Mechanical Ventilation Handout - Allenho

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Principles of Mechanical Ventilation David M. Lieberman, MD Allen S. Ho, MD Surgery ICU Service Stanford University Medical Center September 25, 2006 The Basics

Transcript of Mechanical Ventilation Handout - Allenho

  • Principles of Mechanical VentilationDavid M. Lieberman, MDAllen S. Ho, MDSurgery ICU ServiceStanford University Medical CenterSeptember 25, 2006The Basics

  • Origins of mechanical ventilationNegative-pressure ventilators (iron lungs)Non-invasive ventilation first used in Boston Childrens Hospital in 1928Used extensively during polio outbreaks in 1940s 1950sPositive-pressure ventilatorsInvasive ventilation first used at Massachusetts General Hospital in 1955Now the modern standard of mechanical ventilationThe era of intensive care medicine began with positive-pressure ventilationThe iron lung created negative pressure in abdomen as well as the chest, decreasing cardiac output.Iron lung polio ward at Rancho Los Amigos Hospital in 1953.

  • OutlineTheoryVentilation vs. OxygenationPressure Cycling vs. Volume CyclingModesVentilator SettingsIndications to intubateIndications to extubateManagement algorithimFAQs

  • Principles (1): VentilationThe goal of ventilation is to facilitate CO2 release and maintain normal PaCO2Minute ventilation (VE)Total amount of gas exhaled/min.VE = (RR) x (TV)VE comprised of 2 factorsVA = alveolar ventilationVD = dead space ventilationVD/VT = 0.33VE regulated by brain stem, responding to pH and PaCO2Ventilation in context of ICUIncreased CO2 productionfever, sepsis, injury, overfeedingIncreased VDatelectasis, lung injury, ARDS, pulmonary embolismAdjustments: RR and TVV/Q Matching. Zone 1 demonstrates dead-space ventilation (ventilation without perfusion). Zone 2 demonstrates normal perfusion. Zone 3 demonstrates shunting (perfusion without ventilation).

  • Principles (2): OxygenationThe primary goal of oxygenation is to maximize O2 delivery to blood (PaO2)Alveolar-arterial O2 gradient (PAO2 PaO2)Equilibrium between oxygen in blood and oxygen in alveoliA-a gradient measures efficiency of oxygenationPaO2 partially depends on ventilation but more on V/Q matchingOxygenation in context of ICUV/Q mismatchingPatient position (supine)Airway pressure, pulmonary parenchymal disease, small-airway diseaseAdjustments: FiO2 and PEEPV/Q Matching. Zone 1 demonstrates dead-space ventilation (ventilation without perfusion). Zone 2 demonstrates normal perfusion. Zone 3 demonstrates shunting (perfusion without ventilation).

  • Pressure ventilation vs. volume ventilationPressure-cycled modes deliver a fixed pressure at variable volume (neonates)Volume-cycled modes deliver a fixed volume at variable pressure (adults)Pressure-cycled modesPressure Support Ventilation (PSV)Pressure Control Ventilation (PCV)CPAPBiPAPVolume-cycled modesControlAssistAssist/ControlIntermittent Mandatory Ventilation (IMV)Synchronous Intermittent Mandatory Ventilation (SIMV)Volume-cycled modes have the inherent risk of volutrauma.

  • Pressure Support Ventilation (PSV)Patient determines RR, VE, inspiratory time a purely spontaneous modeParametersTriggered by pts own breathLimited by pressureAffects inspiration onlyUsesComplement volume-cycled modes (i.e., SIMV)Does not augment TV but overcomes resistance created by ventilator tubingPSV aloneUsed alone for recovering intubated pts who are not quite ready for extubationAugments inflation volumes during spontaneous breaths BiPAP (CPAP plus PS) PSV is most often used together with other volume-cycled modes. PSV provides sufficient pressure to overcome the resistance of the ventilator tubing, and acts during inspiration only.

  • Pressure Control Ventilation (PCV)Ventilator determines inspiratory time no patient participationParametersTriggered by timeLimited by pressureAffects inspiration onlyDisadvantagesRequires frequent adjustments to maintain adequate VEPt with noncompliant lungs may require alterations in inspiratory times to achieve adequate TV

  • CPAP and BiPAPCPAP is essentially constant PEEP; BiPAP is CPAP plus PSParametersCPAP PEEP set at 5-10 cm H2OBiPAP CPAP with Pressure Support (5-20 cm H2O)Shown to reduce need for intubation and mortality in COPD ptsIndicationsWhen medical therapy fails (tachypnea, hypoxemia, respiratory acidosis)Use in conjunction with bronchodilators, steroids, oral/parenteral steroids, antibiotics to prevent/delay intubationWeaning protocolsObstructive Sleep Apnea

