Respiratory System Flashcards

Lec 28 & 29

1
Q

What are the 3 processes involved in exchange of air?

A
  1. pulmonary ventilation - inspiration, and expiration (air exchange btwn the atmosphere and lungs) 2. external respiration (air exchange btwn the lungs and blood) 3. internal respiration. (air exchange btwn blood and ISF/cells).
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2
Q

What is pulmonary ventilation the result of?

A

pressure gradients caused by changes in thoracic cavity volume.

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3
Q

What is Boyle’s law?

A

volume and pressure are inversely proportional. so when volume increases pressure decreases and vice versa, provided the temp and number of gas mols stays constant.

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4
Q

What are the pressures involved in pulmonary ventilation? (list)

A
  1. atmospheric pressure (Patm) 2. intrapulmonary pressure (Ppul) 3. intrapleural pressure (Pip)
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5
Q

What is Patm?

A

at sea lvl it’s 760mmHg.

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6
Q

What is Ppul?

A

air pressure inside lungs. btwn breaths it is equal to Patm. during inspiration it decrease and during expiration it increases.

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7
Q

What is Pip?

A

fluid pressure in the pleural cavity which is inbtwn the thoracic wall and lungs. always less than Ppul (has to keep suction) and usually less than Patm - around 4mmHg less = 756 mmHg. Pip usu lower than Patm bc the thoracic wall expands outward and the lungs recoil inward, but they’re held together by plural cavity (like a suction).

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8
Q

What are the types of pulmonary ventilation? (List)

A
  1. quiet inspiration 2. forced inspiration 3. quiet expiration 4. forced expiration.
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9
Q

What is quiet inspiration?

A

active process where mms contract. at start Patm = Ppul (760mmHg) no air moves. then, diaphragm and ext intercostal mms contract which increases the vol of thoracic cavity. lungs resist expansion, causing Pip to decrease (bc vol increases since thoracic cavity expands but lungs dont) 756 –> 754. higher pressure difference btwn Ppul and Pip pushes lungs outward, they expand, and Ppul decreases 760 –> 758mmHg. air moves in down P grad until Ppul = Patm. Summary: mms contract –> thoracic cavity expands –> lungs resist –> Pip decreases –> higher P grad btwn Ppul and Pip causes lungs to expand –> ppul decreases to 758 –> change in pressure causes air to move into lungs down its P grad until Ppul and Patm are equal.

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10
Q

What is forced inspiration?

A

diaphragm, ext intercostals, sternocleidomastoids, pectoralis minors, and scalenes contract (active). big increase in vol of thoracic cavity, therefore pressure gradient increases and more air moves into lungs. Summary: mms contract –> big increase in vol of thoracic cavity –> pressure gradient increases (Ppul decreases) –> more air moves into lungs down presure gradient.

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11
Q

What is quiet expiration?

A

passive process. mms relax –> lungs go back to resting size, thoracic cavity volume decreases –> Pip increases 754 –> 756. Ppul increases 760 –> 762 –> air moves out down pressure gradient. Summary: mms relax –> thoracic cavity vol decreases so Pip increases –> lungs go back to resting size (vol decrease) so Ppul increases –> air moves out of lungs down pressure grad to atmosphere.

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12
Q

What is forced expiration?

A

laboured or impeded breathing. relax diaphragm and ext intercostals but contract int intercostals and abdominals (active). Pip increases (thoracic cavity vol decreases). lung vol decreases so Ppul increases and air moves out. Summary: some mms relax other contract –> decrease in thoracic cavity vol and lung vol –> Pip increases and Ppul increases –> air moves out sown pressure grad.

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13
Q

What is the stretch in the lungs determined by?

A
  1. compliance - effort needed to stretch lungs. low compliance = much effort, high compliance = low effort. 2. recoil - ability to return to resting size after stretch. bc of elastic CT and surfactant.
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14
Q

What is lung collapse prevented by?

A
  1. Pip always below Ppul - pneumothorax. 2. presence of surfactant - lipoprotein/phospholipid mixture. in watery film coating alveoli, decreases surface tension. allows easier stretch of the lungs/ increased compliance. prevents alveolar collapse.
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15
Q

What is pneumothorax?

A

when opening into pleural cavity causes air to move into it which increases Pip and stops suction that was holding lung out, therefore lung collapses while thoracic wall expands. Patm = Ppul = Pip.

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16
Q

What is respiratory distress syndromE?

