Fundamentals of Ventilation

Source: Ventilation Teaching August 2019 (Version 10) — 57 slides Learning levels: Foundation = Band 5 | Intermediate = Band 6 | Advanced = Band 7+

1. Negative Pressure Breathing

1.1 Neural Control of Breathing

Learning level: Foundation

• Breathing is controlled by the brain, mainly the medulla oblongata and pontine respiratory centres
• Other areas (e.g. limbic system) influence respiratory centres via emotions, temperature
• Stimulated primarily by CO2
• Both central and peripheral chemoreceptors detect changes in CO2 levels
• As CO2 increases it diffuses across the blood-brain barrier:
  • CO2 + H2O → HCO3⁻ + H⁺
  • This increases H⁺ ions and reduces pH
  • Central chemoreceptors are triggered, stimulating respiratory centres to initiate contraction of the diaphragm and intercostal muscles

1.2 Anatomy and Pressures

Learning level: Foundation

Key pressures in the respiratory system:

All other pressures are measured in relation to atmospheric pressure. Negative = lower than atmospheric; Positive = higher than atmospheric. If a pressure equals atmospheric pressure, it = 0.

1.3 Pressure Gradients

Learning level: Intermediate

Three key pressure gradients cause breathing:

1.4 The Breathing Cycle — Negative Pressure Ventilation

Learning level: Intermediate

Inspiration:

1. Before inspiration: pleural pressure approximately -5, alveolar pressure 0 — transpulmonary pressure gradient of -5
2. This negative gradient maintains FRC (Functional Residual Capacity = expiratory reserve volume + residual volume — volume of air remaining at end-resting expiratory level)
3. Inspiratory muscles (diaphragm and internal intercostals) contract to expand thorax via bucket handle and pump handle movements
4. This increases the transthoracic pressure gradient by reducing pleural pressure (making it more negative)
5. Must overcome forces of lung elasticity and surface tension of alveolar fluid (both pull lungs inward), but outward pull is still greater
6. As intrapleural pressure drops, transpulmonary gradient widens, causing alveoli to expand
7. Alveolar expansion causes intra-alveolar pressure to drop below atmospheric pressure
8. Negative transrespiratory gradient causes air to move from mouth to alveoli
9. Intrapleural pressure continues to decrease towards end of inspiration
10. Intra-alveolar pressures equilibrate with atmosphere; inspiratory flow stops (becomes 0)
11. Transpulmonary pressure gradient reaches approximately -10

Expiration:

1. Passive process: elastic recoil of lungs + relaxation of diaphragm and internal intercostal muscles
2. Reduction in thoracic volume
3. Intra-pleural pressure rises; alveoli deflate
4. Intra-alveolar pressure increases beyond atmospheric pressure
5. Positive transrespiratory gradient causes air to move from lungs to mouth
6. Expiratory flow stops (0); cycle begins again

For all this to work, forces must be overcome: elastic recoil, surface tension, compliance, and resistance.

2. Forces in the Lungs

2.1 Elasticity

Learning level: Foundation

• Lung parenchyma (alveoli) contains elastic and collagen fibres
• Elasticity = tendency of a material to maintain its shape and offer resistance to stretching forces, and willingness to return to resting position
• Formula: Elastance = Change in pressure applied to lung / Change in volume in the lung
• Concept compared to a spring: increasing force expands the lungs similarly, but stretching capacity is limited; beyond maximum stretch, additional force produces little increase and may cause damage
• Elastic fibres help alveoli expand and recoil
• Altered slightly during expiration due to surface tension

2.2 Surface Tension

Learning level: Intermediate

• Property of the surface of a liquid that allows it to resist an external force due to the cohesive nature of its molecules
• Laplace’s Law: Pressure required to inflate lung = 2 x tension in alveolar walls / radius of alveoli
• The smaller the radius, the higher the surface tension — lungs more difficult to inflate
• Von Neergaard (1929): A saline-filled lung is easier to inflate than an air-filled lung (less pressure required)
• Water molecules on top of lung tissue only have water molecules below/beside them
• Water is polar, forming strong covalent bonds that increase surface tension
• These bonds create an inward force, potentially reducing alveolar surface area (reduced gas exchange)
• Alveoli cannot counteract this inward force through elastic properties alone

2.3 Pulmonary Surfactant

Learning level: Foundation

• Secreted by Type II epithelial cells continuously
• A lipoprotein that reduces the force of surface tension
• Contains a lipid with hydrophilic and hydrophobic ends (hydrophobic ends are water-insoluble and face towards air, pulling away from water)
• Prevents alveolar collapse (atelectasis)
• At end of expiration, as alveoli become smaller, surfactant concentration increases to reduce surface tension

Clinical pearl: Pre-term babies only develop enough surfactant to be effective at 35/40 weeks gestation (begin producing at 24 weeks). Neonates are therefore at high risk of collapse.

