Respiratory Physiology ( 20% ) Flashcards

1
Q

Which one of the following is activated in the lung

  • Renin
  • Angiotensin.
  • Kallikrein.
  • Bradykinin
  • Prostaglandins.
A

Angiotensin. Converted to Ang II by ACE

(remember that COVID attaches to ACE receptors in the lungs)

  • Kallikrein - A serum protease that forms bradykinin from a precursor. It is activated by factor XII
  • Bradykinin - Deactivated by ACE
  • Prostaglandins - Removed from the lungs
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2
Q

Substances metabolized by the lung include all except

  • Serotonin
  • NA
  • ACh.
  • Glutamic acid
  • Bradykinin
A

Glutamic acid.

Part of the Krebs’ cycle which all cells use

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3
Q

Substances synthesised by the lung include all of the following except

  • Arachidonic acid
  • Histamine
  • Kallikrein
  • Angiotensin I
  • Surfactant
A

Angiotensin I

Others are all lung-specific or generic body substances

Angiotensin I is produced by renin (kidneys) acting on angiotensinogen (liver)

Ang I -> Ang II in the lungs (ACE)

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4
Q

substances cleared from the circulation by the lungs include all except

  • angiotensin II
  • serotonin
  • Leukotrienes
  • Bradykinin
  • Prostaglandin
A

angiotensin II

Produced by ACE in the lungs (from Ang I)

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5
Q

Functions of the lung include all of the following except

  • Synthesis of phospholipids
  • Synthesis of proteins
  • Carbohydrate metabolism
  • Inactivation of bradykinin
  • Removal of DA
A

Removal of DA

Presumably this is dopamine

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6
Q

The anatomic dead space

  • Varies with minute ventilation.
  • Is typically 150mL
  • Will increase in C.O.P.D.
  • Is alveolar minus the pathological dead space
  • All of the above
A

Is typically 150mL

It is a fixed volume, representing the conducting part of the lungs, and does not vary with ventilation.

Does not increase in COPD, although physiologic deadspace will

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7
Q

Regarding the alveolar gas equation

  • It gives the value of alveolar pO2 in a given patient
  • R denotes the respiratory rate
  • At sea level, pIO2 = 690mmHg x 0.21 of humidified air
  • At high altitude, paCO2can be less than 35mmHg
  • The alveolar gas equation is only applicable at sea level
A

It gives the value of alveolar pO2 in a given patient

  • R denotes the Respiratory exchange ratio
  • At sea level, pIO2 = 690mmHg x 0.21 of humidified air
    • using 690mmHg means that humidity has already been accounted for
  • At high altitude, paCO2can be less than 35mmHg
    • Should be constant as the body’s metabolic needs don’t change
  • The alveolar gas equation is only applicable at sea level
    • Takes into account FiO2
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8
Q

With respect to dead space

  • Dead space volume is equal to the person’s weight in kg
  • For a constant minute ventilation, alveolar ventilation is decreased as respiratory rate increases
  • Anatomic dead space is less than physiological dead space in healthy persons
  • Physiological dead space is measured by analysis of single breath nitrogen curves
  • Total dead space equals physiological dead space + anatomic dead space
A

For a constant minute ventilation, alveolar ventilation is decreased as respiratory rate increases

This is because TV must reduce to maintain the minute ventilation. As deadspace is fixed at 150ml, any reduction in TV will impact on the alveolar ventilation.

  • Dead space volume is ~ 150mL
  • Anatomic dead space is the same as physiological dead space in healthy persons
    • In diseased lungs, physiological dead space > anatomical dead space
  • Anatomic dead space is measured by analysis of single breath nitrogen curves
    • physiological uses PCO2
  • Total dead space equals physiological dead space + anatomic dead space
    • Both aim to calculate the same thing
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9
Q

The alveolar gas equation

  • Is also known as the Bohr’s equation
  • Can be used to calculate anatomical dead space.
  • Is influenced by diet
  • Is independent of PiO2
  • Requires sampling of gas to determine PACO2
A

Is influenced by diet

https://www.openanesthesia.org/alveolar-gas-equation-altitude/

  • Bohr’s equation calculates physiological dead space
  • Can be used to calculate PAO2
  • Accounts for PiO2
  • Are able to take a Blood sample (ABG) to determine PaCO2, which should equal PACO2
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10
Q

Which one of the following definitions is incorrect

  • The respiratory minute volume equals the amount of air inspired per minute
  • Residual volume is the air left in the lungs after a maximal expiratory effort
  • Vital capacity is the maximal amount of air that can be expired after a normal inspiration
  • Physiological dead space is the amount of air not equilibrating with blood
  • Compliance is the change in lung volume per unit change in airway resistance
A

Compliance is the change in volume per unit change in airway pressure

Above is true, but I think c) is also true, as below

Vital capacity is the maximal amount of air that can be expired after a maximal inspiration

(Expiratory reserve volume is the amount of air that can be expired after a normal expiration)

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11
Q

residual volume in a 70kg man most closely approximates

  • 1L
  • 2L
  • 3L
  • 4L
  • 5L
A

1L

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12
Q

regarding the lung volumes in a 70kg man

  • ERV is > 1.0L
  • IRV is < 3.0 L
  • Residual volume = 1.2L
A

Residual volume = 1.2L

ERV = 1L

IRV = 3L

FRC = 2.5L

VC = 4.5L

TLC = 6L

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13
Q

regarding RQ, which is false

  • ~ 0.82
  • RQ of brain tissue is approximately 1.0
  • RQ of carbohydrate = 1.0
  • RQ of carbohydrate > protein
  • RQ of fat is 0.90
A

RQ of fat is 0.7

  • Carb is 1.0*
  • Protein somewhere in between*
  • Brain = 0.99*
  • Body usually about 0.85 or so, but increases to close to 1 during exercise as carbs are the primary energy source*
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14
Q

