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Critically Ill Children and the Microcirculation Go with the Flow?

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Critically Ill Children and the Microcirculation Go with the Flow? Critically ill children and the microcirculation Go with the flow? Erik Buijs ISBN: 978-94-6169-510-9 Cover design: Joney Habraken. Layout and printing: Optima Grafische Communictie, Rotterdam, the Netherlands © Erik Buijs, Rotterdam, the Netherlands All rights reserved. No part of this thesis may be reproduced, stored in a retrieval system of transmitted in any form or by any means, without prior written permission of the copyright owner. Critically Ill Children and the Microcirculation Go with the Flow? Kritisch zieke kinderen en de microcirculatie Met de stroom mee? Proefschrift ter verkrijging van de graad van doctor aan de Erasmus Universiteit Rotterdam op gezag van de rector magnificus Prof.dr. H.A.P. Pols en volgens besluit van het College voor Promoties. De openbare verdediging zal plaatsvinden op dinsdag 24 juni 2014 om 15.30 uur door Erik Antonius Bernardus Buijs geboren te Utrecht PROMOTIECOMMISSIE Promotoren: Prof.dr. D. Tibboel Prof.dr. C. Ince Overige leden: Prof.dr. J. Bakker Prof.dr. A.P. Bos Prof.dr. A.H.J. Danser CONTENTS PART I INTRODUCTION Chapter 1 Hemodynamic monitoring in critically ill children 9 PART II NON-INVASIVE MICROCIRCULATORY IMAGING Chapter 2 Reproducibility of microvascular vessel density assessment in 29 Sidestream Dark Field (SDF) derived images of healthy term newborns Chapter 3 The microcirculation is unchanged in neonates with severe 43 respiratory failure after the initiation of ECMO treatment Chapter 4 The microcirculation in children with primary respiratory 57 disease requiring venoarterial or venovenous extracorporeal membrane oxygenation: a prospective cohort study Chapter 5 Cardiovascular catecholamine receptors in children: their 79 significance in cardiac disease Chapter 6 Increasing mean arterial blood pressure and heart rate with 103 catecholaminergic drugs does not improve the microcirculation in children with congenital diaphragmatic hernia: a prospective cohort study Chapter 7 Early microcirculatory impairment during therapeutic 127 hypothermia is associated with poor outcome in post-cardiac arrest children: a prospective observational cohort study PART III ARTERIAL LACTATE MONITORING Chapter 8 Arterial lactate as an early predictor for extracorporeal 149 membrane oxygenation in neonates with congenital diaphragmatic hernia Chapter 9 Arterial lactate for predicting mortality in children requiring 167 extracorporeal membrane oxygenation PART IV DISCUSSION & SUMMARY Chapter 10 General discussion 189 Chapter 11 Summary / Samenvatting 215 Appendices Curriculum Vitae 227 List of publications 229 PhD portfolio 231 Dankwoord 233 PART I INTRODUCTION Chapter 1 Hemodynamic monitoring in critically ill children Adapted from: Biomarkers and clinical tools in critically ill children: are we heading toward tailored drug therapy? Erik A.B. Buijs, Alexandra J.M. Zwiers, Erwin Ista, Dick Tibboel, Saskia N. de Wildt. Biomarkers in Medicine (2012); 6: 239-257. Introduction Introduction Around 5,000 children between the age of 1 day and 18 years are admitted to one of the eight dedicated pediatric ICUs in the Netherlands [1]. They form a heterogeneous group: 45-55% present with acute, severe pathology and are deemed as critically ill [1]. The term critical illness denominates life-threatening disease, typically due to the severe dysfunction of the cardiovascular system and/or the respiratory system. 1 Cardiorespiratory dysfunction may result in a mismatch between oxygen consump- 11 tion (VO2) and oxygen delivery (DO2) [2]. Figure 1 shows the equation that describes the VO2-DO2 balance, in which CaO2 and CvO2 stand for arterial and mixed venous blood oxygen content, respectively [3]. For Q, the classical view is that it represents cardiac output. However it is more pragmatic when Q represents blood flow, for instance in case the VO2-DO2 balance in a single organ is to be estimated [3, 4]. As can be deduced from the VO2-DO2 equation, blood flow is key for preserving the VO2-DO2 balance: it is both a prerequisite for DO2 and a component in VO2. Also, blood flow can serve as a physiological compensatory mechanism once VO2-DO2 mismatching is imminent [2]. If blood flow dysfunctions considerably and persistently, a cascade of events will follow that includes cellular dysfunction, organ dysfunction, (multiple) organ failure, and, ultimately, death of the child [5]. Hence, blood flow is one of the essential determinants for cellular homeostasis. Figure 1. The equation describing the balance between oxygen consumption (VO2) and oxygen delivery (DO2). CaO2 represents arterial blood oxygen content and CvO2 represents venous blood oxygen content. The most feasible interpretation of Q is blood flow. The