ARDS AND
MECHANICAL
VENTILATION
DR.ANANTHU MOHAN
Jr3
MCH TVM
ARDS
• Acute onset (<=1 week) of bilateral opacities
on chest that are not explained by cardiac
failure or fluid overload and or ventilation
perfusion mismatch.
• Annual Incidence=60 cases/100000
population.
• Incidence raised after covid _ 19
CAUSES
• Direct lung injury • Indirect lung injury
• Pneumonia • Sepsis
• Aspiration of gastric • severe Trauma (burns)
contents • Multiple transfusions
• Pulmonary contusion • Drug overdose
• Near drowning • Pancreatitis
• Toxic inhalational • post Cardiopulmonary
injury. bypass
BERLIN CRITERIA
• Onset within 1 week of clinical insult
• Bilateral opacities on CXR consistent with
pulmonary edema
• Absence of left atrial hypertension.
• Severity based on pao2/fio2 ratio
• Mild _pao2/fio2 </=300 to >200
• Moderate _pao2/fio2</=200 to >100
• Severe_pao2/fio2 </=100
PATHOPHYSIOLOGY
• The natural history is marked by three
phases.
EXUDATIVE PHASE(1st 7 days)
• Alveolar capillary endothelial cell and
type 1 pneumocytes injured.
• Edema fliud accumulates in alveoli and
interstitium.
• Neutrophils infiltration along with
damaged cells to form hyaline
membrane whorls.
PROLIFERATIVE PHASE
• Last from day 7 to day 21.
• Signs of resolution are evident in this
phase.Initiation of lung repair starts.
• Shift from neutrophils to lymphocyte
predominant pulmonary infiltrates.
• Type2 pneumocytes proliferate and form new
surfactant and they also differentiate in to
type1 pneumocytes.
FIBROTIC PHASE
• The alveolar edema and inflammatory
exudates of earlier phase convert in to
alveolar duct and interstitial fibrosis .
• Intimal fibroproliferation in pulmonary
circulation causes pulmonary
hypertension.
TREATMENT
GENERAL MEASURES
• Recognition and Treatment of Underlying
Conditions:
• Pneumonia
• Sepsis
• Aspiration
• Trauma
• Other medical and surgical disorders
• Minimization of Iatrogenic Harm:
• Unnecessary procedures
• Complications of procedures
• Standardized "Bundled Care" Approaches:
• Prophylaxis against:
• Venous thromboembolism
• Gastrointestinal bleeding
• Aspiration
• Excessive sedation
• Prolonged mechanical ventilation
• Central venous catheter infections
• Prompt Recognition and Management of
Nosocomial Infections.
• Adequate Nutrition:
• Enteral route preferred when feasible.
MECHANICAL VENTILATION
• Heterogeneous Nature of ARDS:
• Primarily affects dependent lung regions.
• Other lung areas are relatively spared.
• Challenges in Ventilation:
• Compliance mismatch between affected and
unaffected areas.
• Full inflation of consolidated areas can lead to
overdistention and injury of healthier lung regions.
• Ventilator-Induced Lung Injury (VILI):
• Demonstrated in experimental models of acute lung injury.
• High-tidal-volume (VT) ventilation is a significant risk factor
for VILI.
• ARDS Network Trial:
• NIH-sponsored, randomized controlled trial.
• Compared low VT (6 mL/kg) to conventional VT (12 mL/kg).
• Trial Outcomes:
• Significantly lower mortality in low VT group (31%) compared
to conventional VT group (40%).
• Substantial improvement in ARDS survival.
• Factors Contributing to Reduced Lung Compliance
in ARDS:
• Presence of alveolar and interstitial fluid.
• Loss of surfactant.
• Consequences of Reduced Lung Compliance:
• Significant alveolar collapse at end-expiration
without increased end-expiratory pressure.
• Impairment of oxygenation.
• Role of Positive End-Expiratory Pressure (PEEP):
• Minimizes the need for high inspired oxygen
concentrations (FIO2).
• Maintains adequate arterial oxygenation (PaO2).
• Prevents alveolar overdistention.