2.4 Compliance

Learning level: Intermediate

• Compliance = Change in volume (L) / Change in pressure (cmH2O)
• Magnitude of the change in lung volume as a result of the change in pulmonary pressure
• Changes throughout inhalation and exhalation
• Affected by either chest wall or lung factors
• Depends on elasticity and surface tension
• Normally measured under static conditions to eliminate resistive factors (zero flow) — this gives the volume/pressure curve
• If compliance doubles, tidal volumes double

If decreased compliance: higher elastic recoil, more pressure needed to inflate lung If increased compliance: expiration difficult due to loss of elastic recoil

Factors affecting compliance:

Cross-reference: The 2025 Advanced Ventilation deck (Section 2.3) covers compliance in more detail, including dynamic vs static compliance distinctions. See 02-advanced-ventilation.md.

2.5 Resistance

Learning level: Intermediate

• Resistance to flow of air caused by friction within the airways
• Two parts:
  1. Tissue resistance (20%) — friction caused by moving organs and chest wall
  2. Airway resistance — friction caused by movement of air through the respiratory system and airways (e.g. secretions, oedema, bronchospasm, ETT size)

Poiseuille’s Law:

• Main factor is the radius — smaller radius = increased resistance
• If there are more airways, resistance reduces (more paths for air)
• Even though bronchioles are smallest, because there are many of them, the bronchi actually have lower total resistance
• Mainly affects expiration (as airways are narrower during expiration)

Properties of air flow:

Clinical pearl: Resistance affects the time constant (does not alter VT). If high resistance, want a slow rate and long expiratory time.

3. Positive Pressure Ventilation

3.1 Mechanism of Positive Pressure Breathing

Learning level: Foundation

Four phases:

1. Initiation of inspiration (triggering):

   • Time-triggered: based on set respiratory rate
   • Pressure-triggered: decrease in pressure in circuit sensed by ventilator
   • Flow-triggered: ventilator delivers constant background flow; any change caused by patient effort is sensed by the flow sensor (detects a negative pressure gradient)
   • Machine trigger (set parameters) vs patient trigger (negative gradient)

2. Inspiratory phase:

   • Inspiratory valve opens
   • Set volume or pressure delivered depending on mode
   • Once reached, inspiratory valve closes

3. Changeover from inspiration to expiration:

   • Once pressure/volume reached and time aspect has occurred, inspiratory valve closes
   • Expiratory valve opens

4. Expiratory phase:

   • Once finished, expiratory valve closes

Largely depends upon the mode the ventilator is set to.

3.2 Indications for Ventilation

Learning level: Foundation

Neurological:

• Low GCS (<8)
• Protect from aspiration
• Loss of airway control/protection
• Head injury (neuroprotection)

Respiratory:

• Respiratory failure
• Increased secretion load (unmanageable)
• Increased WOB
• Inadequate oxygenation (including cardiac insufficiency)
• Apnoeas
• Airway obstruction (e.g. inflammation, foreign body)
• Stridor

Cardiac:

• Cardiac insufficiency

Key consideration: If high PEEP — increased thoracic cavity volume — less room for blood in thoracic cavity (space taken up by air) — reduced venous return — reduced stroke volume — hypotension.

4. Modes of Ventilation

4.1 Overview of Modes

Learning level: Foundation

These can be either volume or pressure controlled.

4.2 Volume Controlled Ventilation (VCV)

Learning level: Intermediate

• A set tidal volume is delivered
• Set RR, set inspiratory time
• Pinsp and PIP are dependent variables — dependent on lung compliance, inspiratory flow, and airway resistance
• Guarantees set minute volume (good for CO2 control, e.g. head injury)

Risk: If compliance reduces, PIP will increase to achieve set VT — risk of VILI (Ventilator-Induced Lung Injury).

