(Circulation. 1997;95:1122-1125.)
© 1997 American Heart Association, Inc.
Articles |
Vasopressin Deficiency Contributes to the Vasodilation of Septic Shock
the Departments of Medicine (D.W.L., H.R.L., E.M.G., S.S., J.A.O.) and Surgery (D.D., M.C.O.), Columbia University, College of Physicians & Surgeons, New York, NY, and the Department of Surgery (R.C.A.), Allegheny General Hospital, Pittsburgh, Pa.
Correspondence to Donald W. Landry, MD, PhD, Columbia University, Department of Medicine, 630 W 168th St, New York, NY 10032.
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Abstract |
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Background The hypotension of septic shock is due to systemic vasodilation. On the basis of a clinical observation, we investigated the possibility that a deficiency in vasopressin contributes to the vasodilation of septic shock.
Methods and Results In 19 patients with vasodilatory septic shock (systolic arterial pressure [SAP] of 92±2 mm Hg [mean±SE], cardiac output [CO] of 6.8±0.7 L/min) who were receiving catecholamines, plasma vasopressin averaged 3.1±1.0 pg/mL. In 12 patients with cardiogenic shock (SAP, 99±7 mm Hg; CO, 3.5±0.9 L/min) who were also receiving catecholamines, it averaged 22.7±2.2 pg/mL (P<.001). A constant infusion of exogenous vasopressin to 2 patients with septic shock resulted in the expected plasma concentration, indicating that catabolism of vasopressin is not increased in this condition. Although vasopressin is a weak pressor in normal subjects, its administration at 0.04 U/min to 10 patients with septic shock who were receiving catecholamines increased arterial pressure (systolic/diastolic) from 92/52 to 146/66 mm Hg (P<.001/P<.05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187 dyne·s/cm5; P<.001). Furthermore, in 6 patients with septic shock who were receiving vasopressin as the sole pressor, vasopressin withdrawal resulted in hypotension (SAP, 83±3 mm Hg), and vasopressin administration at 0.01 U/min, which resulted in a plasma concentration (
30 pg/mL) expected for the level of hypotension, increased SAP from 83 to 115 mm Hg (P<.01).
Conclusions Vasopressin plasma levels are inappropriately low in vasodilatory shock, most likely because of impaired baroreflex-mediated secretion. The deficiency in vasopressin contributes to the hypotension of vasodilatory septic shock.
Key Words: shock • hypotension • vasodilation
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Introduction |
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Endotoxic shock is a syndrome of cardiovascular collapse and multiple organ failure in response to bacterial products.1 The central characteristic of septic shock is systemic vasodilation, the cause of which is multifactorial in view of the fact that abnormalities in vasoconstrictor and vasodilator mechanisms have been reported. Of the latter, Kilbourn et al2 found increased nitric oxide synthesis, and we3 found activation of the vascular smooth muscle K+ATP channel.
Abnormalities in vasoconstrictor mechanisms have been less well examined, but vascular smooth muscle is poorly responsive to norepinephrine in septic shock.4 5 In contrast, the renin-angiotensin system appears to be appropriately activated, and its inhibition worsens the hypotension of sepsis.6 Plasma endothelin is also elevated in septic shock, but the meaning of this observation is yet to be defined.7
Vasopressin does not play a significant role in the control of vascular smooth muscle in normal conditions8 9 10 11 12 13 but becomes critical when blood pressure is threatened.11 12 13 Vasopressin is markedly increased in animal models of acute sepsis,14 15 16 but we recently found that some patients in advanced vasodilatory septic shock are exquisitely sensitive to the pressor action of exogenous hormone (D.W.L., unpublished observation, 1994). This unexpected finding raised the possibility that endogenous plasma vasopressin is inappropriately low in these patients. Thus, we examined the hypothesis that vasopressin deficiency could contribute to the vasodilation of septic shock in humans.
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Methods |
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Subjects were patients admitted to the intensive care units of Columbia-Presbyterian Medical Center and Allegheny Hospital. Patients were not eligible if they were younger than 18 years of age or if pregnancy was suspected, and they did not receive vasopressin if active coronary artery disease or mesenteric ischemia was present. Attending physicians identified candidate subjects, and consecutive patients meeting the entry criteria as stated below were studied. Appropriate consent was obtained, and the study protocol was approved by the institutional review board.
Septic shock was diagnosed by established criteria17 : hypotension (systolic blood pressure 
90 mm Hg in the absence of antihypertensive agents) and low systemic vascular resistance (<800 dyne·s/cm5) before the administration of catecholamines; fever or hypothermia (temperature >101°F or <97°F); tachycardia (heart rate >90 beats/min); tachypnea (respiratory rate >20 breaths/min or the requirement of mechanical ventilation) and either a positive blood culture (63% of patients in the "Septic Shock" column of Table 1, 80
80% of patients in Table 2) or an obvious source of infection (white blood cell count >12 000/mm3 or <4000/mm3 or >10% immature [band] forms); and elevated prothrombin or partial thromboplastin time or reduction of the platelet count to less than half the baseline or <100 000 platelets/mm3.
