Presented by:

Dr. Md. Zareer Tafadar

Post Graduate Resident

Deptt. Of Anaesthesiology & Critical Care

Silchar Medical College & Hospital.

Compliance Resistance & Work Of

Breathing

INTRODUCTIONMechanics Of Respiration

• Inspiration occurs when the alveolar

pressure < atmospheric pressure, and may

be due to,

– lowering alveolar pressure below

atmospheric pressure →negative

pressure respiration

– raising atmospheric pressure above

alveolar → positive pressure

respiration

• Expiration occurs when the alveolar

pressure > atmospheric pressure

Normal Breathing

• Commences with active contraction of inspiratory muscles, which,

a. enlarges the thorax

b. lowers intrathoracic and intrapleural pressures

c. enlarges alveoli, bronchioles, bronchi

d. lowers the alveolar pressure below atmospheric pressure

• Air flows from mouth and nose to alveoli

• Inspiratory muscles provide the force necessary to overcome,

a. elastic recoil of the lungs and chest wall

b. frictional resistance

i. caused by deformation of lung tissue and thoracic cage → tissue resistance

ii. to air flow in the conducting airways → airway resistance

Resistance To Breathing

1. Elastic Resistance ~ 65%

2. Non-elastic resistance ~ 35%

i. Airflow ~ 80%

ii. Viscous ~ 20%

Elastic Resistance to Breathing

Elastic Recoil of the Lungs

• The tendency of elastic lung tissue to recoil from the chest wall results in a

sub-atmospheric intrapleural pressure.

• At FRC, the mean intrapleural pressure ~ 4-5 cmH20 sub-atmospheric

• The intrapleural pressure is normally estimated by an oesophageal balloon

catheter

• This is more accurate in measuring changes rather than absolute pressure,

due to interference from the weight of the heart

Compliance

Definition: The ability of the lungs to expand is expressed using a measure known as the lung

compliance. Lung compliance is the volume change per unit pressure change.

It is represented as C = ΔV/ΔP

Static Compliance

• It is the relationship between volume change of lung and the transpulmonary pressure change,

i.e. airway - intrapleural pressure change, measured under known static conditions (zero

airflow)

• Reflects the elastic resistance of the lung and chest wall.

• Given by CST = Corrected Vt/ (Plateau Pressure- PEEP)

• The normal value for a 70 kg adult ~ 200 ml/cmH20

• The value decreases as lung volume increases, due to the limitations of the non-elastic

components of the lung/chest wall system.

Measurement Of Static Compliance

• The patient takes a breath from a spirometer and holds it until the transpulmonary pressure

difference becomes stable

• This is repeated with different tidal volumes to produce a pressure/volume curve, where

Compliance = the slope of the pressure/volume curve

• This can also be done with the patient apnoeic using PPV

• The patient is inflated with known volumes of gas and the transpulmonary pressure change

determined at equilibrium. This is taken as the mouth - oesophageal balloon gradient.

Factors Affecting Static Compliance

1. Lung Volume - the bigger the lungs the larger the compliance.

2. Pulmonary Blood Volume: pulmonary venous congestion from any cause will

decrease the compliance

3. Age:

4. Restriction Of Chest Expansion: Causes only temporary changes in compliance

5. Recent Ventilatory History

6. Disease

Dynamic Compliance

• Airflow is zero at the point of flow reversal during the normal respiratory cycle.

Measurements of lung compliance made using these points reflect dynamic compliance.

• Reflects the airway resistance as well as elastic properties of the lung and chest wall.

• Given by CDYN = Corrected Vt/ (Plateau Pressure- PEEP)

• In normal lungs at low and moderate frequencies, dynamic and static lung compliance are

about the same value

• However, at higher frequencies in normal lungs, and at normal frequencies in abnormal lungs,

dynamic compliance is less than static compliance. This is due to incomplete filling of alveoli

in the time available.

Measurement of Dynamic Compliance

• Taken from the slope of the transpulmonary pressure/volume loops recorded during tidal

ventilation.

• Using a differential pressure transducer, from an oesophageal balloon to the airway.

• Pneumotachograph: the pneumotachograph measures instantaneous flow, however, this

may be electronically integrated over time to give volume

• Thus, the pressure difference at the no flow points of the P/V loop can be established.

Factors Affecting Dynamic Compliance

• Decreased dynamic lung compliance is seen especially with increased airways resistance, eg.

asthma, chronic bronchitis and emphysema

• Emphysema increases specific lung compliance but decreases dynamic compliance as the

respiratory frequency increases, as slower alveoli fail to fill.

