Circulatory overloading during and following blood transfusion∗

Report on Therapy Circulatory Overloading During and Following Blood Transfusion* A Method of Prevention

Using Packed Red Cells and

Injection of Morphine and Atropine LOUIS PELNER,

M.D.,

F.A.C.C. and SAMUEL WALDMAN, M.D., F.A.C.C. Brooklyn,

I

T

IS difficult to estimate the frequency of circulatory overloading during and following transfusions because such occurrences are seldom reported. Personal experiences indicate that it

occurs much more often than is generally realized. Riddell’ described circulatory overloading as the commonest cause of death following transfusion, and Drummond2 considers it only slightly less important than incompatibility. As will be noted later, this complication following transfusion may selectively occur in patients with chronic congestive heart failure, chronic anemia, prolonged fever and acute or chronic pulmonary disease. If transfusions are definitely required in such patients, packed or sedimented red cells should be used, the transfusion should be given slowly and, in addition, we believe that it should be preceded by an injection of morphine and atropine. Another injection of morphine and atropine should be given about half way through the transfusion. This paper describes the rationale for these prophylactic injections. It seems remarkable that only general cautions against circulatory overloading -are mentioned in the various books on blood transfusions3 One of the best prophylactic measures is the use of concentrated or packed red cells.4 By this method the volume is decreased by about

New York

half and the sodium content is greatly reduced. The point made by Ginsberg, Frank, and Gubner5 that the patient sit upright during the transfusion seems vitiated by the finding by SharpeySchafer6 that reclining reduces the right atria1 pressure. On the other hand, Vugrincic’s7 recent suggestion that less left ventricular work is required to expel blood in the upright than in the recumbent position, would favor the sitting position. Another prophylactic method, besides the one herein described, is based on the finding by McMichael and Sharpey-Schafer8 that digoxin lowers the right atria1 pressure. Scott’s9 recommendation that 1.0 to 1.5 mg of digoxin be given by intravenous injection immediately before transfusion would therefore be a rational procedure. Undoubtedly, Scott means that the amount would only be given before the first transfusion. In this study, we did not consider the administration of hypotonic, hypertonic, or isotonic solutions which would involve electrolyte and solution transfer exchanges creating additional volume alterations. Only reactions were considered.

transfusion

CLINICAL FEATURES AND TREATMENT

OF

CIR-

CULATORY OVERLOAD The

* From the Departments of Medicine, The Swedish Hospital York. OCTOBER,1958

blood

489

clinical

symptoms

resulting

and the Long Island College Hospital,

from Brooklyn,

overNew

490

Circulatory

Overloading

loading of the circulation usually begin with a dry cough and a constriction of the chest. Cyanosis and dyspnea soon appear and if ovcrloading has been marked or continuous, bloodCoincident stained frothy sputum appears. with these symptoms, tachycardia develops, the cervical veins become distended, and coarse and fine rales are heard over the entire chest. The symptoms may appear during or shortly following the transfusion; sometimes follow after a chill and fever.g

sion should be stopped immediately. Morphine gr 1/4 (15 mg) and atropine gr 1/160(0.4 mg) should be given at once. Scott9 recommends gr 1/50 (1.2 mg) of atropine. Oxygen should be given by a face mask or other acceptable method. Venous pressure must be reduced as soon as possible by phlebotomy or application of tourniquets on all four limbs and later followed by phlebotomy if improvement is not apparent. The fully developed pulmonary treated successfully, method descriljed

assumes great importance. The prophylaxis of this condition is obviously very important, since as stated above, this complication is most likely to occur in certain types In these patients, transfusions of patients. If it should be given only if urgently required. that transfusion

is definitely

indi-

cated in this type of patient, then several methods can be used to minimize or protect against the overload effects. Aside from the methods so far recommended, such as using packed washed red cells or sedimented red cells, the sitting-up posture during transfusion and the slow infusion of the blood (about 1 cc/kg/h+“), we have found another simple procedure to have a salutary effect in this type of patient. A hypodermic containing morphine sulfate gr 1/4 (15 mg) and (0.4 mg) is prepared,

are used for transfusion. described, this additional

In each of the patients treatment enabled us

to give the required amount of blood to a patient who was threatened with circulatory overloading. ILLUSI’RATIVE

transfusion should also he considered as evidence of circulatory overload, and the transfu-

