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.
Highlights
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, obstruction of circulatory flow, or impaired cardiac function
While an absolute CVP target is not recommended, the late Dr Max Harry Weil first described the 5-2-0 rule using CVP to evaluate fluid responsiveness [19]
Summary
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 goal in the treatment of shock is, 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) (Figure 1). FFiigguurree22..PPrreessssuurreeRReelalatitoionnshshipips.s.AApaptaietinetnctacnanhahvaevfealfsaellsyeleyleevlaetveadtecdencternaltrvaelnvoeunsopursespsruersesu(Are) i(nAt)hien stehtetinsegttoinf ganoyf aonf ythoefftohlelofwolilnogw: iLnegf:tLveefnttvriecnutlraicruhlyarpehrytproeprthryopahffyecatfinfegctlienfgt vlefnttvriecnutlraircucolamr pcolimanpcleia(nEc)e, m(Eit)r, aml vitarlavlevdailsveeasdeisineacrseeaisnincgrelaesfitnagtrlieafltparetrsisaulrper(eDs)s,upruelm(Do)n, apruylmdiosenaasreyindcisreasienginaclrveeaosilnargparlevsesoulraer (pCr)e, spsuulrme o(nCa),rypuarlmteroyndarisyeaasreteirnycrdeiasseiansgepinuclmreoansianrgy aprutelmryopnraersysuarrete(rBy),prrigeshstuvreen(tBri)c,urliagrhhtyvpeenrttrriocpuhlayr ahffyepcetirntrgocpohmypalifafenccteinogf tchoemripglhiatnhceearotforthtreicruigsphitdhdeiasertasoerintcrriceuasspinigd rdigishetaasteriainl cprreeasssiunrge (rAig)h. t atrial pressure (A)
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