Am J Crit Care 2002 Albright 326 30

7/27/2019 Am J Crit Care 2002 Albright 326 30

1/9

http://ajcc.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECTPersonal use only. For copyright permission information:Published online http://www.ajcconline.org 2002 American Association of Critical-Care Nurses

2002;11:326-330Am J Crit CareTracy N. Albright, Michael A. Zimmerman and Craig H. SelzmanVasopressin in the Cardiac Surgery Intensive Care Unit

http://ajcc.aacnjournals.org/subscriptions/Subscription Information

http://ajcc.aacnjournals.org/misc/ifora.xhtmlInformation for authors

http://www.editorialmanager.com/ajccSubmit a manuscript

http://ajcc.aacnjournals.org/subscriptions/etoc.xhtmlEmail alerts

by AACN. All rights reserved. 2002Copyright

Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049.bimonthly by The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.

journal of the American Association of Critical-Care Nurses (AACN), publishedAJCC, the American Journal of Critical Care, is the official peer-reviewed research

by guest on July 19, 2013ajcc.aacnjournals.orgDownloaded from
http://ajcc.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECThttp://ajcc.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECThttp://ajcc.aacnjournals.org/subscriptions/http://ajcc.aacnjournals.org/subscriptions/http://ajcc.aacnjournals.org/misc/ifora.xhtmlhttp://ajcc.aacnjournals.org/misc/ifora.xhtmlhttp://www.editorialmanager.com/ajcchttp://www.editorialmanager.com/ajcchttp://ajcc.aacnjournals.org/subscriptions/etoc.xhtmlhttp://ajcc.aacnjournals.org/subscriptions/etoc.xhtmlhttp://ajcc.aacnjournals.org/http://ajcc.aacnjournals.org/http://ajcc.aacnjournals.org/http://ajcc.aacnjournals.org/subscriptions/etoc.xhtmlhttp://www.editorialmanager.com/ajcchttp://ajcc.aacnjournals.org/misc/ifora.xhtmlhttp://ajcc.aacnjournals.org/subscriptions/http://ajcc.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT


2/9

Care of patients who have undergone cardiacsurgery is often complicated by profound

hypotension (mean arterial pressure [MAP]70 mm Hg). Often, shock after cardiotomy is associ-

ated with low cardiac output syndrome (also termedlow-output heart failure). These patients are best treated

with volume resuscitation, afterload reduction, andinotropic support. However, some patients remain

hypotensive because of systemic vasodilation. Recentclinical data suggest that a physiological deficiency in

326 AMERICAN JOURNAL OF CRITICAL CARE, July 2002, Volume 11, No. 4

Although nearly 10% of patients experience profound vasodilatory shock after cardiopulmonary bypass,

some patients remain refractory to traditional resuscitation. Among this subset are patients who have

inappropriately low levels of endogenous vasopressin. Thus, vasopressin replacement is an intuitively

attractive intervention. The purposes of this review are to outline the pathophysiology of vasodilatory

shock after cardiopulmonary bypass, to discuss the physiological role of endogenous vasopressin, to

explore the clinical basis for vasopressin replacement, and to review the pharmacology and dosing

guidelines. (American Journal of Critical Care. 2002;11:326-332)

VASOPRESSIN IN THE CARDIAC

SURGERY INTENSIVE CARE UNIT

To purchase reprints, contact The InnoVision Group, 101 Columbia, AlisoViejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax,(949) 362-2049; e-mail, [email protected].

By Tracy N. Albright,RN, CCRN,Michael A. Zimmerman,MD, and Craig H. Selzman,MD. From theCardiothoracic Surgery Service, Veterans Administration Medical Center and the Division ofCardiothoracic Surgery, University of Colorado Health Sciences Center, Denver, Colo.

levels of the hormone vasopressin, also known as

antidiuretic hormone, may be the cause of vasodilatory

shock after cardiotomy.1 Thus, vasopressin replacement

is an intuitively attractive therapy for hypotension that

occurs after cardiopulmonary bypass. In this review,

we outline the pathophysiology of vasodilatory

hypotension in postoperative cardiac surgery patients,

discuss the physiological role of endogenous vaso-pressin, explore the clinical basis for vasopressin

replacement as an adjunct therapy in vasodilatory

shock after cardiopulmonary bypass, and review phar-

macological and administration guidelines.