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In all septic patients, hypotension persisted after fluid administration (pulmonary capillary wedge pressure 
12 mm Hg) and required administration of catecholamines (norepinephrine, epinephrine, dopamine, and/or neosynephrine) to maintain systolic blood pressure >90 mm Hg for 1 to 2 days. Arterial pressure was measured by transduction through an indwelling catheter and cardiac output by the thermodilution technique using a Swan-Ganz catheter in the pulmonary artery.
Cardiogenic shock was diagnosed by a systolic arterial pressure 90 mm Hg, pulmonary capillary wedge pressure >15 mm Hg, and cardiac index of 2 L/min before catecholamine administration18 ; patients with fever, hypothermia, or an obvious source of infection were excluded. All patients required catecholamines to maintain systolic blood pressure >90 mm Hg.
Plasma vasopressin was measured by radioimmunoassay using published protocols.19 For this assay, the reference range (95%) for hemodynamically normal subjects is <2.2 pg/mL for serum osmolality <285 mOsm/kg. Sensitivity was 0.3 pg per tube by dilution method.
Vasopressin (vasopressin injection USP, 8-arginine vasopressin) was administered into a central vein at 0.04 U/min (Table 1
). Intravenous fluids and medications were not changed for the hour before or the first hour of vasopressin administration except that during vasopressin administration, pressor catecholamines were decreased if systolic arterial pressure exceeded 130 mm Hg. Continuous measurements of systolic arterial pressure and heart rate were averaged in 15-minute intervals. In Table 2, "Pre-AVP" values are averages of the hour preceding vasopressin; "AVP" values, from the first hour of vasopressin, are averages of the 15-minute interval in which systolic arterial pressure reached maximum value. In Fig 2, vasopressin administration ("AVP") values are averages of the hour before or after discontinuation; the "No AVP" value is the average of the 15-minute interval during which systolic arterial pressure reached its minimum value. Data were analyzed by unpaired t test (Fig 2) and paired t test (Table 2 and Fig 1). Differences were termed significant if t>5%.
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No AVP, P<.01; for No AVP
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Results |
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Nineteen patients with septic shock were studied. As detailed in "Methods," all subjects had severe hypotension that required administration of catecholamines. Despite catecholamine administration, hemodynamic data showed hypotension due to low systemic vascular resistance (Table 1
). At a time that systolic pressure averaged 92 mm Hg, mean plasma vasopressin concentration was 3.1 pg/mL (Fig 1). In contrast, in a group of patients with hypotension of similar duration and severity due to low cardiac output (cardiogenic shock; Table 1), plasma vasopressin was appropriately increased, with a mean of 22.7 pg/mL (Fig 1), which is in agreement with that of other forms of hypotension of similar magnitude.20 21 To distinguish between increased metabolism of vasopressin versus decreased secretion, we measured plasma vasopressin during infusion of exogenous hormone in two patients with septic shock. At a constant infusion of 0.01 U/min, the steady-state plasma concentration increased to 27 and 34 pg/mL, values expected in subjects given this infusion rate.22 Thus, the low plasma vasopressin in patients with septic shock appears to be due to impaired hormone secretion.
Plasma sodium concentration was normal (mean, 140 mmol/L) in the patients with septic shock (Table 1), and although the osmotically mediated secretion of vasopressin was not formally examined, no patient had clinical evidence of diabetes insipidus. This suggests that patients in septic shock have a specific inhibition of baroreflex-mediated secretion of vasopressin.
To examine whether vasopressin could constrict vascular smooth muscle in vasodilatory septic shock, 10 patients with this condition received vasopressin at 0.04 U/min IV. In normal subjects, significantly higher doses have little vasoconstrictor action9 and do not increase arterial pressure.9 10 In patients in septic shock, however, vasopressin increased systolic arterial pressure from 92 to 146 mm Hg (59% increase) due entirely to its vasoconstrictor effect. Whereas systemic vascular resistance increased 79%, cardiac output decreased 12% (Table 2). The increase in pressure occurred within minutes (<15 minutes) of the administration of hormone and frequently required decreasing or stopping the concomitantly administered catecholamine. Furthermore, in 6 of 10 patients, arterial pressure was maintained on vasopressin alone.
