The Respiratory System

Chapter 13

. External respiration is the sequence of events involved in the exchange of

O2 and CO2 between the external environment and cells of the body.This includes breathing– the movement of air in & out of the lungsO2 and CO2 are then exchanged between the air in the alveoli and blood

of the pulmonary capillaries. O2 and CO2 are transported by the blood from the lungs to the tissues. These gases are exchanged between the blood & the tissues by diffusion.

Internal respiration refers to the metabolic processes occurring in the mitochondria. O2 is used by tissue cells. CO2 is produced.

The respiratory quotient is the CO2 produced divided by the O2 consumed.

Atmosphere

Tissue cell

Alveoli of lungs

Pulmonarycirculation

Systemiccirculation

CO2O2

Food + O2CO2 + H2O + ATP

O2

CO2

CO2

O2

1External respiration

Breathing --Gas exchange betweenthe atmosphere & (alveoli) in the lungs

Exchange of O2 & CO2

between air in the alveoli and the blood

Transport of O2 &

CO2 between the lungs and the tissuesExchange of O2 &

CO2 between the blood and the tissuesInternal respiration

2

3

4

The term respiration has a broad meaning

The respiratory system also carries out nonrespiratory functions. It provides a route for water & heat elimination. It enhances venous return—respiratory pump. It contributes to the maintenance of normal acid-base

balance—elimates CO2.

It enables various kinds of vocalizations. It defends against inhaled foreign matter. It modifies, activates, and inactivates materials passing

through the circulatory system. Activates angiotensin II Inactivates prostoglandins

Nasalpassages

MouthPharynx

LarynxTrachea

Rightbronchus

Bronchiole

Terminalbronchiole

Terminalbronchiole

Respiratorybronchiole

Alveolar sac

Respiratory airways

conduct air between the

atmosphere

& alveoli.reinforced with rings of cartilage.

Below the trachea, the respiratory tract forms progressively smaller and more numerous airways (bronchi to bronchioles to alveoli).

Terminalbronchiole

Respiratorybronchiole

Branch ofpulmonaryartery

Alveolus

Pores of Kohn

Smoothmuscle

Branch ofpulmonary

vein

Pulmonarycapillaries

Alveolarsac

Cartilage is absent in the bronchioles.

The bronchioles are smooth muscle tubes, capable of changing the airflow through them by dilating & constricting.

Bronchioles can control airflow

The alveoli are thin-walled, inflatable sacsThe alveoli are encircled by pulmonary

capillaries, offering tremendous surface area for gas exchange by diffusion.

Alveolar fluid liningwith pulmonary

surfactant

Type II alveolar cell

Type I alveolar cell

Interstitial fluid

Alveolus

Alveolarmacrophage

Erythrocyte

Pulmonarycapillary

Aveoli are formed by a single layer of flattened Type I alveolar cells.

Type II alveolar cells secretes pulmonary surfactant. This substance

facilitates lung expansion.

Surfactant Surfactant is a complex substance containing phospholipids and a

number of apoproteins. This essential fluid is produced by the Type II alveolar cells, and lines the alveoli and smallest bronchioles. Surfactant reduces surface tension throughout the lung, thereby contributing to its general compliance. It is also important because it stabilizes the alveoli. LaplaceÕs Law tells us that the pressure within a spherical structure with surface tension, such as the alveolus, is inversely proportional to the radius of the sphere (P=4T/r for a sphere with two liquid-gas interfaces, like a soap bubble, and P=2T/r for a sphere with one liquid-gas interface, like an alveolus: P=pressure, T=surface tension, and r=radius). That is, at a constant surface tension, small alveoli will generate bigger pressures within them than will large alveoli. Smaller alveoli would therefore be expected to empty into larger alveoli as lung volume decreases. This does not occur, however, because surfactant differentially reduces surface tension, more at lower volumes and less at higher volumes, leading to alveolar stability and reducing the likelihood of alveolar collapse.

