Influence of an acute increase in systemic vascular resistance on transpulmonary thermodilution-derived parameters in critically ill patients

Kozieras, Jan; Thuemer, O.; Sakka, Samir G.

doi:10.1007/s00134-007-0669-0

Cited by 9 publications

(6 citation statements)

References 16 publications

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“…Such findings could be ascribed to the α-mediated effect of reduction in systemic venous capacitance [4]. This hypothesis is in agreement with a previous clinical study that reported an elevation of the central blood volume--measured by transpulmonary thermodilution--in response to an acute norepinephrine-induced increase in systemic vascular resistance [22]. In our study, two findings suggest that many of our patients still had some preload reserve before norepinephrine introduction/increase: (a) the fact that GEDVI and CI both increased, and (b) the fact that the mean baseline SVV was above the presumed threshold value detecting volume responsiveness [20], and this in despite a rather low tidal volume.…”

Section: Discussionsupporting

confidence: 89%

Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension

et al. 2010

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IntroductionWe sought to examine the cardiac consequences of early administration of norepinephrine in severely hypotensive sepsis patients hospitalized in a medical intensive care unit of a university hospital.MethodsWe included 105 septic-shock patients who already had received volume resuscitation. All received norepinephrine early because of life-threatening hypotension and the need to achieve a sufficient perfusion pressure rapidly and to maintain adequate flow. We analyzed the changes in transpulmonary thermodilution variables associated with the increase in mean arterial pressure (MAP) induced by norepinephrine when the achieved MAP was ≥65 mm Hg.ResultsNorepinephrine significantly increased MAP from 54 ± 8 to 76 ± 9 mm Hg, cardiac index (CI) from 3.2 ± 1.0 to 3.6 ± 1.1 L/min/m2, stroke volume index (SVI) from 34 ± 12 to 39 ± 13 ml/m2, global end-diastolic volume index (GEDVI) from 694 ± 148 to 742 ± 168 ml/m2, and cardiac function index (CFI) from 4.7 ± 1.5 to 5.0 ± 1.6 per min. Beneficial hemodynamic effects on CI, SVI, GEDVI, and CFI were observed in the group of 71 patients with a baseline echocardiographic left ventricular ejection fraction (LVEF) >45%, as well as in the group of 34 patients with a baseline LVEF ≤45%. No change in CI, SVI, GEDVI, or CFI was observed in the 17 patients with baseline LVEF ≤45% for whom values of MAP ≥75 mm Hg were achieved with norepinephrine.ConclusionsEarly administration of norepinephrine aimed at rapidly achieving a sufficient perfusion pressure in severely hypotensive septic-shock patients is able to increase cardiac output through an increase in cardiac preload and cardiac contractility. This effect remained in patients with poor cardiac contractility except when values of MAP ≥75 mm Hg were achieved.

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Section: Discussionsupporting

confidence: 89%

Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension

et al. 2010

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“…After NE titration during hemorrhage, GEDV slightly increased (8.2%), which is in accordance to Kozieras et al. , investigating the effect of NE titration on indexed GEDV and left ventricular end‐diastolic area (LVEDAI) in septic patients (25). NE administration resulted in a significant increase in GEDVI and in LVEDAI ( n = 8).…”

Section: Discussionsupporting

confidence: 88%

Effects of norepinephrine on dynamic variables of fluid responsiveness during hemorrhage and after resuscitation in a pediatric porcine model

Renner

Meybohm

Hanß

et al. 2009

Pediatric Anesthesia

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Eight anesthetized piglets were studied at normovolemia, after stepwise blood withdrawal (25 ml x kg(-1)), after infusion of NE to restore mean arterial pressure (MAP), after NE titration was stopped and shed blood was retransfused and finally again after NE titration. Stroke volume (SV) was measured using a thermodilution pulmonary artery catheter. GEDV was measured by transpulmonary thermodilution. PPV and SVV were monitored continuously by pulse contour analysis. In response to NE administration during hemorrhage, MAP significantly increased (P < 0.01), PPV significantly decreased (P = 0.02), whereas SVV, SV and GEDV remained unchanged. After retransfusion, SVV and GEDV significantly correlated with volume induced percentage change in SV. This significant correlation was reversed after NE administration for SVV and persisted for GEDV. In conclusion, NE administration significantly affected PPV and SVV, whereas the volumetric variable GEDV remained unchanged.

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“…Similarly in patients with septic shock, Persichini and colleagues 138 demonstrated that deceasing the dose of norepinephrine, decreased the MCFP with a decrease in venous return and cardiac output. In a cohort of patients with septic shock Kozieras and colleagues 139 demonstrated that norepinephrine increased cardiac index, systemic vascular resistance and central blood volumes (intrathoracic blood volume, global end-diastolic volume), as measured by transpulmonary thermodilution. In this study extra-vascular lung water (EVLW) remained unchanged.…”

Section: Evidence Supporting the Deleterious Effects Of Aggressive Flmentioning

confidence: 99%

A rational approach to fluid therapy in sepsis

Marik

Bellomo

2016

British Journal of Anaesthesia

239

160

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Aggressive fluid resuscitation to achieve a central venous pressure (CVP) greater than 8 mm Hg has been promoted as the standard of care, in the management of patients with severe sepsis and septic shock. However recent clinical trials have demonstrated that this approach does not improve the outcome of patients with severe sepsis and septic shock. Pathophysiologically, sepsis is characterized by vasoplegia with loss of arterial tone, venodilation with sequestration of blood in the unstressed blood compartment and changes in ventricular function with reduced compliance and reduced preload responsiveness. These data suggest that sepsis is primarily not a volume-depleted state and recent evidence demonstrates that most septic patients are poorly responsive to fluids. Furthermore, almost all of the administered fluid is sequestered in the tissues, resulting in severe oedema in vital organs and, thereby, increasing the risk of organ dysfunction. These data suggest that a physiologic, haemodynamically guided conservative approach to fluid therapy in patients with sepsis would be prudent and would likely reduce the morbidity and improve the outcome of this disease.

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Influence of an acute increase in systemic vascular resistance on transpulmonary thermodilution-derived parameters in critically ill patients

Abstract: An acute increase in SVR by increasing norepinephrine dosage results in a reversible increase in central blood volumes (ITBV, GEDV) as measured by transpulmonary thermodilution and supported by echocardiography.

Cited by 9 publications

References 16 publications

Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension

Early administration of norepinephrine increases cardiac preload and cardiac output in septic patients with life-threatening hypotension

Effects of norepinephrine on dynamic variables of fluid responsiveness during hemorrhage and after resuscitation in a pediatric porcine model

A rational approach to fluid therapy in sepsis

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