Physiology Note - Respiratory Mechanics during Positive Pressure Ventilation

 

🫁 Respiratory Mechanics in Positive Pressure Ventilation

By –Dr. Urvi Patel, DrNB critical care medicine resident

Introduction

Respiratory mechanics describe how pressure, flow, and volume interact during breathing and mechanical ventilation.

In positive pressure ventilation (PPV), gas is delivered into lungs against natural recoil. Alters normal mechanics, can cause injury if not optimized. Monitoring mechanics helps set ventilator parameters safely and avoid complications (barotrauma, volutrauma, atelectrauma).

Respiratory mechanics = expression of lung function via pressure & flow.

Measured variables: Pressure, Flow, Volume (via waveforms).

Derived measures: Compliance, Resistance, work of breathing (WOB)

Loops: Pressure–Volume (P–V), Flow–Volume.

These measures can be broadly categorized as: (1) statics, depicting the forces acting on the lungs, related to its volumes and the  elastic behavior; (2) dynamics, reflecting the movement of air and related areas like flow patterns and resistance.

The pressure gradient required for to and fro movement of air in the thorax is determined by the compliance, resistance, and inertia of the lungs; however, the inertial forces are negligible while the patient is on mechanical ventilation.

Useful for:

1.Understanding underlying pathophysiology.

2.        .Optimizing ventilator settings.                                                             

3.Preventing ventilator-induced lung injury (VILI).

 

Pressures

Airway Pressure: measured at proximal airway.

Equation of Motion: Pao = (Elastance × Volume) + (Resistance × Flow) + PEEP.

Alveolar Pressure (Palv): estimated using occlusion maneuvers.

Airway (Paw) & Alveolar (Palv) Pressure changes during PPV- In spontaneous breathing, Airway (Paw) pressure ≈ 0 (atmospheric) and alveolar (Palv) pressure is negative during inspiration to draw air in. In PPV, Airway pressure is actively raised above atmospheric; alveolar pressure becomes positive during inspiration.

Peak Inspiratory Pressure (PIP): Reflects resistance + compliance + tidal volume + PEEP. Flow pattern affects slope. Pressure needed to overcome airway resistance (Raw) + elastic recoil (compliance).

↑ with high resistance (bronchospasm, secretions) or ↓ compliance (ARDS, pulmonary edema).

Pleural Pressure (Ppl): In spontaneous breathing , Pleural Pressure (Ppl) becomes more negative during inspiration.    Becomes positive during inspiration (due to applied pressure).

Transpulmonary Pressure (PL = Palv – Ppl) estimates lung stress. Increases because Ppl decreases (lung distension by suction). Increases because Palv rises (lung distension by applied pressure.

Auto-PEEP / Intrinsic PEEP(PEEPi): Due to air trapping/dynamic hyperinflation , incomplete exhalation ocurrs.  → ↑WOB, ↓trigger sensitivity, hemodynamic compromise.

Extrinsic PEEP (set by clinician): Improves oxygenation, prevents atelectasis, decreases shunt, but can worsen hyperinflation in obstructive disease.

Physiologic PEEP from glottic closure (~3–5 cmH₂O). Applied PEEP maintains alveoli open.

Mean Airway Pressure (Pawmean): avg. pressure across cycle; affects oxygenation.

Esophageal Pressure (Pes): surrogate for pleural pressure.

Transdiaphragmatic Pressure (Pdi) = gastric – esophageal pressure; reflects diaphragmatic load.

Flow & Volume

Inspiratory Flow: may be constant (VCV) or decelerating (PCV).

Expiratory Flow: normally passive; persistent flow at end-expiration = auto-PEEP.

Tidal Volume (VT): derived from flow integration. Generated by patient effort; normally ~6–8 mL/kg. Set or supported by ventilator; risk of excessive VT → volutrauma.

End-Expiratory Lung Volume (EELV): lung volume at end-expiration, can be altered by PEEP.