is ascertained

one-half of the contents al)out five minutes before the transfusion and the other half when the transfusion is approximatelyone-half over. Packed, washed red cells or sedimented red cells

the symptoms

The treatment of circulatory overloading following transfusion must start at the earliest possible moment of detection. The cervical veins should be watched closely, and at the first signs of engorgement the transfusion should be stopped. A dry cough that develops during the

edema cannot always be so that the prophylactic

in Blood Transfusion

atropine sulfate gr 1/~5~ and the patient is given

CASE

HISTORIES

CASE 1. D. C., age 64, a hypertensive patient foi many years, was Seen in the office with complaints of headache and morning nausea and vomiting. The blood pressure was 21 O/l 10, the heart was enlarged, and there was pallor of the skin and mucous mrmbrancs. Urine examination revealed a Specific gravity of 1.006, 3+ albumin, a few red blood cells and a few hyalinc casts in the scdimwt. The blood chemistry determinations were normal except for a urea nitrogen value of 60 mg/lOO cc and a creatinine value of 2.4 m,g/lOO cc. The red blood count was 2.2 million and the hemoglobm examination showed a few was 9 g. An eye ground hemorrhages in each fundus. The patient was placed on a low-protein diet with added vitamins and large quantities of iron. A gastrointestinal x-ray Series was entirely negative except for thickening of the rugae in the Stomach. The patient did not respond to home care with any Significant degree of improvement, So he was hospitalized. On the day after admission, a transfusion of 500 cc of whole blood was given slowly. Followingthe transfusion, it was later determined that the patient coughed for ten minutes but this was not reported. A transfusion of 500 cc of whole blood was started the next day. When about 200 cc were infused, the patient became dyspneic and cyanotic. Loud rales were heard over The patient had developed pulmonary the entire chest. edema due to circulatory overload and the transfusion was Stopped. Morphine, atropine, ccdilanid intraoxygen under high pressure venously, MercuhydrinE, and finally phlebotomy were successively tried without avail. The patient died within 50 minutes. nephritic CASE 2. H. B. age 68, male, a known patient of several years’ duration demonstrated the following clinical findings: Blood pressure 168/100. pallor, moderately enlarged heart, Slight edema of the Blood chemistry findings showed gradually legs. increasing mea nitrogen levels which ranged from 52 mg/lOO cc to 90 mg/lOO cc of blood. The hemoglobin and red crll levels ranged from 9 to 7.5 g and from 3.6 million to 2.4 million, respectively. Treatment at home proved unsuccessful, so the patient was hospitalized. The patient developed acute pulmonary edema while Through heroic receiving one unit of washed red cells. including Several injections of morphine and efforts, an-opine, cedilanid, oxygen and phlebotomy, the patient THE

AMERICAN

JOURNAL

OF

CARDIOLOGY

Pelner and Waldman improved

over

further

the ensuing

transfusion

He was subsequently where

he died.

but it could

hospitalized

He

had

He rrfused

cough

at another

rccrived

According

severe

period.

very

a blood

whether

to the

and died about

efforts

to save him.

two hours

hospital

transfusion, wife,

later

patient

of heroic

June

A. B.,

Hospital

19,

1957.

female,

age

69,

cm May

29,

1957

She

days she had been stools

congestive

was

at

It was stated

infarction. time

was

The

patient

8

g,

but

this

was given

discharged

legs.

four

.January

months

31, 1957),

bases

and

posterior

that

her

hemoglobin

was

not

explained

at

for bleeding weakness

before

peptic

ulcer,

She stated

that

relieved

her present

with

and the passage

for the preceding by food.

On

jet

admission

the

neck

count cells

veins. cu

mm.

blood.

developed sulfate

pretation

was duodenal The

ulcer.

patient

level of 11.5 Pour and

of the neck million

red

strongly

scarring

residue.

first

with

patient

started

to pass loose,

generalized

appeared

pale

larged,

anxious,

veins.

The

hemoglobin

blood

cells.

