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General Health and Disease (GHD) > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

Basic functions of the respiratory system? Overview?

A
  • Gas exchange leading to energy release via aerobic respiration
  • Acid base balance (reg of body pH)
  • Protection from infection
  • Communication via speech
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2
Q

Why do we breathe? Characteristics?

A

To produce energy: - respiration uses oxygen to produce energy, producing CO2 and waste

The only way this works via the integration of the CVS and the respiratory system

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3
Q

Gas exchange? Characteristics?

A

Exchange of gas between lungs and blood (or via blood and cells) occurs via simple diffusion down partial pressure gradients

Part 1: between atmosphere and lungs
Part 2: between lung and blood
Part 3: transport of gases in blood
Part 4: between blood and cells

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4
Q

Basic Respiratory anatomy? Upper and Lower tract?

A

Upper:

  • Pharynx
  • Oesophagus
  • Larynx
  • Tongue

Lower:

  • Trachea
  • Right and Left lung
  • Right and Left bronchus
  • Diaphragm
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5
Q

Lower respiratory tract - lobes and lungs?

A
  • Trachea travels down into the lungs and splits into 2 primary bronchi
  • 5 secondary bronchi 1 to each lobe
  • Right lung has 2 lobes (superior, middle and inferior)
  • Left lung *superior and inferior) also has the cardiac notch where the heart sits
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6
Q

Branching of airways? Structure?

A
  • Larynx
  • Trachea
  • Primary bronchus
  • Secondary bronchus
  • Bronchiole
  • Alveoli
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7
Q

Structure of the lung lobule?

A
  • The bronchiole is surrounded by SM and the bronchial artery, vein and nerve
  • Bronchiole becomes the alveoli that has elastic fibres and capillary beds to allow gas exchange
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8
Q

Alveolar structure?

A

Contains:

  • Elastic fibres
  • Capillaries
  • Endothelial cells of capillaries
  • TII cells (surfactant cells)
  • TI cells
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9
Q

Resistance to air flow? Characteristics?

A

Smooth muscle in bronchial wall regulates diameter of airways:
- contraction reduces diameter and increases resistance and vice versa

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10
Q

Lung volumes and capacities? Names and values?

A
  • Tidal volume: 500mL
  • Total lung capacity: 6000mL
  • Vital capacity: 4600mL
  • Residual volume: 1200mL
  • Expiratory reserve volume: 1100mL
  • Inspiratory reserve volume: 3000mL
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11
Q

Lung volumes and capacities? Definition?

A
  • TV - Tidal Volume. The volume of air breathed in and out of the lungs at each breath.
  • ERV - Expiratory Reserve Volume. The maximum volume of air which can be expelled from the lungs at the end of a normal expiration.
  • IRV - Inspiratory Reserve Volume. The maximum volume of air which can be drawn into the lungs at the end of a normal inspiration.
  • RV - Residual Volume. The volume of gas in the lungs at the end of a maximal expiration.
  • VC - Vital Capacity = tidal volume + inspiratory reserve volume + expiratory reserve volume.
  • TLC - Total Lung Capacity = vital capacity + the residual volume.
  • IC - Inspiratory Capacity = tidal volume + inspiratory reserve volume.
  • FRC - Functional Residual Capacity = expiratory reserve volume + residual volume.
  • FEV1:FVC = Fraction of forced vital capacity expired in 1 second.
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12
Q

Gas laws? Name and explanation?

A
  • Boyle’s Law states that the pressure exerted by a gas is inversely proportional to to its volume (P a 1/V)
  • Henry’s Law states that the amount of gas dissolved in a liquid is determined by the pressure of the gas and it’s solubility in the liquid.
  • Dalton’s Law states that the total pressure of a gas mixture is the sum of the pressures of the individual gases.

Gases always move from areas of high Pa to areas of low Pa

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13
Q

Cross-sectional structure of the lungs?

