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© 2001 International Anesthesia Research Society
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Abstract |
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We retrospectively investigated the effects of continuous arginine vasopressin (AVP) infusion on systemic hemodynamics, acid/base status, and laboratory variables in patients (mean age [mean ± SD]= 66.3 ± 10.1 yr) with catecholamine-resistant septic (n = 35) or postcardiotomy shock (n = 25). Hemodynamic and acid/base data were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Laboratory examinations were recorded before and 24, 48, and 72 h after the start of AVP infusion. For statistical analysis, a mixed-effects model was used. The overall intensive care unit mortality was 66.7%. AVP administration caused a significant increase in mean arterial pressure (+29%) and systemic vascular resistance (+56%), accompanied by a significant decrease in heart rate (-24%) and mean pulmonary arterial pressure (-11%) without any change in stroke volume index. Norepinephrine requirements could be reduced by 72% within 72 h. During AVP infusion, a significant increase in liver enzymes and total bilirubin concentration and a significant decrease in platelet count occurred. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.
Implications: In this retrospective analysis, the influence of a continuous infusion of anendogenous hormone (arginine vasopressin) on systemic hemodynamics andlaboratory variables was assessed in patients with vasodilatory shockunresponsive to conventional therapy. Arginine vasopressin was effective inreversing systemic hypotension. However, adverse effects on gastrointestinalperfusion and coagulation cannot beexcluded.
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Introduction |
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Catecholamine-resistant hypotension is a feared complication in patients with septic shock (SS), postcardiotomy shock (PS), and severe multiple-organ dysfunction syndrome, contributing to mortality rates up to 100%. Excess generation of nitric oxide and vasodilatory prostaglandins and peptides; activation of adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle cells and inflammatory mediators; and use of vasodilatory inotropes contribute to progressive loss of vascular tone (1,2).
Vasopressor catecholamines are the only drugs available for the management of severe hypotension in SS and PS. However, development of adrenergic hyposensitivity with loss of catecholamine pressor effects, resulting in refractory hypotension, is a well known clinical dilemma (3). Further enforcing catecholamine therapy, intensivists often enter a vicious circle in which the significant toxicity of catecholamine administration (e.g., excessive pulmonary hypertension and development of tachyarrhythmias) may contribute to further clinical deterioration and subsequent outcome. Therefore, alternative vasopressor drugs devoid of major systemic side effects would be of vital benefit in advanced states of vascular failure. Arginine vasopressin (AVP) is a potent vasoconstrictor in various hypotensive states, including cardiac arrest, the late phase of hemorrhagic shock, and orthostatic or hemodialysis-induced hypotension (4–7). In addition, in smaller studies (8), AVP has been successfully used to treat hypotension in volume-resuscitated critically ill patients with sepsis and after cardiopulmonary bypass.
Between January 1998 and May 2000, we administered AVP to 60 critically ill patients with catecholamine-resistant SS or PS and severe multiple-organ dysfunction syndrome. This retrospective analysis demonstrates the effects of continuous AVP infusion on systemic hemodynamics, acid/base status, and single-organ variables. This is the largest study reporting on the application of AVP in critically ill patients.
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Methods |
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Between January 1998 and May 2000, all medical records of a 21-bed general and surgical intensive care unit (ICU) were reviewed for patients with advanced multiple-organ dysfunction syndrome caused by SS or PS and who were receiving a continuous IV infusion of AVP (Pitressin®; Monarch Pharmaceuticals, Rochester, NY) because of catecholamine-resistant hypotension. All patients were invasively monitored, including use of a pulmonary artery catheter.
