Use of sodium nitroprusside in post-coronary bypass surgery. A plea for conservatism.

C B Patel, V Laboy, B Venus, M Mathru and D Wier Chest 1986;89;663-667 DOI 10.1378/chest.89.5.663 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/89/5/663

Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1986by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692

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Use of Sodium Post-Coronary

A Plea
Chandrakant Bahman
Dary!

Nitroprusside in Bypass Surgery*

Vicente Ma!i Laboy, Mathru, M.D.;t M.D., F.C.C.P; and

for Conservatism
B. Venus, M.D.t Pate!, M.D., M.D.;t FC.C.P;1

Wier,

In 292

patients surgery,

who

underwent seven patients

coronary

artery

bypass

graft

monly
patients.

described sodium patients.

signs thiosulfate Three

of SNP of was patients SNP

toxicity therapy followed who

observation

were by failed

absent and to
suggests

in those in conthat

(CABG)

developed

sodium

nitro-

Discontinuation

treatment regain

prusside (SNP) tion of infusion

dose ranged

toxicity
varied from 1.8 ill and

in the

postoperative

period.

DuraSNP the loss of

with four
and/or

improvement

between 26 to 160 hrs and total to 12 mg/kgbody weight. All patients required for control ventilatory support in and

sciousness
renal

later

died
complications.

because
Our

of hemodynamic,
may be that toxic the

pulmonary
in unstable post-

were critically postoperative

crease of SNP

period.
dose

Tachyphylaxis the major signs

to SNP of toxicity.

requiring Other

in- recommended

doses We be

of SNP recommend minimized

of hypertension,

CABG
of SNP

patients. infusion

dose

and

duration

consciousness

were

corn-

in critically

ill patients.

ecause titration, the drug

ofits of

rapid sodium choice and

onset, for

short the

duration, (SNP) management

and has

ease become of

of chemical toxicity. acute

data

of

all

patients

who

developed

SNP

nitroprusside

hypertension heart surgery.1 term toms clinician cause operative various plasma gery,5 for (> are 3 h) may

low cardiac output state after Although SNP toxicity during has and to include been SNP of patient distribution is changed,4 are be low more during at risk reported,23 toxicity its thus, inconspicuous;

open long sympthe

CASE
CASE

REPORTS

1 woman chest in revealed leads. and with No showed hemoglobin Patient suffered examination a temperature rate murmur (RR), was pitting (Hb)level with drip, she artery left she period, for returning was the BP started second progressively hemodynamic reexploration from the on 1 p.g/kg/min postoperative increased. main After underwent under she narcotic required for operating SNP day, catheterization, and left coronary insertion quadruple anesthesia. a moderate Later room, drip the she therapy SNP dose the postoperative stabilization. the aneurysm. (IABP), 18/mm; heard edema. vascular was calcium continued which anterior of CPK an was from upon was pain. and anterior hypertensive, chronic admission and and blood the lungs Admission congestion 12.9 g/dl channel to have and admitted Cardiac LDH. scar obstructive revealed rate pressure were chest and to our Critical test ischemic a 60 pack/year pulmonary (HR) (BP), clear. enlarged and pain total and an CABG In dose on became mediastinal for BP patients intra-aortic and the the of an and occlusion 98 percent left balloon ventricular immediate dopamine same hypertencontrol. to required day, bleedapical was There heart was IV Care results (ECG) changes history disease. 90/mm; mm was size. nitrounderof a in of Center showed

therapy fail

A 62-year-old (CCC) a mild examination for recurrent increase

nonspecific deterioration period. Since and patients

enzyme and had

as a possible

Electrocardiographic

during the postinferior of blood flow to smoking and to because sundevelop in two patients signs (CN) level
cardiac,

organs thiosulfate these

tissues levels may

Physical female respiratory Hg. trace film

a well-developed 170/90

CABG toxicity those

of 37#{176} Heart C.

