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HSF > HSF 2 - Unit 2 Physiology: Pulmonary Physiology > Flashcards

HSF 2 - Unit 2 Physiology: Pulmonary Physiology Flashcards

1
Q

what are the functions of the lung?

A

control pH, humidify the air we breathe in, defense, filter the airways

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2
Q

how does the lung maintain pH?

A

through the CO2/HCO3- buffer system: CO2 + H2O –> H2CO3 –> HCO3- + H+ all through carbonic anhydrase

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3
Q

what causes respiratory acidosis? alkalosis?

A

acidosis: hypoventilation; not getting rid of enough CO2 so pushes equation to the right giving more H+ ions, more acidic pH
alkalosis: hyperventilation; getting rid of too much CO2 through fast breathing so pushes equation towards the left and higher pH

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4
Q

how do we humidify air?

A

through the sinuses (nasal especially), this also warms it before it reaches the lower respiratory system

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5
Q

how are the airways filtered? what can be a problem with this in smokers and people with CF?

A

through mucus from goblet cells in the trachea; mucus layer traps the particles from dust or other inhaled things and underneath is a watery saline layer to allow the goblet cells’ cilia to move the mucus towards the pharynx. we end up swallowing most of this unconsciously and it is ultimately eliminated in the stool. CF: thick and sticky mucus so cannot be moved out, more prone to infections because bacteria colonizes in the mucus. smokers: tar in cigarettes make the cilia unable to move while also introducing carcinogens into the body, unable to remove these and also mucus effectively

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6
Q

what are various cell products that defend our respiratory system?

A

Mast: IgE, heparin, proteases, histamine, prostaglandins, chemotactic factors for the immune response
Goblet: mucus, prostaglandins, heparin, histamine

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7
Q

what does IgE do?

A

immune response, amount is in the teens

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8
Q

what do proteases from ______ cells do?

A

Mast/basophil; destroy proteins of foreign bacteria but not selective so other proteins are also destroyed, resulting in damaged lung tissue following an infection; this is a problem with chronic inflammation

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9
Q

what does histamine do?

A

bronchoconstriction and vasodilation (transport of immune factors is faster); BP crashes and leakage of fluid into the tissues but airways close so prevent access by the foreign invaders further into the respiratory system

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10
Q

what does heparin do?

A

prevents blood clotting; if blood clots it could get stuck in the pulmonary arteries

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11
Q

what makes up the lower respiratory tract?

A

trachea, bronchi, bronchioles, respiratory bronchioles, alveoli

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12
Q

what happens as you move lower into the respiratory tract? why can this be an issue but is also necessary?

A

slowly lose the hyaline cartilage rings, problematic because little support so the lungs could close up but necessary to allow gas exchange

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13
Q

what is bronchiectasis? what can cause it?

A

remodeling and thickening of the walls (smooth muscle gets replaced by fibroblasts and scar tissue) of the large airways making the lumen smaller, irreversible, thus reducing airflow and making it harder to remove mucus - promotes infection; caused by recurrent infection and inflammation, which can happen with diseases such as CF, immune deficiency, TB, chronic bronchitis, primary ciliary dyskinesia

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14
Q

what are alveoli composed of?

A

single layer of epithelial cells: type I and type II

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15
Q

what are type I cells?

A

thin cells in the alveoli for gas exchange

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16
Q

what are type II cells?

A

cells in the alveoli that secrete surfactant

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17
Q

what are the chemical properties of the contents of alveoli?

A

holds water, which has 2 dipoles, one neg and one pos, hydrogen bonding causes surface tension and a tendency for the alveoli to close, so surfactant reduces the hydrogen bonding between the water molecules and thus reduces surface tension to keep the alveoli open

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18
Q

what causes respiratory distress syndrome? how can we help ease the symptoms?

A

lack of surfactant, so the alveoli recoil and collapse because of the surface tension of the water within the alveoli; can be treated with positive pressure breathing or administration of surfactant

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19
Q

what is atelectasis? what causes it?

A

collapsing of the airways; caused by pressure on the outside of the lung (buildup of fluid), blockage of the air passages (complete mucus plugs), lack of surfactant, anesthesia

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20
Q

what surrounds alveoli? how is this compromised in certain diseases?

