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Circulation and Breathing > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

How does tissue area affect diffusion of CO2 and O2?

A

The greater the area of tissue, the more gas exchange can occur. Directly proportional.

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2
Q

How does the diffusion constant affect the diffusion of CO2 and O2?

A

The diffusion constant determines the solubility of the gas, therefore the speed by which it will diffuse across cell membranes.
It is inversely proportional to the square root of the molecular weight of the molecule.
More soluble = greater diffusion constant
Small, light molecules have a higher diffusion constant.
Reason why CO2 diffuses more efficiently than O2.

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3
Q

How does tissue thickness affects diffusion of CO2 and O2?

A

The thicker the tissue the lower the diffusion constant.

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4
Q

List 4 respiratory factors that affect diffusion

A

1) Decreased concentration of O2 -> this will decrease the diffusion gradient so diffusion will occur much slower.

2) Hypoventilation reduces diffusion as less O2 is able to enter the lungs and less CO2 is removed from the lungs.

3) Some areas of the lung that are perfused but not ventilation allow deoxygenated blood to bypass the lungs as no diffusion can occur over those capillaries.

4) Inequalities between perfusion and ventilation (eg. the top and bottom of the lung) result in impaired gas exchange as no gas will be able to fully enter/leave blood effectively.

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5
Q

What does TLCO and DLCO stand for and what does this measure?

A

TLCO = Total Lung CO Absorbance
DLCO = Diffusing Capacity of Lung for CO
This test measures the amount of O2 that can be taken up from the air that is breathed in.

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6
Q

What gas is used in TLCO/DLCO tests and why?

A

CO is used as it is very soluble (higher diffusion constant).
It is highly bound to haemoglobin so will not build up in the capillaries as it is taken away from the lung by erythrocytes -> means diffusion gradient is maintained so gas exchange will not reach an equilibrium.

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7
Q

Why does N2 diffuse poorly?

A

It has a low water solubility so only diffuses into bloodstream when in high pressure breathing eg. diving.

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8
Q

Describe the structure of alveoli

A

Small air sacs surrounded by a network of pulmonary capillaries (capillary bed).
These capillaries are highly distensible (extensible), so during exercise they can stretch to increase surface area for maximum diffusion.

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9
Q

Define what transfer factor means

A

Transfer factor refers to the diffusion capacity, which is a measure of how well the lungs can take up oxygen from the air breathed in.

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10
Q

List 4 conditions in which transfer factor could be reduced

A

1) Reduced ventilation due to pulmonary oedema.

2) Reduced perfusion due to pulmonary embolism. The blood clot can prevent blood from reaching the capillaries.

3) Reduced lung area due to pneumonectomy, removal of part of lung.

4) Reduced haemoglobin due to anaemia, as this reduces the carrying capacity of haemoglobin for oxygen.

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11
Q

List 2 conditions in which transfer factor could be increased

A

1) Increased cardiac output due to exercise (heart rate x stroke volume), causes more haemoglobin to travel through pulmonary circulation.

2) Increased haemoglobin concentration. In alveolar haemorrhage leaked blood still absorbed the CO used to test he transfer factor.
In polycythaemia there is a high haemoglobin concentration in the blood, could be because they are chronic smokers or live in high altitudes.

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12
Q

How is the dissolved pO2 measured?

A

It is measured using arterial blood gas. This indicated the pO2 which correlates to the amount of oxygen dissolved in the blood.

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13
Q

How is the saturation of haemoglobin with O2 measured?

A

It is measured using pulse oximeters.

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14
Q

What conditions in the tissues reduce the affinity of haemoglobin for oxygen?

A

1) Low pO2
2) High pCO2
3) Low pH -> due to carbonic acid from high pCO2 so more dissolved CO2 in the bloodstream
4) Higher temperature
5) Higher concentration of 2,3-diphosphoglycerate (DPG). This is a by product of erythrocyte production.

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15
Q

What conditions in the lungs increase the affinity of haemoglobin for oxygen?