Low Compliance• The volume change per unit pressure change is low. The lungs are stiff and are resistant to

expansion

• The patient has low lung volumes and low minute ventilation.

Clinical conditions that decrease lung compliance

Type Of Compliance Clinical Condition

Static Compliance Atelectasis

ARDS

Tension Pneumothorax

Obesity

Retained Secretions

Dynamic Compliance Bronchospasm

Kinking of ET Tube

Airway Obstruction

High Compliance

• Volume change is large per unit pressure change.

• In extreme high compliance situations the exhalation is incomplete due to lack of

elastic recoil of the lungs.

• Usually seen in conditions that increase the patients FRC. Patients have obstructive

lung defect, airflow obstruction, incomplete exhalation and poor gas exchange.

• Emphysema is one such condition where there is destruction of lung tissues,

enlargement of terminal and respiratory bronchioles leading to air trapping and

consequent impairment in gaseous exchange.

Lung Compliance and Elastance

• Elastance, is the reciprocal of compliance, i.e. the pressure change that is required to elicit a

unit volume change. This is a measure of the resistance of a system to expand.

• Elastance = 1/Compliance = Pressure change / Volume change

• Elastance is a measure of the work that has to be exerted by the muscles of inspiration to

expand the lungs. An increased elastance needs to be counteracted by an increased power of

the muscles of inspiration, leading to an increased work of breathing (work of breathing is the

physical work that have to be carried out by the muscles of respiration to overcome the elastic

resistance of the respiratory system and the non-elastic resistance of the airways).

Factors Affecting Elastance of the Respiratory System...

• The elastance of the whole respiratory system depends on the elastance of the chest wall and

that of the lungs.

• Since the chest wall and the lungs have a serial relationship, in forming the respiratory

system, the elastance of the whole respiratory system can be calculated by the addition of the

elastance of the chest wall and the lungs. Since the elastance in each of the lungs and the chest

wall is approximately 5 cmH2O, the elastance of the respiratory system is approximately 10

cmH2O.

Elastance of the Respiratory System Depends on the Elastance of the

Lungs...

• Changes in the elastance (and therefore the compliance) of the chest wall

are uncommon. In contrast, the elastance of the lungs is affected by many

respiratory diseases. Thus, variations in the elastance of the respiratory

system are mainly due to alterations of the elastance of the lungs, which is

governed by two main factors:

– Elastic recoil forces of the lung tissue

– Forces Exerted by Surface Tension at the Air-Alveolar Interface

Factors Affecting Elastic Resistance

1. Elastic recoil forces of the lung tissue

• The elastin fibers forming the pulmonary

interstitium resist stretching and exhibit

the property of returning to its original

length, when stretched .

• This accounts for approximately one

fourth to one third of the elastic resistance

of the lungs and holds the responsibility of

generating the recoil forces necessary to

increase the intra-alveolar pressure during

expiration, which is a passive process.

2. Forces Exerted by Surface Tension at the Air-Alveolar

Interface

• This is responsible for the remaining two-thirds to three-

fourths of the elastance of the lungs.

• Since the alveoli are globular structures, having a thin

lining of fluid, which comes into contact with air, the net

surface tension force acts inwards.

• Laplace’s Law

,

• To prevent the alveoli from collapsing, a transmural

pressure should be acting across the alveolar wall. This

pressure, for a single alveolus, is equal to 2 X surface

tension / radius of an alveolus (2T/r).

• Smaller alveoli have greater tendency to collapse

Surfactant and Reduction in Surface

Tension

• Reduction in the surface tension would

lead to a reduction in the

trasnpulmonary pressure that is

required to keep the alveoli expanded.

Thus, this decreases the power that

needs to be generated by the muscles

of inspiration and hence, the work of

breathing.

• The surface tension in the lungs is

reduced by a chemical agent, known

as surfactant composed of a

phospholipid- Di-Palmitoyl

Phosphatidyl Choline, secreted by the

type II alveolar cells in the lungs.

20

Anatomy Of Alveolar Sacs

Most alveoli occur in clusters called

alveolar sacs

Adjacent alveoli are NOT

completely independent

structures—connected by alveolar

pores (allows equilibrium of

pressure)

They share adjacent walls, so they

are “interdependent,” that is, they

depend on the expansion (inflation)

of neighboring alveoli to help them

inflate

Alveolar Interdependence

• Alveoli are surrounded by other

alveoli and interconnected by

connective tissue.

• If alveolus starts to collapse,

surrounding alveoli are stretched

and they apply expanding forces

on the collapsing alveolus, thereby

help to keep it open, this is called

Alveolar Interdependence.