La Place’s law

  • Explains the observed elastic recoil of the chest
  • Determines the change in volume per unit change in pressure.
  • Tells us the pressure is inversely related to tension.
  • Explains the tendency of small alveoli to collapse
  • All of the above
A

Explains the tendency of small alveoli to collapse

pressure = (4x surface tension) / radius

  • ie the smaller the radius, the greater the internal pressure generated by surface tension (surface tension will be relatively constant for a given substance)*
  • A small alveoli will preferentially collapse and fill a large one, as it has a greater pressure inside it*
  • Pressure is directly related to tension, inversely to radius*
  • Tells us the change in compliance per change in pressure*
  • (Complicance = change pressure / change volume)*
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15
Q

compliance of the lung is reduced by all of the following except

  • emphysema
  • alveolar oedema
  • fibrosis
  • consolidation
  • high expanding pressures
A

emphysema

  • Loss of elastic tissues results in less inwards pressure generated = easier to inflate.*
  • Fibrosis does the opposite - hard to inflate fibrous tissue*
  • Oedema and consolidation make it impossible to inflate some alveoli, so compliance is reduced (collapsed alveoli will tend to produce radial tension on nearby airways, requiring greater*
  • [Compliance = change in volume / change in pressure], so a high pressure -> low compliance. This is shown by the flatter superior portion of the curve*
  • Usual compliance of lung = 200ml/cmH20*
  • (Note saline reduces compliance as it eliminates surface tension)*
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16
Q

lung compliance

  • is normally 100mL/cm water.
  • falls if the lung remains unventilated for long periods
  • rises if the pulmonary venous pressure is increased. Opposite
  • falls as the lung ages. Opposite
  • is the area under the pressure volume curve. Compliance is the slope, work is the area
A

falls if the lung remains unventilated for long periods

  • is normally 200mL/cm water.
  • falls if the pulmonary venous pressure is increased.
  • rises as the lung ages, thought to be due to changes in the elastic tissue
  • Compliance is the slope of the pressure-volume curve, work is the area
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17
Q

work of the lung in breathing

  • is increased with larger tidal volumes
  • is increased with higher flow rates
  • in inspiration need to overcome elastic forces and viscous resistance
  • in expiration need to overcome airway and tissue resistance
  • all of the above
A

all of the above

  • is increased with larger tidal volumes -
    • larger volumes = reduced compliance = more work
  • is increased with higher flow rates
    • higher flow = higher pressure = reduced compliance
  • in inspiration need to overcome elastic forces and viscous resistance
  • in expiration need to overcome airway and tissue resistance
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18
Q

With regards to the normal alveolus

  • Surfactant is produced by type I pneumocytes.
  • Alveolar size has little effect on the surface tension.
  • Surfactant is composed of hydrophilic molecules.
  • Large alveoli have a tendency to collapse into smaller ones. Opposite
  • Surrounding tissues exert a force preventing alveolar collapse
A

Surrounding tissues exert a force preventing alveolar collapse

  • Surfactant is produced by type II pneumocytes.
  • Alveolar size has a great effect on the surface tension.
    • Law of Laplace - pressure is inversely related to radius (size), and directly related to surface tension (usually a constant)
    • Saline and detergent have a constant surface tension regardless of the surface area, however surfactant changes its tension depending on the surface area (increasing area -> increasing tension)
  • Surfactant is composed of bipolar molecules (hydrophilic and hydrophobic ends)
  • Small alveoli have a tendency to collapse into Larger ones.
    • Law of Laplace - smaller radius = larger internal pressure
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19
Q

The following are true regarding lung volumes and compliance except

  • Compliance increases in obstructive lung disease
  • FEV1/FVC ration decreases in obstructive lung disease
  • FRC is the sum of ERV and RV
  • The change in lung volume per unit change in airway pressure is the compliance of the lung.
  • Vital capacity is the largest amount of air that can be expired after a maximal inspiratory effort
A

Bad question - I have changed some options to clarify the answer (reversed a) and b) as these also seemed to be wrong initially, as explained below)

The change in lung volume per unit change in pleural pressure is the compliance of the lung.

Airway pressure is atmospheric at rest, or a combination of forces during inspiration/expiration

  • Compliance increases in obstructive lung disease due to a loss of elastic structures.
    • ​Originally this answer stated ‘decreased’, and this was assumed to be true.
    • ​This one was a little tricky, as emphysema is often used as an example of increased compliance, however..
    • Chronic obstruction often leads to hyperinflation, which will reduce compliance at higher lung volumes, however this needs to be balanced against the above point (overall emphysema will increase compliance)
    • The textbook uses emphysema as its obstructive example, and states that it increases resistence. It is unclear whether something like asthma might reduce compliance due to increased pressures, gas-trapping, and hyperinflation, but I have ignored this as it is not specifically mentioned in the text.
  • FEV1/FVC ratio reduces in obstructive lung disease
    • Obstructive, and so therefore FEV1 is reduced whereas FVC might be unchanged
  • FRC is the sum of ERV and RV - true
  • Vital capacity is the largest amount of air that can be expired after a maximal inspiratory effort - true
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20
Q

Which one of the following definitions is incorrect

  • The respiratory minute volume equals the amount of air inspired per minute
  • Residual volume is the air left in the lungs after a maximal expiratory effort
  • Vital capacity is the maximal amount of air that can be expired after a normal inspiration
  • Physiological dead space is the amount of air not equilibrating with blood
  • Compliance is the change in lung volume per unit change in airway resistance
A

Vital capacity is the maximal amount of air that can be expired after a maximal inspiration

Compliance is the change in lung volume per unit change in transpumonary pressure (which equal pleural pressure at rest as alveolar pressure = atmospheric)