Pathophysiology of Vasodilatory ShockAfter Cardiopulmonary Bypass

Exposure of blood to abnormal surfaces and con-

ditions that exist during cardiopulmonary bypass ini-

tiates a systemic inflammatory response. Kirklin 2

describes a whole body inflammatory response

involving humoral amplification of the coagulationcascade, the kalikrein system, the fibrinolytic system,

and the complement cascade. It is hypothesized that

the deleterious effects of cardiopulmonary bypass are

related to the activation of these proinflammatory

pathways. Adverse effects of bypass include pul-

monary insufficiency, extracellular accumulation of

fluid (third spacing), renal dysfunction, hyperthermia,

coagulopathy, and vasomotor dysfunction.3

CE

Notice to CE enrollees:A closed-book, multiple-choice examinationfollowing this article tests your understandingof the following objectives:

Describe the pathophysiology of vasodilatoryshock following cardiopulmonary bypass

Recognize traditional treatment modalitiesutilized for low cardiac output syndromefollowing cardiopulmonary bypass

Understand the role of vasopressin in thetreatment of refractive vasodilatory shockafter cardiopulmonary bypass, includingdosage and administration guidelines

CE

http://ajcc.aacnjournals.org/http://ajcc.aacnjournals.org/http://ajcc.aacnjournals.org/


3/9

AMERICAN JOURNAL OF CRITICAL CARE, July 2002, Volume 11, No. 4 327

In a recent study, Argenziano et al4 found thatnearly 10% of cardiac surgery patients experience

vasodilatory hypotension after bypass that is not associ-ated with primary cardiogenic shock or sepsis.

Vasodilatory shock is a central component in the sys-temic inflammatory response.5 The hallmarks of

vasodilatory shock include decreased MAP, organ

hypoperfusion, and lactic acidosis.6

A substantialdecrease in systemic vascular resistance (SVR) leads toa generalized maldistribution of blood flow and ulti-

mately to end-stage organ failure.7 Interestingly, ininstances of prolonged hypotension after bypass, vascu-

lar smooth muscle becomes poorly responsive to circu-lating catecholamines. This decreased response may be

due to the down-regulation of adrenergic receptors.5,8

Physiological Role ofEndogenous Vasopressin

Vasopressin, also termed antidiuretic hormone or

arginine vasopressin, is a peptide hormone produced inthe hypothalamus and stored in the posterior lobe of

the pituitary gland. Vasopressin affects numerousorgan systems, including the brain, where it acts as a

neurotransmitter mediating thermoregulation, nocicep-tion, and release of adrenocorticotropic hormone.9,10 In

the pulmonary vasculature, moderate doses of vaso-pressin cause vasodilatation, whereas higher doses

stimulate vasoconstriction.11 Vasopressin also has sev-eral effects on thrombosis and hemostasis, including

promotion of platelet aggregation and release of bothfactor VIIIa and von Willebrand factor from the vascu-

lar endothelium.12,13 In the distal tubule and collecting

duct of the kidney, vasopressin stimulates waterresorption so that concentrated urine is produced.14

High concentrations of vasopressin stimulate smooth

muscle contraction in both the uterus and the gastroin-testinal tract and promote hepatic glycogenolysis.15,16

High concentrations of vasopressin also have a pro-found effect on vascular smooth muscle cells, resulting

in vasoconstriction.17

Crucial in the regulation of fluid balance, vaso-

pressin is released in response to a decrease in bloodvolume or an increase in osmolarity.5 The principal end-

organ effects are mediated by 2 distinct receptor sub-

types. The V1 receptor is present on vascular smoothmuscle cells throughout the body, particularly in skin,skeletal muscle, and thyroid gland vasculature.18 The

direct vasopressor effects are a result of V1-mediated

intracellular signal transduction. G protein-coupled

activation of phospholipase C results in the release ofcalcium from the sarcoplasmic reticulum and a subse-

quent increase in peripheral resistance.17 Of note, themajority of end-organ effects are mediated by the V

