PHYSIO B Respiratory

Question 1

Why is intrapleural pressure negative?

Answer 1

IP is about 756 mmHg so approx -4 mmHg. It is negative bc of the elasticity of the lungs, surface tension and the elasticity of the chest wall. These three factors are tempting to increase thoracic volume and bc of boyle law, increase volume means decrease of pressure. So in other word the increase of thoracic volume means the decrease of IP pressure.

Question 2

What are the transpulmonary and transthoracic pressure?

Answer 2

TP is given by the intrapulmonary p - the IP pressure, it is 760 - (-4) which give +4 mmHg. It is significant that it is positive bc so the lungs are able to inflate.

TTP is given by IP - atmospheric pressure, -4 - 0 which gives -4 which means that naturally since it is negative it wants to deflate.

Question 3

What muscles are involved in inspiration and what happens to the interpleural pressure?

Answer 3

The external costal muscles pull the ribs upward and outward, the diaphragm expands downward pulling on the parietal pleura. This pulling increases the volume therefore the pressure decreases. From about -4 mmHg in a resting condition in becomes about -6 mmHg.

Question 4

What happens to the intrapulmonary pressure during inspiration?

Answer 4

As the thoracic cavity expands so does the lung. The volume increases therefore the pressure decreases. So from 0 mmHg goes to -1 mmHg.

Question 5

Why does air flow inside the lungs?

Answer 5

The intrapulmonary pressure at inspiration is about -1 mmHg, the air will flow inside until the IP pressure is equal to the Patm. So the IP pressure will eventually reach 760 mmHg.

Question 6

What accessory muscles are used during forced inspiration?

Answer 6

Other than the external intercostal and the diaphragm muscle, we use the sternal cleidomastoid, the scalenes and the pectoralis minor.

Question 7

How does exhalation work?

Answer 7

In the medulla the ventral respiratory group which send neurons down to the spinal cord. Other neurons then innervate the external intercostal and the diaphragm. Stretch receptors on the muscles if they detect stretching can inhibit the VGR. So the muscles relax and allow their elasticity to pull them back.

Question 8

How does the pulmonary pressure change during exhalation?

Answer 8

The pressure actually surpasses 760 mmHg by 1 mmHg. Therefore the air flows out in atm until the pressure is equalized.

Question 9

What muscles does forced exhalation use?

Answer 9

Normal exhalation doesn’t use muscles. In forced exhalation the abdominal wall muscles like the external and internal oblique. Also the internal intercostals, which are depressing, so they pull the ribs downwards and inwards forcing even more air out.

Question 10

What is the formula of gas flow?

Answer 10

Gas flow is equal to delta P divided resistance, R.

Question 11

How does pressure and resistance affect gas flow?

Answer 11

Pressure is directly proportional to gas flow. Therefore the higher difference of pressure there is between the lungs and the atm the more flow there will be.
Resistance is inversely proportional to gas flow. Therefore if the smooth muscle cells around bronchioles for example dilates the resistance decreases and the air flow increases.

Question 12

What are the two types of alveolar cells?

Answer 12

Type I pneumocytes: are important in gas exchange, squamous like, more abundant.
Type II pneumocytes: are important for secretion of surfactant, cuboidal shape and less abundant.

Question 13

How does surface tension work?

Answer 13

The water molecules in the alveoli can react with each other but don’t want to react with the gases. So the net vector of movement is downwards towards the alveoli membrane, this causes the layer to become thinner. The thinning the layer causes the alveoli to shrink and eventually collapse.

Question 14

How is the collapsing pressure of the alveoli calculated?

Answer 14

The collapsing pressure is given by 2 x Tension divided by the radius. If the surface tension increases the collapsing pressure of the alveoli. If you decrease the tension the collapsing pressure decreases. In other words surface tension and collapsing pressure are proportional.

Question 15

How does the radius affect the collapsing pressure?

Answer 15

If the radius of a bronchiole is partially clogged by mucous for example the alveoli consequently is hypoventilated. In this case since the radius is smaller the collapsing pressure increases. In other words the radius and the collapsing pressure are inversely proportional.

Question 16

What are alveolar pores?

Answer 16

Also know as the pores of Kohn are pores that connect alveoli to each other. It is significant when for example an alveoli is hypoventilated, a normally ventilated alveoli can send gas to the poorly ventilated alveoli compensating.

Question 17

What is surfactant?

Answer 17

It is a lipid protein complex. 90% lipids and the rest proteins. The head of the surfactant molecule is hydrophilic and the tail is hydrophobic. Proteins attached like albumin, Iga and surfactant proteins which are apoproteins.

