Patient-Ventilator Asynchrony

Definition

"Patient-ventilator dyssynchrony occurs when the trigger, flow, and/or cycling of a mechanical breath is not in time agreement with the initiation and termination of a patient's neural inspiration, respectively, or if the magnitude of mechanical assist does not respond to the patient's respiratory demand." — Fishman's Pulmonary Diseases and Disorders

Prevalence and Clinical Impact

• Frequent asynchronies (>10% of respiratory efforts) are present in 43% of patients undergoing NIV in observational studies.
• Consequences include:
  • Respiratory muscle overload — increased work of breathing
  • Compromised ventilation — inadequate CO₂ clearance or oxygenation
  • Sleep disruption — fragmented sleep architecture
  • Patient discomfort — leading to poor tolerance and NIV failure
  • In invasive MV: risk of ventilator-induced lung injury (VILI) from breath stacking and large tidal volumes

Types of Asynchrony

1. Trigger Asynchrony

• Minimize mask leaks (most common cause in NIV)
• Minimize upper airway resistance (e.g., treat OSA, glottic closure)
• Adjust trigger sensitivity: increase to High for weak efforts; decrease to Low for auto-triggering
• For double-triggering: increase pressure support and/or decrease cycle sensitivity; extend Ti in PC mode

2. Cycling Asynchrony

• Minimize mask leaks first
• Review Ti (or Ti max) settings
• Adjust cycle sensitivity to Low (lower % of peak flow threshold) for premature cycling
• Consider switching to pressure-control (PC) mode

3. Flow Asynchrony

Leading Causes

Monitoring and Detection

• Flow and pressure waveform analysis at the bedside — key clinical tool
• Esophageal electromyography (EAdi): diaphragm electrical activity monitoring allows detection of asynchrony, assessment of respiratory muscle unloading, and direct triggering/cycling (NAVA mode)
• Polysomnography in home NIV patients — detects asynchrony during sleep

Management Summary (Troubleshooting Table)

Special Considerations

Weaning from Mechanical Ventilation

1. When to Consider Weaning: Readiness Criteria

2. Weaning Predictor Tests

Rapid Shallow Breathing Index (RSBI / f/Vt ratio — the Tobin Index)

• Formula: Respiratory frequency (f) ÷ tidal volume in litres (Vt)
• Interpretation: f/Vt < 105 breaths/min/L predicts weaning success
• Sensitivity ≥ 0.90 in multiple studies — excellent as a screening test
• Must be measured during unassisted spontaneous breathing (not on PS or CPAP, which falsely lowers the ratio)
• The higher the f/Vt, the worse the prognosis: patients who fail weaning immediately develop rapid, shallow breathing (↑ RR + ↓ Vt) upon ventilator disconnection

Other indices (less relied upon than SBT outcome)

• Minute ventilation (Ve)
• Negative inspiratory force (NIF / MIP) — reflects respiratory muscle strength
• Vital capacity
• P0.1 (airway occlusion pressure) — reflects neural drive

Relying on these physiologic variables rather than the outcome of an SBT leads to unnecessary delays in extubation. — Harrison's Principles of Internal Medicine

3. Spontaneous Breathing Trial (SBT)

SBT Methods

Passing the SBT — All of the following:

• 25% fewer ventilator days
• 10% decrease in ICU length of stay

4. Algorithm for Discontinuing Mechanical Ventilation

5. Causes of Weaning Failure

• Rapid, shallow breathing — immediately upon disconnection (↑ RR, ↓ Vt)
• Progressive respiratory effort over 30–60 min, reaching >4× normal by the end of a failed trial

Why mechanics worsen during a failed trial:

Cardiovascular stress of weaning failure:

• Extreme negative intrathoracic pressure swings → ↑ RV and LV afterload
• Pulmonary artery pressure ↑ 39%; systemic artery pressure ↑ 27%
• Patients who fail cannot increase O₂ delivery to meet demand → mixed venous O₂ saturation falls (occult cardiac dysfunction is unmasked)

