Ventilator settings in ARDS & COPD & weaning

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A presentation on the basic settings in specific diseases, with particular emphasis on ARDS & COPD; also deals with WEANING from ventilator.

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MECHANICAL VENTILATION IN ARDS & COPD WEANING FROM VENTILATOR Dr Deepa C MD 27 Oct 2011

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RESPIRATORY SYSTEM Ventilating pump - Respiratory control centres in the brain - Connecting tracts and nerves - Chest wall and respiratory muscles Gas-exchange system - Lungs

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INDICATIONS FOR MECHANICAL VENTILATION Ventilatory failure Oxygenation failure Excessive ventilatory workload Impending respiratory failure

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VENTILATORY FAILURE Drug overdose Spinal cord injury Head injury & stroke Neuromuscular dysfunction Sleep disorders Acute airflow obstruction Chest trauma Postoperative – thoracic & upper abdominal Electrolyte imbalance General anaesthesia

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OXYGENATION FAILURE & INCREASED VENTILATORY WORKLOAD Acute lung injury/ARDS Acute severe airflow obstruction Dead space ventilation Shunts Congenital heart diseases Shock High metabolic rate & obesity General anaesthesia & postop

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ACUTE LUNG INJURY & ARDS COPD

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ACUTE LUNG INJURY & ARDS Acute onset dyspnoea Chest radiograph - bilateral alveolar or interstitial infiltrates PCWP < 18 mmHg or no clinical evidence of increased left atrial pressure Poor oxygenation status - PaO ₂ /FiO ₂ < 300 in ALI < 200 in ARDS Diagnostic Criteria for ALI and ARDS

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Chest X-ray in ARDS

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CT thorax – Lungs in ARDS

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CT thorax – Lungs in ARDS

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RECRUITMENT MANOEUVRES PEEP Increasing inspiratory pressure Increasing inspiratory pause Inverse ratio ventilation High frequency oscillatory ventilation Prone position ventilation

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Re-expands collapsed dorsal areas of the lung Chest wall has more favorable compliance curve in prone position Heart moves away from the lungs Net result is usually improved oxygenation Care of patient (suctioning, lines, decubiti) trickier, but not impossible PRONING

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Vasodilator with very short half-life that can be delivered via ETT Vasodilate blood vessels that supply ventilated alveoli and thus improve V/Q No systemic effects due to rapid inactivation by binding to Hb Improves oxygenation but does not improve outcome INHALED NITRIC OXIDE

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COPD - chronic airflow limitation; not fully reversible mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema) and their relative contributions vary from person to person excludes asthma ( reversible airflow limitation) COPD & ASTHMA

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INDICATIONS FOR NIV Moderate to severe dyspnea with use of accessory muscles and paradoxical abdominal motion Moderate to severe acidosis (pH<7.35) and/or hypercapnia (PaCO₂ > 45 mm Hg) Respiratory rate > 25 breaths/ minute

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EXCLUSION CRITERIA FOR NIV Respiratory arrest Cardiovascular instability Change in mental status Non-co-operative patient High aspiration risk Viscous or copious secretions Recent facial or gastro-esophageal surgery Craniofacial trauma Fixed nasopharyngeal abnormalities Burns Extreme obesity

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Success rates of 80-85% Improves CO₂ elimination Improves respiratory acidosis Decreases respiratory rate Unloading of respiratory muscles Lower rate of nosocomial pneumonia Lower intubation rate Reduction in duration of mechanical ventilation Decreases the length of hospital stay & mortality rate BENEFITS OF NIV

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NIV should be considered in patients of COPD in addition to standard medical therapy, when they present in acute exacerbation (pH < 7.35, PaCO ₂ > 45 mm Hg). (Level I) NIV may be useful in appropriately selected patients of hypoxemic respiratory failure . (Level I) CPAP/NIV are recommended in addition to standard medical treatment in cases of cardiogenic pulmonary edema . (Level I) NIV is recommended early in the course of hypoxic respiratory failure in immunocompromised patients, particularly in those with hematological malignancies . (Level I)

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INDICATIONS FOR INVASIVE VENTILATION Unable to tolerate NIV or NIV failure Severe dyspnea with use of accessory muscles and paradoxical abdominal motion Respiratory rate > 35 breaths/ minute Life-threatening hypoxemia (PaO ₂ < 60 mm Hg) Severe acidosis (pH <7.25) and/or hypercapnia (PaCO₂ > 60 mm Hg)

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Respiratory arrest Cardiovascular complications Somnolence, impaired mental status Other complications – metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, barotrauma, massive pleural effusion Contd …

