Beneficial Effects of Short-term Vasopressin Infusion during Severe Septic Shock

2002 ◽  
Vol 96 (3) ◽  
pp. 576-582 ◽  
Author(s):  
Bhavesh M. Patel ◽  
Dean R. Chittock ◽  
James A. Russell ◽  
Keith R. Walley

Background Septic shock is associated with vasopressin deficiency and a hypersensitivity to its exogenous administration. The goal of the current study was to determine whether short-term vasopressin infusion in patients experiencing severe septic shock has a vasopressor sparing effect while maintaining hemodynamic stability and adequate end-organ perfusion. Methods Patients experiencing septic shock that required high-dose vasopressor support were randomized to a double-blinded 4-h infusion of either norepinephrine (n = 11) or vasopressin (n = 13), and open-label vasopressors were titrated to maintain blood pressure. To assess end-organ perfusion, urine output and creatinine clearance, gastric mucosal carbon dioxide tension, and electrocardiogram ST segment position were measured. Results Patients randomized to norepinephrine went from a median prestudy norepinephrine infusion of 20.0 microg/min to a blinded infusion of 17.0 mug/min at 4 h, whereas those randomized to vasopressin went from a median prestudy norepinephrine infusion of 25.0 microg/min to 5.3 microg/min at 4 h (P < 0.001). Mean arterial pressure and cardiac index were maintained in both groups. Urine output did not change in the norepinephrine group (median, 25 to 15 ml/h) but increased substantially in the vasopressin group (median, 32.5 to 65 ml/h; P < 0.05). Similarly, creatinine clearance did not change in the norepinephrine group but increased by 75% in the vasopressin group (P < 0.05). Gastric mucosal carbon dioxide tension and electrocardiogram ST segments did not change significantly in either group. Conclusions The authors conclude that short-term vasopressin infusion spared conventional vasopressor use and improved some measures of renal function in patients with severe septic shock.

2003 ◽  
Vol 98 (3) ◽  
pp. 793-793
Author(s):  
Bhavesh M. Patel ◽  
Dean R. Chittock ◽  
James A. Russell ◽  
Keith R. Walley

1997 ◽  
Vol 22 (3) ◽  
pp. 256-267 ◽  
Author(s):  
Deep Chatha ◽  
James Duffin

The pattern of breathing following a 10-breath voluntary hyperventilation period during hyperoxic rebreathing was compared to that without hyperventilation in 6 subjects (3 male and 3 female). The aim was to measure the posthyperventilation short-term potentiation of ventilation without changes in respiratory chemoreflex drives induced by the voluntary hyperventilation. Hyperoxia was used to reduce the peripheral chemoreflex drive, and rebreathing to prevent the decrease in arterial carbon dioxide tension normally produced by hyperventilation. There were significant differences between the male and female responses. However, in all subjects, ventilation and heart rate were increased during hyperventilation but end-tidal partial pressures of carbon dioxide and oxygen were unchanged. Following hyperventilation, ventilation immediately returned to the values observed when hyperventilation was omitted. Hyperventilation did not induce a short-term potentiation of ventilation under these conditions: changes in chemoreflex stimuli brought about by cardiovascular changes induced by hyperventilation may play a role in the short-term potentiation observed under other circumstances. Key words: rebreathing, hyperventilation, short-term potentiation


2020 ◽  
Author(s):  
Haijun Huang ◽  
Chenxia Wu ◽  
Qinkang Shen ◽  
Hua Xu ◽  
Yixin Fang ◽  
...  