1

receptor. A second receptor, the V2 receptor, is presentin the distal and collecting tubules of the glomeruli

and promotes water resorption. These effects aremediated by an increase in intracellular levels of

cyclic adenosine monophosphate and ultimately byactivation of protein kinase A.14 By increasing water

channel-containing vesicles to the apical membrane,

protein kinase A increases membrane permeability andeventually extracellular fluid volume.19 A third recep-tor, the V

3receptor, is localized in the posterior lobe of

the pituitary gland. Although signal transductioninvolves both activation of G proteins and increases in

the levels of cyclic adenosine monophosphate, itsphysiological role is unknown.11

Under normal physiological conditions, concen-trations of endogenous vasopressin are below the

vasoactive range. Although low-dose exogenous vaso-pressin has little pressor effect in subjects with normal

hemodynamic status, high-dose vasopressin replace-ment markedly increases MAP when the cardiac

baroreflex is impaired, as occurs in septic shock orautonomic insufficiency.20 High-dose vasopressin

directly stimulates contraction of vascular smoothmuscle, causing vasoconstriction of capillaries and

small arterioles. When antidiuresis is advantageous, asin diabetes insipidus, exogenous vasopressin can lead

to conservation of up to 90% of the water that mightotherwise be excreted in the urine. Importantly, the

doses used for antidiuresis are markedly lower thanthose needed for pressor support. Antidiuresis can be

accomplished with single doses of 5 to 10 U, whereas

the vasoconstrictive effects require up to 0.5 U every 5minutes by continuous intravenous infusion.

Clinical Basis for Vasopressin ReplacementRecently, Landry et al20 made an interesting obser-

vation in patients with sepsis. These investigators

found that plasma vasopressin levels were inappropri-ately low in patients with refractory hypotension. In

that study, exogenous vasopressin replacementmarkedly increased arterial pressure (systolic/dias-

tolic) and SVR. Landry et al concluded that when pre-treatment levels are inappropriately low, a vasopressin

deficiency may contribute to refractory hypotension in

septic shock.Argenziano et al1 randomized 10 patients who met

eligibility requirements for a diagnosis of shock after

cardiopulmonary bypass: an MAP of 70 mm Hg orless despite norepinephrine infusion in excess of 8

g/min and a cardiac index (calculated as cardiac out-put in liters per minute divided by body surface area

in square meters) of 2.5 with a left ventricular assistdevice (LVAD) in place. Patients were randomized 5



4/9


minutes after cardiopulmonary bypass was discontin-

ued to receive either vasopressin at 0.1 U/min (n=5) or

a placebo of isotonic sodium chloride solution (n= 5).

Additionally, plasma samples were taken at the time of

randomization to measure the level of endogenous

vasopressin. After 15 minutes, subjects receiving the

placebo had no significant change in arterial pressure,

SVR, or catecholamine dose. Three subjects who ini-tially received placebo were subsequently treated with

vasopressin. In the 8 patients who received vaso-

pressin, MAP increased from 61.3 to 87.4 mm Hg,

and SVR increased from 845 to 1284 dyne sec cm-5.

All patients given vasopressin were successfully

weaned off catecholamines. Of the 8 subjects who

received vasopressin therapy, 5 had endogenous levels

of vasopressin less than 20 pg/mL, far less than the

expected range for after cardiopulmonary bypass

(100-200 pg/mL). No vasopressin-related complica-

tions were reported.

Chart review at Columbia-Presbyterian MedicalCenter in New York yielded 50 patients undergoing

LVAD placement who had had vasopressin adminis-

tered in the operating room or the intensive care unit

within 24 hours of implantation.6 All patients had an

MAP less than 60 mm Hg and a depressed SVR

despite catecholamine support. Administration of

vasopressin at a rate of 0.09 U/min increased MAP

from 58 to 75 mm Hg, increased SVR from 920 to

1200 dyne sec cm-5, and decreased norepinephrine

administration by 32%. No change in LVAD flow was

noted, and no complications were reported.

In a more recent study, Argenziano et al21 exam-ined use of vasopressin in the management of

vasodilatory hypotension after orthotopic heart trans-

plantation. Of 175 patients who underwent orthotopic

heart transplantation, 20 met the criteria for hypoten-

sion after cardiopulmonary bypass. Infusion of vaso-

pressin at a rate of 0.1 U/min significantly increased

MAP (from 60 to 86 mm Hg) and decreased nore-

pinephrine requirements. No complications were

linked to vasopressin therapy directly, although 1

patient died on postoperative day 21 of hemorrhagic

shock and multiple organ failure.