SNP toxicity. patients after failed SNP

post-CABG

We recently reported SNP CABG surgery.6 Because the now

who

of bilateral

roentgenographic 1 mg/dl.

pulmonary treatment (NTG)

to

manifest we
patients

commonly measure
develop

described cyanide
neurologic,

of Her in
glycerin went the

creatinine blockers chest descending;

toxicity,

Despite

or pulmonary received. In patients surgery. suggesting sensitive The tive

*From

complications, a ten-month developed developed post-CABG infusion

irrespective period, we SNP over than toxicity a wide patients the

of SNP identified after

dose seven CABG

emergency right coronary of

exhibited artery;

occlusion ventricular pump postoperative with she IABP underwent After and
After

who Toxicity that to SNP

dosage range, may be more population. bioMedi-

aneurysemectomy

general

purpose cases
the

ofthis report is to present and to summarize the

Department ofCritical Care Medicine,

two representaclinical and

Memorial

ing. sive control

cal Center, Jacksonville, Florida. clinical status began to deteriorate. On the second day, BP was tFellow, Department of Critical Care Medicine. controlled with a 2.5p.gfkg/min intravenous infusion ofSNP At that tAssociate Professor, Departments of Anesthesiology and Surgery, University of Florida Colege of Medicine. time, she was arousable and free of pain. Her chest x-ray film was Supported in part by the Memorial Health, Education and Re- clear and the patient had a vital capacity (VC)of850 ml. Spontaneous search Foundation. respiratory rate (RR) was 20/mm with eight mechanically-assisted Manuscript received October 7; revision accepted December 17. breaths and maintained normal ABGs. The IMV rate was decreased Reprint requests: Dr Venus, Critical Care Medicine, Memorial Medical Center, P0 Box 16325, Jacksonville 32216 to 4/mm. However, ABG levels obtained 30 mm after the change

Concomitantly,

CHEST

I 89 I 5 I MAY,

1986

663

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showed
40/mm and therapy

pH, and

7.28;
shallow.

PaCO2,

53
were

torr; IMV

and rate

PaO2, was day she On SNP, deficit

75 3,

torr. while

Her back

RR receiving in

was

sponded postoperative
postoperatively,

appropriately day, he not normal and the (SCN) developed response. and of labile arterial recurrent tachycardia SNP had

to received

verbal 157 to verbal was for started PVO2

command. gradually mg 32 on of SNP commands. torr. hydralazine SNP He

On

the became ABC drip drip was

second By restless levels therapy and same a rapid ventricular paroxysmal serum day, were disconfor 30 h

Therefore,

increased was was scan

to 8/mm

requirement

increased.

weaning

attempts

cancelled. neurologic tomography wave activity.

with

3.5 p.g/kg/min stimuli. any slow Computer-assisted

intravenous

unresponsive found ofthe (ECG) of cumulative the brain

and within tinued BP h. Blood With the

was

responding limits patient was levels Blood and was

to

noxious

Nofocal abnormality. brain that for and the

examination.

(CAT) Calculation 721 CN therapy g dose she CN was level

failed
showed SNP
toxicity

to show
diffuse dose was method) IV was given pressure. fbllowed 585 was 6 and p.g/L 300

Electroencephalography patient SNP therapy was hours given 6.25 day, 800 g/L. received was of blood mg level with tube more over

control. patient

sent

measurement method). tachycardia manifested of the 7.25 within patient and were status, normal treated patient unsustained

of Later

CN that

thiocyanate ventricular irritability ventricular Because of on tion, 3 4.8 On sustained on dioversion arrest. cardiac dead postoperative p.g/L. the mechanical

(colorometric supraventricular He also episodes which Despite level levels the tachycardia was was were

revealed sent

80

with increased with was lactic limits. an IV

a possible

diagnosis,
the

discontinued. 12.5

sample metric thiosulfate 50 mg blood

measurement patient by eight the another

(spectrophotog sodium Captopril, for control oriented, on and extubated in satisfactory day of CN treat-

lidocaine. maintained ventilaacid episode Carcardiac direct the second Autopsy Brain pronounced level of

followed every On commands and g/L. day

6 h later. alert,

hemodynamic ventilation. pH

via a nasogastric

oxygenation and normal developed severe but he and was

and

following appropriately. 4 it was discontinuation

and
was

obtained measurement infusion and was 8 day

Electrolyte same ventricular with Despite massage, 100 full the mm. day was coronary normal 40