4.3 Pressure Controlled Ventilation (PCV)

Learning level: Intermediate

• Set PIP, PEEP, inspiratory time, RR
• Tidal volume is the dependent variable
• If compliance reduces, tidal volume reduces
• Lower pressures usually achieved than VCV due to decelerating flow
• Decreased tidal volumes easily occur (e.g. with secretions) and can go unnoticed

Decelerating flow pattern:

• Offers highest level of flow at start of breath when patient flow demand is greatest
• Advantages: improved ventilator/patient synchrony, ability to lower PIP, increases MAP (improves lung inflation, gas distribution and oxygenation)
• Disadvantages: increased MAP reduces venous return and cardiac output (hypotension); increases ICP (careful with neuroprotection patients); can reduce expiratory time

4.4 Pressure-Regulated Volume Controlled Ventilation (PRVC)

Learning level: Advanced

• AKA Mandatory Mode
• Delivers a preset tidal volume in a pressure-limited manner using the lowest possible inspiratory pressure with decelerating flow
• Gas flow and pressure change constantly in each breath depending on lung compliance and resistance
• Ventilator automatically weans pressures as required
• Uses tidal volume as feedback control for continuously adjusting the pressure limit
• All breaths are mandatory; RR is fixed

4.5 SIMV (Synchronised Intermittent Mandatory Ventilation)

Learning level: Intermediate

• Can be pressure or volume controlled + PS, or PRVC + PS
• Ventilator delivers a set RR with either a preset PIP or VT
• Mandatory breaths: ventilator does the work
• Spontaneous breaths: variable volumes/pressures (unless PS is set up)

How synchronisation works:

• If patient does not trigger: vent delivers as per programme
• If patient triggers between mandatory breaths: vent allows a normal breath and opens inspiratory valve but provides no assistance unless PS is set up (if PS = Pinsp, every breath is the same)
• If patient triggers at the same time as a mandatory breath: vent synchronises and ensures PIP is delivered
• This avoids breath stacking and improves patient comfort (but no guaranteed tidal volume or Ti)

Advantages:

• Allows weaning
• Patient puts in effort — reduces respiratory muscle fatigue
• Negative pressure generated by patient increases venous return and helps cardiac output

4.6 Pressure Support (PS)

Learning level: Foundation

• Patient-triggered breaths
• Each inspiratory effort is augmented by the ventilator
• Preset level of inspiratory pressure = PS

Advantages over SIMV:

• Further improves weaning
• Preserves respiratory drive, reduces muscle atrophy

Disadvantages:

• Atelectasis can occur (small VTs)
• Requires patient effort

4.7 CPAP/PEEP

Learning level: Foundation

• CPAP = Continuous Positive Airway Pressure
• PEEP = Positive End Expiratory Pressure
• Splints open alveoli to prevent collapse and atelectasis
• Maintains alveolar inflation during exhalation

Benefits:

• Increases FRC by increasing alveolar recruitment
• Improves ventilation and V/Q matching
• Improves oxygenation and reduces WOB
• Reduces FiO2 requirement
• Decreases pulmonary shunting
• Increases lung compliance by recruiting additional lung units

Risks:

• Increased incidence of barotrauma
• Increased MAP — potential decrease in venous return
• Can increase dead space (hyperinflated areas impair perfusion)
• Reduces venous return from the head (increases ICP)
• Alteration of renal function/water balance (increased ADH)

Cross-reference: See 04-oxygen-delivery-and-niv.md for CPAP vs BiPAP in NIV context.

5. Paediatric-Specific Considerations

Learning level: Foundation

5.1 Endotracheal Tubes

• Historically used uncuffed tubes due to paediatric anatomy, but these caused large leaks and poor ventilation
• Current practice: cuffed tubes are used as research shows significantly reduced rates of reintubation and gas leak
• NTT vs ETT: In infants, nasotracheal tubes (NTT/NETT) improve security by reducing unplanned extubations (though Cochrane review showed no significant differences)
• Tube size: Smaller tubes have higher resistance — if there is a large secretion load or a bend in the tube, this has more significant impact

6. Oxygenation and Carbon Dioxide

6.1 Oxygenation

Learning level: Foundation

• Oxygen is a toxic substance
• Carried in blood mainly attached to iron in haemoglobin (4 molecules per Hb)
• Capillary transit time is the most important factor in determining PaO2 (length of time blood remains in the pulmonary capillary)
• To improve oxygenation, transit time needs to be as long as possible for oxygen to diffuse
• To increase transit time: increase space in alveoli — increase MAP (dependent on PIP, PEEP, and inspiratory time)

Strategies to improve oxygenation:

1. Increase diffusion gradient — increase FiO2
2. Increase capillary transit time — increase gas space in alveoli (make bigger and splint open longer)
3. Increase MAP (PEEP more effective than PIP alone due to longer expiratory phase)

6.2 Carbon Dioxide

Learning level: Foundation

• By-product of metabolism
• Carried in blood as CO2 or carbonic acid
• Penetrates membranes 24 times faster than oxygen due to higher water solubility
• Not dependent on time like O2 but by minute ventilation
• Minute ventilation = RR x (VT - dead space)
• Hypercapnia usually due to alveolar ventilation inadequate for metabolic demands
• To improve CO2 clearance: increase RR or increase VT

