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VENTILATOR MANAGEMENT: Are You K idding M e?

VENTILATOR MANAGEMENT: Are You K idding M e?. Susan Marie Baro , DO, FACOS Associate Trauma and Surgical Critical Care Associate Director Surgical Critical Care Physician Director Blood Conservation Program. OBJECTIVES. Review basic modes of ventilation

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VENTILATOR MANAGEMENT: Are You K idding M e?

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  1. VENTILATOR MANAGEMENT:Are You Kidding Me? Susan Marie Baro, DO, FACOS Associate Trauma and Surgical Critical Care Associate Director Surgical Critical Care Physician Director Blood Conservation Program

  2. OBJECTIVES • Review basic modes of ventilation • Understand and treat ARDS and ALI (Acute Lung Injury) • Review recommendations for ventilator settings

  3. TRAUMA AND THE VENTILATOR • Patients with severe trauma are at a high risk for developing respiratory failure • Acute Lung Injury • Acute Respiratory Distress Syndrome • Goals of treatment should be to identify those most likely to develop severe respiratory insufficiency and to institute therapy as soon as possible

  4. ATELECTASIS • Positive pressure and low oxygen concentrations • minimize or reverse the formation of atelectasis during mechanical ventilation and general anesthesia • Within 5 minutes of induction with general anesthesia • increased densities appear in the dependent regions of both lungs

  5. ATELECTASIS • Develops with both IV and Inhalation anesthesia • Develops with both spontaneous and paralyzed mechanical vent • CXR/CT may not show extent • Collapsed lung comprises 4 times more lung tissue than aerated regions • Small amount of compressed lung tissue can account for a significant increase in shunt fraction

  6. ATELECTASIS • 3 Mechanisms of Atelectasis Formation • Compression and absorption • Major cause with anesthesia • Loss of Surfactant • High Inspired Oxygen Concentration • Can be avoided or minimized with vital capacity maneuvers or positive end expiratory pressure (PEEP) • FiO2 1.00 pre-induction and prior to extubation both contribute to atelectasis • Likely explains the hypoxia seen in the PACU • 0.8 and 0.3 both studied and found to have decreased atelectasis

  7. IN TRAUMA • During acute trauma resuscitation patients are generally given 100% oxygen to augment O2 delivery to potentially ischemic tissues • Pre-oxygenation with 100% and early hyper-oxygenation post intubation routinely practiced

  8. THE VENTILATOR (cont.) • Ideally Mechanical Ventilation should: • Potentiate alveolar recruitment • Optimize intrapulmonary gas distribution • Narrow time-constant discrepancies • Thereby distribute pressure and volume to dependent and nondependent regions proportionally

  9. VENTS IN THE OR • If the vent setting in the ICU exceed the capabilities of the OR Vent • Patient should be transported to the OR on the ICU vent • Patient should remain on the ICU vent throughout the procedure • All efforts should be made to avoid de-recruitment

  10. VENTILATOR MODES • Mode • The pattern in which breaths are delivered • Characterized by a group of variables set in different combinations and fashions • Variables: • Respiratory Rate, Tidal Volume or Pressure, Inspiratory Flow, Inspiratory Time/Pause, I:E Ratio, PEEP, Inspiratory Trigger

  11. VENTILATOR MODES • Trigger • Initiates the breath • Time, flow, pressure • Limit • Governs the gas delivery • Pressure, flow volume • Cycle • Terminates the breath • Flow, time, volume, pressure

  12. MORE COMMON VENTILATOR MODES • Controlled Mandatory Ventilation (CMV) • Intermittent Mandatory Ventilation (IMV) • Pressure/Volume Control Vent (PCV) • Assist Control (AC) • Pressure or Volume • BiLevel Positive Airway Pressure (BiPAP) • Airway Pressure Release Vent (APRV) • Synchronized Intermittent Mandatory Vent (SIMV) • Pressure Support Vent (PSV) • Continuous Positive Airway Pressure (CPAP)

  13. LESS COMMON VENTILATOR MODES • Mandatory Minute Vent (MMV) • Adaptive Support Vent (ASV) • Proportional Assist Mode (PAV) • Volume Assured Pressure Support (VAPS) • Pressure Regulated Volume Control (PRVC) • Volume Vent Plus (VVP+) • Inverse Ration Vent (IRV) • NeurallyAdjusted Ventilatory Assist (NAVA)