Time Constant (TC)

Time to inflate or deflate 63% of lung volume.

TC = Compliance × Resistance.

Normal lungs: ~0.1 sec.

Heterogeneous compliance/resistance → “fast” vs “slow” alveoli.

Clinical implication:

Short inspiratory time → incomplete tidal volume delivery → hypoxemia, hypercapnia.

Short expiratory time → gas trapping, auto-PEEP, hyperinflation, ↓compliance, hemodynamic compromise.

 

Derived Measurements

Compliance –

Change in volume per unit change in pressure.

Ø  CRS ( compliance of respiratory system) = VT / (Pplat – PEEP).

Ø  CL (lung compliance) = VT / ΔPL.

Ø  CCW (chest-wall compliance) = VT / ΔPes.

a)     Static compliance (Cstat) : after inspiratory pause (not influenced by resistance). Measured during no airflow (end-inspiratory pause).

Formula: ΔV / (Pplat – EEP).

More reliable, reflects lung elasticity

Clinical Values: Intubated, ventilated adult: Normal Cstat ≈ 70–100 mL/cmH₂O.

Severe ARDS: <25 mL/cmH₂O.

b)     Dynamic compliance (Cdyn)   : measured during active  airflow (affected by resistance). Nonlinear, volume-dependent, shows hysteresis.

Formula Cdyn : ΔV / (PIP – EEP).

Influenced by airway resistance, ET tube, patient effort → less accurate.

Compliance ↓ in ARDS, pneumonia, pulmonary edema, atelectasis, ILD.

Compliance ↑ in emphysema.

Compliance & Recruitment are dependent on patient effort; recruitment is limited if weak effort.         PEEP can recruit alveoli, ↑ compliance, but excessive pressures cause overdistension ↓ compliance.

Fast vs Slow alveoli:

Fast: low Compliance (c ) , low Resistance (R)

Slow: high C, high R.

Clinical implications : Short insp time → low VT.

Short exp time → auto-PEEP.

Elastance (ERS): Recoil pressure per unit volume; inverse of compliance.

Reflects recoil tendency of lung.

Formula: E = 1/C.

High elastance = stiff lung (e.g., ARDS, fibrosis).

Resistance (Raw)

Definition: ΔPressure / ΔFlow.

RI = (PIP – Pplat) / Flow.

RE = (Pplat – PEEP) / Expiratory Flow.

Normal: Spontaneous breathing: 0.6–2.4 cmH₂O/L/sec. Intubated, ventilated: 5–10 cmH₂O/L/sec

Resistance ↑ with artificial airways (ETT, secretions); observed as PIP – Pplat gap.

§  Factors increasing resistance: small ET tube, secretions, bronchospasm, kinking, mucus plug.

Ø  ↑PIP & ↑Pplat with same difference → ↓compliance.

Ø  ↑PIP with wide PIP–Pplat difference → ↑resistance.

 

 

Disease-specific Changes

Condition	Compliance	Resistance	Key Notes
ARDS	↓↓↓	Variable	“Baby lung”; requires low VT and optimal PEEP
COPD/Emphysema	↑	↑↑	Long time constant, risk of gas trapping and auto-PEEP
Asthma	Normal/↓	↑↑↑	Very high Raw, dynamic hyperinflation common
ILD	↓↓	Normal	Very stiff lungs, small 'baby lung' volumes
CCF/Edema	↓	Normal	Surfactant dysfunction, increased hysteresis
Obesity	↓ chest wall compliance, ↓FRC	Normal	High airway pressures required for ventilation
Neonates	↓ lung compliance + compliant chest wall	High	Prone to atelectasis and RDS

 

Work of Breathing (WOB)

From Campbell diagram → elastic + resistive work.

W = (PIP – 0.5 × Pplat)/100 × VT.

In PPV, most work is performed by ventilator.

Normal = 0.3–0.7 J/L if entirely performed by patient

In ventilated/paralyzed patients: ↑ with high resistance, large tidal volume, low compliance, or PEEPi. Excess WOB → fatigue, failure to wean.

