Respiration

Front 1

Function of the nasal septum and the nasal turbinates

Back 1

to clean the air of big dust particles

Front 2

anatomy of airways.

Back 2

From the nose, warmed and moistened air flows through the common passages for air and food, the pharynx, and then continues through the larynx. Air finally reaches the periphery of the lungs via the trachea and bronchi.

The airways consist of a series of tubes that branch and become narrower, shorter and more numerous as they penetrate into the lungs. The trachea divides into 2 main bronchi, each of which divides into lobar and segmental bronchi. The right main bronchus has 3 lobar bronchi (the right lung has 3 lobes), while the left main bronchus divides into only 2 bronchi (the left lung has only 2 lobes). The segmental bronchi divide further into smaller branches. The smallest airways without alveoli are the terminal bronchioles.

Front 3

2 functions of pleural space

Back 3

1. lubrication
2. coupling lungs to chest (most important function).. pull on chest, lungs come with it, lungs open up.. how we breathe

Front 4

Conducting zone and Respiratory zone

Back 4

Conducting zone (no respiration so known as "anatomical dead space"):
-from nose and mouth
-pharynx
-larynx
-trachea
-bronchi
-bronchioles
-terminal bronchioles

Respiratory zone (where we find alveoli)
-Respiratory bronchioles
-Alveolar ducts
-Alveolar sacs

Front 5

4 functions of conducting airways:

Back 5

1. Defense against bacterial infection and foreign particles (mucus and cilia)

2. Warm and moisten air

3. Sound and speech are produced by air passing over the vocal cords

4. Regulation of air flow: smooth muscle around the airways may contract or relax to alter resistance to air flow.

Front 6

Function of the Respiratory Zone

Back 6

The respiratory zone is the site of gas exchange between the air in the alveoli and the blood in the pulmonary capillaries. There are roughly 300 million alveoli in the human lungs, and each alveolus may be associated with as many as 1000 capillaries.

Front 7

Blood Supply to lungs

Back 7

Pulmonary: bringing mixed venous blood (blood that comes from different body organs with different metabolic activities) to the lungs, allowing for the blood to get oxygenated, and then back to the left heart.

Bronchial: supplying oxygenated blood from the systemic circulation to the tracheobronchial tree (this circulation allows for the airways to get oxygenated)

Front 8

3 Alveolar cell types:

Back 8

1. Epithelial type I and II cells: Alveoli are lined by epithelial type I and II cells. Together, all the alveolar epithelial cells form a complete epithelial layer sealed by tight junctions. Little is known about the specific metabolic activities of type I cells. Type II cells produce pulmonary surfactant, a substance that decreases the surface tension of the alveoli.

2. Endothelial cells: Endothelial cells constitute the walls of the pulmonary capillaries. These cells may be as thin as 0.1 micron.

3. Alveolar macrophages: These remove foreign particles that may have escaped the mucociliary defense system of the airways and found their way into the alveoli.

Front 9

Inspiration Muscles:

Back 9

1. Diaphragm (pushes on abdomen, enlarges longitudinal volume of chest, enlarges cross sectional dimension of chest as well)
-innervated by phrenic nerves from cervical segments 3, 4, 5.. cervical nerves 3, 4, 5 keep the diaphragm alive)

2. External intercostals (lift the ribs)

3. Parasternal intercartilaginous muscles (lift the ribs)

Accessory: Sternocleidomastoid and Scalenus

Front 10

Expiration Muscles:

Back 10

NOTE: during respiration at rest, expiration is passive (no muscles)

1. Internal intercostals (depresses ribs)

2. Abdominal muscles (depresses lower ribs, compress abdominal contents)
-rectus abdominis
-external oblique
-internal oblique
-transverse abdominis

Front 11

Summary of events of inspiration:

Back 11

1. Diaphragm and intercostal muscles contract
2. Thoracic cage expands
3. Intrapleural pressure becomes more subatmospheric
4. Transpulmonary pressure increases
5. Lungs Expand
6. Alveolar pressure becomes subatmospheric
7. Air flows into alveoli

Front 12

Summary of events of expiration:

