respiratory system Flashcards
respiratory zone
300 mil alveoli, HUGE SA
rapid exchange b/w alveoli are 1 layer thick
respiratory membrane
thin memb enhances exchange
SA for excahnge
alveoli close to blood
mechanics of breathing
active process of musc contraction
airflow bcs of pressure gradients
inspiratiory muscles act as pump
- lungs expand
- pleural fluid
active vs passive respiration
active resp: during exercise
- abdominal muscles engaged
inspiration: in/external intercostals, diaphragm
boyle’s law
as volume dec, pressure inc
what does airway resistance depend on
- pressure difference
- resistance of airwats
airflow: p1-p2/resistamce
airway resistance depends on DIAMTER
Vt
tidal volume
amount of air moved/breath
f
breath frequency
V
amount of air moved by the lungs/min
Vt x f
Va
alveolar ventilation
volume of air that reaches respiratory zone
VA = (VT - VD) x f
Vd
dead space ventilation
volume of air remaining in conducting aiways
how can V be calculated
V = VA + VD
V = VT x f
VE
minute ventilation
air flow/each…how much air breathed and breaths/min
VE = Vt x f
lung volumes
4 volumes and 4 capacities to diagnose issues
resting tidal volume/VT: vol of normal breath, 500ml
ERV: max are expirated at end of normal expiration, 1000ml
IRV: max air inspired at end of normal inspiration, 3300ml
RV: air left in lungs after max exhalation, 1200ml
FVC
max volume stroke of lungs
force air out of lungs
what does dynamic ventilation depend on
- FVC
- speed of moving a volume of air/breathing rate
- determined by lung compliance/resistance of respiratory passages
FEV1
forced expiratory volume, measured over 1 second
- when divide by FVC, indicates pulmonary airflow capacity
85% = healthy
70% or lower unhealthy
FEV1/FVC x 100%
sex differences
women have dec lung size, airway diameter, static/dynamic lung function
leads to expiratory flow limitations
- inc musc work
- inc resp reserve during max exercise
- dec lung vol, inc expiratory flow in trained women
air composition
0.03% co2
79% n2
21% o2
dalton’s law of partial pressure
each gas contributes to total pressure proportionately to its number of molecules
partial pressure = total pressure x gas fraction
henry’s law of gas exchange
when gas mixes w liquid, each gas will dissolve w proportion to its partial pressure gradient and solubility coefficient
partial pressure in alveoli
tracheal air becomes saturated w water vapur as passes down conductive zone
water molecules disperse gas molecules
- inc total volume of air, bcs add water and gas
- dec gas pressure for given vol of air
factors affecting gas exchange
- partial pressure gradient across barrier
- diffusion capacity: solubility of gas
- characteristics of barrier: SA and thickness
CO2 more soluble than O2
ventilation-perfusion ratio
ratio of alveolar ventilation : pulmonary air flow
- 1 is idea, matches rate
4.2 L air ventilates alveoli/min of rest
5 L of blood flow in capillaries
avg V:P is 0.84…..VA or 0.84L matches 1L of blood flow
high value = too much VE
low value = too much BF
this ratio DECREASES W INTENSE EXERCISE
o2 transport in blood
99% o2 bound to hemoglobin
- amount transported depends on hemo concentration
normal hemo concrentration is 15%
- each hemo transports 1.34ml o2
hemoglobin conc shown in g/100ml
where else is o2 dissolved
small amount o2 dissolved in plasma
3ml/L
things that impact o2 transport
- pH: inc H will weaken o2 and hemo bond, leads to unloading
- right shift via Bohr effect
- more o2 delivery - temperature: inc temp leads to unloading
- right shift - 2,3 DPG: present in RBCs, is anaerobic energy
- 2,3 DPG binds to hemo, reduce hemo o2 affinity
- left shift, dec o2 transport
- only during exercise at altitude or low hgb
myoglobin
facilitates o2 transfer to mitochondria
- cellular PO2 dec rapidly but myoglobin RETAINS high o2 saturation
higher affinity to o2, bcs has iron
greatest amount of o2 releases from myoglobin when tissue PO2 drops below 5mmhg
binds to o2 at low PO2
acidity, co2, temperature do NOT affect myoglobin’s o2 affinity
a-v o2 difference cont
difference b/w o2 content of arterial blood and mixed venous blood
- difference becomes GREATER W EXERCISE
active musc has high capacity to use o2
o2 supply limits aerobic capcity, NOT musc o2 use
co2 transport in blood
70% converted to bicarbonate to move thru blood
co2 + h2o –> h2co3 –> H + HCO3 (bicarbonate)
- via carbonic anhydrase
10% dissolved in plasma
20% bound to hemoglobin
co2 bicarbonate transport
at tissue:
- H binds to hemoglobin
- HCO3 diffuses out of RBC into plasma
- chloride shift when Cl diffuses into RBC
at lung:
- o2 binds to hemoglobin, drives off H
- rxn reverses and releases co2
acid-base balance