A

1) High pO2
2) Low pCO2
3) Higher pH
4) Lower temperature
5) Lower concentration of DPG -> less erythrocyte production in lungs.

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16
Q

In the V/Q ratio, what do these stand for and what is the normal ratio?

A

V = Gas flow
Q = Blood flow
If the ratio is 1 this is when gas flow equals blood flow.
The normal ratio is 0.8.
If gas flow > blood flow, ratio will be higher.
If blood flow > gas flow, ratio will be lower.

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17
Q

What is the conducting zone?

A

Parts of the respiratory anatomy that conduct gas down to the terminal bronchioles. Part of headspace as respiratory exchange does not occur here.

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18
Q

What is dead space?

A

Parts of the tidal volume that do not come into contact with perfused areas of the lung. This means gas exchange cannot take place here.
Normal ventilation but reduced perfusion.

The V (gas flow) is normal, but Q (blood flow) is reduced, which makes the value of V infinite.

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19
Q

What is the respiratory zone?

A

Parts of the anatomy where gas exchange occurs - alveoli.

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20
Q

What is the shunt?

A

1-2% of the cardiac output bypasses the ventilated alveoli. This leads to normal Q value but reduced V, so V/Q ratio is low.
Normal perfusion but reduced ventilation.

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21
Q

Describe the distribution of alveolar ventilation

A

Gravity causes alveoli in the lower regions of the lung to receive more ventilation.
In addition, the intrapleural pressure in the lungs is higher in lower regions, which causes alveoli at the base of the lung to be smaller, and the alveoli at the apex of the lung to be larger. Smaller alveoli are more compliant so has increased alveolar ventilation at base of lung.

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22
Q

What is intrapleural pressure?

A

This is the pressure in the pleural cavity inbetween the pleura.
This maintained pressure prevents lungs from collapsing on expiration.
The intrapleural pressure iso always negative -> always lower than the atmospheric pressure.

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23
Q

What is transpulmonary pressure?

A

This is the difference between the alveolar pressure and the intrapleural pressure.

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24
Q

Describe the distribution of blood flow in the lungs

A

More blood flow in the lower regions of the lung due to gravity.
The intravascular pressure is greater in lower regions, so there is less resistance. More pressure is needed at the apex of the lung to get blood flow to those areas.

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25
Q

Describe the structure of the pulmonary artery

A

The pulmonary artery is shorter and thinner than the aorta.
It contains less smooth muscle and less elastin than the systemic system (the aortic system).
This means it has less capacity to contract.

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26
Q

Describe the structure of the pulmonary vein

A

The pulmonary vein is thinner than the systemic veins and have less smooth muscle.

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27
Q

Describe the pulmonary capillaries

A

These are sandwiched between the alveoli so blood flows through them like a sheet. This provides a large, thin surface area for exchange.

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28
Q

List the 3 characteristics of the lung

A

1) Low pressure - all cardiac output goes through the lungs.

2) Low resistance - Lung blood flow is the same as cardiac output, so to cope with such a high volume of blood the resistance have to be lower.

3) High flow - All cardiac output goes through the lungs. However when blood pressure increases with exercise the pressure in the lungs only slightly rises.
This is because:
Previously collapsed capillaries are opened, and capillaries already open are distend (enlarge).

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29
Q

How is pulmonary blood flow controlled by the autonomic nervous system?

A

Stimulation of vagal fibres to lungs -> decrease pulmonary vascular resistance.
Parasympathetic nerves vasodilate, and M3 receptors on their endothelium are activated.

Stimulation of sympathetic system -> increase in pulmonary vascular resistance.
Sympathetic nerves vasoconstrict, alpha1 receptors on smooth muscle and arteries and arterioles are activated.

Differences in pressure between intra and extra alveolar vessels also helps control pulmonary blood flow.

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30
Q

When is there the lowest total vascular resistance in a breathe?

A

At the end of an expiration (FRC) when there is a balance between the pressure inside the alveoli and pressure from the surrounding capillaries (vasculature).

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31
Q

What are the pressure changes on inspiration to the alveoli?

