ACUTE CIRCULATORY FAILURE Inability for the cells to get enough oxygen in relation to their oxygen needs OXYGEN AVAILABILITY I am in SHOCK Arterial hypotension Altered cutaneous perfusion (mottled, clammy skin) I am in Altered mentation (obtundation, disorientation, SHOCK confusion) Arterial hypotension Altered cutaneous perfusion (mottled, clammy skin) I am in Altered mentation (obtundation, disorientation, SHOCK confusion) Arterial hypotension Altered cutaneous perfusion Decreased (mottled, clammy skin) urine output I am in Altered mentation (obtundation, disorientation, SHOCK confusion) Arterial hypotension Altered cutaneous perfusion Decreased (mottled, clammy skin) urine output GASTRIC TONOMETRY Influence of monitoring systems on outcome Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Gutierrez G et al., Lancet 339:195-9, 1992 EBM ? 260 patients (APACHE II 15-25) pH > 7.35 pH < 7.35 YES NO YES NO Survival 58 % 42 % 37 % 36 % P < 0.01 P = NS I am in Altered mentation (obtundation, disorientation, SHOCK confusion) Hyperlactatemia > 2 mEq/L Arterial hypotension Altered cutaneous perfusion Decreased (mottled, clammy skin) urine output SEVERITY CIRCULATORY SHOCK ELEVATED LACTATE Distributive Hypovolemic Cardiogenic Obstructive Sepsis Hypovolemia Heart Pulm. failure embolism Infection Pericardial Arrhythmias effusion LACTATE Hospital mortality, % 172,723 blood lactate measurements in 7,155 critically ill patients (4 hospitals) 100 90 80 70 60 Initial 50 lactate 40 levels 30 20 10 0 <1.2 1.2-1.5 1.5-2.0 2.0-4.0 4.0-6.0 >6.0 mEq/L or LACTATE mMol/L 6 Single measurement 5 4 3 2 1 0 TIME SKIN RBC BRAIN GUT MUSCLE PRODUCTION 0.8 mmol/kg/h lactate (1300 mmol/day for 70 kg) ELIMINATION LIVER OTHER TISSUES 2/3 1/3 Blood lactate levels are influenced by lactate production more than by lactate clearance PRODUCTION CLEARANCE TIME NATURAL HISTORY OF LACTIC ACIDOSIS AFTER GRAND-MAL SEIZURES Orringer et al, N Engl J Med 297: 796-9, 1977 Lactate levels, mEq/L 14 13 12 11 CLEARANCE 10 9 8 7 6 0 10 20 30 40 50 60 70 Time, min N = 8 pts (adapted) Serial lactate determinations Vincent et al, Crit Care Med 11: 449-51, 1983 In optimal conditions (good response to fluid administration) Lactate, mEq/L 6 5 4 3 2 10 % decrease in 1 hour 1 0 0 1 2 3 4 5 6 7 TIME, hours LACTATE TIME Conclusions: Better outcome associated with decreasing blood lactate concentrations - consistent throughout the clinical studies - not limited to septic patients - valid regardless of the initial value - in all groups, changes relatively slow, so that lactate measurements every 1–2 hrs are probably sufficient in most acute conditions. 2019 104 patients Independent risk factors of 30‐day mortality (multivariable logistic regression) ➢ Δ Lac <2.5%/h, ➢ Baseline lactate >4 mmol/L and ➢ High SAPS III score HEMODYNAMIC STABILIZATION The goals Adequate MAP without vasopressors The three windows of tissue perfusion Normal skin perfusion Urine output > 0.5 mL/kg/h Preserved mental status Lactate levels normal or decreasing Hypotension Mortality lactate measured late No hypotension lactate measured late Hypotension lactate measured early No hypotension lactate measured early Hospital mortality, % 172,723 blood lactate measurements in 7,155 critically ill patients (4 hospitals) 100 90 80 70 60 Initial 50 lactate 40 levels 30 20 10 0 <1.2 1.2-1.5 1.5-2.0 2.0-4.0 4.0-6.0 >6.0 SEVERITY CIRCULATORY SHOCK ELEVATED LACTATE Distributive Hypovolemic Cardiogenic Obstructive Sepsis Hypovolemia Heart Pulm. failure embolism Infection Pericardial Arrhythmias effusion The triangle of shock Arterial hypotension SHOCK Altered tissue Increeased perfusion blood lactate (oliguria, altered mentation, Microcirculatory abnormalities impaired skin perfusion) Vincent JL et al, Crit Care 2012 Arterial hypotension Signs of tissue hypoperfusion ? (oliguria, altered mentation, cutaneous vasoconstriction...) present absent blood lactate > 2 mEq/L < 1.5 mEq/L chronic hypotension ? syncope (if transient) circulatory shock arterial catheter central venous catheter THE FOUR PATHOPHYSIOLOGIC MECHANISMS I am in SHOCK HYPOVOLEMIC hemorrhage, trauma cholera... CARDIOGENIC myocardial infarction terminal cardiomyopathy valvular disease OBSTRUCTIVE severe arrhythmias pulmonary embolism tamponade tension pneumothorax DISTRIBUTIVE inflammatory response (mediators) Arterial pressure = cardiac output x vascular tone ARTERIAL HYPOTENSION CARDIAC OUTPUT HIGH LOW (decreased vascular tone) Hypovolemic Distributive (trauma, bleeding, diarrhea…) (sepsis, anaphylaxis, pancreatitis…) Cardiogenic (heart failure, valvular disease, major arrhythmia…) Obstructive (tamponade, massive pulm. embolism …) SEPTIC SHOCK ALTERED O2 EXTRACTION INCREASED O2 DEMAND IMPAIRED MYOCARDIAL CONTRACTILITY O2 CONSUMPTION O2 DELIVERY 2019 SOSD Br J Anaesth. 