Respi physiology Flashcards
1
Q
Inspiratory reserve volume
A
volume that can be inspired above the tidal volume
2
Q
Dead space
- anatomic
- physiologic
A
- anatomic : total volume of conducting airways
- physiologic : functional, volume that does not participate in air exchange (so includes alveoles)
3
Q
V minute
A
V tidal x FR
4
Q
V alveolaire
A
(V tidal - V dead space) x FR
5
Q
Forced expiratory volume
A
volume that can be expired in 1st second of maximum expiration (obstructive : asthma more decreased FEV compared to FCV)
6
Q
Compliance
A
V/P ; distensibilite .
- sigmoid curve : compliance varies during inspiration (need to go against the surface tension) vs expiration
7
Q
Negative pleural pressure
A
- Lungs want to collapse
- Chest wants to expand
8
Q
Transmural pressure
A
P alveolaire - P intrapleural
=> allows chest expansion
9
Q
Loi de laplace (surface de tension)
A
Collapsing pressure = 2 surface tension / radius
=> the bigger alveoli , low collapse P = stay open
10
Q
Surfactant
A
- Pneumocytes (alveolar cell) type 2
- Composition : Phospholids 80% (DDPPPPC) , 5-10% neutral lipids (cholesterol), 8-10% proteins
11
Q
Types de Cellules alveolaires -
A
Type 1 (95%, gaz exchange) & type 2 (stem cells type 1, surfactant)
12
Q
Basal cells
A
- underneath columnar cells (epithelial of bronchi)
- stem cells of columnar cells + goblet cells
13
Q
Ciliated cells
A
- Nose -pharynx : pseudostratified
-Bronchi : columnar - Bronchioles - cuboidal
300 cilia per cell
14
Q
what do goblet cells do
A
secrete mucous
15
Q
Clara cells
Mast cells
A
- Mucosa of terminal bronchioles, secrete surfactant proteins A, B and D
- Bronchoconstriction
16
Q
What decreases compliance
A
decrease compliance (at FRC greater tendency to collapse vs chest wall)
- Fibrosis , Atelectasia, edema, high lung volume, surfactant deficiency
17
Q
Airflow equation
A
= pressure gradient / airway resistance
18
Q
Loi de poiseuille
A
R = 8 x viscosity x l / pi x r (puissance 4). Resistance depends of radius.
Most resistance medium bronchi
19
Q
What impacts radius
A
Sympathic : bronchodilatation (NE/E adrenal glands)
Para : bronchonstriction (by Ach, due to irritants for example)
20
Q
Compensatory bronchoconstriction
A
decreased CO2 compared to perfused alveoles (no exchange, same as inspiration), leads to bronchoconstriction of nearby ariways so airflow is directed away
*local secretory factors (histamine can also lead to bronchoconstriction)
21
Q
Partial pressure *Loi de Dalton
A
Total pressure x Fractional gas concentration
22
Q
Dissolved gaz
A
Pp x solubility in blood
23
Q
Fick’s law
A
Vx (volume of gaz) = DL (lung diffusing capacity) x delta Pp
24
Q
residual volume
A
volume that remains in the lungs after max expiration
25
expiratory reserve volume
volume that can be expired over the tidal volume
26
volume tidal
volume inspired or expired on each breath
27
inspiratory capacity
VT + IRV
28
vital capacity
maximal breath taken. Volume of max breath expired after max inspiration
29
functinal reserve volume
ERV + RV : volume that remains in the lungs after tidal volume is expired
30
total lung capacity
vital capacity + RV : volume in lungs after max inspiration
31
What increases compliance
emphysema
32
What impacts diffusing capacity in fick's law
- thickness of the barrier
- diffusion coefficient
- surface area
33
which exchange is perfusion limited
O2
34
which exchange is diffusion limited
CO2 (do not equilibrate, exchange persist as long as pressure gradient)
35
Methemoglobin
fe3+, can't bind O2
36
How is oxygen transported
Hb 98% - Fe2+ binds O2 , which is rapid and reversible
dissolved O2 1-2%
37
what causes a right shift of the curve
increased P50, decreased affinity for O2 (so O2 liberated for tissues)
- increased PCO2
- decreased pH (Bohr effect)
- increased Temperature
- Increased 2,3 DPG
38
why is the hb saturation x O2 curve sigmoid
Because of positive oxygen cooperativity : there is an variable in affinity as each O2 binds to the heme site (e.g highest for the 4th)
Facilites O2 loading in lungs (flat portion), and unloading in organs (steep curve)
39
what causes a left shift
Hb is more affine to O2 : decreased CO2, temperature, 2,3 DPG, increased pH,
40
what is the haldane effect
Hb-O2 is a very strong acid (stronger than Hb-CO2), so will cause displacement of CO2 from blood to alveoli ; there will also be a relase of H2 ions and higher pH
41
A-a gradient
PAlveolar-Parterial
42
Decrease in A-a gradient
hypoventilation
43
Increase in A-a gradient
diffusion defect, V/Q mismatch, right to left shunt
44
Hypoxia causes
- anemia
- CO transport
- hypoperfusion
- hypoxemia
45
CO2 transport
- dissolved (minority)
- linked to Hb (20%) carbaminohb
- as hco3 70%, major form. In tissues, CO2 diffuses into RB (free of O2), CO2 then transforms into HCo3- + H+ by AC, then exchanged for chloride (chloride shift)
- H+ buffered by deoxyHb
46
2 hb conformations
- tau state : low O2 state = unloading ; beta chains are pulled apart allow 2,3 DPG to slide between which has a decreased affinity for O2
- r state : relaxed, high O2 state
47
what is the natural shunt
with pulmonary circulation, there is also bronchial circulation for peribronchial plexus, vasavasorum and thx-mediastinal organs (initially oxygenated blood, nutritional supply for airways) - about 80% of this blood will return to LH
48
Impact of inspiration on vessels
Bronchoalveolar bundle : at inspiration (decreased of pleural pressure = pressure of connective tissue), it will distend the bundle so it accomodates more blood flow.
