RESPIRATORY SYSTEM Flashcards
respiration
obtain O2 for body cells & eliminate CO2
* build up of CO2 = toxic ➔ lowers pH
* veins (blue) still have O2 but much less
* arteries (red) still have CO2 but much less
types of respiration
external respiration
* pulmonary circulation: heart & lungs
* systemic circulation: throughout rest of body
internal (cellular) circulation
respiratory system composed of
- nasal passage
- mouth
- pharynx
- larynx trachea (w/ cartilaginous tissue for strength)
- lungs
- diaphragm
always leads to lungs
airways
trachea & larger bronchi: fairly rigid rings of cartilage to prevent collapse
bronchioles:
* no cartilage to hold them open ➔ makes them susceptible to collapse
* walls contain smooth muscles innervated by ANS
* parasympathetic stimulation constricts
* just sympathetic stimulation weakly relaxes
* EP relaxes
alveoli anatomy
alveoli: site of O2/CO2 exchange
* thin-walled flexible sacs
type 1 alveolar cell: large cavity that allows gas exchange
* single layer makes up alveoli walls
type II alveolar cell: produces alveoli fluid lining with pulmonary surfactants:
* weak detergent
* ↓ surface area to prevent collapse
* normalizes pressure
* prevents recoil
* disrupts H-bonding of water lining alveolar wall (mixture of protein & lipid) to prevent large bubble formation from smaller ones
alveolar macrophage protects alveolus & ensures clean air
* guard lumen
pulmonary capillary brings O2/CO2
* encircle each alveolus
* erythrocyte = RBC
* barrier separating alveoli & capillary = extremely thin & short distance to facilitate gas exchange by diffusion
pulmonary ventilation
lungs suspend in pleural sac in thorax
* pleural sac = extremely thin double-walled closed sac separating each lung from thoracic wall
* pleural cavity = interior of pleural sac
* intrapleural fluid = lubricant secreted by surfaces of pleura
* helps lung with movement & prevents friction
* helps with pressure regulation
ventilation pressure
- atmospheric (barometric) pressure: exerted by weight of gas in atm on objects in earth’s surface
-
intra-alveolar (intrapulmonary) pressure: w/in alveoli
-
changes produce flow of air in/out of lungs by diffusion
- if < Patm ➔ air enters lungs
- if > Patm ➔ air exits lungs
- boyles law: P & V are inversely related ➔ ↑P = ↓V
-
changes produce flow of air in/out of lungs by diffusion
-
intrapleural (intrathoracic) pressure: w/in pleural sac
- pressure exerted outside the lungs within the thoracic cavity
- Pintrapleural < P intra-alveolar
inspiration
inhaling
* external intercostal muscles & diaphragm only
* both intra-alveolar & intrapleural pressures drop 1 mmHg ➔ allows for more inflation
* contraction of EIM causes
1. ribs & sternum elevate ➞ ↑ side-to-side & up & out
2. diaphragm lowers ➞ ↑ vertical dimension
expiration
passive expiration during quiet breathing
* diaphragm, ribs, & sternum return to resting position
* inspiratory muscles relax
* restore TC to pre-inspiratory size
* via elastic recoil
* relaxation of diaphragm & intercostals muscles
active expiration ↓ dimensions of TC even more than resting state:
1. contraction of internal intercostals flattens ribs & sternum ➔ ↓ side-to-side & front-to-back dimensions
2. contraction of abdominal muscles pushes diaphragm up ➔ ↓ vertical dimension
intrapulmonary (intra-alveolar) & intrapleural pressures during respiratory cycle
- inspiration: P intra-alveolar < P atm
- expiration: P intra-alveolar > P atm
- at and of both: P intra-alveolar = P atm
- throughout: P intrapleural < P intra-alveolar
- ∴ transmural pressure gradient always exists ➔ lung is always stretched a bit even during expiration
lung volumes
TV = tidal volume: small amount we actually take in during inspiration/expiration
IRV = inspiratory reserve volume: V of air we can use during strenuous situations
- FOF
- exercise
IC = inspiratory capacity: max V we can inspire
ERV = expiratory reserve V ➔ forced expiration after normal expiration
RV = residual V ➔ volume that will be left over after we expire completely
FRC = functional residual capacity ➔ RV + ERV ➔ not actual amount we can use
VC = vital capacity ➔ TLC - minimum amount of air necessary for normal fx; amount of air we can regulate
TLC = total lung capacity
- dead space = non-fresh air; cannot be used by alveoli ➔ does not provide O2
ventilation
pulmonary ventilation (mL/min) = TV (mL/min) x RR (breaths/min)
- not all TV can be used by alveoli & contribute to ventilation ➔ only fresh air
- only ~70% of inspiration = fresh air ∴ only ~350mL fresh air reaches alveoli
alveolar ventilation (L/min) = (TV — dead space) x RR
- alveolar ventilation < total ventilation
