logging in or signing up Mechanical Ventilation- Indication & Monitoring DRARNABMAJI Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 198 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: August 30, 2013 This Presentation is Public Favorites: 1 Presentation Description the basics of mechanical ventilation Comments Posting comment... Premium member Presentation Transcript Image Bitmap: Mechanical Ventilation- Indication & Monitoring Dr Arnab Maji , PGT, CHEST MEDICINE, NRSMCH Feuille de calcul: “… an opening must be attempted in the trunk of the trachea, into which a tube of reed or cane should be put; you will then blow into this, so that the lung may rise again… and the heart becomes strong…” -- Andreas Vesalius (1555) 400 years………………………………………………….. Polio epidemic, 1955, Sweden, Iron Lung In Boston, the nearby Emerson Company made available a prototype positive-pressure lung inflation device, which was put to use at the Massachusetts General Hospital, and became an instant success. Thus began the era of positive-pressure mechanical ventilation (and the era of intensive care medicine). Mechanical Ventilation- Indication & Monitoring: Indication of mechanical ventilation Rule 1. The indication for intubation and mechanical ventilation is thinking of it. Rule 2. Intubation is not an act of personal weakness. Rule 3. Initiating mechanical ventilation is not the “kiss of death.” PowerPoint Presentation: Indication Acute ventilatory failure Impending ventilatory failure Severe hypoxemia Prophylactic ventilatory support Indication of mechanical ventilation: Acute ventilatory failure Sudden increase in PaCO2 to greater than 50 mmHg with accompanying respiratory acidosis (Ph < 7.30) But…………………..this PaCO2 level may be higher in COPD patients. Indication : Impending ventilatory failure Can maintain only marginally normal blood gases but only at the expense of a significantly increased work of breathing Impending ventilatory failure: Parameters for impending ventilatory failure Tidal volume < 3-5 Ml/kg RR - >25-35/minute Minute ventilation - >10 L/min Vital capacity - <15mL/kg MIP/NIF - <-20 cm H2O PaCO2 trend – increasing to over 5o mmHg Vital signs – tachycardia, tachypnea , arrythmia , hypertension, use of accessory respiratory muscle, diaphoresis, cyanosis PowerPoint Presentation: Severe hypoxemia PaO2 <60 mmHg on 50% or more FiO2 or <40 mmHg at any FiO2 ARDS Pulmonary Edema CO Poisoning Parameters for impending ventilatory failure: Indications for prophylactic ventilatory support Prolonged Shock Head injury Smoke inhalation Hypoxic brain Hypoxia of heart muscles CABG Other thoracic or abdominal surgery Severe hypoxemia: Contraindication Only absolute C/I – untreated tension pneumothorax Patient’s informed consent Medical futility Reduction or termination of pain and suffering Indications for prophylactic ventilatory support: Ventilator alarm settings Low exhaled volume alarm Low inspiratory pressure alarm High inspiratory pressure alarm Apnea alarm High respiratory rate alarm High and Low FiO2 alarm Contraindication : Low exhaled volume alarm Set at 100 mL lower than the expired mechanical tidal volume Triggered if patient does not exhale adequate tidal volume Detect a system leak or circuit disconnection Ventilator alarm settings: Low inspiratory pressure alarm Set at 10-15 cm H2O below the observed peak inspiratory pressure Complements the low exhaled volume alarm Detect system leak and circuit disconnection Low exhaled volume alarm: High inspiratory pressure alarm Set at 10-15 cm H2O higher than observed peak inspiratory pressure Cause – Water in the ventilatory circuit Kinking or biting of endotracheal tube Secretions in the airway Bronchospasm Tension pneumothorax Decrease in lung compliance Increased airway resistance coughing Low inspiratory pressure alarm: Apnea alarm Set with a 15 to 20 sec time delay and less time delay with a higher respiratory rate Ventilator provides full ventilatory support until the alarm condition no-longer exists High inspiratory