Nick thought E), I thought c) + e)

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21
Q

Pulmonary compliance

  • Is decreased in emphysema
  • Is defined as the change in pressure per unit change in volume
  • Compliance is slightly greater when measured during deflation than when measured during inflation
  • Is increased by pulmonary fibrosis
  • Is independent of lung volume
A

Compliance is slightly greater when measured during deflation than when measured during inflation

ie a lower pressure is needed to maintain a given volume

  • Is increased in emphysema
  • Is defined as the change in volume per unit change in pressure
  • Is decreased by pulmonary fibrosis (harder to pull fibrosis open)
  • Is dependent of lung volume - higher or lower volumes have reduced compliance
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22
Q

With regard to pulmonary function

  • Tidal volume is the volume of each maximal inspiration
  • Residual volume is the volume remaining at the end of passive expiration
  • Residual volume can be measured directly
  • Vital capacity is equivalent to the total inspiratory reserve volume, tidal volume and expiratory reserve volume
  • Tidal volume is measured by the single breath nitrogen technique
A

Vital capacity is equivalent to the total inspiratory reserve volume, tidal volume and expiratory reserve volume

  • Tidal volume is the volume of each normal inspiration
  • Residual volume is the volume remaining at the end of maximal expiration
    • Functional residual capacity is the volume following a normal (passive) expiration
    • Expiratory reserve volume is the difference between a normal and maximal expiration
  • Residual volume cannot be measured directly
  • Anatomic dead space is measured by the single breath nitrogen technique (Fowlers Technique)
    • ​Bohrs technique measure physiologic deadspace and utilises CO2 production
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23
Q

increased lung compliance is associated with

  • increasing age
  • increasing pulmonary venous pressure
  • high expanding volumes
  • interstitial fibrosis
  • low lung volumes associated with hypoventilation
A

increasing age

  • and also emphysema*
  • Very high and low lung volumes cause reduced compliance*
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24
Q

Surfactant

  • Is produced by class II pneumocytes
  • Is increased in smokers
  • Helps keep the alveoli moist
  • Decreases alveolar stability in preterm babies
  • Maturation is impaired by glucocorticoids
A

Is produced by class II pneumocytes

Keep alveoli dry, as surface tension tends to suck fluid out of capillaries (as well as trying to cause alveoli to collapse), causing pulmonary oedema (this is what happens in respiratory distress of the newborn, where there is a lack of surfactant

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25
Q

With respect to lung volumes

  • FRC can be measured with a spirometer
  • He dilution measures the total volume of gas in the lung, including any trapped behind closed airways
  • The volume of gas left in the lungs after a maximal expiration is the functional residual volume
  • Vital capacity is the volume exhaled when a maximal inspiration is followed by a maximal expiration
  • TLC is the volume of the lung available to partake in gas exchange
A

Vital capacity is the volume exhaled when a maximal inspiration is followed by a maximal expiration

  • FRC cannot be measured with a spirometer
  • He dilution measures the total volume of gas in the lung that is able to diffuse and equilibrate with the atmosphere
  • The volume of gas left in the lungs after a maximal expiration is the residual volume (FRC is after a normal expiration)
  • TLC is the volume of the lung available to partake in gas exchange
    • Alveolar gas is the volume for gas exchange - TLC includes deadspace
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26
Q

Surfactant

  • Increases surface tension
  • Surface tension is proportional to their concentration
  • Is produced by type I alveolar cells
  • Is increased in cigarette smoking
  • Prevents pulmonary oedema
A

Prevents pulmonary oedema

As the surface tension wants to pull fluid out of capillaries

  • reduces surface tension
  • Surface tension is proportional to their concentration
    • Tension is proportional to area, which is presumably inversely proportional to their concentration
  • Is produced by type II alveolar cells
  • Is decreased in cigarette smoking
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27
Q

surfactant

  • increases compliance
  • is produced by type I pneumocytes
  • is absorbed by type II pneumocytes
A

increases compliance

  • By reducing surface tension*
  • Produced by Type II pneumocytes (absorption not mentioned)*
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28
Q

Given that the intrathoracic pressure changes from -5cmH2O to -10 with inspiration and a tidal volume of 500mL, what is the compliance of the lung

  • 0.01
  • 0.1
  • 1.0
  • 10
  • 100
A

100

  • Compliance = change in volume over change in pressure*
  • = 500 / 5*
  • = 100*
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29
Q

What is the compliance of a lung if a balloon is blown up with 500mL of air with a pressure change from -5 to -10

  • 0.1
  • 1
  • 10
  • 100
  • 200
A

100

Compliance = change in volume over change in pressure

= 500 / 5

= 100

(a normal lung compliance is 200ml/cmH20)

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30
Q

With regards to pulmonary gas exchange

  • Transfer of nitrous oxide is perfusion limited
  • Transfer of oxygen is typically diffusion limited.
  • At altitude the profound systemic hypoxaemia favours oxygen diffusion.
  • The diffusion rate for CO2 is double that of oxygen.
  • Diffusion is inversely proportional to the partial pressure gradient
A

Transfer of nitrous oxide is perfusion limited

Carbon monoxide is diffusion limited

  • Transfer of oxygen is typically perfusion limited.
  • At altitude the profound systemic hypoxaemia favours oxygen diffusion.
    • Reduced atmospheric oxygen -> Partial pressure gradient is reduced, therefore diffusion will also be reduced
  • The diffusion rate for CO2 is 20x that of oxygen
  • Diffusion is directly proportional to the partial pressure gradient
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31
Q

Fick’s law of diffusion is dependent on all except

  • Thickness of membrane barrier
  • Solubility of the gas
  • The molecular weight of the gas
  • The posture of the subject
  • The area of the membrane
A

The posture of the subject

32
Q

Regarding the diffusing capacity of the lung

  • Oxygen passage is diffusion limited
  • Diffusion is directly proportional to the surface area of the alveolocapillary membrane and inversely proportional to the thickness
A

Diffusion is directly proportional to the surface area of the alveolocapillary membrane and inversely proportional to the thickness

33
Q

Regarding the rate of diffusion through tissue, which is correct?