7. Complications of Ventilation

Learning level: Intermediate

7.1 Airway Complications

• Aspiration
• Ventilator-acquired pneumonia
• Cilia paralysis, irritation, oedema (from ETT)
• Trauma of insertion

7.2 Mechanical Complications

• Atelectasis (hypoventilation)
• Hyperthermia (from overheated inspired air)
• V/Q mismatch (overexpansion and compressed arteries)
• Pneumothorax
• Oxygen toxicity
• Unintended air trapping (can cause hypotension and reduced cardiac output)
• Reduced surfactant production
• Ventilator asynchrony
• VILI (barotrauma, volutrauma — alveolar overdistension, atelectrauma — collapse and reopening of alveoli cyclically)

7.3 Physiological Complications

• Reduced cardiac function / hypotension
• Decreased venous return
• Fluid overload
• Respiratory muscle weakness
• Immobility
• GI issues (ulcers, malnutrition)

8. Humidification

Learning level: Foundation

• Upper airway is bypassed by ETT/tracheostomy
• Cilia have reduced function due to paralysis from medications and presence of tube
• Rest of airway may not be able to supply enough moisture and heat to delivered gases
• Humidification and heating are essential
• Prevents complications: hypothermia, sticky secretions, destruction of airway epithelium, atelectasis
• Target temperature: 37 degrees Celsius
• Mucous membranes in upper airway (nose and mouth) normally release moisture

9. Weaning

Learning level: Intermediate

9.1 When to Begin Weaning

• As soon as possible
• Patient should be stable: no infection, scans completed, no neuroprotection needed
• Look for: improvement in secretions, improvement in CXR, improving blood gases
• Sedation and paralysis are also weaned alongside ventilator settings (e.g. cough reflex, secretion management, responsiveness if TBI/neuro)

9.2 Process

• Change modes so patient puts in more effort — monitor for fatigue and changes in VTs
• Consider Swedish nose (heat-moisture exchanger)

9.3 Extubation Criteria

• GCS > 8
• Cough, gag, and respiratory drive present
• Secretion load — can they manage independently?
• Dexamethasone: give to reduce inflammation for upper airway obstruction — more effective if started 12-24 hours pre-extubation
• Consider: WOB, diaphragm function, spontaneous breathing trial (SBT)
• Sedation weaned, paralysis off

10. Ventilator Graphics

Learning level: Advanced

10.1 Pressure-Time Waveform

• Shows pressures generated within airways during each ventilator cycle
• At start of breath, pressure is generated to overcome airway resistance (note: no volume gained at this time)
• PEEP start line will be higher than baseline
• Pressure rises to reach the peak
• At end of inspiration, airflow is 0
• Passive expiration follows
• Inspiratory rise time = amount of time it takes to reach desired airway pressure or peak flow rate

Rise time troubleshooting:

• If rise time is too fast: peak/spike appears — need to increase rise time (valve makes air come out more slowly)
• If rise time is too slow: curve is more rounded — will cause decreased VT as unlikely to get full pressure

10.2 Flow-Time Waveform

• Decelerating flow pattern: longer inspiratory time; also possible square waveform (constant flow = volume controlled mode)
• Expiratory part determined by: elastic lung recoil, airway resistance, respiratory muscle effort by patient
• If curve reaches 0: good set pressure achieved
• If vertical line before reaching 0: inspiratory phase not finished; larger VT achievable if flow continues

Air trapping on flow-time:

• If expiratory arm is longer and flatter (does not descend as much vertically) = low peak expiratory flow
• If it does not reach 0 at beginning of next inspiration = gas trapping is occurring
• Treatment: bronchodilator, long expiratory time (increased resistance, struggling to get air out)

10.3 Volume-Time Waveform

• Plateau at top if inspiratory pause time is set
• Top part = inspiratory VT
• For pressure-controlled machines, volume-time and flow-time are important as both show changes in VT and compliance (dependent variables)
• Air trapping on volume: exhaled volume should return to baseline; if not = air trapping or leak

10.4 Pressure-Volume Loop

Learning level: Advanced

• Generated every breath (ventilator or patient triggered)
• Normal shape = rugby ball shaped
• Loop moves anticlockwise for positive pressure breaths and clockwise for negative pressure breaths
• The slopes represent compliance: flatter curve = lower compliance
• A line down the middle: left area = expiratory resistance, right area = inspiratory resistance

Inflection Points:

Ideal Pressure-Volume Curve and the “Safe Window”:

• Safe window exists between the lower zone of atelectasis and upper zone of overdistension
• Tidal volumes should fit within this area
• Set PEEP above the lower inflection point
• Reduce pressures to avoid overinflation
• In disordered lung, the safe window may be too small for conventional tidal volumes

Cross-reference: The HFOV deck (03-hfov-and-nitric-oxide.md) uses this concept to justify HFOV as a strategy when the safe window is too narrow for conventional ventilation.