A
  • Right/Left lung

- Right/Left pleural cavity

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14
Q

Anatomy of the pleural sac? Structure?

A

The lungs and interior of the thorax are covered by pleural membranes between the surfaces of which is an extremely thin layer of intrapleural fluid

  • left/right pleural sac
  • parietal pleura
  • visceral pleura
  • pleural cavity filled with intrapleural fluid`
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15
Q

Functions of the pleural membranes? Functions?

A
  • Stick the lungs to the rib cage
  • Visceral pleura is “stuck” to the surface of the lungs
  • Visceral pleura is “stuck” to the parietal pleura via the cohesive forces of the pleural fluid
  • Parietal pleura is “stuck” to the rib cage and diaphragm

The lungs will therefore follow the movements of these bones and muscles

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16
Q

Muscles of Breathing? Overview?

A

These muscles are responsible for creating the pressure gradient that determines air flow (remember, air flows from high pressure to low pressure)

Inspiration:

  • Sternocleidomastoids
  • Scalenes
  • External intercostals
  • Diaphragm

Expiration:

  • Internal intercostals
  • Abdominal muscles
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17
Q

Mechanism of breathing action? Diaphragm?

A
  • At rest, the diaphragm is relaxed
  • Diaphragm relaxes and the thoracic volume decreases
  • Diaphragm contracts and the thoracic volume increases
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18
Q

Mechanics of breathing? Ribs?

A

Pump handle: motion increases anterior-posterior dimensions of rib cage

Bucket handle: motion increases lateral dimensions of rib cage

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19
Q

Relevant pressures within the lungs?

A

Intra-thoracic Pa: pressure inside the thoracic cavity (inside lung)

Intra-pleural Pa: pressure inside the pleural cavity

Transpulmonary Pa: difference between alveolar Pa and intra-pleural Pa

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20
Q

Pressure changes within the lungs during inspiration and expiration?

A

During inspiration:

  • the alveolar pressure decreases and increases by 1 mmHg ending at 0 Pa difference
  • the interapleural pressure drops by -3 mmHg

During expiration:

  • the alveolar Pa increases by 1 and drops by 1 ending at a 0 Pa chnage
  • the intrapleural Pa increases back to -3 mmHg (from -6)
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21
Q

Importance of the relationship between pleural membranes?

A

Normal:

  • the intrapleural Pa is subatmospheric (-3mmHg), which drives air into the lungs
  • elastic recoil tries to pull chest wall outward and creates and inward pull

Pneumothorax:

  • stab wound
  • lung collapses
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22
Q

Bulk flow of air equation and explanation? lung elasticity explanation?

A
  • Bulk flow of air between the atmosphere and alveoli is proportional to the difference between the atmospheric and alveolar pressures and inversely proportional to the airway resistance: F = (Patm- Palv)/R
  • The lungs are stretched and are attempting to recoil, whereas the chest wall is compressed and attempting to move outward. This creates a subatmospheric intrapleural pressure and hence a transpulmonary pressure that opposes the forces of elastic recoil
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23
Q

Surfactant? definition and function?

A

Detergent like fluid produced by Type II Alveolar cells

  • Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse
  • surface tension occurs wherever there is an air-water interface and refers to the attraction between water molecules
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24
Q

How does surfactant work? Example? Principle of surface tension?

A

Water molecules is attracted to other water molecules, forming larger droplets

All of these droplets causes the overall force to be brought inwards that causes surface tension within the alveoli

Surfactant’s role us to surround the other water molecules to stop the attraction

Increases lung compliance, reduces lung’s tendency to recoil, makes breathing easier and more effective in small alveoli

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25
Q

How does surfactant prevent alveolar collapse?

A

Pa is greater in the smaller alveoli than the larger ones and so air flows into the larger alveoli

Surfactant reduces surface tension which equalises the large and small alveoli, which allows greater gas exchange due to increased SA

26
Q

Pulmonary ventilation? Definition?

