Respiratory System PhysiologyDr. Amjed Hassan lecture 2 · Web viewpressures as gases in the...

Respiratory System PhysiologyDr. Amjed Hassan lecture 2

Compliance of the Respiratory System

Lung Compliance

Lung compliance expresses the dispensability of the lungs, that is, how

easily the lungs expand when trans-pulmonary pressure increases. It is

expressed by the following equation:

C = ΔV/ΔP

where

C = lung compliance

ΔV = increase in lung volume (mL)

ΔP = increase in trans-pulmonary pressure (mm Hg).

– Compliance is inversely related to stiffness.

– Compliance is inversely related to the elastic recoil, or elastance, of the

lung. Recoil causes the lungs to return to their previous volume when

stretching ceases following an increase in trans-pulmonary pressure. It is

mediated by surface tension in the alveoli and by elastic fibers in the

lung connective tissue.

Compliance of the Lung–Chest Wall Combination

Because the lungs and chest wall expand and contract together, the

overall compliance of the respiratory system is that of the lung–chest wall

combination. The compliance of the lung–chest wall combination is

lower than the compliance of the lungs alone or chest wall alone.

– The compliance of the lung–chest wall combination varies with lung

volume. Compliance is highest at the normal resting volume (functional

residual capacity [FRC]) and decreases at both very low and very high

volumes.

– At low volumes, compression of the chest wall reduces compliance.

– At high volumes, the increased stretch of elastic tissues in the lung

parenchyma causes the lungs to get stiffer (less compliant). High trans-

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pulmonary pressure is required to drive this increase in volume, but it is

not responsible for the decrease in compliance.

Changes in lung compliance in disease states

– Lung compliance is decreased in pulmonary fibrosis because the

interstitium surrounding the alveoli becomes infiltrated with inelastic

collagen.

– Lung compliance is increased in emphysema because many small

alveoli are replaced by fewer but larger coalesced air spaces that have less

elastic recoil.

Surface Tension in the Alveoli

Surface tension is due to the cohesive forces between water molecules at

the air–water interface in the alveoli of lungs. It acts to contract the

alveoli and is a major contributor to the force of elastic recoil of the lung.

If there were no opposing force, surface tension would cause the alveoli

to collapse (atelectasis).

However, the collapsing force is opposed by trans-pulmonary pressure,

which is always positive, allowing the alveoli to remain open.

According to the law of Laplace, the trans-pulmonary pressure P (in

dynes/cm2) required to prevent collapse of an alveolus is directly

proportional to surface tension T (in dynes/cm), and inversely

proportional to alveolar radius r (in cm), as expressed by

P = 2T/r

– All alveoli in a given region of the lungs have about the same trans-

pulmonary pressure. If they all had the same surface tension, the Laplace

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relationship predicts that the smaller alveoli would collapse and force

their volume into larger alveoli. However, surface tension is reduced by

pulmonary surfactant, and the reduction is greater in small alveoli than in

larger ones because small alveoli concentrate the surfactant. Thus, the

increased tendency to collapse because of small radius is just balanced by

a greater reduction in surface tension.

Surfactant

Surfactant is a complex substance, consisting of proteins and

phospholipids (mainly dipalmitoyl lecithin), that is produced in type II

pneumocytes. It lines alveoli and lowers surface tension by the same

mechanism as detergents and soaps (i.e., it coats the water surface and

reduces cohesive

interactions between water molecules).

As an extension of its role in lowering surface tension, surfactant also

produces the following effects:

– It increases compliance at all lung volumes, which allows for easier

lung inflation and greatly decreases the work of breathing.

– It reduces the otherwise highly negative pressure in the interstitial

space, which reduces the rate of filtration from pulmonary capillaries.

This assists in maintaining lungs without excessive water.

Failure of surfactant production and/or excessive surfactant breakdown

occurs in neonatal respiratory distress syndrome (RDS).

Effect of Alveolar Radius on the Pressure Caused by Surface

Tension. Note from the preceding formula that the pressure generated as a

result of surface tension in the alveoli is inversely affected by the radius

of the alveolus, which means that the smaller the alveolus, the greater the

alveolar pressure caused by the surface tension. Thus, when the alveoli

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have half the normal radius (50 instead of 100 micrometers), the

pressures noted earlier are doubled. This is especially significant in small

premature babies, many of whom have alveoli with radii less than one

quarter that of an adult person.