Back 12

1. Diaphragm and external intercostal muscles stop contracting
2. Chest wall moves inwards
3. Intrapleural pressure goes back towards preinspiratory value
4. Transpulmonary pressure goes back towards preinspiratory value
5. Lung recoil towards preinspiratory volume
6. Air in lungs is compressed
7. Alveolar pressure becomes greater than atmospheric pressure
8. Air flows out of the lungs

Front 13

Tidal volume:

Back 13

breathing at rest

Front 14

Residual volume:

Back 14

you can never breathe out all the air in your lungs.. even if you breathe out as hard as you can you will be left with this volume

Front 15

Inspiratory Reserve volume

Back 15

From tidal volume to maximal inspiration

Front 16

Expiratory Reserve volume

Back 16

from tidal volume to maximal voluntary expiration

Front 17

Vital Capacity

Back 17

From residual volume to total lung capacity

Front 18

Inspiratory Capacity

Back 18

From FRC to max inspiration

Front 19

FRC

Back 19

functional residual capacity (amount of air remaining in the lungs after a normal tidal expiration)

*functional residual capacity (the volume where whole respiratory system is in equilibrium, at rest) occurs at the volume where the positive pressure of the lungs wanting to collapse is equal and opposite to the negative pressure of the chest that wants to expand.
(each is about 5 cm H2O)

Front 20

Minute Ventilation

Back 20

The amount of air inspired into the lungs over some period of time is called ventilation. Usually, it is measured for one minute, and therefore we call it minute ventilation (VE). Therefore, VE is the amount of air inspired (or expired) during one minute:

VE = VT x f

where VT is the tidal volume, and f is the number of breaths per minute.

Front 21

Alveolar Ventilation

Back 21

In a normal adult male, VT = 500ml, and f =12 breaths/minute. Therefore, VE = 6000ml/min. However, not all the air inhaled into the lungs reaches the gas exchanging area (the respiratory zone). Some of the air remains in the conducting airways, i.e. in the anatomical dead space (Figure 12). The volume of the anatomical dead space in the adult subject is about 150ml. Thus, the amount of air that reaches the respiratory zone per minute and available for gas exchange, the alveolar ventilation (VA), is: VA= (500-150 ml) x 12= 4200 ml/min.

Front 22

Physiological Dead Space

Back 22

Under some pathological conditions, a certain amount of inspired air, although reaching the respiratory zone, does not take part in gas exchange. In this case, alveoli either receive a decreased blood supply or no blood supply at all. These alveoli represent alveolar dead space. The sum of alveolar and anatomical dead space is called the physiological dead space (VD). Therefore, the difference between minute and alveolar ventilation is the dead space ventilation that is wasted from the gas exchange point of view, i.e. VD=VE – VA, or in terms of volume, VD=VT-VA.

Front 23

Normal Alveolar Ventilation

Back 23

VA matches CO2 and keeps PaCO2 at a constant level

Front 24

Alveolar Hyperventilation

Back 24

This occurs when more O2 is supplied and more CO2 removed than the metabolic rate requires (VE exceeds the needs of the body). As a consequence, alveolar partial pressures of O2 (PACO2) rises and that of CO2 (PACO2) decreases. Note that ventilation has to be considered with respect to the metabolism so ventilation during exercise is not hyperventilation.

Front 25

Alveolar Hypoventilation

Back 25

A fall in the overall level of ventilation can reduce alveolar ventilation below that required by the metabolic activity of the body. Under the condition of alveolar hypoventilation, the rate at which O2 is added to alveolar gas, and the rate at which CO2 is eliminated, is lowered, so that the alveolar partial pressure of O2 (PAO2) falls and PACO2 rises. As a result of this, the blood in the pulmonary capillary is less oxygenated, and PaO2 falls below normal values. Similarly, PaCO2 rises above the normal value. Alveolar hypoventilation may occur during severe disorders of the lungs (e.g. chronic obstructive lung disease), or when there is damage to the respiratory muscles. It can also occur when the chest cage is injured and the lungs collapse, or when the central nervous system is depressed.

Front 26

3 factors that affect diffusion rate

Back 26

directly proportional to surface area
directly proportional to pressure difference
inversely proportional to thickness

Front 27

How can we explain how O2 and CO2 diffusion rates are the same despite the much greater difference in pressure of O2 compares to CO2?