A

Total air movement in and out of the lungs

27
Q

Alveolar ventilation? Definition?

A

Fresh air getting to the alveoli and therefore available for gas exchange

28
Q

Anatomical dead space volume? Characteristics?

A
  • 150 mL

- volume of gas occupied by the conducting airways and the gas is not available for exchange

29
Q

Inhalation and exhalation process - air volumes?

A

Exhalation: 500mL loss; - which is 150mL dead space and 350mL stale air and the remaining 150mL (stale air) is present in the conducting airways

Inhalation: 500mL gain;
- 150mL stale air from the dead space enters the lungs, and only 350mL of fresh air enters the alveoli, and another 150mL of fresh air is trapped in the dead space

30
Q

Hypoventilation vs Hyperventilation? Differences?

A

Hypoventilation: Higher TV and lower frequency (but alveolar ventilation is still normal)

Hyperventilation: Lower TV and higher frequency (but the alveolar ventilation is much lower)

Hyperventilation is bad in a clinical sense

31
Q

Dalton’s Law? Definition?

A

The pressure of an entire gaseous mixture is equal to the sum of the pressures of the individual gases in that mixture

Atmospheric Pa - 760 mmHg
Composition of air: 78% N, 21% O2 and 0.04% CO2

32
Q

Alveolar ventilation and partial pressues? PO2 and PCO2?

A

Normal ventilation: 4.2L/min

  • PO2: 100 mmHg
  • PCO2: 40 mmHg

Hyperventilation: >4.2L/min

  • PO2: 120 mmHg
  • PCO2: 20 mmHg

Hypoventilation: < 4.2L/min

  • PO2 30 mmHg
  • PCO2 100 mmHg
33
Q

Compliance? Definition?

A

Change in volume relative to change in pressure

  • It represents the stretchability of the lungs
    e. g. how much does volume change for any given change in pressure
34
Q

Difference between low and high compliance?

A

HIGH COMPLIANCE = large increase in lung volume for small decrease in interpleural pressure

LOW COMPLIANCE = small increase in lung volume for large decrease in interpleural pressure

Changes in disease and age

35
Q

Pressure, volume and distribution of ventilation? Differences in orientation?

A
  • The pressure volume curve varies between apex and base of the lung. At the base the volume change is greater for a given change in pressure.
  • Alveolar ventilation declines with height from base to apex.
  • Compliance is lower at the apex due to being more inflated at FRC. At the base the lungs are slightly compressed by the diaphragm hence more compliant on inspiration.
  • A small change in intrapleural pressure therefore brings about a larger change in volume at the base compared with the apex.
36
Q

Gas transport in the blood? Process?

A
  • Blood transport O2 from the lungs to the tissues, used to produce energy and then the waste and CO2 is removed
  • Haemoglobin carries O2 (200ml/L)
  • Bulk of CO2 is transported in various forms
37
Q

Blood supply to the lungs? Pulmonary circulation?

A
  • Consists of L and R pulmonary arteries originating from the RV
  • These both supply the capillary network around the alveoli and returns oxygenated blood to the LA, via the pulmonary vein (high flow - low pressure)
38
Q

The rate of diffusion across the alveoli? Factors?

A
  • Directly proportional to the partial pressure gradient
  • Directly proportional to the solubility of the gas
  • Directly proportional to the available SA
  • Inversely proportional to the thickness of the membrane
  • Most rapid over short distances
39
Q

Gas exchange in the alveoli and blood? Partial Pa?

A 
Alveoli: 
- PO2 (100)
- PCO2 (40)
Blood at lungs:
- PO2 (40)
- PCO2 (46)
Blood at cells
- PO2 (100)
- PCO2 (40)
Cells:
- PO2 (<40)
- PCO2 (>46)
40
Q

Alveoli to RBC transfer? Characteristics?

A

The alveoli has a very thin membrane which allows simple diffusion of o2 to the passing RBCs in the bloodstream

41
Q

Haemoglobin? Characteristic?