Question 18

How is surfactant made and how is it secreted?

Answer 18

Type II pneumocytes store the surfactant in globules called lamellar bodies. When it is pushed out it is called tubular myelin which is a strand made of many surfactant molecules. The hydrophilic heads interact with the water molecules while the tail tries to pull away since it is hydrophobic. This causes and upward pulling force decreases surface tension.

Question 19

What is compliance? Why is it different from elasticity?

Answer 19

It is defined as the change in volume over the changing pressure. It is a measure of stretch ability. It is how easy it is to stretch something. While elasticity is the ability to resist stretch.

Question 20

What affects compliance?

Answer 20

Elasticity of the lungs, the surface tension and the elasticity of the chest wall. The lungs are very compliant but have just the right amount of elasticity to recoil, for example in pulmonary fibrosis the tissue is less willing to expand so less compliant but more elastic since it resists stretch. Same thing but inverse if the compliance is abnormally high it is easy to expand but harder to exhale since the elasticity and the ability to recoil is decreases.

Question 21

What are the main pulmonary volumes?

Answer 21

Tidal volume: in resting conditions average of 500 ml.

Inspiratory reserve volume: extra volume above the tidal volume which is about 3L.

Expiratory reserve volume: maximum volume that can be expired below tidal volume which is about 1.1L.

Residual volume: volume that remains in lung even after a forced expiration which is about 1.2L.

Question 22

What is the Laplace equation?

Answer 22

It describes the relationship between the pressure within the alveoli and the surface tension. When we inspire we increase the radius of the alveoli and therefore surface tension is working against the alveoli. During expiration surface tension is less relevant since the radius is decreasing. The equation is P=KL/TS x r

Question 23

What is alveolar interdependence?

Answer 23

If an alveolus is collapsing the force is being counterbalanced by the elastic retraction force of the neighboring alveoli.

Question 24

What are the areas of perfusion of the lungs?

Answer 24

Zone 1: apex, worse perfused area, it is possible to have complete absence of flow.

Zone 2: intermediate area, there is flow but reduced.

Zone 3: better perfused area, vessels are full of blood.

Question 25

What is ventilation and perfusion? And what is their ratio?

Answer 25

Ventilation is the amount of air going in and out contributing to gas exchange.

Perfusion is the amount of blood going through pulmonary capillaries. In other words the cardiac output.

Their ratio V/P.

Question 26

What is alveolar ventilation rate and what is the formula?

Answer 26

Alveolar ventilation rate is equal to the tidal volume minus the dead space, times the respiration rate. So 500ml - 150 ml times 12.

Question 27

How can high oxygen and low CO2 partial pressures affect ventilation and perfusion? What does the body do to compensate?

Answer 27

If V/P is higher than normal, so higher than 0.8, the partial pressure of O is higher and CO2 lower. The O in the blood stimulates the production of nitric oxide in the smooth muscle cells of the pulmonary capillaries which cause vaso dilation, thus increasing the perfusion. This helps bring back the V/P ratio back to normal.

Question 28

How can low oxygen and high CO2 partial pressure affect ventilation and perfusion? What does the body do to compensate?

Answer 28

If we have poor ventilation the V/P ratio is under 0.8 and the partial pressure of O is low and CO2 partial pressure is high. There is going to be a decrease in nitrous oxide production due to the low levels of O. This initiates vaso constriction lowering perfusion and bringing the V/P ratio back to normal.

Question 29

What happens to the ventilation and perfusion if the cardiac output is higher than normal?

Answer 29

An increase cardiac output increases perfusion therefore increasing the amount of oxygen moving into the blood and the amount of CO2 moving in the alveoli. The increase of CO2 partial pressure acts on the smooth muscle cells of the bronchiole tubes causing dilation decreasing resistance and thus increasing flow, so more oxygen can enter and more CO2 can leave.

Question 30

What happens to the ventilation and perfusion if the cardiac output is lower than normal?

Answer 30

For example a pulmonary embolism can decrease perfusion in the pulmonary capillaries. The gas exchange is minimal, very little oxygen moving in the blood and very little CO2 moving in the alveoli. The low partial pressure of CO2 causes the constriction of the bronchiole tube redirecting the air flow to a normally perfused and ventilated alveoli.

Question 31

How does a thick or thin respiratory membrane affect gas exchange, ventilation and perfusion?

Answer 31

Thick membrane due to for example left heart failure creates a longer distance for gases to travel. This causes abnormal gas exchange.
A thin membrane causes an increase in gas exchange so partial pressure of O is high and CO2 low can cause alcolosis.

Question 32

What is alpha 1 antitrypsin?

