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![Mode Of Ventilation
● In order to adhere to a strategy of LTVV, it is probably easier to use a
volume limited approach. However, a pressure limited mode is an
acceptable alternative, as long as the resulting tidal volumes are
stable and consistent with the strategy of LTVV
● Regardless of whether volume limited or pressure limited ventilation
is chosen, fully supported modes of mechanical ventilation (eg, assist
control) are generally favored over partially supported modes (eg,
[SIMV]. This is particularly true early in the course of disease
● Ultimately, the choice of mode depends primarily on clinician comfort
and familiarity](https://image.slidesharecdn.com/ventilotrymanagemantofards-220316110231/75/Ventilotry-managemant-of-ards-33-2048.jpg)
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Ventilotry managemant of ards
- 1. Ventilatory Management of ARDS(ACUTE RESPIRATORY DISTRESS SYNDROME) Dr. Avinash Kumar JR-2 Moderator-Dr J.N. Thakur Dr Aditya Kejriwal
- 2. Introduction • First reportedin 1967 in adults by Ashbaugh & coworkers • Mortality rate of 35 to 40 % • Death usually due to sepsis or multiorgan faliure rather than primary respiratory causes.
- 3. Introduction(cont.) SYNONYMS • Shock lung •Non-cardiogenic pulmonary oedema • Adult respiratory distress syndrome • Acute lung injury • Wet lung • Leaky - capillary pulmonary edema
- 4. New and Improved •Adult Respiratory Distress Syndrome • Acute Respiratory Distress Syndrome
- 5. -European Society ofIntensive Care Medicine with endorsement from American Thoracic Society and Society of Critical Care Medicine -Devided three mutually exclusive severity categories: Mild,Moderate and Severe -Took into account: timing, chest imaging, origin of edema, oxygenation
- 6. Definition ARDS is definedby the presence within 7 days of a known clinical insult or new or worsening respiratory symptoms of a combination of acute hypoxemia (PaO₂/FiO₂ ≤ 300 mmHg), in a ventilated patient with PEEP of at least 5cm H₂O, & bilateral opacities not fully explained by heart failure or volume overload.
- 7. Comparison of AECC& Berlin definition of ARDS AECC Definition Berlin Definition Timing Acute onset Onset is within 1 week of a Known clinical insult or new or worsening respiratory symptoms Oxygenation ALI:PaO₂/FiO₂ ≤ 300 mmHg ARDS:PaO₂/FiO₂ ≤ 200 mmHg Mild: 200˂PaO₂/FiO₂ ≤ 300 mmHg with PEEP ≥ 5 cm H₂O Moderate: 100˂PaO₂/FiO₂ ≤ 200 mmHg with PEEP ≥ 5 cm H₂O Severe: PaO₂/FiO₂ ≤ 100 mmHg with PEEP ≥ 5 cm H₂O Chest Radiograph Bilateral infiltrates Bilateral opacities not fully explained by effusions, lobar or lung collapse or nodules Edema PAWP ≤ 18 mmHg or no clinical evidence of left atrial hypertension Respiratory faliure not fully explained by cardiac faliure or fluid overload Risk factor Not included in definition If no risk factor for lung injury is identified then objective assesssment like echocardiography to exclude hydrostatic edema is needed.