Back 27

CO2 diffuses more readily than O2 (about 20x more)

Front 28

Transit Time

Back 28

Although the transit time of blood through the pulmonary capillaries is only 0.75 seconds at rest, diffusion is so rapid that the PO2 of the air and that of the blood reach equilibrium before the blood has passed even half way along the pulmonary capillary. During the transit time, blood in the capillaries is in contact with the air in the alveoli. Diffusion of the gases occurs along the pressure gradient. In a normal lung, diffusion of both O2 and CO2 is accomplished within 1/3 of the red blood cell transit time. Therefore, in a resting person with an impaired rate of diffusion (e.g. a patient with pulmonary edema) PO2 and PCO2 may be normal (because CO2 and O2 may still be able to diffuse during the transit time). However, when blood flow increases in this person and the transit time consequently becomes shorter (e.g. during exercise), arterial PO2 may decrease and arterial PCO2 may increase.

Front 29

Pulmonary Blood Pressure

Back 29

Systole: 25mmHg
Diastole: 8mmHg

Front 30

Vascular Resistance (difference between pulmonary and systemic)

Back 30

Blood flow depends on vascular pressure and resistance, i.e. flow=pressure/resistance. There is a total pressure drop from pulmonary artery to left atrium of about 10 mm Hg, compared to ~100mmHg for the systemic artery to right atrium. Therefore, the pulmonary resistance is only 1/10 that of the systemic circulation. The low vascular resistance in the pulmonary circulation relies on the thin walls of the vascular system. The low vascular resistance and high compliance of the pulmonary circulation allows the lung to accept the whole cardiac output at all times.

Front 31

2 ways of accommodating increased blood flow without an increase in arterial pressure:

Back 31

1. Distention: increasing the caliber of already open blood vessels

2. Recruitment: opening previously closed blood vessels

Front 32

Effects of drugs on pulmonary blood vessels

Back 32

-Serotonin, histamine, and norepinephrine: cause contraction of smooth muscles which increases resistance

-acetylcholine and isoproteranol: relax smooth muscles which decreases resistance

*Nitric oxide produced by endothelial cells relaxes vascular smooth muscle leading to vasodilation.

Front 33

Effects of gravity on pulmonary blood flow:

Back 33

Pulmonary blood flow is affected by gravity and it differs with body posture. In the upright position, blood flow increases almost linearly from top to bottom of the lungs. The vessels are more distended toward the bottom of the lungs because gravity increases vascular pressure. Near the top of the lungs, the pulmonary capillaries may be completely compressed if alveolar pressure is greater than blood pressure in the capillaries.

-Top: pulmonary arterial pressure< alveolar pressure, so the capillaries are compressed. Occurs only in cases of low arterial pressure or positive ventilation.

-Middle: pulmonary arterial pressure> alveolar pressure > venous pressure. So the flow depends only on the difference between arterial and alveolar pressures.

-Bottom: pulmonary arterial pressure> venous pressure> alveolar pressure. So the flow depends on the arterio-venous pressure difference.

Front 34

Effects of lung volume on pulmonary vascular resistance

Back 34

-Above FRC, the alveolar vessels are stretched longitudinally and thus, their diameter decrease leading to an increase in vascular resistance.

-Below FRC, the extra-alveolar vessels collapse because they are not stretched by the pulmonary tissues.

*resistance is lowest at FRC

Front 35

Effects of gravity on ventilation

Back 35

Gravity also affects the distribution of ventilation. In an upright lung at rest, in normal gravity, the alveoli at the top of the lungs are more opened than the bottom ones (think of a “Slinky” held in normal gravity). Therefore, during breathing the alveoli from the bottom of the lungs are opened wider than those at the top, i.e. preferential ventilation of the bottom of the lungs.

Front 36

Is the effect of gravity greater on ventilation or blood flow?

Back 36

blood flow

Front 37

O2 physically dissolved in plasma

Back 37

Because O2 is relatively insoluble in H2O, the amount of O2 dissolved in blood is very small, and linearly proportional to PO2. In 100 ml of plasma, there is 0.3 ml of O2 (i.e. 0.3 volume %) when equilibrated with PO2 of 100 mm Hg. O2 consumption (VO2) by the body cells, even at rest, is much greater than what can be supplied from the amount dissolved in blood. At rest, O2 is about 300 ml O2/min. Therefore, if O2 were only found in plasma, the tissue demand for O2 would never be met.