  • It is proportional to the square of the surface area.
  • It is inversely related to thickness which is only 0.3μm in places
  • CO2 diffuses much more rapidly than O2 because it has a lower molecular weight.
  • It is an active process described by Fick’s law.
A

It is inversely related to thickness which is only 0.3μm in places

  • It is proportional to the surface area (not the square)
  • CO2 diffuses much more rapidly than O2 because it is much more soluble
  • It is a passive process described by Fick’s law.
34
Q

Diffusion in the lung can be limited by all of the following except:

  • Exercise.
  • Hypoxia
  • Thickening of the blood-gas barrier
  • Low altitude
A

Low altitude

  • Exercise can limit it by reducing the capillary transit time*
  • Hypoxia can limit it by reducing the A-a gradient*
  • High-altitude can limit it due to hypoxia*
35
Q

Which is correct regarding gas exchange in the lung:

  • Carbon monoxide rapidly reaches maximum Pco in blood so it is diffusion limited
  • Under normal circumstances oxygen exchange is diffusion limited
  • Because nitrous oxide is highly soluble in blood it is diffusion limited
  • None of the above
A

None of the above

  • Carbon monoxide binds to Hb and therefore has a very low PP in the blood, and never reaches maximum
  • Under normal circumstances oxygen exchange is perfusion limited
    • Only diffusion limited in disease, or hard-exercise at altitude
  • Because nitrous oxide is highly soluble in blood it is perfusion limited (only limited by the amount of blood that can be supplied)
36
Q

Using Fick’s law of diffusion through a tissue slice, if gas X is twice as soluble and 4 times a dense as Y then the ratio of diffusion rates of X to Y will be

  • There will be no difference
  • 0.5
  • 2
  • 8
A

There will be no difference

Diffusion is relative to [solubility / the square root of its molecular weight (density)]

Therefore 2 / square root 4 = 1

37
Q

Examples of gases that display perfusion limited exchange in normal individuals include all except:

  • Oxygen
  • Carbon dioxide
  • Carbon monoxide
  • Nitrous oxide
A

Carbon monoxide

= diffusion limit

NO is perfusion limited

Binds to Hb and hence creates almost no ‘backpressure’ in the blood. Essentially means that even at very slow rates of blood flow, it is absorbed enough that it is just the diffusion that limits it.

All others create a backpressure/reduce their concentration gradient more quickly, so they require the blood flow to be higher to maintain exchange

38
Q

In control of ventilation the medullary chemoreceptors respond to

  • Oxygen tension
  • Hydrogen ion concentration
  • CO2 tension
  • H+ concentration and CO2 tension
  • H+ concentration and oxygen and CO2 tension
A

Hydrogen ion concentration

CO2 diffuses across the BBB, but H+ and HCO3- cannot.

CO2 then combines with water in the CSF to create H+ and HCO3-

This H+ is sensed by central chemoreceptors.

39
Q

The main respiratory control neurons

  • Send out regular bursts of impulses to expiratory muscles during quiet respiration.
  • Are unaffected by stimulation of pain receptors.
  • Are located in the pons.
  • Send out regular bursts of impulses to inspiratory muscles during quiet respiration
  • Are unaffected by impulses from the cerebral cortex
A

Send out regular bursts of impulses to inspiratory muscles during quiet respiration

  • Do not send out regular bursts of impulses to expiratory muscles during quiet respiration - Expiration is passive
  • Can be modified by stimulation of pain receptors.
  • Are located in the medulla
  • Are affected by impulses from the cerebral cortex (respiration can be overtaken by voluntary control)
40
Q

With regards to ventilation

  • The autonomic control centre is located in the midbrain
  • Brainstem respiratory neurons only discharge during inspiration.
  • Arterial pO2 must be below 80mmHg to produce increased discharge from peripheral chemoreceptor
  • Medullary chemoreceptors monitor O2 concentrations in the CSF.
  • In metabolic alkalosis ventilation is depressed.
A

In metabolic alkalosis ventilation is depressed.

Low CO2 in the blood (as it is buffered out) causes a rise in pH in the CSF -> hypoventilation

  • The autonomic control centre is located in the Medulla
  • Brainstem respiratory neurons only discharge during inspiration and can discharge in expiration if needed
  • Arterial pO2 must be below 100mmHg to produce increased discharge from peripheral chemoreceptor
    • Start responding at very low levels <500mmHg, but rate increases rapidly below 100mmHg
  • Medullary chemoreceptors monitor H+ concentrations in the CSF.
41
Q

The following physiological events are in a random sequence, which is the usual sequence : (a) decreased CSF pH, (b) increased PaCO2, (c) increased CSF PCO2, (d) stimulation of medullary chemoreceptors, (e) increased PACO2

  • a b c d e
  • d a c b e
  • c d e b a
  • e b c a d
  • e c b d a
A

e b c a d

  1. Increased PACO2
  2. Increased PaCO2
  3. Increased CSF CO2
  4. Decreased CSF pH
  5. Stimuation of chemoreceptors
42
Q

With regard to the neural control of respiration

  • There are 3 neural mechanisms regulating respiration
  • The dorsal group of respiratory centre has excitatory neurons
  • The ventral group of respiratory centre is located in the pons.
  • The main respiratory control centre is located in the pons.
  • Voluntary control system is located in the cerebral cortex
A