Digitalis

mercurial

injection

was given

a packed

OCTOBER,

1958

red cell

transfusion

half

the

start

atroof this

about

June

I4

x-ray

of the midway

was 14.15

g

series

revealed

a

with a slight five-hour

was discharged

On

May

liver

improved

hydrin,

of the

half

inter-

tion,

of the

:1

heart

unit of washed

the ensuing morphine

six days, and

were

dis-

cnculation

kept under

con-

diuretic.

a transfusion

of 250

cc of

by slow, intravenous

was precipitated

before

Aminophyllin,

sulfate,

and

mercu-

atropine

sulfate

this attack. another cells

transfusion

was given,

sulfate 3.

been

and

atropine other

preceded

all received

was one

red cells was given and accompanied as

by the patient level

detailed without

was

12.2

of

injecgiven

one-half

Thereafter,

injections

the hemoglobin

about

cc

by one-

sulfate half

when

given.

packed

of 250

preceded

The

at a point

atropine

red blood

were a

edematous

was slight

had been

edema

as in case had

not

of a mercurial

morphine

morphine

transfusion

million

cc at a

was

disease,

(2

Decholina

finished.

the transfusion,

At discharge,

of 250

block

There

The

patient

to treat

exactly

These

a

she

heart

legs were

enlarged. veins.

was

4,

admission

she

to the

was 160/I 10 and there The

pulmonary

red

distention and

addition,

heart

red cells was given

packed

On

1957,

In

and

of admission,

September

with

2.92

loss.

arteriosclerotic

bases.

The

oxygen,

On

stools

day

required

washed.

29,

was admitted

The patient had a which ulcerated and re-

hernia,

blood

injections

transfusion

the

30,

1, 1957.

was not

packed Frank

the were

series

black

age 72,

pressure

at both

the

drip.

for

(May

female,

of the cervical

washed,

a hemoglobin

was continued On

on

patient

hiatus

trol with weekly of

was 7..6 g with

was given.

and

cells.

on Sept.

large

the blood

the

during

jet

weakness. and

before

method.

i/d) and

On admission the hemoglobin level was 7.2 g block). with 3.6 million red blood cells. The heart was en-

to a duodenal

admission

a

time was I4 sec.

and

The

in

tention

of these.

portion

niche.

esophageal

and

red blood

x-ray

C. B.,

Hospital

few rales

and morphine

secondary

present

The

failure,

blood

positive three

large

tional the

a

19, 1957.

myocardial

stools.

transfusions,

after

was discharged

before

developed patient

1.6 million

was

ulcer

(gr

prepared

of the duodenum,

chronic

g.

days the

with

of the

a definite

of

g) it was decided

sulfate

14, a gastrointestinal spasm

for

(on

Her

mercuhydrin,

deformity

without

enlarged.

edema

June

periodically

to this hospital,

had seven

5 cc daily

because

by a modified

level

red blood

treated

hospital

tarry

A gastrointestinal

occasion.

a constant

duodenum

j

patient

pulmonary

hemoglobin

this

year she had epigastric

was

stool

aminophyllin,

on each

showed

Her

The

frank

She required

the

heart

was 5.5 g of hemoglobin per

occult

1957

The

4,

half was given

sulted

her pulse was 100, she was pale and had engorgement her

Imferon,

June

minutes

wall

of generalized

black

admission

live

the

In this manner, seven transcells were given without mishap of any

million

CASE 4.

and was

to another

symptoms

of many

The

Swedish

further.

digitalis

she was admitted

on

was

to

because

transfusion.

type.

with 4.87

She

improved.

About

the

of packed

gastric

examination

lung with

anticoagulants,

given

fusions

On

‘/i50)

the

clear

and still anemic.

level (5.75

and the other

on June

the

X-ray

both

was

done

to start

of morphine

(gr

became

not

and

during

for complaints

of

consistent

sulfate

times

apprehensive

cell transfusion

A hypodermic

and

The morphine

chest

was

hemoglobin

to give packed pine

her

However,

falling

persistent

four

foul-smelling

elsewhere edema

steadily

on

previous

black,

patient.

changes

discharged

the

intramuscularly.

through

to the

before

frank

dyspnea

mercuhydrin,

three

1, it was decided

transfusion

and dizziness.

and

hypertensive

electrocardiogram

pain

loose, jet

orthopnea,

was a known

and

for

by weakness

she was hospitalized

dyspnea,

showed

that

passing

accompanied

In 1954, of

stated

was admitted

repeated

was markedly

amount

in case reports

days

developed

extreme

and oxygen.

be

Phlebotomy

On June

demise is often not recognized found in the literature.

Swedish

two

auscultation.

in spite

to

she

with

aminophyllin,

and atropine

ensuing

this,

associated

received

had

at the end of the trans-

this type of patient. Unfortunately, the connection between transfusions and the patients’

CASE 3.