A

Structure: 2 alpha chains and 2 beta chains
- 98% O2 bound to haemoglobin
Each haemoglobin contains 4 haem groups, each of which contains one Fe which binds one o2 and so each haemoglobin can bind 4 molecules
- The degree of haemoglobin binding depends on oxygen partial pressure

42
Q

Blood with haemoglobin vs blood without haemoglobin?

A

Hb effectively sequesters O2 from the plasma, thus maintaining a partial pressure gradient that continues to suck O2 out of the alveoli, until the Hb becomes saturated with O2.

Partial pressure of O2 in plasma is fundamental in determining how much O2 binds to Hb.

43
Q

Oxygen-haemoglobin dissociation curve?

A

Haemoglobin is almost 100% saturated at the normal systemic arterial PO2 of 100 mm Hg. The fact that saturation is already more than 90% at a PO2 of 60 mm Hg permits a relative normal uptake of oxygen by the blood even when alveolar PO2 is moderately reduced.

Haemoglobin is 75% saturated at the normal systemic venous PO2 of 40 mm Hg. Thus, at rest only 25% of the oxygen dissociates from haemoglobin and enters the tissues.

44
Q

Factors affecting the oxygen-dissociation curve? Factors?

A
  • pH (reduced pH, reduced affinity and vice versa)
  • PCO2 (increased CO2, reduced affinity and vice versa)
  • Temperature (increase temp, reduced affinity and vice versa)
  • DPG (addition of DPG, reduces affinity)
45
Q

Carbon dioxide transport? Process?

A

CO2 transport is much simpler than the transport of O2. CO2 is much more soluble than O2 and after CO2 diffuses from the tissues into the blood down it’s partial pressure gradient, 7% remains dissolved in the plasma and is transported in simple solution.

The remaining 93% moves into the red blood cells where 23% forms carbamino compounds with the now desaturated haemoglobin while the remainder is converted to bicarbonate ions, exchanged for Cl- across the RBC membrane and transported in the plasma in the form of HCO3-

46
Q

Distribution of blood flow in lungs - influenced by? perfusion? alveolar? resistance chnages?

A

The distribution of blood flow in the lung is influenced by both hydrostatic (blood) pressure and alveolar pressure.

At the base of the lungs blood flow is high since perfusion pressure exceeds alveolar pressure and hence vascular resistance is low.

At the apex of the lungs blood flow is low because perfusion pressure is less than alveolar pressure. This compresses the arterioles and vascular resistance is increased.

47
Q

Matching ventilation and perfusion? Characteristics?

A

In the upright position the ratio of ventilation to perfusion within the lung changes from the base of the lung (bottom) to the apex (top) owing to the effect of gravity.

Over 75% of the height the healthy lung performs quite well in matching blood and air (right y-axis). The majority of the mismatch takes place in the apex. This is then auto regulated to keep the ventilation perfusion ratio close to 1.0

48
Q

Autoregulation of ventilation:perfusion?

A

Ventilation > perfusion:

  • alveolar PO2 rises, PCO2 falls
  • causes pulmonary vasodil and bronchial constrict

Perfusion > ventilation:

  • alveolar PO2 falls, PCO2 rises
  • pulmonary vasoconstrict and bronchial dilation
49
Q

Ventilatory control? Innervation and brain centres?

A
  • requires stimulation of the (skeletal) muscles of inspiration. This occurs via the phrenic (to diaphragm) and intercostal nerves (to external intercostal muscles)
  • subconcious, but can have voluntary modulation
  • entirely dependent on signalling from the brain (sever spinal cord above origin of phrenic nerve (C3-5) breathing ceases)
50
Q

Rhythmic breathing and voluntary override? Overview?

A

Breathing depends upon cyclical activation of the phrenic and intercostals nerves stimulating contraction of the inspiratory muscles (diaphragm/external intercostals). This neural activity is triggered by the medullary inspiratory neurones but with voluntary override

51
Q

Respiratory centres have rhythm modulated by? factors affecting rhythm?

