Respiratory System Flashcards
1
Q
function of conchae
A
- increases surface area of mucus that air is exposed to
- create turbulence → swirls air around/slows air down→ particles stick to mucus
2
Q
how does the nasal cavity prepare air for respiration?
A
- thick hairs (i.e. vibrissae) at entrance → filters/cleans air
- lined with respiratory epithelium (i.e. pseudostratified ciliated columnar epithelium + goblet cells + basal cells) → particles stick to wet/warm mucus → humidifies and heats air
- very rich blood supply under epithelium → heat from blood into air → warms air
- glands under epithelium → secrete water → humidifies air
3
Q
olfactory epithelium
A
- at roof of nasal cavity
- sniffing → causes turbulence → carries air up to olfactory epithelium
- axons of olfactory receptor cells → through perforations in overlying bone (i.e. cribriform plate) → brain
4
Q
impairments to mucocilliary escalator
A
- allergies, bronchitis, colds → excess mucus, cilia cannot cope → mucus is not cleared → coughing, increased risk of infection
- smoking → toxins paralyse cilia (disappear with long term smoking), makes mucus thicker → mucus is not cleared → coughing, increased risk of infection
5
Q
order of conductive airways
A
nasal cavities → pharynx → larynx → trachea → main stem bronchi → lobar bronchi → segmental bronchi → smaller bronchi → terminal bronchioles
6
Q
order of respiratory airways
A
nasal cavities → pharynx → larynx → trachea → main stem bronchi → lobar bronchi → segmental bronchi → smaller bronchi → terminal bronchioles
7
Q
generations of respiratory tree
A
- trachea → 0
- main stem bronchi → 1
- lobar bronchi → 2
- segmental bronchi → 3
- smaller bronchi → 4-9
- bronchioles → 10-15
- terminal bronchioles → 16-19 (i.e. the point at which risk of critical infection transitions from low → high)
- respiratory bronchioles → 20-23
- alveolar ducts → 24-27
- alveolar sacs → 28
8
Q
features of bronchial wall
A
- cartilage, smooth muscle → keeps the bronchi open
- ciliated columnar epithelium + goblet cells, mucus glands → secrete and move mucus, condition air for gas exchange
9
Q
features of bronchiolar wall
A
- smooth muscle → controls flow of air
- ciliated cuboidal epithelium, club cells → move/destroy particles that haven’t been filtered, condition the air for gas exchange
10
Q
features of alveolar wall
A
- type I pneumocyte → squamous epithelium, very thin cytoplasm
- type II pneumocyte → cuboidal epithelium, secretes surfuctant
- alveolar macrophages → last minute defence, ingests particles
11
Q
lung segments
A
- divisions of the lungs with each division supplied by a segmental bronchus
- each has its own air/blood supply and connective tissue capsule
- damage in one segment will not impact the others
- generally 8 on the left, 10 on the right
12
Q
responsibility of ribs in quiet breathing
A
ribs responsible for ~25% of air movement in/out of lungs
13
Q
responsibility of diaphragm in quiet breathing
A
- responsible for ~75% of air movement in/out of lungs in quiet breathing
- smaller proportion during exercise
14
Q
structure of diaphragm
A
- dome-shaped platform, forms floor of thorax
- central part → thin sheet of connective tissue/aponeurosis (i.e. central tendon)
- lateral margins → fast acting skeletal muscle, innervated by phrenic nerve
15
Q
innervation of respiratory muscles
A
- internal intercostal muscles → internal intercostal nerves (T1-L1)
- external intercostal muscles → external intercostal nerves (T7-L1)
- diaphragm → phrenic nerve (C3-C5)
- abdominal muscles → abdominal nerve (T7-L1)
16
Q
residual volume
A
- volume remaining in the lungs following maximal expiration
- some air remains trapped in small airways, prevents airways from fully collapsing
- cannot be measured with spirometer
- assessed by dilution method involving breathing helium gas
17
Q
minimal volume
A
volume of air remaining in the lungs after a complete collapse of the lung
18
Q
functional residual capacity
A
expiratory reserve volume + residual volume
19
Q
vital capacity
A
inspiratory reserve volume + tidal volume + expiratory reserve volume
20
Q
respiratory frequency
A
- number of times you breathe in a minute
- ~12 breaths/min
21
Q
dead space ventilation
A
- dead space volume (0.15L) x respiratory frequency
- ~1.8L/min
22
Q
alveolar ventilation
A
- (tidal volume - dead space) x respiratory frequency
- ~4.2 L/min
23
Q
minute ventilation
A
- tidal volume x respiratory frequency
- dead space volume + alveolar volume
- ~6.0 L/min
- hyperventilation → >6 L/min
- hypoventilation → <6 L/min
24
Q
FEV1
A
- forced expiratory volume in 1 second
- ~4.0L
- smaller FEV1 indicates increased resistance
25
FVC
- forced vital capacity
- ~5.0L
26
FEV1/FVC
- ~80% in healthy lung
- lower/higher indicates problem
27
elasticity
- ability to recover original size and shape after deformation
- due to elastin and collagen in lung tissue
- forms a matrix that supports airways, alveoli, and vessels
- in inhalation → fibres stretch → outwards pulling force (i.e. radial traction) → opens airways → reduces resistance to airflow
- in exhalation → inwards pulling force → passively returns stretched airways to resting state
28
compliance
- term used in respiratory physiology (i.e. not elasticity)
- compliance = 1/elasticity = change in volume/change in pressure