Finally, in a third study, Argenziano et al 4

prospectively studied several preoperative variables

in a group of 145 patients that included both patients

undergoing orthotopic heart transplantation and

patients having an LVAD implanted. The authors

noted that low ejection fraction and preoperative use

of an ACE inhibitor were independent risk factors

for hypotension after cardiopulmonary bypass. They

also found that vasodilatory shock after bypass was

associated with inappropriately low serum concentra-tions of vasopressin (12.0 pg/mL). Retrospectively,

40 of the 145 patients met the standard criteria for

vasodilatory shock. Patients treated with low-dosevasopressin infusions (0.1 U/min) had a significant

increase in MAP and a decrease in norepinephrinerequirements. Similar findings in children have been

reported.22

Clinical PerspectivesCollectively, clinical evidence suggests that vaso-

pressin therapy may be a valuable alternative or adjunct

for patients with refractory vasodilatory shock after car-diopulmonary bypass. However, these data must be

interpreted cautiously. Large, randomized, double-blind

trials that compare vasopressin with catecholamineshave yet to be done. Central to the issue of refractory

hypotension after cardiopulmonary bypass is the con-cept of vasopressin deficiency. Vasopressin levels in

healthy hydrated humans are normally less than4 pg/mL,23 whereas water deprivation stimulates an

increase to about 10 pg/mL.24 Plasma levels of vaso-

pressin in patients after bypass are in the range of 100 to200 pg/mL, whereas hemorrhagic shock promotes levels

as high as 1000 pg/mL.25-27 Several investigators reportedinappropriately low vasopressin levels in different popu-

lations of patients. Although this deficiency was initially

described in patients with septic shock, similar indices(


5/9


vasoconstrictor (Table 1). Interestingly, in outliningthe new Advanced Cardiac Life Support standards, the

American Heart Association adopted vasopressin asits first-line drug in the treatment of ventricular tachy-

cardia/fibrillation refractory to initial defibrillation.With its use in advanced life support and in vasodila-

tory shock, vasopressin is gaining popularity for use

in treating critically ill patients. Critical care nursesmust gain a basic understanding of the pharmacologyof vasopressin and its clinical indications.

Pharmacokinetics

Vasopressin is distributed throughout the extracel-lular space. With a half-life of 10 to 35 minutes, the

pressor effects after a single dose last about 30 to 60minutes.28 When the goal is to maintain continuous

hemodynamic support, vasopressin must be given by

continuous intravenous infusion. Vasopressin is inacti-vated and metabolized by the kidney and liver; 5% to

15% is excreted in the urine.29

Compatibility, Dosing, and Current Indications

Approved uses for vasopressin by either intra-

venous or intramuscular injection include diabetesinsipidus, abdominal distention, gastrointestinal

bleeding, and refractory ventricular f ibri llat ion.Desmopressin is a synthetic, longer-acting analog of

vasopressin. It has minimal vasopressor activity with

an antidiuretic-to-vasopressor ratio 4000 times that ofvasopressin.30 Clinically, desmopressin is used to treat

nocturnal enuresis, hemophilia A, and von Willebranddisease. Furthermore, it is useful for treating bleeding

due to platelet dysfunction associated with uremia andcardiopulmonary bypass. These hemostatic effects are

related to increased release of von Willebrand factor

from vascular endothelial cells, thus promoting moreeffective platelet adhesion.12