Further, surfactant does not normally begin to be secreted into the alveoli

until between the sixth and seventh months of gestation, and in some

cases, even later than that. Therefore, many premature babies have little

or no surfactant in the alveoli when they are born, and their lungs have an

extreme tendency to collapse, sometimes as great as six to eight times

that in a normal adult person. This causes the condition called respiratory

distress syndrome of the newborn. It is fatal if not treated with strong

measures, especially properly applied continuous positive pressure

breathing.

The work of inspiration can be divided into three fractions: (1) that

required to expand the lungs against the lung and chest elastic forces,

called compliance work or elastic work; (2) that required to overcome the

viscosity

of the lung and chest wall structures, called tissue resistance work; and

(3) that required to overcome airway resistance to movement of air into

the lungs, called airway resistance work.

Energy Required for Respiration. During normal quiet respiration, only 3

to 5 per cent of the total energy expended by the body is required for

pulmonary ventilation. But during heavy exercise, the amount of energy

required can increase as much as 50-fold, especially if the person has any

degree of increased airway resistance or decreased pulmonary

compliance. Therefore, one of the major limitations on the intensity of

exercise that can be performed is the person’s ability to provide enough

muscle energy for the respiratory process alone.

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Airflow through the Bronchial Tree

Airflow through the bronchial tree obeys the same principles as blood

flow through blood vessels except that the viscosity of air is much lower

than that of blood. Airflow is related to the driving pressure and the

resistance to flow by

Q = ΔP/R

where Q is airflow (mL/min), ΔP is pressure gradient between the

mouth/nose and alveoli (cm H2O),

and R is airway resistance (cm H2O/mL/min).

– Airflow is directly proportional to the pressure difference between the

mouth/nose and the alveoli and inversely proportional to airway

resistance.

Airway Resistance

Resistance is derived from Poiseuille’s equation as expressed by

R = 8ηL/πr4

where R is airway resistance, r is radius of the airway (cm), η is viscosity

of air, and L is length of the airway.

– Like the circulatory system, the length of the bronchial tree is relatively

constant, as is the viscosity of inspired air. Therefore, any changes in

resistance to airflow are mainly due to changes in the radius of the

airways. Because resistance is inversely proportional to the airway radius

to the fourth power, small changes in diameter cause large changes in

resistance.

– The large airways offer little resistance to airflow. The small airways

individually have high resistance, but their enormous number in parallel

reduces their combined resistance to a small value. Therefore, the sites of

highest resistance in the bronchial tree are normally in the medium

airways.

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Regulation of Airway Resistance. Airway resistance is primarily

regulated by modulation of airway radius by the parasympathetic and

sympathetic nervous systems.

– Parasympathetic nervous system: Vagal stimulation releases

acetylcholine that acts on muscarinic (M3) receptors in the lungs, leading

to bronchoconstriction. This increases the resistance to airflow.

– Sympathetic nervous system: Postganglionic sympathetic nerves release

norepinephrine that act on β2 receptors, leading to broncho-dilation. This

decreases the resistance to airflow

Lung Volumes and Capacities

– Lung volumes are a way to functionally divide volumes of air that

occur during different phases of the breathing cycle (Fig. 12.5). They are

all measured by spirometry, except for residual volume.

They vary with height, sex, and age.

– Lung capacities are the sums of two or more lung volumes.

– Tidal, inspiratory, and expiratory reserve volumes and inspirational and

vital capacities are used in basic pulmonary function tests.

Lung Volumes

– Tidal volume (TV) is the volume of air that moves in or out of the

lungs during one normal, resting inspiration or expiration.

– Inspiratory reserve volume (IRV) is the volume of air that can be

inspired beyond a normal inspiration.

– Expiratory reserve volume (ERV) is the volume of air that can be

expired beyond a normal expiration.

– Residual volume (RV) is the volume of air left in the lungs and

airways after maximal expiration.