Catecholamine-resistant shock was defined as the failing effect of a stepwise increase of norepinephrine by 0.2 µg · kg-1 · min-1 over a 2-h period on mean arterial pressure (MAP). All patients were volume-resuscitated according to the response of stroke volume index to volume loading. Normovolemia was assumed if a trial of further volume loading with colloids produced no effect on stroke volume index. The pulmonary capillary wedge and central venous pressure where stroke volume index was maximal was used as the therapeutic target for additional volume resuscitation. An AVP infusion was given continuously, with doses ranging from 4 to 6 U/h. No bolus injections were used. After initiating AVP infusion, norepinephrine therapy was targeted to maintain MAP 
70 mm Hg in all patients. When MAP exceeded 70 mm Hg, norepinephrine infusion was stepwise decreased according to MAP. Norepinephrine was not completely withdrawn in any patient. AVP infusion was continuously reduced and tapered off when norepinephrine requirements decreased <0.3–0.4 µg · kg-1 · min-1. In this situation, weaning from AVP occurred first and individually according to the patient’s response to a stepwise decrease in AVP. In patients successfully weaned from AVP, further weaning from norepinephrine occurred individually according to the response of MAP to small stepwise reductions in norepinephrine infusion. During the observation period, 80% of the study patients were on continuous venovenous hemofiltration with constant ultrafiltration rates between 20 and 30 mL/min.
The following data were collected from all patients: demographics (including age, sex, admission diagnosis, and length of ICU stay), multiple-organ dysfunction score (MODS) (Appendix 1), ICU mortality, and length of AVP administration.
Hemodynamic data, including heart rate, MAP, mean pulmonary arterial pressure, and norepinephrine requirements, were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Arterial acid/base status and arterial lactate concentrations (Rapidlab 860; Chiron Diagnostics, Medfield, MA), as well as pulmonary artery catheter measurements—including cardiac index, stroke volume index, and pulmonary capillary wedge pressure—were measured before and 1–3, 4–8, 12–16, 24 ± 5, 48 ± 5, and 72 ± 5 h after the start of AVP infusion. Systemic vascular resistance was calculated from recorded data.
In all patients, laboratory examinations to evaluate hepatic, renal, and hematologic organ systems, as well as creatine kinase MB (CK-MB) and troponin I (TROP) serum concentrations were obtained at least once daily.
The primary study end point was the assessment of changes in systemic hemodynamics during continuous infusion of AVP in catecholamine-resistant SS and PS. To evaluate possible differences at baseline and during AVP infusion, patients were further separated into survivors and nonsurvivors and into patients with SS or PS.
The secondary study end point was to compare alterations in acid/base status and single-organ laboratory variables during AVP infusion in survivors and nonsurvivors.
Demographic data were compared with the use of Student’s t-tests, 
2 tests, or Mann-Whitney U-tests, as appropriate. Repeated measurements were analyzed with a mixed-effects model (SAS PROC MIXED; SAS Institute, Cary, NC) to account for death-related dropouts (9). Variables that did not meet normality assumptions (systemic vascular resistance, aspartate aminotransferase, and alanine aminotransferase; bilirubin, lactate, CK-MB, and TROP serum concentrations; and thrombocyte count) were log-transformed. If trends were significant, comparisons with baseline were performed with the same model. Because of the explorative character of the study, no corrections for multiple comparisons were used. P values <0.05 were regarded as statistically significant. Data are given as mean ± SD.
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Results |
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During the review period, 60 patients with catecholamine-resistant hypotension were treated with AVP (4–6 U/h) for a median period of 31 h (range, 0.5–384 h). Thirty-five patients were in SS, and 25 patients were in PS. The mean age was 66.3 ± 10.1 yr; mean MODS was 11.2 ± 1.4. The overall ICU mortality of the study population was 66.7%.
Characteristics of study subgroups are shown in Table 1. There were no significant differences in age and MODS between survivors and nonsurvivors. ICU stay was significantly longer in survivors. We found no differences in MODS, ICU stay, and mortality between SS and PS patients. Patients with PS were significantly older and demonstrated nearly 20% less ICU mortality when compared with SS patients.
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Table 2 presents serial hemodynamic variables and changes in norepinephrine requirements during continuous infusion of AVP in all patients (survivors and nonsurvivors). AVP caused a significant decrease in mean heart rate (-24%) and a significant increase in MAP (+29%) because of an increase in systemic vascular resistance (+56%). The decrease in heart rate was accompanied by a significant decrease in cardiac index (-21%) without any changes in stroke volume index. Mean pulmonary artery pressure significantly decreased (-11%) during the observation period, and norepinephrine requirements were reduced by 76% within 72 h. There were no significant differences in heart rate, MAP, pulmonary capillary wedge pressure, cardiac index, or stroke volume index between survivors and nonsurvivors at baseline and during the observation period. However, nonsurvivors exhibited less of a decrease in mean pulmonary artery pressure and a smaller increase in systemic vascular resistance. In addition, norepinephrine requirements were significantly larger at baseline and during AVP infusion in nonsurvivors when compared with survivors.