- 8. Clinical disorders associatedwith development of ARDS • Direct lung injury – Pneumonia – Aspiration of gastric contents – Pulmonary contusion – Fat emboli – Near drowning – Reperfusion edema (post transplant) – Inhalational injury • Indirect lung injury – Sepsis – Severe trauma – Cardiopulmonary bypass – Drug overdose – Acute pancreatitis – Multiple blood product transfusions
- 9. Pathophysiology – Acute exudativephase (1-7days) – Proliferative phase (3-10 days) – Chronic/fibrotic phase ( 1-2 weeks) – Recovery phase
- 10. Acute Inflammation Affects Alveolar CapillaryMembrane Increased Permeability Recruitment Of Neutrophils Inflammatory Mediators Loss Of Gas Exchange Surface Area Inactivation Of Surfactant Collapse & Consolidation Pulmonary Oedema Hypoxia Pulmonary Vasoconstriction Profound Hypoxaemia Type 1 Respiratory Failure Patho Physiology
- 11. Consequences of lunginjury include: – Impaired gas exchange – Decreased compliance – Increased pulmonary arterial pressure – V/Q mismatch – Increased dead space – Impairs carbon dioxide elimination – High minute ventilation
- 12. Clinical Features ofARDS • Rapid onset • Severe dyspnea • Severe tachypnea • Arterial hypoxemia refractory to O2 therapy • Decreased pulmonary compliance
- 13. Differential Diagnosis of ARDS ManyDiseases Can Present Acutely With Bilateral Infiltrates and Hypoxemia ARDS CHF Pneumonia Alveolar Hemorrhage Aspiration T. Sisson
- 14. ARDS - Principlesof Therapy • Treat underlying cause • Lung protective ventilation • Promoting oxygen transport & adequate gas exchange • Fluid management • Pharmacotherapy & nutrition • Need for tracheostomy • Avoid secondary injury & initiate mobilization
- 15. Need for Mechanical Ventilation •Persistent hypoxemia (SpO2 ˂ 90%) on non rebreathing facemask oxygen or NIV • Excessive work of breathing • Hemodynamic instability • NIV/CPAP –limited role in immunosuppressed • Strategy – Open up the lung & keep it open
- 16. Initial ventilator settings •Mode- VCV or PCV as starting mode • Tidal vol.-initial 8mL/Kg PBW • Reduce by 1mL/Kg every 2hrs until 6mL/Kg • Inspiratory airway pressure < 30 cm H2O • Initially high FiO2 to be titrated down with PEEP between 5-10 cm H2O • RR <35/min, pH goal 7.35-7.40
- 17. Promoting oxygen transport &adequate gas exchange • Recuritment Maneuver • Prone positioning • High frequency ventilation • ECMO • Inhaled nitric oxide
- 18. ARDS Management Mechanical Ventilation: ● Low tidal volume ventilation ● Open lung ventilation High peep recruitment ● Inverse ratio ventilation Unconventional approach: ● APRV ● HFV General Measures: ● Prone positioning ● Nitric oxide ● NMBA ● Fluid Management ● ECMO
- 19. Strategies of mechanicalventilation of adults in ARDS Low tidal volume ventilation (lung protective ventilation) Permissive hypercapnia Open lung ventilation
- 20. Low Tidal volumeVentilation ● Low tidal volume ventilation (LTVV) is also referred to as lung protective ventilation. ● For patients with acute respiratory distress syndrome (ARDS), low tidal volume ventilation (4 to 8 mL/kg PBW) is recommended ● Adjust the tidal volume to achieve an inspiratory plateau airway pressure =30 cm H2O
- 21. Low tidal volumeventilation (LTVV) Benefit Evidence suggests that the early application of and adherence to LTVV decrease mortality, as well as other clinically important outcomes in patients with ARDS
- 22. Low tidal volumeventilation (LTVV) Benefit ● The multicenter ARMA trial randomly assigned 861 mechanically ventilated patients with ARDS to receive LTVV (initial tidal volume of 6mL/kg PBW) or conventional mechanical ventilation (initial tidal volume of 12 mL/kg PBW)
- 23. Low tidal volumeventilation (LTVV) Harm ● LTVV is generally well tolerated ● It was not associated with any clinically important adverse outcomes in the ARMA trial. ● With respect to physiologic adverse outcomes, LTVV caused hypercapnic respiratory acidosis in some patients ● Hypercapnic respiratory acidosis was an expected and generally well tolerated consequence of LTVV
- 24. Low tidal volumeventilation (LTVV) Harm Two major concerns were expressed after publication of the ARMA trial (1) Auto-PEEP ● The higher respiratory rater in LTVV may create auto-PEEP by decreasing the time available for complete expiration (2) Sedation ● Work of breathing and patient-ventilator synchrony may increase when tidal volumes are <7 mL/kg of PBW. ● While asynchrony may require increased sedation soon after the initiation of LTVV, the need for increased sedation does not appear to persist
- 25. Low tidal volumeventilation (LTVV) Application
- 26. Permissive Hypercapnia ● LTVVfrequently requires permissive hypercapnic ventilation (PHV), a ventilatory strategy that accepts alveolar hypoventilation in order to maintain a low alveolar pressure and minimize the complications of alveolar overdistension (eg, ventilator associated lung injury) ● Hypercapnia and respiratory acidosis are a consequence of this strategy ● Minimum accepted PH = 7.25 ● The degree of hypercapnia can be minimized by using the highest respiratory rate that does not induce auto-PEEP and shortening the ventilator tubing to decrease dead space
- 27. Open Lung ventilation(OLV) ● A strategy that combines low tidal volume ventilation (LTVV) with a recruitment maneuver and subsequent titration of applied PEEP to maximize alveolar recruitment ● The LTVV and set limits on plateau pressure aim to mitigate alveolar overdistension, while the applied PEEP seeks to minimize cyclic atelectasis. ● Together, these effects are expected to decrease the risk of ventilator-associated lung injury.