A

As alveoli expand, pulmonary capillaries are compressed and elongated, this increases intra alveolar resistance.
BUT the chest wall also expands, so extra alveolar vessels do not have much pressure on them. This means resistance decreases.
This means total vascular resistance is low but still increases.

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32
Q

Define FRC

A

Functional residual capacity, the volume remaining in the lungs after a normal, passive exhalation.

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33
Q

What are the pressure changes in forced expiration?

A

In forced expiration the vascular resistance increases.
The large positive intra pleural pressures needed to force air out causes compression of extra alveolar vessels from the chest wall.
This increases vascular resistance.
Intra alveolar pressure falls through because the alveoli are not expanded.

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34
Q

Define TLC

A

Total lung capacity, volume of lungs at maximum inspiration (usually about 6 litres)

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35
Q

In inspiration you move from FRC towards ___ ?

A

FRC towards TLC

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36
Q

In passive expiration you move from TLC towards ___ ?

A

TLC towards FRC

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37
Q

In forced expiration you move from TLC towards __ ?

A

TLC towards RV

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38
Q

Define RV

A

Residual capacity, volume of air left in lungs after a normal exhalation.

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39
Q

Outline what happens in pulmonary hypertension

A

Pulmonary hypertension is a result of the constriction of the pulmonary arteries that supply blood to the lungs.
This means it becomes harder to pump blood towards the lungs.
This stress leads to enlargement of the right heart. This means fluid can eventually build up in the liver and other tissues such as the legs (more filtration).
Results in an elevation of pulmonary arterial pressure of more than 25 mmHg (rest) / 30 mmHg (exercising).

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40
Q

Describe the perfusion and ventilation at the apex of the lung

A

In the apex of the lung the alveolar pressure is greater than the arteriolar pressure.
More ventilation than perfusion.
The apex is hypo perfused compared its alveolar ventilation.

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41
Q

Describe the perfusion and ventilation in the middle of the lung

A

In the middle of the lung the arterial pressure is greater than the alveolar pressure BUT venous pressure is still lower than alveolar pressure.
This means perfusion depends on the gradient from arterial to alveolar pressure.
Vessels collapse when venous pressure is below alveolar pressure, limiting flow.
But since arterial pressure rises above alveolar pressure as you move lower down the lung the perfusion increases.

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42
Q

Describe the perfusion and ventilation of the base of the lung

A

In the base of the lung the arterial and venous pressure is greater than the alveolar pressure.
More perfusion than ventilation.
The base is hyper perfused compared to its alveolar ventilation.

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43
Q

How does the V/Q change across the lung?

A

V/Q is lowest in in apex and highest in the base.

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44
Q

What is the response to hypoxic vasoconstriction? (where there is low pO2)

A

Low pO2 environment.
Pulmonary arterioles constrict blood away from a shunt or hypoventilated alveoli towards ventilated alveoli to increase gas exchange in increase pO2.

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45
Q

What is the response to hypocapnic bronchoconstriction? (where there is low pCO2)

A

Low pCO2 environment.
Bronchioles divert ventilation away from a deadspace/hyperventilated alveoli and towards alveoli that are better perfused to remove more CO2.

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46
Q

Define hypoxia

A

Deficiency in the amount of oxygen reaching the tissues.
Can have hypoxia (due to anaemia) but still have high pO2 - when enough oxygen is in the blood but not enough goes to right parts of the body.

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47
Q

Define hypoxemia

A

Abnormally low oxygen concentration in arterial blood.

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48
Q

What is hypoxemic hypoxia?

A

When there is a low conc of O2 in the blood.
Due to:
1) Low inspired O2
2) Hypoventilation
3) Impairment of diffusion
4) Right to left shunts (collapsed alveoli, also gravity causing apex to be under perfused)
5) Typically pulmonary embolism can cause this.

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49
Q

What is anaemia hypoxia?

A

Reduction of oxygen carrying capacity of blood as total haemoglobin/blood is altered,
Decrease of functional haemoglobin - pO2 could be normal but O2 content is less.
Reduced number of erythrocytes (haemorrhage).

