Note
Studied by 18 peopleChapter 11 – Ventilation Vocabulary
Learning Objectives
Understand physiologic functions provided by ventilation (gas exchange support, CO(2) removal, O(2) supply).
Explain pressure gradients that drive gas flow, diffusion, and lung inflation.
Identify forces (elastic, resistive, surface–tension) that oppose gas movement.
Describe the role of surface tension in lung recoil and alveolar stability.
Relate lung, chest-wall, and total (respiratory-system) compliance.
List factors affecting airway resistance and work of breathing (WOB).
Explain why ventilation is not uniformly distributed throughout the lung.
Discuss how time constants govern alveolar filling/emptying.
Calculate alveolar ventilation, anatomic/alveolar/physiologic dead space, and VD/VT.
Key Terminology & Symbols
(VT) = tidal volume (L or mL) – gas moved during one inspiration or expiration.
(f_B) = breathing frequency (breaths min(^{-1})).
(VE) = minute ventilation – total gas moved per minute.
VE = f_B \times VT(VA) = alveolar ventilation – fresh gas reaching perfused alveoli per minute.
VA = (VT - VD) \times f_B(VD) = dead-space volume (mL); subdivided into anatomic ((VD{anat})) & alveolar ((VD{alv})).
(VD/VT) = physiologic dead-space fraction (efficiency index).
Pressures (cm H(_2)O)
(PAO): airway-opening (mouth) pressure.
(PA): alveolar pressure.
(P_{pl}): pleural (intrapleural) pressure.
(P_{BS}): body-surface (≈ atmospheric) pressure.
Trans- pressure differences
Transrespiratory: P{TR}=PAO-P{BS}
Transairway: P_{TAW}=PAO-PA
Transalveolar: P{TA}=PA-P{pl}
Transpulmonary: P{TP}=PAO-P{pl}
Transthoracic: P{TT}=PA-P{BS}
Compliance (C): ease of volume change.
C=\Delta V/\Delta PResistance (R): pressure cost of flow.
R=\Delta P/\dot{V}Time Constant (TC): speed of local filling/emptying.
TC = R \times C
Ventilation vs. Respiration
Ventilation = mechanical movement of gas into/out of lungs.
Respiration = cellular O(2) utilization & CO(2) production.
In health, ventilatory control keeps (PaCO2) & (PaO2) stable across activity levels.
Disease can impair ventilation (hypoventilation) and ↑ muscular effort (↑ WOB).
Mechanics of Ventilation
Ventilatory cycle = inspiration (active) + expiration (passive at rest).
Healthy lungs: inspiratory load minimal; expiration driven by elastic recoil.
Structural loads:
Compliance of lung & chest wall
Airway/tissue resistance
Removing CO(2), replenishing O(2) are ultimate functional goals.
Pressure Gradients & Gas Flow
Gas moves from high to low pressure; thoracic volume changes establish gradients.
End-expiration (rest):
(PA = 0), (P{pl} \approx -5) cm H(2)O.
Positive end-expiratory (P{TP}) (≈ 5 cm H(2)O) holds lungs at Functional Residual Capacity (FRC).
Inspiration: thoracic expansion → (P{pl}) ↓ (more negative) → (P{TP})/(P_{TA}) ↑ → air flows inward.
Magnitude of inspiratory flow ∝ (+\Delta P_{TAW}).
Expiration: recoil ↑ (P{pl}) (less negative) → (P{TP}) ↓ → outward flow.
Driving force stored in combined elastance of lung + chest wall.
During vigorous inspiration, (P{pl}) can reach −50 cm H(2)O.
Forces Opposing Lung Inflation
Elastic Tissue Forces
Elastic + collagen fibers resist stretch; larger (\Delta P) yields larger (\Delta V) until anatomical limits.
Deflation path differs → hysteresis (inflation curve > deflation curve).
In diseased lungs, reopening collapsed alveoli contributes vastly to hysteresis.
Surface-Tension Forces
Liquid film in alveoli tends to shrink (Laplace effect).