- 28. Open Lung ventilation(OLV) ● On balance, most trials do not show convincing benefit and some show possible harm such that it is better to avoid the routine application of open lung strategies as an initial strategy in patients with ARDS ● Any use of OLV strategies should be limited to those with severe ARDS refractory to standard LTVV strategies; in addition, when employed patients should be closely observed for an oxygenation response, so that the clinician can decide whether it is appropriate to continue or abandon the OLV trial.
- 29. High PEEP ● Theroutine use of a high PEEP strategy in ARDS patients as an initial strategy is not recommended. ● However, in patients refractory to standard methods of mechanical ventilation, some experts use a high PEEP strategy such as that employed in the ALVEOLI or LOVS trials
- 30. High PEEP ● Itis thought that use of higher levels of PEEP benefit patients by opening collapsed alveoli, which in turn serves to decrease alveolar overdistension because the volume of each subsequent tidal breath is shared by more open alveoli. ● If the alveoli remain open throughout the respiratory cycle, cyclic atelectasis is also reduced. Alveolar overdistension and cyclic atelectasis are the principal causes of ventilator- associated lung injury
- 31. High PEEP ● Theapplication of high PEEP does not appear to be associated with improved mortality except perhaps in those with severe gas exchange abnormalities ● Further study is needed to determine the optimal level of PEEP and the ARDS population in whom a clear mortality benefit might be expected
- 32. Mode of Ventilation ●Patients with ARDS can be supported using either a volume limited or a pressure limited mode of Ventilation ● In most patients with ARDS, a volume limited mode will produce a stable airway pressure and a pressure limited mode will deliver stable tidal volumes, assuming that breath to breath lung mechanics and patient effort are stable ● Abrupt changes in the airway pressure in a patient receiving volume limited ventilation, or in tidal volumes in a patient receiving pressure limited ventilation, should prompt an immediate search for a cause of an acute change in compliance (eg, pneumothorax or an obstructed endotracheal tube)
- 33. Mode Of Ventilation ●In order to adhere to a strategy of LTVV, it is probably easier to use a volume limited approach. However, a pressure limited mode is an acceptable alternative, as long as the resulting tidal volumes are stable and consistent with the strategy of LTVV ● Regardless of whether volume limited or pressure limited ventilation is chosen, fully supported modes of mechanical ventilation (eg, assist control) are generally favored over partially supported modes (eg, [SIMV]. This is particularly true early in the course of disease ● Ultimately, the choice of mode depends primarily on clinician comfort and familiarity
- 34. Inspiratory time adjustment (Inverseratio ventilation) ● Refractory hypoxemia can occur even if the applied PEEP and FiO2 are optimized. In this situation increasing the I:E ratio by prolonging inspiratory time may improve oxygenation. ● Increasing the I:E ratio will increase the mean airway pressure and may improve oxygenation in some patients
- 35. Inspiratory time adjustment (Inverseratio ventilation) ● There are potential costs associated with prolonging the inspiratory time that should be considered. When the inspiratory time is increased, there is an obligatory decrease in the expiratory time. This can lead to air trapping, auto-PEEP, barotrauma, hemodynamic instability, and decreased oxygen delivery. ● In addition, a prolonged inspiratory time may require significant sedation or neuromuscular blockade. particularly if the inspiratory time suppress the expiratory time (inverse ratio ventilation)