pressure alarm: High respiratory rate alarm Set at 10-15 bpm over the observed respiratory rate. Indicates tachypnea – a sign of respiratory distress Apnea alarm: Initial ventilator settings MODE – FVS, PVS FVS – AC/VCV, almost always initially PVS – BiPAP , PSV during weaning, SIMV VCV PCV Dual control mode – mandatory breaths that are volume targeted, pressure limited and time cycled High respiratory rate alarm: Respiratory rate RR – 10-12 bpm RR of >20 bpm in PSV are associated with auto-PEEP and should be avoided Estimate pt’s minute volume requirement RR = estimated minute volume / tidal volume Minute volume (male) = 4* BSA Minute volume (female) = 3.5* BSA Respiratory rate : Situation If CO2 production is elevated (due to an increase in metabolic rate or increased physiological dead space) the minute volume is needed to be increased Increased minute volume Increase tidal volume Increase respiratory rate PowerPoint Presentation: Tidal volume Usually set b/w 10-12 ML/kg of IBW IBW calculation Male IBW in lb = 106+[6*(height in inches – 60)] Female IBW in lb = 105+[5*(height in inches – 60)] Convert IBW to Kg by dividing pounds by 2.2 Situation : Where comes the low volume lung protective ventilation? Tidal volume: Alveolar capillary stress fracture Pulmonary interstitial emphysema, pneumomediastinum , pneumothorax Inflammatory lung injury indistinguishable from ARDS Multi-organ injury from release of inflammatory mediators in the blood stream Where comes the low volume lung protective ventilation?: Ventilation with low tidal volumes was associated with a 9% (absolute) reduction in mortality when the end- inspiratory “plateau pressure” was <30 cm H2O lung protective ventilation with low tidal volumes is considered a beneficial strategy for all patients with acute respiratory failure. PowerPoint Presentation: Lower tidal volume – why? Minimize the airway pressure and the risk of barotrauma To increasing expiratory time in COPD patients sply Conditions that may require Lower Tidal Volume ARDS Pulmonary Edema Emphysema Pneumonectomy PowerPoint Presentation: Positive End-Expiratory Pressure Low tidal volumes can result in airway collapse, particularly at the end of expiration. Repeated opening and closing of airways at the end of expiration can become a source of lung injury (possibly by generating excessive shear forces that can damage the airways epithelium) Airways collapse can be mitigated by adding positive end-expiratory pressure (PEEP). This pressure acts as a stent to keep small airways open at the end of expiration Permissive Hypercapnia Another consequence of low volume ventilation is a reduction in CO2 elimination via the lungs, which can lead to hypercapnia and respiratory acidosis. Allowing hypercapnia to persist in favor of maintaining low volume ventilation is known as permissive hypercapnia Lower tidal volume – why?: Permissive hypercapnia The limits of tolerance to hypercapnia and respiratory acidosis are unclear, but individual reports show that PaCO2 levels as high as 375 mm Hg and pH levels as low as 6.6 are remarkably free of serious side effects as long as tissue oxygenation is adequate. One of the more troublesome side effects of hypercapnia is brainstem respiratory stimulation with subsequent hyperventilation, which often requires neuromuscular blockade to prevent ventilator asynchrony. arterial PCO2 levels of 60 to 70 mm Hg and arterial pH levels of 7.2 to 7.25 are safe for most patients. Often, the perceived risk of hypercapnic acidosis in individual patients is determined by the perceived benefit of maintaining low-volume ventilation to protect the lungs from volutrauma . Hickling KG, Walsh J, Henderson S, et al. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia : a prospective study. Crit Care Med 1994;22:1568–1578. Positive End-Expiratory Pressure Low tidal volumes can result in airway collapse, particularly at the end of expiration. Repeated opening and closing of airways at the end of expiration can become a source of lung injury (possibly by generating excessive shear forces that can damage the airways epithelium): Gas leakage and Circuit Compressible Volume Tidal volume delivered to pt < ventilator delivered tidal volume Causes – Leakage in the ventilator circuit Gas leakage in the endotracheal tube cuff Circuit compressible volume loss Permissive hypercapnia: FIO2 Initially 100% Then adjust as per ABG report After stabilization, FIO2 is best kept below 50% to avoid oxygen induced lung injury Gas leakage and Circuit Compressible Volume: PEEP In refractory hypoxemia Increases the FRC PEEP adjusted based on ABG, FIO2 requirements, tolerence of PEEP, CVS response. FIO2: I:E ratio Usually 1:2 to 1:4 A larger I:E ratio is basically a longer E ratio used where there is possibility of air-trapping and auto-PEEP generation. How do we detect auto-PEEP? When end-expiratory pressure does not touch the base line (i.e. 0 cm H2O/ PEEP level when PEEP is applied) Inverse I:E ration – to correct refractory hypoxemia in ARDS patients with very low compliance I:E ratio: How to increase I:E ratio?? Parameters I/D I TIME E TIME I:E Flow rate I D I I D I D D Tidal volume I I D D D D I I RR I NEGLIGIBLE D D D NEGLIGIBLE I I I – INCREASE, D - DECREASE PowerPoint Presentation: Vital signs - HR Tachycardia Bradycardia Hypoxemia Endotracheal suctioning Hypovolemia Inadequate coronary blood flow Pain Heart block Anxiety Abnormal SA node function Fever Hypothermia AMI/ drug reactions Morphine sulfate How to increase I:E ratio??: BP Hypertension Hypotension Fluid overload Secondary to PPV Stress Hypovolemia Anxiety Sepsis Pain Shock CHF CCF CVS disorders Polycythemia Vital signs - HR: Temperature Hyperthermia - infection, tissue necrosis, leukemia, increased metabolic rate Hypothermia - CNS problem, metabolic disorcders , drugs and toxins, Induced Induced Hypothermia – head Injury, CABG Temperature correction during ABG analysis BP: Clinical assessment (Inspection, Auscultation) Diminished or Absent – airway obstruction, Atelectasis , Main stem intubation, Effusion, Pneumothorax Wheezing – obstruction Inspiratory crackles – consolidation, Pulmonary edema Coarse crackles – excessive secretions Temperature : Fluid balance PPV - CO renal perfusion urine output PPV - ADH, ANF FLUID RETENTION INTAKE/OUTPUT CHART MAINTENANCE IS MUST INTAKE = OUTPUT + 500 mL in 24 hours Clinical assessment (Inspection, Auscultation): ABG analysis and Anion Gap determination What is the pH? Acidemia or Alkalemia ? What is the primary disorder present? Is there appropriate compensation? Is the compensation acute or chronic? Is there an anion gap? If there is a AG check the delta gap? What is the differential for the clinical processes? Fluid balance : Assessment of ventilator status By PaCO 2 - BEST Hypoventilation and respiratory acidosis are present when PaCO2 is increased with a current decrease in pH. To be corrected by increasing RR or Tidal Volume Metabolic causes should be corrected first before changing the ventilatory settings Excessive work of breathing ( minute ventilation in excess of 10 L/min ) is an obstacle to weaning. ABG analysis and Anion Gap determination: Assessment of oxygenation status Arterial oxygen tension (PaO2) Alveolar-arterial oxygen gradient (A-a)DO2 PaO2/PAO2 PaO2/FiO2 Assessment of ventilator status: PARAMETERS CRITERIA INTERPRETATION PaO2 80-100mmHg Normal 60-79mmHg Mild hypoxemia 40-59mmHg Moderate hypoxemia <40mmHg Severe hypoxemia PaO2/FiO2 >200 Normal <200 Presence of shunt P(A-a)O2 Room Air Should be less than 4 for every 10 years of age, otherwise hypoxemia 100% O2 Every 50 mmHg difference approximates 2% shunt PaO2/PAO2 FiO2 equal or >30% >75% normal <75% hypoxemia Assessment of oxygenation status: PaO2 P(A-a)O2, PaCO2 P(A-a)O2 – N almost PaCO2 - HYPOVENTILATION O2 +Improve ventilation P(A-a)O2 – PaCO2 – N/ V/Q mismatch O2 therapy shunt PEEP Diffusion defect Low alveolar-arterial oxygen gradient alveolar capillary thickness alveolar surface area oxygen PowerPoint Presentation: Oxygen saturation monitoring Simple