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Airflow obstruction Low I:E ratios Increased respiratory rate Low flows Leads to dynamic hyperinflation (DHI) AUTO-PEEP or INTRINSIC PEEP

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AUTO-PEEP or INTRINSIC PEEP

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DYNAMIC HYPERINFLATION Expiratory flow obstruction Increased rate Decreased expiratory time

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DIMINISH DHI Diminish minute ventilation Low V T (6-8 mL/kg) Low RR (8-10 /min) Maximize expiratory time (Low I:E ratio) High flows

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GOALS OF VENTILATION IN COPD Diminish dynamic hyperinflation Diminish work of breathing Controlled hypoventilation (permissive hypercapnia)

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Provide V E that does not cause alkalosis Initiate low tidal volume : 6- 8 mL/kg RR : 8-12/min I:E with prolonged expiration to minimise DHI Adjust PEEPe to match at least 85% of PEEPi (diminish work of breathing) FiO ₂ to achieve PaO ₂ > 55 - 60 mmHg Insp. flow - initially 60L/min, then ↑ till the demands are satisfied Trigger : 2L/min or -2cm H ₂ O

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PERMISSIVE HYPERCAPNIA Control the ventilation to keep adequate pressures up to a pH > 7.20 and/or a PaCO ₂ upto 80 mmHg Head pathologies and raised ICP Severe HTN Severe metabolic acidosis Hypovolemia Severe refractory hypoxia Severe pulmonary HTN Coronary artery disease CONTRAINDICATIONS

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Neuromuscular disorders – dependent areas atelectatic Traumatic brain injury – aim for normoacpnia (NOT hypocapnia ) Pressure mode vs Volume mode Which is BETTER/IDEAL ? Are Dual modes an answer? Are they PERFECT ?

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Defined as effective spontaneous breathing without any mechanical assistance for 24 hours or more The spontaneous breaths are unassisted by mechanical means Supplemental oxygen, bronchodilators, pressure support, or continuous positive airway pressure are often used to support and maintain adequate spontaneous ventilation and oxygenation WEANING SUCCESS

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PaO₂ >60 mm Hg with FiO₂ < 0.5 and PEEP ≤ 5 cm H₂O PaCO ₂ < 45 mm Hg pH : 7.35–7.45 A minimal spontaneous Vt > 5-10 ml/kg Vital capacity > 10 ml/kg Minute ventilation (either spontaneous or assisted) less than 10 L/min (assuming PaCO ₂ is normal) Negative inspiratory force > -20 to -30 cm H ₂ O Rapid, shallow breathing index (RSBI) - f/Vt < 105 Predictors of weaning success

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General approaches for weaning SIMV Pressure Support Ventilation (PSV) - prolonged weaning process because of slowly resolving lung disease Spontaneous Breathing Trials (SBT) no positive pressure to the airway a low level of CPAP a low level of PSV ( eg ., 5 - 8 cm H ₂ O)

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Explain the process to the patient and encourage co-operation Begin during day time, allow patient to rest at night and between trials of weaning Place patient in propped-up position PEEP = 5, PS = 0 – 5, FiO ₂ < 40% Breathe independently for 30 – 120 min ABG obtained at end of SBT

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Tachypnea (RR >35 breaths/min for ≥ 5min) Hypoxemia (SpO ₂ by pulse oximeter < 90%) Tachycardia (HR >140 beats/min or sustained rate increase > 20%) Bradycardia (sustained rate decrease by > 20%) Hypertension (systolic BP > 180 mm Hg) Hypotension (systolic BP < 90 mm Hg) Agitation, diaphoresis, anxiety, respiratory distress (use of accessory muscles, abdominal paradox..) Optional ABG criteria: Increase in PaCO ₂ >10 mm Hg or decrease in pH > 0.1 Criteria for the discontinuation of a weaning trial

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Rapid breathing

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EXTUBATION Control of airway reflexes Patent upper airway (air leak around tube?) Minimal oxygen requirement Minimal rate Minimize pressure support (0-10 cm H ₂ O) “Awake ” patient

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TROUBLESHOOTING

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Remove patient from ventilator Initiate manual ventilation Perform physical examination and assess monitoring indices Check patency of airway If death is imminent, consider and treat most likely causes Once patient is stabilized, undertake more detailed assessment and management

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PATIENT-RELATED CAUSES Artificial airway problems Secretions Bronchospasm Pneumothorax Pulmonary embolism Dynamic hyperinflation Abnormal respiratory drive Drug-induced problems Abdominal distension Agitation VENTILATOR-RELATED CAUSES System leak Circuit malfunction Inadequate FiO ₂ Inadequate ventilator support PATIENT-VENTILATOR ASYNCHRONY

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