Repeat of SNP

evening, Hz

level
ment

on day

5 following She transferred

hypotension. developed including was on 16 mg/L. mitral valve.

continued out of the

to improve CCC on

attempted cardiac did CN p.g/L. and edematous. not SCN level life

day

advanced patient Blood 516.8 grafts but

support obtained

condition. CASE 2 man was and of admitted infarction. electrocardiographic infarction. papillary left examination. contained coronary was wall was quadruple After He drip at also required akinesis also operation, noted with noted. coronary the therapy artery on preserved Later artery patient the bypass was a subtotal was heart A to the hospital After new muscle four examination holosystolic dysfunction. IV and catheterization The stenosis totally anterior same graft maintained drip intact he was study. septal day, and left occluded. anterior in its midporAlso, + Inferior and the mitral and and lateral patient valve at 4 on IAPB with deelectrocardiography 12 p.glkg/mmn with days, a diagnosis the demonejection conWhile at patient

respond level

after

A 65-year-old acute became inferior hypotensive

myocardial

patent of showed was essentially

functioning

COMMENTS

strated
murmur firmed receiving ratio, he

an extension
was the therapy underwent heard. with presence

Two-dimensional ofischemic dopammne diagnostic

From

October

1984

to

July

1985,

292

patients this toxinfarcunderwent

underwent 1:1 period,

se-

CABG surgery in our hospital. seven patients were identified were

unstable

During with SNP

lected
scending
lion. mitral and wall

coronary
coronary
right insufficiency posterior motion The

icity.
tion

All
and

admitted cardiac

with
cardiovascular

acute

myocardial
status,

angiographic artery main

emergency

catheterization,

and

later

had inforof age, heavy

ventriculographic

CABG

surgery. mation ofthese five had history smokers. required

Table 1 summarizes patients. All were of hypertension

the clinical over 60 years and four were

underwent replacement. 1:1 ratio. SNP

on IABP

with p.gfkg dopamine 15

All had extensive coronary artery disease and four or more coronary grafts. Three of them IABP for hemodynamic support before and

1 g/kg/min.

Neurologically,

re- required

Table

1-Clinical

Information

ofPatients

with

SNP

Toxicity
Pump time

History Age Patient 1

2

No. IABP used Yes No Yes Yes of CABG 4 4 5 4

(mm)

Admission Sex F F M M diagnosis AMI COPD AM! DM AM! DM AM! Acute Mit. Reg.

History hypertension No Yes Yes Yes

of

of smoking Yes No Yes Yes

.
X-clamp 50 35 45 81

(yrs) 62 72 71 65

Total 85 70 110 128

Outcome Survived Survived Died Died

3 4

61

Unstable angina

Yes

No

No

67

129

Survived

Renal
failure 6 7 AM!
=

71 58 acute myocardial

M M

Unstable angina AM! infarction; COPD

Yes Yes chronic obstructive

Yes No pulmonary

No No disease;

4 4 DM

39 88 diabetis mellitus

79 114

Survived Died

664

Sodium

Nitroprusside

after

CABG

Surgery

(Pate! at al)

Downloaded from chestjournal.chestpubs.org by guest on December 17, 2011 1986 American College of Chest Physicians

after surgery. Table cardiac, and pulmonary mm after starting SNP responsive oxygenated. cardiac When showed dose, to indices verbal Blood

summarizes the neurologic, status of the patients. Thirty drip (period I) all patients were and level 1.8 were adequately was controlled to 3.2 Lmin

sodium status died renal later

thiosulfate of four complications. patients. because

(period Those ofhemodynamic, Three

III) who

improved remained pulmonary had

the

mental comatose

and/or high Four II levels of 10.3 serum had SNP g/dl were had

commands

individuals

pressure ranged from

SNP toxicity tachyphylaxis five patients

was suspected (period to SNP. Despite increase were still hypertensive

levels at initiation ofSNP infusion. and creatinine serum creatinine levels at period x m2. high All patients had Hb levels below II), all infusion. in SNP during and had below in all abnormal Cheyneinstabilwas
(SGOT)

