use of sodium nitroprusside in post coronary bypass surgery
TRANSCRIPT
DOI 10.1378/chest.89.5.663 1986;89;663-667Chest
C B Patel, V Laboy, B Venus, M Mathru and D Wier bypass surgery. A plea for conservatism.Use of sodium nitroprusside in post-coronary
http://chestjournal.chestpubs.org/content/89/5/663
can be found online on the World Wide Web at: The online version of this article, along with updated information and services
) ISSN:0012-3692http://chestjournal.chestpubs.org/site/misc/reprints.xhtml(without the prior written permission of the copyright holder.reserved. No part of this article or PDF may be reproduced or distributedChest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights
ofbeen published monthly since 1935. Copyright1986by the American College is the official journal of the American College of Chest Physicians. It hasChest
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
CHEST I 89 I 5 I MAY, 1986 663
Use of Sodium Nitroprusside inPost-Coronary Bypass Surgery*A Plea for ConservatismChandrakant B. Pate!, M.D.;t Vicente Laboy, M.D.;t
Bahman Venus, M.D., FC.C.P;1 Ma!i Mathru, M.D., F.C.C.P;� and
Dary! Wier, M.D.t
In 292 patients who underwent coronary artery bypass graft
(CABG) surgery, seven patients developed sodium nitro-
prusside (SNP) toxicity in the postoperative period. Dura-
tion of infusion varied between 26 to 160 hrs and total SNP
dose ranged from 1.8 to 12 mg/kg body weight. All patients
were critically ill and required ventilatory support in the
postoperative period. Tachyphylaxis to SNP requiring in-
crease of SNP dose for control of hypertension, and loss of
consciousness were the major signs of toxicity. Other corn-
ecause ofits rapid onset, short duration, and ease of
titration, sodium nitroprusside (SNP) has become
the drug of choice for the management of acute
hypertension and low cardiac output state after open
heart surgery.1 Although SNP toxicity during long
term (> 3 h) therapy has been reported,23 its symp-
toms are nonspecific and inconspicuous; thus, the
clinician may fail to include SNP toxicity as a possible
cause for deterioration of patient during the post-
operative period. Since distribution of blood flow to
various organs and tissues is changed,4 and because
plasma thiosulfate levels are low during CABG sun-
gery,5 these patients may be more at risk to develop
SNP toxicity. We recently reported SNP toxicity in two
patients after CABG surgery.6 Because those patients
failed to manifest the commonly described signs of
SNP toxicity, we now measure cyanide (CN) level in
post-CABG patients who develop neurologic, cardiac,
or pulmonary complications, irrespective of SNP dose
received. In a ten-month period, we identified seven
patients who developed SNP toxicity after CABG
surgery. Toxicity developed over a wide dosage range,
suggesting that post-CABG patients may be more
sensitive to SNP infusion than the general population.
The purpose ofthis report is to present two representa-
tive cases and to summarize the clinical and bio-
*From the Department ofCritical Care Medicine, Memorial Medi-
cal Center, Jacksonville, Florida.tFellow, Department of Critical Care Medicine.
tAssociate Professor, Departments of Anesthesiology and Surgery,University of Florida Colege of Medicine.Supported in part by the Memorial Health, Education and Re-search Foundation.
Manuscript received October 7; revision accepted December 17.Reprint requests: Dr Venus, Critical Care Medicine, MemorialMedical Center, P0 Box 16325, Jacksonville 32216
monly described signs of SNP toxicity were absent in those
patients. Discontinuation of SNP therapy and treatment
with sodium thiosulfate was followed by improvement in
four patients. Three patients who failed to regain con-
sciousness later died because of hemodynamic, pulmonaryand/or renal complications. Our observation suggests that
recommended doses of SNP may be toxic in unstable post-
CABG patients. We recommend that the dose and duration
of SNP infusion be minimized in critically ill patients.
chemical data of all patients who developed SNP
toxicity.
CASE 1
CASE REPORTS
A 62-year-old woman was admitted to our Critical Care Center
(CCC) for recurrent chest pain. Cardiac enzyme test results showed
a mild increase in CPK and LDH. Electrocardiographic (ECG)
examination revealed an anterior scar and ischemic changes in
inferior leads. Patient was hypertensive, had a 60 pack/year history of
smoking and suffered from chronic obstructive pulmonary disease.
