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A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation

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A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation Journal of Clinical Medicine Review A Physiologic Approach to Hemodynamic Monitoring and Optimizing Oxygen Delivery in Shock Resuscitation Amy Russell 2, Emanuel P. Rivers 3,4, Paresh C. Giri 1, Anja K. Jaehne 3 and H. Bryant Nguyen 1,2,* 1 Division of Pulmonary, Critical Care, Hyperbaric, Allergy, and Sleep Medicine, Loma Linda University, Loma Linda, CA 92354, USA; [email protected] 2 Department of Emergency Medicine, Loma Linda University, Loma Linda, CA 92354, USA; [email protected] 3 Department of Emergency Medicine, Henry Ford Hospital, Detroit, MI 48202, USA; [email protected] (E.P.R.); [email protected] (A.K.J.) 4 Surgical Critical Care, Henry Ford Hospital, Detroit, MI 48202, USA * Correspondence: [email protected]; Tel.: +1-909-558-4023 Received: 25 May 2020; Accepted: 27 June 2020; Published: 30 June 2020 Abstract: The approach to shock resuscitation focuses on all components of oxygen delivery, including preload, afterload, contractility, hemoglobin, and oxygen saturation. Resuscitation focused solely on preload and fluid responsiveness minimizes other key elements, resulting in suboptimal patient care. This review will provide a physiologic and practical approach for the optimization of oxygen delivery utilizing available hemodynamic monitoring technologies. Venous oxygen saturation (SvO2) and lactate will be discussed as indicators of shock states and endpoints of resuscitation within the framework of resolving oxygen deficit and oxygen debt. Keywords: shock; resuscitation; hemodynamic monitoring; fluid responsiveness; stroke volume; venous oxygen saturation; lactate; oxygen delivery 1. Introduction Circulatory shock is defined as inadequate oxygen delivery to meet metabolic and oxygen demands [1]. Mechanisms underlying this physiologic emergency are related to decreased cardiac output (CO) due to either decreased circulating volume (hypovolemic shock), obstruction of circulatory flow (obstructive shock), or impaired cardiac function (cardiogenic shock). A fourth recognized mechanism is based on the altered distribution of blood flow leading to perfusion failure (distributive shock). The occurring oxygen debt and tissue hypoperfusion, regardless of the underlying etiology of the shock, lead to cellular ischemia and injury and potentially to multi-organ dysfunction syndrome (MODS) and eventual death. By its definition, the goal in the treatment of shock is, therefore, to increase oxygen delivery (DO2) to meet oxygen demand in order to resolve the global tissue hypoperfusion. Oxygen delivery is determined by CO and blood oxygen content (CaO2) (Figure1). Therefore, resuscitation of shock at the bedside is dependent on optimizing the components of CO and CaO2: Preload, afterload, contractility, hemoglobin, and oxygen saturation. J. Clin. Med. 2020, 9, 2052; doi:10.3390/jcm9072052 www.mdpi.com/journal/jcm J. Clin. Med. 2020, 9, 2052 2 of 18 J. Clin. Med. 2020, 9, x FOR PEER REVIEW 2 of 18 Figure 1. Determinants of oxygen delivery (DO2). CO–Cardiac output; CaO2–Oxygen content; Figure 1. Determinants of oxygen delivery (DO2). CO–Cardiac output; CaO2–Oxygen content; Hgb– Hgb–Hemoglobin concentration; SaO2–Oxygen saturation; PaO2–Partial pressure of oxygen. Hemoglobin concentration; SaO2–Oxygen saturation; PaO2–Partial pressure of oxygen. Unfortunately, recent literature discussing shock resuscitation focuses only on preload, specifically fluidUnfortunately, responsiveness [2recent–4]. The literature passive legdiscussing raise (PLR) shock maneuver resuscitation has been popularized focuses only as a non-invasiveon preload, methodspecifically of simulating fluid responsiveness a fluid bolus [2–4]. due The to fears passive of administrating leg raise (PLR) anmaneuver actual bolus has been [5]. Additionally, popularized thereas a non-invasive has been much method debate of regardingsimulating what a fluid amounts bolus todue a fluidto fears bolus of administrating and what type an of fluidactual should bolus be[5]. used. Additionally, there has been much debate regarding what amounts to a fluid bolus and what type of fluidIn thisshould review, be used. we will provide the reader with a practical review on shock resuscitation beyond the fluidIn this bolus review, and assessmentwe will provide of fluid the responsiveness,reader with a practical discussing review the on physiologic shock resuscitation basis for variousbeyond bedsidethe fluid hemodynamic bolus and assessment monitoring of fluid tools responsive available toness, optimize discussing oxygen the delivery.physiologic While basis fundamental, for various webedside believe hemodynamic that these concepts monitoring are important tools available for clinicians to optimize to apply