control of cardiac output

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Introduction to Critical Care

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What’s so Special about the ICU?Ventilators Hemodynamic Monitoring Vasoactive Drugs “Applied Physiology”

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Basic Ventilator ManagementIndications for Ventilation Inability to Ventilate (high pCO2) COPD Inability to Oxygenate (low pO2) ARDS Mixed common

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Orotracheal Nasotracheal Cricothyrotomy TracheostomyIntubation

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Ventilator OrdersInitial Ventilator Orders : Volume cycled FiO2 Rate Mode (AC, SIMV, PC, PS, CPAP) PEEP TV Consider NG tube, art line, restraints Check the CXR!!

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Ventilator ChangespO2: keep FiO2 <60% PEEP FiO2 pCO2 TV Rate

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Ventilator ChangespO2 = 380 FiO2=100% What now?

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Ventilator ChangesRemember the “Rule of 7s” Each % change of FiO2 of 1 results in a change of pO2 of 7 pO2 - 100  FiO2 = ------------------- 7

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PaO2 >60 on FiO2 < 0.5 with PEEP <5 Minute vent <10 L/min NIF more negative than -20 VC >800 mL TV >300 mL Use T-piece or CPAP with PSWeaning

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Oxygen Mask Check ABG Cough / Deep Breathing Incentive SpirometerAfter Extubation

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ARDS 1. Impaired Oxygenation: PaO2/FiO2 ratio < 200 (normal > 450) 2. Bilateral pulmonary infiltrates on CXR 3. PCW < 18 (no CHF)ARDS is an acute clinical illness characterized by severe hypoxemia and bilateral infiltrates on chest X-ray in the absence of pulmonary edema.

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Infection è sepsis Trauma è hemorrhagic shock Multiple transfusions Low flow state from any cause Aspiration pneumonia Acute pancreatitis Smoke inhalation and many more…..Causes

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Levy G, Shabot MM, Hart M, et al: Transfusion associated non-cardiogenic pulmonary edema. Transfusion 1986;26: 278.Levy G, Shabot MM, Hart M, et al: Transfusion associated non-cardiogenic pulmonary edema. Transfusion 1986;26: 278.

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PathophysiologyLarge alveolar surface area = 70 m2 (skin = 1.7 m2) Lung sensitive to noxious stimuli - inhaled and circulating Lung receives entire cardiac output every minute Affected by multiple inflammatory mediators and cells

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Thromboxane A2 Prostacyclin Leukotrienes Platelet-activating factor (PAF) Bradykinin C3a, C5a Tumor necrosis factor IL-1, IL-6 Elastase, Collagenase Oxygen free radicalsNothing New…...Still can’t do anything about ‘em!Leucocytes Macrophages Monocytes Endothelial cells Mast cells Bosophils Fibroblasts PlateletsInflammatory MediatorsCells

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Causes & Time of Death After Multiple Trauma

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Goal: Reduce Alveolar distentionMarcy & Marini. Chest 1991;100:494 New Ventilator Strategies - I

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Pressure controlled ventilation Pressure release ventilation Low volume pressure-limited ventilation Inverse ratio ventilation Prone ventilationNew Ventilator StrategiesPermissive hypercapnia

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Permissive HypercapniaTolerate mild to moderate respiratory acidosis (elevated PCO2) in order to reduce airway pressures.Lower tidal volumes Lower respiratory rates Lower peak and mean airway pressures

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Prone PositioningStocker et al. Chest 1997;111:1008

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Extracorporeal CO2 Removal (ECCO2R)Guinard et al. Clin Invest Crit Care 1997;111:1000Status: Ineffective

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Extra-corporeal membrane oxygenation (ECMO)Other New Ventilator StrategiesHigh frequency ventilation (>60/min)High Positive End-Expiratory Pressure (PEEP) ventilationExtra-Corporeal CO2 Removal (ECCOR)Partial Liquid Ventilation

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Partial Liquid VentilationLeach et al. Crit Care Med 1993;21:1270.

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Partial Liquid VentilationPartial Liquid VentConventional VentStatus: Unproven

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Surfactant replacement Ketoconazole Prostaglandin E1 Non-steroidal anti-inflammatory agents High dose steroids (again)New Pharmacologic StrategiesInhaled nitric oxide (NO)

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Pharmacologic Treatment of ARDSKollef & Schuster. NEJM 1995;332:27.

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Last Updated: 8th March 2018

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