A

extensive and redundant network of capillaries and elastic fibers; when diseases destroy these you lose air and blood vessels, resulting in a higher BP; seen in emphysema with pulmonary hypertension because there is no where for the blood to go

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21
Q

how big is the gap for gas exchange?

A

0.1-1.5 micrometers between the alveoli and the capillaries; separated by a very small interstitial space

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22
Q

what is Boyle’s law?

A

P1V1 = P2V2; decreasing volume increases the rate of collisions of oxygen molecules with the lung interior and increases pressure

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23
Q

what happens to the volume and pressure of the lungs during inspiration? expiration?

A

inspiration: volume increases so pressure decreases; atmospheric pressure is greater than the alveolar pressure so air follows the gradient and moves in
expiration: volume decreases so pressure increases; atmospheric pressure is less than the alveolar pressure so air follows the gradient and moves out

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24
Q

what are the pleural membranes?

A

visceral and parietal, separated by an intrapleural space that is filled with pleural fluid that provides lubrication between the 2 membranes and is also cohesive so they stick together and move fluidly during breathing

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25
what is the pressure in the intrapleural space?
negative; due to the thoracic cavity's tendency to go out and the lungs tendency to recoil in
26
what are the Pip changes during breathing?
starts at -4 (4 under atmospheric) because of opposite pulling of the lungs and the thoracic cavity and the lymphatics draining the area; continues to go more negative during inspiration because no air going into the cavity but air coming into alveoli - can't equalize; during expiration volume goes back down so the pressure goes back to -4
27
what are the PA changes during breathing?
goes down at first during chest expansion as air comes in, at the end of inspiration it equalizes then goes back up
28
what happens during a pneumothorax?
the cohesion is broken between the parietal and visceral membranes, so it equalizes to atmospheric pressure and the lung collapses due to its elastic recoil tendency
29
what happens during a hemothorax?
aka tension pneumothorax; causes more intense pain and pressure in the lung, pulling in more air and cannot expel it; building up pressure in the lung so must be punctured to release it, then seal and provide positive pressure for reinflation
30
what is an example of positive pressure breathing?
mechanical ventilation, CPAP for people with sleep apnea to keep airways open
31
what is compliance work?
(inspiration) distensibility or stretchiness of the lung and its ability to move; elastic work
32
what is airway resistance work?
(expiration) overcome tissue and airway resistance (obstructions), flow is proportional to change in pressure/resistance : increase change in pressure you increase the flow and an increase resistance you decrease flow
33
what are the 2 types of work during breathing?
compliance and airway resistance
34
what are the determining factors of lung compliance?
property of the tissue (stretchable, scar tissue), volume of the lung, surfactant, obesity (abdominal fat makes it harder on the diaphragm to move downward and reduces compliance so have to work harder)
35
what is the compliance equation?
change in volume over the change in pressure (slope of the line in transpulmonary pressure versus volume graph)
36
what is emphysema? what are its causes?
effects the alveoli, get destruction of them so lose elastic recoil and can get narrowing of the bronchioles,, causing air trapping, V/Q mismatch, reduced DLCO, and loss of capillaries; caused by smoking (chronic irritants and infection; smoke leads to neutrophils and macrophages which leads to proteases and inflammation and ROS) or alpha 1 antitrypsin (protease inhibitor) deficiency; all results in a loss of surface area in the alveoli and total lung, lowered ability to exchange gas and increased compliance because fewer alveoli to oppose opening of the lung
37
what is pulmonary fibrosis?
thickened alveolar membrane slows gas exchange, lowering lung compliance and decreasing alveolar ventilation; fibrous scar tissue (stiff lung), DLCO reduced; can be caused by inhalation of particulates (asbestos, coal dust, silica, etc.) which leads to repetitive alveolar injury and thus increased production of fibroblasts and collagen (ECM)