She

atropine

he de-

Following

edema

morphine,

Both of the patients described chronic anemia due to uremia. must be given with great caution in

Comment: above had Transfusions

rate.

cyanosis.

this was a factor

patient’s

and dyspnea

fusion,

slow

pulmonary

not be determined

in his death. veloped

12-hour

therapy.

491

of

addi-

daily for by the above. incident.

g with

4.0

cells.

Comment: In both case 3 and case 4, it was possible to give the required amount of blood to

Circulatory

492 patients

in chronic

Overloading

heart failure with very little

cardiac reserve by the simple expedient of giving the prophylactic injections of morphine and atropine as described in this paper. sLll,sequently, we have used this method many times with salutary effects in every patient in which it was tried.

in Blood Transfusion mia that are of considerable

importance

if trans-

fusions arc being planned as part of the trratment. The total circulating blood vol~~rnc is reduced.‘7 This reduction has been variously estimated to be from 14 to 33 per cent below normal, depending, of course, on the degree of anemia.‘* The reduction of the blood volume is apparently proportionate to the reduction of hemoglobin and is not dependent on the cause of

The number of actual published instances of circulatory overloading following transfusion is few. Plummer” reported five deaths from this cause, and Pygottr” and DeGowini3 each describe two fatalities. Drummond14a reported five deaths from pulmonary edema following transfusion. Reports of fatalities are no indication of the actual incidence of this complication, since many patients recover if the situation is recognized early and intensively treated. There are several disorders in which it is relatively easy to produce pulmonary lowing transfusion9 Patients with

edema folheart dis-

ease, especially those with left ventricular strain, and patients with chronic anemia are the most likely subjects. Prolonged fevers, such as typhoid fever, or even a simple febrile reaction can place a burden on the circulation. Patients with pulmonary diseases, either acute or chronic lung infection, chest injuries and pneumothorax are predisposed to this complication of transfusion. The effect of rapid intravenous infusions in normal individuals is well documented.*4b Following such infusions the venous pressure rises, the heart becomes dilated, and much of the infused fluid remains for a time in the pulmonary vessels.15J6 The experiments cited were with saline infusions, but even more pronounced effects would undoubtedly follow blood transfusions. The effect could well prove disastrous in organic heart disease, especially stenotic lesions of mitral and aortic valves and patients with borderline compensation. In prolonged fevers, anemia is often combined with a toxic myocarditis. The presence of lung disease causes an additional right heart strain, so that circulatory overloading can occur more easily. Circulatory Changes in Chronic Anemia: There are various circulatory changes in chronic ane-

anemia. The cardiac output is increased,rg also depending on the reduction of hemoglobin, and has been said to average a 50 per cent increase. Brannon et a1.20 found that 7 g of hemoglobin per 100 cc was the critical level, above which no change in cardiac output was noted, while below this level there was a large increase in cardiac output. Although some authorities20’23 have reported normal venous pressure and normal right atria1 pressures, others 21have found higher values than normal. Scott,9 writing in the Keynes’ manual on blood transfusion, states dogmatically that there can be no reasonable doubt that the venous pressure, and presumably also the right atria1 pressure, is raised in many cases of severe chronic anemia. This statement is based largely on the clinical finding of cervical venous distention many cases of severe chronic anemia. PREVENTION

Rate

OF

of

OVERLOAD

InfuCon:

In

DURING

chronic

in

TRANSFUSION

anemia,

the

transfusion must be administered by the slowdrip method, at a rate not exceeding 2 cc/kg body weight/hour, and if the anemia is severe, only 1 cc/kg/hour would be a safer rate of infusion. Scott9 states that a constant watch should be kept for increasing distention of the cervical veins, and the transfusion should be stopped immediately if this occurs. Digitalis: In an attempt to lower the risk of circulatory overload in chronic anemic patients, Sharpey-Schafer6 recommends that the transfusion be carried out in the reclining position, because this reduces the pressure in the right atrium. McMichael and Sharpey-Schafer* noted that digoxin also lowers the right atria1 pressure, and Scott9 believes that an intravenous injection of 1 .O to 1.5 mg of digoxin immediately before transfusion is a rational procedure. Luisada and Cardi, however, caution against THE

AMERICAN

JOIJRNAI.