Common causes of weaning failure:

• Unresolved underlying disease
• Respiratory muscle weakness / fatigue
• Excessive respiratory load (↑ resistance, ↓ compliance, auto-PEEP)
• Cardiovascular dysfunction / occult heart failure
• Neurological impairment / impaired drive
• Metabolic derangements (hypophosphataemia, hypomagnesaemia → muscle weakness)
• Psychological dependence (in prolonged ventilation)

6. Risk Factors for Extubation Failure Despite Passing SBT

• Age > 65
• Congestive heart failure
• COPD
• APACHE-II score > 12
• BMI > 30
• Significant secretions

• 2 medical comorbidities

• 7 days on mechanical ventilation

7. Prolonged Weaning

• Tracheostomy — reduces dead space, improves comfort, facilitates secretion clearance
• Progressive SBT duration increases — gradually extend unassisted breathing time each day
• Inspiratory muscle training
• Optimizing nutrition — avoid overfeeding (↑ CO₂ production worsens ventilatory demand)
• Management of comorbidities (heart failure, infection, thyroid, electrolytes)

Ventilation in ARDS

Overview

Pathophysiologic Basis: Why the ARDS Lung is Vulnerable

Mechanisms of VILI

Lung-Protective Ventilation: The ARDSNet Protocol

Part I — Ventilator Setup

Use predicted (ideal) body weight, not actual body weight — actual BW can be ~20% higher due to fat and oedema, leading to dangerous over-ventilation.

Part II — Oxygenation Goal: PaO₂ 55–80 mmHg or SpO₂ 88–95%

Part III — Plateau Pressure Goal: ≤30 cmH₂O

• Check Pplat with a 0.5-second inspiratory pause
• If Pplat > 30 cmH₂O → reduce Vt by 1 mL/kg (minimum 4 mL/kg PBW)
• If Pplat < 25 cmH₂O and Vt < 6 mL/kg → increase Vt by 1 mL/kg

No plateau pressure is known to be truly "safe" — the data show a continuous relationship between Pplat and mortality with no safe threshold.

Part IV — pH Goal: 7.30–7.45

PEEP in ARDS

1. Prevent atelectrauma — keeps terminal units open, avoiding cyclic collapse/reopening
2. Improve oxygenation — recruits collapsed alveoli, reduces shunt

Evidence on High vs. Low PEEP

• ALVEOLI, LOVS, EXPRESS trials: Higher PEEP (combined with low Vt) did not reduce 60-day mortality vs. lower PEEP strategies
• Meta-analysis of the three trials: Higher PEEP improved survival in moderate-to-severe ARDS (PaO₂/FiO₂ < 200) but not in mild ARDS
• Higher PEEP improved secondary outcomes: reduced rescue therapy use (LOVS), shorter MV duration and less organ failure (EXPRESS)

The optimal PEEP level in ARDS remains unclear. Higher PEEP is safe and may benefit severe ARDS; PEEP increments should only be applied when they produce reliable alveolar recruitment. — Fishman's Pulmonary Diseases and Disorders

Recruitment Maneuvers

Prone Positioning

• Redistributes perfusion toward non-dependent (now ventral) lung regions, better matching ventilation to perfusion
• Reduces dorsal compression atelectasis
• PROSEVA trial: Prone positioning ≥16 hours/day in severe ARDS (PaO₂/FiO₂ < 150) reduced 28-day mortality from 32.8% → 16.0%
• Indicated in moderate-to-severe ARDS (PaO₂/FiO₂ < 150 on FiO₂ ≥ 0.6, PEEP ≥ 5, on lung-protective ventilation)