38
how is resistance determined?
length of the respiratory system, viscosity, and radius of the tubes
39
what is Poiseulle's law?
``` R = 8nl/pi*r^4 R=resistance n=viscosity l=length r=radius ```
40
what are the determining factors for the radius of the respiratory tubes?
1) mechanical connections (connective tissues and alveoli) 2) physical (mucus) 3) neural control (autonomic nervous system) 4) paracrine and endocrine agents (CO2, histamine, prostaglandins, leukotrienes, etc.)
41
what are the different lung volumes?
tidal volume, inspiratory reserve volume, expiratory reserve volume, residual volume
42
what are the different lung capacities?
vital capacity, inspiratory capacity, functional residual capacity, total lung capacity
43
FVC
forced vital capacity
44
FEV1
forced expiratory volume in 1 second; should be close to 80%
45
what are obstructive diseases? what are some examples of obstructive respiratory diseases?
hard to get the air out; asthma and COPD
46
what are restrictive diseases? what is an example of a restrictive respiratory disease?
hard to get the air in; fibrosis
47
COPD
chronic obstructive pulmonary disease, typically includes bronchitis and emphysema; causes: smoking (chronic irritants, infection); alpha 1 antitrypsin (protease inhibitor) deficiency
48
asthma
inflammation, spastic contraction of the smooth muscle in the bronchioles, reduced timed expiratory volume, air becomes trapped in the lungs (over time have increased RV and barrel shaped chest); foreign substance in the lungs leads to the release of IgE and then Mast cell degranulation (histamine, leukotrienes, bradykinin, etc.) and then leads to smooth muscle contraction, mucus secretion (can also come from hypersensitivity to exercise or cold); will have a lower FEV/FVC value, can be improved with a beta agonist
49
how to interpret PFT results
if FEV1/FVC <75% = obstructive | if FEV1/FVC >75% , normal FVC is normal, low FVC (<75%) = restrictive lung disease
50
what is closing volume?
volume of gas in the lungs in excess of the residual volume at the time when small airways in the dependent portions of the lungs close during exhalation
51
what is closing capacity? what can change it?
closing volume + residual volume; increases with age and smoking
52
FRC decreases with ...
laying down, anesthesia, obesity
53
what happens if FRC < CC
closing of some of the airways occurs; increases the work of breathing and alveoli not properly ventilated, V/Q mismatch
54
what is the total pulmonary ventilation?
"minute ventilation"; = ventilation x tidal volume ; usually around 6000 ml/min
55
what is alveolar ventilation?
= ventilation rate x (tidal volume - dead space volume); physiological dead space (anatomical dead space + alveolar dead space); usually around 4200 ml/min or 4.2 L/min
56
VA =
0.863mmHg*L/ml * (VCO2(ml/min) / PACO2 (mmHg))
57
how much blood can the lung hold?
450 mL (9% of total blood)
58
blood can be ____ into and out of pulmonary circulation
shifted; in: capillaries open, veins expand (heavy exercise and left heart failure) out: hemorrhage
59
what is starling's hypothesis
fluid movement due to filtration across the wall of a capillary is dependent on the balance between the hydrostatic pressure gradient and the osmotic pressure gradient across the capillary
60
what is the net filtration pressure?
Kf [( Pc - Pi ) - ( Oc - Oi )] * SA
61
what is Kf?
the capillary filtration coefficient - permeability of the membrane
62
what is SA?
the surface area of alveolar capillary barrier
63
what happens if the net filtration pressure is positive? negative?
pos: fluid will move from capillary to interstitial space neg: fluid will move from interstitial space to capillary
64
what are the 3 problems leading to pulmonary edema?
nephrotic syndrome, pulmonary capillary membrane damage, left heart failure
65
nephrotic syndrome
plasma protein lost in the urine
66
pulmonary capillary membrane damage
leakage of plasma proteins into the interstitial space
67
what is an example of pulmonary edema? what are characteristics of it?
congestive heart failure; less oxygen exchange at the lungs, less oxygen for the heart tissue, heart continues to get weaker and weaker
68
what 2 things can lead to left heart failure? what happens after this?
MI, high systemic resistance; blood backs up into the pulmonary circulation, causing the pulmonary pressure to build and resulting in pulmonary edema