A
  • Emotion (via limbic system in the brain)
  • Voluntary over-ride (via higher centres in the brain)
  • Mechano-sensory input from the thorax (e.g. stretch reflex)
  • Chemical composition of the blood (PCO2, PO2 and pH) – detected by chemoreceptors.
52
Q

Respiratory centre flow chart of action? flow chart?

A
  • Located in the medulla and pons of the brain
  • Factors affecting rhythm influence the VRG and DRG (dorsal/ventral respiratory group)
  • the most significant factor is chemoreceptor input
  • the VRG innervates the tongue, pharynx, larynx and epiratory muscles
  • the DRG (via the phrenic or intercostal nerves) innervate the inspiratory muscles
53
Q

Chemoreceptors? Types and overview on how they work?

A

Types:
- Central and Peripheral

Central:

  • medulla
  • responds directly to the H+ (reflects PCO2)
  • primary ventilatory force

Peripheral:

  • carotid and aortic bodies
  • responds to plasma H+ and PO2
  • secondary ventilatory drive
54
Q

Central chemoreceptors in the medulla? Characteristics and what it detects?

A
  • Detect changes in H+ in CSF
  • Causes reflex stim of ventilation following rise in H+ (driven by raised PCO2 = hypercapnea)

CO2 + H20 = H2CO3 = H+ + HCO3-

Ventilation is reflexly inhibited by a decrease in arterial PCO2

55
Q

Process of central chemoreceptor action? Process?

A

When arterial PCO2 increases carbon dioxide crosses the blood-brain barrier not H+

Central chemoreceptors monitor the PCO2 indirectly in the cerebrospinal fluid.

Bicarbonate and H+ are formed and the receptors respond to the H+

Feedback via the Respiratory Centres increases ventilation in response to increased arterial PCO2 .

Decreased arterial PCO2 slows ventilation rate.

56
Q

Peripheral chemoreceptors? Characteristics and what it detects?

A
  • Located in the carotid and aortic bodies
  • Detect changes in arterial PO2 and H+
  • Causes reflex stim of ventilation following significant fall in arterial PO2 or a rise in H+
  • respond to arterial PO2 not oxygen content
  • increased H+ usually accompanies a rise in arterial PCO2
57
Q

Oxygen-haemoglobin dissociation curve? Description?

A
  • Haemoglobin is highly saturated across many mmHg of PO2
  • And so a large fall in mmHg will occur before the peripheral chemoreceptors to detect a change and influence a response
58
Q

Good Chemoreceptor reflex slide

A

GHD - Resp 4

59
Q

Emotion and the respiratory centres? the link?

A

Limbic system input allows emotional responses to alter breathing e.g. rapid, shallow breathing often accompanies anxiety

60
Q

Other aspects of controlling breathing? Characteristics?

A

Descending neural pathways from cerebral cortex to respiratory motor neurons allow a large degree of voluntary control over breathing

Respiration is inhibited during swallowing to avoid aspiration of food or fluids into the airways. Swallowing is followed by an expiration in order that any particles are dislodged outwards from the region of the glottis

61
Q

Pharmacological influences on ventilatory control? Drug examples and their influence?

A
  • Barbiturates – e.g. thiopental (iv. anaesthesia). Inhibit phrenic nerve activity, decrease depth of breathing (alv. ventilation)
  • Opioids – e.g. morphine. sensitivity to pH and therefore response to PCO2 . Also peripheral chemoreceptor response to PO2
  • Benzodiazepines – e.g. diazepam (anxiolytic, sedative). Similar effects to opioids but much less severe. Relatively safe and widely used.
  • Nitrous oxide – Little effect on response to PCO2 but significantly depresses response to falling PO2. Caution with COPD patients! Widely used.

General Health and Disease (GHD) (31 decks)

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