Answer 32

It is a molecule produced by the lung which inhibits elastase from breaking down elastic molecules in the alveoli. This can cause emphysema.

Question 33

What is the partial pressure of oxygen and CO2 in the atmosphere and in the alveoli?

Answer 33

Oxygen:160 mmHg in the atmosphere and 104 mmHg in the alveoli.
CO2: 40 mmHg in the alveoli.

Question 34

What is the partial pressure of oxygen and CO2 in the blood coming from the pulmonary artery?

Answer 34

The partial pressure of oxygen in the blood vessels is about 40 mmHg in normal conditions. The partial pressure of CO2 is about 45 mmHg.

Question 35

How does solubility affect gas exchange? How soluble are oxygen and CO2 and why is it important?

Answer 35

Henrys law states that the solubility of a gas is dependent upon the rate constant multiplied by the pressure. The solubility of CO2 is twenty time more soluble than oxygen. So even though the partial pressure of oxygen is much higher than CO2, the rate of exchange is compensated by the higher solubility of CO2.

Question 36

How is CO2 transported in the blood?

Answer 36

20% of it is attached to the globin chains of hemoglobin and it is called carboaminohemoglobin, 70% is in bicarbonate form and the rest is free in the blood plasma.

Question 37

What is deoxyhemoglobin and what is it bound to?

Answer 37

It is hemoglobin in deoxygenated blood. It is bound to very little oxygen, a lot of CO2, protons and 2,3 BPG which helps stabilize it.

Question 38

What is the concept of positive cooperatability?

Answer 38

As oxygen binds hemoglobin, the pockets of hemoglobin get progressively bigger making it easier for the next oxygen molecule to bind.

Question 39

What happens after hemoglobin binds to oxygen?

Answer 39

As oxygen binds to hemoglobin it changes its shape too let go of certain molecules like 2,3 BPG, CO2 and protons.

Question 40

Hoe does the CO2 in form of bicarbonate move in the alveoli?

Answer 40

The bicarbonate enters the RBC letting out Cl- to balance it. The bicarbonate then binds to the protons that hemoglobin previously had and produce carbonic acid. Carbonic acid then disassociates in CO2 and water. Carbonic anhydrase speeds up this process. The CO2 then can go in the alveoli.

Question 41

What is oxyhemoglobin?

Answer 41

It is hemoglobin what is bound to oxygen and has released CO2. It is in the R state and has high affinity to oxygen.

Question 42

What does slow replacement of alveolar gas mean?

Answer 42

Every new breathing cycle there is not a complete replacement of new air. In each cycle some air is left behind, this is called Residual Capacity and is about 2.3 L. This all means that multiple breaths are needed to completely replace the alveolar air. In normal conditions it takes about 20 seconds to remove half of the air.

Question 43

What is hypercapnia? What is hypocapnia?

Answer 43

Hypercapnia: It is an increase in arterial partial pressure of CO2 bc of impaired alveolar ventilation.

Hypocapnia: It is a decrease in arterial partial pressure of CO2 bc of alveolar hyperventilation.

Question 44

What is dead space?

Answer 44

It is a space that affects alveolar ventilation bc such space filled with air doesn’t participate in gas exchange. There are two types: anatomical dead space and physiological dead space. The first is the volume trapped inside the conduction airways, and the latter is the volume that doesn’t participate bc of other reasons like bad ventilation and perfusion. 30% of total volume.

Question 45

What is the Haldane effect?

Answer 45

It is the opposite of the Bohr effect and says that binding of oxygen to hemoglobin in the lungs tends to displace CO2 from the blood.

Question 46

Why is carbon monoxide very dangerous?

Answer 46

CO is a toxic product coming form the incomplete burning of organic compounds. It is odorless and doesn’t alter oxygen partial pressure. It has 200 times greater affinity for hemoglobin than oxygen, this means that a very small amount of CO can saturate all available hemoglobin.

Question 47

What is the pneumotaxic center?

Answer 47

It is located dorsally in the superior portion of the pons. Mainly controls rate and depth of breathing by sending impulses to DRG.
Its primary effect is the adjustment of the breakpoint of the ramp inspiratory signal (it controls the shutdown of the respiratory ramp).
It can limit the duration of inhalation and thus increase the respiratory rate (the more active it is, the shorter the ramp duration).
Its activity can increase the frequency up to 30-40 breathing acts per minute.

Question 48

What is an anatomical shunt?

Answer 48

It is a part of circulation that bypasses the alveolus, causing a mixture of oxygenated and deoxygenated blood. This can cause hypoxemia. It doesn’t increase the PaCO2 bc chemoreceptors feel the increase in CO2 and modulate ventilation accordingly.