Surfactant (type II cells) lowers surface tension, stabilizes alveoli, prevents collapse, minimizes hysteresis.
When area ↓ (small alveolus), surfactant effectiveness ↑ —self-adjusting.
Chest-Wall Forces
Chest wall tends to spring outward; lung tissue tends to recoil inward.
At FRC these opposing tendencies balance ((P{pl}) ≈ −5 cm H(2)O).
Compliance
Normal combined lung compliance: CL \approx 0.2\;L\;cm^{-1}H2O
Pathology:
Emphysema/obstruction: destroyed elastic tissue → ↑ (C_L) (floppy lungs, easy to inflate, hard to deflate).
Fibrosis/restriction: excess stiff tissue → ↓ (C_L).
Combined behaviors:
Parallel lungs: C{total}=C{R}+C_{L}
Lungs + chest wall in series: C{rs}=\frac{C{CW}\times C{L}}{C{CW}+C_{L}}
Airway & Tissue Resistance
Tissue viscous resistance: energy to displace parenchyma.
Airway resistance (Raw) – majority arises in large AWs (nose, mouth, trachea):
80 % of total R in upper & large central airways (turbulent flow).
20 % in <2 mm bronchioles (laminar).
Combined Raw:
Parallel: R{total}=\frac{R{R}\times R{L}}{R{R}+R_{L}}
Series: R{total}=R{upper}+R_{bronchi}
Static vs Dynamic Mechanics
Static: flow = 0; muscle effort = 0 (e.g., inspiratory pause during MV).
Measures pure elastic recoil (no resistive component).
Dynamic: ongoing flow; values influenced by frequency & time constants.
At zero mouth flow, inter-compartment “pendelluft” may persist.
As respiratory rate ↑, both effective C and R ↓ (frequency dependence).
Exhalation Mechanics & Flow Limitation
Airway caliber governed by transmural pressure ((P{tm}=P{inside}-P_{outside})).
Equal-Pressure Point (EPP): location where intraluminal pressure = extraluminal pressure → downstream compression; sets maximal flow.
Small, non-cartilaginous airways more prone to collapse (dynamic compression).
Forced expiratory tests (e.g., FVC) display effort-independent portion due to dynamic compression.
Work of Breathing (WOB)
Mechanical work: W = F \times x; respiratory muscles generate force measured as transpulmonary pressure ((P_{TP})).
Ventilator work assessed by transrespiratory pressure ((P_{TR})).
Pressure–volume (P–V) curve used to set optimal PEEP (point just above lower inflection).
Disease impact:
Restrictive (↓ C): ↑ elastic work.
Obstructive (↑ R): ↑ resistive work (especially during high flow).
Metabolic Cost
O(2) cost of breathing (OCB) < 5 % of total O(2) uptake in health.
Disease can raise OCB > 30 % → fatigue, failed weaning.
In shock, MV may be instituted to re-allocate O(_2) delivery to vital organs.
Ventilation–Perfusion Distribution
Ventilation ((\dot V)) & perfusion ((\dot Q)) are uneven → regional (\dot V/\dot Q) mismatch.
Overall lung average: \dot V/\dot Q \approx 0.8.
Upright position: bases (dependent) receive more blood & slightly more ventilation → best matching.
Apical alveoli larger at rest (higher (P_{TP})) but accept less (\Delta V).
Clinical pearl: in unilateral disease, place good lung down to improve matching.
Gravity–Related Factors
Thoracic expansion: mechanics favor greater movement at bases.
(P{TP}) gradient: (P{pl}) is more negative at apex (−10 cm H(_2)O) vs base (−2.5 cm).
Time Constants & Regional Filling
TC = R \times C governs % volume change per unit time.
1 TC → 63 % filling/emptying, 2 TC → 86 %, 3 TC → 95 %.
Ventilator settings:
Pressure-control: set inspiratory time ≥ 3 TC to deliver ≥ 95 % target volume.
Expiratory time likewise ≥ 3 TC for passive emptying.