oxygen when delivery. facedwith While patients fundamental, having complexwe believe hemodynamic that these concepts presentations. are important We will for firstclinicians discuss to measurementsapply when faced of preloadwith patients as this having is the initialcomplex target hemodynamic of resuscitation. presentations. We then review We will the techniquesfirst discuss of measurements determining fluid of preload responsiveness as this basedis the oninitial the classicaltarget of Frank–Starling resuscitation. andWe Guytonthen review curves. the Optimizing techniques preload of determining thus requires fluid measuring responsiveness stroke volumebased on (SV) the and classical CO with Frank–Starling a number of available and Guyt technologies.on curves. OnceOptimizing preload preload is addressed, thus afterloadrequires andmeasuring contractility stroke are volume targeted. (SV) Finally, and CO the with resuscitation a number endpoints of available venous technologies. oxygen saturation Once preload (SvO 2is) andaddressed, lactate areafterload applied and to determine contractility if shock are persists,targeted. requiring Finally, further the resuscitation increased oxygen endpoints delivery venous with inotrope,oxygen saturation blood transfusion, (SvO2) and and lactate/or oxygen are applied supplementation to determine (e.g., if mechanical shock persists, ventilation requiring support). further increased oxygen delivery with inotrope, blood transfusion, and/or oxygen supplementation (e.g., 2.mechanical Measuring ventilation Preload support). 2.1.2. Measuring Left Ventricular Preload End-Diastolic Volume and Pressure Preload is the first target for the resolution of shock. Left ventricular end-diastolic volume (LVEDV) is2.1. the Left reference Ventricular standard End-Diastolic for the assessmentVolume and ofPressure preload. LVEDV can be measured or estimated using eitherPreload transthoracic is the echocardiographyfirst target for the (TTE) resolution or transesophageal of shock. Left echocardiography ventricular end-diastolic (TEE). The volume apical four-chamber(LVEDV) is the view reference visualizes standard the left ventricle.for the assessment The LVEDV of measurement preload. LVEDV is based can on be images measured obtained or inestimated end-diastole using corresponding either transthoracic with the echocardiogr R-wave on anaphy electrocardiogram. (TTE) or transesophageal LVEDV is calculated echocardiography based on (TEE). The apical four-chamber view visualizes the left ventricle. The LVEDV measurement is based on images obtained in end-diastole corresponding with the R-wave on an electrocardiogram. LVEDV J. Clin. Med. 2020, 9, 2052 3 of 18 J. Clin. Med. 2020, 9, x FOR PEER REVIEW 3 of 18 tracingis calculated the endocardium based on tracing at end-diastole the endocardium and applying at end-diastole a modified and Simpson’s applying rule a [modified6]. This assessment Simpson’s isrule user-dependent [6]. This assessment with respect is user to-dependent skill and appropriatewith respect image to skill acquisition. and appropriate Additionally, image acquisition. LVEDV is measuredAdditionally, at a singularLVEDV timeis measured point, not at addressing a singular the ti needme point, for serial not assessmentsaddressing requiredthe need to for evaluate serial responseassessments to interventions. required to evaluate Alternatively, response pressure to interventions. instead of Alternatively, volume is often pressure measured, instead which of volume has its ownis often set ofmeasured, limitations. which Left has ventricular its own end-diastolicset of limitations. pressure Left (LVEDP) ventricular measured end-diastolic by the leftpressure heart catheterization(LVEDP) measured can be by afalse the representationleft heart catheterizat of LVEDVion in can common be a false pathological representation states such of LVEDV as chronic in leftcommon heart failurepathological with low states compliance. such as chronic Compliance left he isart equal failure to thewith change low compliance. in volume dividedCompliance by the is changeequal to in the pressure change (C in= volumeDV/DP). divided With a decrease by the change in ventricular in pressure compliance (C = ΔV/ (stiΔffP).ening With of thea decrease ventricle) in seenventricular in left ventricularcompliance hypertrophy,(stiffening of thethe left ventricle) ventricular seen pressure in left ventricular can be elevated hypertrophy, in the presence the left ofventricular hypovolemia. pressure can be elevated in the presence of hypovolemia. 2.2.2.2. Pulmonary CapillaryCapillary WedgeWedge PressurePressure andand LeftLeft AtrialAtrial PressurePressure UsingUsing aa pulmonary pulmonary artery artery catheter catheter (PAC) (PAC) we can we measure can measure left atrial left pressure atrial (LAP)pressure via pulmonary(LAP) via capillarypulmonary
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