Transmural pressure**
49
Vasodilatators
- NO
- PGI2 (prostacycline)
- beta 2 - R (NE-E)
- M3 (parasympathetic, Ach) - via NO pathway
- Bradykinin
- ANP
- Adenosine
50
Vasoconstrictors
- PGE
- Thromboxane A2
- alpha 1 - R
- Endothelin 1
- PDE5 (variable)
- serotonin
- leukotrienes
- histamine
- hypoxia (alveolar hypoxia induces vasoconstriction pf pulmonary arteries so blood flow is decreased to poorly ventilated areas)
- decreased pH and oxygen
51
V / Q higher vs lower
Apex : V lower, Q much lower => highest V/Q = PO2 is going to be much higher (more efficient gaz exchange as ventilation is better)
Base : V higher, Q much higher => lower V/Q ; pCO2 is higher (blood brings more CO2)
52
Where is the blood higher in animals
caudo-dorsal
53
compensatory bronchoconstriction
alveoli not perfused (e.g emboli) - due to increased Palveolar O2 and decreased PCO2 which approximates air
54
Causes of V/Q = O and meaning
- Obstruction of airways
- Right to left shunt ; no gaz exchange
PO2 and PCO2 of capillary will be of mixed blood
55
Causes of V/Q = infinity and meaning
pulmonary embolism or CV collapse
- dead space (no gaz exchange)
- PCO2/PO2 alveolar gaz = air
56
Causes of decreased v/q
- r to left shunt
- obstruction of airways
- pneumonia
- pleural space
- chronic bronchitis
57
What is the hering breur reflex
- Due to lung stretch receptors : smooth muscle of the airway
A distension of the lungs, will cause a decreased of RR (by vagal nerves, which go to dorsal respiratory group)
58
other receptors in regulation of RR
- muscle and joint receptors (activated during movement of limbs ex exercice)
- irritant receptors
- j juxtacapillary receptors : in alveolar wall, close to capillaries, sensitive to engorgement of capillaries
59
What substances are involved in pulmonary hypertension?
Decreased NO
Decreased prostacyclin
Increased endothelin-1
Increased thromboxane A2
Increased serotonin
60
How is cyanide toxicity treated?
1. Hydroxycobalamine
2. Nitrates/Thiocyanate
61
What is the effect of cyanide toxicity on venous blood?
The venous O2 will increase (cherry red blood) due to the non-use of iron
62
What is the mechanism behind cyanide toxicity?
Inhibits cytochrome C oxidase → prevents mitochondrial aerobic respiration (blocks the ETC)
63
How does the lung adapt to accommodate more blood during exercise?
Increases pulmonary blood flow (blood vessel dissension)
2. Decreases physiologic dead space (blood vessel recruitment)
64
How is bradykinin metabolized in the lung?
Degraded by ACE - 80%
65
How is serotonin metabolized in the lung?
There is uptake and storage - almost completely removed
## Footnote
Serotonin is taken up by lung tissue and stored, leading to its near-total removal from circulation.
66
How much norepinephrine is metabolized in the lung?
30% is removed
## Footnote
Norepinephrine undergoes significant metabolism in the lung, with a notable portion being removed from the bloodstream.
67
What happens to prostaglandins in the lung?
Prostaglandins E1, E2, F2α, and leukotrienes are inactivated
## Footnote
Various prostaglandins and leukotrienes are inactivated in the lung, indicating a metabolic role of lung tissue in regulating these compounds.
68
What is Bernoulli’s equation for use in calculating tricuspid regurgitation?
4xV^2 where V is the regurgitant jet
69
Which conditions will not respond to 100% oxygen supplementation?
Cyanide toxicity, Shunt, V/Q to infinity (ventilation but no perfusion)
70
What is normal tidal volume?
10-15 ml/kg
71
Positive end-expiratory pressure (PEEP) will increase which lung volume?