Front 38

O2 bound to hemoglobin

Back 38

the total amount of O2 bound to Hb is 19.5 vol. %

(Note that the O2 that is bound to Hb does not contribute to the PO2 of the blood. Only molecules physically dissolved in the blood plasma are responsible for PO2. However, the PO2 of the plasma does determine the amount of O2 that combines with Hb)

Front 39

The O2 disassociation curve

Back 39

The HbO2 dissociation curve determines the amount of O2 carried by Hb for a given partial pressure of O2. The curve is flat at high values of PO2 (at alveolar levels of PO2) and steep at low values of PO2 (at peripheral tissue levels of PO2). The implications of this are as follows: at high values of PO2, the amount of O2 bound to Hb, or HbO2, stays roughly constant, when alveolar PO2 drops by 20 mmHg, from 100 mmHg to 80 mmHg. PO2 has to drop to 60 mmHg in order for HbO2 to drop significantly.

At low values of PO2, as seen in the peripheral tissues, a small drop in PO2 unloads the O2 from Hb to the tissue. The fact that HbO2 dissociates into Hb and O2 more readily at lower PO2 values is of crucial importance: at the tissue level, PO2 may get as low as 1-3 mmHg. A drop in PO2, for example, from 40 to 20 mmHg results in a decrease in %HbO2 from about 75% to 35%. (Compare this to a drop in PO2 from 100 to 80 mmHg, where % HbO2 changes by less than 3 %!) This takes place at the tissue level, where metabolic processes need O2. This is an important mechanism that operates automatically in matching tissue O2 supply to tissue O2 need.

Front 40

The Bohr Effect (effect of HbO2 dissociation curve)

Back 40

The Bohr Effect is the shift of the HbO2 dissociation curve to the right when blood CO2 or temperature increases, or blood pH decreases.

* Therefore, you can disassociate HbO2 at higher PO2 (you can get more oxygen without having a very low concentration)

when we exercise, we increase our CO2 and acid production and generate heat. The curve shifting to the right means that for a given drop in PO2, an additional amount of O2 is released from Hb to the working tissues. The same effect is seen when 2,3-diphosphoglycerate (2,3-DPG), an end product of red blood cell metabolism, increases. 2,3-DPG levels may increase during chronic hypoxia (due to high altitude or lung disease).

A decrease in temperature, an increase in pH, and a decrease in CO2 have the opposite effect on the dissociation curve, shifting it to the left. Keep in mind that all of these factors, however, have little effect on the total amount of O2 combined with Hb above 80 mm Hg.

Front 41

Carbon monoxide poisoning:

Back 41

-CO has an extremely high affinity for the O2 binding sites in hemoglobin (210-fold).

-Therefore it reduces the amount of O2 bound to hemoglobin.

-It also shifts the O2-hemoglobin curve to the left, thus decreasing the unloading of O2 to the tissue.

-In CO poisoning, there is little stimulation to increase ventilation because PaO2 remains normal.

Front 42

CO2 is carried in three forms in the blood:

Back 42

1. Physically dissolved in blood (10%): According to Henry’s Law, CO2 from the tissues diffuses into the plasma where it is physically dissolved.

2. Combined with Hb to form HbCO2 (11%): Contrary to O2 that combines with the heme portion of Hb, CO2 combines with the globin portion; hence there is no competition for binding on Hb.

3. As bicarbonate (79%): CO2 combines with H2O to produce carbonic acid (H2CO3). This reaction is very slow in plasma, but as CO2 diffuses into the erythrocytes, the reaction is aided by the enzyme carbonic anhydrase (CA)

Front 43

The Haldane Effect (Hb transportation of CO2)

Back 43

In the tissue capillaries, Hb free of O2 (the O2 has diffused to the tissues) may combine with H+

*deoxygenated blood will transport more CO2 than oxygenated blood. (b/c when Hb doesn’t have O2 it can bind hydrogen ions, then CO2 will become even more bicarbonate to create more hydrogen to keep equilibrium)

Front 44

Arterial Hypoxia

Back 44

Blood hypoxia refers to deficient blood oxygenation, i.e. low PaO2 and low % Hb saturation. In hypoxic conditions, if PaO2 decreases below 60 mm Hg, O2 content in arterial and venous blood becomes lower than the normal values at sea level.

