NON-INVASIVE VENTILATION (NIV) 

Effects on Respiratory Mechanics

Mechanism

Effect

Inspiratory pressure support

Work of breathing

Positive end-expiratory pressure (PEEP/EPAP)

FRC, atelectasis

Alveolar recruitment

Oxygenation

Improved tidal volume

PaCO₂

Reduced respiratory muscle load

Prevents fatigue


 Cardiovascular Effects

Effect

Mechanism

Preload

Intrathoracic pressure

LV afterload

Transmural pressure

Beneficial in cardiogenic pulmonary edema

Improves cardiac output

### Excessive pressure hypotension


 TYPES / MODES OF NIV

A. CPAP (Continuous Positive Airway Pressure)

 Single continuous pressure throughout respiratory cycle
•Prevents alveolar collapse
Uses
Cardiogenic pulmonary edema
Obstructive sleep apnea
Mild hypoxemic respiratory failure

Standard Starting CPAP

Parameter

Initial Setting

CPAP pressure

5 -10 cm H₂O( CPAP by 2 cm H₂O)

FiO₂

Start 0.4–0.6, titrate to SpO₂

Interface

Oronasal mask preferred

Target SpO₂

92–96% (88–92% in COPD)


 BiPAP (Bilevel Positive Airway Pressure)

Two pressure levels:

Parameter

Function

IPAP

Inspiratory support VT, PaCO₂

EPAP

Equivalent to PEEP oxygenation

Pressure Support (PS) = IPAP – EPAP


 Advanced Modes (ICU Ventilators)

• PSV-NIV
• NIV-SIMV (rare)
• AVAPS (Average Volume Assured Pressure Support)
• iVAPS

Used mainly in chronic hypercapnic respiratory failure


 INTERFACES USED IN NIV

Interface

Advantages

Disadvantages

Nasal mask

Comfort, speech

Mouth leak

Oronasal (full-face)

Most common, effective

Claustrophobia

Total face mask

pressure sores

Air leak

Helmet NIV

Better tolerance

CO₂ rebreathing, noise

—> Helmet NIV increasingly used in ARDS (e.g., COVID)


 INDICATIONS 

A. STRONG EVIDENCE / GOLD-STANDARD INDICATIONS

1. Acute Exacerbation of COPD (AECOPD)

Criteria
• pH < 7.35
• PaCO₂ > 45 mmHg
• Moderate–severe dyspnea

Guidelines: GOLD, ERS/ATS Class I recommendation

2. Acute Cardiogenic Pulmonary Edema

Mechanism
Preload
LV afterload
• Recruits alveoli


B. MODERATE EVIDENCE INDICATIONS

3. Hypoxemic Respiratory Failure (Selected)

• Pneumonia (carefully selected)
• Early ARDS (PaO₂/FiO₂ > 150)
• Immunocompromised patients

 High failure rates close monitoring mandatory

4. Post-Extubation Respiratory Failure

• Especially in COPD, CHF
• Prophylactic NIV reduces re-intubation

5. Weaning Facilitation

  • Difficult weaning in COPD
    • NIV after extubation prevents failure


 CHRONIC USE INDICATIONS

• Obesity hypoventilation syndrome
• Neuromuscular diseases (ALS, MG, DMD)
• Chest wall deformities
• Stable chronic hypercapnic COPD


 CONTRAINDICATIONS

A. ABSOLUTE

  • Cardiac or respiratory arrest
     Inability to protect airway
     Severe encephalopathy (GCS < 8)
     Active vomiting / GI bleeding
     Facial trauma or surgery
     Uncontrolled agitation

B. RELATIVE

 Hemodynamic instability
 Excessive secretions
 Severe hypoxemia (P/F < 100)
 Recent upper GI surgery


INITIATION OF NIV – STEPWISE

A. Patient Selection (MOST IMPORTANT)

Ideal patient:
Awake
Cooperative
Hemodynamically stable
Moderate respiratory distress
Able to clear secretions


