Mechanics of Breathing & Volumes and Ventilation

By Jackson Lee Primary Course 17/03/2010

Syllabus
MECHANICS OF BREATHING
1. General Instructional Objectives a)An understanding of the elastic properties (static mechanics) and the flow resistive properties of the a)An airways (dynamic mechanics) as well as the forces acting on the ventilatory system. b)The application of this knowledge to changes with anaesthesia and intensive care. b)The 2. Required Abilities 1.To describe the inspiratory and expiratory process involving the chest wall, diaphragm, pleura and 1.To lung parenchyma. 2.To define compliance (static, dynamic and specific) and relate this to the elastic properties of the 2.To lung. 3.To explain the concepts of time constants and relate these to "fast" and "slow" alveoli. 3.To 4.To describe the elastic properties of the chest wall and to plot pressure volume relationships of the 4.To lung, chest wall and the total respiratory system. 5.To describe the properties of surfactant and relate these to its role in influencing respiratory 5.To mechanics. mechanics. 6.To explain the vertical gradient of pleural pressure and its significance. 6.To 7.To explain the physics of gas flow and the significance of the relationship between resistance and 7.To flow in the respiratory tract. 8.To describe the factors affecting airway resistance, and how airway resistance may be measured. 8.To resistance, 9.To define closing capacity and its relationship to airway closure and explain its clinical significance 9.To and measurement. measurement. 10.To 10.To describe the work of breathing and its components. 11.To 11.To describe altered lung mechanics in common disease states. states.

Syllabus
VENTILATION - PERFUSION INEQUALITIES
General Instructional Objectives 1.An understanding of the normal matching of ventilation and perfusion, the mechanisms 1.An causing ventilation-perfusion inequality and an appreciation of its clinical significance ventilationRequired Abilities 1.To describe West's zones of the lung and explain the mechanisms responsible for them. 1.To 2.To explain the shunt equation. 2.To equation. 3.To describe and explain regional ventilation-perfusion inequalities, their clinical 3.To ventilationinequalities, importance, importance, and changes with posture. posture. 4. To outline the methods used to measure ventilation-perfusion inequalities. ventilationinequalities. 5. To explain venous admixture and its relationship to shunt. 6. To explain the clinical significance of changes in anatomical and physiological dead space. space. 7. To explain the effect of ventilation-perfusion inequality on oxygen transfer and carbon ventilationdioxide elimination.

Gross Factors
Lungs within thorax separated from thorax by potential intra-pleural space intraThe lungs are elastic with tendency to recoil in. Chest wall has tendency to spring out Together these produce a negative intra-pleural intrapressure. At FRC the two opposing forces are balanced

Muscle of Respiration
Inspiration: Diaphragm Innervated by phrenic nerve C3,4,5. Normal tidal volume 1-2 cm 1 Forced: 10 cm Moves abdominal content downward increased vertical dimension Ribs are moved outwards increase transverse dimension External intercostal Slopes forwards and downwards Pulls upwards and forwards increase lateral and AP diameter. bucket handle Scalene and Sternocleidomastoid Elevation first two ribs Important in exercise, resp failure or stress

Expiration
Generally is passive due to the elastic property of lung and chest wall to return to equilibrium. Abdominal muscles: Contracts to move the diaphragm upwards Internal costal muscles: pull the ribs down and inward. Important to prevent bulging of intercostal space.

Lung Volumes

Tidal Volume (TV): amount of air entering and leaving with normal breath. ~500ml resting Inspiratory Reserve Volume (IRV): volume that can be inspired above TV (TLC (TV + FRC)) (~2000 ml) Expiratory Reserve Volume (ERV): Additional volume that can be expired from a normal end expiratory breath to RV (1500ml) Residual Volume (RV): gas in lungs after maximal expiration (1500-1900ml) Inspiratory Capacity: Volume able to be inspired from FRC Vital Capacity (VC): Maximal forced expiration from TLC (4500-5000ml) Total Lung Capacity ( TLC): total lung volume (around 6000ml)

FRC
The amount of air remain in the lung after a quiet expiration. The equilibrium point of the lung and chest wall Residual volume + Expiratory reserve volume ~ 2.2 L or 30 mL/kg

Factors influencing FRC

Height Obesity FRC Gender: female have FRC 10% less than male Age: increase by around 16 mL per year Diaphragm tone: FRC decrease in paralysed patient ~400 mL Posture: The abdominal content can push against the diaphragm Lung disease:
Increase recoil decrease FRC fibrotic lung disease Decrease recoil increase FRC asthma, emphysema