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50
Q

What is stagnant hypoxia?

A

Failure to transport enough oxygen due to inadequate blood flow.
eg, pulmonary embolism, heart failure.

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51
Q

What is histotoxic hypoxia?

A

Impaired use of oxygen by cells.
Poisoning at tissue levels (eg. cyanide) which disables oxidative phosphorylation - O2 not taken up by cells as the final hydrogen acceptor).
In cyanide, it binds to cytochrome C oxidase ( in electron transport chain) which prevents it from transporting any electrons.
This stops production of ATP so O2 is not taken up by cells as it isn’t needed.

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52
Q

What property of respiratory muscles allows them to be overridden by the body?

A

They do not have automaticity (unlike cardiomyocytes).
Means they are completely innervated by the autonomic nervous system.

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53
Q

What part of the brain does the breathing pattern originate from?

A

The medulla - it is the central controller.

54
Q

What is the dorsal respiratory group responsible for?

A

The dorsal respiratory group is active during inspiration. It is a collection of nerve cells on the back of the medulla.
It carries out rhythmic pattern firing down the phrenic nerve (sympathetic) -> this causes the diaphragm too move down/contract.

Also sends a negative response to ventral respiratory group so that expiratory signals aren’t fired at the same time.

55
Q

What is responsible for the relaxation of muscle in passive expiration?

A

Nothing - it is a completely passive process :P

56
Q

What is the ventral respiratory group responsible for?

A

The ventral respiratory group is active during active expiration (forcing air out of lungs, reaching RV).
This means it activates the accessory muscles during exercise.

57
Q

What is the pons and what is it responsible for in breathing?

A

The pons is part of the brainstem, is a horseshoe shaped mass of transverse nerves that connect the medulla with the cerebellum.
It fine tunes the rate and depth to give normal breathing.

58
Q

Give 2 examples of problems with the brainstem and explain why they are so severe.

A

1) Bleeding in the brain.
This increases intracranial pressure, so the brainstem is pushed downwards into the foramen magnum. This pressure on the dorsal respiratory group stops respiration from occurring.

2) When being hung
The force of patient transects the spinal cord att he foramen magnum. Means there will be no impulse from the brainstem to the lungs, so breathing stops.

59
Q

What is central hypoventilation and how does it occur?

A

Occurs commonly in brainstem strokes.
It is where pattern generation in the dorsal respiratory group is not present BUT voluntary ventilation still functions.

Involuntary respiration is impossible, therefore during sleep patient will not be able to breathe.
Have to use a ventilator to breathe.

60
Q

How is ventilation matched to the metabolic activity of the body?

A

The homeostasis of O2 and CO2 has to be monitored in the arterial blood by chemoreceptors.

61
Q

What are central chemoreceptors? (neural)

A

Located in the ventral medulla.
Stimulated by high concentration of H+ ions (low pH).
This is caused by CO2 dissolving to carbonic acid in the CSF, as the blood brain barrier is impermeable to charged molecules (eg. H+) but CO2 can diffuse across.
Not many buffers present in CSF so small increase in CO2 = large increase in H+.

A response to this is increased ventilation, which allows pCO2 to return to normal.

62
Q

What factors can affect the central chemoreceptor response of increased ventilation?

A

1) Hypoxia can increase the sensitivity to pCO2, so increase the ventilation response. There is a synergistic effect of hypoxia and hypercapnia.

2) Sleep, respiratory depressants and very high pCO2 reduce ventilatory response to pCO2.

63
Q

What factor does not affect the central chemoreceptor response of increased ventilation

A

1) Increasing the concentration of O2 does not affect the ventilation rate.

64
Q

How is ventilation controlled in a patient with chronic lung disease?

A

Ventilation is not effective at reducing the pCO2.
This is because HCO3- is transported to the CSF, and this acts as a buffer, allowing the pH of the CSF to normalise. Overall, higher CO2 levels can be tolerated.