B. Initial Settings (BiPAP)

Parameter

Starting Value

IPAP

10–12 cmH₂O

EPAP

4–6 cmH₂O

RR backup

10–14/min

FiO₂

Target SpO₂ 88–92% (COPD), 92–96% (others)

Gradually titrate:
• IPAP to improve VT & CO₂
• EPAP for oxygenation


MONITORING DURING NIV 

A. Clinical

• RR
• Accessory muscle use
• Dyspnea
• Mental status improves


B. Gas Exchange

ABG at 1–2 hours

Success indicators:
pH
PaCO₂
PaO₂


PREDICTORS OF NIV SUCCESS vs FAILURE

A. Predictors of SUCCESS

pH improves within 1–2 hrs
RR decreases
Patient comfortable
Good mask fit
Stable hemodynamics


B. Predictors of FAILURE 

HACOR Score for Predicting NIV Failure

HACOR =

  • H Heart rate
  • A Acidosis (pH)
  • C Consciousness (GCS)
  • O Oxygenation (PaO₂/FiO₂ ratio)
  • R Respiratory rate


 TOTAL SCORE

  • Minimum = 0
  • Maximum = 26


INTERPRETATION 

HACOR Score

Interpretation

Clinical Action

≤5

Low risk of NIV failure

Continue NIV

>5

High risk of NIV failure

Consider early intubation

>8–10

Very high risk

Strong indication for intubation

 Cut-off ≥5 at 1 hour of NIV is the most commonly used threshold.


 TIMING OF ASSESSMENT 

  • Baseline (before NIV)
  • After 1 hour of NIV MOST PREDICTIVE
  • Repeat at 12 hours and 24 hours
  • HACOR is NOT a replacement for clinical judgment



CLINICAL APPLICATION 

 Indications for using HACOR

  • NIV in:
    • ARDS
    • Pneumonia
    • Early COVID hypoxemia
    • Immunocompromised patients


 When NOT reliable

  • Hypercapnic respiratory failure (e.g., COPD exacerbation)
  • Sedated patients (GCS unreliable)
  • Hemodynamic instability


 HACOR vs ROX INDEX 

Feature

HACOR

ROX Index

Modality

NIV

HFNC

Components

5 (multi-system)

3 (SpO₂/FiO₂, RR)

Best timing

1 hr

2–12 hr


## Delay in intubation mortality


 COMPLICATIONS OF NIV

Complication

Mechanism

Aspiration

Loss of airway reflex

Pressure sores

Mask pressure

Gastric distension

Air swallowing

Barotrauma

High pressures

Eye irritation

Air leak

Hypotension

Preload


NIV IN ARDS – CONTROVERSIAL BUT IMPORTANT

• NIV failure common in moderate–severe ARDS
• Best outcomes when:
– P/F > 150
– Early initiation
– Helmet NIV preferred

# Intubate early if no rapid improvement


WHEN TO INTUBATE (DO NOT DELAY)

Immediate intubation if:
• Cardiac arrest
• Severe hypoxemia
• Airway compromise
• NIV failure at 1–2 hrs


How to WEANING FROM NON-INVASIVE VENTILATION (NIV)

WHEN TO CONSIDER NIV WEANING (READINESS CRITERIA)

A. Clinical Stability

Awake, alert, cooperative
Hemodynamically stable (no/inotrope minimal)
RR ≤ 25/min
No severe accessory muscle use
Minimal dyspnea (Borg ≤ 3)


B. Gas Exchange Targets

Parameter

Target

SpO₂

≥ 90% (COPD: 88–92%)

PaO₂

≥ 60 mmHg

FiO₂

≤ 0.4

pH

≥ 7.35

PaCO₂

Stable or improving


C. Ventilator Settings (Low Support)

Parameter

Acceptable

IPAP

≤ 10–12 cmH₂O

EPAP

≤ 5–6 cmH₂O

Backup rate

Off or minimal


 Strategy 1: Gradual Reduction of NIV Duration (Most Common)