  • Assist/Control ModeControl ModePt receives a set number of breaths and cannot breathe between ventilator breathsSimilar to Pressure ControlAssist ModePt initiates all breaths, but ventilator cycles in at initiation to give a preset tidal volumePt controls rate but always receives a full machine breathAssist/Control ModeAssist mode unless pts respiratory rate falls below preset valueVentilator then switches to control mode

    Rapidly breathing pts can overventilate and induce severe respiratory alkalosis and hyperinflation (auto-PEEP)Ventilator delivers a fixed volume

  • IMV and SIMV Volume-cycled modes typically augmented with Pressure SupportIMVPt receives a set number of ventilator breathsDifferent from Control: pt can initiate own (spontaneous) breathsDifferent from Assist: spontaneous breaths are not supported by machine with fixed TVVentilator always delivers breath, even if pt exhalingSIMVMost commonly used modeSpontaneous breaths and mandatory breathsIf pt has respiratory drive, the mandatory breaths are synchronized with the pts inspiratory effort

  • Vent settings to improve FIO2Simplest maneuver to quickly increase PaO2Long-term toxicity at >60%Free radical damageInadequate oxygenation despite 100% FiO2 usually due to pulmonary shuntingCollapse AtelectasisPus-filled alveoli PneumoniaWater/Protein ARDSWater CHFBlood - Hemorrhage

    PEEP and FiO2 are adjusted in tandem

  • Vent settings to improve PEEP Increases FRCPrevents progressive atelectasis and intrapulmonary shuntingPrevents repetitive opening/closing (injury)Recruits collapsed alveoli and improves V/Q matchingResolves intrapulmonary shuntingImproves complianceEnables maintenance of adequate PaO2 at a safe FiO2 levelDisadvantagesIncreases intrathoracic pressure (may require pulmonary a. catheter)May lead to ARDSRupture: PTX, pulmonary edemaPEEP and FiO2 are adjusted in tandemOxygen delivery (DO2), not PaO2, should be used to assess optimal PEEP.

  • Vent settings to improve Respiratory rateMax RR at 35 breaths/min Efficiency of ventilation decreases with increasing RRDecreased time for alveolar emptyingTVGoal of 10 ml/kgRisk of volutraumaOther means to decrease PaCO2Reduce muscular activity/seizuresMinimizing exogenous carb loadControlling hypermetabolic statesPermissive hypercapneaPreferable to dangerously high RR and TV, as long as pH > 7.15RR and TV are adjusted to maintain VE and PaCO2I:E ratio (IRV)Increasing inspiration time will increase TV, but may lead to auto-PEEPPIPElevated PIP suggests need for switch from volume-cycled to pressure-cycled modeMaintained at

  • Alternative ModesI:E inverse ratio ventilation (IRV)ARDS and severe hypoxemiaProlonged inspiratory time (3:1) leads to better gas distribution with lower PIPElevated pressure improves alveolar recruitmentNo statistical advantage over PEEP, and does not prevent repetitive collapse and reinflationProne positioningAddresses dependent atelectasisImproved recruitment and FRC, relief of diaphragmatic pressure from abdominal viscera, improved drainage of secretionsLogistically difficultNo mortality benefit demonstratedECHMOAirway Pressure Release (APR)High-Frequency Oscillatory Ventilation (HFOV)High-frequency, low amplitude ventilation superimposed over elevated PawAvoids repetitive alveolar open and closing that occur with low airway pressuresAvoids overdistension that occurs at high airway pressuresWell tolerated, consistent improvements in oxygenation, but unclear mortality benefitsDisadvantagesPotential hemodynamic compromisePneumothoraxNeuromuscular blocking agents

  • Treatment of respiratory failurePreventionIncentive spirometryMobilizationHumidified airPain controlTurn, cough, deep breatheTreatmentMedicationsAlbuterolTheophyllineSteroidsCPAP, BiPAP, IPPBIntubationThe critical period before the patient needs to be intubated

  • Indications for intubationCriteriaClinical deteriorationTachypnea: RR >35Hypoxia: pO2 55mm HgMinute ventilation

  • Indications for extubationClinical parametersResolution/Stabilization of disease processHemodynamically stableIntact cough/gag reflexSpontaneous respirationsAcceptable vent settingsFiO2< 50%, PEEP < 8, PaO2 > 75, pH > 7.25General approachesSIMV WeaningPressure Support Ventilation (PSV) WeaningSpontaneous breathing trialsDemonstrated to be superiorNo weaning parameter completely accurate when used aloneMarino P, The ICU Book (2/e). 1998.