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Table 3 compares serial hemodynamic variables and changes in norepinephrine requirements in patients with SS or PS during continuous infusion of AVP. There were no differences in heart rate, MAP, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, or norepinephrine requirements between groups. Patients with PS demonstrated significantly lower cardiac and stroke volume indices and a significantly higher systemic vascular resistance at baseline and during AVP infusion.
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Arterial pH, lactate concentrations, base excess, and laboratory variables to assess organ function in survivors and nonsurvivors at baseline and during AVP infusion are presented in Table 4. Nonsurvivors demonstrated significantly lower arterial pH and base excess and significantly higher arterial lactate and total bilirubin concentrations at baseline and during the observation period when compared with survivors. There were no significant differences in liver enzymes, platelet count, cardiac enzymes, or serum creatinine concentrations between survivors and nonsurvivors. However, we observed a significant decrease in platelet counts (P < 0.0001), CK-MB (P = 0.0023), and TROP (P < 0.0001) and a significant increase in aspartate aminotransferase (P = 0.024), alanine aminotransferase (P = 0.032), and total bilirubin concentrations (P < 0.0001) during AVP infusion in all patients.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this retrospective analysis, AVP proved to be a powerful vasopressor in patients with catecholamine-resistant hypotension and severe multiple-organ dysfunction syndrome caused by sepsis or after cardiac surgery. AVP administration caused a significant increase in systemic vascular resistance and MAP, accompanied by a significant decrease in heart rate and mean pulmonary arterial pressure and without any change in stroke volume index. AVP administration led to a pronounced decrease in norepinephrine requirements starting almost within minutes after the onset of continuous infusion in most patients.
The pharmacologic mechanisms of AVP-mediated increases in arterial pressure are still a matter of speculation. However, four molecular pathways have already been discussed. First, stimulation of vascular smooth muscle V1-receptors by AVP increase cytoplasmic ionized calcium via the phosphatidyl-inositol-bisphosphate cascade, leading to arteriolar vasoconstriction (8). Second, blockage of activated ATP/potassium channels within the muscle cell membrane facilitates myocyte depolarization and thus vasoconstriction (10). Third, under pathophysiologic conditions, AVP attenuates endotoxin and interleukin-1ß-stimulated generation of nitric oxide and its second messenger, cyclic guanosine monophosphate, thus inhibiting excessive arteriolar vasodilatation (11). Fourth, during endotoxemia, AVP enhances adrenergic responsiveness through stimulation of smooth muscle V1-receptors (12). The last three mechanisms may be especially important in counteracting excessive vasodilatation in shock caused by sepsis or after major surgery.
Because similar dosages of AVP usually demonstrate no pressor effect in normotensive subjects, several authors have postulated that AVP deficiency in critically ill patients is probably mediated by a defective baroreflex system with subsequent development of compensatory "AVP pressor hypersensitivity" (13,14). However, in acute hypotensive states (i.e., cardiac arrest, hypotension during combined general and epidural anesthesia, or phosphodiesterase inhibitor-induced hypotension) in which primary AVP deficiency seems to be unlikely, AVP is also a potent arterial vasoconstrictor (4,15,16). Argenziano et al. (17) demonstrated a reversal of vasodilatory shock with AVP regardless of AVP plasma concentrations before administration. In addition, in normotensive subjects, AVP-induced vasoconstriction is accompanied by a reflectory decrease in heart rate and cardiac output, preventing any increase in MAP (18). Furthermore, in critically ill patients, partial restoration of adrenergic hyporesponsiveness could imitate AVP hypersensitivity. These findings suggest that hypotension per se, rather than an impaired baroreflex system or AVP deficiency, is a precondition for the pressor effect of AVP.
In this study, we observed a significant decrease in mean pulmonary arterial pressure during infusion of AVP; such a decrease has not been described in humans before. This decrease was already present four hours after the start of AVP infusion, suggesting a causal relationship with AVP administration. Experimental studies in animals have demonstrated that AVP-induced pulmonary vasodilatation is probably mediated by a nitric oxide-dependent mechanism (19,20). However, in our patients, the simultaneous significant reduction in norepinephrine requirements during AVP infusion may have contributed to the observed decrease in mean pulmonary arterial pressure.