- during hyperventilation alveolar ventilation = ~0 ➔ very little fresh air reaches alveoli, just reusing dead air
feedback mechanisms within lung match local airflow w/ local blood flow
gas exchange
- simple diffusion between pulmonary capillary & alveoli in extremely close proximity
- major determinant of rate of transfer = PP gradients of O2 & CO2
- SA of alveolar capillary membrane: ROT↑ as SA↑
- constant at resting conditions
- ↑ during exercise
- ↓ w/ pathologies
- thickness of alveolar-capillary membrane: ROT ↑ as thickness ↓
- normally remains constant
- ↑ w/ pathologies (pulmonary edema, pulmonary fibrosis, pneumonia)
- diffusion constant: ROT ↑ as diffusion constant ↑
- diffusion constant CO2 = 20x O2
- balances w/ smaller particle pressure gradient of CO2
alveolar air composition
- diff than atm: atm ➔ alveoli:
- %N ↓ ➔ same amount just diff ratio
- %O2 ↓
a. diffusing out for cellular resp
b. not all air = fresh air - % CO2 ↑
a. byproduct of cellular resp
b. deadspace - % H2O ↑ ➔ ↑ water vapor (moisture) traveling down resp airway
- biggest change in terms of relative proportion = CO2
- O2 & CO2 exchange across pulmonary & systemic capillaries through partial pressure gradients
gas transport
- most O2 transported bound to hemoglobin in erythrocytes: RBC
- hemoglobin = protein w/ 4 subunits (2⍺ + 2β) each surrounding a heme group (iron center)
- higher affinity for O2
- erythrocytes ≠ mitochondria ➞ must use glycolysis ∴ need energy for active pumps
gas transport: O2 vs CO2
O2:
- 98.5% bound to hemoglobin
- very low solubility in blood
- can loosely & reversibly bind to hemoglobin
CO2:
- majority as bicarbonate
- bicarbonate (60%) > bound to hemoglobin (30%) > physically dissolved (10%)
- higher solubility
- HCO3- produced as byproduct from rxn H2O + carbonic anhydrase (ca)
oxygen hemoglobin dissociation curve
- plateau of curve is where PPO2 is high (lungs)
- steep part of curve (0-60) exists at systemic capillaries where hemoglobin unloads O2 onto tissue cells
- PPO2 = main factor in determining % hemoglobin saturation
- ↑ % saturation where ↑ PPO2 (lungs)
- ↓ % saturation where ↓ PPO2 (tissue cells)
- O2 dissociates from hemoglobin at tissue cells
the bohr effect
- influence of CO2 and acid on the release of O2
- CO2/H+ can combine reversibly with Hb at sites other than the O2-binding site ➞ changes the molecular structure of Hb that reduces its affinity for O2
- ↑ CO2 & H+ at tissues shifts dissociation curve right
- allows hemoglobin to give up 1 O2 at ↓ PP
- during exercise less binding to O2 & more binding to CO2
haldane effect
- ↓ O2 in tissues causes Hb to pick up CO2 & H+
- ↑ O2 in lungs causes release of CO2/H+ from Hb
chloride shift (hamberger phenomenon)
Cl- moves into RBC to offset HCO3- coming out into plasma
- HCO3- is more soluble in blood than CO2
- too much CO2 would change blood pH ➞ HCO3- less harmful
- carbonic anhydrase catalyzes both formation & dissociation of HCO3- (reversible)
- facilitates CO2 transport to alveoli
sickle cell anemia
single V-E mutation in β chain of hemoglobin causes defective rigid mol that makes RBC still & sickle-shaped
- defective Hb mol = less efficient binding ∴ less O2 for cells
- blocks vessels
- ↓ SA:V ratio
- more rigid = more prone to break ➞ more rapid turnover of RBC but body cannot replace fast enough ∴ ↓ O2 carrying capacity
hypoventilation
underventilation results in↑ PCO2 ➞ respiratory acidosis
- more CO2 = more carbonic acid
- ex: pneumonia
hyperventilation
rapid ventilation results in ↓ PCO2 & respiratory alkalosis
- CO2 (as HCO3-) helps maintain pH in certain ranges ➞ enzymes depend on pH & temp to be optimal
respiratory control centers in brain stem
- control by est rhythmic breathing pattern
- neural networks control rhythmic firing or motor nerves to diaphragm (phrenic nerve) & intercostal muscles
-
medullary respiratory centers
- dorsal respiratory group (DRG): inspiratory neurons active in normal quiet breathing
- ventral respiratory group (VRG): inspiratory & expiratory neurons activated upon demand
- pre-botzinger complex: on top of VRG = where rhythm is generated
- pons respiratory centers (PRG): modulate activity of medullary centers to promote smooth breathing rhythms
- hering breuer reflex: stretch receptors in smooth muscles of bronchioles that inhibit medullary centers to prevent over-inflation
chemical influences on ventilation rate
A. pO2: only something strenuous causes ventilation
- 100➞80 mmHg = no change in ventilation
- normal pp in alveoli: 104 goes down to 40
- < 40pp ➞ ventilation
B. pCO2: linear relationship w/ ventilation to get rid of CO2
- PPCO2: 46 in blood ➞ 40 in alveoli
- < 40 ➞ ventilation ↓
- more CO2 ➞ more ventilation