Surfactant is formed relatively late in fetal life; thus premature infants born without adequate amounts experience respiratory distress and may die

Rightlung

Leftlung

Thoracic wall

Diaphragm

Parietal pleura

Visceral pleura

Parietal cavityfilled withintrapleural fluid

The lungs occupy much of the thoracic cavity. Each has several lobes. Lung tissue is highly branched airways, alveoli, pulmonary blood vessels, and large amounts of elastic connective tissue.

A pleural sac separates the lungs from the thoracic wall The pleural cavity is the inside of the pleural sac and is filled with fluid

The diaphragm separates the thoracic cavity from the abdominal cavity.

The diaphragm is used for breathing.

Vacuum760 mm

Mercury (Hg)

Pressure exerted byatmospheric air aboveEarth’s surface

Pressure is measured in

mm of mercury.

Atmospheric pressure760 mm Hg

Intra-alveolar pressure 760 mm

Hg

Intrapleural pressure

Airw

ays

Thoracic wall

Plural wall

Lungs

756 mm Hg

There are several pressures inside & outside the lungs.

Atmospheric pressure (760 mm of Hg at sea level) is produced by the weight of the air on the Earth.

Atm Pressure ~ = Intra-alveolar (intrapulmonary) pressure

Intrapleural pressure is in the intrapleural cavity.

It has a slight vacuum compared to normal atm pressure & averages 756 mm Hg at rest.

The lungs stretch to fill the large thorax due, in part, to: intrapleural fluid’s cohesiveness. transmural pressure pushes the lungs outward.

760

760 760

Collapsed lung

760

760

756

760

Puncture woundin chest wall

760 760

Traumatic pneumothorax

760

756

756

760

760 760

Spontaneous pneumothorax

760

756

760

756

Hole in lung

Changes in the intra-alveolar pressure produces the flow of air into and out of the lungs.

If pressure in the lungs is less than atmospheric pressure, air enters the lungs.

If the opposite occurs, air exits from the lungs.

Volume = 1/2Pressure = 2

Volume = 1Pressure = 1

Volume = 2Pressure = 1/2

Piston

Closed container with a given number of gas molecules

Boyle’s law states an inverse relationship between the pressure exerted by a quantity of gas and its volume.

Assuming temperature remains constant.

Equilibrated;no net movement of air

760

756

Before inspiratio

n

759

754

During inspiration

760

761

756

During expiration

760760

Inspiration & expiration are dependent on changing the size of the the thorax:

Increasing throcic volume

Decreasing throcic volume

Inspiration Expiration

Atmpressure

Intra-alveolarpressure

Intrapluralpressure

Transmural pressuregradient across thelung wall

Intra-Aveolar and Intrapleural Pressures

Inspiration begins with the contraction of the respiratory muscles:

The diaphragm (phrenic nerve) & the external intercostal muscles account for 75 % of the enlargement of the thoracic cavity during quiet respiration

The lungs expand to fill the expanded space.

This increase in volume lowers the intra-alveolar pressure drawing in air under atmospheric pressure.

Accessorymuscles ofInspiration:

Musclesof activeexpiration

Majormuscles ofinspiration

Sternocleido-mastoidScalenes

Externalintercostalmuscles

Diaphragm

Internalintercostalmuscles

Abdominalmuscles

Externalintercostalmuscles(relaxed)

Contractions of external intercostal muscles causes elevation of ribs, which increases side-to-side dimension of thoracic cavity

Lowering of diaphragm on contraction increases verticaldimension of thoracic cavity

Elevation of ribs causes sternum

to move upward and outward, which increases front-to

back dimension of thoracic cavity

Before inspirationInspiration

Elevatedrib cage

Contractionof externalintercostalmuscles

Sternum

Diaphragm(relaxed)

Contractionof diaphragm

The onset of expiration begins with the relaxation of the inspiratory muscles.Relaxation of the diaphragm and the muscles of the chest wall,

plus the elastic recoil of the alveoli, decrease the size of the chest cavity.