AVP proved to be equally effective in reversing hypotension caused by SS or PS with an almost identical hemodynamic response. Reversal of hypotension was accompanied by a decrease in heart rate and mean pulmonary arterial pressure without any change in myocardial performance (assessed by stroke volume index), despite a simultaneous significant reduction in norepinephrine requirements. The latter observation is of particular interest because AVP, in contrast to norepinephrine, is devoid of major positive inotropic effects on the myocardium (18). Perhaps AVP improved myocardial perfusion and thus prevented any deterioration in myocardial performance, either by increasing myocardial perfusion pressure or by inducing selective coronary vasodilatation at dosages used in these patients. Coronary vasodilatation, probably caused by stimulation of various V1- and V2-receptors, has been demonstrated in animal experiments (21). We observed no new myocardial ischemic events during AVP administration in this study. Increased concentrations of serum CK-MB and TROP at baseline significantly decreased during the observation period in both survivors and nonsurvivors. Although four patients developed new onset supraventricular tachyarrhythmias, we observed eight other patients spontaneously converting into sinus rhythm during application of AVP. Decreased adrenergic myocardial stimulation because of a significant reduction in norepinephrine requirements and a possible improvement of myocardial perfusion may have contributed to this observation.
Nonsurvivors demonstrated more severe lactic acidosis, most likely as a consequence of a more pronounced deterioration of tissue perfusion when compared with survivors. Survivors showed a progressive improvement in acid/base status throughout the observation period. Because 80% of patients were on continuous venovenous hemofiltration, no differences in serum creatinine concentrations were observed.
A significant increase in liver enzymes and bilirubin concentrations occurred in all patients during the observation period. Because AVP is a potent gastrointestinal vasoconstrictor, this finding might indicate adverse effects on gastrointestinal perfusion (22). However, the observed increases in liver enzymes and bilirubin concentration may have also been a consequence of shock-associated hepatic dysfunction.
We noted a significant decrease in platelet count during this study that was almost identical in survivors and nonsurvivors. Although disseminated intravascular coagulation with increased platelet consumption is a common finding in patients with shock, the observed decrease in circulating platelets may in part be related to the infusion of AVP; in animal experiments, AVP facilitates platelet adhesion and aggregation as a consequence of V1-receptor stimulation, with subsequent platelet calcium loading (23,24).
In conclusion, AVP proved to be a powerful vasopressor in patients with catecholamine-resistant SS or PS and severe multiple-organ dysfunction syndrome. AVP consistently led to a significant increase in MAP and a decrease in heart rate, mean pulmonary arterial pressure, and norepinephrine requirements, without any change in myocardial performance. Because negative side effects on gastrointestinal perfusion and coagulation cannot be excluded, we suggest that the administration of AVP should still be restricted to patients with catecholamine-resistant vasodilatory shock. Future studies should focus on the influence of AVP on single-organ functions and its effect on overall mortality in these critically ill patients.
APPENDIX
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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-
Parillo JE. Pathogenetic mechanisms of septic shock. N Engl J Med 1993; 328: 1471–7.
[Free Full Text] -
Morales DL, Gregg D, Helmann DN, et al. Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock. Ann Thorac Surg 2000; 69: 102–6.
[Abstract/Free Full Text] - Chernow B, Roth BL. Pharmacologic manipulation of the peripheral vasculature in shock: clinical and experimental approaches. Circ Shock 1986; 18: 141–55.[Web of Science][Medline]
- Lindner KH, Dirks B, Strohmenger HU, et al. Randomized comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet 1997; 349: 535–7.[Web of Science][Medline]
-
Morales DL, Madigan J, Cullinane S, et al. Reversal by vasopressin of intractable hypotension in the late phase of hemorrhagic shock. Circulation 1999; 100: 226–9.