OF

CARDIOI.r)OY

Pelner

and

rapid

digitalization in patients with mitral They state that in these patients the stenosis. elevated pulmonary pressure is caused by a high right ventricular output in the presence of mitral obstruction. Rapid digitalization may precipitate pulmonary edema by increasing the right ventricular output while the outflow from the In one lungs is impeded by the mitral block. morphine and venesection such instance, lowered the pulmonary pulmonary edema. Morphine: The

pressure and cleared

empirical

use

the

of morphine

and

atropine in the treatment of pulmonary Although edema has been known for decades. the evidence for the use of morphine rests on fairly solid ground, the evidence for the use of atropine is more tenuous. Morphine terminates most of the mild and some of the severe attacks of pulmonary edema, especially when associated with hypertension, uremia, coronary thrombosis, or mitral stenosis.23 Morphine must be used with great circumspection, if at’all, in patients with cerebral The vascular disease or chronic car pulmonale. mechanism of action of morphine is not entirely It depresses the respiratory center and known. It has decreases the suction effect of dyspnea.23 been stated that in pharmacologic doses, morphine causes no apparent change in cardiovasPulmonary atria1 pressures cular dynamics.24 in cardiac patients studied by catheterization decreased in 26 of 34 patients, but there was an In increase in the pressure in eight patients.25 coronary patients, morphine may act by alleviation of anxiety and by interruption of harmful reflexes. Morphine decreases the basal metabolic rate, and thus could conceivably reduce the work of the heart and possibly also the venous pressure.23 In any event, morphine is probably one of the most effective drugs in the treatment of pulmonary edema, even though we may not know exactly how it acts. A&opine: The value of atropine in acute pul-

43.3

Waldman were responsible

for its use in pulmonary

edema.

There is another possibility, however, that these authors do not stress in their excellent review, Antonini and BiancalanFr reported patients with traumatic injury to the brain and spinal cord, in whom severe pulmonary edema ocIn these instances, the pulmonary curred. edema was thought to be due to pulmonary transudation because of direct neurogenic vasoIt has been dilatation of the pulmonary vessels. noted28 that pulmonary edema can occur in nervous illness in which autonomic imbalance Cookezg reported on the demay play a part. velopment

of pulmonary

edema

in a healthy

patient with ureteral colic who had been given Likewise, two patients with multiple eserine. sclerosis who were being treated with neostigmine developed attacks of pulmonary edema.30 Paine, Smith, and Howard,28 after a review of these instances, state that serious physiologic disturbances may follow parasympathetic stimulation even from ordinary movements or mild reactions of apprehension. One of the most useful of the anticholinergic drugs is atroIf parasympathetic stimulation, from pine. whatever

origin, can cause pulmonary

transuda-

tion and finally pulmonary edema, atropine In practical use, may help reverse the process. also, morphine when used alone in patients with pulmonary edema, may induce dreaded nausea and vomiting, which may not occur if atropine is used with the morphine. It would be unusual indeed, if so simple a prophylactic method for the prevention of circulatory overloading as we describe had not in We did not find it menfact been tried before. tioned in any of the literature on transfusions available to us. However, even if the method described in this article should not prove to be completely unique, we feel that it is still worth reporting, because an important hazard of transMany practitioners have defusion is stressed. veloped a cavalier therapy.

attitude

toward

this form of

monary edema is questioned by some experts, even though it has been found of value cliniIts use was first reportedz6 from England cally. in 1927, but its beneficial effect was known many years earlier. Luisada and Cardiz3 believe

It is stressed that circulatory overloading following transfusion is especially liable to occur in

that the drying and the results

certain types of patients: heart disease patients especially with left ventricular strain, chronic

OCTORER,

1958

effect of atropine on secretions obtained in bronchial asthma

SUMMARY

494

Circulatory

Overloading

in Blood

anemia patirnts, also those with prolonged fvvrr, pulmonar)r discascs, cithcr acute or chronic, ancl with chest injuries. Two fatalities from circulatory overloading arc dcscril)cd. A method of prevention is detailed which consists of administrring packed red cells and a prophylactic in-

12.

,jection of morphine and during the transfusion.

14a.

atropine,

I)cforF and

don,

V.

13.

:

R.

M. J.

Transfusion

on

in

and fatalities

(section

II);

Williams

in &o/1

b. DEGOWIN,

R.,

of hlood

Baltimorr.

HARDIN.

R.

TmnsJu,ion.

WIENFR,

C..

transfusion

.J.