Voluntary control system is located in the cerebral cortex

  • There are 3 neural mechanisms regulating respiration???
  • The dorsal group of respiratory centre has excitatory neurons
    • Dorsal = inspiration
  • The ventral group of respiratory centre is located in the Medulla
    • Ventral = expiration
  • The main respiratory control centre is located in the Medulla
    • ​Pons contains the apneustic and pneumotaxic centres
43
Q

for the chemical control of respiration

  • the carotid bodies respond to changes in pH, pCO2 and O2
  • the aortic bodies respond to changes in pH, pCO2 and O2
  • pO2 is only detected by central chemoreceptors.
  • severe hypoxia strongly stimulates central chemoreceptors.
  • the central chemoreceptors respond to changes in plasma pH.
A

the carotid bodies respond to changes in pH, pCO2 and O2

  • the aortic bodies respond to changes in pCO2 and O2
    • Only the carotid bodies respond to pH
  • pO2 is only detected by peripheral chemoreceptors.
  • severe hypoxia strongly stimulates peripheral chemoreceptors.
  • the central chemoreceptors respond to changes in CSF pH.
44
Q

with regard to chemoreceptors, which is false

  • the medullary chemoreceptors respond to a change in blood pCO2
  • the medullary chemoreceptors respond to blood H+
  • the predominant peripheral chemoreceptors are located in the carotid and aortic bodies
  • the peripheral chemoreceptors respond to pO2
  • the peripheral chemoreceptors respond to blood H+
A

the medullary chemoreceptors respond to CSF H+

Indirectly respond to blood pCO2 as this is what diffuses across the BBB

45
Q

which one of the following is false

  • medullary chemoreceptors monitor the CO2 concentrations of the CSF
  • HCO3 penetrate the BBB slowly
  • E neurons in the brain stem usually only become active when ventilation is increased
  • In metabolic acidosis CO2 response curves for fixed values of alveolar CO2 are shifted to the left
  • Type I cells in the carotid bodies are not stimulated by hypoxia caused by CO poisoning
A

medullary chemoreceptors monitor the H+ concentrations of the CSF

46
Q

carotid body stimulation occurs with

  • decreased BP
  • decreased pO2
  • increased pO2
  • increased pH
  • increased BP.
A

decreased pO2

  • Carotid and Aortic bodies are chemoreceptors*
  • Carotid sinus and aortic arch are involved in BP regulation*
47
Q

With regard to the distribution of pulmonary blood flow

  • Typically there is a zone at the apex that is not perfused.
  • The mean pulmonary arterial pressure is 8mmHg
  • In some areas flow is determined by the arterial/alveolar pressure difference
  • Hypoxia leads to pulmonary vasodilation.
  • The net balance of Starling forces act to keep the alveoli dry.
A

In some areas flow is determined by the arterial/alveolar pressure difference

  • Typically there is a zone at the apex that is poorly perfused.
  • The mean pulmonary arterial pressure is about 15mmHg
  • Hypoxia leads to pulmonary Vasoconstriction
  • The net balance of Starling forces act to Promote fluid to go from cap -> alveoli by a net filtration pressure of just 1mmHg.
48
Q

Pulmonary vascular resistance

  • Increases as venous pressure rises
  • Is increased in both very low and high lung volumes
  • Is decreased by histamine
  • Is increased by muscular pulmonary arterioles which regulate blood flow to various regions of the lungs.
  • Increases with recruitment
A

Is increased in both very low and high lung volumes

  • falls as venous (or arterial) pressure rises
  • Is increased by histamine
  • Can be increased by muscular pulmonary arterioles which regulate blood flow to various regions of the lungs
    • Nick thinks can be, I think there is hypoxic vasoconstriction at the level of the capillaries, but do not believe arteriole smooth muscle plays a role in blood flow
  • decreases with recruitment (of additional capillary beds)
49
Q

Regarding pulmonary blood flow

  • Low blood pH causes vasodilation
  • At high altitude, generalized vasodilation causes a rise in pulmonary arterial pressure.
  • Vasoconstriction may occur when the alveolar pO2 is reduced below 55mmHg.
  • Inhaled nitrous oxide reduces pulmonary vasoconstriction
  • Endothelins are potent vasodilatory peptides
A

Inhaled nitrous oxide reduces pulmonary vasoconstriction

(However NO synthase inhibitors augment vasoconstriction. Who the fuck knows why)

  • Low blood pH causes vasodilation Vasoconstriction
  • At high altitude, generalized vasoconstriction causes a rise in pulmonary arterial pressure.
  • Vasoconstriction may occur when the alveolar pO2 is reduced below 70mmHg.
    • Starts below 100mmHg, but pronounced at <70
  • Endothelins are potent vasoconstricting peptides.
50
Q

which of the following causes increased pulmonary vascular resistance

  • altitude
  • forced expiratiion
A

altitude

Due to hypoxic vasoconstriction.

51
Q

Regarding ventilation/perfusion differences in the lungs

  • In healthy individuals, anatomical dead space is less than physiological dead space.
  • The relative change in blood flow from apex to base is less than relative change in ventilation.
  • V/Q differences are due to gravity.
  • V/Q ratio is low at the bases.
  • All of the above
A

V/Q ratio is low at the bases.

