Respiratory Flashcards

(46 cards)

1
Q

Ficks Law

A

The shorted the distance through which diffusion takes places and the greater the surface area of which this can occur will affect diffusion rate.

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2
Q

Basic functions

A
  • Homeostasis of CO2, O2 and blood pH
  • Speech generation
  • Warm, humidify and clean insiparted air
  • Nose is olfactory organ
  • Activates hormones (angiotensin 2), inactivates hormones (prostaglandins)
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3
Q

Key points about anatomy

A

Type 1 alveolar cells - form the walls

Type 2 alveolar cells - produce the watery lining, which will decrease surface tension and O2 needs to dissolve in water before lung

Note the very close proximity of the capillaries to the alveolar walls (decrease diffusion distance)

Inner lung surface is about 50 times larger than surface of the skin, this means it is easier for diffusion and this is able to happen via the great amounts of branching that the bronchi’s perform

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4
Q

Pulmonary surfactant

A

Pulmonary surface reduces the lungs tendency to recoil and increases pulmonary compliance. Does this more in smaller alveoli because the surfactant molecules are closer.
It improves ling stability to prevent small alveoli to collapse into the larger ones

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5
Q

Law of LaPlace

A

Magnitude of inward directed pressure in a bubble = 2xsurface tension/radius of bubble

Therefore, with the same surface tension their will be smaller pressure in larger balloon. Meaning smaller alveoli would collapse into the larger ones.

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6
Q

Inspiration of molecules blocked by cells

A

Blocks inspiration of molecules over certain lengths

Nasal cavity capable of cleaning particles larger than 10 nano-meters

Large airways 5-10

Respiratory bronchioles stop particles between 1 and 5

Suspended in air >0.5

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7
Q

Dynamic airway closure

A

Frictional losses causes the pressure in the air ways to drop. If this falls below the surrounding elevated intrapleural pressure the small compliant airways are compressed closed, blocking further expiration and trapping air in alveoli. The amount of air left in the alveoli after this is called residual volume.

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8
Q

Tidal Volume

A

Tidal volume = difference between end expiratory and end inspiratory (quite breathing)

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9
Q

Vital capacity

A

Vital capacity= total amount of air moved in and out of the lung (- res volume)

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10
Q

Functional residual capacity

A

Functional residual capacity = amount of air in lungs after quite expiration (COPD indicator)

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11
Q

Residual volume

A

Residual volume = amount of air left in lungs after force expiration (minimal lung volume)

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12
Q

Expiratory reserve volume

A

Expiratory reserve volume = amount of air exhaled after normal breathing

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13
Q

Why does tidal volume increases first during exercise

A

Tidal volume increases first. Any increases in tidal volume will increase alveolar ventilation by the same amount. Increase in respiratory rate will increase alveolar ventilation by a smaller amount due to the anatomical dead space (air left from preceding respiration).

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14
Q

Difference between physiological dead space and anatomical dead space

A

Physiological is when there is more perfusion than there is ventilation. Anatomical shut is when there is more ventilation than perfusion (some old air left)

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15
Q

How does Asthma cause small airway closure

A

There is increased small airway resistance (from inflammation) which causes a loss of pressure in the small airways. This causes early small airway closure meaning there is an increase in RV and decrease in FVC

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16
Q

How does Emphysema cause small airway closure

A

The breakdown of alveoli walls causes a decrease in lung recoil, increases intrapleural pressure. Meaning that early small airway closer occurs with decreases FVC and increased RV

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17
Q

What is henrys law

A

At a given temperature the amount of a gas is proportional to the partial pressure of that gas.

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18
Q

Factors that effect the rate of gas transfer

A

Diffusion coefficient (higher in Co2 than O2 = pp can be lower)
Partial pressure gradient
Surface area
Thickness of membrane

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19
Q

Diffusion Coefficient (D) and how does this relate to O2 and CO2 exchange

A

Rate of gas transfer directly proportional to this.

It is a constant value related to solubility of a gas and its molecular weight

D for Co2 is 20 times that of O2 because it is much more soluble and also heavier due to the extra Carbon. However this difference is offset by the differences in pp for O2 and CO2 meaning equal amounts of O2 and CO2 are exchanged.

20
Q

Transport of CO2 and O2 in the blood

A

Only 1.5% of O2 is dissolved in blood, the rest is carried in RBC by haemoglobin

CO2 transported as bicarbonate

21
Q

What is the Bohr effect

A

The influence of CO2 and acid on the release of O2 from haemoglobin.
Increased offloading of O2 with increased CO2 and H+

22
Q

Carrying capacity of O2 in haemoglobin

A

1 g Hb can hold 1.34 ml O2

23
Q

Other respiratory pigments

A

Myoglobin - monomer with one heme. Stores O2 in aerobic muscle and offloading occurs at lower pp.