    Numerical ParametersNormal RangeWeaning ThresholdP/F> 400> 200Tidal volume5 - 7 ml/kg5 ml/kgRespiratory rate14 - 18 breaths/min< 40 breaths/minVital capacity65 - 75 ml/kg10 ml/kgMinute volume5 - 7 L/min< 10 L/min

    Greater Predictive ValueNormal RangeWeaning ThresholdNIF (Negative Inspiratory Force)> - 90 cm H2O> - 25 cm H2ORSBI (Rapid Shallow Breathing Index) (RR/TV)< 50< 100

  • Spontaneous Breathing TrialsSettingsPEEP = 5, PS = 0 5, FiO2 < 40%Breathe independently for 30 120 minABG obtained at end of SBTFailed SBT CriteriaRR > 35 for >5 minSaO2 30 secHR > 140Systolic BP > 180 or < 90mm HgSustained increased work of breathingCardiac dysrhythmiapH < 7.32SBTs do not guarantee that airway is stable or pt can self-clear secretionsSena et al, ACS Surgery: Principles and Practice (2005).

    Causes of Failed SBTsTreatmentsAnxiety/AgitationBenzodiazepines or haldolInfectionDiagnosis and txElectrolyte abnormalities (K+, PO4-)CorrectionPulmonary edema, cardiac ischemiaDiuretics and nitratesDeconditioning, malnutritionAggressive nutritionNeuromuscular diseaseBronchopulmonary hygiene, early consideration of trachIncreased intra-abdominal pressureSemirecumbent positioning, NGTHypothyroidismThyroid replacementExcessive auto-PEEP (COPD, asthma)Bronchodilator therapy

  • Continued ventilation after successful SBTCommonly cited factorsAltered mental status and inability to protect airwayPotentially difficult reintubationUnstable injury to cervical spineLikelihood of return trips to ORNeed for frequent suctioningInherent risks of intubation balanced against continued need for intubation

  • Need for tracheostomyAdvantagesIssue of airway stability can be separated from issue of readiness for extubationMay quicken decision to extubateDecreased work of breathingAvoid continued vocal cord injuryImproved bronchopulmonary hygieneImproved pt communicationDisadvantagesLong term risk of tracheal stenosisProcedure-related complication rate (4% - 36%)

    Prolonged intubation may injure airway and cause airway edema1 - Vocal cords. 2 - Thyroid cartilage. 3 - Cricoid cartilage. 4 - Tracheal cartilage. 5 - Balloon cuff.

  • Ventilator management algorithimInitial intubation FiO2 = 50% PEEP = 5 RR = 12 15 VT = 8 10 ml/kg

    SaO2 < 90%SaO2 > 90%SaO2 > 90%Adjust RR to maintain PaCO2 = 40Reduce FiO2 < 50% as toleratedReduce PEEP < 8 as toleratedAssess criteria for SBT dailySaO2 < 90%Increase FiO2 (keep SaO2>90%)Increase PEEP to max 20Identify possible acute lung injuryIdentify respiratory failure causesAcute lung injuryNo injuryFail SBTAcute lung injuryLow TV (lung-protective) settingsReduce TV to 6 ml/kgIncrease RR up to 35 to keep pH > 7.2, PaCO2 < 50Adjust PEEP to keep FiO2 < 60%SaO2 < 90%SaO2 > 90%SaO2 < 90%Dx/Tx associated conditions (PTX, hemothorax, hydrothorax)Consider adjunct measures (prone positioning, HFOV, IRV)SaO2 > 90%Continue lung-protective ventilation until:PaO2/FiO2 > 300Criteria met for SBTPersistently fail SBTConsider tracheostomyResume daily SBTs with CPAP or tracheostomy collarPass SBTAirway stableExtubateIntubated > 2 wks

    Consider PSV wean (gradual reduction of pressure support)Consider gradual increases in SBT duration until endurance improvesProlonged ventilator dependencePass SBTPass SBTAirway stableModified from Sena et al, ACS Surgery: Principles and Practice (2005).

  • ReferencesSena, MJ et al. Mechanical Ventilation. ACS Surgery: Principles and Practice 2005; pg. 1-16.Marino, PL. The ICU Book. 2nd edition. 1998.Byrd, RP. Mechanical ventilation. Emedicine, 6/6/06.

    Interesting to compare the viewpoints and biases of medicine/endocrinology articles, and the surgery articlesDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsDisorders characterized by systemic effects of M protein, and direct effects of bone marrow infiltration

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressorsThis concept is hugely important in cancer in that methylation silencing genes is equivalent to a mutation

    Common examples of methylation-induced silencing:Imprinted genes (Prader-Willi, Angelmann Syndromes)Inactivated 2nd X chromosome in femalesDNA methylation results in histone deacetylation, compacted chromatin, and repression of gene activityMethylation can have a profound effect in tumorigenesis by silencing tumor suppressors