Vasopressin can be diluted to a concentration of

100 to 1000 U/L in 5% dextrose in water or isotonicsodium chloride solution.31 The normal infusion

mixture is 100 U per 250 mL. Infusion with vaso-pressin is often used as adjunctive therapy to treat-

ment with catecholamines and phosphodiesterase

inhibitors. No incompatibilities have been reported,and these drugs can conveniently be infused through

the same central catheter.Because treatment of vasodilatory shock is current-

ly not an approved use of vasopressin, dosing guidelinesfor such use have not been firmly established. Research

to date indicates that a dosing range of 0.01 up to 0.1U/min is most effective in patients with vasodilatory

shock without causing any adverse effects. Patients inthe studies reported here received a continuous infusion

for up to 24 hours. Vasopressin results in a decrease insplanchnic blood flow and has been used to treat gas-

trointestinal bleeding. Continuous infusion to treatvariceal bleeding and other types of upper gastrointesti-

nal hemorrhage, which are uses approved by the Foodand Drug Administration, start at a rate of 0.2 U/min

and may be increased each hour by 0.2 U/min. The opti-

mal upper limit dose is 1 U/min, but up to 2 U/min maybe tolerated. Infusion continues up to 12 hours afterbleeding is controlled. The dosage is then cut in half for

an additional 12 to 24 hours before cessation.32

By comparison, doses used to treat variceal bleeding (up

to 2 U/min) are much higher than the doses used to treathypotension that occurs after cardiopulmonary bypass.

Conversely, doses used to treat vasodilatory shock aremarkedly higher (up to 0.1 U/min) than those used for

other conditions. For example, primary nocturnal enure-sis requires only 20 g given intranasally. Similarly,

hemophilia A and von Willebrand disease require only

300 g per dose.

Precautions and Contraindications

While ongoing investigation continues to charac-terize the appropriate dosing regimen for patients who

have had cardiothoracic surgery, caution must be usedwhen administering this drug. Contraindications

include anaphylaxis or hypersensitivity to vasopressinand chronic nephritis with nitrogen retention. Because

Table 1 Clinical indications for vasopressin

Indication

VasopressinDiabetes insipidus

Abdominal distentionProvocative testing

(growth hormoneand corticotropinrelease)

Gastrointestinalbleeding

Vasodilatory shock

after cardio-pulmonary bypass

Refractory cardiacarrest

DesmopressinPlatelet dysfunctionNocturnal enuresis

Hemophilia A, vonWillebrand disease

DosageRoute of

administration

5-10 U

5-10 U10 U

0.2-0.9 U/min

0.01-0.1 U/min

40 U

0.3 g/kg20 g0.2 g300 g0.3 g/kg

Intramuscular orsubcutaneous

IntramuscularIntramuscular

Intravenous(continuous)

Intravenous

(continuous)

Intravenous

IntravenousIntranasalOralIntranasalIntravenous



6/9


of the antidiuretic effect of vasopressin, patients withheart failure, asthma, epilepsy, and migraine must be

followed up closely. The most serious adverse effectsinclude myocardial ischemia and ventricular dys-

rhythmias (Table 2). Vasopressin should be infusedthrough a central catheter because peripheral

extravasation could cause tissue necrosis and gan-

grene. Although the doses of vasopressin currentlybeing used are not suff icient to have deleteriouseffects on a fetus, vasopressin should be used in

pregnancy only when clearly indicated.29

SummaryAlthough approximately 10% of patients undergo-

ing cardiopulmonary bypass have profound vasodila-tory hypotension, a subset of these patients is

refractory to traditional therapies of fluid replacementand administration of catecholamine vasopressors.

This lack of response may be due in part to anendogenous vasopressin deficiency related to deple-

tion in patients with chronic heart failure.

Alternatively, baroreflex-mediated secretion may beimpaired. Clinical studies to date suggest that an infu-sion of vasopressin at a rate of 0.01 to 0.1 U/min sig-

nificantly improves MAP and SVR without toxiceffects. Because additional research must be done

before vasopressin administration can be safely rec-ommended in patients with vasodilatory shock after

cardiopulmonary bypass, patients undergoing treat-ment must be closely followed up and monitored for

potential adverse effects. Familiarity with the physiol-ogy of endogenous vasopressin and the pharmacology

of replacement therapy will help critical care

providers meet this challenge.

REFERENCES

1. Argenziano M, Choudhri AF, Oz MC, Rose EA, Smith CR, Landry DW. A

prospective randomized trial of arginine vasopressin in the treatment of

vasodilatory shock after left ventricular assist device placement.

Circulation. 1997;96(9 suppl):II-286-II-290.

2. Kirklin JK. Prospects for understanding and eliminating the deleterious

effects of cardiopulmonary bypass.Ann Thorac Surg. 1991;51:529-531.

3. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Chenoweth DE,

Pacifico AD. Complement and the damaging effects of cardiopulmonary

bypass.J Thorac Cardiovasc Surg. 1983;86:845-857.

4. Argenziano M, Chen JM, Choudhri AF, et al. Management of vasodilatory

shock after cardiac surgery: identification of predisposing factors and use

of a novel pressor agent.J Thorac Cardiovasc Surg. 1998;116:973-980.

5. Rozenfeld V, Cheng JW. The role of vasopressin in the treatment of

vasodilation in shock states.Ann Pharmacother. 2000;34:250-254.

6. Morales DL, Gregg D, Helman DN, et al. Arginine vasopressin in the treat-

ment of 50 patients with postcardiotomy vasodilatory shock. Ann Thorac

Surg. 2000;69:102-106.

7. Parrillo JE, Parker MM, Natanson C, et al. Septic shock in humans:

advances in the understanding of pathogenesis, cardiovascular dysfunction,

and therapy.Ann Intern Med. 1990;113:227-242.

8. Chernow B, Roth BL. Pharmacologic manipulation of the peripheral vas-

culature in shock: clinical and experimental approaches. Circ Shock.

1986;18:141-155.

9. Doris PA. Vasopressin and central integrative processes.

Neuroendocrinology. 1984;38:75-85.

10. Pittman QJ, Wilkinson MF. Central arginine vasopressin and endogenous

antipyresis. Can J Physiol Pharmacol. 1992;70:786-790.

11. Eichinger MR, Walker BR. Enhanced pulmonary arterial dilation to argi-

nine vasopressin in chronically hypoxic rats. Am J Ph ys io l.

1994;267:H2413-H2419.

12. Bichet DG, Razi M, Lonergan M, et al. Hemodynamic and coagulation

responses to 1-desamino[8-d-arginine] vasopressin in patients with con-

genital nephrogenic diabetes insipidus.N Engl J Med. 1988;318:881-887.

13. Mannucci PM, Canciani MT, Rota L, Donovan BS. Response of factor

VIII/von Willebrand factor to DDAVP in healthy subjects and patientswith hemophilia A and von Willebrands disease. Br J Haematol .

1981;47:283-293.

14. Snyder HM, Noland TD, Breyer MD. cAMP-dependent protein kinase

mediates hydrosmotic effect of vasopressin in collecting duct. Am J

Physiol. 1992;263:C147-C153.

15. Inaba K, Umeda Y, Yamane Y, Urakami M, Inada M. Characterization of

human platelet vasopressin receptor and the relation between vasopressin-

induced platelet aggregation and vasopressin binding to platelets. Clin

Endocrinol (Oxf). 1988;29:377-386.

16. Keppens S, de Wulf H. The activation of liver glycogen phosphorylase by

vasopressin.FEBS Lett. 1975;51:29-32.

17. Thibonnier M, Bayer AL, Leng Z. Cytoplasmic and nuclear signaling path-

ways of V1-vascular vasopressin receptors.Regul Pept. 1993;45:79-84.

18. Laszlo FA, Laszlo F Jr, De Wied D. Pharmacology and clinical perspec-

tives of vasopressin antagonists.Pharmacol Rev. 1991;43:73-108.

19. Knepper MA, Nielsen S. Kinetic model of water and urea permeability regu-

lation by vasopressin in collecting duct.Am J Physiol. 1993;265:F214-224.

20. Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency con-

tributes to the vasodilation of septic shock. Circulation. 1997;95:1122-1125.

21. Argenziano M, Chen JM, Cullinane S, et al. Arginine vasopressin in the

management of vasodilatory hypotension after cardiac transplantation. J

Heart Lung Transplant. 1999;18:814-817.

22. Rosenzweig EB, Starc TJ, Chen JM, et al. Intravenous arginine-vaso-

pressin in chil dren wi th vasodi la tory shock af ter card iac surgery.

Circulation. 1999;100:II182-II186.

23. Cowley AW, Cushman WC, Quillen EW, Skelton MM, Langford HG.

Vasopressin elevation in essential hypertension and increased responsive-

ness to sodium intake.Hypertension. 1981;3:I93-I100.