Unequal TCs:
High R &/or C → long TC (slow unit).
Low R &/or C → short TC (fast unit).
Mode implications:
VC with constant flow distributes volume more uniformly when TCs differ but C equal.
PC may give safer distribution when Cs differ but Rs equal.
Efficiency of Ventilation & Dead Space
Unavoidable wasted gas:
Anatomic dead space (conducting airways) ≈ 1 mL · lb⁻¹ IBW (≈ 2.2 mL · kg⁻¹).
Alveolar dead space: ventilated but unperfused or high (\dot V/\dot Q) units (e.g., embolism, apices).
Physiologic dead space: VD{phys}=VD{anat}+VD_{alv}
Bohr (modified) equation for bedside VD/VT (ventilator pts): VD/VT = \frac{PaCO2 - \dot{PE}CO2}{PaCO_2}
(\dot{PE}CO2) = mixed-expired CO(2) (often substituted by end-tidal).
Normal VD/VT \approx 0.3 (0.2–0.4).
> 0.6 signals poor weaning potential; high wasted ventilation.
Breathing strategy: slow & deep lowers dead-space fraction; fast & shallow increases it.
Minute & Alveolar Ventilation
Typical resting values:
(VT \approx 500\,\text{mL}), (f_B \approx 12\,\text{min}^{-1}) → VE \approx 6\,L\,min^{-1}
Drivers of VE: metabolic CO(2) production ((\dot V{CO2}) ≈ 200 mL min⁻¹) & body size.
Because of VD, VA<VE; VA is sole determinant of arterial CO(_2).
Effectiveness of Ventilation
Target: maintain arterial pH via adequate CO(_2) removal.
Relationship:
PaCO2 \propto \frac{\dot V{CO2}}{VA}With constant metabolism, ↑ PA (alveolar) ventilation → ↓ (PaCO_2); ↓ VA → hypercapnia.
Ethical / Practical Implications
High WOB & OCB can precipitate fatigue; timely mechanical ventilation preserves energy.
Setting ventilator parameters (PEEP, inspiratory time) demands understanding of pressure gradients, compliance, and time constants to avoid volutrauma/barotrauma.
Proper patient positioning (good lung down) exploits gravity to optimize (\dot V/\dot Q) matching.
Monitoring VD/VT at bedside guides weaning and detects pulmonary vascular pathology (e.g., embolism).
End of Study Notes – Chapter 11: Ventilation
Learning Objectives
Physiologic Functions of Ventilation:
Ventilation, as the mechanical movement of gas into and out of the lungs, primarily supports gas exchange by removing carbon dioxide (CO2) and supplying oxygen (O2) to the body. Its ultimate functional goals are to remove CO2 and replenish O2. Alveolar ventilation specifically refers to the fresh gas reaching perfused alveoli per minute, which is the sole determinant of arterial CO2. The overall target is to maintain arterial pH via adequate CO2 removal.
Pressure Gradients Driving Gas Flow, Diffusion, and Lung Inflation:
Gas flow is driven by pressure gradients, moving from areas of high pressure to areas of low pressure, which are established by changes in thoracic volume.
End-expiration (rest): Alveolar pressure (PA) is 0 cm H2O (atmospheric), and pleural (intrapleural) pressure (P{pl}) is approximately -5 cm H2O. A positive transpulmonary pressure (P{TP} ext{ } ext{(} ext{≈} ext{ } 5 ext{ } cm ext{ } H_2O)) holds the lungs at Functional Residual Capacity (FRC).
Inspiration: Thoracic expansion causes (P{pl}) to decrease (become more negative), leading to an increase in transpulmonary pressure (P{TP}) and transairway pressure (P{TAW}). This pressure difference drives air inward. The magnitude of inspiratory flow is proportional to (+\Delta P{TAW}).
Expiration: Elastic recoil increases (P{pl}) (making it less negative) and decreases (P{TP}), leading to outward gas flow. The driving force for expiration is stored in the combined elastance of the lung and chest wall.
