Compliance Resistance & Work Of Breathing

1. Compliance Resistance & Work Of
Breathing
Presented by:
Dr. Md. Zareer Tafadar
Post Graduate Resident
Deptt. Of Anaesthesiology & Critical Care
Silchar Medical College & Hospital.

2. INTRODUCTION
Mechanics 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

3. 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

4. • 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

5. Resistance To Breathing
1. Elastic Resistance ~ 65%
2. Non-elastic resistance ~ 35%
i. Airflow ~ 80%
ii. Viscous ~ 20%

6. 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

7. 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.

8. 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.

9. 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

10. 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.

11. 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.

12. 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

13. 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.

14. 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).

15. 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.

16. 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

17. 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.

18. 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

19. 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. 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

21. 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. 22
Loss of alveolar walls results in
Loss of surface area for diffusion
Loss of interdependence (greater tendency to
collapse = local regions of atelectasis)

23. Summary of forces acting on the lung to
keep the alveoli open.
23

24. 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

25. 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

26. 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.

27. • 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

28. 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.

29. • 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.

30. 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

31. 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

32. • 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. 33
Airway Resistance
Midsize airways are normally the source of major resistance
Segmental Terminal bronchioles
bronchioles
0 5 10 15 20
0.10
0.08
0.06
0.04
0.02
0.00
Resistance
Airway Generation

34. 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.

35. • 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

36. 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

37. 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.

38. 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.

39. 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.

40. 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.

41. 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.

42. 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.

44. 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

45. 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
5 15 30
500
250
5 15 30
Example: Emphysema,
Surfactant Therapy
Example: ARDS, CHF,
Atelectasis
500
250

46. P-V Loop Demonstrating Airway Resistance
Airway Resistance
5 15 30
500
250
•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.

47. 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.

48. Assessing Raw Using Flow-Volume Loop
– A : normal Raw & exp
flow
– B : increased Raw &
reduced exp flow
– C : markedly
increased Raw &
reduced exp flow

51. Evaluation of Raw Using Waveforms
• 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.

52. 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.

53. 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

54. 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.