Respiratory system and exercise Flashcards
pulmonary ventilation
gas exchange mouth to lungs
external respiration
gas exchange from lungs to blood
internal respiration
gas exchange from blood to cells
cellular respiration
process to get ATP - anerobic/aerobic
VE (2)
minute ventilation - the volume of air inspired/expired each minute
VE = breathing rate X tidal volume
VD
dead space - amount of air in the airway that does not undergo gas exchange = approx 150 mL
VT
tidal volume - amt of air that is inspired or expired in a normal breath
f
frequency
VD/VT
ratio of dead space to tidal volume
VA
alveolar ventilation - volume of air available for gas exchange
VA = (VT-VD) xF
PAO2
partial pressure of oxygen at the alveoli
PaO2
partial pressure of oxygen in the arterial blood
SaO2%
percent saturation of arterial blood with oxygen
PACO2
partical pressure of CO2 at the alveoli
(A-a)PO2diff
oxygen or PO2 pressure gradient beween the alveoli and the arteries
PaO2
partial pressure of oxygen in the arterial blood
paCO2
partial pressure of CO2 in arterial blood
PvCO2
partial pressure of CO2 in venous blood
SvO2%
percent saturation of venous blood with oxygen
PvO2
partial pressure of oxygen in venous blood
conductive zone (3)
nose and mouth to trachea to bronchi to bronchioles
- air is adjusted to body temperature, filtered and humidified
- anatomical dead (VD) space
respiratory zone (2)
terminal bronchioles to alveolar sacs to alveoli
- external respiration
300 million alveoli provide the surface for
gas exchange between lung tissue and blood (size of a tennis court)
location of capillaries and alveoli
side by side with thin surfaces to faciliate rapid gas exchange
amt of gases that diffuse from alveoli to/from blood each min at rest
250ml o2 and 200 ml co2
two types of cells that compose the alveoli
type 1 - pavement cells that form the walls of alveolus, gas exchange
type 2 - produce pulmonary surfactant to decrease surface tension 3.5ml/min
why do we need surfactant?
the water in the lungs wants to make them collapsed
smooth muscles of the pulmonary system is under the control of
autonomic nervous system
- increased parasympathetic - bronchoconstriction
- increased sympathetic - bronchodilation - activation of beta 2 receptiors (N/NE decrease resistance and increase flow)
regulation of air flow
V=P/R
flow = changing pressure/resistance
thoracic cavity is lined with
pleural sac which extends around each lung
visceral pleura
connective tissue that covers the lung
parietal pleura
connective tissues that lines the thoracic cavity
intrapleural
filled with fluids that lets us to expiration process as the rib cage is always trying to pull out but the lungs want to deflate
atmospheric pressure
760mmHg at sea level
intrapulmonary pressure
760 mmHg
intra pleural pressure and purpose
756 mmHg
always subatmospheric due to the inward recoil of lungs and outward revoil of chest wall
intrapleural fluid prevents two pleural layers from seperating
transpulmonary pressure
diff between the intrapulmonary and intrapleural pressure
boyle’s law
pressure is inversely related to volume
P1V1=P2V2
MUSCLES for inspiration
diaphragm and intercostal
muscles for expiratoin
abdominals and intercostal
pressure difference between chest and atmospheric before inspiration, at inspiration and atexpiration
same, lower and higher by 2
inspiration mechanics (3)
expansion of thoracic cavity
- contraction of diaphragm and exernal intercostal muscles
- increased volume of alveolus, decreased pressure relative to atmospheric pressure
expiration mechanics (2)
passive recoil of thorax
decreased volume of alveolus, increased pressure relative to atmospheric pressure
forced expiration (3)
faster rate of volume decrease
contraction of internal intercostal and abdominal muslces
during exercise
pulmonary circulation (2)
serves the external respiratory function
alveoli receive the largest supply of all organs
bronchial circulation (2)
supplies the internal respiration needs of the lung tissues
part of systemic circulation
2 respiratory circulation
pulmonary and bronchial
measuring lung volume
blow in a tub of water liked to a pulley with a pencil that draws on a graph with the y axis of air volume and rotates at a fixed rate
inspiratory reserve volume
greatest amt of air that can be inspired at the end of a normal inspiration
expiratory reserve volume
greatest amount of air that can be expired at the end of a normal expiration
residual volume
amt of air left in lungs following a max exhalation
inspiratory capacity (2)
greatest amount of air that can be inspired from a resting expiratory level
IC =IRV +VT
vital capacity (2)
greatest amount of air that can be exhaled following a max inhalation
VC=IRV+VT+ERV
functional residual capacity FRC (2)
amount of air left in the lungs at the end of a normal expiration
FRC = ERV + RV
total lung capacity (4)
greatest amount of air that can be contained in the lungs
TLC = VC+RV
= IC + FRC
= IRV + VT + ERV + RV
if you breathed less how do you compensate for alveolar ventilation?
you increase in volume
which is more effeficient? Raising the volume or the frequency of breathing?