Physical examination upon admission revealed a well-developed
female with a temperature of 37#{176}C. Heart rate (HR) was 90/mm;
respiratory rate (RR), 18/mm; and blood pressure (BP), 170/90 mm
Hg. No murmur was heard and the lungs were clear. There was a
trace of bilateral pitting edema. Admission chest roentgenographic
film showed pulmonary vascular congestion and enlarged heart size.
Her hemoglobin (Hb)level was 12.9 g/dl and creatinine was 1 mg/dl.
Despite treatment with calcium channel blockers and IV nitro-
glycerin (NTG) drip, she continued to have chest pain and under-
went emergency catheterization, which exhibited total occlusion of
the right coronary artery and left anterior descending; 98 percent
occlusion of the left main coronary artery; and an apical left
ventricular aneurysm. After insertion of an intra-aortic balloon
pump (IABP), she underwent quadruple CABG and ventricular
aneurysemectomy under narcotic anesthesia. In the immediate
postoperative period, she required a moderate dose of dopamine
with IABP for hemodynamic stabilization. Later on the same day,
she underwent reexploration for postoperative mediastinal bleed-
ing. After returning from the operating room, she became hyperten-
sive and was started on 1 p.g/kg/min SNP drip therapy for BP control.
After the second postoperative day, the SNP dose required to
control BP progressively increased. Concomitantly, the patient’s
clinical status began to deteriorate. On the second day, BP was
controlled with a 2.5 p.gfkg/min intravenous infusion ofSNP At that
time, she was arousable and free of pain. Her chest x-ray film was
clear and the patient had a vital capacity (VC)of850 ml. Spontaneous
respiratory rate (RR) was 20/mm with eight mechanically-assisted
breaths and maintained normal ABGs. The IMV rate was decreased
to 4/mm. However, ABG levels obtained 30 mm after the change
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
664 Sodium Nitroprusside after CABG Surgery (Pate! at al)
showed pH, 7.28; PaCO2, 53 torr; and PaO2, 75 torr. Her RR was
40/mm and shallow. Therefore, IMV rate was increased back to 8/mm
and weaning attempts were cancelled. On day 3, while receiving
therapy with 3.5 p.g/kg/min intravenous SNP, she was unresponsive
to noxious stimuli. No focal neurologic deficit was found in the
examination. Computer-assisted tomography (CAT) scan ofthe brain
failed to show any abnormality. Electroencephalography (ECG)
showed diffuse slow brain wave activity. Calculation of cumulative
SNP dose revealed that the patient received 721 mg over 80 h. With
toxicity a possible diagnosis, SNP therapy was discontinued. Blood
sample was sent for measurement of blood CN level (spectrophoto-
metric method) and the patient was given therapy with 12.5 g sodium
thiosulfate IV followed by another 6.25 g dose 6 h later. Captopril,
50 mg was given every eight hours via a nasogastric tube for control of
blood pressure. On the following day, she was more alert, oriented,
and fbllowed commands appropriately. CN level obtained on day 3
was 585 p.g/L and day 4 it was 800 �g/L. Repeat measurement of CN
level on day 5 following discontinuation of SNP infusion and treat-
ment was 300 �g/L. She continued to improve and was extubated on
day 6 and transferred out of the CCC on day 8 in satisfactory
condition.
