Marieke Poterman
University Medical Center Groningen
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BJA: British Journal of Anaesthesia | 2014
Jaap Jan Vos; Marieke Poterman; E.A. Mooyaart; Marloes Weening; Michel Struys; Thomas Scheeren; A.F. Kalmar
BACKGROUND For a majority of patients undergoing anaesthesia for general surgery, mean arterial pressure (MAP) is only measured intermittently by arm cuff oscillometry (MAPiNIAP). In contrast, the Nexfin(®) device provides continuous non-invasive measurement of MAP (MAPcNIAP) using a finger cuff. We explored the agreement of MAPcNIAP and MAPiNIAP with the gold standard: continuous invasive MAP measurement by placement of a radial artery catheter (MAPinvasive). METHODS In a total of 120 patients undergoing elective general surgery and clinically requiring MAPinvasive measurement, MAPiNIAP and MAPcNIAP were measured in a 30 min time period at an arbitrary moment during surgery with stable haemodynamics. MAPiNIAP was measured every 5 min. RESULTS Data from 112 patients were analysed. Compared with MAPinvasive, modified Bland-Altman analysis revealed a bias (sd) of 2 (9) mm Hg for MAPcNIAP and -2 (12) mm Hg for MAPiNIAP. Percentage errors for MAPcNIAP and MAPiNIAP were 22% and 32%, respectively. CONCLUSIONS In a haemodynamically stable phase in patients undergoing general anaesthesia, the agreement with invasive MAP of continuous non-invasive measurement using a finger cuff was not inferior to the agreement of intermittent arm cuff oscillometry. Continuous measurements using a finger cuff can interchangeably be used as an alternative for intermittent arm cuff oscillometry in haemodynamically stable patients, with the advantage of beat-to-beat haemodynamic monitoring. CLINICAL TRIAL REGISTRATION NCT 01362335 (clinicaltrials.gov).
European Journal of Anaesthesiology | 2015
Marieke Poterman; Jaap Jan Vos; Hugo Vereecke; Michel Struys; Henk Vanoverschelde; Thomas Scheeren; A.F. Kalmar
BACKGROUND Phenylephrine and norepinephrine are two vasopressors commonly used to counteract anaesthesia-induced hypotension. Their dissimilar working mechanisms may differentially affect the macro and microcirculation, and ultimately tissue oxygenation. OBJECTIVES We investigated the differential effect of phenylephrine and norepinephrine on the heart rate (HR), stroke volume (SV), cardiac index (CI), cerebral tissue oxygenation (SctO2) and peripheral tissue oxygenation (SptO2), and rate-pressure product (RPP). DESIGN A randomised controlled study. SETTING Single-centre, University Medical Center Groningen, The Netherlands. PATIENTS Sixty normovolaemic patients under balanced propofol/remifentanil anaesthesia. INTERVENTIONS If the mean arterial pressure (MAP) dropped below 80% of the awake state value, phenylephrine (100 &mgr;g + 0.5 &mgr;g kg−1 min−1) or norepinephrine (10 &mgr;g + 0.05 &mgr;g kg−1 min−1) was administered in a randomised fashion. MAIN OUTCOME MEASURES MAP, HR, SV, CI, SctO2, SptO2 and rate-pressure product (RPP) analysed from 30 s before drug administration until 240 s thereafter. RESULTS Phenylephrine and norepinephrine caused an equivalent increase in MAP [&Dgr; = 13 (8 to 22) and &Dgr; = 13 (9 to 19) mmHg, respectively] and SV [&Dgr; = 6 ± 6 and &Dgr; = 5 ± 7 ml, respectively], combined with a significant equivalent decrease in HR (both &Dgr; = −8 ± 6 bpm), CI (both &Dgr; = −0.2 ± 0.3 l min−1 m−2) and SctO2 and an unchanged RPP (&Dgr; = 345 ± 876 and &Dgr; = 537 ± 1076 mmHg min−1). However, SptO2 was slightly but statistically significantly (P < 0.05) decreased after norepinephrine [&Dgr; = −3 (−6 to 0)%] but not after phenylephrine administration [&Dgr; = 0 (−1 to 1)%]. In both groups, SptO2 after vasopressor was still higher than the awake value. CONCLUSION In normovolaemic patients under balanced propofol/remifentanil anaesthesia, phenylephrine and norepinephrine produced similar clinical effects when used to counteract anaesthesia-induced hypotension. After norepinephrine, a fall in peripheral tissue oxygenation was statistically significant, but its magnitude was not clinically relevant.