- how much pressure required to pull apart, stiffness
- more pressure required → less compliant
- less pressure required → more compliant
29
Laplace's law
- measures the surface tension induced pressure within the alveoli
- P = 2T/R
- P → pressure, T → surface tension, R → radius of alveolus
- the smaller the radius, the greater the deflating pressure
30
COPD
- chronic obstructive pulmonary disease
- increased compliance → less pressure required to inflate lungs
- at FRC, lung is somewhat inflated, diaphragm is flattened, mid-sternal space reduced
- cannot take deep breaths → limited inspiratory reserve volume
- caused by smoking → loss of elastic fibres
31
Fibrosis
- decreased compliance → more pressure required to inflate lungs
- at FRC, lungs are deflated, mid-sternal space widened
- fluffy white matter (i.e. fibrotic tissue) at bottom of lung
- caused by toxins/contaminants (e.g. coal mining) → inflammation → scar tissue
32
dead space
- formed by conducting zone (i.e. trachea, main stem bronchi, lobar bronchi)
- volume of air that fills conducting airways, does not participate in gas exchange
- ~150 mL per breath
- ~2.2 mL per kg
- causes contamination of freshly inhaled air, diluting oxygen content
33
funnel effect
- air flow ∝ 1/cross-sectional area
- cross-sectional area increases from trachea → alveoli by 500x
- conducting zone → fast and turbulent air flow
- respiratory zone → slow and laminar (i.e. in smooth, parallel layers) air flow
34
parasympathetic control of airflow
- innervated by branches of vagus nerve
- bronchoconstriction
- releases acetylcholine
- acts on muscarinic receptor → smooth muscle constriction
35
sympathetic control of airflow
- innervated by sympathetic nerves from thoracic spinal segment
- bronchodilation
- releases noradrenaline
- acts on beta-adrenoceptors → smooth muscle relaxation
36
Hering-Breuer Reflex
- mechanoreceptors in bronchioles detect stretch → activates vagus afferents (i.e. sensory nerves of vagus nerve) → signal sent to medulla oblongata respiratory centres
- activates sympathetic efferents → signal sent to NA-β-adrenoceptor (i.e. noradrenaline) on bronchioles → bronchodilation
37
pulse pressure
systolic pressure - diastolic pressure
38
pulmonary pressure
- systolic/diastolic → 22/10 mmHg
- mean → 14mmHg
- low pressure system
- only has to pump blood to one organ (i.e. lungs)
39
tracheobronchial circulation
- branch of aorta delivers oxygenated blood → tracheobronchial tree
- deoxygenated blood from tracheobronchial tree → branch of vena cava and branch of pulmonary vein
- branch to pulmonary vein (i.e. anatomical shunt/design fault) delivers deoxygenated blood into left side of heart, contaminates oxygenated blood
40
regional variations
top of lung → hydrostatic pressure is the lowest (i.e. poorly perfused), P(A) > P(a) > P(v)
middle of lung → hydrostatic pressure is greater, P(a) > P(A) > P(v)
bottom of lung → greatest hydrostatic pressure (i.e. best perfused), P(a) > P(v) > P(A)
- P(a) → pulmonary blood pressure/hydrostatic pressure
- P(v) → arterial venous difference, driving force for blood flow
- P(A) → alveolar pressure
41
pulmonary hypertension
- hypoxia → vasoconstricton → increased pulmonary vascular resistance → increased afterload to overcome
- increased pulmonary arterial pressure → strain on right ventricle → right heart failure → stretched, baggy, weak
42
pulmonary oedema
- left ventricular myocardial infarction (e.g. due to blood clot), right heart normal → congestion → increased pulmonary venous pressure
- increased hydrostatic pressure → oedema → systemic hypoxia (i.e. not enough oxygen to the body) → tired, weak, breathlessness (i.e. dyspnoea)
43
PO2 differential across tissue
- alveoli → 100mmHg
- capillary → 40mmHg
- 60mmHg difference
- diffuses into capillaries
- large driving force (i.e. 10x bigger than CO2)
44
PCO2 differential across tissue
- alveoli → 40mmHg
- capillaries → 46mmHg
- 6mmHg difference
- diffuses into alveoli
- small driving force
45
carrying capacity of blood for oxygen
- 1L of blood (i.e. 150g Hb) carries 200mLs of oxygen
- 1g of Hb can transport 1.39mL of oxygen when fully saturated
- at PO2 of 80mmHg, 1L of blood carries 0.2mL of aqueous oxygen
46
oxygen transport in blood
- binds with haemoglobin (predominantly)
- dissolves in solution
47
carbon dioxide transport in blood
- dissolves in solution (20x more soluble in blood than O2)
- as HCO3- (i.e. predominantly, 85% of carbon dioxide, catalysed by carbonic anhydrase, 60% diffused into plasma, 20% in red blood cells, 5% in plasma (i.e. not enzymatically regulated))
- combines to amine groups (i.e. NH2) of proteins (CO2 + Hb-NH2 ↔ Hb-NHCOO- (i.e. carbamino protein) + H+)
- as H2CO3 and CO3- ions (low levels)
48
oxygen dissociation curve - saturation
- sigmoidal relationship due to cooperative binding
- at lower PO2 → smaller percent oxygen saturation of haemoglobin, lower affinity, tissues have lower PO2 (i.e. due to oxygen consumption) → encourages oxygen release
- at higher PO2 → higher percent oxygen saturation of haemoglobin, higher affinity, alveoli have higher PO2 (i.e. due to oxygen rich air entering) → encourages oxygen uptake
- ~25% reduction in saturation from lungs to tissues
- independent of amount of Hb present
49
why does Hb’s affinity for oxygen change?