Means that patients that have chronic hypoventilation rely on hypoxic drive as opposed to hypercapnic drive.
This oxygen therapy has to be controlled to prevent a build up of CO2.

65
Q

What are peripheral chemoreceptors? (neural)

A

Located in the carotid arteries, aorta and aortic bodies, (bifurcation of internal and external carotid arteries).
Stimulated by lack of O2 (also by a higher H+ concentration, synergistic effect with high pCO2 levels).
Releases neurotransmitter to increase signalling through afferent nerve to the dorsal respiratory centre.
A response to this is an increase in ventilation to return to the normal pO2 level.

HOWEVER the lack of O2 must be very severe in order to affect breathing.
This is because according to the O2 dissociation curve when there is less O2, haemoglobin has a higher affinity for O2. Therefore small decreases in O2 will not have an affect as the body will hold onto as much O2 as possible.

66
Q

What are pulmonary stretch receptors?

A

Located in airway smooth muscle.
Prevents hyperinflation of the lungs (air trapped causing lungs to overinflate) leads to shallow, short inspiration to increase expiratory time = Hering-Breuer reflux.
This will be more important in neonates with more compliant chest walls.

67
Q

What are airway/irritant receptors?

A

Located in the epithelial cells of upper and lower airways.
Responds to poisonous/harmful agents with bronchoconstriction, hypoventilation, coughing and sneezing.

68
Q

What are pulmonary vascular receptor/J receptors?

A

Located throughout the respiratory tract and the smooth muscle and endothelial cells of vasculature.
Responds to pulmonary vascular congestion with an increased respiratory rate, to increase the O2 absorbed in the blood and the CO2 removed from the blood.

Can be responsible for breathlessness and heart failure, and cheyne stokes breathing - recurrent apnoea.

69
Q

What does apnoea mean?

A

Breathing stopping temporarily.

70
Q

What do joint and muscle receptors (proprioeceptors) do in breathing?

A

Present in joints and muscles.
Moving limbs stimulates ventilation.

71
Q

What do temperature receptors do in breathing?

A

Increased temperature of the skin stimulates ventilation.

72
Q

What do pain receptors do in breathing?

A

Causes brief apnoea then hyperventilation.

73
Q

What does the diving reflex do in breathing?

A

Immersing the face in cold water results in apnoea or decreased heart rate.

74
Q

Outline what happens in ventilation as a response to exercise

A

1) Neural central chemoreceptors and temperature receptors are stimulated by hypercapnia, lowers pH in CSF due to more H+. These send more afferent action potentials.

2) Impulse is sent to the dorsal respiratory centre. This increases frequency of efferent action potentials, so more contraction of diaphragm. Also reduces ventral respiratory centre so expiration doesn’t occur at the same time.

3) Ventilation increases immediately to match the O2 uptake with increased CO2 output, to restore pH to normal - if extreme then will be hyperventilation.

4) Venous CO2 increases. Lungs are able to excrete excess CO2 from arteries.
Ventilation can be increased up to 20 times, but limiting factor is cardiac output -> heart rate x stroke volume.

5) After CO2 has been removed from lungs the pH returns to normal, so the impluses are sent with less frequency. This is a negative feedback loop.

75
Q

Volatile acids are in _______ form and can be removed by the _____ .

A

Gaseous, lungs.

76
Q

Non-volatile fixed acids are in ________ form and can be removed by the _______ .

A

Solution, kidneys.

77
Q

Define acids

A

H+ donors

78
Q

Define bases

A

H+ acceptors

79
Q

Define buffers and give an example

A

A buffer is a weak acid and its conjugate base.
An example is within the blood, the weak acid = carbonic acid, the conjugate base = bicarbonate HCO3-

80
Q

Why are only weak acids used in buffers?

A

Because weak acids can reversibly absorb H+ ions, but strong acids fully dissociate.

81
Q

What pH range does the body need to be kept at?

A

pH range in body is 7.35-7.45.
Below 7.35 = acidosis
Above 7.45 = alkalosis

82
Q

What are the main intracellular buffers?