A

happens in newborns that have inadequate surfactant so alveoli collapse bc they have low compliance so theres high effort leading to exhaustion and death.

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17
Q

What is the air flow and airway resistance formula and the variables?

A

F= ∆P/R. F= air flow ∆P= Patm-Ppul R= airway resistance.

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18
Q

What is airway resistance determined by?

A

diameter of bronchi/bronchioles. asthma, bronchitis, emphysema increase airway resistance. expiration is more difficult than inspiration. bc inspiratory mechanics open airways and expiratory mechanics close airways. so with increase resistance to already constricted bronchioles, expiration is harder. SNS - dilates bronchiolar smooth mm (bronchodilation) PSNS - constricts bronchiolar smooth mm (bronchoconstriction).

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19
Q

What are respiratory volumes in pulmonary ventilation and how are they measured?

A

1 respiration is 1 inspiration and 1 expiration. measured using spirometer.

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20
Q

What are the respiratory volumes of pulmonary ventilation?

A
  1. Tidal volume - normal breath. vol of air in quiet inspiration OR quiet expiration ˜500 mL. 2. inspiratory reserve volume - excess air inspired on top of TV in a max/deepest breath (so max inspiration) ˜3000mL. 3. expiratory reserve volume - excess air expired on top of TV in max expiration ˜1200 mL (so max expiration). 4. residual volume - vol of air in lungs left over after ERV/max expiration ˜1200 mL. 5. Minute respiratory volume - TV x RR; 55mL x 12 breaths/min = 6L/min on avg. 6. forced expiratory volume in 1 second - volume expired in 1 sec, with max effort after max inhalation.
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21
Q

What are respiratory capacities?

A

comparing 2 or more respiratory volumes.

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22
Q

What are the respiratory capacities?

A
  1. Inspiratory capacity - TV + IRV. 2. vital capacity - largest vol in and out of lungs. TV + IRV + ERV. 3. total lung capacity - either TV + IRV + ERV +RV OR VC + RV.
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23
Q

How do you measure %VC?

A

measure FEV1 while measuring vital capacity and get %VC. always correction for body size. usu FEV1 = ˜80% VC

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24
Q

What does measuring %VC allow diagnoses of?