non-invasive method ABG – Isolated measurement, single time Pulse Oximetry – continuous assessment So single ABG f/b continuous oximetry to have a PaO2 trend But result may be inaccurate Simple method to check accuracy: If HR on the oximeter varies significantly from the actual pulse as measured by palpation or cardiac monitor, please do varify accuracy PowerPoint Presentation: SpO2 of >95% has a strong correlation with PaO2 of >70 mmHg with a sensitivity of 100% but but SpO2 becomes less accurate as SpO2 decreases and overestimates pt’s oxygenation status Oxygen saturation monitoring: Factors that affect the accuracy of pulse oximetry Factors Type of inaccuracy Sunlight SpO2 measures lower than actual SpO2 Nail polish Fluorescence light Intravenous dyes Dyshemoglobins (meth, sulfa, carboxy -hemoglobin) SpO2 measures higher than actual SpO2 Low perfusion states (profound shock) SpO2 of >95% has a strong correlation with PaO2 of >70 mmHg with a sensitivity of 100% but but SpO2 becomes less accurate as SpO2 decreases and overestimates pt’s oxygenation status : O2 oxygenation alveoli perfusion metabolism + oxygen glucose energy back to lungs capillary vein CO2 Physiology Ventilation The Standard of Care Capnography Transport Cell Metabolism Factors that affect the accuracy of pulse oximetry: Factors that affect CO2 levels: INCREASE IN ETCO 2 DECREASE IN ETCO 2 Increased muscular activity Decreased muscular activity Increased cardiac output (during resuscitation) Decreased cardiac output (during resuscitation) Effective drug therapy for bronchospasm Bronchospasm Hypoventilation Hyperventilation The Standard of Care Capnography Physiology: Normal EtCO 2 O2 CO2 Normal The Standard of Care Capnography PowerPoint Presentation: Terminology Capnogram a real-time waveform record of the concentration of carbon dioxide in the respiratory gases Capnograph Capnogram waveform plus numerical value CO2 38 mmHg The Standard of Care Capnography Normal EtCO2: Terminology EtCO 2 – End Tidal CO 2 The measurement of exhaled CO 2 in the breath Normal Range | 35-45 mmHg CO2 The Standard of Care Capnography Terminology: Normal Waveform A B C D E A 38 mmHg CO 2 TIME End of inspiration Beginning of exhalation End of exhalation Beginning of new breath Alveolar plateau The Standard of Care Capnography Clearing of anatomic dead space Terminology: Normal Common Waveforms mmHg 39 16 RR The Standard of Care Capnography Normal Waveform: Hyperventilation Hypoventilation Common Waveforms mmHg 48 8 RR mmHg 24 35 RR The Standard of Care Capnography Common Waveforms: 4 Main Uses of Capnography The Standard of Care Capnography Severity of asthma patients Monitoring head injured patients Cardiac arrest Tube confirmation Common Waveforms: Terminology The Standard of Care Capnography Sidestream An indirect method of measuring exhaled CO 2 in non-intubated patients Mainstream Direct method of measuring exhaled CO 2 with intubated patients 4 Main Uses of Capnography: Shark Fin Asthmatic Waveforms mmHg 45 18 RR COPD patients have a difficult time exhaling gases This is represented on the capnogram by a shark fin appearance The Standard of Care Capnography Terminology: Moderate Attack Mild Attack EtCO 2 & Asthma mmHg 28 38 RR mmHg 36 20 RR The Standard of Care Capnography Asthmatic Waveforms: Severe Attack EtCO 2 & Asthma mmHg 49 9 RR Time To Get MOVING!!! The asthmatic who looks tired and has a shark fin appearance on the capnogram… IS HEADED FOR RESPIRATORY ARREST The Standard of Care Capnography EtCO2 & Asthma: The Head Injured Patient The Standard of Care Capnography Carbon dioxide dilates the cerebral blood vessels, increasing the volume of blood in the intracranial vault and therefore increasing ICP Recognizing the head injured patient and titrating their CO 2 levels to the 30-35 mmHg range can help relieve the untoward effects of ICP EtCO2 & Asthma: Titrate EtCO 2 The Head Injured Patient mmHg 30 16 RR The Standard of Care Capnography Titration IS NOT hyperventilation. Intubating a head injured patient and using