Tag Archives: septic shock

Prostacyclin in Septic Shock: Conclusion

However, there is increasing evidence that discrete tissue hypoxia may exist on the regional level despite supranormal D02 lack of O2 supply dependency, and normal lactate values For example we can estimate gastrointestinal tissue oxygenation by gastric mucosal tonometry. A recent short report has shown PGI2 to increase D02 and gastric mucosal pH without an increase in whole body V02
We believe that our protocol for hemodynamic stabilization with sufficient volume,inotropic, and vasopressor support to achieve “supranormal” O2 delivery and adequate perfusion pressure pressures provides a reasonable basis on which to test an agent such as PGI2. We recognize that there is no single protocol for resuscitation in septic shock and that these are trade-offs when potentially competing drugs are administered. For instance, we cannot rule out that the norepinephrine given to maintain arterial pressures may have counterbalanced to some degree the vasodilating effects of PGI2. However, in severe septic shock, alpha-agonists vasoconstrictors such as norepinephrine or high doses of dopamine, are necessary to achieve adequate organ perfusion pressures. www.canadian-familypharmacy.com other Norepinephrine has been shown to be effective in septic shock not only to improve kidney function but also to increase D02 and V02 Even with the norepinephrine given in the present study, systemic vascular resistance remained only about half normal, suggesting that these patients were not overly vasoconstricted.
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Prostacyclin in Septic Shock: Discussion

Prostacyclin in Septic Shock: DiscussionWe believe that the higher baseline levels of D02 in our patients are at least in part responsible for the differences in V02 with prostacyclin infusion between the present study and the previous ones. It has been demonstrated that supranormal levels of D02 improved survival rate in a variety of critically ill patients, possibly by improvement of tissue oxygenation A supranormal D02 does not guarantee a concomitant increase in V02 or higher survival rate 2 which may explain our high mortality rate, 87 percent. At our D02 levels closer to 800 ml/min/m2, near the value found by Mohsenifar et al to be needed for the V02 to become independent of D02 in ARDS, we found neither the substantial increase in V02 nor the increase in O2 extraction that Bihari et al reported from a much lower baseline D02 of 375 (nonsurvivors) or 420 ml/min/m2 (survivors). A “pathological” O2 supply dependency at suboptimal
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Prostacyclin in Septic Shock: Therapy

The primary finding of this study was that in patients with septic shock with supranormal O2 delivery, prostacyclin infusion produced a modest further increase in D02 without a matching increase in V02. In fact, when V02 was measured independent of the D02, now considered by some to be preferable in studies comparing these two variables, there was no increase in V02 at all. These findings are in contrast to recent studies that have shown a “pathological” increase in V02 with a prostacyclin-induced increase in D02 in patients with respiratory distress, particularly those who subsequently died. Altogether, however, the total number of such patients studied with prostacyclin remains quite small. Furthermore, the present data address two key issues: methodologic coupling of data and the maintenance of above-normal levels of D02 in patients with septic shock.
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Prostacyclin in Septic Shock: Results

Prostacyclin in Septic Shock: ResultsTable 3 lists the hemodynamic variables, and Table 4 lists the O2 transport variables, at baseline, with PGI2 infusion, and 30 and 60 min after infusion. The PGI2 infusion produced marked vasodilatation as evidenced by significant reductions in systemic vascular resistance (33 percent), MAP (18 percent), pulmonary capillary wedge pressure (12 percent), and calculated coronary artery perfusion pressure (20 percent) (p<0.05). The effects were demonstrable up to 30 min after stopping the infusion (Tables 3 and 4).
The PGI2 infusion also led to a significant fall in arterial oxygen tension from 115 ± 24 to 79 ± 15 mm Hg (p<0.01), with significant increases in the calculated alveolar-arterial oxygen tension gradient from 149 ±85 to 185 ±79 (p<0.01), and pulmonary shunt from 13 ±7 percent to 17 ±7 percent (p<0.01). Despite these changes, a 17 percent increase in cardiac index after the administration of PGI2 resulted in a 14 percent increase in D02 which was already at baseline 750 ml/min/m2.
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Prostacyclin in Septic Shock: Statistical Analysis

Before baseline measurements were obtained, the conditions of the patients were stabilized hemodynamically with adequate volume loading until there was no further increase in cardiac output. All patients received additional inotropic support with dobutamine in an attempt to achieve D02 >600 ml/min/m2 (Table 2). Because of the frequency of undesired side effects of dobutamine that may occur with much higher doses,2 such as tachycardia or tachyarrhythmia, which we did encounter in some patients, we limited the dobutamine infusion to a modest 18 Mg/ kg/min, and we reduced it when tachycardia (HR >130) occurred. Then, if the mean arterial blood pressure (MAP) did not reach 70 mm Hg, norepinephrine was added, “titrated” as low as possible, to obtain the desired MAP (Table 2).
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Prostacyclin in Septic Shock: Hemodynamic and Oxygen Transport Measurements