Vasopressin at 0.04 U/min causes the plasma concentration to increase 100 pg/mL,22 which is substantially higher than the concentrations of 20 to 30 pg/mL that we found in the patients in cardiogenic shock (Fig 2) and those that others have found for this degree of hypotension.20 21 To test whether this lower concentration could increase arterial pressure in septic shock, we infused the hormone at 0.01 U/min (shown above to provide a concentration of 30 pg/mL). Thus, in the six patients who were receiving vasopressin as the sole pressor, the hormone was stopped and within minutes, systolic arterial pressure declined from 126 to 83 mm Hg (P<.01) (Fig 2). The subsequent administration of vasopressin at 0.01 U/min resulted in a significant and sustained increase in systolic arterial pressure from 83 to 115 mm Hg (P<.01). Although systemic vascular resistance was not measured in these patients, the acute increase in arterial pressure was due to vasoconstriction because vasopressin only decreases cardiac output (see Table 2 and Reference 9).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Plasma vasopressin was found to be inappropriately low in patients with advanced vasodilatory septic shock, indicating impaired baroreceptor-mediated vasopressin secretion. Furthermore, a dose of exogenous vasopressin that provides a plasma concentration expected for the degree of hypotension resulted in a marked pressor response in these patients. These results indicate that the low endogenous levels of hormone in septic shock contribute to the vasodilation of sepsis.
The reason for impaired baroreflex-mediated vasopressin secretion in septic shock is unknown. First, autonomic failure is a possibility. Deficient baroreflex-mediated secretion of vasopressin is well documented in primary autonomic failure,23 24 and sympathetic function appears to be impaired in septic shock.25 In support of autonomic dysfunction in our patients with septic shock, vasopressin did not cause the marked bradycardia observed under normal conditions (Table 2 ).23 26
A second potential explanation for inappropriately low vasopressin levels in human septic shock is depletion of the secretory stores of the neurohypophysis. This has been observed with strong osmotic stimuli,27 28 29 and endotoxin is a most potent vasopressin secretagogue.16 In animal models of acute septic shock,14 15 16 an enormous rise in plasma vasopressin during the 1 to 2 hours after endotoxin/bacterial administration (even before hypotension14 ) is followed by a rapid decline over the next few hours; no study has monitored plasma vasopressin in animals with septic shock of more than a few hours' duration.
Needless to say, the mechanisms responsible for the profound vasodilation of septic shock are of great interest. Previous work has demonstrated abnormal activation of vasodilatory mechanisms in experimental models of septic shock.2 3 The findings reported herein document an abnormality of a vasoconstrictor mechanism critical for arterial pressure maintenance and provide the basis for new inquiries into the pathogenesis of the vasodilation in septic shock.
Received October 28, 1996; revision received January 6, 1997; accepted January 15, 1997.
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References |
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 T. N. Albright, M. A. Zimmerman, and C. H. Selzman Vasopressin in the Cardiac Surgery Intensive Care Unit Am. J. Crit. Care., July 1, 2002; 11(4): 326 - 330. [Abstract] [Full Text] [PDF]
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W. L. Jackson Jr, A. F. Shorr, C. L. Holmes, K. R. Walley, and J. A. Russell Vasopressin and Cardiac Performance Chest, May 1, 2002; 121(5): 1723 - 1724. [Full Text] [PDF]
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 M. I. Rudis and C. Chant Update on Vasopressors and Inotropes in Septic Shock Journal of Pharmacy Practice, April 1, 2002; 15(2): 124 - 134. [Abstract] [PDF]
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J. D. Tobias Arginine Vasopressin for Refractory Distributive Shock in Two Adolescents J Intensive Care Med, January 1, 2002; 17(1): 48 - 52. [Abstract] [PDF]
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C. L. Holmes, B. M. Patel, J. A. Russell, and K. R. Walley Physiology of Vasopressin Relevant to Management of Septic Shock Chest, September 1, 2001; 120(3): 989 - 1002. [Abstract] [Full Text] [PDF]
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D. W. Landry and J. A. Oliver The Pathogenesis of Vasodilatory Shock N. Engl. J. Med., August 23, 2001; 345(8): 588 - 595. [Full Text] [PDF]
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M. W. Dunser, A. J. Mayr, H. Ulmer, N. Ritsch, H. Knotzer, W. Pajk, G. Luckner, N. J. Mutz, and W. R. Hasibeder The Effects of Vasopressin on Systemic Hemodynamics in Catecholamine-Resistant Septic and Postcardiotomy Shock: A Retrospective Analysis Anesth. Analg., July 1, 2001; 93(1): 7 - 13. [Abstract] [Full Text] [PDF]