- Hb4 (i.e. deoxyhaemoglobin) + O2 → Hb4O2 + O2 → Hb4O4 + O2 → Hb4O6 + O2 → Hb4O8 (i.e. oxyhaemoglobin, fully saturated)
- CO2 + H2O ↔ H2CO3 (i.e. carbonic acid) ↔ H+ HCO3- (i.e. bicarbonate)
- CO2 + H2O ↔ H2CO3 catalysed by carbonic anhydrase, highly concentrated in red blood cells, can go in either direction
- at tissues → more CO2, more H+, lower pH → causes conformational changes that decrease haemoglobin affinity for oxygen → oxygen release
- at lungs → less CO2, less H+, higher pH → causes conformational changes that increase haemoglobin affinity for oxygen → oxygen uptake
50
oxygen dissociation curve - content
- dependent on PO2 and amount of haemoglobin present
- less capacity for carrying oxygen
- anaemia (i.e. reduced blood cells, haemoglobin) → saturation may be 100%, but blood oxygen content is reduced
51
carbon dioxide dissociation curve - content
- two curves since HbO2 has less affinity for CO2 than Hb (i.e. deoxyHb)
- HbO2/arterial blood → displaced to the right (i.e. Haldane shift)
- actual curve is steeper than expected since arterial and venous points are joined
- cannot be saturated → dependent on PCO2, high CO2 solubility and methods of transport
52
Bohr shift
- Bohr shift → for a given PO2, haemoglobin has a lower affinity for oxygen, less saturated, more oxygen given up
- represented by a rightward shift
- e.g. at tissues
- increased CO2, increased [H+] (i.e. lower pH), increased temperature (i.e. heat generated by metabolism), increased DPG (i.e. diphosphoglycerate, product of metabolism, binds to Hb, contributes to offloading of O2)
53
chloride shift
- HCO3- moves out/into of cell down its concentration gradient
- entrance/exit of Cl- ions maintains cellular electroneutrality
at tissue -> HCO3- moves out of cell, Cl- ions enter cell
at lung -> HCO3- moves into of cell, Cl- ions exit cell
54
fetal haemoglobin
- leftward shift in oxygen dissociation (saturation) curve
- higher affinity for oxygen than adult haemoglobin at a given PO2
- O2 saturation within maternal blood entering the placenta is low
- helps movement of oxygen across placenta to foetus
- prevents hypoxia in foetus
55
myoglobin
- leftward shift in oxygen dissociation (saturation) curve
- functions as O2 store within muscle tissue
- higher affinity for oxygen than haemoglobin at a given PO2
- only binds one O2
56
location of peripheral chemoreceptors
- outside central nervous system
- located in aortic bodies (i.e. at aortic arch) carotid bodies (i.e. at bifrucation of carotid artery)
- connected to brain stem via vagal and glossopharyngeal nerves (i.e. C5/C6)
57
stimulants of peripheral chemoreceptors
- hypoxia (i.e. reduced PO2)
- hypercapnia (i.e. increased PCO2)
- combination of hypoxia and hypercapnia (i.e. very effective)
- haemorrhage (i.e. loss of blood and ability to carry oxygen)
- acidosis (i.e. decreased blood pH)
- increased sympathetic activity (i.e. decreased blood supply to carotids)
- sodium cyanide (i.e. mimics lack of oxygen)
58
reflex response of peripheral chemoreceptors
- fast response time
- increases rate and depth of breathing (i.e. minute volume increases)
59
location of central chemoreceptors
- inside central nervous system
- located within the medulla oblongata
- three chemo-sensitive regions on ventral surface
- neurons and/or astrocytes <0.5mm beneath the surface
- close to basilar artery
60
stimulants of central chemoreceptors
H+ ions liberated when CO2 diffuses across the blood brain barrier and dissolves in CSF
61
reflex response of central chemoreceptors
- slow response time as protons cannot cross blood-brain barrier, and low levels of carbonic anhydrase in CSF
- increases minute volume
- hypercapnia (i.e. increased PCO2) increases minute volume in a non-linear manner (i.e. dog leg effect)