CASE 2
A 65-year-old man was admitted to the hospital with a diagnosis of
acute inferior myocardial infarction. After four days, the patient
became hypotensive and electrocardiographic examination demon-
strated an extension of infarction. A new holosystolic ejection
murmur was heard. Two-dimensional electrocardiography con-
firmed the presence ofischemic papillary muscle dysfunction. While
receiving therapy with dopammne 12 p.glkg/mmn IV and on IAPB at 1:1
ratio, he underwent diagnostic left heart catheterization with se-
lected coronary angiographic examination. The left anterior de-
scending coronary artery contained a subtotal stenosis in its midpor-
lion. The right main coronary artery was totally occluded. Also, 4 +
mitral insufficiency was noted on ventriculographic study. Inferior
and posterior wall akinesis with preserved anterior septal and lateral
wall motion was also noted. Later the same day, the patient
underwent quadruple coronary artery bypass graft and mitral valve
replacement. After operation, the patient was maintained on IABP at
1:1 ratio. He also required therapy with 15 p.gfkg dopamine drip and
SNP drip at 1 �g/kg/min. Neurologically, he was intact and re-
sponded appropriately to verbal command. On the second
postoperative day, SNP requirement gradually increased. By 30 h
postoperatively, he had received 157 mg of SNP He became restless
and was not responding to verbal commands. ABC levels were
within normal limits and PVO2 was 32 torr. SNP drip was discon-
tinued and the patient was started on hydralazine drip therapy for
BP control. Blood was sent for measurement of CN and serum
thiocyanate (SCN) levels (colorometric method). Later that same day,
the patient developed supraventricular tachycardia with a rapid
ventricular response. He also manifested increased ventricular
irritability and recurrent episodes of unsustained paroxysmal
ventricular tachycardia which were treated with IV lidocaine.
Because of labile hemodynamic status, the patient was maintained
on mechanical ventilation. Despite normal oxygenation and ventila-
tion, arterial pH level was 7.25 and lactic acid level
4.8 p.g/L. Electrolyte levels were within normal limits.
On the same evening, the patient developed an episode of
sustained ventricular tachycardia and severe hypotension. Car-
dioversion with 100 Hz was attempted but he developed cardiac
arrest. Despite full advanced cardiac life support including direct
cardiac massage, the patient did not respond and was pronounced
dead after 40 mm. Blood CN level obtained on the second
postoperative day was 516.8 p.g/L. SCN level was 16 mg/L. Autopsy
showed patent coronary grafts and functioning mitral valve. Brain
was essentially normal but edematous.
COMMENTS
From October 1984 to July 1985, 292 patients
underwent CABG surgery in our hospital. During this
period, seven patients were identified with SNP tox-
icity. All were admitted with acute myocardial infarc-
tion and unstable cardiovascular status, underwent
emergency cardiac catheterization, and later had
CABG surgery. Table 1 summarizes the clinical infor-
mation ofthese patients. All were over 60 years of age,
five had history of hypertension and four were heavy
smokers. All had extensive coronary artery disease and
required four or more coronary grafts. Three of them
required IABP for hemodynamic support before and
Table 1-Clinical Information ofPatients with SNP Toxicity
Patient
Age
(yrs) Sex
Admission
diagnosis
History of
hypertension
History
of
smoking
IABP
used
No.
of
CABG
Pump time
(mm)
. -
X-clamp Total Outcome
1 62 F AMI
COPD
No Yes Yes 4 50 85 Survived
2 72 F AM!
DM
Yes No No 4 35 70 Survived
3 71 M AM!
DM
Yes Yes Yes 5 45 110 Died
4 65 M AM!
Acute
Yes Yes Yes 4 81 128 Died
5 61 M
Mit. Reg.
Unstable
angina
Renalfailure
Yes No No 6 67 129 Survived
6 71 M Unstable Yes Yes No 4 39 79 Survived
7 58 M
angina
AM! Yes No No 4 88 114 Died
AM! = acute myocardial infarction; COPD chronic obstructive pulmonary disease; DM diabetis mellitus
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
ST =
*1 =
tIl =
UI! =
sinus tachycardia; NSR normal sinus rhythm; AF atrial fibrillation
Data obtained 30 minutes after starting SNP drip
Data obtained at the time SNP toxicity was suspected
Data obtained 12 hours after discontinuation and treatment of SNP toxicity
CHEST I 89 I 5 I MAY, 1986 665
after surgery. Table 2 summarizes the neurologic,
cardiac, and pulmonary status of the patients. Thirty
mm after starting SNP drip (period I) all patients were
responsive to verbal commands and were adequately
oxygenated. Blood pressure level was controlled and
cardiac indices ranged from 1.8 to 3.2 L�min x m2.