A
  1. obstructive disorders - asthma, ephysema, cystic fibrosis. hard to expire bc obstruct air mvmt in bronchioles, so increased resistance. means that RV will increase and VC will decrease, bc not expiring as much. FEV1 is less than 80% VC. 2. Restrictive disorders - scoliosis, pneumothorax. restrict lung expansion, which affects inspiration bc lung vol cant increase therefore lung pressure cant decrease to allow air to move in. IC is low, VC is low, FEV1 is low but FEV1 = 80% VC (bc theyre both lower).
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25
What is external respiration and what is it aided by?
O2 from alveoli to blood and co2 from blood to alveoli. aided by; 1. thin respiratory membrane. 2. large surface area - caps and alveoli. rbcs move single file through caps, so get max rbc exposure to gases. 3. bl velocity is slow compared to gas diffusion rates so rbcs have time to pick up/release gases.
26
What is internal respiration?
involves diffusion of O2 from blood to ISF then cells, and diffusion of CO2 from cells to ISF then blood.
27
What is the partial pressure of gases?
the pressure exerted by a single gas in a mixture of gases. ex. O2 is 21% of air so Po2 is 0.21 x 760 = 160mmHg. pressure gradients promote gas mvmts, gases move from high p to low p.
28
What are the 2 ways O2 is carried (list)?
1. dissolved in plasma and carried through caps. (1.5%) 2. bound to Hb and carried through caps
29
How is O2 dissolved in plasma at lung capillaries (ext resp)?
O2 moves from high P 105mmHg in lungs alveoli to low P 40mmHg in cap.
30
How is O2 dissolved in plasma at tissue capillaries (int resp)?
O2 moves from high P in arterial cap at 95 mmHg to low P in ISF at 40 mmHg and then cells at less than 40 mmHg. when O2 leaves cap the resting venous Po2 changes to 40 mmHg (bc O2 leaving).
31
How is O2 bound to Hb?
each Hb has 4 Fe which each bind 1 mol of O2, so each Hb can have 4 O2. Hb is deoxygenated Hb, add o2 and becomes HbO2 which is oxygenated Hb.
32
What does the O2-Hb dissociation curve show?
relationship btwn Po2 (amount of O2) and saturation of Hb with O2 (Hb%). so shows how much O2 is on Hb for a given amount of dissolved O2.
33
What does the plateau on the O2-Hb dissociation curve signify?
range of P02 at the lungs where Hb picks up O2 , so btwn 60 and 100 mmHg Po2. Hb is 97% saturated. if alveolar Po2 decreases slightly below normal there would be little change to Hb%. at high altitudes if alveolar Po2 is above 60 mmHg Hb carries normal amount of O2.
34
What does the steep portion of the O2-Hb dissociation curve signify?
range of Po2 at the tissues where O2 is unloaded from Hb. at rest; ISF Po2 is 40 mmHg and Hb is 75% saturated. (97 - 75 = 22% O2 unloaded to cells), so most of the Hbs are still oxygenated. high metabolism/exercise; ISF P02 is 20 mmHg and Hb is 40% saturated. 97 - 40 = 57% of O2 unloaded to cells, so much less oxygenated Hb in blood.
35
What happens when the dissociation curve shifts to the right?
for a given Po2 (amount of O2) get less Hb saturation. so O2 either unloads more easily or loads less easily.
36
Why does the shift to the right happen?
increase in Pco2, decrease in pH which is related to Pco2 increase and lactic acid, means decreased ability for o2 to bind to Hb when H+ is bound to globin (Bohr effect). increased temp. all occur when cell metabolism increases (ie exercise - Hb releases more O2).
37
What happens when the dissociation curve shifts to the left?
for a given Po2/amount of o2, get more Hb saturation. so O2 loads more easily or unloads less easily.
38
Why does the shift to the left happen?
decrease in Pco2, increase in pH, decrease in temp. all conditions at the lung (decreased temp due to evaporative cooling).
39
What are the ways that CO2 is carried?
1. dissolved in plasma (8%) 2. bound to Hb (20%) 3. As bicarbonate ions HCO3- (72%)
40
How is CO2 dissolved on the plasma at the lungs during external respiration?
Pathway: blood/capillary --> lungs/alveoli. resting arterial Pco2= 45 mmHg. alveolar Pco2= 40 mmHg (Co2 goes down P grad from bl to alveoli). venous Pco2= 40 mmHg (bc CO2 unloading into lungs so there is less afterwards)
41
How is CO2 dissolved in the plasma at the tissues during internal respiration?
Pathway: cell --> ISF --> capillary/blood. arterial Pco2= 40mmHg (before co2 loaded fro mtissues). ICF Pco2= more than 40 mmHg. ISF Pco2= 40 mmHg. (co2 goes down P grad). venous Pco2= 45mmHg (after co2 loaded into capillary).
42
How is CO2 bound to Hb?
carbamino Hb, CO2 binds to globin. CO2 binds to deoxy Hb better than oxyHb. so at tissues where Hb has been deoxygetnated, CO2 binds readily.
43
How is CO2 transported as bicarbonate ions (HCO3-) inside the RBCs at the tissues?
Rxn to become bicarbonate ion: CO2 + H2O --carbonic anhydrase in rbc--> H2CO3 --> H + HCO3-. H + Hb --> HbH (Hb is a buffer). HCO3- transported out of the RBC in exchange for Cl-, so venous blood rbcs have more Cl-.
44
What is the chloride shift?
when HCO3- leaves the rbc, Cl- comes in to replace it to keep the cell neg. this allows for more HCO3- to be made.
45
How is CO2 transported as bicarbonate ions (HCO3-) inside the RBCs at the lungs?