Thomas, Plmma

Spring-field.

1939.

M.

MCGRAW.

M.

and

16.

B.:

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F.

Davis.

A.

Hlood and

C.

S. and WF.INSTEIN, .I. d.: Williams

tiw.s and Suhrf?tutrc. mow, 4a.

EVANS? R.

S.:

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Usr

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147:

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in

1941.

19.

The

action

Quart.J. 0.

Scwr~,

R.

(section Williams 10.

MARRIOTT.

of

and

11.

and

1,.

in Bloxf

H.

I>. and

in

20.

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(rd.

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21.

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VOIX, systcrn

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for

the

estimating 70 : 1209.

J.A..\f.A.

studivs in

thr

hlood

volume

in

to thr hematopoirtic liver

: 401,

18

of

blood

in relation

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of

and blood

extract

thrrapy.

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I.II.JESTRANU.

G.

and

on the work

of six

to

chronic of

anemia

right

Cardiac

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421,

:

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CARDI,

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chez

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and clinical

Grunr

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les cardiaques.

man-

1356.

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LENEGRE,

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in scverr

N. F.. and I~EITRICK, .T. E.:

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ALTSCHULE. M. I).

output

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Cwcula!zon 1 ? : 113,

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the

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E;,. P.:

Pathology.

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in patients

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LUISAD.4 , A. A. and

and Stratton.

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H. .l., CRANE,

agcment.

Ai/

.4. .r., WARREN, .r. V.. and

(Xzn. SC. 5: 125.

STEWART,

rrst.

1925-26.

atria1

332.

Clinical

darin-

‘l’he cardiac

S~~ARPEY-SCHAFER.

SW.BAT,

dur

misccllanrous

N.:

STENSTROM.

L’action

do la mor-

des cavites

droit

tltl

.4rch. nml. GOPUT42:

THE AMERICAN JOURNAL

:

VII.

.1. Clirz. Ir,w1/. 18:

of the heat

BRANNON, 1;. S., MERRILI..

vdcma.

25.

and

vrra.

130,

Inivct. 16:

of anemia.

volume. anemias

hemolysis

and polycythcmia

./. Cl+.

24.

blood

hypochromic

loss.

ma”.

and

thr

1939.

anemia.

G. Kcyncs).

A report 1936.

and

.I. Clzn. Znrwst. 17: 7,

Clinical Changes

on thr

1

&it.

of thr*

1938.

D.,

and

to intramuscular

niqllc

transfusion

Volume

for the rrlicf

: 1043. 1940. S. : Blood transfusion.

G.:

VI.

StudiFs

1949. A.:

dynamics 401,

M.

in anemia.

STEAU. li. A., JR.:

23. of blood

The cffccts

intravenously

.4 new

E.:

P.:

1:.

1944.

and Wilkins,

PLUMMER, N. fatalities.

123.

of .on

.4v1. .I.

R.:

Il.

Thr

volnmc.

hlood volumr

mpd. .rcnndinnu. 63:

50: 280,

SHARPEY-SC:HAI'~R.

Complications

II);

:M. J.

IJNDEM.AN,

11wrrt. 26:

digoxin

II.

amount

and

thr

Pathogrncsis

intravenous

13:

Mel. B.:

ratv in blood Rrrl.

and

hrart.

on the cardiovascular

in blood

the

studies

22. .I.

cffcct

prcssurr

of fluids administrrrd

ALTSCHULE.

effects

Pro-

195.5. 8. MCMICHARL,

R..

changes

621,

upright.

J.

of thr

Inurst. 17:

C/in.

administrwd

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Thr

venous

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01

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1945.

Am.

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6. SHARPEY-SCHAFER,

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J.A..Zl.rl.

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J.

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T. B..

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Balti-

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rrythrocytes

793. red

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330.

in transfusion

122:

and DAVE.

V.. FRANK,

cedurc

7.

blood

.J.A.M.A.

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5. ~INSRERG.

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:

11

1943.

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Blood Ikrir~a-

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MATIIEK,

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‘vlrfl,

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WHITE,

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d. STRUMIA,

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1949. c.

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1949.

Saunders.

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:

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2: 319,1943. R. B.:

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1939.

2. T)RUMMOND,

3a.

I’.:

sion.

b. MEEK,

Blood Tmncft~r~on.Oxford,

H.:

Death

PYCZOTT,

,\I. .I. 2: 319.

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