When SNP toxicity was suspected (period II), all
showed tachyphylaxis to SNP. Despite increase in SNP
dose, five patients were still hypertensive and had
elevated SVR. Breathing pattern was abnormal in all
patients. Five were tachypneic and one had Cheyne-
Stokes respiration. Because of hemodynamic instabil-
ity and/or hypoventilation, none of the patients was
successfully weaned from the ventilator. However,
PaO�/FIo2 ratio was above 250 in all patients, pointing
to adequate pulmonary function. During SNP infu-
sion, P�O2 was below 42 torn in all patients. Except for
one case, all patients had normal pH and base deficit
levels at all times. Tachyphylaxis to SNP developed in
all patients and was the first clue to SNP toxicity. When
SNP toxicity was suspected, SNP therapy was discon-
tinued and sodium thiosulfate was administered in all
patients. Discontinuation of SNP and treatment with
sodium thiosulfate (period III) improved the mental
status of four patients. Those who remained comatose
died later because ofhemodynamic, pulmonary and/or
renal complications. Three individuals had high serum
creatinine levels at initiation ofSNP infusion. Four had
high serum creatinine levels at period II of SNP
infusion. All patients had Hb levels below 10.3 g/dl
during SNP infusion. Also, serum albumin levels were
below 3.1 g/dl in all patients. Four patients had
abnormal serum glutamic-oxaloacetic transam inase
(SGOT) and all had high lactate dehydrogenase (LDH)
levels. During the three periods of SNP infusion all
patients were afebrile, their white blood cell counts
were within normal limits, and they showed no evi-
dence ofsepsis. Table 3 provides information regarding
SNP infusion and CN and SCN levels in seven patients
who developed SNP toxicity. All patients had toxic
levels ofCN. The SCN level was measured in five cases
and was within the accepted range in all of them.
DISCUSSION
Initial reports of toxicity associated with SNP infu-
sion were described when it was employed to induce
Table 2-Clinical and Laboratory Data ofPatients with SNP Toxicity
PaOd
Patient
Neurological
status
HR
(beats)nm) Rhythm
BP
(mm Hg)
Cl
(L/min M2)
SVR
(dynesec cm5)
RR
(breath/mm)
P�02
(mm Hg)
Fi02
ratio
(mm Hg)
Creat.
(mg/dl)
BUN
(mg/dl)
Base
deficit pH
Lactic
acid
(meq/L)
1 1* Alert 97 ST 136/74 2.5 1100 18 39 220 1.0 70 0.8 7.34 -
lit Comatose 101 ST 188/83 3.1 1880 28 41 210 1.9 69 5.6 7.44 1.1
IIII Alert 78 NSR 125/58 3.0 1120 24 40 215 1.6 76 1.6 7.41 1.2
2 I Alert 70 NSR 148/66 1.9 1836 20 30 210 0.9 19 0.3 7.42 -II Agitation, 102 ST 148/65 1.6 1984 32 34 215 0.9 32 4.0 7.44 1.5
hallucination
III Alert 98 ST 161/77 2.6 1684 22 33 220 1.0 41 2.5 7.49 1.3
3 I Awake 103 ST 114162 2.0 1590 0 43 220 1.9 18 2.7 7.38 -II Restless- 139 ST 154/69 2.8 1232 40 42 210 2.5 65 6.1 7.37 2.6
unresponsive
III Comatose 118 ST 110/48 4.1 701 0 39 220 3.5 92 2.9 7.38 1.5
4 I Awake 73 NSR 108/41 1.6 1104 18 35 210 2.2 29 4.3 7.47 -
II Restless- 116 ST 176/68 2.6 1430 38 32 200 1.7 39 7.4 7.25 4.8
unresponsive
III Response 79 NSR 128/61 2.3 771 #{149}28 29 240 1.5 32 3.1 7.46 1.4
to command
5 I Alert 77 NSR 150/100 2.6 1560 0 33 210 1.9 17 1.8 7.41 -
II Restless- 115 AF 170/106 2.1 1788 40 34 200 2.4 33 0.2 7.42 2.4
unresponsive
III Awake 79 NSR 160/99 2.8 1380 22 35 220 2.6 34 1.2 7.36 -
6 I Awake 86 NSR 155/69 3.1 1100 20 32 210 1.1 15 0.4 7.50 -
II Agitated- 102 ST 162/85 2.6 1010 38 34 220 0.9 17 0.6 7.39 -
confused
III Alert 89 NSR 144/76 3.2 1200 26 35 230 1. 1 20 1.3 7.45 -
7 I Unresponsive 92 ST 102/57 3.2 800 0 35 220 1.2 14 4.0 7.38 -
II Coma 98 ST 150/63 2.4 1400 36 34 210 1.4 15 +2.0 7.47 -
III Coma 87 NSR 108/53 3.1 1100 32 32 230 1.3 20 +7.0 7.52 -
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
Table 3-Nitroprusside Dose and Levels ofits Metabolites in Patients with SNP Toxicity
666 Sodium Nitroprusside after CABG Surgery (Pate! at a!)
SNP dose
(mg)
- Duration
Blood levels**�,- . .