capnography gives a means to closely monitor CO 2 levels. Keep them between 30 and 35 mmHg The Head Injured Patient: EtCO 2 and Cardiac Arrest The Standard of Care Capnography The capnograph of an intubated cardiac arrest patient is a direct correlation to cardiac output Increase in CO 2 during CPR can be an early indicator of ROSC The Head Injured Patient: Termination of Resuscitation The Standard of Care Capnography EtCO 2 measurements during a resuscitation give you an accurate indicator of survivability for patients under CPR Non-survivors < 10 mmHg Survivors > 30 mmHg ( to discharge) EtCO2 and Cardiac Arrest: ET Tube Verification Verification of proper tube placement There is simply NO BETTER WAY to confirm proper tube placement than with waveform capnography…. PERIOD!!! no waveform = no tube!!! The Standard of Care Capnography Termination of Resuscitation: Obstruction Troubleshooting mmHg 39 16 RR The Standard of Care Capnography An obstructed ET tube may have an erratic EtCO 2 value with a very irregular waveform ET Tube Verification: Inadequate Seal Troubleshooting mmHg 39 16 RR The Standard of Care Capnography As air escapes around the cuff during BVM respirations the waveform will distort, alerting you to a possibly deflated or damaged ET cuff Troubleshooting: Rebreathing Troubleshooting mmHg 42 16 RR The Standard of Care Capnography A capnogram that does not touch the baseline is indicative of a patient who is rebreathing CO 2 through insufficient inspiratory or expiratory flow Troubleshooting: Monitoring of lung mechanics – proximal airway pressure Troubleshooting: P peak = (Resistance + elastance ) Peak pressure varies directly with airway resistance and lung elastance The effects of theses two can be distinguished by occluding the expiratory tubing – inflation holding Monitoring of lung mechanics – proximal airway pressure: P plateau = Elastance ( P peak – P plateau ) = Airway Resistance Ppeak = (Resistance + elastance): Acute respiratory deterioration Peak Inspiratory Pressure Decreased Air Leak Hyperventilation No Change Pulmonary Embolism Extrathoracic process Increased Plateau Pressure No change Airway obstruction Aspiration Bronchospasm Secretions Tracheal tube obstruction Increased Decreased Compliance Abdominal distension Atelectasis Auto-PEEP Pneumothorax Pulmonaryuedema Bronchodialator responsiveness PowerPoint Presentation: Thoracic Compliance Compliance = reciprocal of elastance C stat = V T / P plateau C stat = 0.5 L/ 10 cmH2O Normal = 0.05 - 0.08 L/cmH2O Stiff lung when C stat = 0.01 – 0.02 L/cmH2O (Pulmonary edema, ARDS) PowerPoint Presentation: Pitfalls in Compliance calculation PEEP corrections Compliance of connector tubings – 3mL/cm H2O Exhaled Volume Compliance measurement only during passive ventilation Thoracic Compliance: Different types of patient Pitfalls in Compliance calculation: COPD and Asthma Goals: Diminish dynamic hyperinflation Diminish work of breathing Controlled hypoventilation (permissive hypercapnia) Different types of patient: Diminish DHI Why? COPD and Asthma: Diminish DHI How? Diminish minute ventilation Low Vt (6-8 cc/kg) Low RR (8-10 b/min) Maximize expiratory time Diminish DHI: Diminish work of breathing How: Add PEEP (about 85% of PEEPi) Applicable in COPD and Asthma. Diminish DHI: Controlled hypercapnia Why? Limit high airway pressures and thus diminish the risk of complications Diminish work of breathing: Controlled hypercapnia How? Control the ventilation to keep adequate pressures up to a PH > 7.20 and/or a PaCO2 of 80 mmHg Controlled hypercapnia: Controlled hypercapnia CI: Head pathologies Severe HTN Severe metabolic acidosis Hypovolemia Severe refractory hypoxia Severe pulmonary HTN Coronary disease Controlled hypercapnia: Development in most of the fields of medicine appears to occur according to sound scientific principles. However exceptions can be found and the development of mechanical ventilatory support is one of them. ------- J. Rasanen Thank you…….. 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