Principle: Increase spontaneous breathing time off NIV

Day

NIV Usage

Day 1

Continuous NIV except meals

Day 2

NIV at night + intermittent daytime

Day 3

Night-only NIV

Day 4

Stop NIV

Preferred in COPD, AHF, hypercapnic failure


Strategy 2: Gradual Reduction of NIV Pressure Support

Stepwise decrease in IPAP

Step

Action

Step 1

Reduce IPAP by 2 cmH₂O every 6–12 h

Step 2

Maintain EPAP

Step 3

When IPAP ≤ 8–10 trial off NIV

Useful in pressure-dependent patients

Feeding a Patient on Non-Invasive Ventilation (NIV)

Core Principles

  • NIV ≠ absolute contraindication to enteral feeding
  • Aim to maintain nutrition without increasing aspiration risk or NIV failure

 DO NOT feed if:

  • GCS < 13
  • Active vomiting
  • Copious secretions
  • Severe hypoxemia or hypercapnic encephalopathy


B. NIV Factors

Factor

Safe Feeding Range

IPAP

≤ 20 cmH₂O

EPAP

≤ 8–10 cmH₂O

Mask fit

Minimal leak

NIV tolerance

Stable for ≥ 6–12 h

High pressures gastric insufflation & aspiration risk

Route of Feeding on NIV

Oral Feeding (Preferred if feasible)

  • Allow small, slow meals Keep head elevated ≥45°.Restart NIV immediately after meals except in aerophagia,Marked gastric distension

Why NIV is needed immediately after meals

Pathophysiology

After meals:

  • Oxygen consumption, CO₂ production, Diaphragmatic splinting due to gastric distension, Work of breathing

 High-risk patients (COPD, OHS, neuromuscular disease) may decompensate rapidly if NIV is delayed.


B. Enteral Feeding (Most ICU Patients)

1️⃣ Nasogastric Tube (NGT)

Most commonly used

Problems

  • Mask leak around tube,Gastric distension,Aspiration risk

Risk reduction

  • Use fine-bore (8–10 Fr) NGT,Prefer continuous feeding,Elevate head end 30–45°

2️⃣ Post-Pyloric Feeding (Nasojejunal) – BEST for High Risk

Preferred when available

Indications

  • High aspiration risk
  • Poor gastric emptying
  • High NIV pressures
  • Recurrent feed intolerance

ESPEN & SCCM recommend post-pyloric feeding if NIV > 48 h(always recheck current recommendations)



Q.How NIV decreases afterload


1️⃣ Key Concept: What Is LV Afterload?

LV afterload ≈ LV transmural systolic pressure

LV afterload=PLV −Pintrathoracic

Where:

  • PLV = intracavitary LV systolic pressure
  • Pintrathoracic ≈ pleural pressure

 It is the pressure the LV must generate to eject blood


2️⃣ NIV Increases Intrathoracic Pressure

  • CPAP / EPAP positive pressure throughout respiratory cycle
  • IPAP (in BiPAP) intermittent higher positive pressure during inspiration


3️⃣ How Increased Intrathoracic Pressure LV Afterload

 A. Reduction in LV Transmural Pressure

LV transmural pressure=PLV −Ppleural

When NIV increases pleural pressure:

  • External pressure on LV rises
  • LV does not need to generate as high intracavitary pressure
  • Afterload decreases


 B. Reduction in Aortic Transmural Pressure

  • Aorta lies within thorax
  • Increased intrathoracic pressure:
    • Raises external pressure on aorta
    • Aortic wall tension

Wall stress2hPtransmural ×r

Thus:

  • pressure gradient between LV and aorta
  • resistance to LV ejection

 CPAP vs BiPAP – Afterload Effect

Mode

Afterload Reduction

CPAP

Continuous afterload reduction

BiPAP

Afterload reduction + inspiratory unloading

 Both reduce afterload via EPAP component


 GUIDELINES REFERENCED

• ERS/ATS NIV Guidelines
• GOLD COPD Guidelines
• Surviving Sepsis Campaign
• Harrison’s Principles of Internal Medicine
• NEJM / Intensive Care Medicine reviews