69
how does the body try to keep pulmonary arterial pressure low?
during normal increases in LA pressure, pulmonary capillaries and venuoles open
70
what is the normal range for left arterial pressure?
0-10
71
what do the different ratios in V/Q mean? what does the lung want to do?
V/Q = 1 ventilation is equal to perfusion V/Q>1 perfusion is low V/Q<1 ventilation is low; lung tries to match so that V/Q = 1
72
how do we compensate for high V/Q? low?
bronchoconstriction; vasoconstriction (low O2 will induce hypoxic vasoconstriction)
73
what is hydrostatic pressure of the lung?
caused by the weight of the blood above it in the vessels due to gravity
74
which zones of the lung will be present with varying kinds of cardiac output?
as decrease Q, V increases and alveoli expand and restrict blood flow; normal Q will have lung in mostly zones 2 and 3 low Q will have lung in all 3 zones high Q will have 2 and 3, more 3 than 2
75
what is Dalton's law?
total pressure of a mixture of gases is the sum of the pressures of the individual gases (sum of the partial pressures)
76
what is the partial pressure of oxygen in the air?
atmospheric pressure * 21% O2
77
what is Henry's law?
at a constant temp, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid
78
what is the tracheal PO2?
aka PIO2 = FiO2 * (Patm - PH2O)
79
what is DLO2?
diffusing capacity of the lung for O2
80
what is PAO2?
= FiO2 * [(Patm - PH2O) - (PACO2 / RQ)]
81
what is RQ?
= CO2 / O2
82
what is Fick's law of diffusion?
diffusion rate is proportional to (change in pressure * SA * diff. coefficient) / membrane thickness
83
which hemoglobin structure is tight binding? relaxed binding?
tight: deoxy; domed shape relaxed: oxy; planar shape
84
what can reduce the affinity for oxygen of hemoglobin?
CO2
85
how much Hb is in blood?
normal blood contains 15 g Hg/dl; 1 g Hg can bind 1.34 ml of O2
86
what is hematocrit?
ratio of red blood cells to plasma, normal range is 40-50%
87
what is anemia?
decrease in hemoglobin, decrease in oxygen carrying capacity of the blood
88
cause of sickle cell
substitution of valine for glutamic acid in 6th amino acid; autosomal recessive mode of inheritance
89
what is polycythemia vera?
bone marrow defect (somatic gene mutation) that causes an abnormal increase in RBCs and thus a sluggish blood flow and blood clots
90
what determines PO2 in the blood? what does PO2 determine?
composition of air, alveolar ventilation, efficiency of gas exchange; amount of O2 dissolved in plasma, oxygen saturation of hemoglobin (SO2)
91
what is P50?
pressure at which hemoglobin is 50% saturated (usually around PO2 = 27 mmHg)
92
SO2 at PO2 of 20, 40, 60, 80, 100
20: 35 40: 75 60: 90 80: 95 100: 98
93
what is the Bohr effect?
the decrease in oxygen affinity of hemoglobin in response to decreased blood pH resulting from increased carbon dioxide concentration; right shift of curve and oxygen more readily dissociates from hemoglobin
94
what can also decrease oxygen's affinity for hemoglobin?
2,3 DPG; is formed during hypoxic conditions
95
what is the solubility of oxygen in the blood?
0.003ml O2/ mmHg/dl
96
what effect does CO have on hemoglobin?
takes up same binding site that oxygen holds, has a higher affinity than oxygen, shifts curve to left
97
what are the different ways CO2 is carried in the blood?
dissolved in the plasma (7%), bound to hemoglobin (23%), in the form of bicarbonate (70%)
98
what is the Haldane effect?
the promotion of carbon dioxide dissociation that results from the oxygenation of hemoglobin
99
what part of the brain stem generates the signal to breathe?
medulla
100
what different groups are part of the medulla that influence breathing?
central rhythm generator neurons, DRG (normal breathing, inspiration) and VRG (inspiration and expiration)
101
apneustic center
promotes inspiration
102
pneumotaxic center
shuts off inspiration
103
what does the pons modulate?
the medulla and the ANS
104
what are the peripheral chemoreceptors?
carotid body (through glossopharyngeal), aortic body (through vagus); sense O2, H+, CO2
105
how do peripheral chemoreceptors get activated by low PO2?
glomus cell senses low PO2, closes K+ channels and opens Ca++ channels to depolarize and result in ACh being released and binds on afferent fiber of glossopharyngeal nerve
106
what is the Hering Breuer reflex?
over-inflation of the lung stimulates stretch receptors (vagal afferent nerves) and inhibit inspiration at the DRG

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