/kg body of SNP Cyanide Thiocyanate
Patient Total weight drip (hrs) (�.&g/L) (mg/L)
1 721 12 80 800 -2 447 5.5 160 575 17
3 682 8.4 55 3660 19
4 157 2.2 30 517 16
5 431 6.1 74 555 24
6 126 1.8 26 546 -7 661.6 8.2 81 1600 21
*Normal ranges for our laboratory:
Thiocyanate, serum during SNP infusion, 6-29 mg/L; toxic range, >100 mg/L. Cyanide, blood during SNP infusion, 50-500 �.tg/L; toxic range =
>500 p.g/L.
hypotension during � Later, its long-term
use for treatment of acute hypertensive crisis, post-
operative hypertension, and finally as a vasodilator in
the treatment of cardiac failure was described.910
During long-term SNP therapy, two potential prob-
lems exist. First, the patient is exposed for prolonged
periods to increased concentration of CN. Second,
thiocyanate (SCN) accumulates in the extracellular
fluid and can produce toxic effects.” Despite high CN
levels, the level of SCN was not high in any of our
patients. Toxic effects such as psychosis, hypotension,
coma, and death are known to occur with a SCN
plasma concentration greater than 100 g/” The
symptoms and signs of CN poisoning described in the
literature are nonspecific and include nausea, vomit-
ing, restlessness, air hunger, tachypnea without cyano-
sis, irregular pulse, dry skin, partial paralysis, confu-
sion, convulsion, and somnulence. Since early states of
SNP toxicity are subclinical, attempts have been made
to measure blood CN and SCN levels for prevention of
toxicity. However, these measurements are not readily
available. Therefore, blood level measurement can be
used for treatment but not for prevention of toxicity.
Furthermore, M ichenfelden’� has questioned the
value of plasma CN levels because of the paucity of
information concerning the relationship between
blood and tissue CN levels and the fact that the high
affinity CN has for methemoglobin can cause a higher
level in blood than tissues. He suggests the use of
metabolic indicators of CN toxicity (ie, blood pH,
blood lactate, PVO�) for diagnosing CN toxicity. How-
ever, our observation suggests that metabolic indica-
tons are not sensitive enough to identify early CN
toxicity in critically ill patients. Despite toxic levels of
CN, our patients failed to show extraordinarily high P�
02. Only one patient showed significant metabolic
acidosis with a moderate blood lactate level.
Another suggested measure for prevention of SNP
toxicity is to limit the dose of SNP infusion. The safe
daily dose and maximum amount of SNP permitted
during long-term therapy is not well-substantiated.
Michenfelder and Tinker� have recommended 0.5 mg/
kg/h as the maximum dose of SNP for long-term
infusion in man. Vesey and Cole’3 recently studied 30
patients receiving SNP for 12 to 314 hours and sug-
gested that the maximum safe sustained dose rate for
long-term SNP infusion is near to 240 �g/kg/hr (5.8
mg/kg/day), and the maximum total dose of SNP is in
the region of7O mg/kg for a period ofless than 14 days.
Our patients developed SNP toxicity while receiving
doses well below that considered to be safe. This
suggests that post-CABG critically ill patients are
supensensitive to SNP infusion. The inability of post-
CABG patients to metabolize CN can be due to several
factors:
1) Nutritional status is an important determinant of
the thiosulfate pool. Thiosulfate is essential as a sulfur
donor for conversion of CN to TCN and as a substrate
for the isolation and purification of mitochondrial
rhondanase system.’4 In the post-CABG surgery pe-
nod, the state of semistarvation is present. In fact,
Ivankovitch et al5 have shown that during CABG
surgery, the plasma thiosulfate level is significantly
decreased and its excretion is increased in the immedi-
ate postoperative period.