As Q is greater at the bases than V

  • In healthy individuals, anatomical dead space is more or equal than physiological dead space.
  • The relative change in blood flow from apex to base is more than relative change in ventilation.
    • ie blood flow increases more than ventilation does from apex to base
  • V/Q differences are due to gravity. ​
  • All of the above
52
Q

In regional ventilation and perfusion of the lung

  • Upper regions of the lung ventilate better than the lower regions.
  • When supine the apical and basal ventilation is equal
  • V/Q ratio increases down the lung.
  • The highest alveolar pO2 is at the base of the lung .
  • Blood flow is uniform throughout the normal lung.
A

When supine the apical and basal ventilation is equal

  • Upper regions of the lung ventilate worse than the lower regions.
    • Bases have more ventilation AND more blood flow (relatively more blood flow than ventilation though)
  • V/Q ratio decreases down the lung.
    • Ventilation drops, but perfusion drops more (ie the denominator gets bigger, relatively speaking)
  • The highest alveolar pO2 is at the apex of the lung
    • Highest V/Q ratio at the apex, so the ventilation is relatively more than the perfusion (so there is less blood for the O2 to diffuse into, away from the alveoli)
  • Blood flow varies throughout the normal lung, and when upright is least at the apex, and most at the bases
53
Q

The haemoglobin oxygen dissociation curve moves up and to the left with

  • Increased hydrogen ion concentration
  • Hypothermia
  • Increased 2,3 DPG
  • Hypercarbia
  • All of the above
A

Hypothermia

Remember. acidosis, heat, and increased CO2 (all things that occur in exercising muscle) shift the curve to the right.

54
Q

The haldane effect refers to

  • The increased capacity for deoxygenated blood to carry CO2
  • The dissociation constant for the bicarbonate buffer system
  • The chloride shift that occurs to maintain electrical neutrality
  • The carriage of dissolved CO2 according to Henry’s law
  • The shape of the CO2 dissociation curve
A

The increased capacity for deoxygenated blood to carry CO2

Via two mechanisms:

  1. DeoxyHb more able to form carbamino compounds than oxyHb
  2. H+ binds to deoxy Hb, shifting the equation to the right and allowing more CO2 be turned into HCO3 (and this more CO2 to dissolve)
55
Q

Regarding buffers of the body

  • Initial correction of pH disturbance is best achieved by the kidneys.
  • The phosphate buffer system is the predominant buffer in the blood.
  • Bones contribute to the buffer system by taking up HCO3
  • Hb is an important buffer of the blood
  • All of the above are correct
A

Hb is an important buffer of the blood

Hb binds H+ in its deoxy form

  • Initial correction of pH disturbance is best achieved by the Lungs (kidneys take 2-3 days to take effect)
  • The phosphate buffer system is the predominant intracellular buffer.
  • Bones contribute to the buffer system by taking up HCO3
  • All of the above are correct
56
Q

In CO2 transport

  • The HCO3 content of venous blood is reduced compared to arterial blood
  • The osmolarity of RBCs in venous blood is increased compared to arterial blood
  • The haematocrit of venous blood is 3% less than arterial blood
  • The solubility of CO2 in blood is less than O2.
  • CO2 does not react with plasma proteins.
A

The HCO3 content of venous blood is reduced compared to arterial blood

Reduces frorm 90% to 60% of CO2 carriage, presumably because of the rise in carbamino compoundsa and dissolved CO2 in venous blood

  • The osmolarity of RBCs in venous blood is increased compared to arterial blood
    • Stays the same, as HCO3- is replaced by CL- (otherwise the RBC would expand/explode)
  • The haematocrit of venous blood is 3% less than arterial blood
    • Presumably the same as the Hb content does not differ.
  • The solubility of CO2 in blood is more (like 20x) than O2.
  • (5% in arteries, 20% in veins) of CO2 is bound to plasma proteins
57
Q

Regarding the O2 dissociation curve

  • Each gram of pure Hb can bind 1 mol of O2
  • 2,3 DPG levels fall at high altitude.
  • an increase in the affinity of Hb for O2 in an acid environment is called the Bohr effect.
  • a right shift implies a lower pO2 is required for O2 binding.
  • the p50 is an index of the affinity of Hb for O2
A

the p50 is an index of the affinity of Hb for O2

Is the pO2 that will give 50% saturation (normally 27mmHg)

  • Each gram of pure Hb can bind 1.39ml of O2 (each molecule Hb binds 4 molecules O2)
  • 2,3 DPG levels i**ncrease at high altitude (this allows for increased venous offloading of O2 despite a lower PO2 [causes a right-ward shift of Hb-diss curve ie less affinity])
  • an decreased affinity of Hb for O2 in an acid environment is called the Bohr effect (allows increasd offloading of O2 to the tissues that are acidotic/hypoxic)
  • a right shift implies a higher pO2 is required for O2 binding.
58
Q

Haemoglobin dissociation curve shifts

  • To the right with CO poisoning.
  • To the left with a rise in temperature
  • To the left with a rise in pH
  • To the right with a decrease in 2,3 DPG
  • To the left with anaemia.
A

To the left with a rise in pH

Acidosis->right; alkalosis -> left

  • To the left with CO poisoning (increased affinity, harder to offload O2)
  • To the right with a rise in temperature
  • To the right with an increase in 2,3 DPG
  • Does not change with anaemia - the O2 concentration does though (the pO2 also does not change)
59
Q

In CO2 transport

  • There is slightly more carbon dioxide in dissolved in the blood than oxygen.
  • Venous blood can carry more CO2 than arterial blood
  • Chloride shift allows CO2 to dissociate
  • There is equal amounts of CO2 transported as dissolved CO2 and carbamino compounds
  • 2,3 DPG concentration in RBC will alter the cells ability to catalyse CO2.
A

Venous blood can carry more CO2 than arterial blood

  • There is a lot more CO2 dissolved than O2*
  • Chloride shift maintains electroneutrality when HCO3- diffuses out of RBC after being produced by carbonic anhydrase*
  • 5% of CO2 is each dissolved and as carbamino compounds in arterial blood, but in venous blood 10% is dissolved and 30% carbamino compounds*
  • Carbonic anhydrase concentration alters RBC ability to catalyse CO2*
60
Q

