that perfusion with acidic
solutions
produces
electrocardiographic
changes analogous to those produced during
infusion with potassium.9-11 Rise in plasma
potassium was demonstrated uniformly
throughout the induction of acidosis, but cardiac toxicity was manifest at lower levels of
2918
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hyperpotassemia. This potentiation of potassiumi toxicity by acidosis has also been
suggested by stu(lies in patients with diabetie
acidosis.1-'
Hyponatremiia may augment the changes
produced by an iincrease inl plasma potassium.13 Metabolic a(idosis is often associated
with increased renial sodium excretion. In
.addition, increased (Ilantities of sodium may
enter the eell to btiffer the fall in initraelletlkar pII. Together, these may lead to a fall
in 1)lasnma sodium concentration. Finally.
studies on isolated car(liac muscle as well as
in intact animals and human subjects have
shown that hypo al( einiia, also, potentiates the
effect of hyperpotassemia.'4-16
Dehydration, inc reased catabolism, and hypotension, all of wlhic(.l may accompany uremia,
cannot be so clearly related to cardiac toxicity. With sustained increased catabolism,
as in fever with iiif(ctiouis, hyperpotasseinia
may occur. Hypoteiisiioni frequently leads to
mvocardial isehemia; iiicreased sensitivity to
potassium has been demoii'trated in hypoxic
states.'7
JllIperpotasseinia constitutes a serious medical emergency. Its, managemeiit includes
hemodialysis, cationi exchlange resins, intravenlous iiifusion of hypertonic glucose antd
insullin, hypertonic saline, calcium salts and,
nost recently, molar sodium lactate.1'19"
These agents fall into 2 major groups. The
first, which includes dialy-sis, resinls, and glu(oseienfusions, acts through the direct removal of potassium from the extracellular
fluid. The second group, comprising hypertonic saline and calcium infusions, niay also
encourage intracellular transfer of potassium,
but produces an additional effect through replacement of ions, deficiency of which potentiates hyperpotassemia.
Receimt reports have appeared on the use of
molar sodium lactate in the treatment of
advanced cardiac toxicity dtie to hyjperpotasseilnia, with prompt reversal of electrocardiographic (hlianges and rapid cliuiical improvement.'8' 19 The authors suggest the possibility
of a specific action of lactate iOI ill addition
to the effect of this therapy oii acidosis, extra-
SCHWARZ, COHEN, LUBASH, RUBIN
cellular fluid volume, and intracellular potassium shifts.
Our observations imidicate that correction
of the bicarbonate deficit with sodium bicarbonate lowers plasma potassium directly,
aplp)arently through intracellular transfer of
1)otassiumu ions. We were led to employ 5
per cent sodium bicarbonate because of the
severe clinical acidosis that the 4 patients
1resented in addition to the electrocardio(rraphic signs of hyperpotasseinia. Treatment
of acidosis in this manner reversed the electrocardiographic signs. These effects were
identical to those reported by Bellet'8 19 with
the use of sodium lactate.
Iii eachll instamice, plasma potassium was
lowered. Since urinary potassium excretion
was miegligible during the perio(d of infusion.
it miiay be assumed that this was accomplished
ini large measure tlhrougofh intracellular tramlsfer, although expansion of normal extracellular volume may have playe1d a small role. Iii
addition, blood plI rose in the 3 instances im
which values were obtained. The plasma car1)o01 dioxi(de conmbining power changed only
slightly immediately following the bicarbonate infusion. The administration of additional sodium was probably not important,
since initial plasma values were only slightly
reduced. The results of treatment were similar whether or not there was a significant alteration in plasma sodium. The effect of
liicarbonate infusiomi appears to be independ(lit of correction of dehydration, since the
iniitial plasma volume was not reduced in 3
of the 4 patients.
The mechanism by which sodium bicarbonate acts in this instance seems to depend,
therefore, upon its effectiveness in reducing
the plasma concentration of potassium ions,
and possibly hydrogen ions. The latter is
accomplished directly by means of repletion
of buffer alkali, and is best demonstrated by
serial pH determniuiationls. _Moreover, correction of extracellular alkali (leficit is acconpanied by restoration of intracellular bicarbonate as well. Since potassiuml is the major
intracellular cation, correctioum of intracellular acidosis is associated with a shift of po-
SEVERE ACIDOSIS AND HYPERPOTASSEMIA
tassium as well as bicarbonate into the cell,
and hence a reduction in plasma potassium
concentration.