Functional residual capacity
72
What is the major side effect of positive end expiratory pressure (PEEP)?
Increased thoracic pressure → decreased venous return
73
What is indicated by a PaO2 <65?
Right to left shunt
## Footnote
SEVERE pulmonary disease → need for positive pressure ventilation
74
What are the causes of hypoxemia? Which will not respond to oxygen therapy?
Hypoventilation (Decreased PAO2)
Diffusion Defect
V/Q Mismatch
Shunts
Low FiO2
*Shunt will not respond to 100% O2
75
How is hypoxia different in the lung compared to other tissues?
Lung hypoxia causes vasoconstriction to send blood to better aerated areas, whereas it causes vasodilation in other tissues.
76
What part of the lung has the highest ventilation?
The base
## Footnote
The apex is the lowest due to the effects of gravity.
77
Where is the V/Q ratio the highest? The lowest?
The apex is the highest. The base is the lowest.
78
PO2 and PCO2 are (highest/lowest) in which part of the lung?
Apex: PO2 is highest, PCO2 is lowest.
## Footnote
Due to higher V/Q, gas exchange is more efficient. Base: PO2 is lowest, PCO2 is highest due to lower V/Q, gas exchange is less efficient.
79
How are PO2 and PCO2 affected in airway obstruction?
V/Q = 0.
## Footnote
Will approach their values in mixed venous blood.
80
How are PO2 and PCO2 affected in pulmonary embolism?
V/Q = infinity.
## Footnote
Will approach their values in inspired air.
81
The dorsal respiratory group controls (inspiration/expiration)?
Inspiration.
## Footnote
Generates a rhythm for breathing.
82
The ventral respiratory group controls (inspiration/expiration)?
Expiration.
## Footnote
Not active during normal breathing.
83
The pneumotaxic center (inhibits/stimulates) inspiration?
Inhibits. (apneustic center)
84
How are the following affected by high altitude? Alveolar and arterial PO2, Acid/Base status, [Hemoglobin], [2,3 DPG], Right Ventricle
Alveolar PO2 is decreased, so arterial PO2 is also decreased. Respiratory alkalosis occurs due to hypoxemia stimulating peripheral chemoreceptors → hyperventilation. Increased [hemoglobin] due to hypoxemia stimulating EPO production. Increased [2,3 DPG], HGB-O2 curve shifts right → facilitates O2 offloading. Right ventricle hypertrophy occurs due to increased pulmonary vasoconstriction.
85
which conditions are not o2 responsive
- shunt
- cyanide
86
Which receptors are thought to play a role in the cough mechanism
- RAR (rapidly adapting pulmonary irritant receptor)
- Bronchial C fibers
- Pulmonary C fibers
87
What substances activate the cough receptors/reflex
neurokinin, substance P, CGRP
88
Cough reflex
1. activation of receptors with release of neuroh (neurokinin, substance p etc)
2. vagus nerve
3. medulla (posterior aspect)
4. consequence :
- following inspiration, near closure of the glottis
- effector : contraction of abdominal wall muscles (external oblique, internal oblique, rectus abdominis) : expulsion of air (glottis opened upward)
89
MOA + side effect of codeine
Mu receptor agonist
Sedation : constipation , sedation, anorexia
90
MOA + side effect of hydrocodone
My receptor agonist (more potent than codein)
91
Dextromertophan
NMDA receptor antagonist
(not recommended in dogs, as it does not reach effective oral concentration)
AE : CNS IV , vomiting with PO
92
Butorphanol
Kappa receptor agonist, Mu receptor agonist-antagonist
No release of histamine so no GI signs
Potent anti-tussive
AE : sedation, respiratory distress, anorexia, diarrhea
93
Lomotil (diphenoxylate hydrochloride + atropine)
agonist opiods , anti-cholinergic
Constipation, sedation, bloat
94
Acetylcystein
Mucolytics
- interaction of exposed sulfhydryl group on disulfid bonds on mucoprotein
(broncho-constriction in cats, airway irritant)
95
Beta adrenergic receptor agonists - molecules
non selective : epinephrine
selective : terbutaline, salbutamol, albuterol, isoproterenol
96
MOA B2 receptors agonists
increase adenylate cyclase activity, increased cAMP, relaxing of bronchiolar smooth muscle
mast cells : inhibition of mediator release (stabilizing effect)
increase mucociliary clearance
97
Side effect b2 agonist
tachycardia, muscle tremors, twitching, nervousness
CI : late pregnancy and hypokaliemia
98
MOA of Methylxanthines (Theophylline)
inhibition of PDE 3-4
Adenosine receptor antagonist
Intracalcium handling and histone deacetylcyclate activation
99
AE theophylline
- CNS stimulation, urinary diuresis, cardiac stimulation, mild GI upset
- Metabolism of theo inhibited by erythromycine and enrofloxacin => decrease 30% dose
increased by phenobarbital and rifampin
