Phenylephrine-induced recruitable preload from the venous side

Jacobs, Rita; Lochy, Stijn; Malbrain, Manu L N G

doi:10.1007/s10877-018-0225-1

Cited by 15 publications

(8 citation statements)

References 30 publications

(31 reference statements)

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“…Over the first Resuscitation phase and the following Optimization phase, the use of vasopressors (like norepinephrine) could be considered [ 126 ]. During SAP, hypotension is partially due to vasodilation and an hyperdynamic circulatory state usually follows fluid resuscitation [ 127 , 128 ].…”

Section: Fluid Resuscitation: An Individualized Approachmentioning

confidence: 99%

Intravenous fluid therapy in patients with severe acute pancreatitis admitted to the intensive care unit: a narrative review

Crosignani

Spina

Marrazzo

et al. 2022

Ann. Intensive Care

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Patients with acute pancreatitis (AP) often require ICU admission, especially when signs of multiorgan failure are present, a condition that defines AP as severe. This disease is characterized by a massive pancreatic release of pro-inflammatory cytokines that causes a systemic inflammatory response syndrome and a profound intravascular fluid loss. This leads to a mixed hypovolemic and distributive shock and ultimately to multiorgan failure. Aggressive fluid resuscitation is traditionally considered the mainstay treatment of AP. In fact, all available guidelines underline the importance of fluid therapy, particularly in the first 24–48 h after disease onset. However, there is currently no consensus neither about the type, nor about the optimal fluid rate, total volume, or goal of fluid administration. In general, a starting fluid rate of 5–10 ml/kg/h of Ringer’s lactate solution for the first 24 h has been recommended. Fluid administration should be aggressive in the first hours, and continued only for the appropriate time frame, being usually discontinued, or significantly reduced after the first 24–48 h after admission. Close clinical and hemodynamic monitoring along with the definition of clear resuscitation goals are fundamental. Generally accepted targets are urinary output, reversal of tachycardia and hypotension, and improvement of laboratory markers. However, the usefulness of different endpoints to guide fluid therapy is highly debated. The importance of close monitoring of fluid infusion and balance is acknowledged by most available guidelines to avoid the deleterious effect of fluid overload. Fluid therapy should be carefully tailored in patients with severe AP, as for other conditions frequently managed in the ICU requiring large fluid amounts, such as septic shock and burn injury. A combination of both noninvasive clinical and invasive hemodynamic parameters, and laboratory markers should guide clinicians in the early phase of severe AP to meet organ perfusion requirements with the proper administration of fluids while avoiding fluid overload. In this narrative review the most recent evidence about fluid therapy in severe AP is discussed and an operative algorithm for fluid administration based on an individualized approach is proposed.

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Section: Fluid Resuscitation: An Individualized Approachmentioning

confidence: 99%

Intravenous fluid therapy in patients with severe acute pancreatitis admitted to the intensive care unit: a narrative review

Crosignani

Spina

Marrazzo

et al. 2022

Ann. Intensive Care

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“…On average, a higher dose of phenylephrine would increase MAP even more but simultaneously decrease CI as higher SVRI increasing the afterload would probably lead to reduced CI and would produce even more pronounced re ex bradycardia. Also, a favourable effect of venoconstriction, that is pooling blood to the heart, would be outweighed by higher venous resistance to ow and preload would eventually decrease (32).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Crystalloid Co-Loading on Circulatory Stability During General Anaesthesia Induction in ASA II/III Patients for Major Abdominal Surgery: A Randomized Controlled Trial

Kos

Kamenik

Dinevski

2022

Preprint

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BackgroundWe studied the effect of crystalloid co-loading with simultaneous infusion of vasopressor phenylephrine on circulatory stability during general anaesthesia induction with propofol in ASA II/III patients. We analysed the postinduction phase because circulatory instability is most prevalent in this period and more prominent in multimorbid patients. Prevention rather than treatment might be a better strategy to avoid complications associated with even short periods of instability.Methods46 ASA II/III patients were randomly assigned to two treatment groups. During the induction, the control group received an infusion of phenylephrine only and the test group received the same phenylephrine regimen and also a crystalloid co-load. Cardiac index (CI), mean arterial pressure (MAP), stroke volume index (SVI), systemic vascular resistance index (SVRI), stroke volume variation (SVV) and heart rate (HR) were recorded for 18 minutes and the dynamics of change between groups analysed.ResultsCI decreased in both groups after the induction but less in the test group, almost reaching statistical significance (p=0,052). MAP also decreased more in the control group; however, not reaching statistical significance. HR decreased in both groups, significantly more in the test group (p=0,041). SVRI almost identically increased in both groups. SVI decreased in the control group, whereas it significantly increased after initial decrease in the test group (p=0,006). SVV slowly decreased under 10% in the test group and increased over 10% in the control group.ConclusionsOur results show that phenylephrine combined with crystalloid co-loading enables better circulatory stability than phenylephrine alone.Trial registrationThe study was registered on 15th of March 2017 at ISRCTN registry: http://www.isrctn.com/ISRCTN46293288 and was retrospectively registered.Clinical trial number is ISRCTN46293288.

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“…To reduce fluid administration, the early use of vasopressors may be needed. Early application of vasopressors has the potential to reduce intravascular volume deficit by recruiting blood from the venous compartment, while avoiding the detrimental effects of fluid administration [17]. Delaying vasopressor use until fluid resuscitation has demonstrably failed to correct shock, on the other hand, may delay resolution, and assumes that fluid resuscitation is safer than vasopressor use, an assumption which is contrary to the available data [18,19] and which may be driven in part by resource constraints.…”

Section: Restrictive Fluid Administrationmentioning

confidence: 99%