What is the physiology behind a ventilator?

Understanding Ventilator Physiology

Core Physiological Principle

The primary physiological purpose of mechanical ventilation is to decrease the work of breathing by providing positive pressure support that replaces or augments the patient's respiratory muscle effort, allowing blood flow to be redirected to other vital organs while maintaining adequate gas exchange. 1, 2

Fundamental Physiological Mechanisms

Positive Pressure vs. Normal Breathing

Mechanical ventilation fundamentally differs from normal physiological breathing by using positive pressure rather than the negative intrathoracic pressure generated by diaphragmatic contraction 3. This creates several key physiological effects:

• Pressure gradient reversal: Instead of creating negative pressure to draw air in, ventilators push air into the lungs using positive pressure 3
• Work redistribution: The ventilator assumes the work normally performed by respiratory muscles (diaphragm and intercostals), reducing oxygen consumption by these muscles 1, 2
• Hemodynamic effects: Positive pressure affects venous return, cardiac output, cerebral perfusion pressure, and renal venous drainage 3

Gas Exchange Optimization

The ventilator maintains adequate oxygenation and CO2 elimination through several mechanisms:

• Mean airway pressure increase: Positive pressure throughout the respiratory cycle improves ventilation-perfusion matching 1
• Alveolar recruitment: Positive end-expiratory pressure (PEEP) prevents alveolar collapse and recruits underventilated lung units, similar to its use in intubated patients 1
• FiO2 delivery: Ventilators can deliver precise oxygen concentrations higher than achievable with standard oxygen supplementation 1

Ventilator Modes and Their Physiological Basis

Volume-Controlled Ventilation

In volume-controlled modes, a preset tidal volume is delivered regardless of the pressure required, with the resulting airway pressure determined by lung compliance and airway resistance 1, 4:

• The ventilator guarantees minute ventilation by delivering a fixed volume 1
• Tidal volume should be based on ideal body weight to prevent overdistention 1
• This mode ensures alveolar ventilation even when compliance or resistance changes 1

Pressure-Controlled Ventilation

Pressure-controlled modes deliver breaths to a preset pressure target, with the resulting tidal volume varying based on lung mechanics 1:

• The decelerating flow profile may improve ventilation distribution 1
• Better leak compensation occurs compared to volume control 1
• Inspiratory pressure (IPAP) generates ventilation while expiratory pressure (EPAP) recruits lung and offsets intrinsic PEEP 1

Assist-Control Mode (ACV)

In assist-control ventilation, the ventilator delivers a preset number of mandatory breaths, but patient-triggered breaths receive identical support 1, 5:

• Prevents central apneas during sleep due to backup respiratory rate 5
• Patient triggering is permitted but delivers the same breath as mandatory breaths 1
• Synchronization occurs between patient-triggered and machine-delivered breaths 1

Pressure Support Ventilation (PSV)

The patient's respiratory effort triggers both the start and end of each breath, with respiratory frequency and timing determined entirely by the patient 1:

• Requires less sedation than fully controlled ventilation 1
• Can reduce ventilation-perfusion mismatch and decrease ICU stay duration 1
• Risk: No backup rate means no breaths occur if patient effort ceases 1

Critical Physiological Interactions

Triggering Physiology

Ventilator triggering must align with the patient's intrinsic respiratory center output to minimize work of breathing 2, 6:

• Flow sensors detect changes in bias flow to identify inspiratory effort 1
• Intrinsic PEEP (PEEPi) in COPD patients requires isometric respiratory muscle contraction before triggering can occur 1
• Applying external PEEP (typically 3-5 cm H2O) offsets intrinsic PEEP, reducing trigger effort and improving comfort 1

Cycling and Synchrony

Problems at inspiration-expiration switchover create patient-ventilator dyssynchrony 2, 6:

• Dyssynchrony imposes high pressure loads on respiratory muscles, promoting fatigue and increasing sedation needs 6
• Neuromuscular blocking agents may be required in severe ARDS to prevent excessive transpulmonary pressure generation and breath stacking 1
• Careful monitoring of airway pressure and flow graphics is essential to detect and correct dyssynchrony 6

PEEP Physiology

PEEP maintains end-expiratory lung volume, preventing cyclic alveolar collapse and improving oxygenation 1:

• Recruits underventilated lung similar to its use in intubated patients 1
• Offsets intrinsic PEEP in obstructive lung disease, reducing inspiratory work 1
• In hyperinflated COPD patients, excessive PEEP may adversely affect inspiratory muscle function by further increasing lung volume 1
• EPAP levels of 3-5 cm H2O are typically used, as higher levels are rarely tolerated 1

Ventilation-Perfusion Matching

The ventilator improves V/Q matching through:

• Recruitment of collapsed alveoli: PEEP opens previously unventilated lung units 1
• Redistribution of ventilation: Pressure-controlled breaths may improve distribution compared to volume control 1
• Reduction of shunt fraction: Improved mean airway pressure reduces intrapulmonary shunting 1

Common Physiological Pitfalls

Rebreathing Risk

With single-circuit ventilators using passive exhalation, EPAP levels of 3-5 cm H2O do not completely eliminate rebreathing, especially at high respiratory rates 1:

• Consider this in tachypneic patients who fail to improve or develop worsening hypercapnia 1
• Ensure exhalation ports are patent; occlusion by secretions exacerbates hypercapnia 1

Hemodynamic Compromise

Positive pressure ventilation reduces venous return and can compromise cardiac output 3:

• Monitor for hemodynamic instability, particularly in volume-depleted patients 1
• Judicious fluid management is essential in states of altered capillary permeability 1

Ventilator-Induced Lung Injury (VILI)

Even assisted ventilation can cause VILI through high tidal volumes and transpulmonary pressures if unrecognized 1:

• Monitor for alveolar overdistention by limiting plateau pressures and driving pressures 3
• Patient self-inflicted lung injury (P-SILI) can occur when vigorous inspiratory efforts generate excessive transpulmonary pressure 1, 3

Diaphragm Dysfunction

Prolonged controlled ventilation without respiratory muscle activity leads to diaphragm atrophy and ICU-acquired weakness 1:

• Reduce sedation and transition to partial support as soon as gas exchange and mechanics improve 1
• Neuromuscular blockade should be reserved for severe ARDS in the first 48 hours only 1