Stress & Strain : Moderate, unless excessive effort or obstruction. ↑ Stress (transpulmonary pressure) & strain (ΔV/FRC); risk of VILI if thresholds exceeded.

Graphical Tools

Pressure-Volume (P-V) Curve

Normal - Sigmoidal; slope = compliance.

Lower Inflection Point (LIP): alveolar recruitment starts → guides minimum PEEP.

Upper Inflection Point (UIP): overdistension begins → avoid high VT/pressures.

Deflation limb may guide optimal PEEP.

Used to optimize PEEP and tidal volume.

 

Practical difficulties: observer variability, hysteresis, optimal PEEP debate.

Applications in Disease

-ARDS: Basis of “baby lung” concept; need careful PEEP titration.

-Emphysema: Increased compliance → P–V curve shifts towards pressure axis.

-Asthma: No reliable P–V curve data; resistance is key problem.

-ILD: Low compliance → curve shifts downward.

-CCF: Fluid-filled alveoli, increased hysteresis.

-Obesity: Low FRC, decreased chest wall compliance.

 

Flow-Volume Loop

Detects obstruction, flow limitation, secretions, bronchodilator response.

Clinical Applications

·       Setting PEEP: guided by P-V curve, stress index, esophageal pressure.

·       ARDS: recruitment vs. overdistension balance critical.

·       Adaptive Support Ventilation (ASV): uses mechanics to minimize WOB.

·       Hemodynamics: pleural pressure influences venous return & cardiac function.

Stress Index: A coefficient that describes the shape of the pressure-time curve during volume-controlled ventilation with a constant flow. It helps to assess whether a patient's lungs are being adequately recruited or are at risk of over-distension.

* Stress Index = 1: The pressure curve is linear, suggesting adequate alveolar recruitment without over-distention.

* Stress Index > 1: The pressure curve is concave upward, indicating over-distention. A decrease in PEEP or tidal volume may be necessary.

* Stress Index < 1: The pressure curve is concave downward, suggesting potential for further tidal recruitment. Increasing PEEP may be beneficial.

Key Pulmonary Effects of Positive Pressure Ventilation

1.      Increase in Functional Residual Capacity (FRC) / Lung Volume

Applying PEEP (positive end-expiratory pressure) increases FRC by keeping alveoli or airways open at end expiration, preventing collapse. This allows for more alveolar recruitment (more alveoli participating in gas exchange).

2.      Improvement in Gas Exchange / V/Q Matching

With alveolar recruitment, regions of lung that were collapsed or poorly ventilated become ventilated → less shunt. Also, positive pressure can reduce pulmonary oedema (in certain parts) by redistributing lung water from alveolar interstitium into more compliant interstitial compartments (that don’t contribute to gas diffusion) → thinner alveolar septa and thus improved diffusion.

3.      Effect on Lung Compliance and Work of Breathing

As alveoli are recruited and lung volume increases, compliance often improves (i.e. the lung becomes “easier” to inflate per unit volume) because part of the lung that was stiff/collapsed is now open. The Improved compliance reduces the work of breathing (for assisted breathing) and helps in oxygenation.

4.      Dead Space & Lung Zones

At high airway pressures, there may be expansion of alveolar dead space: alveoli that are ventilated but not perfused. For example, overdistension can compress capillaries. overdistension or very high lung volumes (beyond optimal), alveolar vessels are squeezed, increasing pulmonary vascular resistance (PVR).

5.      Overdistension / Lung Injury Risks

If pressures (tidal or plateau) or volumes are too large, alveoli overdistend → mechanical stress, damage to alveolar walls. This can worsen V/Q matching: overdistended alveoli may be ventilated but poorly perfused or have altered blood flow distributions.  Also leads to “biotrauma”: inflammatory mediator release, potentially worsening injury.