21

22

Loss of alveolar walls results in

Loss of surface area for diffusion

Loss of interdependence (greater tendency to

collapse = local regions of atelectasis)

Summary of forces acting on the lung to

keep the alveoli open.

23

Elastic Recoil of the Thoracic Cage

• Thoracic cage compliance is calculated from total compliance of the thoracic cage , and from

pulmonary compliance when measured simultaneously, where,

• 1/CTOT = 1/CL + 1/CCW

Normal Values

1. Total thoracic compliance CTOT ~ 0.1 l/cmH20

2. Compliance of lung CL ~ 0.2 l/cmH20

3. Compliance of chest wall CCW ~ 0.2 l/cmH20

Thoracic Cage Compliance Is Decreased In :

a. kyphoscoliosis

b. scleroderma

c. muscle spasticity

d. abdominal distension, obesity - especially when supine

Resistance

Non-Elastic Resistance to Breathing

This is composed of,

a. airway flow resistance ~ 80%

b. pulmonary tissue resistance, or viscous resistance ~ 20%

Airway Resistance

• Definition: It is the pressure that is required to overcome the resistance to gas flow through

the airways during respiration.

Normal value for a healthy adult ~ 0.5-1.5 cmH20/l/s

Types of Flow Patterns

Laminar Flow

• Below critical flows, gas proceeds through a straight tube as a series of concentric cylinders

that slide over one another. Fully developed flow has a parabolic profile with a velocity of

zero at the cylinder wall and a maximum velocity at the center of the advancing “cone.”

• Peripheral cylinders tend to be stationary, and the central cylinder moves fastest.The

advancing conical front means that some fresh gas reaches the end of the tube before the tube

has been completely filled with fresh gas.

• A clinical implication of laminar flow in the airways is that significant alveolar ventilation

can occur even when the tidal volume ( Vt) is less than anatomic dead space. This

phenomenon, noted by Rohrer in 1915, is important in high-frequencyventilation.

Hagen-Poiseuille Equation For Gas Flow In a Straight Unbranched Tube

R=( PB – PA) / (8 X Length X Viscosity)/ π (Radius)4

where Pb= Atm. Pr., Pa= Alveolar Pressure, R= flow rate

Turbulent Flow

• High flow rates, particularly through branched or irregularly shaped tubes, disrupt the orderly

flow of laminar gas.

• Turbulent flow usually presents with a square front so fresh gas will not reach the end of the

tube until the amount of gas entering the tube is almost equal to the volume of the tube. Thus,

turbulent flow effectively purges the contents of a tube.

• Four conditions that will change laminar flow to turbulent flow are

– 1) high gas flows,

– 2) sharp angles within the tube,

– 3) branching in the tube,

– 4) change in the tube's diameter.

• During turbulent flow, resistance increases in proportion to the flow rate. Turbulent flow

occurs when there is a net forward flow, but there are many local eddy currents (little

circulations that occur).

• Turbulent flow of air is observed in the upper airways where the radius is larger and the

airflow is more rapid.

Reynolds Number

• The Reynolds number is used as an index to determine whether flow is laminar or turbulent. It

is a unitless number that is defined as:

Re = 2rvd/η,

where r is radius, v is velocity, d is density, and η

is viscosity.

< 2000 - Laminar.

> 4000 - Turbulent.

2000 – 4000 – Both

• According to this equation, turbulent flow is likely if the tube has a large radius, a high velocity, a high density, or a low viscosity

Factors Affecting Airway Resistance:

Poiseuille’s Law : Δ P = V/r4

where P= Pressure required to maintain airflow

V= Volume of airflow

r = Radius of airway

Thus the airway resistance may be increased by any condition where the caliber of the airway

decreases.

• Viscosity and Density of the gas mixture:

• Length, and lumen radius of artificial and patient’s airways: Airway resistance

and lumen radius are exponentially related to the fourth power. Because of this

relationship any small amount of bronchospasm, secretion accumulation, in the

endotracheal tube, water in the ventilator tubing, or other obstruction considerably

increases airway resistance

• Flow rate: The higher the flow, the greater the amount of turbulence and

consequent increase in the airway resistance. Conversely, a slow flow rate

minimizes turbulence and airway resistance.

• Flow pattern: Laminar flow decreases airway resistance whereas turbulent flow

increases it.

• Lung Volume: In general, as lung volume increases, resistance decreases. This is

due to radial traction exerted on the airways. When the volume of the lung

increases, the radius of the conducting airways increases and the result is lower

airway resistance.