The intrapleural pressure increases and the lungs are compressed. The intra-alveolar pressure increases. When it increases to a level above atmospheric pressure, air is

driven out - an expiration. Forced expiration can occur by the contraction of expiratory

muscles. These skeletal muscles are ones in the abdominal wall and the

internal intercostal muscles. Their contraction further increases the pressure gradient between

the alveoli & the atmosphere.

Relaxation of external intercostalmuscles

Return of diaphragm, ribs, and sternum to resting position on relaxation of inspiratory muscles restores thoracic cavity to preinspiratory size

Contractions of abdominal muscles cause diaphragm tobe pushed upward, further reducing vertical dimension of thoracic cavity

Contraction of internal intercostal

muscles flattens ribs & sternum, further reducing side-

to-side and front to-back dimensions of

thoracic cavity

Passive expiration

Active expiration

Contractionof internalintercostalmuscles

Relaxation ofdiaphragm

Contractionof diaphragm

Position of relaxedabdominal muscles

Airway resistance in the respiratory tract influences the rate of airflow.

F = P/R where P is the difference

between the atmospheric and intra-alveolar pressures. The greater the difference the greater the flow

However, if the resistance (R) increases, the airflow is decreased (inversely proportional).

The autonomic nervous system control of bronchiolar dialation is the major determinant of resistance Sympathetic stimulation and epinephrine from the

adrenal medula cause bronchodilation.

Airway resistance is increased abnormally with chronic obstructive pulmonary disease.

760

756

756

756

756

760.5

761

760

786 786

786 791 786

788

786

Expiration is more difficult than inspiration. Chronic bronchitis involves long-term

inflammationAsthma involves muscle spams and/or

inflammationEmphysema is the collapse of the alveoli.760

770

770

770

770

772

775

760

772775

772

774

772

769

786

772 772

The lungs have elastic behavior.The lungs have elastic recoil, rebounding if they are

stretched. Compliance is the effort required to stretch or distend

the lungs. A thin balloon is more compliant than a thick balloon

A highly-compliant lung stretches further for a given increase in pressure than a lung with less compliance.

Pulmonary elastic behavior depends on the pulmonary elastic behavior and alveolar surface tension.

Numerous factors decrease lung compliance.

The work of breathing normally requires 3% of total energy expenditure. Factors such as a decrease

of pulmonary compliance and an increase in airway resistance can increase this percentage.

During each quiet breathing cycle, about 500 ml of air is inspired and expired. The lungs do not completely empty about each expiration.

Surface tension

H2O

An alveolus

This tension is determined by the thin liquid film that lines the outside of each alveolus.

This film allows the alveolus to resist expansion.

This film also squeezes the alveolus, producing recoil.

A coating of pulmonary surfactant prevents the alveoli from collapsing from this surface tension.

Insufficient pulmonary surfactant can produce newborn respiratory distress syndrome.

Aveoli are interconnected.

Thus aveoli must expand & contract as a unit.

Interconnectedalveoli

Alveolus startsto collapse

Collapsing alveolus pulled open

Airways

Alveoli

Pulmonary surfactantmolecule

Airways

Alveoli

Surfactant equalizes

the inward pressure

differences in between

large & small aveoli

created by surface tension

Variations in lung volume

Total lung capacityat maximum inflation

Variation in lungwith normal,quiet breathing

Minimal lung volume(residual volume) atmaximum deflation

Normal expiration(average 2,200 ml)

normal inspiration(average 2,200 ml)

Avg. 500 ml

Figure 13.19bPage 477

TV = Tidal volume (500ml)IRV = Inspiratory reserve volume (3,000 ml)IC = Inspiratory capacity (3,500 ml)ERV = Expiratory reserve volume (1,000 ml)RV = Residual volume (1,200 ml)FRC = Functional residual capacity (2,200 ml)VC = Vital capacity (4,500 ml)TLC = Total lung capacity (5,700 ml)

Time Time (sec)

Lung volumes and capacities can be measured by a spirometer.