2014 Nov;113(5):740-7 Salvage / Rescue Optimisation Stabilisation De-escalation Echo/Doppler CVP Monitoring ScvO2 Cardiac Output Signs of fluid responsiveness Fluid challenge SOSD SOSD JL Vincent & D De Backer TIME SOSD Oxygen Central venous catheter Maintenance Tracheal intubation? Fluid challenge (CVP) Diuretics? Fluids Initial fluid loading Arterial catheter Ultrafiltration? Norepinephrine Norepinephrine Taper down for MAP 65-70 mmHg for adequate MAP norepinephrine Cardiac outputCO / SvO2/ ScvO2 Echocardiography Non-invasive ventilatiion In shock states High flow oxygen In shock states 442 patients mechanical ventilation either with FiO2 at 1·0 (hyperoxia) or FiO2 set to target a SaO2 of 88–95% (normoxia) during the first 24 h …in nature, and by contrast with virtually all other biochemical abnormalities, no animal is ever exposed to hyperoxia. A recommendation to keep SpO2within the low-normal range of 92–96% in all critically ill patients is easily achievable with minimum effort and little cost. The VIP rule (Weil and colleagues) entilate Oxygen administation V mechanical ventilation ? nfuse IV fluids I Blood transfusions ? Vasopressor agents ? Pump Dobutamine ? 2018 ‘Fluid overload’ Too much fluid, but where? The patient has anasarca, but develops septic shock... 2018 The terms hypervolemia and fluid overload are often used interchangeably, yet they do not have the same meaning. “Fluid overload” may vaguely refer to excess total body water content associated with edema, but it would be better if the term were avoided completely. The word “hypervolemia” is sufficient to indicate an excess in circulating blood volume and, if present, needs to be properly documented before a strategy of fluid restriction and/or diuretics is applied. AN EDEMATOUS PATIENT MAY BE HYPOVOLEMIC Beware of the terms ➢ Hypervolemia ➢ Fluid overload SOSD Oxygen Central venous catheter Maintenance Tracheal intubation? Fluid challenge (CVP) Diuretics? Fluids Initial fluid loading Arterial catheter Ultrafiltration? Norepinephrine Norepinephrine Taper down for MAP 65-70 mmHg for adequate MAP norepinephrine Cardiac outputCO / SvO2/ ScvO2 Echocardiography Br J Anaesth. 2014 Nov;113(5):740-7 Salvage / Rescue Optimisation Stabilisation De-escalation Echo/Doppler CVP Monitoring ScvO2 Cardiac Output Signs of fluid responsiveness Fluid challenge MOF Hypovolemia + vasopressors FLUID ADMINISTRATION INCREASE IN INCREASE IN CARDIAC FILLING PRESSURES CARDIAC OUTPUT EDEMA FORMATION INCREASE IN ARTERIAL PRESSURE IMPROVED TISSUE PERFUSION DECREASE IN HEART RATE INCREASED URINE OUTPUT Does this patient need IV fluid ? Arterial pressure 85/45 mmHg maybe Heart rate 117 / min maybe Cardiac output 3.9 L/min maybe Urine output 10 mL/h maybe ScvO2 60 % maybe Lactate 3.1 mEq/L maybe Central venous pressure 6 mmHg maybe MORE FLUIDS ? Fully controlled Spontaneous breathing mechanival ventilation (with or without mechanical ventilation) Anesthetized or Deeply sedated/paralyzed Pulse Pressure Variation (PPV) Stroke Volume Variation (SVV) End-expiratory pause Sigh AIRWAY PRESSURE MECHANICAL cmH2O VENTILATION 0 SPONTANEOUS FLUID RESPONSIVENESS Transient increase in intrathoracic pressure Transient decrease in venous return (+ reduced RV ejection) AIRWAY PRESSURE AIRWAY Decreased RV stroke volume Decreased LV stroke volume (after a few beats) Transient decrease in pulse pressure ARTERIAL PRESSURE ARTERIAL FLUID RESPONSIVENESS STROKE VOLUME END-DIASTOLIC VOLUME FLUID RESPONSIVENESS AP monitoring Pulse Pressure Variation (PPV) CO monitoring Stroke Volume Variation (SVV) FLUID RESPONSIVENESS PPV / SVV REQUIREMENTS Mechanical ventilation No spontaneous breathing activity No major arrhythmia Relatively large tidal volume No significant tachypnea No intraabdominal hypertension 2018 Anesth Analg 2019 CI Healthy volunteers (young) 4.0 3.2 10 16 PAOP, mmHg Respiratory variation in IVC diameter Limited ability to predict fluid responsiveness, particularly in spontaneously ventilating patients. A negative test cannot be used to rule out fluid responsiveness. 2017 Neuromuscular blockade agents were routinely used N = 319 pts MORE FLUIDS ? Fully controlled Spontaneous breathing mechanival ventilation (with or without mechanical ventilation) Anesthetized or Deeply sedated/paralyzed Fluid Pulse Pressure Variation (PPV) challenge Stroke Volume Variation (SVV) End-expiratory pause Sigh FLUID ADMINISTRATION WILL FLUIDS BE BENEFICIAL ? Obviously yes Not sure Fluid loading Fluid challenge The goal of fluid administration Minimal increase Increase in cardiac filling pressures in cardiac output No increase Increase in edema in DO2 Improved tissue perfusion FLUID ADMINISTRATION What we desire The LOWEST hydrostatic pressures associated