Front 45

5 causes of hypoxia:

Back 45

1) Inhalation of low PO2 (e.g. at high altitude).

2) Hypoventilation: PaO2 decreases and PaCO2 increases. It means that alveolar ventilation in relation to the metabolic CO2 production is reduced. Hypoventilation occurs due to: diseases affecting the central nervous system, neuromuscular diseases, barbiturates, other drugs and narcotics.

3) Ventilation/perfusion imbalance in the lungs: this occurs when the amount of fresh gas reaching an alveolar region per breath is too little for the blood flow through the capillaries of that region.

4) Shunts of blood across the lungs: venous blood bypasses the gas exchanging region of the lungs and returns to systemic circulation, deoxygenated.

5) O2 diffusion impairment (e.g. thickening of the alveolar-capillary membrane, or pulmonary edema).

Front 46

"The Breaking Point"

Back 46

If you stop ventilation voluntarily, you will find that in spite of your efforts to prevent it, breathing will eventually start again. This occurs because the arterial PCO2 has reached about 50 mm Hg and arterial PO2 has reached about 70 mm Hg, at which point voluntary control is over-ridden. This is called the breaking point. The over-riding of the voluntary control by the automatic control depends upon the information from the receptors sensitive to CO2 and O2 levels (in arterial blood and/or cerebro-spinal fluid).

Front 47

Medulla

Back 47

-contains pacemaker cells

-mainly located in 2 groups:
1. ventral respiratory group that generates the basic rhythm
2. dorsal respiratory group that receives several sensory inputs
-the ventral and the dorsal groups also connect to each other.

*Respiratory neurons in the medulla generate the basic respiratory rhythmicity

Front 48

Pons (upper)

Back 48

-cells located in the rostral (upper) pons “turn-off” inspiration
-this leads to smaller tidal volume and increased breathing frequency
-cutting the pneumotaxic centers causes breathing to become deep and slow (this is the same effect as cutting the vagus nerves which bring afferent info)

Front 49

Pons (lower)

Back 49

Cells located in the lower pons (called the apneustic center) send excitatory impulses to the respiratory groups of the medulla, thus promoting inspiration.

Front 50

What happens if upper pons and vagus nerve are cut?

Back 50

Removing influence of both the upper pons and the vagus nerves causes apneuses (tonic inspiratory activity interrupted by short expirations). This type of breathing is seen in some severe types of brain injury.

Front 51

Chemoreceptors

Back 51

PO2, PCO2, and pH in arterial blood are detected by chemoreceptors. If these pressures or pH are changed, ventilation will also change in attempt to return the gas pressures to their normal values. Information from the chemoreceptors is carried to the respiratory neurons. In turn, the activity of respiratory neurons will increase if PaO2 is too low (less than 60 mm Hg) or PaCO2 is higher than 40 mm Hg. The activity of the respiratory neurons will decrease if PaO2 is higher than 100 mm Hg or PaCO2 is lower than 40 mm Hg.

Front 52

Central Chemoreceptors

Back 52

-Central chemoreceptors are located on the ventral surface of the medulla

-They detect the pH of the cerebrospinal fluid (CSF) surrounding them (PCO2 and pH of the CSF are influenced by those of arterial blood).

-The central chemoreceptors give rise to the main drive to breathe under normal conditions.

Front 53

Peripheral Chemoreceptors:

Back 53

-Peripheral chemoreceptors are mainly sensitive to changes in PO2, but are also stimulated by increased PCO2 and decreased pH.

-They are located in the carotid bodies (i.e. the bifurcation of the common carotid arteries) and in the aortic bodies (next to the ascending aorta). The carotid and aortic bodies are made up of blood vessels, structural supporting tissue, and numerous nerve endings of sensory neurons of the glossopharyngeal (in carotid bodies, IX nerve) and vagus nerves (in aortic bodies, X nerve). The afferent fibers of these receptors project to the dorsal group of respiratory neurons in the medulla.