Spirogram

Floating drum

AirWater

Expiredair

Inspired air

Figure 13.22aPage 479

Obstructive lung disease

Figure 13.22bPage 479

Restrictive lung disease

Normal totallung capacity

“Old” alveolar air that has exchanged O2 and CO2 with the blood

Fresh atmospheric air that has not exchangedO2 and CO2 with the blood

150

During expiration

350

150

500 ml “old” alveolar airexpired

Fresh airfrom inspiration

150dead space

volume (150 ml)

After inspiration,before expiration

Alveolar air

150

350

150

During inspiration

Alveolar ventilation is less because of the anatomic dead space.

Pulmonary ventilation is the tidal volume x respiratory rate.Due to dead space:alveolar ventilation =

(tidal volume - dead space volume) x respiratory rate

Breathing patterns (e.g., deep and slow) can affect alveolar ventilation.

An alveolar dead space also exists, but it is usually small.

There are local controls on the smooth muscle of the airways.

An accumulation of CO2 in the alveoli decreases airway resistance.

An increase of O2 in the alveoli causes pulmonary vasodilation.

It causes vasoconstricion of pulmonary arterioles

Gas exchange occurs by partial pressure gradients. The exchange of O2 and CO2 as the pulmonary and tissue

capillaries is by simple diffusion. Air is a mixture of gases. The partial pressure of each gas depends on its percentage in the

total atmospheric pressure. For example, nitrogen is 79% of the air. Its partial pressure is 0.79 x 760 = 600.4

A partial pressure gradient is established when there are two partial pressures for a gas in different regions of the body.

For example the partial pressure of O2 is greater in the alveoli (e.g., 100) diffuses down its partial pressure gradient towards into the blood of the pulmonary capillaries where the pressure is 40

Composition andpartial pressure inatmospheric air

Totalatmosphericpressure= 760 mm Hg

79% N2

Partial pressureN2 = 600 mm Hg

21% O2

Partial pressureO2 = 160 mm Hg

Partial pressure of N2

in atmospheric air:PN2 = 760 mm Hg X 0.79

= 600 mm Hg

Partial pressure of O2

in atmospheric air:PO2 = 760 mm Hg X 0.21

= 160 mm Hg

Across pulmonarycapillaries:O2 partial pressure gradientfrom alveoli toblood = 60 mm Hg(100 –> 40)

O2 partial pressure gradient from blood toalveoli = 6 mm Hg(46 –> 40)

Across pulmonary capillaries:O2 partial pressure gradientfrom blood to alveoli = 6 mm Hg(46 –> 40)

O2 partial pressure gradient from tissue cell to blood = 6 mm Hg (46 –> 40)

Inspiration

Expiration

Pulmonarycirculation

Systemiccirculation

Alveoli

Diffusion gradientsfor O2 & CO2

betweenthe lungs & tissues

Tissuecell

Atmospheric air

Area in which blood flow (perfusion)is greater than airflow (ventilation)

Helpsbalance

Helpsbalance

Small airflow

CO2 in area

Relaxation of local-airwaysmooth muscle

Dilation of local airways

Airway resistance

Airflow

O2 in area

Contraction of local pulmonary smooth muscle

Constriction of blood vessels

Vascular resistance

Blood flow

Large bloodflow

Area in which blood flow (ventilation)is greater than blood (perfusion)

Helpsbalance

HelpsbalanceLarge airflow

Small blood flow

CO2 in area

Contraction of local airway smooth muscle

Constriction of local-airway

Airway resistance

Airflow

O2 in area

Relaxation of local pulmonary smooth muscle

Dilation of local blood vessels

Vascular resistance

Blood flow

The partial pressures for O2 & CO2 in the pulmonary capillaries equilibrate with the partial pressures for these gases in the alveoli by simple diffusion,.The greater the partial pressure gradients between

the alveoli and the blood, the greater the rate of transfer for the gases.