pulmonary ventilation removes H from blood by HCO3 rxn
inc VE results in co2 exhalation
- dec PCO2 and H conc
- ph inc/basic
dec VE results in buildup of co2
- inc pco2 and h conc, more acidic
rest-to-work transitions
when constant load, submaximal exercise:
- VE inc rapidly initially, then slow to steady state
PO2 and PCO2 relatively unchanged
increase in alveolar ventilation is slower than inc in metabolism
ventilatory equivalent
ratio of gas expired/min to volume o2 consumption/min
VE/VCO2
has linear relationship during light/mod exercise
- up to 55% vo2 max
remains constant during steady state exercise
prolonged exercise in heat will inc VE, but not inc CO2
- inc blood temp will affect respiratory control centre
non-steady state exercise
VE inc proportionately to VO2
as intensity inc, VE disproportionately increases compared to VO2
- VE/VO2 can reach 40L
incremental exercise
in untrained ppl:
- linear inc, initial 50-75% vo2max
- after this, exponential rate (ventilatory threshold)
in elites:
- VT occurs at higher percentage of vo2max
- PO2 dec to 30-40mmHg, hypoexmia
- bcs ventilation/perfusion mismatch, short RBC transit time and high CO
ventilatory threshold
inflection pt where VE inc exponentially
bcs co2 release from lactic acid
elite athletes will reach VT later
where does VE inc the most in breathing
tidal volume
control of ventilation at rest
inspiration is active, expiration is passive
resp muscles controlled by somatic motor neurons in spinal cord
activity of motor neurons controlled by respiratory control centre in medulla oblongata
respiratory control centre
in brain stem:
- medulla oblongata, connected to SC and brainstem
- pons
3 distinct rhythm centres of RCC
- prebotz: inspiration
- interacts w other centres at rest of reg breathing - RTN/PFRG: expiration
- pontine resp centre: rate and pattern
all act as pacemaker of breathing rate
normal rhythm bcs of interactions b/w clusters
where does RCC get info from
from higher brain centres/neural input and periphery/humoral input
humoral input
input from periphery
chemoreceptors: specialized neurons detect changes in environ/blood
central chemoreceptors: in medulla, detect pco2, h concentration, CSF
peripheral chemoreceptors: aortic arch and common carotid artery…detect PO2, PCO2, H, K in blood
neural input
from higher brain centres and afferent pathways
motor cortex alters breathing in proportion to exercise
afferent input from muscle spindles, GTOs, joint pressure receptors
important in reg breathing during submax and steady state
what is greatest respiratory stimuli during rest
PCO2 in arterial blood
- small inc in PCO2 in inspired air causes large inc in VE
stimulates both central and peripheral chemoreceptors
ph affects VE:
- acidosis reflects CO2 retetnion
- breathing inc to remove co2
plasma o2 and VE
changes in PO2 have small effect on VE
environ changes that dec o2 will stim PERIPHERAL CHEMORECEPTORS ONLY
- carotid bodies
- monitor arterial blood as moves to brain, protect against dec PO2
stim ventilation during exercise to:
- inc temp
- inc acidity
types of peripheral chemoreceptors
aortic body: detects inc PCO2 and ph
carotid body: detects inc PCO2, dec PO2, and ph
will inc VE
cortical influence
anticipation of exercise stimulates respiratory neurons in medulla
rapid inc in VE
peripheral influence
sensory input from joints, tendons, muscles
influences ventilatory adjustments to exercise
ventilatory control during submax vs heavy exercise
submax exercise:
- primary drive is higher brain centres/central command
- fine tuned by humoral and neural input
heavy exercise:
- linear inc in VE
- bcs inc H in blood stims carotid bodies
integrated regulation of ventilation during exercise
simultaneous effects of many chem and neural stimuli
phase 1: start exercise, neurogenic stim from cerebral cortex and feedback from active musc stims medulla to ABRUPTLY inc VE
- neural
phase 2: after short plateau, VE rises exponentially to achieve steady lvl
- humoral
phase 3: fine tuning of steady state ventilation thru peripheral feedback
recovery: gradual dec of short term potentiation of resp centre
training effects on respiratory muscles
no effect on lung structure or function at rest
normal lung is capable of meeting gas exchange demand
- don’t need adaptation for homeostasis
elite endurance athletes experience hypoexmia
- bcs lungs fail to adapt to training
- FATIGUE at greater than 90% vo2max
maximum voluntary ventilation
rapid and deep breathing for 15s, extrapolate to 1 min
- eval ventilatory capacity
exercise doesn’t maximally stress healthy person
trained resp muscles:
- inc endurance
- inc max voluntary vent
- inc inspiratory musc function