Consequence of FRC
FRC below Closing Volume
Atelectasis/V/Q mismatch/shunt Atelectasis/V/Q arterial hypoxia

Increase Work of Breathing

Decreased compliance, opening of collapsed alveoli Increased airway resistance

Decrease oxygen reserve Increase pulmonary vascular resistance

Dead Space
This is the amount of air in the respiratory system that does not participate in gas exchange. Anatomical dead space: This is the volume of air in the conducting airway. Alveolar dead space: This is the volume of air in unperfused alveoli. Physiological dead space: This is sum of anatomical and alveolar dead space.

Closing Capacity
Airways and alveoli in the dependent part of the lungs are always smaller than those at the top. As the lung volume is reduced closer to residue volume the dependent airway begins to collapse. The lung volume at which dependent airways begins to collapse is known as the closing capacity (CC). Closing volume = CC-RV CCCC increases with age generally less than FRC in young adult FRC = CC supine age 44 FRC = CC erect age 66 Independent of body position

Significance of CC
FRC < CC means pulmonary blood flow is delivered to closed airway in dependent airways. Creates a shunt increased Aa gradient This means for a given alveolar O2 there will be a decrease of arterial PO2 Given that CC does not change with position but FRC does the effect is more marked in elderly supine patients

Determination of Dead Space & CC

Fowlers Method
Ask the subject to take a single breath of 100% O2 after maximal expiration. a. Phase I- the beginning of expiration. This gas is coming from the anatomic dead space and is pure oxygen. The phase is barely seen on the tracing. b. Phase II- seen as the first steep slope on the tracing. The gas is coming from both the bronchial and alveolar areas and shows an abrupt increase in N2%. (50% dead space & 50% alveolar) c. Phase III- the plateau phase in which the gas is coming from the alveoli. The percent of nitrogen changes slowly and evenly producing a flatter line. d. Phase IV- the percent of nitrogen once again increases sharply due to closure of the airway and emptying of the apices (high in amount of nitrogen).

Bohrs Method Measuring Physiological Dead Space

VT = VA + VD Total dead space is the sum of alveolar and anatomical dead space VA = VT - VD VT Fe = VAFA Amount of CO2 produced VT Fe = (VT - VD )FA VT Fe = FAVT - FA VD FA VD = FAVT - VT Fe FA VD = VT (FA - Fe )

Enghoff modification: replace PACO2 with measured PaCO2

Compliance
Compliance = Volume change per unit pressure change C = V/ P ml/cmH20 Is the slope of the volume-pressure volumecurve The steeper the curve the higher the compliance easier to be stretched. Slope flatter at high volumes stiffer Normal value of LUNG ALONE = 200ml/cmH20 Elastance = 1/compliance = stiffness or resistance to deformation

Compliance
Static compliance: The change in volume per unit pressure change when the flow of gas has ceased
Measured by inspiration to a certain volume and then relaxing against a closed airway for as long as possible, intrapleural pressure is measure by oesophagus

Dynamic compliance: Measure of volume V pressure change during normal breathing without breath holding.
Calculation is made when there is no gas flow at mouth at the end of insp & exp parts. It is frequency dependent and decrease with resp rate due to lung units have different time constant.

Specific Compliance: Compliance per unit volume of the lung i.e. static compliance/FRC

Factors Affecting Lung Compliance

Surface tension
Most important >50% of normal lung recoil Presence of surfactant FRC: age, body size, posture

Lung Size
Large difference in volume comparing neonate and adult. Pressure is less different

Tissue elastic fibres

Account for 20% Emphysema, pulmonary oedema, fibrosis

Gravity Pulmonary congestion

Lung volume (Optimal at FRC) FRC)

Lobar, lung resection Collapse or consolidation

Surface Tension (Dynes)

This is the imbalance of intermolecular forces at the liquid and gas interface. The attraction forces between water molecules is stronger than with air. Water would therefore reduce its surface area as small as possible Given lung has a surface area of 5050100 m2 it is a considerable force to overcome.