24. Morton JJ, Padfield PL, Forsling ML. A radioimmunoassay for plasma

arginine-vasopressin in man and dog: application to physiological and

pathological states.J Endocrinol. 1975;65:411-424.

25. Wu W, Zbuzek VK, Bellevue C. Vasopressin release during cardiac opera-

tion.J Thorac Cardiovasc Surg. 1980;79:83-90.

26. Levine FH, Philbin DM, Kono K, et al. Plasma vasopressin levels and uri-

nary sodium excretion during cardiopulmonary bypass with and withoutpulsatile flow.Ann Thorac Surg. 1981;32:63-67.

27. Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin

relevant to management of septic shock. Chest. 2001;120:989-1002.

28. Stump DL, Hardin TC. The use of vasopressin in the treatment of upper

gastrointestinal haemorrhage.Drugs. 1990;39:38-53.

29. Arky R, ed. Physicians Desk Reference. 53rd ed. Montvale, NJ: Medical

Economics Co; 1999:2776-2778.

30. Key DW, Bloom DA, Sanvordenker J. Low-dose DDAVP in nocturnal

enuresis. Clin Pediatr (Phila). 1992;31:299-301.

31. Trissel LA, ed. Handbook of Injec table Drugs . 6th ed. Bethesda, Md:

American Society of Hospital Pharmacists; 1990.

32. Rice TL. Treatment of esophageal varices. Clin Pharm. 1989;8:122-131.

Table 2 Possible adverse effects of therapeutic vasopressin

Decreased cardiac outputAnginaMyocardial ischemiaVentricular dysrhythmiaBronchial constrictionTremor

Facial pallor

VertigoMetabolic acidosisAbdominal crampsNausea/vomitingGastric infarctionWater intoxication



7/9


To receive CE credit for this test (ID# A021104), mark your answers on the form below, complete theenrollment information, and submit it with the $12 processing fee (payable in US funds) to American

Association of Critical-Care Nurses (AACN). Answer forms must be postmarked by July 1, 2004. Within 3to 4 weeks of AACN receiving your test form, you will receive an AACN CE certificate.

This continuing education program is provided by AACN, which is accredited as a provider of continuing education in nursing by the AmericanNurses Credentialing Centers Commission on Accreditation. AACN has been approved as a provider of continuing education by the State Boardsof Nursing of Alabama (#ABNP0062), California (01036), Florida (#FBN2464), Iowa (#332), Louisiana (#ABN12), Nevada, and Colorado. AACNprogramming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

1. a 2. a 3. a 4. a 5. a 6. a 7. a 8. a 9. a 10. a 11. a 12. a 13. a 14. a 15. a

b b b b b b b b b b b b b b b

c c c c c c c c c c c c c c c

d d d d d d d d d d d d d d d

Program evaluation

Agree Neutral Disagree

Objective 1 was met

Objective 2 was met

Objective 3 was met

The content was appropriate

My expectations were met

This method of CE is effective

for this content

The level of difficulty of this test was:

easy medium difficult

To complete this program, it took me

hours/minutes.

Mail this entire page to: AACN, 101 Columbia, Aliso Viejo, CA 92656, (800) 899-2226

Name

Address

City State ZIP

E-mail address

AACN member number

I would like to receive my certificate via e-mail (check box)

CE Test Instructions

CE

CE Test FormVasopressin in the Cardiac Surgery Intensive Care UnitObjectives

1. Describe the pathophysiology of vasodilatory shock following cardiopulmonary bypass

2. Recognize traditional treatment modalities utilized for low cardiac output syndrome following cardiopulmonary bypass

3. Understand the role of vasopressin in the treatment of refractive vasodilatory shock after cardiopulmonary bypass, including dosage and

administration guidelines

Mark your answers clearly in the appropriate box. There is only one correct answer. You may photocopy this form.