Prostacyclin in Septic Shock: Hemodynamic and Oxygen Transport MeasurementsAll patients had pulmonary and radial artery catheters placed for hemodynamic monitoring (Swan-Ganz catheters: Edwards Laboratories, Los Angeles; transducers 5265 039: Viggo-Spec-tramed, Bilthoven, The Netherlands; electronically derived means, with reference to the midaxillary line; cardiac output [thermodilution at temperature between 6°C and 12°C]: SAT II cardiac output computer, Edwards Laboratories).
Cardiovascular pressures and cardiac output were determined immediately before withdrawal of arterial and mixed venous blood. The blood samples were immediately measured for oxygen tension and pH (ABL 2, Radiometer, Copenhagen), and hemoglobin concentration and oxygen saturation (Hemoximeter Osm 3, Radiometer, Copenhagen). Canadian health and care mall All blood gases were corrected to the blood temperature as measured in the pulmonary artery.
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Prostacyclin in Septic Shock: Methods

In a prospective, single cohort design, we studied 15 patients in large tertiary-care ICU. All procedures were approved by our institutional research review committee and informed consent was received. Clinical data of the patients are shown in Table 1. All required ventilatory support and pulmonary artery catheterization due to septic shock. Patients exhibited at least five of the following clinical criteria of septic shock: persistent arterial hypotension with a systolic blood pressure <90 mm Hg, increasing volume need (>4 L of fluid per 24 h), systemic vascular resistance <700 dynesXsXcm’, temperature above 38.5°C or below 35.0°C, white blood cell count above 12X109 or below 4X109 cells per liter, either positive blood culture or a known site of sepsis, decrease of the thrombocytes >30 percent/24 h not due to bleeding, tachypnea, or mental disturbances with agitation and confusion.

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Prostacyclin in Septic Shock

Prostacyclin in Septic ShockThere is little doubt that tissue hypoxia is linked to multiple organ dysfunction syndrome and eventual mortality in patients with septic shock. It is still not known, however, how much systemic O2 delivery (D02) really is “adequate” for organ viability and patient survival or why some patients fail to extract sufficient O2 even when it seems to be abundantly delivered. Thus, the search continues for therapy to improve hypoxia, occult or otherwise, in patients with sepsis.
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Urine Hydrogen Peroxide During Adult Respiratory Distress Syndrome in Patients With and Without Sepsis – Conclusion

Urine Hydrogen Peroxide During Adult Respiratory Distress Syndrome in Patients With and Without Sepsis - ConclusionThe additional source of H0O2 in patients with sepsis is undoubtedly related to the extra noxious stimuli provided by endotoxin which is known to further prime leukocytes and activate cyclo-oxygenase systems. Yet another possibility for the observed higher levels of H202 may be a reflection of increased production of H202 by different bacterial strains. In any case, since urine H202 levels in the ARDS-only group were about 70 percent of those in the ARDS-sepsis group, these findings suggest that the ARDS abnormality alone is the major producer of this oxygen metabolite in patients with both ARDS and sepsis. www.mycanadianpharmacy.com

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Urine Hydrogen Peroxide During Adult Respiratory Distress Syndrome in Patients With and Without Sepsis – Discussion

However, within-group correlations were as follows: 0.969 for patients with ARDS only; 0.943 for survivors with ARDS and sepsis; and 0.961 for nonsurvivors with ARDS and sepsis. In general, there were not enough urine data at every lung injury score in each group to make meaningful statistical comparisons at each score. However, at a lung injury score of 3, the data showed significantly higher urine H202 concentrations in both ARDS-sepsis groups compared with the ARDS-only group. At lung score of 2, the urine H202 concentration of the survivor patients with ARDS and sepsis remained significantly increased compared with the patients with ARDS only. The difference, between the groups, in urine H202 level at these lung injury scores (3 and 2) are reflected in the significantly (p<0.05) poorer correlation (0.754) when correlating all data from the three groups.
The urine H202 concentrations in the healthy subjects and non-ARDS patient groups were not significantly different from each other or from the ARDS-sepsis and ARDS-only groups at the time when their lung injury scores were zero (Table 4). canadian neightbor pharmacy

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