PRONE VENTILATION
• Early trials showed improved oxygenation but no
mortality benefit.
• A 2013 trial demonstrated a significant reduction in
28-day mortality for patients with severe ARDS
(PaO2/FIO2 <150 mm Hg).
• Increased use of prone positioning:
• Many centers are adopting prone positioning for
severe ARDS due to the mortality benefit.
• Challenges and risks of prone positioning:
• Requires an experienced critical care team.
• Repositioning can be hazardous, leading to:
• Accidental extubation
• Loss of central venous catheters
• Orthopedic injuries
FLUID MANAGEMENT IN
ARDS
• Importance of Maintaining Low Left Atrial Filling
Pressure:
• Minimizes pulmonary edema.
• Prevents further decline in arterial oxygenation and
lung compliance.
• Improves pulmonary mechanics.
• Shortens ICU stay and duration of mechanical
ventilation.
• Management Strategies:
• Aggressive fluid restriction.
• Diuretic administration.
NEURO MUSCULAR
BLOCKADE
• Neuromuscular Blockade Trial:
• Multicenter, randomized, placebo-controlled trial.
• Early neuromuscular blockade (cisatracurium) for
48 hours.
• Demonstrated increased survival and ventilator-
free days in patients with severe ARDS.
• No increase in ICU-acquired paresis.
• Implications:
• Suggests that selective use of neuromuscular
blockade might be beneficial.
• Specifically in ARDS patients with ventilatory
dyssynchrony despite adequate sedation.
GLUCOCORTICOIDS
• Glucocorticoids have been tried for early and late
ARDS.
• The goal was to reduce pulmonary inflammation.
• Few studies show a significant mortality benefit.
• Current evidence does not support routine
glucocorticoid use in ARDS.
OTHER THERAPIES
• Clinical trials of surfactant replacement and other
therapies for ARDS have been disappointing.
• Pulmonary vasodilators (inhaled nitric oxide,
inhaled epoprostenol sodium) can temporarily
improve oxygen levels.
• These vasodilators have not been shown to
improve survival or reduce time on mechanical
ventilation.
PROGNOSIS
• Hospital mortality rates in the LUNG SAFE trial
varied by ARDS severity:
• Mild ARDS: 34.9%
• Moderate ARDS: 40.3%
• Severe ARDS: 46.1%
• While there's variability, ARDS outcomes show a
trend toward improvement over time.
• Most ARDS deaths (>80%) are due to
nonpulmonary causes, primarily sepsis and
nonpulmonary organ failure.
• Improved ARDS survival is likely linked to
advancements in treating sepsis/infections and
multiple organ failure
• Advanced age is a significant risk factor for ARDS
mortality.
• Mortality is substantially higher in patients >75
years (∼60%) compared to those <45 (∼20%).
• Patients >60 years with ARDS and sepsis have a
threefold higher mortality risk.
• Preexisting organ dysfunction (chronic liver disease,
alcohol abuse, immunosuppression) increases ARDS
risk.
• Direct lung injury (pneumonia, contusion,
aspiration) nearly doubles the mortality risk
compared to indirect causes.
• Surgical and trauma patients, especially those
without direct lung injury, generally have better
ARDS survival.
FUNCTIONAL RECOVERY IN
ARDS
• Most patients recover maximal lung function within
6 months of ARDS.
• One year post-extubation: Over one-third have
normal spirometry and diffusion capacity.
• Most others have only mild pulmonary function
abnormalities.
• Lung function recovery is strongly correlated with
the initial extent of lung injury.
• Less recovery is associated with:
• Low static respiratory compliance
• High PEEP requirements
• Longer mechanical ventilation
• High lung injury scores
• Five years post-ARDS, despite often normal/near-
normal pulmonary function, exercise limitation and
decreased physical quality of life are frequently
observed.
MECHANICAL VENTILATION
• Mechanical ventilation refers to devices that deliver
positive-pressure gas, of varying oxygen content, to
patients with acute or chronic respiratory failure
ASSIST CONTROL
VENTILATION
• Assist-control (AC) ventilation allows clinicians to
control nearly all ventilator settings.