A

Proteins and phosphate

83
Q

What are the main extracellular buffers?

A

Bicarbonate HCO3-

84
Q

What does the pKa of a buffer indicate?

A

pKa = log of the Ka
This is the pH at which the buffer works best.

85
Q

What is the dissociation constant of carbonic acid?

A

CO2 + H2O
-> H2CO3 ->

86
Q

Using the Henderson-Hasselbach equation and rearranging, what is the equation for the blood pH?

A

pH = 6.1 + log[HCO3-] / [H2CO3]

87
Q

What is the concentration of HCO3- determined by?

A

The activity of the kidney.

88
Q

What is the concentration of CO2 is determined by?

A

The activity of the lungs.

89
Q

What is unique about the buffer system of the blood?

A

Normally buffers can be exhausted, but kidneys and lungs can deal with infinite excess by excreting acid or base

90
Q

What is the role of the lungs in the dissociation constant of carbonic acid?

A

The lungs remove carbonic acid from the blood in the form of carbon dioxide during expiration.

91
Q

What is the role of the kidneys in the dissociation constant of carbonic acid?

A

In normal metabolism there is continuous production go H+.
Renal tubules contain lots of carbonic anhydrase and this forms carbonic acid from CO2 and H2O.
This carbonic acid then dissociates to HCO3- and H+.
The bicarbonate is reabsorbed into the blood and the H+ passes into tubules and is eliminated from the body in urine.

92
Q

Which has the ability to change the acid base balance more, kidneys or lungs?

A

The lungs excrete 10,000 mEq of H2CO2 in 24 hours compared to 100 mEq of fixed acid from kidneys in 24 hours.

Means changes in ventilation will change the acid base balance with more magnitude than change to excretion of solutes in the kidneys.

93
Q

Outline respiratory acidosis

A

This occurs due to hypoventilation, when the pCO2 rises in the body.
This means there will be more dissociation of carbonic acid, so more H+ ions present in the blood.
This means the pH falls.
The kidney counteracts this by reabsorbing the HCO3- from the carbonic acid dissociation and excretes the H+. This in then decreases the H+ concentration.
This normalises the ratio of HCO3-/pCO2, with an excess of the base HCO3- .

94
Q

What are the causes of respiratory acidosis?

A

1) COPD,
2) Obesity
3) Neuromuscular disorders
4) Chest wall deformities
5) Exhaustion
6) CNS depression following stroke/opioids.

95
Q

Outline respiratory alkalosis

A

This occurs due hyperventilation, when pCO2 falls in the body.
This means there is less dissociation of carbonic acid, so less H+ ions are present in the blood.
This means the pH rises.
The kidney counteracts this by excreting more HCO3- in order too cause more dissociation of the carbonic acid. This in turn increases the H+ concentration.
The ratio of HCO3- and pCO2 normalises with a deficit of the base HCO3- .

96
Q

What are the causes of respiratory alkalosis?

A

1) Pulmonary embolism
2) Salicylates
3) Anxiety
4) Stroke/CNS lesions

97
Q

Outline metabolic acidosis

A

This occurs due to tissue hypoxia/ketoacidosis, when the HCO3- concentration falls when mopping up excess H+.
This means the pH falls.
The lung counteracts this by increasing ventilation to lower the pCO2 in the body. This means less carbonic acid can dissociate so the H+ in the body is conserved and no more is added.
The ratio of HCO3-/pCO2 will then normalise with a deficit of the base HCO3- .

98
Q

What are the causes of metabolic acidosis?

A

1) Increased acid production - diabetic ketoacidosis, hypoxia
2) Loss of HCO3- through diarrhoea
3) Inability of kidney to excrete acid - chronic kidney disease

99
Q

Outline metabolic alkalosis

A

This occurs due to excessive ingestion of alkali/loss of gastric acid, when the HCO3- concentration rises.
This means the pH rises.
The lung counteracts this with mild hypoventilation as this will increase the pCO2 in the body, so the H+ concentration will increase due to carbonic acidic the blood.
The ratio of HCO3-/pCO2 normalises with an excess of the base HCO3- .