  14. MODES • Mandatory • CMV • IMV • Spontaneous/Triggered • CPAP • PSV • Hybrid • AC • SIMV • BiPAP • APRV

  15. CONTROLLED MANDATORY VENTILATION (CMV) • Preset TV at a time triggered RR • Vent controls the TV and RR • May require sedation (possibly paralysis) for patient comfort • Can be pressure controlled or volume controlled

  16. INTERMITTENT MANDATORY VENTILATION (IMV) • Patient initiates own breath • Different from CMV • Periodic volume/pressure targeted breaths occur at set interval (time triggered) • Between breaths, patient breathes spontaneously at any desired baseline pressure/volume without getting a mandatory breath • Vent always gives breath even if patient exhaling - Get stacking of breaths

  17. CPAP • Triggered/Spontaneous Mode • Helpful to improve oxygenation in patient with refractory hypoxemia and low FRC (functional residual capacity) • Adjusted to provide the best oxygenation with the lowest possible pressure and the lowest FiO2 • PEEP without the preset vent rate or volume

  18. PSV • Patient triggered, pressure limited flow cycle • Inspiration initiated by negative pressure/flow change (patient) • Expiration initiated by decreased flow (patient) • Purely spontaneous

  19. ASSIST CONTROL (AC) • Mandatory breath either patient triggered (spontaneous respiration) or time triggered (preset RR) • Spontaneous effort • With respiratory assist • Assist Mode • Patient initiates all breathes but the vent cycles at initiation to give preset TV • Patient controls rate but always gets a full breath

  20. SYNCHRONIZED INTERMITTENT MADATORY VENTILATION(SIMV) • Vent delivers controlled breath (mandatory) at or near time of patients spontaneous breath (time triggered) • Mandatory breath is synchronized with patients spontaneous breathing effort to avoid breath stacking • Patient triggered • If patient fails to initiate breath within a predetermined interval, vent will provide a mandatory breath at the end of the time period

  21. BiPAP • 2 levels of pressure set • Hi and Low levels are set • At either pressure level patient can breath spontaneously • May be supported with Pressure Support • Initial settings • IPAP ~ 8 cm H2O • EPAP ~ 4 cm H2O

  22. APRV - BiVENT • A bi-level form of ventilation with sudden short releases in pressure to rapidly reduce FRC and allow for ventilation • Provides 2 levels of CPAP and allows spontaneous breathing at both levels when spontaneous effort is preserved • Set Phigh and Plow • Both pressure levels are time triggered and time cycled

  23. APRV - BiVENT • Inverse I:E Ratio • Set Thigh and Tlow • Allows spontaneous breathing patient to breath at a high CPAP level but drops briefly ( ~1 sec) periodically to allow low CPAP level for extra CO2 elimination (airway pressure release)

  24. APRV - BiVENT • Mandatory breaths occur when the pressure limit rises from the lower CPAP level to the higher CPAP level • Allows Inverse Ratio Vent (IRV) with or without spontaneous breathing • Improves patient-ventilator synchrony if spontaneous breathing is present • Improves mean airway pressure

  25. APRV - BiVENT • Improves oxygenation by stabilizing collapsed alveoli • Allows patient to breath spontaneously while continuing lung recruitment • Lowers PIP

  26. APRV - BiVENT • Disadvantages • Variable Tidal Volume • Could be harmful to patients with high expiratory resistance (COPD, Asthma) • Some form of Auto PEEP usually present • Caution with hemodynamically unstable pateints • Can get asynchrony if spontaneous breaths out of synch with release time

  27. PEEP PHYSIOLOGY • Re-inflates collapsed alveoli and maintains alveolar inflation during exhalation • PEEP leads to decreased alveolar distending pressures • Increases FRC by alveolar recruitment • Improves ventilation • Increases ventilation and perfusion • Improves oxygenation • Decreased work of breathing

  28. PEEP DISADVANTAGES • High intra-thoracic pressures can cause decreased venous return • May produce pulmonary barotrauma • May worsen air trapping in obstructive pulmonary diseases • Increases intracranial pressure • Can cause alterations in renal function and water metabolism

  29. RUN OF THE MILL VENT SETTING • Tidal Volume ~ 8 ml/kg PBW/IBW • Decrease Tidal Volume to 6 ml/kg in ARDS • Respiratory Rate 12 – 16 breaths per minute • PEEP 5 – 10 cm H2O • Peak flow rate that creates an Inspiratory to Expiratory (I:E) ratio of 1:2 to 1:3 • Lowest Fraction of Inspired Oxygen (FiO2) sufficient enough to meet oxygenation goals