The blood passing through the lungs gains O2 and eliminates some of its CO2.

This blood passes through the left side of the heart and enters the systemic circulation. It arrives at the tissues with the same gas content (e.g., 100 for O2 and 40 for CO2) established at lung equilibration.

Other factors contributing to the pressure gradient affect the rate of gas transfer.As surface area increases the diffusion rate increases.

The alveoli collectively offer a tremendous surface area. Increased pulmonary blood pressure, from an increased

cardiac output, increases the area. The walls of the alveoli and pulmonary capillaries are thin for

rapid gas transfer. Pulmonary edema, pulmonary fibrosis, and pneumonia

thicken the barriers for gas exchange. Gas exchange is also directly proportional to the diffusion

coefficient for a gas. This coefficient is twenty times as great for CO2 compared to

O2, as CO2 is more soluble.

Gas exchange across systemic capillaries also occurs down partial pressure gradients.The O2 in the systemic capillaries has a high partial pressure (100) compared to tissue cells (40). O2 diffuses into the tissue cells (100 40).

The partial pressure for CO2 in the systemic capillaries is low (40) compared to the tissue cells (46). CO2 diffuses into the blood (46 40).

Having equilibrated with the tissue cells, the blood leaving the systemic capillaries is low in O2 & high in CO2.

This blood is then pumped by the right side of the heart to the lungs.

At in the lungs, the blood acquires O2 & releases CO2.

Most O2 in the blood is transported by binding with hemoglobin.Hemoglobin combines with O2 to form oxyhemoglobin. This is a reversible process, favored to form

oxyhemoglobin in the lungs. Hemoglobin tends to combine with O2 as O2 diffuses

from the alveoli into the pulmonary capillaries. A small percentage of O2 is dissolved in the plasma.The dissociation of oxyhemoglobin into hemoglobin

and free molecules of O2 occurs at the tissue cells. The reaction is favored in this direction as O2 leaves

the systemic capillaries and enters tissue cells.

Alveoli

Pulmonarycapillary blood

= O2 molecule

= Partially saturated hemoglobin molecules

= Fully saturated hemoglobin molecules

Hemoglobin increases the concentation gradient of O2 in pulmonary capillaries.

The partial pressure of O2 is the main factor determining the % hemoglobin saturation. The plateau part of the curve is where the partial pressure of O2 is high (lungs).

The steep part of the curve exists at the systemic capillaries, where hemoglobin unloads O2 to the tissue cells.

Average restingPO2 at

systemiccapillaries

Normal PO2

at pulmonarycapillaries

Hemoglobin saturation curve

Hemoglobin promotes the net transfer of O2 at both the alveolar and tissue levels.There is a net diffusion of O2 from the alveoli to the blood.

This occurs continuously until hemoglobin is as saturated as possible (97.5% at 100 mm of Hg).

At the tissue cells hemoglobin rapidly delivers O2 into the blood plasma and on to the tissue cells. Increases in CO2 & acidity increase unloading

This shift of the curve to the right (more dissociation) is called the Bohr effect.

Increased temperature as well as BPG also produces this shift.

Hemoglobin has more affinity for carbon monoxide compared to O2.

Figure 13.30Page 491

Arterial PCO2 & acidity,normal body temperature(as at pulmonary level)

PCO2 Acid (H+)

Temperatureor2,3-Bisphosphoglycerate

(from normal tissue levels)

Most CO2 (about 60%) is transported as the bicarbonate ion. 30% of the CO2 is bound to hemoglobin in the blood. This is another means of transport.Haldane effect increases the ability of hemoglobin to bind

with CO2.About 10% of the transported CO2 is dissolved in the plasma. 60% of CO2 is transported as carbonic acid which is formed by

carbonic anhydrase from CO2 & H20 Carbonic acid dissociates into H+ & bicarbonate ions This process is reversible and CO2 is reformed in the in the

lungs.The chloride shift Erythrocytes passively transport

bicarbonate ions out of the cell & Cl- in.