2) Because of continuous exposure to cyanide,
smokers have lower plasma thiosulfate levels and
therefore can develop SNP toxicity with lower doses of
the � A large percentage of patients undergoing
CABG surgery are smokers’6 and therefore they may
be more susceptible to CN toxicity.
3) Thiosulfate sulfur transferase (rhodanase) cata-
lyzes the transfer ofa sulfur atom from a donor such as
thiosulfate to a nucleophilic acceptor such as CN, thus
transforming CN to SCN. The rhodanase system may
be compromised in critically ill patients and exhibit
limited ability for detoxification of CN to SCN.
4) The metabolism of CN to SCN also depends on
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
CHEST I 89 I 5 I MAY, 1986 667
vitamin B-i2, a rhodanase system cofactor.’7 Long-
term infusion ofSNP is shown to decrease vitamin B-i2
levels)8 Thus, low serum vitamin B-12 level in these
patients may increase the likelihood for development
of CN toxicity.
5) Serum albumin can carry sulfane sulfur in a form
highly available to, and reactive with, CN. In mam-
mals, the serum albumin-sulfane sulfur complex is
suggested to be the primary CN detoxification �
The low serum albumin which is usually seen after
CABG surgery may decrease the availability of this
buffer system and cause CN toxicity.
6) Abnormal hepatic and failing renal function is not
uncommon in critically ill patients. Detoxification and
excretion of CN may become impaired because of
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
patient’s ability to convert CN to SCN was hampered
by some or all the above-mentioned mechanisms.
Furthermore, the LD 50 for cyanide may have been
significantly lowered in these critically ill patients.
Experience with prophylaxis and treatment of CN
toxicity during SNP infusion in man is limited. Hy-
droxycobalmin (vitamin B-12) has been suggested as
being useful for prevention and treatment.Z1 However,
the issue is not settled and the proper dosage and its
possible toxic effects have not been established. Injec-
tion of thiosulfate constitutes a major antidote for CN
poisoning. The rationale is that the CN will be con-
vented to SCN, which is much less toxic and will be
excreted. It is free ofside effects, is not antagonistic to
the desired hemodynamic effects of SNP and can
prevent CN toxicity if infused concomitantly with
SNP.2’ All of our patients received sodium thiosulfate
(150 to 200 mg/kg) once high blood CN levels were
recognized. However, only four patients responded to
the treatment. Non-responders later died with multi-
organ failure. It is possible that several factors contnib-
uted to the deteriorating clinical picture of those
patients who did not respond. Therefore, cyanide
toxicity may be one of several contributing factors to
the deteriorating status of critically ill patients.
Our observation suggests that during long-term
therapy, recommended SNP doses which may be
tolerated by stable patients, may prove toxic in cniti-
cally ill patients. The fact that our post-CABG patients
developed toxicity on therapy with a wide range of
SNP doses suggests that reaction of these patients to
SNP therapy is unpredictable. Development of tachy-
phylaxis to SNP requiring increase of the SNP dose
should make the clinician suspicious of toxicity.
Despite the potential for toxicity and the lack of
knowledge regarding safe dosage regimens, physicians
prescribe this drug without proper monitoring. Until
more information is available, we recommend that in
critically ill post-CABG patients, the dose and dura-
tion of SNP infusion be minimized and an alternative
drug started as soon as possible.