  30. PREDICTED BODY WEIGHT (PBW) or IDEAL BODY WEIGHT (IBW) • Males: IBW inKg 50 kg + 2.3 kg for each inch over 5 feet • Females: IBW in Kg 45.5 kg + 2.3 kg for each inch over 5 feet

  31. ACUTE RESPIRATORY FAILURE Acute Lung Injury (ALI) Acute Respiratory Distress Syndrome (ARDS) Acute onset B/L Infiltrates on CXR PaO2/FiO2 ratio < 200 Non cardiogenic pulmonary edema • Acute onset • B/L Infiltrates on CXR • PaO2/FiO2 ratio < 300 • Non cardiogenic pulmonary edema

  32. VENTILATOR ASSOCIATED LUNG INJURY • Iatrogenic • High volume, low PEEP vent settings • Induce parenchymal damage through over-distension or “stretch” of the aerated lung • Cause repeated opening and closing or “shear” of the collapsed de-recruited lung • Results in disruption of the normal alveolar integrity and can perpetuate the inflammatory response

  33. ALI/ARDS Multicenter Trial • Randomized to • “Traditional” TV Vent • 12 ml/kg and • end inspiratory Plateau Pressure of < 50 cm H2O • “Low Volume” TV Vent • 6 ml/kg with • end inspiratory plateau pressure of < 30 cm H2O • Study stopped after 861 patients secondary to significantly decreased mortality in the study arm group • 39.8 vs 31% (p=0.007)

  34. RECOMMENDATIONS FOR VENT SETTINGS • Low Tidal Volumes: 6 – 8 ml/kg • Limit Peak/Plateau Pressure: < 35 cm H2O • Set PEEP above the lower inflection point on the pressure – volume curve • Adjust I:E Ratio and Respiratory Rate as needed to achieve the above • Wean FiO2 to obtain PaO2 80 – 100 mm Hg • or an oxygen saturation of 93- 97% • Early conversion to pressure limited mode

  35. RISK FACTORS FOR ARDS • Shock • Pulmonary Contusions • Fractures • Multiple Tranfusions • Pneumonia • ISS > 16 • Trauma Score < 13 • Surgery to Head • DIC Early Findings • +/- Admission lactate, pH, base deficit, and serum bicarbonate • Gastric Aspiration • Near Drowning • Smoke Inhalation • Fat Emoblism • Sepsis • Blunt Injury

  36. ARDS IN TRAUMA • Trauma is 2o only to sepsis in regard to risk factors for ARDS • 12-39% • Of the 14 main risk factors identified as highly associated with subsequent ARDS • 8 may be seen early in the trauma patient with 3 more seen in days to weeks

  37. ARDS • Early ARDS (< 48 hours) • Characterized by hemorrhagic shock and capillary leak • Late ARDS ( > 48 hours) • Follows pneumonia and is more closely associated with MSOF

  38. ARDS (cont.) • Initial Stages • Increased capillary permeability results in lung edema • Positive pressure must exceed the sum of interstitial pressures and superimposed hydrostatic pressure to re-open lung units • Following the Initial Phase • Alveolar edema becomes organized and is replaced by fibrinous material • Recruitment maneuvers to open collapsed alveoli become less effective as the response to pressure increases • Favors over-distension • Therefore – Lung recruitment needs to be instituted early!

  39. ARDS and RECRUITMENT • Greatest frequency of opening lung units • Occurs at ~ 25 cm H2O • Maximal frequency of estimated transpulmonary opening pressure • Between 20 – 25 cm H2O • Different regions of the lung are recruited at differing pressures • Ranges from 10 – 45 cm H2O • Majority of de-recruitment • Occurs at PEEP values spanning 0 – 15 cm H2O

  40. ARDS PROGRESSION • Over-distension creates dead space • Progressive over-distension initiates capillary compression • Blood flow is then redistributed to less ventilated regions • Subsequently aggravating hypoxemia

  41. ARDS PROGRESSION (cont.) • Recruitment require sufficient airway pressures to exceed the critical opening pressure of the airways • Also requires time in addition to critical opening pressure • As pressure is reached and maintained, time allows redistribution of delivered gas volume

  42. ARDSp vs ARDSexp • Pulmonary (Primary or Direct Insult) ARDS • ARDSp • ExtraPulmonary (Secondary or Indirect) ARDS • ARDSexp

  43. ARDS ARDSp ARDSexp Atelectasis of alveolar architecture Accompanied by microvascular congestion Stiffer thoraco-abdominal cage and a more compliant lung Likely improves with PEEP • Consolidation • Alveolar filling of fibrin, edema, blood cells, and collagen • Stiffer lungs • May not improve with PEEP

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