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 M. P. Talbot, I. Tremblay, A. Y. Denault, and S. Belisle Vasopressin for refractory hypotension during cardiopulmonary bypass J. Thorac. Cardiovasc. Surg., August 1, 2000; 120(2): 401 - 402. [Full Text] [PDF]
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H.-J. Weig, K.-L. Laugwitz, A. Moretti, K. Kronsbein, C. Stadele, S. Bruning, M. Seyfarth, T. Brill, A. Schomig, and M. Ungerer Enhanced Cardiac Contractility After Gene Transfer of V2 Vasopressin Receptors In Vivo by Ultrasound-Guided Injection or Transcoronary Delivery Circulation, April 4, 2000; 101(13): 1578 - 1585. [Abstract] [Full Text] [PDF]
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D. L.S. Morales, D. Gregg, D. N. Helman, M. R. Williams, Y. Naka, D. W. Landry, and M. C. Oz Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock Ann. Thorac. Surg., January 1, 2000; 69(1): 102 - 106. [Abstract] [Full Text] [PDF]
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P. T. Murray, M. E. Wylam, and J. G. Umans Nitric Oxide and Septic Vascular Dysfunction Anesth. Analg., January 1, 2000; 90(1): 89 - 89. [Full Text] [PDF]
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S. M. Brabant, M. Bertrand, D. Eyraud, P.-L. Darmon, and P. Coriat The Hemodynamic Effects of Anesthetic Induction in Vascular Surgical Patients Chronically Treated with Angiotensin II Receptor Antagonists Anesth. Analg., December 1, 1999; 89(6): 1388 - 1388. [Abstract] [Full Text] [PDF]
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E. B. Rosenzweig, T. J. Starc, J. M. Chen, S. Cullinane, D. M. Timchak, W. M. Gersony, D. W. Landry, and M. E. Galantowicz Intravenous Arginine-Vasopressin in Children With Vasodilatory Shock After Cardiac Surgery Circulation, November 9, 1999; 100 (2009): II-182 - II-186. [Abstract] [Full Text] [PDF]
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S. M. Brabant, D. Eyraud, M. Bertrand, and P. Coriat Refractory Hypotension After Induction of Anesthesia in a Patient Chronically Treated with Angiotensin Receptor Antagonists Anesth. Analg., October 1, 1999; 89(4): 887 - 887. [Full Text] [PDF]
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D. Morales, J. Madigan, S. Cullinane, J. Chen, M. Heath, M. Oz, J. A. Oliver, and D. W. Landry Reversal by Vasopressin of Intractable Hypotension in the Late Phase of Hemorrhagic Shock Circulation, July 20, 1999; 100(3): 226 - 229. [Abstract] [Full Text] [PDF]
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Y. Hamu, Y. Kanmura, I. Tsuneyoshi, and N. Yoshimura The Effects of Vasopressin on Endotoxin-Induced Attenuation of Contractile Responses in Human Gastroepiploic Arteries In Vitro Anesth. Analg., March 1, 1999; 88(3): 542 - 542. [Abstract] [Full Text] [PDF]
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K.-L. Laugwitz, M. Ungerer, T. Schoneberg, H.-J. Weig, K. Kronsbein, A. Moretti, K. Hoffmann, M. Seyfarth, G. Schultz, and A. Schomig Adenoviral Gene Transfer of the Human V2 Vasopressin Receptor Improves Contractile Force of Rat Cardiomyocytes Circulation, February 23, 1999; 99(7): 925 - 933. [Abstract] [Full Text] [PDF]
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J. A. M. Avontuur, F. Boomsma, A. H. van den Meiracker, F. H. de Jong, and H. A. Bruining Endothelin-1 and Blood Pressure After Inhibition of Nitric Oxide Synthesis in Human Septic Shock Circulation, January 19, 1999; 99(2): 271 - 275. [Abstract] [Full Text] [PDF]
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S. E. Buijk, H. A. Bruining, J. A. Oliver, and D. W. Landry Vasopressin Deficiency Contributes to the Vasodilation of Septic Shock • Response Circulation, July 14, 1998; 98(2): 187 - 187. [Full Text] [PDF]
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 Vasopressin and Septic Shock Journal Watch Cardiology, April 28, 1997; 1997(428): 14 - 14. [Full Text]
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I. A. Reid Role of Vasopressin Deficiency in the Vasodilation of Septic Shock Circulation, March 4, 1997; 95(5): 1108 - 1110. [Full Text]
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 M. Bucher, J. Hobbhahn, K. Taeger, and A. Kurtz Cytokine-mediated downregulation of vasopressin V1A receptors during acute endotoxemia in rats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2002; 282(4): R979 - R984. [Abstract] [Full Text] [PDF]
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 K.-L. Laugwitz, H.-J. Weig, A. Moretti, E. Hoffmann, P. Ueblacker, I. Pragst, K. Rosport, A. Schomig, and M. Ungerer Gene Transfer of Heterologous G Protein-Coupled Receptors to Cardiomyocytes : Differential Effects on Contractility Circ. Res., April 13, 2001; 88(7): 688 - 695. [Abstract] [Full Text] [PDF]
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