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Fluid challenge Revisited. D. Matamis M.D I.C.U PAPAGEORGIOU Hospital Thessaloniki Greece. Physiology. DO 2 – VO 2 - SvO 2. Determinants of Tissue Oxygenation. Relationship between Ht and DO2. VO 2 -VCO 2 production during shivering. VO 2 -VCO 2 production during agitation.
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Fluid challenge Revisited D. Matamis M.D I.C.U PAPAGEORGIOU Hospital Thessaloniki Greece
DO2/VO2 imbalance Decrease in O2 delivery DO2=CO x CaO2 x 10 Increase in O2 Consumption VO2= CO x (a-v)DO2 O2 reserves 25% of the Ο2 delivered in the periphery is used Is it reasonable? - CaO2 =20 ml/dl - (a-v)DO2 = 5 ml/dl -SvO2 75%, Marathon Runners Deep Divers (mammals, Birds) Tissue Hypoxia
Critically ill patients are suffering Trauma Severe Sepsis Extensive Surgery If we increase DO2 Mortality Goals of the hemodynamic optimization DO2 ? SvO2 ?, SvcO2 ? C.O ? Tissue Hypoxia -The Concept of Supra-normal Values
SvcO2 jugular SvO2 hepatic SvO2 renal SvO2 coronary sinus SvO2 mesenteric SvO2 Regional SvO2
PRO CON
Fluids are primarily required to reverse hypovolemia • Hypovolemia may be due to external or internal fluid losses • External fluid losses (Bleeding, losses from G.I, U.T (diabetes, diabetes insipidus), skin or peritoneal surface) • Internal fluid losses (exudation, transudation or redistribution of the body fluids – distributive shock, especially in sepsis) • Volume replacement is essential to restore C.O and perfusion to vital organs and tissues
Misconceptions about fluid administration • We should stop fluid administration because the CVP is high • We should stop fluid administration because there is evidence of lung edema on the chest X ray • We should stop fluid administration because the patient has already received a large volume in a short period of time • Tachycardia is mainly due to volume deficit and we should prompt increase the fluid administration • I gave fluids to increase the CVP to 12 mmHg to exclude an underlying hypovolemia
Clinical end points of fluid challenge • To increase SV and C.O • To increase ABP • To increase urine output • When the decision of fluid loading is based on clinical criteria and /or CVP measurements, 50% of the patients do not respond by a significant increase in SV and CO
Methods of preload assessment Static indices • CVP • PAOP Dynamic indices • Pulse Pressure Variation (PPV), or Stroke Volume Variation (SVV) • Aortic blood flow velocity • IVC collapsibility • Passive Leg Rising (PLR) • 2D ECHO of the heart chambers
CVP-PAOP CVP (Pressure) reflect the preload of the RV=RV Volume • Limitations • RV compliance • Ventricular inter-dependence • Lung hyperinflation – PVR PAOP (Pressure) = LA pressure=LVED Pressure = LVED Volume • Limitations • LV Compliance • Tachycardia, MV disease, • Lung Hyperinflation (High PEEP, auto PEEP)
Am J Respir Crit Care Med2000. 162:134-138 PPmax PPmean PPmax – PPmin PPV = PPmean The pulse pressure variation is the variation in pulse pressure over the ventilatory cycle, measured over the previous 30 second period.
Dynamic indices - Aortic Blood Velocity Chest 2001.119:867
SVmax SVmin SVmean Dynamic indices - SVV Dynamic parameters of volume responsiveness – Stroke Volume Variation SVmax – SVmin SVV = SVmean
SV increases during inspiration SV decreases during inspiration Dynamic indices - SVV Stroke volume
Dynamic indices - SVV Many studies have shown that SVV is a very accurate predictor of fluid responsiveness SVV > 15% a positive response to fluid loading is very likely SVV< 10% a positive response to fluid loading is very unlikely
Limitations of the SVV - Sustained cardiac arrhythmia - In Spontaneous Breathing patients (false negative) - In ARDS patients ventilated with small Vt (<8ml/kg)(false negative) - RV failure (false positive) - Drugs ( Esmolol)
In cases of false negative SVVis there an alternative solution? - When giving fluids is not risky (Surgery patients) • Give fluids and monitor SV and CO • If SV and CO up Responder • If SV and CO stable Inotropes - When giving fluids is risky (ARDS patients) • PLR maneuver for 1-2 minutes
Positive response Negative response Passive leg raising and fluid responsiveness Crit Care Med 2006;34:1402
Attention !!!!!! • Patients should not receive fluids because the SVV or PPV or IVC collapsibility is high • We - healthy individuals - are all fluid responders • The first question must be << does my patient need an increase in SV or in CO>> • Dynamic parameters will never answer this question • Clinical examination +++ • Biological tests (lactates, SvO2, C.O)
Cardiac Output Evaluation The absolute value of C.O. is meaningless. Hypo, Hyperthermia, Drugs) ICU patients Frequent modifications of Mechanical Ventilation and PEEP, TR, Sedation, General Anesthesia, Surgery, Variations of body temperature in the O.R., Substantial blood losses. SvO2, ScvO2, (a-v)DO2, DO2, VO2. Adequacy of C.O and oxygen transport, quality of tissue oxygenation.
Pulse contour Cardiac Output (PCCO):Flaws & Limitations • Aortic Valve disease • Arrhythmias • Quality of the arterial waveform • Frequent & rapid changes in arterial compliance • Need for frequent calibrations - every 4h or before important acquisitions Minimally invasive???
7 randomized trials 1016 patients included Major problem: crossover of the patients Time of intervention Pre or postoperative in the ICU Timing of inotropic support Maximizing Oxygen delivery in critically ill patients: A methodologic appraisal of the evidence. Heyland et al. Crit Care Med 1996;24:517-24
21 randomized controlled trials Mortality reduction with hemodynamic optimization when treated early before MSOF when group mortality is >20% Crit. Care Med 2002;30:1686-92