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Table 12.1 contains the normal approximate lung volumes and expresses

them as a percentage of total lung capacity (TLC).

Lung Capacities

– Inspirational capacity (IC) is the maximum volume of air that can be

inspired with a deep breath following a normal expiration. It is the sum of

TV and IRV.

– Functional residual capacity (FRC) is the volume of the lungs after

passive expiration with relaxed respiratory muscles. It is the sum of ERV

and RV.

– Vital capacity (VC) or forced vital capacity (FVC): is the maximum

volume of air that can be expired in one breath after deep inspiration. It is

the sum of TV, IRV, and ERV.

– Total lung capacity (TLC) is the total volume of air that can be

contained in the lungs and airways after a deep inspiration. It is the sum

of all four lung volumes: TV, IRV, ERV, and RV.

Note: TLC and FRC cannot be measured by spirometry because residual

volume is needed for their calculation.

Table 12.2 contains the normal lung capacity volumes.

Forced Expiratory Volume (FEV1) is the volume of air that can be

forcibly expired in the first second following a deep breath

It is usually > 70% of the FVC (FEV1/FVC > 70%).

– In obstructive lung disease (e.g., asthma and COPD), FEV1

is reduced proportionally more than FVC; therefore, FEV1 /FVC < 70%.

– In restrictive lung disease (e.g., fibrosis), both FEV1 and FVC are

reduced. This means that FEV1 /FVC is normal or increased.

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Figure: old spirometry technique

Figure: lung volumes and capacities

Dead Space

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Dead space is volume within the bronchial tree that is ventilated but does

not participate in gas exchange.

– Anatomical dead space is the volume of the conducting airways

(pharynx, trachea, and bronchi) that do not contain alveoli and therefore

cannot participate in gas exchange. It is ~150 to 200 mL.

– Physiological dead space is the total volume of the bronchial tree that is

ventilated but does not participate in gas exchange.

Fig. 12.6 Volume exhaled versus time during a forced exhalation.

The total volume exhaled is the forced vital capacity (FVC), and the

volume exhaled in the first second is the forced expiratory volume

(FEV1).

– In healthy lungs, physiological dead space is approximately equal to

anatomical dead space.

However, physiological dead space may be increased in lung diseases

where there are mismatches between ventilation (V) and perfusion

(pulmonary blood flow [Q]).

– Physiological dead space can be calculated using Bohr’s equation.

This calculation assumes that the partial pressure of CO2

(Paco2) in the alveoli is the same as that in systemic arterial blood.

Ventilation Rate

Minute ventilation refers to the total ventilation per minute. It is

expressed as

Minute ventilation = TV × breaths/min

Alveolar ventilation refers to ventilation of alveoli that participate in gas

exchange per minute. It is

expressed as Alveolar ventilation = (TV – physiological dead space) ×

breaths/min.

Distribution of Pulmonary Blood Flow

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When a person is upright, the force of gravity affects the distribution of

pulmonary blood flow within the lungs (but not the total amount of blood

flow) because vascular pressures progressively fall at locations above the

heart. This distribution of blood flow is described in terms of “zones” of

the lung.

Zone 1: Lung Apex. If pulmonary artery pressure is not high enough to

support the column of blood

from the right ventricle all the way to the apices of the lungs, the

uppermost blood vessels collapse, and there is no flow in this region. This

does not normally occur in healthy lungs but may occur if right

ventricular pressure is extremely low (e.g., due to hemorrhage). Also, if

alveolar pressure is

increased to the point where it exceeds vascular pressure, blood vessels

collapse (e.g., due to positive pressure ventilation).

Zone 2: Middle of the Lung. In zone 2, blood flow is intermittent.

Pulmonary artery pressure drives blood flow at its peak during systole,

but not during the rest of the cardiac cycle.

Zone 3: Lung Base. Zone 3 has no gravitational impediment to blood

flow because regions located below the heart always have vascular

pressures greater than alveolar pressure. Therefore, blood flow

is continuous.

Gas Exchange and Transport

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Partial Pressures

In a gas mixture, each gas species exerts a pressure, the partial pressure of

that gas. The sum of the partial pressures of the gases in a mixture equals

the total gas pressure.