1. O2 + deoxyHb --> oxyHb/HbO2. so deoxygenated Hb becomes oxygenated. deoxyHb= HbH or HbCO2. since HbO2 binds CO2 and H poorly, CO2 is released (haldane effect) and H is released. so CO2 and H are kicked off Hb bc HbO2 doesnt bind well to them like Hb does. So at lungs Hb becomes oxygenated, letting CO2 loose 2. H + HCO3- --> H2CO3 --carbonic anhydrase--> Co2 + H2O. therefore HCO3- decreases in rbc, so HCO3- that was outside moves into the rbc (down grad) and exchanges with Cl- (reverse chloride shift). CO2 then moves from rbc --> plasma --> alveolar air --> out.
46
What controls respiration? (list)
1. respiratory centres in medulla 2. pontine respiratory centres 3. other factors a. lung stretch receptors b. voluntary control c. chemical control d. other.
47
How do the respiratory centres in the medulla control respiration?
set the rate, depth and rhythm of breathing. 2 groups of neurons. has inspiratory and expiratory neurons.
48
What are the 2 groups of neurons in the respiratory centres in the medulla and what do they do?
1. VRG= ventral respiratory group - generates rate, expiratory and inspiratory neurons. 2. DRG= dorsal respiratory group - receives chemoreceptor input and modifies VRG output.
49
What are the inspiratory neurons and what do they do?
impulses are sent down SC to; a. phrenic nerve which innervates the diaphragm b. thoracic nerves which innervate the external intercostal mms.
50
What are the expiratory neurons and what do they do?
fire to inhibit the inspiratory neurons and expiration occurs passively. (so stop inhalation by turning off inspiratory neurons)
51
How does the medulla affect quiet breathing? What happens if the VRG is damaged?
inspiratory neurons active for around 2 sec = inspiration. expiratory neurons inhibit inspiratory neurons output for around 3 sec = expiration. VRG also active for forced inspiration and expiration to recruit more mms. respiration may cease of VRG damaged or suppressed (ie alc or morphine).
52
What do the pontine respiratory centres do?
work with medulla centres to make breathing smooth. damage= gasping, irregular breathing.
53
How do lung stretch receptors affect breathing?
in smooth mm of bronchi and bronchioles. Hering-Breuer Reflex.
54
What is the Hering-Breuer reflex?
receptors are overstretched on inspiration --> impulses via vagus nerve --> inhibit inspiratory neurons --> relaxes mms (expiration - prevents over inflation).
55
How does voluntary control affect breathing?
primary motor cortex signals to skel mms involved in breathing (via corticospinal pathway) so bypasses medulla. if the medulla is damaged a person must consciously remember to breathe. if a person holds their breath - Pco2 increases and eventually he medulla will override voluntary control and the person iwll inspire.
56
What are the types of chemoreceptors (list)?
1. peripheral chemoreceptors - carotid and aortic bodies 2. central chemoreceptors - medulla oblongata (dominant control)
57
How do the peripheral chemoreceptors affect breathing?
weakly sensitive to Pco2, but very sensitive to H+. so if bl H+ increases which means pH decreased, the ventilation rate will increase and vice versa (ie. H+ decreases= vent rate decrease). since bl is buffered it takes a large change in H+ to change the pH. Po2 - stimulates receptors when Po2 reaches around 50-60 mmHg (end of plateau) which is an emergency situation. Po2 decreases due to lung disease or low atm Po2
58
How do central chemoreceptors affect breathing?
respond indirectly to arterial Pco2. resting arterial Pco2 = 40 mmHg. CO2 crosses the bl brain barrier easily, but H+ and HCO3- do not. in cerebrospinal fluid - CO2 + H2O --carbonic anhydrase--> H2CO3 --> H + HCO3-. so H is detected. CSF is poorly buffered so small change will stimulate a response. so will know that theres too much CO2 if theres lots of H bc CO2 is being converted.
59
What are other factors that affect ventilation?
1. increased temp --> increased vent. 2. decreased temp --> decreased vent. 3. increased emotion --> increased vent 4. increased proprioceptor discharge --> increased vent. 5. sudden increase BP --> decreased vent 6. sudden decrease in BP --> increase vent 7. sudden pain --> stops vent 8. chronic pain --> increased vent 9. sudden cold --> stops temporarily 10. stretching anal sphincter --> increased vent.
60
What is hyperventilation?
too much CO2 released. decreases arterial Pco2 which causes cerebral vasocon (intrinsic metabolic response). vasocon reduces Po2 in brain (bc less bl and O2 to brain) and get dizziness.
61
What is hypoventilation?
not enough Co2 released. increases arterial Pco2 which results inmore free H in blood leads to acidosis (decrease in pH)
62
What is carbon monoxide?
produced by the incomplete burning of gas. (cars, furnaces).
63
What is carbon monoxide poisoning?
CO binds 210x more strongly to Fe in Hb compared to O2. Hb with CO bound to it is carboxyhemoglobin (HbCO). so what happens is the total O2 carries by Hb decreases (bc its taken up by CO). but theres no change in the Po2 or Pco2, so vent rate doesnt change. the body is suffocating but the NS doesnt detect a change in amount of O2 carries on Hb, it can only detect changes to Po2 and Pco2. Summary: less HbO2, bc of more HbCO, so not enough O2 getting to tissues, but body doesnt know bc amount of O2 in the plasma is the same.