• AC is used when patients cannot participate in
breathing (e.g., deep sedation, respiratory failure,
critical illness).
• Most AC is in volume control mode: Clinician sets
tidal volume (VT) and respiratory rate, ensuring
minimum minute ventilation (VE).
• Inspiratory flow rate is set by the clinician; if too
low, it can cause patient distress and increased
work of breathing.
• Clinician also sets PEEP and FIO2.
• In AC volume control: VT is an independent variable
(set by the clinician).
• Plateau pressure is a dependent variable,
determined by lung compliance, and must be
monitored to prevent barotrauma.
• PCV: Inspiratory (driving) pressure is set.
• In PCV: The ventilator raises airway pressure to the
set amount above PEEP until inspiratory flow
decreases below a set threshold, ending inhalation.
• Resulting VT varies depending on lung compliance.
• Because lung compliance can change, VT and
minute ventilation must be monitored.
• PCV is used to limit peak airway and plateau
pressures in situations where high pressure is
harmful (e.g., ARDS, post-thoracic surgery).
• In PCV: Inspiratory flow rate and volume are
dependent variables (not set by the clinician), unlike
in VC.
PRESSURE SUPPORT
VENTILATION
• Pressure support ventilation (PSV) is similar to PCV,
but has no set respiratory rate; all breaths are
patient-triggered.
• The clinician sets FIO2, PEEP, and maximum
inspiratory pressure.
• In PSV: Patient inspiratory effort triggers increased
positive pressure to the set level.
• Pressure is maintained until flow decreases below a
set threshold (often ~20% of peak flow).
• Tidal volume is monitored (not assured), depends
on lung compliance, and requires sustained patient
effort.
• Tidal volume, minute ventilation, and respiratory
rate must be closely monitored to detect
hypopnea/apnea and hypoventilation.
• PSV is often used for less sedated patients who can
participate in breathing (e.g., weaning from
ventilation, airway support).
NON INVASIVE
VENTILATION
• Noninvasive ventilation (NIV) delivers positive
pressure via a mask (nasal or full-face).
• Delivery methods include:
• CPAP (continuous positive airway pressure)
• BiPAP (bilevel positive airway pressure)
• NIV is beneficial for acute respiratory failure with
quickly treatable underlying causes, reducing the
need for prolonged invasive ventilation
• . Examples of NIV use: Moderate acute hypercarbia
(pH 7.25-7.35) due to COPD exacerbations (reduces
intubation and hospital stay).
• Acute cardiogenic pulmonary edema (adjunct to
diuresis and vasodilators).
• Chronic respiratory failure (restrictive lung diseases,
COPD with chronic hypercapnia; nocturnal NIV
reduces hospital admissions).
CONTRA INDICATIONS FOR
NIV
• Inability to protect the airway such as severe
encephalopathy
• High risk for aspiration such as vomiting or severe
upper GI bleeding
• Facial trauma or surgery
• Upper airway obstruction
• Significant hemodynamic instability
COMPLICATIONS OF
MECHANICAL VENTILATION
AIRWAY
• Endotracheal intubation and mechanical
ventilation, especially prolonged (>7 days), can
cause pulmonary and extrathoracic complications.
Upper airway complications: Vocal cord trauma
(edema, avulsion, paralysis)
• Tracheal stricture (due to granulation tissue)
• Tracheomalacia
• Vocal cord injury can lead to postextubation stridor
(PES) and potential need for reintubation.
DUE TO POSITIVE PRESSURE VENTILATION
• High positive intrathoracic pressure (plateau
pressures >30 cmH2O, high PEEP) can cause lung
barotrauma: Worsening acute lung injury
• Pneumomediastinum
• Pneumothorax
• Pneumoperitoneum
• Positive-pressure ventilation can improve left-sided
heart failure but may worsen right-sided heart
failure and pulmonary hypertension due to:
1.Inadequate right ventricular preload
2.Increased right ventricular afterload and
pulmonary vascular resistance.
• Blunted central venous return can cause upper and
lower extremity edema, especially with aggressive
IV fluids and vascular leak in critical illness.