Partial pressure for an individual gas = the fraction of that gas in the gas

mixture × total gas pressure Calculation of Partial Pressure of Oxygen

(Po2) in Dry Inspired Air O2 comprises 21% of air; total gas pressure =

760 mm Hg (at sea level)

At high altitude, the Po2 is reduced because barometric pressure is lower.

Correction of Po2 for the Presence of Water Vapor

Dry air entering the lungs becomes completely saturated with water as air

passes through moist airways. This displaces some of the other gases and

slightly reduces their partial pressures.

Partial pressure of water vapor (PH2o) is 47 mm Hg at body temperature.

Total pressure of gases other than water = 760 mm Hg − 47 mm Hg

= 713 mm Hg

Therefore, the Po2 in warm, humidified inspired air is

Gas Exchange

Diffusion of Gases

O2 and carbon dioxide (CO2 ) diffuse between alveolar gas and

pulmonary capillary blood according to standard physical principles

– The total amount moved per unit of time is proportional to the area

available for diffusion and to the difference in partial pressure between

alveolar gas and pulmonary capillary blood, and inversely proportional to

the thickness of the diffusion barrier.

– Gas will diffuse from the alveoli (higher partial pressures) to the

pulmonary capillaries (lower partial pressures) until they equilibrate and

no partial pressure gradient exists. As a result, blood entering the

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pulmonary veins from the pulmonary capillaries has virtually the same

partial

pressures as gases in the alveoli.

– The diffusion barrier, composed of alveolar epithelial cells (type I

pneumocytes) and capillary endothelial cells, is very thin, which ensures

that the diffusion distance between alveolar gas and pulmonary capillary

blood is very short. This allows blood in the pulmonary capillaries to

equilibrate with alveolar gas during the short time (< 1 sec) that the blood

is in the capillaries.

Figure . Ultra structure of the respiratory membrane where diffusion occurs.

Partial Pressure Changes of Oxygen and Carbon Dioxide

Following Gas Exchange

Partial Pressure Changes of Oxygen

– The Po2 of humidified inspired air is 150 mm Hg.

– The Po2 of alveolar air is 100 mm Hg. This is due to the diffusion of

O2

from alveolar air into pulmonary capillary blood.

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– The Po2 of systemic arterial blood is 95 mm Hg. It is almost the same

as the Po2 of alveolar air because the partial pressure of pulmonary

capillary blood equilibrates with alveolar air. However, ~2% of the

cardiac output bypasses the pulmonary circulation, which accounts for the

slight discrepancy in partial pressures.

– The Po2 of venous blood is 40 mm Hg because O2 has diffused from

arterial blood into the tissues.

Partial Pressure Changes of Carbon Dioxide

– The Pco2 of humidified inspired air is almost zero.

– The Pco2 of alveolar air is 40 mm Hg because CO2 from venous blood

entering the pulmonary capillaries diffuses into alveolar air.

– The Pco2 of systemic arterial blood is 40 mm Hg because pulmonary

capillary blood equilibrates with alveolar air.

– The Pco2 of venous blood is 46 mm Hg. It is higher than systemic

arterial blood due to the diffusion of CO2 from the tissues into venous

blood following cellular respiration.

Ventilation and Perfusion Ratios for Optimum Gas Exchange

Ventilation/perfusion ratio is the ratio of alveolar ventilation V to

perfusion (pulmonary blood flow)Q.

– In healthy lungs, the V/Q ratio is close to 1:1, resulting in optimum gas

pressures and oxygenation in systemic arterial blood.

Distribution of V/Q Ratios

There are regional differences in alveolar ventilation and blood flow in

the upright individual.

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– Alveolar ventilation is higher at the base of the lungs than the apices

because the base is more compliant and changes more in volume during

each breathing cycle.

– Blood flow is very low at the apex of the lung and very high at the base

due to the effects of gravity.

The differences in regional blood flow are greater than the differences in

regional ventilation. This creates different V/Q ratios at various levels of

the lung. Typical values are as follows:

– Apex V/Q is ~3:1.

– Middle of lungs (heart level) V/Q is ~1:1.

– Base of lungs V/Q is ~1:2.

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