Clinical examination: a trigger but not a substitute for hemodynamic evaluation

Backer, Daniel De; Vieillard‐Baron, Antoine

doi:10.1007/s00134-019-05538-9

Cited by 13 publications

(11 citation statements)

References 10 publications

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“…Alterations in CRT and mottling scores can be used for basic monitoring as they correlate with outcome [ 6 , 7 ] and rapidly respond to therapeutic interventions. However, they are poorly correlated with cardiac output (CO), do not identify the source of tissue hypoperfusion, and cannot direct the necessary interventions [ 8 ].…”

Section: Personalization Of Monitoringmentioning

confidence: 99%

A plea for personalization of the hemodynamic management of septic shock

et al. 2022

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Although guidelines provide excellent expert guidance for managing patients with septic shock, they leave room for personalization according to patients’ condition. Hemodynamic monitoring depends on the evolution phase: salvage, optimization, stabilization, and de-escalation. Initially during the salvage phase, monitoring to identify shock etiology and severity should include arterial pressure and lactate measurements together with clinical examination, particularly skin mottling and capillary refill time. Low diastolic blood pressure may trigger vasopressor initiation. At this stage, echocardiography may be useful to identify significant cardiac dysfunction. During the optimization phase, echocardiographic monitoring should be pursued and completed by the assessment of tissue perfusion through central or mixed-venous oxygen saturation, lactate, and carbon dioxide veno-arterial gradient. Transpulmonary thermodilution and the pulmonary artery catheter should be considered in the most severe patients. Fluid therapy also depends on shock phases. While administered liberally during the resuscitation phase, fluid responsiveness should be assessed during the optimization phase. During stabilization, fluid infusion should be minimized. In the de-escalation phase, safe fluid withdrawal could be achieved by ensuring tissue perfusion is preserved. Norepinephrine is recommended as first-line vasopressor therapy, while vasopressin may be preferred in some patients. Essential questions remain regarding optimal vasopressor selection, combination therapy, and the most effective and safest escalation. Serum renin and the angiotensin I/II ratio may identify patients who benefit most from angiotensin II. The optimal therapeutic strategy for shock requiring high-dose vasopressors is scant. In all cases, vasopressor therapy should be individualized, based on clinical evaluation and blood flow measurements to avoid excessive vasoconstriction. Inotropes should be considered in patients with decreased cardiac contractility associated with impaired tissue perfusion. Based on pharmacologic properties, we suggest as the first test a limited dose of dobutamine, to add enoximone or milrinone in the second line and substitute or add levosimendan if inefficient. Regarding adjunctive therapies, while hydrocortisone is nowadays advised in patients receiving high doses of vasopressors, patients responding to corticosteroids may be identified in the future by the analysis of selected cytokines or specific transcriptomic endotypes. To conclude, although some general rules apply for shock management, a personalized approach should be considered for hemodynamic monitoring and support.

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Section: Personalization Of Monitoringmentioning

confidence: 99%

A plea for personalization of the hemodynamic management of septic shock

et al. 2022

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“…Post analyses of potential confounding by norepinephrine dose (5) We assessed patients by dose of norepinephrine using the median (0.205, IQR 0.1225-0.3975) and histogram (Fig. 3, Panel A).…”

Section: Baseline Characteristicsmentioning

confidence: 99%

Do blood pressure changes following a small bolus of propofol correlate with fluid responsiveness as assessed with stroke volume variation – an experimental study

Stefaniak

Spychalski

Owczuk

2022

Preprint

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Background For many years, in everyday practice at intensive care units (ICUs) and in high-risk surgery patients, there has been a need for objective and repetitive methods to assess patients’ volemia. Hypotension consecutive to propofol administration may be dependent on volemia. In oligovolemic patients, propofol-induced sympathetic nervous system depression may cause a decrease in blood pressure greater than that in normovolemic patients. The aim of the study was to determine whether blood pressure decrease after a small bolus of propofol will correlate with fluid responsiveness evaluated with stroke volume variation (SVV) obtained with a PiCCO (Getinge AB, Göteborg, Sweden) device. Methods We enrolled 50 intensive care unit (ICU) patients whose lungs were mechanically ventilated. The patients were temporarily sedated with midazolam infusion for the length of the trial. Prior to propofol injection, the following parameters were acquired for every patient: heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), invasive blood pressure and infusion rate of catecholamines and noradrenergic vasopressors. The PiCCO device was calibrated, and stroke volume variation (SVV) was calculated and recorded. Each patient received consecutive propofol boluses of 0.25 mg kg− 1, 0.5 mg kg− 1, and 1.0 mg kg− 1. After each bolus, systolic and diastolic invasive blood pressure, heart rate (HR), continuous cardiac output (CCO), continuous cardiac index (CCI), stroke volume index (SI), and stroke volume variation (SVV) were recorded every fifteen seconds for ten minutes. Results We found a statistically significant weak-to-moderate positive correlation after propofol 1 mg kg− 1 between ΔSBP and SVV for every timepoint (p < 0.05). Additionally, we discovered statistically significant differences (t test, p = 0.004), with a mean difference of -15.42 mmHg (95% CI, -25.73 to -5.11), between ΔSBP (135) in patients receiving > 0.2 mcg kg− 1 min− 1 norepinephrine and patients receiving ≤ 0.2 mcg kg− 1 min− 1 norepinephrine. Conclusion We found that a 1 mg kg− 1 bolus of propofol cannot predict fluid responsiveness in ICU patients receiving norepinephrine infusion. We believe, however, that these findings open a new field for further study in noninvasive haemodynamic measurements. Trial registration Prior to the study, Independent Bioethical Committee consent was sought and obtained (NKKBN/91-147/2019). This study was registered at ClinicalTrails.gov (NCT03917446) on 17th April 2019, retrospectively registered.

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“…8,9 Accordingly, these signs of skin hypoperfusion should be used to trigger advanced hemodynamic evaluation rather than replace it. 10…”

Section: Clinical Signs Of Tissue Hypoperfusion (Including Skin Bloodmentioning

confidence: 99%