Key pressure definitions:
Airway-opening (mouth) pressure: (PAO)
Alveolar pressure: (PA)
Pleural (intrapleural) pressure: (P_{pl})
Body-surface (≈ atmospheric) pressure: (P_{BS})
Trans-pressure differences:
Transrespiratory: P{TR}=PAO-P{BS}
Transairway: P_{TAW}=PAO-PA
Transalveolar: P{TA}=PA-P{pl}
Transpulmonary: P{TP}=PAO-P{pl}
Transthoracic: P{TT}=PA-P{BS}
Forces Opposing Gas Movement (Lung Inflation):
Elastic Tissue Forces: Elastic and collagen fibers within the lung tissue resist stretch. As volume changes ( \Delta V), larger pressure differences ( \Delta P) are required, up to anatomical limits. The inflation and deflation paths differ, demonstrating hysteresis (inflation curve > deflation curve).
Surface-Tension Forces: A liquid film lines the alveoli, tending to shrink due to surface tension (Laplace effect).
Chest-Wall Forces: The chest wall naturally tends to spring outward, opposing the inward recoil tendency of the lung tissue. At FRC, these opposing tendencies balance, resulting in a (P{pl}) of approximately -5 cm H2O.
Airway & Tissue Resistance:
Tissue viscous resistance: Energy is required to displace the lung parenchyma.
Airway resistance (Raw): The majority (80%) arises in the upper and large central airways due to turbulent flow, while 20% occurs in bronchioles less than 2 mm in diameter due to laminar flow.
Role of Surface Tension in Lung Recoil and Alveolar Stability:
The liquid film lining the alveoli creates surface tension, which tends to cause the alveoli to shrink (Laplace effect) and contributes to the lung's tendency to recoil inward. This force, if unopposed, could lead to alveolar collapse.
Surfactant, produced by type II alveolar cells, is crucial because it:
Lowers surface tension, which reduces the inward collapsing force.
Stabilizes alveoli, particularly by minimizing surface tension more effectively in smaller alveoli (when surface area decreases, surfactant effectiveness increases, making it self-adjusting).
Prevents alveolar collapse and minimizes hysteresis (the difference between inflation and deflation curves).
Relating Lung, Chest-Wall, and Total (Respiratory-System) Compliance:
Compliance (C) is defined as the ease of volume change: C=\Delta V / \Delta P.
Normal combined lung compliance (CL) is approximately 0.2 L cm^{-1}H2O.
The lung and chest wall are considered to be in series in terms of their mechanical properties. Therefore, the total respiratory system compliance (C{rs}) is calculated as: C{rs} = \frac{C{CW} \times CL}{C{CW} + CL}, where (C_{CW}) is chest wall compliance.
Pathological conditions affect compliance:
Emphysema/obstruction: Destroyed elastic tissue leads to increased lung compliance ( \uparrow C_L) (producing 'floppy' lungs that are easy to inflate but difficult to deflate).
Fibrosis/restriction: Excess stiff tissue leads to decreased lung compliance ( \downarrow C_L).
Factors Affecting Airway Resistance and Work of Breathing (WOB):
Factors affecting Airway Resistance (Raw):
Airway caliber: The majority of resistance is in large airways (nose, mouth, trachea), with turbulent flow. Smaller bronchioles (<2 mm) have laminar flow but can contribute significantly if their diameter is reduced.
Flow type: Turbulent flow in large airways accounts for ~80% of total resistance, while laminar flow in smaller airways accounts for ~20%.
Fluid viscosity and length of airways.
Transmural pressure: Airway caliber is governed by transmural pressure (P{tm} = P{inside} - P{outside}). Small, non-cartilaginous airways are prone to collapse (dynamic compression) if (P{tm}) becomes negative, especially during forced expiration.
Factors affecting Work of Breathing (WOB):
Mechanical work is generated by respiratory muscles to overcome forces opposing lung inflation. It is measured as transpulmonary pressure (P{TP}). Ventilator work is assessed by transrespiratory pressure (P{TR}).