Neuroglobin - found in neurons

24
Q

CO2 Transport

A
  • Co2 produced in tissues
  • Diffuses into plasma and some will then move into RBC
  • Some can sty in ICF but some will bind to haemoglobin by binding onto the globin chains (not the heme molecule)
  • Majority of Co2 in RBC with water and under presence of carbonic anhydrase forms carbonic acid, this dissociates into Hydrogen ion and bicarbonate ion.
  • Hydrogen ion can also now bind onto globin chains and therefore don’t change pH of RBC
  • And the bicarbonate is transported into plasma via chloride shift.
  • After reaching alveoli the Co2 in plasma and ICF will diffusion out, some of the Co2 on the globin chains will detach and diffuse. Some H+ will leave globin chains and with bicarbonate will form Co2 and water via carbonic anhydrase

Net result is that majority of the produce CO2 in the tissues is transported as bicarbonate ions within the plasma

25
What is the devonport diagram
It shows the relationship between PCO2, bicarbonate levels and the effect they have on blood pH
26
What is the Haldane effect
Once hB has offloaded more O2 from heme group, its affinity for Co2 and H ion is increased which will bind to the globin chains.
27
How do the Haldane and Bohr effects work together
Bohr causes offload of more O2 at increased levels of Co2 and acidity. This will then rigger Haldane effect as the globin chains then have increased affinity to Co2 and H. This allows increased efficiency as Co2 and H are going to the lungs as well.
28
Medullary controllers of respiration
- Rostral ventromedial medulla - Peacemaking activity, once depolarise thy create peacemaking potential (on/off rhythm for the other two) - Dorsal respiratory group - Fire to diaphragm, inspiratory nerve and stop activity during increased activity - Ventral respiratory group - Increased respiration - Inspiration and expiration nerves
29
Pons respiration centres
- Pneumotaxic center - Apneustic center Both fine tune the on/off rhythm
30
Responses for change in non CO2 acidosis
- Chemical buffer system (fast response) - Respiratory compensation (few mins), noted above - Cannot compensate for own fault, respiratory failure - Renal compensation (hours to days) - If the acidosis continues for long time - Kidneys hang onto bicarbonate (increase bicarbonate), with reference to Devonport diagram if you cant change PCO2 then increasing bicarbonate will increase pH.
31
Apnea and Dysapnea
During apnea a person subconsciously forgets to breathe. This can be either central (mexulla) or obstructive (tongue blocks) During dyspnea a person consciously feels thatr ventilation is inadequate
32
What happens to pp with exercise
During exercise PO2 increases and PCO2 decreases
33
Is the diffusion rate of Co2 faster than O2
Although Co2 has a much higher coefficient of diffusion (more soluble and heavier due to carbon), this is offset due to there begin a much bigger pp gradient for O2 than Co2
34
Why does the pp of O2 drop slightly from pulmonary capillaries to systemic capillaries
This is due to the presence of anatomical shunts (allows venous blood to enter arterioles)
35
How does CO2 transport alter blood pH
Some of the Co2 in the plasma (with the presence of water) will follow the same process and form carbonic acid. This will dissociated into hydrogen ion and bicarbonate. The H cannot bind to anything therefore increasing the blood pH. Increased amounts of this can causes acidosis (too much Co2, hypoventilation)
36
Decrease in arterial pO2
Peripheral chemoreceptors relate to the emergency life saving mechanism of the hypoxic drive to breath. This occurs if pp O2 drops below 60 and causes an increases in ventilation (resulting in an increase of pp O2). This is important because hypoxia can cause irreversible changes to neurons in the brain
37
Increase in arterial pCO2
- Causes the blood to become more acidic - This is a recoverable change but will decreases brain function above 70 pp CO2 - Weakly detected within the peripheral chemoreceptors - The central chemoreceptors detect this change due to increase H ions in the brain ECF. CO2 can easily diffuse across the blood brain barrier which will then lead to increased H
38
Increase arterial H (not from CO2)
Known as metabolic acidosis Not detected by central as H cannot cross BBB Peripheral monitor this but not as fast and signal medulla to drive resp - Chemical buffer system (fast response) - Respiratory compensation (few mins), noted above - Cannot compensate for own fault, respiratory failure - Renal compensation (hours to days) - If the acidosis continues for long time - Kidneys hang onto bicarbonate (increase bicarbonate), with reference to Devonport diagram if you cant change PCO2 then increasing bicarbonate will decrease pH.
39
What are the causes for increased respiration during exercise
It is not simply PCo2 or PO2 It is a combination of: - Joint and muscle receptors - Body temperature - Adrenaline - Cerebral cortex
40
Non respiratory factors that effect respiration
- Protective reflexes (sneezing, coughing) - Pain - Emotion - Speaking signing and whistling (voluntary)
41
Some patients with severe lung disease and chronic elevated arterial PCO2 do not show any increase in ventilation. Why?
In the presence of a prolonged increase of H+ in the brain ECF as a result of longstanding CO2 retention, and associated increase in arterial bicarbonate levels due to renal compensation of respiratory acidosis, enough bicarbonate may cross the blood-brain barrier to buffer the excess H+, and the brain ECF ph is restored to normal levels despite the fact that arterial PCO2 and ECF PCO2 remain high.
42
Oxygen therapy for such patients has to be carefully | monitored. Why?
Because such patients may rely on the life saving mechanism of the peripheral chemoreceptors (PO2 under 60 mm HG) for ventilation. This is called ‘hypoxic drive to breathe’. O2 therapy will increase arterial PO2 above 60 mm Hg and thus decrease the patients drive to breathe. They may stop breathing all together and need to be mechanically ventilated.
43
Does tidal volume or respiratory rate increase first with exercise
Tidal volume increases first. Any increases in tidal volume will increase alveolar ventilation by the same amount. Increase in respiratory rate will increase alveolar ventilation by a smaller amount due to the anatomical dead space. Air left from preceding respiration will remain in the alveoli after small airway closure so increasing respiration rate will have less of an effect.
44
Why is ventilation not based on PO2
Think about haemoglobin curve
45
Acute Asthma attack
- Increased physiological shunting - Decrease PO2 - Hyperventilate to compensate which causes decrease PCO2 and increased pH
46
What is pursed lip breathing
Ex with pursed, decreases air trapping and work of breathing