[Abstract/Free Full Text] - Kochar MS. Hemodynamic effects of lysine-vasopressin in orthostatic hypotension. Am J Kidney Dis 1985; 6: 49–52.[Web of Science][Medline]
- Lindberg JS, Copley JB, Melton K, et al. Lysine vasopressin in the treatment of refractory hemodialysis-induced hypotension. Am J Nephrol 1990; 10: 269–75.[Web of Science][Medline]
- Rozenfield V, Cheng JWM. The role of vasopressin in the treatment of vasodilation in shock states. Ann Pharmacother 2000; 34: 250–4.[Abstract]
- Laird NM, Ware JH. Random effects models for longitudinal data. Biometrics 1982; 38: 963–74.[Web of Science][Medline]
-
Salzman AL, Vromen A, Denenberg A, Szabo C. KATP-channel inhibition improves hemodynamics and cellular energetics in hemorrhagic shock. Am J Physiol 1997; 272: H688–94.
[Abstract/Free Full Text] -
Umino T, Kusano E, Muto S, et al. AVP inhibits LPS- and IL-1beta stimulated NO and cGMP via v1-receptor in cultured rat mesangial cells. Am J Physiol 1999; 276: F433–41.
[Abstract/Free Full Text] -
Hamu Y, Kanmura Y, Tsuneyoshi I, Yoshimura N. The effects of vasopressin on endotoxin-induced attenuation of contractile responses in human gastroepiploic arteries in vitro. Anesth Analg 1999; 88: 542–8.
[Abstract/Free Full Text] -
Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency contributes to the vasodilatation of septic shock. Circulation 1997; 95: 1122–5.
[Abstract/Free Full Text] - Landry DW, Levin HR, Gallant EM, et al. Vasopressin pressor hypersensitivity in vasodilatory septic shock. Crit Care Med 1997; 25: 1279–82.[Web of Science][Medline]
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De Kock M, Laterre PF, Andruetto P, et al. Ornipressin (Por 8): an efficient alternative to counteract hypotension during combined general/epidural anesthesia. Anesth Analg 2000; 90: 1301–7.
[Abstract/Free Full Text] - Gold JA, Cullinane S, Chen J, et al. Vasopressin as an alternative to norepinephrine in the treatment of milrinone-induced hypotension. Crit Care Med 2000; 28: 249–52.[Web of Science][Medline]
- Argenziano M, Choudhri AF, Oz MC, et al. A prospective randomized trial of arginine vasopressin in the treatment of vasodilatory shock after left ventricular assist device replacement. Circulation 1997; 96 (Suppl 2): 286–90.
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Aylward PE, Floras JS, Leimbach WN, Abboud FM. Effects of vasopressin on the circulation and its baroreflex control in healthy men. Circulation 1986; 73: 1145–54.
[Abstract/Free Full Text] -
Evora PR, Pearson PJ, Schaff HV. Arginine vasopressin induces endothelium-dependent vasodilatation of the pulmonary artery: V1-receptor-mediated production of nitric oxide. Chest 1993; 103: 1241–5.
[Abstract/Free Full Text] -
Russ RD, Walker BR. Role of nitric oxide in vasopres-sinergic pulmonary vasodilatation. Am J Physiol 1992; 262: H743–7.
[Abstract/Free Full Text] - Okamura T, Ayajiki K, Fujioka H, Toda N. Mechanisms underlying arginine vasopressin-induced relaxation in monkey isolated coronary arteries. J Hypertens 1999; 17: 673–8.[Web of Science][Medline]
- Varga C, Pavo I, Lamarque D, et al. Endogenous vasopressin increases acute endotoxin shock-provoked gastroin-testinal mucosal injury in the rat. Eur J Pharmacol 1998; 352: 257–61.[Web of Science][Medline]
- Filep J, Rosenkranz B. Mechanism of vasopressin-induced platelet aggregation. Thromb Res 1987; 45: 7–15.[Web of Science][Medline]
- Pedersen OS, Reichelt KL. The effect of arginine vasopressin, lysine vasopressin or oxytocin on ADP or arginine vasopressin-induced Ca2+ increases in human platelets. Clin Physiol 1999; 19: 305–10.[Web of Science][Medline]
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Goris RJA, te Boekhorst TPA, Nuytinck JKS, Gimbrere JSF. Multiple-organ failure. Arch Surg 1985; 120: 1109–15.
[Abstract/Free Full Text]
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