Front 54

3 types of receptors in the lungs that respond to mechanical stimuli:

Back 54

1) Pulmonary Stretch Receptors;

2) Irritant Receptors;

3) Juxta-capillary or J receptors (C-fibres);

Afferent fibres from all of these receptors travel in the vagus nerves. If the vagus nerve is sectioned, the result is slow, deep breathing.

Front 55

Pulmonary Stretch Receptors:

Back 55

Pulmonary stretch receptors are located in smooth muscles of the trachea down to the terminal bronchioles. They are innervated by large, myelinated fibres, and they discharge in response to distension of the lung. Their activity is sustained as long as the lung is distended. Activity of these receptors phasically increases as lung volume increases during each inspiration.

Front 56

Hering-Breuer Inflation Reflex:

Back 56

decrease in respiratory frequency due to a prolongation of expiratory time. In other words, an increase in lung volume tends to inhibit the beginning of the next inspiratory effort (negative feedback mechanism). The Hering-Breuer reflex is weak in adults unless the tidal volume exceeds 1 L as in exercise, but is noticeable in infants and animals.

Front 57

Irritant Receptors:

Back 57

The irritant receptors are located between airway epithelial cells in the trachea down to the respiratory bronchioles. They are stimulated by noxious gases, cigarette smoke, histamine, cold air, and dust. They are innervated by myelinated fibers, and their stimulation leads to bronchoconstriction and hyperpnea (increased depth of breathing). The irritant receptors may be important in the reflex bronchoconstriction triggered by histamine release during an allergic asthmatic attack.

Front 58

Juxta-Capillary Receptors:

Back 58

The name of these fibres originates from their location in the alveolar walls close to the capillaries. They are innervated by non-myelinated fibres and have short lasting bursts of activity. They are stimulated by an increase in pulmonary interstitial fluid, like what may occur in pulmonary congestion and edema. The reflex effects caused by these receptors include rapid and shallow respiration, although intense stimulation causes apnea. These receptors may play a role in dyspnea (sensation of difficulty in breathing) associated with left heart failure and lung edema or congestion.

Front 59

Transpulmonary Pressure (Pl)

Back 59

Measured from the difference between Palv and Ppl. When there is no air flow, closed nose and mouth, Palv and the pressure measured at the mouth are the same. Thus,

Pl = Palv - Ppl

Front 60

Transrespiratory-system pressure (Prs)

Back 60

Measured as the difference between Palv and Pbs:

Prs = Palv – Pbs

Hence, Prs is the sum of the pressures generated by its two components, lung and chest:
Prs = Pl + Pw

Front 61

Compliance of the lungs:

Back 61

The compliance of the lungs, or chest wall, or total respiratory system, is a parameter that refers to the ease with which each of these structures can be distended. The standard procedure for measuring the respiratory system compliance in humans is to determine the static pressure-volume relationship while lung volume is decreased step by step from TLC

Compliance is expressed as the volume change in the lungs for a unitary change in pressure. The pressure required to maintain a given volume of gas inside the lungs increases as the volume increases. Compliance of the lungs is also altered in diseases such emphysema and fibrosis

Front 62

Fibrosis vs. Emphysema

Back 62

in fibrosis, lungs are stiff, there is a flatter compliance compared to a normal subject.
-restrictive: for a given volume, the flow is always going to be higher

in emphysema, lungs are floppy, for a given pressure change, much bigger change in lung volume (steeper compliance compared to a normal subject). very difficult for these patients to deflate their lungs.
-obstructive: no recoil. the patient is unable to empty their lungs either (can’t generate enough flow). has a lower flow for a given volume

Front 63

Airway Resistance

Back 63

Raw = (Palv - Pao) / Flow

In order to have gas flow through the airways, the pressure at the airway opening (Pao) must be different to that in the alveoli (Palv)

Airway resistance is therefore related to airway caliber and is an important determinant of lung function. In certain diseases (such as asthma) airway resistance can become very high making breathing difficult.

Front 64

Surface Tension

Back 64

Tension arises because the molecules in the surface of the film tend to arrange themselves in the configuration involving the lowest energy. Being more attracted to themselves than to air, they like to “hold hands” rather than freely associate with air molecules. This causes a tension to be generated across the film surface. If the surface is curved, such as on the inside of an alveolus or airway, this tension can produce a pressure.