volume
forced expiratory volume
forced expiratory volume in 1s
FEV/FVC indicates 3
pulmonary airflow capacity - pulmonary expiratory power and overall resistance to air movement upstream in lungs
85% - healthy
equal or less than 70 - some level of airway obstruction
exercise induced asthma (2)
airway narrowing - induced during or after exercise
- exercise triggers/exacerbates underlying asthma (chronic inflammation leading to bronchoconstriction)
how can exercise induced asthma be diagnosed?
how do they treat it?
eucapnic hyperventilation/spirometry test - if FEV/FVC is reduced by more than 15% pre vs post
corticosteroids and beta 2 antagonists
how long do EIA symptoms take to subside
30-90 min after exercise
eucapnic
prevents you from fainting
salbutamol
short acting beta 2 adrenergic receptor agonist - cause airway smooth muslces to relax
How do people cheat with EIA medication?
beta 2 also vasodilates the heart and corticosteroids leads to greater mobilization of energy
exercise induced bronchospasm (2)
narrowing of airway thats induced during or after exercise
- hyperventilation during exercise induces a loss of heat/drying of the airway which leads to an increased intracellullar osmolarity and subsequent release of acute inflammatory mediators list - mast cells
what can induce acute inflammatory mediators
air pollutants
what sports is EIB common in? (3)
cross country skiing, hockey, swimmers
how to diagnose EIB
FEV reduction of 10% post exercise
diagnose EIB can be treated with
beta 2 agonist
residual volume allows for
continuous gas exchange between breaths
Dalton’s law of partial pressure
partial pressure: molecules of each specific gas in a mixture of gases exert their own partial pressure
partial pressure are altered at the alveoli level due to 3
fresh air mixing with air in dead space
humidification of air in alveolus
temp adjustments (charles law)
henry’s law
mixture of gases is in contact with a liquid, each gas dissolves in the liquid in proportion to its partial pressure and solubility until equilibrium is achieved and the gas partial pressures are equal in both locations
gas always diffuses from an area of ________ partial pressure to an area of _______ partial pressure
high to low
ficks law of diffusion (3)
governs gas diffusion across a fluid membrane
gas diffuses across fluid membrane
- directly proportional to tissue area, a diffusion constant, and pressure differentail of the gas on each side of the membrane
- inversely proportional to tissue thickness
external respiration of gas exchange (3)
o2 travels from high to low pressure as it dissolves and diffuses through alveolar membranes into blood
co2 exists under greater pressure in returning venous blood than alveoli, net diffusion of co2 from blood 2 lungs
n2 essentially unchanged
PaO2 when it leaves the heart
95
internal respiration of gas exchange (3)
PO2 in muslce cell is about 40mmHg and PCO2 is 45mmHg
O2 leaves blood and diffuses toward cells (myoglobin is dropping off oxygen as well) , CO2 flows from cells into blood
into venous circuit to return to heart then lungs
Q difference before and after exercise
5l/min to 40l/min
3 options of co2
stay in the plasma, enter BC and attach to hemoglobin
turn into bicarbonate acid
2 way to transport oxygen
dissolved in fluid portion of blood
bound to hemoglobin
quantity of dissolved oxygen in blood
solubility of O2 is 0.00304ml/dlmmHg
about 0.3ml in arterial blood
if this was the only way, with a VO2 of 250mlo2/min (RMR) you would need a Q of 83l/min
hemoglobin
protein portion of RBC binds with oxygen, has 4 iron containing pigments called heme and a protein called globin
quantity of oxygen on hemoglobin (3)
70x more than dissolved O2 in plasma
hbo2 = hb x 1.34o2/gram x sbo2%
males: hb of 15-16g/dl, females 13-14g/dl
we can bring up the hemoglobin concentration to
19g/dl
oxygen carrying capacity of hemoglobin relies on the principle of
cooperativity - binding of one molecule of oxygen facilitates the binding of the other three. relatioship is responsible for sigmoidal curve
usually after circulation, how much oxygen has been used?
25%
a-vo2 difference
difference between oxygen content of arterial blood and mixed venous blood
pAo2 vs pao2
104mmHg then mixed with venous blood if 95
3 ways to transport co2 in blood
dissolved in plasms (5-10%)
bound to hemoglobin - carbaminohemoglobin (20%)
bicarbonate ions (HCO3) (70-75%)
- chloride shift (make sure that everything is neutral)
control of ventilation is centered in
medulla oblongata and pons region of the brainstem
central pattern generator cells
pre botzinger complex like the SA nod which determines the rate of your breathing at he inspiratory centre
expiratory centre is influenced by
exercise
what nerve controls the diaphragm
phrenic - if damagesd you wont be able to breath on your ownor severedat c3-c5
centres in the pons
pneumotaxic centre - constant which in combination of situation controls the apneustic center which has a constant effect on this inspiratory center.