Abstract Background: The effect of early vasopressin initiation on clinical outcomes in patients with septic shock is uncertain. A systematic review and meta-analysis was performed to evaluate the impact of early start of vasopressin support within 6 hours after the diagnosis on clinical outcomes in septic shock patients.Methods: We searched the PubMed, Cochrane, and Embase databases for randomized controlled trials (RCTs) and cohort studies from inception to the 1st of October 2020. We included studies involving adult patients (> 16 years)with septic shock. All authors reported our primary outcome of short-term mortality and in the experimental group patients in the studies receiving vasopressin infusion within 6 hours after diagnosis of septic shock and in the control group patients in the studies receiving no vasopressin infusion or vasopressin infusion 6 hours after diagnosis of septic shock, clearly comparing with clinically relevant secondary outcomes(use of renal replacement therapy(RRT),new onset arrhythmias, ICU length of stay and length of hospitalization). Results were expressed as odds ratio (OR) and mean difference (MD) with accompanying 95% confidence interval (CI).Results: Five studies including 788 patients were included. The primary outcome of this meta-analysis showed that short-term mortality between the two groups was no difference (odds ratio [OR] = 1.09; 95% CI, 0.8 to 1.48; P =0.6; χ2 =0.83; I2 = 0%). Secondary outcomes demonstrated that the use of RRT was less in the experimental group than that of the control group (OR =0.63; 95% CI, 0.44 to 0.88; P =0.007; χ2 =3.15; I2 =36%).The new onset arrhythmias between the two groups was no statistically significant difference (OR =0.59; 95% CI, 0.31 to 1.1; P =0.10; χ2 =4.7; I2 =36%). There was no statistically significant difference in the ICU length of stay(mean difference = 0.16; 95% CI, - 0.91 to 1.22; P = 0.77; χ2 = 6.08; I2 =34%) and length of hospitalization (mean difference = -2.41; 95% CI, -6.61 to 1.78; P = 0.26; χ2 = 8.57; I2 =53%) between the two groups.Conclusions: Early initiation of vasopressin in patients within 6 hours of septic shock onset was not associated with decreased short-term mortality, new onset arrhythmias, shorter ICU length of stay and length of hospitalization, but can reduce the use of RRT. Further large-scale RCTs are still needed to evaluate the benefit of starting vasopressin in the early phase of septic shock.


2003 ◽  
Vol 98 (3) ◽  
pp. 793-793 ◽  
Author(s):  
Tetsuya Iijima ◽  
Takeshi Oguchi ◽  
Satoshi Kashimoto

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A572-A573
Author(s):  
Albert Chang ◽  
Dharscika Arudkumaran ◽  
Deviani Umadat ◽  
Deirdre A Cocks Eschler

Abstract Background: Vasopressin is a hormone produced in the hypothalamus and secreted by the posterior pituitary. Underproduction or resistance to vasopressin can lead to diabetes insipidus (DI) resulting in the imbalance of fluid status and serum sodium levels. Synthetic vasopressin is a common second line agent used in the critical care setting for its vasopressor effects with an added clinical benefit by increasing cerebral perfusion pressure. There have been reported cases of transient DI after discontinuation of vasopressin in neurosurgical patients, however only few cases have been reported in septic shock patients without neurological involvement. We present a case of transient DI during treatment for septic shock after attempts to wean off vasopressin infusion. Presentation: A 41-year-old female with history of type 2 diabetes mellitus, quadriplegia following a motor vehicle accident at age 11 was admitted to the surgical intensive care unit for urosepsis after placement of right ureteral stent. The patient was started on broad spectrum intravenous (IV) antibiotics and vasopressors norepinephrine and vasopressin. After 8 days of vasopressin treatment, with each effort to wean IV vasopressin, the patient was noted to have significant polyuria with urine output reaching as much as 800 mL/hr and increase in her serum sodium to a maximum of 148 mmol/L (n 145 mmol/L). During episodes of excessive diuresis, urine sodium reached 87 mmol/L, urine osmolality was 72 mOsm/kg (50-1400 mOsm/kg), and serum osmolality was 288 mOsm/kg (n 300 mOsm/kg). The patient received three doses of 1 microgram of desmopressin 24 hours apart while weaning off vasopressin. This helped slow excessive diuresis while also maintaining normal serum sodium levels. Urine output decreased to approximately 150 mL/hr after each administration of desmopressin. The serum sodium levels eventually stabilized between 135-140 mmol/L and urine output held steady around 200 cc/hr. The patient did not require additional desmopressin and was hemodynamically stable off all vasopressors. Discussion: The pathophysiology behind transient diabetes insipidus following vasopressin infusion is still unclear. It is known that in septic shock, there is depletion of vasopressin stores which suggests central DI. Yet, pharmacologic doses of vasopressin are speculated to downregulate V2 receptors in the renal distal convoluted tubules and collecting ducts which suggests nephrogenic DI. Our patient responded to desmopressin which indicates that she at least had a central component of DI. There is no consensus on the duration of vasopressin required to precipitate transient DI, but vasopressin infusion was administered for at least 24 hours in other cases prior to onset. We present a rare case of transient diabetes insipidus after prolonged vasopressin infusion that clinicians should be aware of in the critical care setting.


2012 ◽  
Vol 72 (5) ◽  
pp. 1228-1238 ◽  
Author(s):  
Pablo Tapia ◽  
Eduardo Chinchón ◽  
Danny Morales ◽  
Jimmy Stehberg ◽  
Felipe Simon

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