SNP 3.1
and

infusion. g/dl serum

all had

Also,

serum

albumin

elevated SVR. Breathing pattern was abnormal patients. Five were tachypneic and one had Stokes respiration. Because of hemodynamic ity and/or hypoventilation, none of the patients successfully weaned ratio was above pulmonary was below
all patients

in all patients. glutamic-oxaloacetic

high lactate

Four patients transam inase

dehydrogenase (LDH)

levels. patients were dence SNP

During were within ofsepsis. infusion

developed

the three afebrile, normal Table and CN

SNP

periods of SNP their white blood and they showed

infusion all cell counts no evi-

from 250

the

ventilator.

However, pointing SNP Except

base

limits,

PaO/FIo2
to adequate sion, PO2
one case,

in all patients,

function. During 42 torn in all patients.

had normal pH and

infufor who deficit levels

3 provides and SCN

toxicity.

information regarding levels in seven patients

All patients had toxic

levels at all times. Tachyphylaxis to SNP developed in and all patients and was the first clue to SNP toxicity. When SNP toxicity was suspected, SNP therapy was discontinued patients. and sodium thiosulfate Discontinuation of
Table

ofCN. The SCN level was within the accepted

DISCUSSION

was measured range in all

in five of them.

cases

was administered SNP and treatment 2-Clinical

and
Laboratory

Initial reports of toxicity in all sion were described when with Data ofPatients with SNP
PaOd

associated it was

with employed

SNP to

infuinduce

Toxicity

HR

Fi02 BP Rhythm ST ST NSR NSR ST ST ST ST ST NSR ST NSR NSR AF NSR NSR ST NSR ST ST NSR NSR
(mm

Lactic Creat. BUN (mg/dl) 1.0 1.9 1.6 0.9 0.9 1.0 1.9 2.5 3.5 2.2 1.7 1.5 1.9 2.4 2.6 1.1 0.9 1. 1 1.2 1.4 1.3 15 20 15 17 20 14 +2.0 +7.0 33 34 0.4 0.6 1.3 4.0 7.38 7.47 32 17 65 92 29 39 3.1 1.8 0.2 1.2 32 41 18 2.7 6.1 69 76 19 70 Base deficit 0.8 5.6 pH 7.34 acid (meq/L)
-

Neurological
Patient 1 1* lit IIII 2 I II III 3 I II III 4 I II III to 5 I II III 6 I II III 7 I II III ST *1 tIl UI!
=

(beats)

Cl Hg) (L/min M2) 2.5 3.1 3.0 1.9 1.6 2.6 2.0 2.8 4.1 1.6 2.6 2.3 2.6 2.1 2.8 3.1 2.6 3.2 3.2 2.4 3.1 sinus rhythm; SNP was drip suspected and

SVR (dynesec 1100 1880 1120 1836 1984

cm5)

RR
(breath/mm)

P02
(mm

ratio

status Alert Comatose Alert Alert Agitation, hallucination Alert Awake Restlessunresponsive Comatose Awake Restlessunresponsive Response command Alert Restlessunresponsive Awake Awake Agitatedconfused Alert Unresponsive Coma Coma sinus Data Data Data tachycardia; obtained obtained obtained

nm)
97 101 78 70 102 98 103 139 118 73 116 79 77 115 79 86 102 89 92 98 87

Hg)

(mm

Hg) 220

(mg/dl)

136/74 188/83

18 28 24 20 32 22 0 40 0 18 38

39 41 40 30 34 33 43 42 39 35 32 29 33 34 35 32 34 35 35 34 32

210 215 210 215 220 220 210 220 210 200 240 210

7.44
7.41 1.6 0.3 4.0 7.44 7.49 2.5 7.38 7.37

1.1 1.2 7.42 1.5 1.3

125/58
148/66 148/65 161/77 114162 154/69 110/48 108/41 176/68 128/61 150/100 170/106