• Bronchial Smooth Muscle Activity:

– The contraction of bronchial smooth muscle decreases the airway radius, causing an

increase in airway resistance. Relaxation of the bronchial smooth muscle increases the

airway radius and causes a decrease in airway resistance.

– The tone of bronchial smooth muscle is determined by autonomic input. Adrenergic

stimulation, mainly by norepinephrine acting on β2 receptors and by nitric oxide, causes

bronchial smooth muscle relaxation. Substances such as acetylcholine, histamine, and

prostaglandin F2α cause bronchial smooth muscle contraction.

33

Airway Resistance

0 5 10 15 20

0.00

0.02

0.04

0.06

0.08

0.10

Res

ista

nce

Airway Generation

Terminal bronchiolesSegmental

bronchioles

Midsize airways are normally the source of major resistance

Airway branchings parallel design reduces

the frictional resistance to airflow • Respiratory bronchioles have small

individual radii. Yet the parallel

arrangement of these small airways

results in a large total cross sectional

area creating little resistance to

airflow.

• In airway disease the smaller airways

are the major site of resistance to flow

of air because of a reduction in their

luminal size.

• Clinical Conditions That Increase Airway Resistance

Type Clinical Condition

COPD Emphysema

Chronic Bronchitis

Bronchiectasis

Mechanical Obstruction Post Intubation Obstruction

Foreign Body Aspiration

Endotracheal Tube

Infection Laryngotracheobronchitis

Epiglottitis

Bronchiolitis

Miscellaneous Asthma

Bronchospasm

Effects of Increased Airways Resistance

1. Lung hyper-inflation → increased FRC and residual volume

2. Dyspnoea

3. Decrease in respiratory rate

4. Mechanical disadvantage of respiratory muscles

5. V/Q mismatch

Differential Diagnosis Of Types Of Increased Airway Resistance,

a. Increased airway resistance in expiration only → airway collapse

b. Airway obstruction rapidly reversed by therapy → bronchoconstriction, ±

i. mucosal congestion, oedema

ii. mucus, exudate, etc., in the lumen

Pulmonary Tissue Viscous Resistance

• Due mainly to the movement of pleural layers between lobes, and between the

lungs and chest wall during inspiration & expiration

• Accounts for < 20% of the total non-elastic resistance in health

• Increased in pulmonary fibrosis, carcinomatosis, etc., but rarely to significant or

limiting values.

• Measurements of thoracic cage viscous resistance, rib cage & abdominal contents,

is difficult.

• There is also the inertia of lung/thorax system and the air mass, however, this is

very small.

Work Of Breathing

Definition: It is the work required by the respiratory muscles to overcome the mechanical

impedance to respiration. It is the sum of work requires to overcome both elastic and airflow

resistance.

• There are two categories that the physical work of breathing can be broken down into. One

type is resistance work in which an increase in resistance results in an increase in work.

• Compliance work is the other type of breathing work done. A decrease in compliance of the

lungs requires an increase in work of them.

Airway Resistance & Work of Breathing

• As given in the equation Raw = ΔP/V (Raw = Airway resistance

ΔP = PIP-Pplat

V= Flow )

• The pressure change ΔP, can be treated as the amount of work imposed on the patient.

Thus the work of breathing is directly proportional to the airway resistance and an increase in

the airway resistance increases the work of breathing.

• If the work of breathing remains constant then an increase in the airway resistance will

decrease the flow. In the clinical setting if the patient is unable to overcome the airway

resistanc eby increasing the work of breathing then hypoventilation may result in decrease of

the minute ventilation of the patient.

Compliance & Work of Breathing

• Since compliance is inversely related to pressure change, a decrease in compliance will result

in increase in the work of breathing. In the clinical setting, atelectasis is one of the most

frequent causes of increased work of breathing.

• If the change in pressure remains constant then the decrease in compliance will cause a

decrease in the tidal volume and minute ventilation.

• Thus in low compliance situations such as ARDS the decrease in minute ventilation is

characterized by low tidal volume and high respiratory rates

In summary, the work of breathing can be increased by

– increased airway resistance,

– reduced lung compliance, or

– reduced thorax compliance.

Work of Breathing during Normal Respiration

• During normal quite breathing, respiratory muscles work during inspiration to expand

the lungs, whereas expiration is a passive process.

• Normally lungs are highly compliant and airway resistance is low, so only 3% of total

energy is used by the body during quite breathing.

Clinical Application

Work of breathing may be increased:

1. When pulmonary compliance is decreased.– more work is required to expand the

lung. eg Pulmonary Fibrosis

2. When airway resistance is increased: more work is required to overcome the

resistance. Eg. COAD.