C. pH effects ventilation ➞ ability to get O2
- blood pH drops too low ➞ acidosis
- blood pH rises to high ➞ alkalosis
chemoreceptors
central chemoreceptors:
- located in medulla near resp control center (brainstem)
- excitatory input to inspiratory neurons
- more activation than peripheral
peripheral chemoreceptors:
- carotid bodies located in carotid sinus
- aortic bodies located in aortic arch
- chemical factors sense [CO2], [O2], & [H+]
- only respond to [O2] if PO2 < 40mmHg
- PO2 influence mostly important in situations like suffocation or high altitudes
*PO2 doesn’t directly activate resp centers ➞ activates through [H+] - both active at all times
effect on peripheral chemoreceptor vs central chemoreceptor:
↓ PO2 in arterial blood
effect on peripheral chemoreceptor:
- stimulates only when arterial PO2 < 60mmHg
- even at 40 O2-hemoglobin saturation ~75%
- hemoglobin designed to carry a lot of O2 in blood even when PO2 ↓
- emergency mechanism
effect on central chemoreceptor:
- directly depresses + resp center itself when < 60 mmHg
- inhibits system
effect on peripheral chemoreceptor vs central chemoreceptor:
↑ PCO2 in arterial blood
(↑H+ in the brain ECF only for central)
effect on peripheral chemoreceptor: weakly stimulates
effect on central chemoreceptor:
- strongly stimulates
- dominant control of ventilation
- levels > 70-80 mmHg inhibit resp control centers & central chemoreceptors
- no CO2 in BBB ➞ [H+] in ECF stimulates central chemoreceptors
effect on peripheral chemoreceptor vs central chemoreceptor:
↑ [H+] in arterial blood
effect on peripheral chemoreceptor:
- stimulates
- important in acid-base balance
effect on central chemoreceptor: no effect ➞ cannot penetrate BBB
type 1 alveolar cell
- large cavity that allows gas exchange
- single layer makes up alveoli walls
type II alveolar cell
produces alveoli fluid lining with pulmonary surfactants:
- weak detergent that ↓ surface area to prevent collapse
- normalizes pressure
- prevents recoil
- disrupts H-bonding of water lining alveolar wall (mixture of protein & lipid) to prevent large bubble formation from smaller ones
pulmonary surfactants
- in fluid lining of alveoli produced by type II alveolar cells
- weak detergent that ↓ surface area to prevent collapse
- normalizes pressure
- prevents recoil
- disrupts H-bonding of water lining alveolar wall (mixture of protein & lipid) to prevent large bubble formation from smaller ones
tidal volume
TV = small amount we actually take in during inspiration/expiration
- normal breathing
- V of air entering/leaving during single breath
- ~500 mL
inspiratory reserve volume
IRV = extra volume of air that can be maximally inspired over & above TV
* V of air we can use during strenuous situations
* FOF
* exercise
* maximal con-traction of the diaphragm, external intercostal muscles, and accessory inspiratory muscles.
inspiratory capacity
IC = max volume we can inspire after normal quiet expiration
* IC = IRV + TV
* normal V + extra volume for strenuous situations
expiratory reserve volume
ERV = extra volume that can be actively expired by maximally contracting the internal intercostals beyond that normally passively expired at the end of a resting TV
* forced expiration after normal expiration
residual volume
RV = volume left over after max expiration
functional residual capacity
volume in lungs after normal passive expiration
vital capacity
VC = maximum V that can be moved out during a single breath following a maximal inspiration
* TLC — minimum amount of air necessary for normal fx
* amount of air we can regulate
* maximum volume change possible within the lungs
* IRV + TV + ERV
total lung capacity
TLC = maximum volume of air that the lungs can hold
* VC + RV
* dead space = non-fresh air; cannot be used by alveoli ➔ does not provide O2
medullary respiratory centers
- dorsal respiratory group (DRG): inspiratory neurons active in normal quiet breathing
- ventral respiratory group (VRG): inspiratory & expiratory neurons activated upon demand
pre-botzinger complex
where rhythm is generated
* on top of VRG
normal breathing process is controlled by
dorsal respiratory group (DRG) & ventral respiratory group (VRG)
pons respiratory centers (PRG)
regulate activity of medullary centers to promote smooth breathing rhythms
hering breuer reflex
stretch receptors in smooth muscles of bronchioles that inhibit medullary centers to prevent over-inflation
dorsal respiratory group (DRG)
part of medullary respiratory center consisting of inspiratory normal quiet breathing
ventral respiratory group (VRG)
part of medullary respiratory center consisting of inspiratory & expiratory neurons activated upon demand