REFERENCES
1 Bixler ‘fl, Gardner TJ, Donahoo JS, Brawley RK, Potter A, Gott
VL. Improved myocardial performance in postoperative cardiac
surgical patients with sodium nitroprusside. Ann Thorac Surg
1978; 25:444-48
2 Michenfelder JD, Tinker JH. Cyanide toxicity and thiosulfate
protection during chronic administration of sodium nitroprus-
side in the dog: correlation with a human case. Anesthesiology
1977; 47:441-48
3 Rieves RD: Importance of symptoms in recognizing nitro-
prusside toxicity. South Med J 1984; 77:1035-37
4 Rudy LW Jr, Heymann MA, Edmunds LH Jr. Distribution of
systemic blood flow during cardiopulmonary bypass. J Appl
Physiol 1973; 34:194-99
5 Ivankovitch AD, Braverman B, Stephens TS, Shulman M,
Heyman HJ. Sodium thiosulfate disposition in humans: relation
to sodium nitroprusside toxicity. Anesthesiology 1983; 53:11-17
6 Sarvotham SS, Patel C, Venus B, Mathru M. IV nitroglycerin vs
nitroprusside treatment of myocardial ischemia. Crit Care Med
1985; 13:212-13
7 McDowall DG, Keaney NP, Turner JM, Lane JR. Okuda Y. The
toxicity ofsodium nitroprusside. Br J Anaesth 1974; 46:327-32
8 Jack RD. Toxicity of sodium nitroprusside. Br J Anaesth 1974;
46:952
9 Mukherjee D, Feldman MS, Helfant R. Nitroprusside therapy.
Treatment of hypertensive patients with recurrent resting chest
pain, ST-segment elevation, and ventricular arrhythmias. JAMA
1976; 235:2406-09
10 Franciosa JA, Guiha NH, Limas CJ, Rodriguera E, Cohn JN.
Improved left ventricular function during nitroprusside infusion
in acute myocardial infarction. Lancet 1972; 1:650-54
1 1 Garvin CE The fatal toxic manifestations of the thiocyanates.
JAMA 1939; 112:1125-27
12 MichenfelderJD. Cyanide release from sodium nitroprusside in
the dog. Anesthesiology 1977; 46:196-201
13 Vesey CJ, Cole PV. Blood cyanide and thiocyanate concentrations
produced by long term therapy with sodium nitroprusside. Br JAnaesth 1985; 57:148-55
14 Sorbo BH. Crystalline rhodanese. I. Purification and phys-
icochemical examination. Acta Chem Scand 1953; 7:1129-36
15 Darby PW, Wilson J. Cyanide, smoking and tobacco amblyopia.
Br J Opththal 1967; 51:336-38
16 Braun SR, Birnbaum ML, Chopra PS. Pre- and postoperative
pulmonary function abnormalities in coronary artery revasculari-
zation surgery. Chest 1978; 73:316-20
17 Wokes F, Picard CW. The role ofvitamin B,2 in human nutrition.
Am J Clin Nutrit 1955; 3:383-90
18 Lipma J, Hesdorffer C, Costa FF, Roos CP, Edelman J, Plit M.
Vitamin B,, levels in the prolonged use ofsodium nitroprusside.
Crit Care Med 1984; 12:161-63
19 Vennesland B, Castric PA, Conn EE, Solomonson LP, Volini M,
Westley J. Cyanide metabolism. FABS Proc 1982; 41:2639-48
20 Braverman B, Ivankovich AD, Shah G. Thiosulfate pharmacoki-
netics in normal and anuric dogs. Proc Soc Exp Biol Med 1982;
170:273-80
21 Posner MA, Rodkey FL, Tobey RE. Nitroprusside-mnduced
cyanide poisoning: antidotal effect of hydroxocobalammn. Anes-
thesiology 1976; 44:330-35
22 Ivankovich AD, Braverman B, Klowden AJ, Heyman HJ. Preven-
tion of nitroprusside toxicity with thiosulfate in dogs. Anesth
Analg 1982; 61:120-26
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from
DOI 10.1378/chest.89.5.663 1986;89; 663-667Chest
C B Patel, V Laboy, B Venus, M Mathru and D Wierconservatism.
Use of sodium nitroprusside in post-coronary bypass surgery. A plea for
December 17, 2011This information is current as of
http://chestjournal.chestpubs.org/content/89/5/663Updated Information and services can be found at:
Updated Information & Services
http://www.chestpubs.org/site/misc/reprints.xhtmlonline at: Information about reproducing this article in parts (figures, tables) or in its entirety can be foundPermissions & Licensing
http://www.chestpubs.org/site/misc/reprints.xhtmlInformation about ordering reprints can be found online:
Reprints
the right of the online article.Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to
Citation Alerts
slide format. See any online figure for directions. articles can be downloaded for teaching purposes in PowerPointCHESTFigures that appear in Images in PowerPoint format
© 1986 American College of Chest Physicians by guest on December 17, 2011chestjournal.chestpubs.orgDownloaded from