CO2 transport

Tissue cell Alveolus

Plasma

From systemiccirculationto pulmonary

circulation

The DRG has inspiratory neurons that signal to the inspiratory muscles.

The VRG activate inspiratory & expiratory muscles for exercise .

Pre-Botzinger complex apperas to contro rhythm

The apneustic center in the pons prevents increases depth of breathing –keeps inspiratory muscles active.

The pneumotaxic center has final say and limits depth of inhalation.

Respiratory centers in the brain stem establish a rhythmic breathing pattern.

The Hering-Breuer reflexstretch receptors in the lungs are activated when the lungs inflate with air from an inspiration.

Effects of hyperventilation and hypoventilation on arterial PO2 & PCO2

Hypoventilation Hyperventilation

Normal alveolarand arterial PO2

Normal alveolarand arterial PCO2

PCO2

PO2

Output from the DRG goes through the phrenic nerve to the diaphagm

Input from other areas–some excitatory, some inhibitory

Inspiratory neuronsin DRG(rhythmically firing)

Phrenic nerve DiaphragmSpinal cord

Medulla

The magnitude of ventilation is adjusted in response to three chemical factors.

Carotid sinus

Carotid bodies

Aortic bodies

Heart

Peripheral and central chemoreceptors detect chemical changes in the blood & signal the medulla to change respiratory rate

Respiratory rate increases by: Primary CO2-generated hydrogen ions in the brain

are normally the primary regulators of ventilation. Secondary A decrease in the partial pressure of

arterial O2 or an increase in the partial pressure of arterial CO2 or in hydrogen ions in the blood also can increase the breathing rate.

These responses keep the partial pressure of O2 and CO2 remarkably constant.

A very low partial pressure of O2 in the blood depresses the respiratory center.

Arterial PCO2Relieves

Brain ECF PCO2

Brain ECF H+

CentralChemo-

receptors

Medullaryrespiratory

center

Ventilation

Arterial PCO2

PeripheralChemo-

receptors

Weakly

Brain ECF when arterial PCO2>70-80

mm Hg

Low levels of O2 can trigger increased external respiration

Arterial PO2 <60 mm Hg

Emergencylife-saving

mechanism

Medullaryrespiratory

center

Ventilation

Arterial PO2

Centralchemoreceptors

Peripheralchemoreceptors

Noeffect

on

Relieves

Figure 13.38Page 5O2

Acidosis Arterial non-CO2-H+

PeripheralChemo-receptors

Medullaryrespiratorycenter

CentralChemo-receptors

Cannot penetrateblood-brain barrier

No effecton

Ventilation

Arterial PCO2

Arterial -CO2-H+

Relieves

Other factors on the control of respiratory rate include:Measuring O2 concentrations is not useful since most O2 is

bound to hemoglobinBy default the C02 concentrations are more reliable

Adjustments of H+ concentrations are a rapid mechanism for controlling blood pH.

Removal of CO2 from the lungs increases blood pH Exercise significantly increases ventilation, but the

mechanisms are not clear. Factors such as increased body temperature and epinephrine release may contribute.

Ventilation can be influenced by factors unrelated to gas exchange such as protective reflexes and pain.

Respiratory failures During apnea there is a transient interruption of

ventilation. Most common during REM sleep In respiratory arrest it does not continue.

Results in sudden infant death syndromeNeuronal controls are often not well developed

During dyspnea there is “shortness of breath.” It often accompanies other conditions such as

pulmonary edema with congestive heart failure. Is not directly linked to a physical shortness of breath