European Journal of Anaesthesiology | 2017
Marieke Poterman; Thomas Scheeren; Marieke I. van der Velde; P. Buisman; Silvie Allaert; Michel Struys; A.F. Kalmar
BACKGROUND Induction of anaesthesia with propofol and remifentanil often induces unwanted bradycardia and hypotension, raising concerns regarding tissue oxygenation. The electrophysiological cardiac effects of remifentanil can be reversed by atropine. OBJECTIVE To investigate if prophylactic administration of atropine can attenuate the negative haemodynamic effects of propofol and a high dose of remifentanil during induction of anaesthesia. DESIGN A double-blind, randomised controlled trial. SETTING Single-centre, University Medical Center Groningen, The Netherlands. PATIENTS Sixty euvolaemic patients scheduled for surgery under general anaesthesia. INTERVENTIONS Anaesthesia was induced and maintained with a target-controlled infusion of propofol with a target effect-site concentration (Ce) of 2.5 &mgr;g ml−1, remifentanil (target-controlled infusion), (Ce 8 ng ml−1) and cis-atracurium. Methylatropine (500 &mgr;g) or 0.9% saline was administered at immediately before induction of anaesthesia. MAIN OUTCOME MEASURES The changes (&Dgr;) in mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), rate pressure product, cerebral tissue oxygenation and peripheral tissue oxygenation between induction of anaesthesia (T0) and 10 min later (T10). RESULTS Atropine significantly attenuated the changes in the outcome measures between T0 and T10. Median (inter-quartile range) changes were MAP, &Dgr; = −24 (−40 to −21) vs. &Dgr; = −37 mmHg (−41 to −31) (P = 0.02); HR, &Dgr; = 0 ± 13 vs. −19 ± 11 bpm (P < 0.01); CI, &Dgr; = −0.4 ± 0.7 vs. −0.9 ± 0.6l min−1 m−2 (P < 0.01) and rate pressure product, &Dgr; = −3241 (−5015 to −613) vs. &Dgr; = −5712 mmHg min−1 (−6715 to −3917) (P < 0.01). Cerebral tissue oxygenation and peripheral tissue oxygenation did not change in either group. Maximum HR after atropine was 102 (86 to 116) vs. 85 bpm (76 to 95). CONCLUSION Administration of atropine, before induction of anaesthesia with propofol and high-dose remifentanil, can significantly reduce the decreases in HR, MAP and CI. TRIAL REGISTRATION Clinicaltrials.gov identifier: NCT01871922.
Anesthesia & Analgesia | 2014
A.F. Kalmar; Marieke Poterman; Thomas Scheeren
To the Editor The articles by Park et al. 1 and Sjöstrand et al.2 deal with the accuracy of the noninvasive hemoglobin (SpHb) measurement of the Masimo Radical 7 monitor. While we agree that SpHb may be of value as a trend monitor to decrease the number of invasive measurements, appropriate timing of the determination of the baseline value is essential. Although SpHb readings are stable after mere seconds in steady-state conditions, induction of general anesthesia or variations in fractions of inspired oxygen (Fio2) in our experience almost systematically induce an increase in SpHb (Fig. 1), often by as much as 40%, even in ASA physical status I and II patients scheduled for elective surgery. Likewise, the methodology described by Sjöstrand et al.2 of using SpHb may certainly be of interest for pharmacokinetic studies, but if it were to be translated to clinical situations, the sources of drift in SpHb should be addressed first. Massive fluid resuscitation in emergency settings is often accompanied by induction of general anesthesia and changes in Fio2. Colloid administration may even independently decrease SpHb accuracy,3 casting additional bias. While changes in perfusion index affect signal reliability, our observed systematic increase in SpHb in patients with only minor comorbidity and adequate perfusion index suggests there may be a more fundamental causality. This may be either related to concomitant changes in Fio2 and thus peripheral oxyhemoglobin saturation or to vasodilation following induction of anesthesia. Determination of the baseline value (and in newer models manual recalibration of the device) using an invasive gold standard assessment would likely be performed early Copyright
Canadian Journal of Anaesthesia-journal Canadien D Anesthesie | 2015
Jaap Jan Vos; Marieke Poterman; Pieternel Papineau Salm; Kai Van Amsterdam; Michel Struys; Thomas Scheeren; A.F. Kalmar
BMC Anesthesiology | 2014
Paul A. van Beest; Jaap Jan Vos; Marieke Poterman; A.F. Kalmar; Thomas Scheeren
Perioperative medicine (London, England) | 2014
Jaap Jan Vos; Marieke Poterman; Laura Hannivoort; Victor W. Renardel de Lavalette; Michel Struys; Thomas Scheeren; A.F. Kalmar
European Journal of Anaesthesiology | 2017
Marieke Poterman; Thomas Scheeren; Marieke I. van der Velde; P. Buisman; Silvie Allaert; Michel Struys; A.F. Kalmar
Critical Care | 2014
Pa Van Beest; Jaap Jan Vos; Marieke Poterman; A.F. Kalmar; Thomas Scheeren
Archive | 2015
Jaap Jan Vos; Marieke Poterman; Pieternel Papineau Salm; Kai Van Amsterdam; Michel Struys; Thomas Scheeren; A.F. Kalmar