100
Q

What are the causes of metabolic alkalosis?

A

1) Vomiting -loss of gastric acid
2) Diuretics - excretion of ions
3) Steroid excess - loss of kidneys
4) Congential kidney diseases

101
Q

What does renal failure to produce HCO3- or excrete H+ cause?

A

Not able to remove H+ so H+ accumulates. This lowers the pH.
This results in metabolic acidosis.
This is compensated by hyperventilation in the lungs so the pCO2 in the body decreases. This reduces the carbonic acid dissociation so more H+ is not added to the body.
The HCO3-/pCO2 ratio normalises with a base deficit.

102
Q

What does vomiting (loss of HCl from stomach) cause?

A

Loss of H+ ions increases the pH.
This results in metabolic alkalosis.
This is compensated by slight hypoventilation in the lungs so the pCO2 in the body increases. This increases the dissociation of carbonic acid so more H+ can be added into the body.
The HCO3-/pCO2 ratio normalises with a slight base excess.

103
Q

What does diarrhoea (loss of HCO3-) cause to acid base balance?

A

Loss of HCO3- ions causes an increase in H+ ions, which decreases there pH.
This results in metabolic acidosis.
This is compensated by hyperventilation in the lungs so the pCO2 in the body decreases so there is less carbonic acid dissociation so H+ isn’t added to the body.
The HCO3-/pCO2 ratio normalises with a base deficit.

104
Q

What can a pulmonary embolism cause to acid base balance?

A

Hyperventilation in the lungs causes a decrease of pCO2 in the body, so less carbonic acid is present to dissociate.
Means there are less H+ ions so the pH increases.
This results in respiratory alkalosis.
This is compensated by the kidney excreting more HCO3-, which causes more carbonic acid dissociation to increase the H+ levels in the body.
The HCO3-/pCO2 ratio is normalised with a base deficit.

105
Q

What can obesity cause to acid base balance?

A

Hypoventilation in the lungs causes an increase in pCO2 in the body, so more carbonic acid is present to dissociate.
Means there are more H+ ions so the pH decreases.
This results in respiratory acidosis.
This is compensated by the kidney excreting H+ and reabsorbing HCO3- (to prevent more dissociation of carbonic acid), to decrease H+ levels in the body.
The HCO3-/pCO2 ratio is normalised with a base excess.

106
Q

Why is air taken by the mouth rather than nose during heavy breathing?

A

Because there is less resistance to the air flow through the mouth.

107
Q

Outline the pathway of the conducting zone?

A

Air passes through nose and mouth.
Then passes through pharynx then the larynx.
Afterwards, air passes to the trachea, which splits into 2 bronchi, which further splits into bronchioles (alveoli are on the end).

108
Q

What are the changes to the thorax during quiet inspiration?

A

1) Sternum moves forwards like a “pump handle”. This increases the anteroposterior diameter of the thorax.

2) The ribs then move up and out like “bucket handles”. This increases the transverse diameter of the thorax.

3) External intercostal muscles contracts internal intercostal muscle relax, further increases volume.

3) The volume of the thorax increases, which decreases the pressure inside the lungs. The intra pleural pressure also decreases.

4) Pressure inside the lungs in lower than the pressure outside lungs. Causes air to be sucked into the lungs during inspiration.

109
Q

What are the changes to the thorax during normal expiration?

A

1) Relaxation of all respiratory muscles.

2) Elastic recoil of the thoracic cage allows the thorax to decrease in volume. Intra pleural pressure in the lungs also increases.

3) Pressure inside the lungs is greater than the pressure outside the lungs. Causes are to be forced out of the lungs.

110
Q

What are the changes to the thorax during deep and forced inspiration?

A

In addition to other changes…
1) Accessory muscles also act on the thoracic cage. The scalene and sternocleidmastoid muscles in the neck pull on the first and second ribs.

2) If upper limbs are fixed, pectoral muscles can act on the rib cage to elevate the ribs further.