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SUMMARY
In 4 uremic patients with severe clinical
acidosis associated with electrocardiographic
evidence of hyperpotassemia, intravenous administration of 5 per cent sodium bicarbonate
resulted in correction of the acidosis, fall in
plasma potassium, and reversal of electrocardiographic signs. The effect of this treatment
did not depend on changes in plasma sodium,
renal excretion of potassium, or on correction
of dehydration.
In the treatment of severe acidosis, reversal of electrocardiographic signs of hyperpotassernia parallels more closely the correct ion of blood pH than it does alteration in
plasma carbon dioxide combining power. The
results suggest that the infusion of hypertonic
sodium bicarbonate in patients with hyperpotassemia, acidosis, and electrocardiographic
signs of cardiac toxicity has proved a safe
and practical measure in the emergency management of this common problem in the uremie syndrome.
ACKNOWLEDGMENT
We are indebted to Mrs. Ruth Aronson and Miss
Carolyn Register for their technical assistance.
SUMMARIO IN INTERLINGUA
In 4 patientes uremnic con sever acidosis
clinic, associate con signos electrocardiographic de hyperkalemia, le administration
intravenose de bicarbonato de natrium de 5
pro cento resultava in le correction del acidosis, un reduction del kalium del plasma, e un
reversion del signos electrocardiographic. lie
effecto de iste tractamento non dependeva de
alterationes in le natrium del plasma o in le
excretion renal o del correction del dishydratation.
In le tractamento de sever acidosis, le reversion del signos electrocardiographic de
hyperkalemia es plus strictemente correlationate con le correction del pH del sanguine
que con alterationes in le potentia del plas-
219
ma de comnbinar dioxydo de carbon. Le
resultatos suggere que le infusion de hypertonic bicarbonato de natrium in patientes con
lhyperkalemia, acidosis, e signos electrocardiographic de toxicitate cardiac es un practic
e salve mesura de urgentia.
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Quantitative analysis of the electrocardio-
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SCHWARZ, COHEN, LUBASH,
h)X(
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An experimental study. J. Lab. & Cliii. Med.
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9.
Berkowitz, D., Wagner, B. M., and Uricchio, J. F.: Acute Peptic Ulceration following
Cardiac Surgery. Ann. Int. 2Med. 46: 1015 (June), 1957.
Acute peptic ulceration following cardiac surgery has been demonstrated in 4 patients and clinically suspected in 3 others. This was a most serious conmplication, 4
of the patients having died. Another survived only after emergency gastric resection.
Promnpt diagnosis is essential for a favorable outcome and iany be attained only by a
constant alertness to the possibility of an acute ulcer in any postoperative cardiac
patient who is not doing well. Early surgery rather than a mnore conservative programl]
of therapy may be lifesaving in these patients and should not be withheld merely
because the patient has recently undergone cardiac surgery. The exact mechanisilm
responsible for an acute ulceration of the gastrointestinal tract following surgery is not
well understood but it is believed that it represents a response to the alarm reaction
described by Selye. Prolonged hypotension with resulting ischemia is an important
factor in the pathogenesis and since many patients following cardiac surgery develop
prolonged periods of hypotension, this particular complication is not altogether unexpected. It should b? emphasized that this complication generally arises without any
obvious background of peptic ulceration and without any prodromnata. Melena, helmltemnesis, shock, or evidence of perforation may be the initial findings. In a group of
patients who died following cardiac surgery fromim various causes, necropsy findings
revealed an incidence of acute ulcerative lesions of the gastrointestinal tract of greater
than 15 per cent.
W EN DKOS
Severe Acidosis and Hyperpotassemia Treated with Sodium Bicarbonate
Infusion
KUNO C. SCHWARZ, BURTON D. COHEN, GLENN D. LUBASH and ALBERT
L. RUBIN
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Circulation. 1959;19:215-220
doi: 10.1161/01.CIR.19.2.215
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX
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