centres in the medulla oblongata
expiratory (ventral respiratory group) and inspiratory (dorsal respiratory group) center
inspiratory center receives signals from
directs
pons
neural activity of inspiratory muslces
expiratory centor which stimulates expiratory and inspiratory muslces
active contraction of inspiratory muslces
starts when inspiratory center is stimulated due to need for more forceful breathing
4 factors affecting pulmonary ventilation
higher brain centres
systemic receptors
mechanoreceptors
chemoreceptors - peripheral and central
higher brain centres that control breathing
cerebral cortex and hypothalamus
cerebral cortex and ventilation (4)
motor cortex
conscious control of stimulation of inhibition
overruled if PCO2 is high enough
stimulates expiratory then inspiratory muslces
hypothalamus (3)
sympathetic nerve system centres
strong emotions or pain and stiumulate or inhibit the inspiratory center which affects the expiratory center
systematic receptors (2)
airway irritant receptors respond to fumes, mucus, particulates, pollutants by inhibition, cough, sneeze, bronchial constriction which stimulates the expiratory and inspiratory center
lung stretch receptors - hering breuer reflex overinflation - inhibition which stimulates the apneustic cener and the inspiratory centre
2 chemoreceptors
central - CSP and medulla sense a decrease in pH and increased in PCO2 to peripheral - arterial blood, carotid and aortic bodies sense increase in PCO2, K, decrease in PO2 and pH
both stimulate inspiratory centre then the expiratory one
why does K stimulate the peripheral chemoreceptors
signifies lots of muscle contraction
mechanoreceptors 2
procrioceptive receptors (joint and muslce mecano receptors) sensitive to bodily movements and stimulate expiratory and inspiratory centers
what sensor is more likely to increase VE
PCO2, PaCO2 has to drop about half before VE goes up
central chemoreceptor located in
chemosensitive area of medulla oblongata (ventral portion near respiratory control centre), far more sensitive to change in PCO2 than peripheral, but peripheral sensors are faster to react to changes
short term, light to mod exercise effect on pulmonary ventilation
- VE
VT x2
VD
VE - disproportionate increase at the start - anticipatroy response (Cerebral cortex) and afferent activity from mechanoreceptors - hypernea
VT and f increase to increase VE
VT encroach more into IRV than ERV
VD changes little with bronchodilation - decreased VD/VT beneficial for increasd VA - smaller increase in VE required
Short term light to mod exercise on external respiration
VA
Aa PO2
SaO2
increased VA maintains PAO2
A-a PO2 reflects efficiency of oxygen transfer (no change - higher if mod intensity, lower if low intensity)
SaO2 maintained at 97%
short, light mod exercise effect on internal respiration (4)
amt of o2 delivered to tissues does not change
increase avo2 diff due to increased cellular o2 extraction - decreased Pvo2 and SvO2
paCO2 decreased as a result of VE
slight increase in pvco2
Bohr effect
rightward shift resulting from increased PCO2 and decreased pH
Increased avo2 diff occurs because
increased pO2 gradient and rightward shift in oxygen dissociation curve
rightward shift means
O2 can be released from Hb without any increase in local tissue blood flow
will heat impact the oxygen dissociation curve?
Yes, it will result in a rightward shift
long term, mod to heavy exercise effect on pulmonary ventilation
increased VE (ventilator drift)
- related to increased temp
- primarily influences breathing frequency
long term, mod to heavy exercise effect on external respiration
VA
PaO2
AaPO2
increased VA parallels VE
PaO2 goes down until ventilator drift initiates
insufficiency in AaPO2 is not sufficient to limit exercise
long, mod heavy exercise effect on internal respiration (3)
same changes with light/mod but at increased magnitude
- increased avo2 diff, decreased Svo2%
- increased VE, decreased paCO2
incremental aerobic exercise to VO2max on pulmonary ventilation
VE
VT
increase VE - a point where no longer proportional to VO2, disproportionate increase
reduced - rarely exceed 60% of VC
at higher exercise intensities, what takes on a more important role in terms of raising VE
frequency - can increase to 45breaths/min during strenuous exercise in healthy young adults and 70 in some elite endurance athletes
ventilatory thresholds
point during incremental exercise where the rectilinear raise in VE breaks from linearity - disproportionally increased in relation to VO2
VT1 and VT2
close association
anaerobic threshold
disporportionate increase in lactate accumulation and/or ventilator parameters during incremental exercise shown as lactate thresholds or ventilatory thresholds
how to determine vt1/vt2
identify inflection points
align multiple graphs
in theory, what causes ventilatory threshold
in theory - excess CO2 resulting from excess hydrogen buffering (anaerobic glycolysis)
therefore VT1 and VT2 will occur slight after LT1 and LT2
does not always seem to happen
does LT cause VT
no, VT can precede LT if subjects were depleted of muslce glycogen prior to anaerobic threshold test
mcardle’s syndrome and relationship of LT and VT
deficiency in enzyme glycogen phosphorylase
- these ind cant produce lactate but still experience distinct breakpoints in VE
5 possible causes of ventilatory thresholds
increased chemoreceptor activity (k, PCO2)
increased afferent neural activity from skeletal muslce proprioceptors
increased temp
increased catecholamines
limitations in the change of VT, f and VD/VT