Laplace Law
For a bubble (2 air-fluid interfaces) airP = 4T/R For a fluid lined alveolus (one airairfluid interface) P = 2T/R P = pressure (cmH20) T = surface tension, CONSTANT (without surfactant) R = radius As P 1/R then R P And there would be a tendency for small alveoli to collapse and empty into larger alveoli The lung would be unstable

Surfactant
Composition:
Phospholipid 90% (Dipalmitoyl Phophatidylcholine DPPC) (Dipalmitoyl 10% protein

Produced:
Type 2 Alveolar epithelial cells

Function
Reduce Ts in alveoli
lung recoil and work of breathing

Stabilise alveoli of different sizes

Prevent emptying of small alveoli into large alveoli

Prevent pulmonary oedema via decrease transudation

Compliance of Lung and Chest Wall

1/CT = 1/CL + 1/CCW Compliance of lung and chest wall are both 200 mL/cmH2O 1/200 + 1/200 = 1/100 The total lung and chest wall compliance is 100 mL/cmH2O

Determinants of Compliance
Lung Factors
Decrease Compliance (Stiff lungs)
Pulmonary fibrosis Pulmonary/alveolar oedema Increased blood in lungs 2nd increase pulm venous pressure (LVF, MR etc) Increased Surface tension loss of surfactant (premature,drowning) ARDS

Chest Wall Factors

Decrease Compliance (stiff chest wall) Bone disorders RA Deformity kyphosis, scoliosis kyphosis, Burns Diaphragmatic paralysis Increased intraabdominal pressure (obesity, pregnancy, pneumoperitoneum, ascites, pneumoperitoneum, ascites, peritonitis) Position supine, prone, trendelenburg

Increased Compliance
Emphysema destruction of parenchyma decreased surface area and decreased elastic tissue

Regional Variation in Lung Ventilation

In an erect subject the ventilation at the bases is greater than the apices.
The base has a lower resting volume so a larger change in volume It has a better compliance

The weight of the lung requires that to support it the pressure below needs to be higher than that above. The intrapleural pressure at the apices (-10 cmH2O) and at (the base (-2 cmH2O) (-

Regional Variation in Lung Ventilation

Basal Alveoli
Intrapleural Pressure = -2cmH20 Resting volume is low On steep part of V-P curve and hence is very Vcompliant and expands more per unit pressure change than the apex

Alveoli at Apex
More negative resting expanding pressure = 10cmH20 Resting Volume high On flat part of V-P slope, low compliance Vhence increase in volume per unit pressure is less than base and hence its proportion of alveolar ventilation is less. Note: with position change the weight and ventilation redistributes to the dependent side

Time Constants of the Lung

A lung unit can be considered as an airway with the alveoli it supplies The resistance and compliance of a lung unit affect the rate of air flow into and out of the unit and the time to filling/emptying of that unit. A higher resistance airway will fill/empty slower A lower compliance (stiffer) unit will fill quicker And Vice-Versa ViceThe time-dependent filling/emptying of a lung unit can be expressed by its TIME timeCONSTANT = RC R: Resistance C: Compliance And is used to describe the rate of change of an Exponential Process TC = the time it would take to complete the process if it continued at its original rate An exponential process (eg flow of gas into lung unit) is 95% complete after 3 Time Constants

Time Constants of Lung Units

For normal lung tissue Resistance = 2cmH20/L/sec Total Compliance = 100ml/cmH20 Which gives a Time Constant of 0.2 seconds Therefore 95% of filling/emptying is complete in 0.6 seconds

SLOW ALVEOLI
Resistance length of TC Compliance TC

(slower filling/emptying)

FAST ALVEOLI
R TC C TC

(faster filling/emptying)

The presence of lung units with different time constants means that gas flow can still occur between units at the end of insp/exp when there is not gas flow at the mouth It also means that regional ventilation depends on RR with RR leading to ventilation of the long TC lung units as a percentage of Tidal Volume.

Gas Flows
Physics of Gas Flow For gas to flow a pressure difference must exist The pressure difference required to achieve a certain flow is dependent on the type of flow
Laminar Turbulent Transitional

For Laminar flow driving pressure is proportional to flow P = kV (where k is a constant) For Turbulent flow driving pressure is proportional to flow squared P = kV2

Poiseuilles Law
Describes Laminar gas flow in a straight circular tube Volume flow rate = V= P r4 -----------8 l P = driving pressure r = radius = viscosity l = length

Most significant factor is the radius! and from Ohms Law as: Resistance (R) = Driving pressure / Flow = P / V Then 8l Resistance = R = -----------r4