Question 49

What is the apneustic center?

Answer 49

It is located in the of medulla. Signals directed to DRG. It inhibits or
delay the interruption of ramp signal, so the opposite of pneumotaxic. When it is activated it sends signals to the DRG and causes the immediate interruption of ramp signal, blocking the inspiration phase.
Threshold of activation: lung volume exceeds 1.5L (three times the tidal volume).
It is a defensive mechanism, necessary to avoid the overfilling of the lungs.

Question 50

What is the Dorsal Respiratory Group (DRG)?

Answer 50

It is located in the dorsal portion of the medulla. It mainly
controls inspiration.Most of its neurons are located within the tractum solitarium. Other neurons are located in the reticular substance of the medulla. It integrates signals from the periphery and send outputs to primary respiratory muscles.
It generates RAMP SIGNALS —> not instantaneous, but progressive increase of action potential (slope). There is a constant increase in the frequency. It lastsfor about 2sec (normal breathing), then it stops for 3sec. The trigger that goes to inspiratory muscles is only to start the inspiration. Expiration is only due to elastic recoil of the system.
To increase the frequency it would be sufficient to increase the slope or decrease the time of expiration by stopping earlier the signal.

Question 51

What is the Ventral Respiratory Group (VRG)?

Answer 51

It is located in the ventrolateral part of the medulla. It modulates the expiratory phase. It is anterior and lateral to the dorsal respiratory group. Neurons located in this group are inactive during normal breathing in DRG.Some neurons in this group generate inhalation while others exhalation. This center contributes to both phases of breathing.
It is important in sending powerful exhaling signals to the abdominal muscles during forced exhalation. Active for example during heavy exercise.

Question 52

What is the Hering-Breuer respiratory flex?

Answer 52

It is a defensible reflex triggered when the volume of air increases above threshold which is around 1.5 L so 3 times the normal tidal volume.
The mechanoreceptors detect the increase of stretch and signal the respiratory centers to signal themselves to stop the RAMP signal in order to inhibit further inhalation.

Question 53

What do chemoreceptors do if there is high PaCO2 in the blood?

Answer 53

The formation of carbonic acid from the CO2 and water leads to the disassociation of bicarbonate and H+. This stimulates the central chemoreceptors, its then going to stimulate the DRG or the pneumaxic, telling the body to exhale by stimulating the respiratory muscles.

Question 54

What do chemoreceptors do if the PaCO2 is significantly low?

Answer 54

This will cause a significant decrease in the disassociation of carbonic acid therefore less H+. The stimuli to the central chemoreceptors and to the DRG and VRG are going to significantly decrease. This will cause a slower rate of contraction of muscles thus decreasing the ventilation. Since the ventilation is decrease we are retaining more CO2, stabilizing the normal respiration rate.

Question 55

Where are the peripheral chemoreceptors located?

Answer 55

They are located beneath the bifurcation of the left and right ICA into the ECA and ICA. They are called the Carotid bodies.
Other peripheral chemoreceptors are found under the aortic arch and they are called Aortic bodies.

Question 56

What do the peripheral chemoreceptors respond to?

Answer 56

Respond to the PaCO2, PaO and to the pH. The most significant one is the O2, if its Pa is under 60 mmHg.

Question 57

What are the two cells in the carotid or aortic bodies?

Answer 57

Sustenacular cell and Glomus cell.

Question 58

What do we find in the glomus cells? What do they do?

Answer 58

There are vesicles of neurotransmitters specifically dopamine. We also have specialized potassium channels that can be sensitive to O and protons. If we have very low O levels, high CO2 and pH low it will stimulate the K channels. If the K levels rise in the cell they open Ca channels letting Ca inside causing the fusion of the dopamine vesicles to the membrane thus releasing the dopamine. This causes the stimuli of certain nerve endings, if in the carotid body it will stimulate C.N IX aka glossopharyngeal, if in the Aortic body … C.N X aka vagus. They takes these signals to the DRG therefore stimulating the muscles thus more ventilation.

Question 59

What happens to the metabolic acids that stimulate the glomus cells since they cannot be exhaled?

Answer 59

The kidneys would intervene by urinating out the metabolic acids, and bring more bicarbonate in the blood stream.

Question 60

What are the immersion, sneezing and sniffing reflex?

Answer 60

Immersion: activated when there is a stimuli of facial or nose receptors. It induces apnea and bradycardia.

Sneezing: It is due to stimulation of nasal receptors.

Sniffing: It shifts the pattern of respiration, the receptors located along the nasopharyngeal region are activated.