1684
1590 1232 701 1104 1430 771

2.6 1.5
-

2.9 7.38 4.3 7.47 7.4 7.25 7.46

4.8 1.4 7.417.42

7.36 -

#{149}28
0 40 22 20 38 26 0 36 32 atrial fibrillation

1560
1788 1380 1100 1010 1200 800 1400 1100 AF

200
220 210 220 230 220 210 230

2.4

160/99
155/69
162/85

7.50

7.397.45-

144/76 102/57

150/63 108/53
normal after SNP

7.52 -

30

minutes time after

starting toxicity discontinuation

= =

at the 12 hours

treatment

of SNP

toxicity

CHEST

I 89

I 5 I MAY,

1986

665

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Table

3-Nitroprusside
SNP (mg) dose

Dose

and

Levels

ofits Metabolites

in

Patients

with

SNP

Toxicity

Blood

levels*
*

,
/kg

Duration of SNP drip 80 160 55 30 74 26 81 (hrs)

.
Thiocyanate (mg/L)

body

Cyanide (.&g/L)

Patient 1 2 3 4 5 6 7 *Normal Thiocyanate, >500 p.g/L. ranges for serum our

Total 721

weight 12 5.5 8.4 2.2 6.1 1.8 8.2

800
575 3660 517 555 546

17 19 16 24

447
682 157 431 126 661.6 laboratory: SNP infusion, 6-29

21

1600

during

mg/L;

toxic

range,

>100

mg/L.

Cyanide,

blood

during

SNP

infusion,

50-500

.tg/L;

toxic

range

hypotension use for

during treatment

of

acute

Later, hypertensive

its

long-term crisis,

operative hypertension, and finally as a vasodilator the treatment of cardiac failure was described.910 During long-term SNP therapy, two potential lems exist. periods to thiocyanate fluid and levels, patients. coma, plasma symptoms the can First, the increased (SCN) produce patient is exposed concentration of accumulates in toxic effects. SCN such are

daily dose and maximum amount of SNP permitted post- during long-term therapy is not well-substantiated. in Michenfelder and Tinker have recommended 0.5 mg/ kg/h as the maximum dose of SNP for long-term prob- infusion in man. Vesey and Cole3 recently studied 30 patients gested long-term our the Our receiving that the SNP and of7O SNP maximum infusion the for for 12 to 314 hours and sugsafe sustained dose rate for is near to 240 g/kg/hr (5.8 total dose of SNP is in

for prolonged CN. Second,

the extracellular Despite high in any of hypotension, with g/ a

CN mg/kg/day), region patients well that patients

maximum

level of Toxic effects

was not high as psychosis, to occur than 100 poisoning and include tachypnea partial attempts SCN level levels

mg/kg developed

a period ofless than 14 days. SNP toxicity while receiving considered critically to be safe. ill patients inability be due can This are

and death concentration and signs

known greater

SCN doses The suggests CABG

below that post-CABG to SNP to metabolize

of CN

described nausea, without

in the supensensitive vomitcyano-

infusion. CN

The

of postto several

literature are ing, restlessness, sis, irregular sion, convulsion, SNP toxicity. available. used for Furthermore, value of information blood and affinity level metabolic blood ever, tons lactate, our are not in toxicity to measure

nonspecific air hunger, pulse, are

dry skin, and somnulence. CN these blood but not and

paralysis, Since early have are

subclinical,

factors: 1) Nutritional status is an important determinant of confustates of the thiosulfate pool. Thiosulfate is essential as a sulfur been made donor for conversion of CN to TCN and as a substrate not readily can of toxicity. the paucity of for the rhondanase be nod, the Ivankovitch surgery, isolation and purification of system.4 In the post-CABG state the of et al5 plasma semistarvation have shown thiosulfate is that level mitochondrial surgery In pefact,

blood However, Therefore, treatment

for prevention

measurements for prevention

measurement questioned of the that

present.