macrocirculation and the microcirculation Blood flow is regulated at three different levels within the circulation: the systemic circulation –i.e. towards and away from organs–, the regional circulation–i.e. between and within organs–, and tissue circulation –i.e. within organs at cellular level– [6]. Blood flow at the central and regional levels is also referred to as the macrocirculation; blood flow at tissue level as the microcirculation. The macrocirculation encompasses the heart and all the blood vessels with a diameter >100µm [7]. Its main function is to assure blood flow at the systemic and the regional level. Also, the macrocirculation should ensure blood supply to the microcirculation: macrocirculatory driving pressure –which is determined by cardiac output– generates microcirculatory blood flow. In clinical practice, inotropic, lusitropic, and chronotropic agents are often primarily administered to improve blood flow at macrocirculatory level. By doing so, it is anticipated that DO2 will enhance as well. Dopamine, for example, increases the strength of myocardial contraction –i.e. inotropic action– as well as the contraction rate –i.e. chronotropic action–, whilst milrinone affects the ability of the myocardium to relax –i.e. lusitropic action– [8]. The microcirculation consists of three entities: arterioles, capillaries, and venules 1 [7]. This is where gases, nutrients, water, hormones, drugs, and waste products are 12 exchanged between the blood and the tissue cells [9]. Adequate microcirculation is pivotal for normal cellular function and, therefore, also for organ function [7]. Whilst microcirculatory functioning relies heavily on the macrocirculation, the reverse is also true: the microcirculation determines partly macrocirculatory functioning. For instance, already in the 1960s Guyton described that three factors govern the regulation of car- diac output: 1) the function of the heart itself, 2) the resistance to blood flow through the peripheral tissue circulation, and 3) the degree of filling of the circulatory system [10, 11]. The latter is determined by the microcirculation as well given its function as a volume reservoir for blood [12]. So, cardiac output –and therefore macrocirculatory function– is to a great extent influenced by the microcirculation [10]. Thus, the macrocirculation and the microcirculation form a physiologically complex, dynamic entity in which the microcirculation is dependent on macrocirculation and vice versa. When VO2-DO2 mismatching is impending, macrocirculatory function is, amongst others, maintained initially by two mechanisms: the regulation of vascular resistance to preserve arterial blood pressure and the enhancement of venous return / cardiac preload through redistribution of blood [10, 11]. Unfortunately, this initial response is a temporary compromise because it goes at the expense of microcirculatory reduction in the non-vital and, to a lesser extent, the vital organs [12]. Ultimately, in the face of severe disease, the microcirculation must be restored in order to maintain the VO2-DO2 balance. Moreover, research in critically ill adults with distributive or cardiogenic shock indicat- ed that the microcirculation can be affected independently from the macrocirculation [13, 14]. Likewise, restoring the macrocirculation in adults with shock does not always imply that the microcirculation is restored as well [15]. Hence, it is advocated that both the macrocirculation and the microcirculation should be monitored and treated if necessary. This concept is increasingly supported by studies in adults using goal-directed therapy with endpoints such as arterial lactate [16]. Circulatory monitoring in the neonatal and pediatric ICU Neonatal and pediatric ICUs offer advanced treatment and 24-hour monitoring. The purpose of monitoring is two-fold: to assess the nature, severity, and progression of disease –i.e. patient status monitoring– and to determine the type, timing, dose, and Introduction effectiveness of treatment –i.e. therapeutic monitoring– [17]. Adequate monitoring is a prerequisite for adequate treatment. Macrocirculatory monitoring, and in particular cardiac output monitoring, is one of the keystones of hemodynamic monitoring [18, 19]. In this respect, circulatory monitor- ing represents the cornerstone of intensive care management in critically ill children [20]. In adults, the pulmonary artery catheter is deemed the gold standard of invasive 1 macrocirculatory monitoring [21]. Its true value is, however, increasingly debated and 13 it is argued that it should be used only during specific disease conditions [21]. In criti- cally ill children, the use of the pulmonary artery catheter is less feasible. Cardiac output monitoring in children in general is, among other things, hindered by technical and size constraints, potential toxicity of indicators,
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