With respect to gas transport in the blood

  • Arterial pO2 measures the amount of oxygen bound to haemoglobin
  • Normal arterial blood with a pO2 of 100mHg contains 3mL of dissolved oxygen per litre
  • Haldane effect refers to the shift of Chloride ions into the RBC to maintain electrical neutrality after carbon dioxide diffuses out of cells
  • The great bulk of carbon dioxide in blood is found as dissolved carbon dioxide and carbamino compounds
  • Oxygen capacity is the total amount of oxygen that can be carried in 100mL of blood
A

Oxygen capacity is the total amount of oxygen that can be carried in 100mL of blood

usually 20ml O2 /100ml blood

  • Oxygen saturation measures the amount of oxygen bound to haemoglobin
  • Normal arterial blood with a pO2 of 100mHg contains 0.3mL of dissolved oxygen per litre (ie fuck all)
  • Chloride shift refers to the shift of Chloride ions into the RBC to maintain electrical neutrality after carbon dioxide diffuses out of cells
    • Haldane effect is the increased ability of deoxygenated blood to carry CO2
  • The minority of carbon dioxide in blood is found as dissolved carbon dioxide and carbamino compounds - most is in the form of bicarbonate
61
Q

Regarding CO2 transport in the blood

  • 50% is in the dissolved form
  • the Haldane effect is the fact that oxygenation of the blood increases its ability to carry CO2
  • ionic dissociation of carbonic acid requires the presence of carbonic anydrase to be a fast process
  • an increase in pCO2 in blood shifts the oxygen dissociation curve to the left
  • approximately 30% of the venous arterial difference is attributable to carbamino compounds
A

approximately 30% of the venous arterial difference is attributable to carbamino compounds

  • 5% is in the dissolved form (in arterial blood, 10% in venous)
  • the Haldane effect is the fact that deoxygenation of the blood increases its ability to carry CO2
  • ionic dissociation of carbonic acid is always fast (H2CO3 <-> HCO3- + H+)
    • ​[H20 + CO2 <-> H2CO3] requires the presence of carbonic anydrase to be a fast process
  • an increase in pCO2 in blood shifts the oxygen dissociation curve to the right
62
Q

Oxygen transport

  • The oxygen dissociation curve shifts left with a fall in pH
  • More oxygen is supplied to tissues by a fall in 2,3 DPG levels
  • 2,3 DPG levels are increased by ascent to 7000m
  • oxygen dissociation curve shifts right with a drop in temperature
A

2,3 DPG levels are increased by ascent to 7000m

  • The oxygen dissociation curve shifts right with a fall in pH
  • More oxygen is supplied to tissues by a rise in 2,3 DPG levels
    • 2,3 DPG binds to deoxy Hb, and lowers affinity of the remaining Hb for O2 (ie it helps dissociate O2 in the tissues)
  • oxygen dissociation curve shifts left with a drop in temperature
63
Q

The oxygen Hb dissocation curve

  • The p50 is roughly 83.5
  • Oxygenation status of haemoglobin has no effect
  • In the low part of the curve, large amounts of oxygen is liberated to the tissues for small decreases in the O2
  • In the flat part of the curve, there is large changes in the saturation for small changes in pO2
  • A fall in pH shifts the curve to the left
A

In the low part of the curve, large amounts of oxygen is liberated to the tissues for small decreases in the O2

  • The p50 is roughly 27mmHg O2
  • Oxygenation status of haemoglobin has an effect apparently.
  • In the flat part of the curve, there is small changes in the saturation for large changes in pO2
  • A fall in pH shifts the curve to the right
64
Q

A 28yo woman takes an OD of sedatives, causing her to hypoventilate. Her pCO2 is now 80mmHg, given that she is breathing room air, which of the following is likely to be correct

  • PaO2 is ~ 70mmHg
  • PaO2 is ~ 35mmHg
  • SaO2 ~50%
  • SaO2 ~80%
  • SaO2 ~27%
A

SaO2 ~80%

Inspired O2 = 21% (if using kPa) or 149mmHg

Therefore PAO2 = 149 - (80 / 0.8)

= 49

PaO2 40 = 75%

Therefore 50 ~ 80%

65
Q

What is the pO2 of alveolar air with a CO2 of 64 and a respiratory quotient of 0.8

  • 35
  • 52
  • 69
  • 72
  • 80
A

PAO2 = 149 - ( 64 / 0.8 )

= 149 - 80

= 69

Note that if using kPA, FiO2 is 21 (im fairly sure), but is 149 if using mmHg (the larger numbers)

66
Q

A shift of the haemoglobin/oxygen dissociation curve to the right is associated with:

  • Increased p50
  • Increased affinity of haemoglobin for oxygen
  • Decrease in 2,3 DPG
  • Decrease in blood temperature
  • Increase in pH
A

Increased p50

  • Decreased affinity of haemoglobin for oxygen
  • Increase in 2,3 DPG
  • Increase in blood temperature
  • Decrease in pH (increase in H+)
67
Q

causes of hypoxic hypoxia include all of the following except

  • pulmonary shunting
  • morphine
  • pulmonary fibrosis
  • fatigue
  • congestive heart failure
A

First 4 all cause hypoxic hypoxia, through hypoventilation, lung disease, or shunt.

CHF could cause it through pulmonary oedema, or could be classified under circulatory hypoxia depending on the specifics.

I think this is a poor question.

1) Hypoxic hypoxia: Global hypoventilation, V/Q mismatch, right to left shunting, high altitude, pulmonary obstruction, or lung disease.
2) Anaemic hypoxia: aneamia, Hb disorders, CO poisoning
3) Circulatory hypoxia: shock, resulting in impaired O2 delivery to tissues
4) Histotoxic hypoxia: unable to metabolise O2, eg cyanide poisoning.