6.      Intrinsic PEEP / Dynamic Hyperinflation

When expiration is incomplete (e.g. due to obstructed airways, increased respiratory rate, or dynamic collapse), gas is trapped. This produces intrinsic (auto)-PEEP. Consequences: elevated alveolar pressure at end expiration; increased work of breathing (to overcome that residual pressure); risk of further overdistension; adverse effects on both ventilation and hemodynamics.

Spontaneous Breathing vs. Positive Pressure Ventilation

Parameter	Spontaneous Breathing	Positive Pressure Ventilation (PPV)
Airway Pressure	Subatmospheric during inspiration (negative intrathoracic pressure draws air in).	Supratmospheric during inspiration (air pushed into lungs).
Alveolar Pressure (Palv)	Falls below atmospheric during inspiration, returns to 0 at end-expiration.	Rises above atmospheric during inspiration; can remain elevated at end-expiration with PEEP.
Transpulmonary Pressure (PL = Palv – Pes)	Generated by pleural pressure decrease from diaphragm contraction.	Generated by applied airway pressure; risk of excessive stress/strain if high.
Pleural Pressure (Pes / Ppl)	Becomes more negative during inspiration.	Becomes more positive (especially with PEEP); reduces venous return.
Compliance (C = ΔV/ΔP)	Reflects natural lung-chest wall interaction; optimized at FRC.	Altered by ventilator settings; improved with recruitment (PEEP) but ↓ with overdistension.
Airway Resistance (Raw)	Flow driven by patient effort; resistance mainly in conducting airways.	Flow driven by ventilator; resistance becomes evident (PIP – Pplat gap).
Tidal Volume (VT)	Determined by patient effort, respiratory drive, and mechanics.	Set/delivered by ventilator; excessive VT → volutrauma.
PEEP / Auto-PEEP	No external PEEP; intrinsic auto-PEEP rare (unless disease present).	Applied PEEP ↑ end-expiratory lung volume; auto-PEEP common with short expiratory times.
Work of Breathing (WOB)	↑ with ↓ compliance, ↑ resistance, or auto-PEEP.	Done by ventilator (controlled modes); patient effort may add in assisted modes.
Stress & Strain	Usually within physiologic limits unless disease present.	↑ Stress (PL) and strain (ΔV/FRC); can cause VILI if thresholds exceeded.
Flow Patterns	Inspiratory flow decelerates naturally; expiration passive.	Flow shape set by mode (square in VCV, decelerating in PCV); expiration may be incomplete → trapping.
Hemodynamics	Negative intrathoracic pressure enhances venous return and cardiac output.	Positive intrathoracic pressure reduces venous return, preload, and cardiac output (especially with high PEEP).

 

✅ Take-home message:

In PPV, monitoring compliance, resistance, pressures, and time constants is essential. The respiratory mechanics guide ventilator adjustments, disease assessment, and prevention of VILI. Each disease alters mechanics differently, and interpreting PIP, Pplat, compliance, and Raw trends provides the best bedside clues help Tailoring therapy.

 

Reference

1)Lucangelo U, Bernabe´ F, Blanch L. Lung mechanics at the bedside: make it simple. Curr Opin Crit Care 2007;13(1):64-72.

2) Cairo JM. Initial patient assessment. Pilbeam’s mechanical ventilation: Physiological and clinical applications, ch. 8 6th ed., St. Louis: Elsevier; 2016. pp. 118–141.

3) Respiratory Mechanics in Mechanically Ventilated Patients, Dean R Hess

Respiratory Care 2014 59:11, 1773-1794

4)Gertler R. Respiratory Mechanics. Anesthesiol Clin. 2021 Sep;39(3):415-440. doi: 10.1016/j.anclin.2021.04.003. PMID: 34392877; PMCID: PMC8360707.

5) Respiratory Mechanics: To Balance the Mechanical Breaths!!Manu Sundaram1, Manjush Karthika2 Indian Journal of Critical Care Medicine (2021): 10.5005/jp-journals-10071-23700