M ichenfelden plasma CN levels concerning tissue CN

has because

during CABG is significantly in the to immedicyanide, levels and

the relationship levels and the fact He

CN has blood

for methemoglobin than tissues. of for CN diagnosing suggests enough ill patients. failed to show showed blood measure the dose PVO) sensitive

can cause suggests the blood toxicity. metabolic identify CN that to

and ofdecreased ate postoperative between 2) Because the high smokers have a higher use Howindicaof therefore the

its excretion period. of continuous lower plasma

is increased exposure thiosulfate

indicators observation

toxicity (ie,

pH,

CABG
be more

can develop SNP A large percentage surgery are smokers6 susceptible sulfur ofa transfer to

toxicity with lower doses of of patients undergoing and therefore they may (rhodanase) from a donor catasuch as

early levels high metabolic

CN

3) Thiosulfate
the

CN toxicity. transferase atom

toxicity in critically CN, our patients

Despite toxic extraordinarily significant lactate for level.

of lyzes

sulfur

02.
acidosis

Only one
with is to Another

patient a moderate limit

P thiosulfate to a nucleophilic acceptor such transforming CN to SCN. The rhodanase be compromised in critically ill patients SNP safe limited ability for 4) The metabolism
Sodium

as CN, thus system may and exhibit SCN. depends

(Pate! at a!)

suggested

prevention infusion.

of The

toxicity
666

of SNP

detoxification of CN
Nitroprusside

to

of CN to SCN also
Surgery

on

after CABG

Downloaded from chestjournal.chestpubs.org by guest on December 17, 2011 1986 American College of Chest Physicians

vitamin term levels)8 patients of CN 5) highly mals,

B-i2, infusion Thus, may toxicity.

a ofSNP

rhodanase is shown

system to decrease vitamin likelihood

cofactor.7 vitamin

LongB-i2

critically tion drug started

ill

post-CABG infusion as soon be

patients, minimized as possible.

the and

dose an

and

dura-

of SNP

alternative

low serum increase the can and

B-12 level in these for development sulfur CN. complex seen of in a form In mamis after this

Serum albumin available to, the serum to be serum surgery system Abnormal

carry sulfane reactive with, sulfur CN which

REFERENCES 1 Bixler VL. surgical 1978; 2 protection side in the RD: toxicity. LW Jr, blood 1973; HJ. SS, 13:212-13 DG, ofsodium RD. Toxicity D, Keaney NP, Turner nitroprusside. of Feldman elevation, Guiha ventricular The fatal Cyanide Cole by 1985; BH. PW, Opththal SR, surgery. F, Picard Clin Nutrit Hesdorffer B,, levels Med B, PV. long Blood term NH, infarction. toxic sodium MS, and Limas function JM, nitroprusside. Helfant with ventricular CJ, during Lancet manifestations from 46:196-201 and with thiocyanate sodium I. Scand and PS. in coronary 73:316-20 role ofvitamin Roos use EE, FABS AD, anuric FL, antidotal 44:330-35 Braverman toxicity B, Klowden with AJ, thiosulfate Heyman in HJ. dogs. PrevenAnesth Shah dogs. Tobey effect G. Proc RE. B,2 in human nutrition. concentrations nitroprusside. Purification 1953; tobacco Preand artery and 7:1129-36 amblyopia. postoperative revascularisodium R. Lane JR.Okuda 1974; AD, Sodium Patel treatment nitroprusside C, 1977; 3 Rieves prusside Rudy systemic Physiol 5 Ivankovitch Heyman to 6 sodium Sarvotham nitroprusside 1985; 7 8 9 McDowall toxicity Jack 46:952 Mukherjee Treatment
pain,

fl,

Gardner patients

TJ, myocardial with JD,

Donahoo sodium JH. with of MA, during

JS,

Brawley

RK, Ann toxicity of case. in LH

Potter Thorac and

A,

Gott Surg

albumin-sulfane the primary albumin may

Improved 25:444-48

performance nitroprusside. Cyanide a human symptoms

in postoperative

cardiac

suggested The low CABG buffer 6)

detoxification is usually the availability function

Michenfelder during dog: 47:441-48

Tinker chronic correlation

thiosulfate nitroprus-

decrease

administration

sodium

and cause CN toxicity. hepatic and failing renal ill patients. become

Anesthesiology recognizing Jr. Distribution nitroof

is not and of

uncommon excretion

in critically of CN may

Detoxification impaired because

Importance South Heymann flow 34:194-99 Braverman thiosulfate

MedJ 1984;