Compliance: In restrictive diseases (decreased compliance), there is greatly increased elastic work of breathing.
Resistance: In obstructive diseases (increased resistance), there is greatly increased resistive work of breathing, especially during high flow rates.
Metabolic cost: The oxygen cost of breathing (OCB) can be significantly elevated in disease, potentially exceeding 30% of total oxygen consumption, leading to fatigue. In severe cases like shock, mechanical ventilation may be instituted to re-allocate O_2 delivery to vital organs.
Why Ventilation is Not Uniformly Distributed Throughout the Lung:
Ventilation ( \dot V) and perfusion ( \dot Q) are unevenly distributed throughout the lung, leading to regional ( \dot V/ \dot Q) mismatch, even in healthy individuals. This non-uniformity is primarily due to gravity-related factors:
Gravity–Related Factors & Thoracic Expansion: In an upright position, the bases (dependent regions) of the lungs receive more blood flow and slightly more ventilation compared to the apices. This leads to better matching of ventilation and perfusion in the bases.
Pleural Pressure (P{pl}) Gradient: The pleural pressure is more negative at the apex (approx. -10 cm H2O) than at the base (approx. -2.5 cm H2O). This means apical alveoli are larger at rest (due to higher (P{TP})) but are less compliant, accepting less change in volume ( \Delta V) during inspiration. Conversely, basal alveoli are smaller at rest but more compliant, accepting a greater ( \Delta V) during inspiration.
How Time Constants Govern Alveolar Filling/Emptying:
A time constant (TC) is defined as the product of resistance (R) and compliance (C): TC = R \times C.
It governs the speed and percentage of volume change (filling or emptying) per unit time in a lung unit. Specifically:
After one TC, a lung unit will have completed 63% of its volume change.
After two TCs, it will have completed 86%.
After three TCs, it will have completed 95%.
Ventilator Settings Implications: To ensure adequate gas delivery, an inspiratory time of at least 3 TCs should be set in pressure-control ventilation to deliver ≥95\% of the target volume. Similarly, an expiratory time of ≥3 TCs is needed for passive emptying.
Unequal Time Constants: Lung units can have unequal TCs. Units with high resistance and/or high compliance will have a long TC (referred to as 'slow units'), filling or emptying slowly. Units with low resistance and/or low compliance will have a short TC ('fast units'), filling or emptying quickly.
Mode Implications: For instance, volume-controlled (VC) ventilation with constant flow may distribute volume more uniformly when time constants differ but compliance is uniform. Pressure-controlled (PC) ventilation may provide safer distribution when compliances differ but resistances are uniform.
Calculation of Alveolar Ventilation, Anatomic/Alveolar/Physiologic Dead Space, and VD/VT:
Alveolar Ventilation (VA): The fresh gas reaching perfused alveoli per minute. It is calculated as: VA = (VT - VD) \times f_B
(VT) = tidal volume (L or mL) – gas moved during one inspiration or expiration.
(VD) = dead-space volume (mL).
(f_B) = breathing frequency (breaths \min^{-1}).
Dead Space Volume (VD): Represents wasted gas that does not participate in gas exchange.
Anatomic Dead Space (VD_{anat}): The volume of the conducting airways (nose, mouth, pharynx, trachea, bronchi). It is approximately 1 mL per pound of ideal body weight (\approx 2.2 mL per kg of IBW).
Alveolar Dead Space (VD_{alv}): The volume of ventilated alveoli that are either unperfused or poorly perfused (e.g., due to pulmonary embolism or in apical regions with high ( \dot V/ \dot Q)).
Physiologic Dead Space (VD{phys}): The sum of anatomic and alveolar dead space: VD{phys} = VD{anat} + VD{alv}.
Physiologic Dead-Space Fraction (VD/VT) - Efficiency Index: This ratio indicates the proportion of tidal volume that is 'wasted' ventilation. It is calculated using the modified Bohr equation at the bedside (for ventilator patients): VD/VT = \frac{PaCO2 - \dot{PE}CO2}{PaCO_2}
$$(Pa