ID#: A021104

Form expires: July 1, 2004Contact hours: 2.0

Passing score: 7 correct (70%)Test writer: Kim Brown, RN, MSN, CS-FNP, CEN

Category: ATest Fee: $12

AMERICANJOURNAL OFCRITICALCARE



8/9


6. Where is the hormone vasopressin endogenouslyproduced?a. Hypothalamus

b. Posterior pituitaryc. Anterior pituitaryd. Parathyroid

7. Which of the following is an indication for the use ofvasopressin in addition to the treatment of vasodilatoryshock?a. Diabetes mellitusb. Gastrointestinal bleedingc. Acute cerebral vascular accidentd. Acute tubular necrosis

8. Which of the following best describes dosing

recommendations given by the authors for the use ofvasopressin in vasodilatory shock?a. 0.2 to 0.9 U/min continuous IV infusionb. 20 micrograms intranasallyc. 0.01 to 0.1 U/min continuous IV infusiond. 5 to 10 U intramuscularly

9. Which of the following is notan adverse effect ofvasopressin administration?a. Decreased cardiac outputb. Metabolic alkalosisc. Myocardial ischemiad. Cardiac arrhythmias

10. Which of the following statements is true regardingvasopressin?a. Its half-life is 45 to 60 minutesb. It is metabolized by the kidneys and liverc. 50% is excreted in the urined. Normal infusion mixture is 100 to 200 U/L

1. Which of the following are notutilized in the initialtreatment of low cardiac output syndrome followingcardiac surgery?

a. Afterload reductionb. Inotropic supportc. Beta blockaded. Volume resuscitation

2. A deficiency of which of the following hormones maybe present in vasodilatory shock after cardiotomy?a. Antidiuretic hormoneb. Thyroid stimulating hormonec. Vasopressind. Both a and c

3. During cardiopulmonary bypass, which of the followingphysiologic responses is initiated?a. Systemic inflammatory responseb. Humoral amplification of the coagulation cascadec. Humoral amplification of the complement cascaded. All of the above

4. Which of the following is notan adverse effect ofcardiopulmonary bypass?a. Extracellular accumulation offluidb. Renal dysfunctionc. Hepatocellular dysfunctiond. Hyperthermia

5. Which of the following is a hallmark of vasodilatoryshock?a. Organ hypoperfusionb. Decreased mean arterial pressurec. Decreased systemic vascular resistanced. All of the above

CE Test QuestionsVasopressin in the Cardiac Surgery Intensive Care Unit



9/9

AMERICAN JOURNAL OF CRITICAL CARE,November 2002, Volume 11, No. 6 503

CORRECTIONS

In the article titled Celebrating the 100th

Birthday of the Electrocardiogram: LessonsLearned From Research in Cardiac Monitoring

(July 2002;11:378-386), on page 382, 2nd col-umn, 3rd paragraph, 10th line, it reads, Of inter-

est, ST-segment elevation is present in lead aVR

with less elevation than in V1. . . . The wordthan was inadvertently added during our internal

editorial process and should be deleted because itimparts just the opposite meaning than the author

intended. The criterion that has been recentlydescribed in the literature to indicate a left main

coronary artery stenosis is as follows: If, duringa transient myocardial ischemic event involving

ST-segment depression, there is ST-segment ele-vation in lead aVR that is greater than the ST-

segment elevation normally seen in lead V1, aleft main coronary artery stenosis is likely. This

criterion is illustrated in the electrocardiogramshown in Figure 4B (p384).

In Figure 4 (p384) of this article, the last twosentences of the legend belong in the Figure 3

legend. These sentences describe how the STtrend is displayed, with time represented on the x

axis, and millimeters of ST-segment deviation onthe y axis.

In the article titled Vasopressin in the CardiacSurgery Intensive Care Unit (July 2002;11:326-

332), on page 327, 2nd column, last sentence ofthe first true paragraph, the wrong dosing regi-

men is given. The sentence should read as fol-lows: Antidiuresis can be accomplished with

single doses of 5 to 10 U, whereas the vasocon-strictive effects require up to 0.5 U every 5 min-

utes. Additionally, Table 1 (p329) incorrectly lists

the continuous infusion rate for vasodilatory shockafter cardiopulmonary bypass as 0.01 to 1.0

U/min. This should be 0.01 to 0.1 U/min. In thecontinuing education test (p332) for this article,

choice C in question 8 should read as follows: 0.01to 0.1 U/min continuous IV infusion.

b J l 19 2013j j lD l d d f

Documents

Am J Crit Care 2002 Albright 326 30