“Bird Beak” Sign:

• Occurs when there is overdistension (too much pressure/volume)
• On the PV loop, see a beak-like shape at the upper end

Inspiration detail:

1. As pressure builds, little volume change until LIP reached (low compliance)
2. Alveoli open (nondependent then dependent regions); small pressure rise = large volume gain (high compliance)
3. Continues until UIP reached
4. Beyond UIP: more pressure needed for small volume gain (low compliance again)

Compliance changes on PV loops:

• Increased compliance (e.g. surfactant, younger age): curve shifts left, more vertical
• Decreased compliance (e.g. ARDS, fibrosis): flatter curve
• In pressure-controlled ventilation: PIP does not change but VT reduces with decreased compliance
• If long horizontal line at 0 degrees: PEEP needs increasing as no volume is being achieved

Hysteresis:

• The area separating the inspiratory and expiratory curves
• The output of the system depends not only on current input but also on history of past inputs
• Develops when volume change is sustained for some time after force is removed
• E.g. increased airway resistance due to secretions causes collapse of small airways that must be overcome to inflate lungs
• Expiratory resistance is generally larger

10.5 Patient-Triggered Breaths on Graphics

• Patient triggers breath, then PS is given to top up
• If patient manages the entire breath with no ventilator top-up needed, it would not be visible on the ventilator display

10.6 Identifying Leaks

• Leak (ETT cuff, pneumothorax, vent connections, water in circuit)
• Leads to loss of PEEP
• PIP decreases; expiratory wave will not return to baseline

10.7 Identifying Asynchrony

• Causes: neurological injury, improperly set sensitivity trigger
• Pressure wave: extra inhale/exhale in middle of waveforms, erratic flow volumes
• Leads to: increased RR, increased WOB, patient discomfort, fatigue

Double Trigger:

• Small double loop at top of pressure curve
• If patient effort continues, vent triggers twice immediately — results in high pressures and volumes
• May need to: change mode of ventilation, increase sedation, or increase VTs

10.8 Auto-PEEP

Learning level: Advanced

• Positive end-expiratory pressure caused by progressive accumulation of air (air trapping) due to incomplete expiration prior to next breath
• Often occurs in patients with high RR or high minute ventilation, or if PEEP > 10
• Occurs when inspiration starts before end of previous exhalation

Consequences:

• Increased WOB when patient initiates breath (larger negative pressure needed to reach trigger point)
• Diaphragm flattens, reducing effectiveness of contraction
• Gas trapping leads to increased PaCO2
• Increased inspiratory time can decrease I:E ratio and favour auto-PEEP development
• Air trapping causes increased PIP (increasing end-expiratory pressure and end-inspiratory lung volumes)
• Over several breaths: breath stacking — FRC increases, tidal volume occurs at less compliant portion of PV curve
• Can cause: increased alveolar pressure, pneumothorax, impeded venous return

On graphics:

• Pressure and volume flow loop curves will not meet axes

Management:

• Identify cause: removal of secretions, bronchodilator, larger ETT, decrease RR
• Aim to reduce gas trapping

11. References

• D. Hess, 2014. Respiratory Mechanics in Mechanically Ventilated Patients. Respiratory Care, 59(11)
• D. Grinnan and J. Truwit, 2005. Clinical review: Respiratory mechanics in spontaneous and assisted ventilation. Critical Care, 9(5)
• Gupta, R. and Rosen, D., 2016. Paediatric Mechanical Ventilation in the intensive care unit. BJA Education, 16(12), pp. 422-426
• Paediatric Ventilation Guidelines 2010: https://www.health.gov.fj/wp-content/uploads/2014/05/Ventilation-Guidelines-for-PICU_Oct-2010.pdf
• Open Textbook BC — The Process of Breathing: https://opentextbc.ca/anatomyandphysiology/chapter/22-3-the-process-of-breathing/
• Deranged Physiology — Interpreting flow-volume and pressure-volume loops
• Draeger webinar (DiBlasi)
• Life in the Fast Lane (LITFL) — HFOV
• Various SlideShare and journal resources (see original slides 56-57)