VENTILATOR ASSOCIATED
PNEUMONIA
• Mechanical ventilation increases pneumonia risk
due to:
• Compromised airway defenses
• Sedation and depressed cough
• Microaspiration
• Ventilator-associated pneumonia (VAP): Occurs in
up to 15% of mechanically ventilated patients, with
~50% mortality.
• Diagnostic criteria (≥48 hours post-intubation):
• New pulmonary opacities on chest x-ray.
• Clinical changes (fever, increased sputum, leukocytosis,
increased ventilator support).
• Positive lower respiratory tract culture (deep suction,
bronchoalveolar lavage, or protected brushing).
• Common pathogens: Staphylococcus aureus,
Pseudomonas aeruginosa, and other enteric gram-
negative rods.
• Empiric antibiotic therapy:
• Broad-spectrum β-lactam (piperacillin-tazobactam,
cefepime, ceftazidime).
• Consider vancomycin/linezolid (MRSA) or carbapenem
(multidrug-resistant gram-negative rods) based on local
ICU data and patient risk.
• De-escalate and limit treatment to 7 days based on
culture results.
• VAP prevention strategies:
• Effective interventions:
• Head-of-bed elevation (30-45°).
• Specialized endotracheal tubes with subglottic suction.
• Minimizing ventilator circuit changes.
• Hand hygiene.
• Practices with uncertain but reasonable value:
• Limiting deep tracheal suctioning.
• Daily sedation interruption.
• Routine oral and dental care.
OTHER COMPLICATIONS
• Mechanical ventilation and related therapies
(sedation, neuromuscular blockade) can cause
extrathoracic complications:
• Gastrointestinal stress ulcers and bleeding
• Deep venous thrombosis (DVT) and pulmonary
embolism (PE)
• Sleep disruption and delirium
• Critical illness-associated myopathy (potentially
leading to prolonged ventilation)
• To minimize these risks, ICUs should implement
care bundles including:
• Daily sedation interruption
• Daily assessment for extubation readiness
• DVT prophylaxis
CRITERIA FOR EXTUBATION
• Underlying Disease Improvement: The primary
condition that necessitated intubation (e.g.,
pneumonia, acute respiratory distress syndrome)
should be showing signs of resolution.
• Neurological Status:
• Awake and Responsive: The patient should be awake
and able to follow simple commands.
• Minimal Sedation: Sedative medications should be
minimized or discontinued to assess the patient's own
respiratory drive.
• Respiratory Parameters:
• Oxygen Requirements: Fraction of inspired oxygen
(FiO2) should be low (≤ 0.5 or 50%).
• Positive End-Expiratory Pressure (PEEP): PEEP should be
minimized (< 8 cmH2O).
• Oxygen Saturation (SaO2): SaO2 should be maintained
above 88% on minimal oxygen support.
• Hemodynamic Stability: Blood Pressure: Stable
blood pressure within an acceptable range.
• Heart Rate: Stable heart rate.
• Secretion Management: The patient should be able
to effectively clear their own secretions through
coughing or suctioning.
• Spontaneous Breathing Trial (SBT)
• Purpose: To assess the patient's ability to breathe
independently without the support of the
ventilator.
• Procedure:
• Ventilator Settings: Ventilator settings are adjusted to
minimal support, typically with a low level of positive
pressure to overcome the resistance of the endotracheal
tube (usually 5-7 cmH2O).
• Duration: The SBT usually lasts from 30 to 120 minutes.
• Success Criteria:
• Comfort: The patient should appear comfortable during
the trial, with no signs of significant anxiety or distress
(e.g., diaphoresis, increased respiratory effort).
• Respiratory Rate: Respiratory rate should remain within
an acceptable range (typically < 35 breaths per minute).
• Oxygen Saturation: SaO2 should be maintained above
90%.
• Hemodynamic Stability:
• Systolic blood pressure should remain within a normal range
(usually between 90 and 180 mmHg).
• Heart rate should remain stable with a change of less than 20
beats per minute.
• Success Rate: Patients who successfully pass an SBT
have a high probability (typically > 70%) of
successful extubation.
THANK YOU