68
Q

The most important short term response to high altitude is

  • Hyperventilation
  • Polycythaemia
  • Chronic mountain sickness
  • Acidosis
  • Decreased EPO release
A

Hyperventilation

Increases pO2, but also creates a metabolic alkalosis in the short-term which limits the degree to which it can be utilised (CO2 production does not change)

69
Q

All of the following are effects of hypoxia except

  • Increased EPO secretion
  • Increase in respiratory minute volume
  • Increase sensitivity to pCO2
  • Increased HR
  • Pulmonary vasodilation
A

Pulmonary vasodilation

Pulmonary vasculature constricts in response to hypoxia (can cause pulmonary hypertension at altitude due to global constriction of the pulmonary circuit)

70
Q

On climbing Everest

  • EPO secretion rises after 2-3 days
  • Nifedipine alleviates the symptoms of mountain sickness
  • Alveolar pCO2 levels rise
  • pCO2 levels fall because of decreased oxygen content of the air
  • initially the oxygen-Hb dissociation curve shifts to the left
A

EPO secretion rises after 2-3 days

  • acetazolamide alleviates the symptoms of mountain sickness as it causes urinary HCO3 loss, creating a metabolic acidosis, allowing further hyperventilation to occur
  • Alveolar pCO2 levels fall due to hyperventilation
  • pCO2 levels fall because of decreased oxygen content of the air
    • Not directly - low O2 -> hyperventilation -> low CO2
  • initially the oxygen-Hb dissociation curve shifts to the right due to an icnrease in 2,3 DPG (in response to the respiratory alkalosis)
71
Q

Regarding ventilation during exercise

  • Pulmonary blood flow is increased from 5.5L/min –> 55L/min
  • Abrupt increase in ventilation at onset of exercise is due to increased respiratory rate
  • Increases in ventilation are proportional to increased CO2 production
  • CO2 excretion increases from 200mL/min up to 8000mL/min
  • There is a fall in blood pH during moderate exercise
A

Increases in ventilation are proportional to increased CO2 production

Not specifically mentioned, but as the CO2 does not vary with exercise, this must be true

  • Pulmonary blood flow is increased from 5.5L/min –> ~30L/min (CO increse about 7x)
  • Abrupt increase in ventilation at onset of exercise is unknown why this happens, ?due to movement of muscles
  • CO2 excretion increases from 200mL/min up to 3000mL/min
  • There is no change in blood pH during moderate exercise
    • Only at severe exercise dose lactate production overcome the ability to ventilate CO2 off
72
Q

In SCUBA diving

  • A person needs to breathe higher concentrations of oxygen
  • There is an increase in barometric pressure of 1 atm for every 15m of water
  • Nitrogen acts as an inert gas
  • Normal V/Q differences in the lung are exaggerated
  • Decompression sickness is caused by oxygen toxicity
A

Nitrogen acts as an inert gas

Answer not specifically in Wests, however nitrogen is generally used as the inert gas in SCUBA except very deep dives, where helium is used to prevetion nitrogen narcosis.

  • A person needs to breathe higher pressures of oxygen
  • There is an increase in barometric pressure of 1 atm for every 10m of water
  • Normal V/Q differences in the lung are reduced (less gravitational effects)
  • Decompression sickness is caused by nitrogen toxicity
73
Q

exposure to altitude

  • shifts the O2-Hb dissociation curve to the right due to alkalosis
  • is associated with an increase in RBC 2,3 DPG
  • is associated with a decrease in p50
  • is associated with a respiratory acidosis
  • has no effect on EPO secretion
A

is associated with an increase in RBC 2,3 DPG

  • shifts the O2-Hb dissociation curve to the right due to increased 2,3 DPG
  • is associated with an increase in p50
  • is associated with a respiratory alkalosis
  • after 2-3 days causes a rise in EPO secretion
74
Q

with regard to high altitude

  • there is a linear decrease in inspired oxygen pressure with increasing altitude
  • the partial pressure of water vapour in moist inspired air decreases with PIO2
  • at 19 200m, barometric pressure = 47mmHg, PIO2 is then 9mmHg
  • at the peak of Everest, barometric pressure ~ 380mmHg, PIO2 is then approximately 70mmHg
  • in permanent residents of the Andes, arterial and venous pO2 is half normal levels
A

at the peak of Everest, barometric pressure ~ 380mmHg, PIO2 is then approximately 70mmHg

  • PiO2 = (Patm - Ph2o) x FiO2*
  • = (380-47) x 0.21*
  • =* 69.93

And PAO2 = PiO2 - (PaCO2 / 0.8 )

75
Q

A permanent inhabitant at 4500m

  • Has a high alveolar pO2 level
  • Has a decreased 2,3 DPG
  • Shows increased ventilation
  • May have a normal HCO3
  • Is highly sensitized to the stimulatory effects of hypoxia
A

May have a normal HCO3

“at high altitude…renal compensation occurs by increased excretion of bicarbonate, thus returning the HCO3/CO2 ratio towards normal. After a prolonged stay at high altidue, renal compensation may be nearly complete”

  • Has a low alveolar pO2 level
  • Has a increased 2,3 DPG
  • Shows increased ventilation
    • Generally this occurs and is prolonged, however “Interestingly, people who are born at high altitude have a diminished ventilatory response to hypoxia that is only slowly corrected by subsequent residence at sea level. Conversely, those born at sea level who move to high altitudes retain their hypoxic response intact for a long time.”
  • has reduced sensitivity to the stimulatory effects of hypoxia
76
Q

When walking at a steady pace, the increase in respiratory rate is due to

  • Decreased pO2
  • Increased CO2
  • Increased pH
  • Increased pH CSF
  • None of the above
A

I think none of the above

Increase in ventilation in exercise occurs very early, before any parameters such as CO2, pH, or O2 levels begin to change.

These are kept very constant except in extreme exercise, and cannot account for the marked increase in respiratory rate.