77:1035-37 bypass. TS,

Edmunds cardiopulmonary B, Stephens Anesthesiology B, Mathru

decreased hepatic and renal rhodanase activity. #{176} In our patients, presumed CN toxicity occurred at a SCN level of below 25 mg/dl. This suggests that our patients ability to convert CN to SCN was hampered by some Furthermore, significantly Experience toxicity droxycobalmin being useful the issue possible or all the above-mentioned mechanisms. the LD 50 for cyanide may have been lowered in these critically ill patients. with prophylaxis and treatment of CN SNP infusion in man is limited. suggested However, Hyas (vitamin for prevention B-12) has been and treatment.Z1

Appl M,

Shulman relation 53:11-17 1983;

disposition M. ischemia.

in humans: IV nitroglycerin Crit

toxicity. Venus of myocardial

vs Med

Care

Y.The
1974; therapy. resting chest JAMA E, Cohn infusion thiocyanates. in JN.

during

J Br Anaesth

46:327-32

Anaesth Br

Nitroprusside recurrent arrhythmias.

is not settled and the proper dosage toxic effects have not been established. constitutes a major rationale is that the which is much less ofside effects, effects infused received hemodynamic toxicity if patients antidote CN will toxic and antagonistic

and its Injecfor CN be conwill be to can with were to multiand

10

of hypertensive 235:2406-09 JA, left CE 1939; myocardial 112:1125-27

patients

ST-segment

tion of thiosulfate poisoning. The vented to SCN, excreted. the desired prevent CN SNP.2 All (150 to 200 recognized. the treatment. organ uted failure. to the

1976; Franciosa Improved in acute 11 12 13 Garvin JAMA the Vesey produced Anaesth 14 15 16 Sorbo

Rodriguera nitroprusside 1972; of 1:650-54 the

It is free

is not

of SNP concomitantly sodium

MichenfelderJD. dog. CJ,

release 1977; cyanide therapy rhodanese. Acta

nitroprusside

Anesthesiology

of our

thiosulfate

mg/kg) once high However, only four Non-responders It is possible deteriorating

blood CN levels patients responded later died with factors picture

Br phys-

57:148-55 Crystalline examination. Wilson

1967;

that several clinical

contnibof those

icochemical Darby Br

Chem smoking Chopra

J.

Cyanide, 51:336-38 ML, abnormalities 1978; The 3:383-90

patients who did not respond. Therefore, cyanide toxicity may be one of several contributing factors to the deteriorating status of critically ill patients. Our therapy, tolerated observation recommended by stable that during long-term SNP doses which may be patients, may prove toxic in cnitisuggests

Braun pulmonary zation

Birnbaum function Chest CW. 1955;

17 18

Wokes Am

Lipma Vitamin
Crit

J,
Care

C, Costa FF, in the prolonged 1984; Castric 12:161-63 PA, Conn

CP, Edelman J, Plit M. ofsodium nitroprusside. Solomonson Proc Soc 1982; Exp Thiosulfate Biol LP, Volini M,

cally ill patients. The fact that our post-CABG patients developed toxicity on therapy with a wide range of 19 SNP doses suggests that reaction of these patients to 20 SNP therapy is unpredictable. Development of tachyphylaxis to SNP requiring increase suspicious for toxicity of the SNP lack dose
21

Vennesland Westley Braverman netics 170:273-80 Posner cyanide thesiology MA,

J.

Cyanide B, and

metabolism. Ivankovich

41:2639-48 pharmacokiMed 1982;

in normal

should make the clinician Despite the potential knowledge prescribe more regarding this drug information

of toxicity. and the

Rodkey

Nitroprusside-mnduced Anes-

of
22

poisoning: 1976; AD, nitroprusside 1982; 61:120-26

of hydroxocobalammn.

safe dosage regimens, physicians without proper monitoring. Until is available, we recommend that in

Ivankovich tion Analg of

CHEST

I 89 I 5 I MAY,

1986

667

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Use of sodium nitroprusside in post-coronary bypass surgery. A plea for conservatism. C B Patel, V Laboy, B Venus, M Mathru and D Wier Chest 1986;89; 663-667 DOI 10.1378/chest.89.5.663 This information is current as of December 17, 2011
Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/89/5/663 Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.

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