Turbulent or Laminar?
Reynolds Number : density d: diameter : velocity : viscosity Re < 1000 consider laminar Re > 1500 (>2000) almost entirely turbulent

Laminar Smooth, cylindrical rigid tubes Occurs at low flows Fast moving central spike with decreasing velocity from axis to edge Density is less important Pressure is proportion to flow

Turbulent Not Smooth, cylindrical rigid tubes Usually occur at fast flow rate No high axial flow velocity Density is important Pressure is proportional to flow squared

Where in Bronchial Tree does Laminar and turbulent flow occur

Bronchial tree is a rapidly branching system and turbulence occurs at branch points

True Laminar Flow

Only in very small airways Here Re is very low ( approx 1 in terminal airways) Low velocity, low radius (but high combined calibre)

True Turbulent Flow

At trachea Especially with exercise when velocity is high

Transitional Flow
Mixture of laminar and turbulent Most airways Evidence of this by decreased resistance with Helium Hence driving pressure (P) is determined by flow rate and its square

P = k1 V + k2 V 2

Respiratory Resistance
Airway resistance Tissue resistance Inertia (negligible)

Sites of Airway Resistance (AWR)

From Poiseuilles law one would think most resistance would be at small airways because of tiny radius Most resistance/pressure drop (>80%) is within the first 7 airway generations Airways < 2mm diameter (gen 8+) contribute <20% resistance The large number of small airway therefore a large overall cross sectional area Small airways constitute a silent zone where considerable small airways disease can be present before a measurable resistance

Lung volume and AWR

Like extra-alveolar blood vessels extralung volume radial traction increased calibre resistance Conductance = reciprocal of resistance Airway Conductance V Lung volume a linear Closing Capacity: At very low lung volumes small dependent airways can close completely. Pts with high airway resistance often breath at high lung volumes to help reduce AWR

Factors Influencing Airway Resistance

Radius of airway
Intramural: secretions, foreign bodies, oedema or intra-luminal lesions intraMural: Smooth muscle tone Cholinergic: ACh Adrenergic: beta 2 receptors Non-adrenergic Non cholinergic VIP, SP and Neurokinin A NonExtramural: Compression by tumours, tension pneumothorax, dynamic airway compression during forced expiration.

Lung Volume Anatomical site

Highest resistance bronchi due to the small cross sectional area. Turbulent Laminar Transitional

Types of Flow

Measurement of Airway Resistance

AWR = pressure difference Mouth Alveoli flow rate Mouth pressure and flow rate are easily measured Alveolar pressure can be measure by 1. Deduction from measurement by a whole body plethysmograph using Boyles Law P1V1 = P2V2 = K 2. Estimated from oesophageal pressure during normal breathing

Work of Breathing
Work = Pressure * Volume (joules) During normal tidal breathing the inspiratory muscles do all work and expiration is passive. Inspiratory muscles do work against 1. Frictional Forces (airway and tissue resistance) 35% of work, lost as heat 2. Elastic Forces 65%, stored as potential energy During Expiration the inspiratory muscles relax, elastic materials return to their original length and release stored potential energy which is used to overcome frictional airway and tissue forces and lost as heat. Normal Value of WOB = 3 watts= 3joules/min, 3ml of 02

Diagram of intrapleural pressure change during inspiration and expiration of normal tidal breath from FRC.

Area (1) = work against Elastic Forces, stored as potential E ( increased work with TV or if low lung compliance (high elastance)) Area (2) = work against non-elastic nonforces (airway and tissue resistance) lost as heat ( with faster flow rates/RR or AWR) Total Work of Breathing (WOB) = sum of elastic and non-elastic nonwork Area (3) = Expiration, work against nonnon-elastic forces, lost as heat

How to Minimise WOB

Work = Pressure * Volume To minimise work aim to reduce pressure to achieve a certain volume Increase compliance = volume change per unit pressure change Minimise resistance = pressure change per unit flow Breathing from FRC maintains lung on steep part of compliance curve Control RR RR flow/velocity resistance WOB (non(nonelastic) RR and TV advantageous in obstructive lung disease as minimises frictional work and increases stored potential, also maximises alveolar ventilation as % of MV and decreases dead space. In Restrictive Lung disease (low complaince/stiff lung) RR (small rapid breaths) minimises WOB the majority of which is from elastic work. From Poiseuilles law and Reynolds no. multiple ways of minimising AWR and hence WOB

The End