Front 65

LePlace's Law (surface tension)

Back 65

Alveoli can be modeled to some degree of approximation as being like a collection of soap bubbles. The pressure, P, inside the soap bubble of radius R, resulting from a surface tension T, is given by LaPlace’s Law:

P=4T/R

This equation shows that the pressure inside a small bubble is greater than that inside a large bubble

Front 66

Pulmonary Surfactant

Back 66

The soap bubble analogy suggests that small alveoli should collapse into large ones. This means that the gas exchanging regions of the lung is unstable. However, alveolar collapse is prevented from happening by a substance called pulmonary surfactant, secreted by alveolar type II cells. Pulmonary surfactant has 2 principal roles:

1) Making the surface tension inside the alveoli change with the lung volume in a way that prevents the pressure inside the small alveoli from exceeding that of the large alveoli. (Surfactant has biophysical properties that allow it to decrease the surface tension to a greater extent in the smaller than in the larger alveoli, thereby stabilizing the lungs).

2) Reducing overall surface tension so that we are able to breathe. If the surface tension in the liquid lining layer was equal to that of water, we simply would not be able to inflate our lungs.

Front 67

How does breathing change with exercise?

Back 67

-both tidal volume and frequency increase
-tidal volume only increases to a point however, and frequency can keep increasing
-peak expiratory flow rate increases more than peak inspiratory flow rate

Front 68

Minute ventilation vs. metabolic rate during exercise:

Back 68

In both untrained and trained subjects, minute ventilation (VE) increases linearly with metabolic rate (VO2) up to about 50% to 65% of VO2 max. Thereafter, VE increases at a rate disproportionately greater than the change in VO2. Note that an effect of endurance training is to delay the ventilatory inflection point (Tvent).

Front 69

Is Ventilation a limiting factor in aerobic performance at sea level? (VE/Q)

Back 69

No, ventilation does not limit aerobic performance because you can increase ventilation 35 fold from resting ventilation whereas you can only increase cardiac output 5-6 fold from rest.

Also there is an enormous surface area so there is a large capacity for gas exchange.

Front 70

The Central Chemoreceptors During Exercise

Back 70

During exercise, there is an alkalotic (↑pH) response in the medullary ECF. This decreases the ventilatory response. Therefore, the role of the central chemoreceptors is important at rest but not so much during exercise.

Front 71

The Peripheral Chemoreceptors During Exercise

Back 71

-PaO2 remains rather constant during exercise. Therefore the increase in ventilation cannot come from the stimulation of the peripheral chemoreceptors by changes in O2.

-PaCO2 is often seen to decrease during exercise. Therefore the increase in ventilation cannot come from the stimulation of the peripheral chemoreceptors by CO2.

-However, during exercise, arterial pH does decrease (lactic acid) and PaO2 fluctuates subtly with arterial pulse waves. Therefore, it is possible that during exercise, these fluctuations in PaO2 increase the sensitivity of the peripheral chemoreceptors to CO2 and H+.

Front 72

Peripheral Mechanoreceptors during Exercise

Back 72

-The pulmonary mechanoreceptors, the muscle spindles, the Golgi tendons, and the skeletal joint receptors were thought to play a role in the increase in VE during exercise.

-Stimulation of these mechanoreceptors does produce an increase in VE, but it is small compared to the large and abrupt increases observed during exercise.

Front 73

Control of breathing before and after exercise:

Back 73

-VE is known to start increasing even before the exercise has started. This control is thought to be neural. A similar control is thought to operate at the end of exercise because a very rapid decrease in VE is observed.

-Humoral control is believed to be responsible for the ventilatory response during the exercise event.

Front 74

Asthma:

Back 74

Chronic inflammatory disease of the airways, clinically characterized by airway obstruction, and enhanced airway responsiveness to contractile agonists and/or allergens.

Front 75

Emphysema:

Back 75

Enlargement of the air spaces due to the destruction of the walls of the alveoli. The lungs actually self-destruct, attacked by proteolytic enzymes secreted by leukocytes in response to a variety of factors. The airways tend to collapse because of the loss of radial traction.

Front 76

Fibrosis:

Back 76

Progressive distortion of the alveolar architecture with inflammation and accumulation of fibrotic tissue.