Work of Breathing during Normal Respiration

• During normal quite breathing, respiratory muscles work during inspiration to expand

the lungs, whereas expiration is a passive process.

• Normally lungs are highly compliant and airway resistance is low, so only 3% of total

energy is used by the body during quite breathing.

Clinical Application

Work of breathing may be increased:

1. When pulmonary compliance is decreased.– more work is required to expand the

lung. eg Pulmonary Fibrosis

2. When airway resistance is increased: more work is required to overcome the

resistance. Eg. COAD.

Compliance Diagram of Lungs

The Pressure-Volume Loop

• Since compliance is determined by

ΔV/ΔP, the P-V loop provides useful

information on the characteristics of a

a patients compliance.

• There are 2 different curves according

to different phases of respiration.

• The curves are called :

Inspiratory compliance curve

Expiratory compliance curve

• The total work of breathing of the cycle

is the area contained in the loop.

Triangle APAE

– Represents the amount of

mechanical work to

overcome the compliance

[elastic forces] of the chest

Area ACBPA represents

amount of work to

overcome Raw during

Insp

Triangle APAD represents

amount of work to

overcome Raw during

Exp

The insp area [area w/in

the hysteresis] represents

total WOB due to Raw

15 305

250

500

15 305

A slope is drawn from the beginning point dividing the expiratory and inspiratory limb.

A shift of the slope towards the pressure axis indicates a decrease in compliance

whereas shift towards the volume axis indicates an increase in compliance.

Increased Compliance Decreased Compliance

Example: Emphysema,

Surfactant Therapy

Example: ARDS, CHF,

Atelectasis

500

250

P-V Loop Demonstrating Airway Resistance

15 305

Airway Resistance

•As airway resistance increases, the loop will become wider.An increase in expiratory resistance is

more commonly seen. Increased inspiratory resistance is usually from a kinked ETT or patient

biting.

500

250

When the forward path is different from the reverse path, then this

is referred to as hysteresis. Hysteresis is a common

phenomenon in nature and in the lung. Hysteresis is best

observed when starting with a collapsed lung.

– A : normal Raw & exp

flow

– B : increased Raw &

reduced exp flow

– C : markedly

increased Raw &

reduced exp flow

Assessing Raw Using Flow-Volume Loop

• Exp flow is low &

slow, taking a long

time to rid the lungs

of volume.

• Te is barely

adequate to allow for

lung emptying

before next breath

• This pt may have

COPD or severe

asthma.

Evaluation of Raw Using Waveforms

Anaesthetic Implications

Response to Increased Resistance

• Anaesthetised patients retain a remarkable ability to compensate for increases in airflow

resistance

• Following increases in inspiratory resistance, there is an instantaneous augmentation of the

force of contraction of the diaphragm. This is consistent with muscle spindle activity.

• The time course for this response is such that PaCO2 appears to be the likely mediator

• In combination these allow the anaesthetised patient to compensate for inspiratory loading of

the order of ~ 8.0 cmH2O

• There is even greater ability to compensate for increases in expiratory resistance up to 10

cmH2O there is no activation of the expiratory muscles, awake or anaesthetised.

• The additional work is performed by the inspiratory muscles, shifting the tidal loop further up

the compliance curve, allowing the increased elastic recoil to overcome the increased

resistance.

Effect On Compliance

• Compliance is significantly decreased, with little difference with or without

paralysis.

• The majority of the change occurs in the lung, there being little alteration of

chest wall compliance.

• Pressures ≥ 30 cmH2O inflate the lung to only 70% of the preoperative

total lung capacity. This reduction occurs early in anaesthesia and is not

progressive

• There is no general agreement on a direct effect of anaesthetics on

pulmonary surfactant. Some studies have shown a decreased activity

• Alternative explanations include :

– a. breathing at a reduced lung volume

– b. pulmonary collapse in the dependent regions*

– c. the reduced compliance is a cause of the decreased FRC

Effect On Work of Breathing

• An increase in respiratory muscle loading secondary to an increase in

physiologic and/or imposed WOB results in increased force and duration of

diaphragmatic contraction, increased oxygen consumption and respiratory

muscle fatigue.

• Insertion of an oral airway during spontaneous mask breathing reduces

inspiratory WOB significantly from that without an airway.

• The addition of CPAP significantly reduces WOB, probably because of

“stenting” of the pharyngeal soft tissue, preventing the tissue from being

sucked together by negative intraluminal pressure.

• ETT with a relatively smaller diameter increases flow resistance and the

resistive WOB although Vt is maintained by associated increases in

inspiratory time. LMA exerts much less resistance.