111
Q

What are the changes to the thorax during forceful expiration?

A

In addition to other changes…
1) Abdominal wall muscles become active. These raise the intra abdominal pressure, which forces the abdominal viscera against the diaphragm, and pushing it into the thoracic cavity.

112
Q

Describe the structure and function of the pleura

A

The pleura are membrane that fold to form a two membrane structure that separates the lung and chest wall.
Space between the membranes is the pleural cavity. This is filled with pleural fluid. It is a lubricant that allow the pleurae to slide over each other in ventilation.

The outer parietal pleura is attached to chest wall.
The inner visceral pleura is attached to the lungs.

The pressure between these two membranes is called intrapleural pressure.

113
Q

In the ventral medulla, what complex is also responsible for generating respiratory rhythm?

A

The pre-Bötzinger complex

114
Q

Outline exercise hyperpnoea and why it occurs

A

Exercise hyperpnoea is when feed forward control leads to anticipation of exercise.
Suggestions of exercise cause rate and depth of ventilation to increase.

Prevents a build up of CO2 occurring, as body has to wait for CO2 to be detected before increasing ventilation, but exercise releases a large amount of CO2 which could be dangerous if in the blood.

115
Q

How can muscle afferents affect the depth and rate of ventilation?

A

Peripheral afferent muscle fibres are able to increase the depth and rate of ventilation independent of CO2 concentration - instead it is affected by muscular contraction.
The body is able to detect stretch within large muscle groups.

116
Q

What is dispnoea?

A

Mismatch of the demand and supply of oxygen.
Expectations of the breathing system are not what the body was expecting.

117
Q

What 3 factors affect the volume of air that reaches the alveolar surface?

A

1) Respiratory rate - number of breaths per minute.

2) Tidal volume (respiratory depth) - number of breaths per minute.

3) Dead space volume - volume of gas that does not reach the gas exchange surface (150ml)

118
Q

What is the relationship between dead space volume and the volume of air that reached alveoli?

A

More dead space = Less air to alveoli

119
Q

How do you calculate minute ventilation?

A

Tidal Volume x Respiratory Rate

120
Q

What is minute ventilation?

A

The total volume of gas entering the lungs per minute.

121
Q

How do you calculate alveolar ventilation?

A

(Tidal Volume - Deadspace) x Respiratory Rate

122
Q

What is alveolar ventilation?

A

The volume of gas per unit time that reaches the alveolar gas exchange surface.

123
Q

How do you calculate deadspace ventilation?

A

Deadspace x Respiratory Rate

124
Q

What is deadspace ventilation?

A

The volume of gas per unit time that does not reach the gas exchange surface.

125
Q

What happens to airway resistance when the volume of the lung decreases?

A

The airway resistance increases, because the elastin and collagen fibres attached to the small airways slacken when the lung volume decreases.

126
Q

Which nervous pathways control airway resistance and how?

A

The sympathetic and parasympathetic pathways.

Sympathetic = decreases bronchial muscle tone so bronchodilaton occurs
Parasympaththetic = increases muscle tone so bronchodilator doesn’t occur

127
Q

Which drugs can decrease the airway resistance by causing bronchodilation?

A

Beta 2 agonist - Salbutamol = activates the beta 2 adrenoreceptors so promotes more bronchodilation.

Anti-cholinergics - Tiotropium, Ipratropium = antagonists to the M3 muscarinic receptors, so prevents constriction, leading to bronchodilation.

128
Q

What does the Peak Expiratory Flow Rate (PEFR) measure?

A

Measures the maximum speed of expiration of an individual using a peak flow meter.

129
Q

What does the Forced Expiratory Volume in 1 second measure?

A

Measures the volume of air that can be expelled from maximum inspiration to maximum expiration in the first second.

130
Q

What does the FEV1/FVC ratio measure?

A

It is the volume of air expelled in 1 second as a ratio of the total volume of air expelled from maximum inspiration.

FEV1 ÷ total volume of air from a maximum inspiration

Circulation and Breathing (7 decks)

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