- 38. Fluid management • Conservativefluid management not at cost of organ perfusion • Both crystalloids & colloids along with vasopressors (if required) can be used • Among colloid HES is Not used due risk of renal damage
- 39. Pharmacotherapy & nutrition •Glucocoricoids – Weigh risk & benefits for individual pts. – To be used within 2 wks of onset – Methlprednisolone 1mg/kg bolus followed by 1mg/kg/day infusion to be used if not on NMBA – If no response in 5 days discontinue – If favourable response continue for 14 days, thereafter half dose for 7 days followed by one fourth dose for 7 days & then stop
- 40. Tracheostomy • Should beperformed once the patient is off high Fio2 & PEEP support but still needs continuous ventilator support due to high Minute ventilation
- 41. Weaning & mobilization •Weaning attempts to be started once FiO2 & PEEP support decrease & minute ventilation requirement comes down • Early mobilization & physiotherapy to prevent long term neuromuscular disability
- 42. Benefits of Proneposition • The dependent lung units are susceptible to collapse in ARDS superadded by wt. Of heart ,abdominal viscera & congested lung. • Turning to prone alleviates the potential compressive reduction in regional shear stress. • Together these reduce the risk of ventilator induced lung injury.
- 43. Benefits of Proneposition • Systemic inflammatory mediators causing organ faliure & mortality in VILI are significantly reduced by mechanical ventilation in prone . • Drainage of posterior dependent lung units is improved in prone position reducing ventilator associated pneumonia. • More ventilator free days in proned pts. reduces further risk of ventilator associated pneumonia → mortality↓
- 44. Contraindication for proneposition • Absolute – Severe acute arrhythmia – Pelvic fracture – Intracranial hypertension – Spine instability – Recent sternotomy / heart surgery • Relative – Tracheostomy within first 24 hrs – Bronchopleural fistula – Hemoptysis/alveolar haemorrhage – Ophthalmic surgery/increased intraocular pressure – Pregnancy/ intraabdominal pressure >20mmHg
- 45. Complications of proneposition • Pressure ulcers on face, chest & knee. • ET tube obstruction, or decannulation, or extubation ( most serious/fatal event, 0-2.4%). • Operative wound dehiscence. • Brachial plexus injury, compression of retinal vessels. • Diet intolerance. • Central catheter extubation or avulsion. • Transient desaturation & transient hypotension. • Difficulty in instituting CPR.
- 46. Summary/ Key Points ARDSis Diagnosed by Clinical Parameters: ♦ Acute Onset in Appropriate Setting ♦ Bilateral Infiltrates ♦ Reduced Oxygenation ♦ No Evidence of CHF Differential Diagnosis Includes: ♦ Congestive Heart Failure ♦ Alveolar Hemorrhage ♦ Pneumonia ♦ Aspiration Pathophysiology Includes: ♦ Systemic Inflammation ♦ Injury to the Alveolar Membrane ♦ Alveolar Flooding with Plasma Fluid ♦ Inactivation of Surfactant Respiratory Distress ↑ Resp. Rate Hypoxemia ↓ Compliance Bilateral Infiltrates
- 47. Summary/ Key Points ManagementProblems: ♦ Decreased Compliance ♦ Refractory Hypoxemia ♦ High Mortality Strategies to Manage: ♦ Decreased Compliance ♦ Refractory Hypoxemia ♦ High Mortality Risk Factors for Mortality: ♦ Multi-organ Failure ♦ Underlying Cause of ARDS Low Tidal Volume Ventilation Permissive Hypercapnea Best PEEP Curve Prone Positioning ECMO
- 48.
- 49. Question 1.Berlin definition . 2.DefinePermissive hypecapnia. 3.Benifit of low tidal volume ventilation. 4.Contraindication of prone position. 5.Fluid management in ARDS.