use of sodium nitroprusside in post coronary bypass surgery

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

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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



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



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 -



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



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.

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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

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