Rescue / Salvage Strategies

Modes Allowing Spontaneous Breathing

• APRV: sustained high pressure (P-high) to recruit + brief release to a low pressure (P-low) for CO₂ clearance, without allowing derecruitment
• Theoretical benefits: reduced sedation, preserved diaphragm function, improved haemodynamics
• Controlled data are limited; risk of patient self-inflicted lung injury (P-SILI) in vigorous spontaneous breathers

Fluid Management

Summary: Priorities in ARDS Ventilation

1. Vt 6 mL/kg PBW — non-negotiable foundation
2. Pplat ≤ 30 cmH₂O — reduce Vt further if needed
3. Permissive hypercapnia — tolerate high PaCO₂ to protect the lung
4. Adequate PEEP — prevent atelectrauma; higher PEEP in moderate-severe disease
5. Prone positioning — for PaO₂/FiO₂ < 150 early and sustained
6. Conservative fluids after resuscitation
7. Rescue strategies — stepwise escalation for refractory hypoxaemia

LRTI with Septic Shock: Antibiotic Dosing

• Source (community vs. hospital/ventilator-acquired)
• Risk factors for MDR organisms (MRSA, Pseudomonas aeruginosa)
• Host factors (immunocompetence, prior antibiotics, comorbidities)

Step 1 — Severity Assessment: ATS/IDSA Criteria for Severe Pneumonia

• Invasive mechanical ventilation
• Haemodynamic compromise requiring vasopressor support

• RR ≥ 30 breaths/min
• PaO₂/FiO₂ ≤ 250
• Multi-lobar infiltrates
• Confusion/disorientation
• BUN ≥ 20 mg/dL
• WBC < 4,000 cells/mm³
• Platelets < 100,000 cells/mm³
• Core temperature < 36°C
• Hypotension requiring aggressive fluid resuscitation

A. Community-Acquired Pneumonia (CAP) with Septic Shock

Standard Regimen (No MDR Risk Factors)

Penicillin allergy: Replace β-lactam with aztreonam 2 g IV every 8 h

Add MRSA Coverage if:

• Prior respiratory isolation of MRSA
• Recent hospitalisation + IV antibiotics within 90 days
• Post-influenza necrotising pneumonia
• Locally validated MRSA risk factors

For CA-MRSA (toxin-producing), linezolid alone or vancomycin + clindamycin (toxin inhibition) is preferred.

Add Pseudomonas aeruginosa Coverage if:

• Prior respiratory isolation of P. aeruginosa
• Recent hospitalisation + IV antibiotics within 90 days
• Structural lung disease (bronchiectasis, cystic fibrosis)
• Locally validated epidemiologic risk factors

B. Hospital-Acquired Pneumonia (HAP) / VAP with Septic Shock

Group A — Early-Onset HAP, No MDR Risk Factors

Group B — Late-Onset HAP / VAP, or MDR Risk Factors Present

C. Septic Shock — Unknown Source (Empirical Broad Coverage)

D. Special Populations

Aspiration Pneumonia (LRTI with anaerobic component)

Neutropenic Patients

Legionella Suspected

• Azithromycin 500 mg IV → 250 mg IV every 24 h, or
• Levofloxacin 750 mg IV every 24 h (preferred over macrolide for Legionella)

Key Principles in Septic Shock

1. Blood cultures × 2 before antibiotics — do not delay antibiotics to obtain cultures
2. Broad then narrow — start broad empirically; de-escalate at 48–72 h based on cultures and clinical response
3. Timing is critical — antibiotic administration within 1 hour of septic shock recognition
4. Avoid monotherapy in ICU/severe CAP — combination always required
5. Adjust for renal function — vancomycin, aminoglycosides, carbapenems all require dose adjustment in AKI (common in septic shock)
6. PK/PD optimisation — in septic shock, consider extended/continuous infusions of β-lactams and loading doses of vancomycin to achieve therapeutic targets rapidly
7. Duration — typically 5–7 days for CAP; 7–8 days for HAP/VAP; extend to 14–21 days for Legionella, S. aureus bacteraemia, or slow responders