Exam 5 - Pulmonary Ventilation & Circulation Flashcards
Transpumlomary pressure
- difference between alveolar and pleasurable pressure
- measure of force that collapses lung (recoil pressure)
- increase in trans pulm pressure = more recoil pressure
Normal pleural pressure
-5 cm H20
Holds lungs open at rest
Inspiration
- chest cavity expands…-7.5 cm H20 pleural pressure
- 500 mls air in (normal tidal volume)
Expiration
- recoil back to resting
- 500 mls air out
Normal alveolar pressure
- 0 cm H20
- atmospheric pressure
Change in alveolar pressure driven by:
- Change in pleural pressure
- expansion/collapse of alveoli
Change in pleural pressure driven by:
- change in thoracic cavity size
Length of expiration
- 2-3 seconds
- passive process
- inspiration is only 2 sec….active process
What determines how fast alveolar pressure changes:
- resistance
- pressure gradient (transpulmonary pressure)
- compliance of lungs
Lung compliance
- 200 mls air for each 1 cm H2O increase
- transpulmonary pressure rises during inspiration
Compliance curve
- shape determined by elastic forces of lungs
- easier to move air out vs in (lungs want to collapse)
- Inspiration: compliance starts low then high
- Expiration: compliance starts high then low
Elastic forces affecting lung compliance
- elastic forces of lung: -elastin/collagen fibers
- 1/3 of elastic forces - elastic forces of air-fluid interface: -2/3 of forces
- Becomes problem if no surfactant
- 1-2 H2O molecules on alveoli
- easier to breathe without interface
Surfactant
- reduces water surface tension
- secreted by type II epithelial cells
- contains phospholipids
- reduce tension 8-50%
Alveoli lined with water
- on inside
- helps with expiration
- makes inspiration harder
Emphysema
- merging of alveoli
- good for collapsing pressure
- lose more surface area…doesn’t make up for collapsing pressure
Collapsing pressure
2 x surface tension / alveolar radius
- if collapsing pressure increases…harder to bring air in
- normal is 4 cm H2O
- if no surfactant… 18
- if radius halved…36
Premature babies surfactant
- forms in 6th or 7th month of gestation
- radius less than 1/4 of adult
- collapsing pressure 6-8 x greater than adult
- respiratory distress syndrome can be fatal
- treated with surfactant
Lungs+Thorax compliance
- half of that of just lungs
- 110 mls / cm H2O (vs 200)
3 factors of energy needed to breath
- force requires to expand lungs against elastic forces
- increase compliance = less energy
- tissue resistance work
- airway resistance work (asthma)
- 3-5% of total energy is for NORMAL ventilation (can increase 50x)
- limitation of exercise is muscle energy for respiration
Spirometer
- measures pulmonary volumes
Tidal volume
- normal breath volume
- 500 mls
Inspiratory reserve volume (IRV)
- full force of inspiration above tidal volume
- 3000 mls
Expiration reserve volume (ERV)
- Max expiration after tidal volume
- 1100 mls
Residual volume (RV)
- Air remaining after forced exhale
- always there to prevent lungs from collapsing
- keeps normal pO2 and pCO2
- 1200 mls
Inspiratory capacity (IC)
- TV + IRV
- 3500 mls
Functional residual capacity (FRC)
- ERV + RV
- 2300 mls
Vital capacity
- IRV + TV + ERV
- 4600 mls
- Total we can actually move
Total lung capacity (TLC)
- VC + IRV
- 5800 mls
Raw
Airway resistance to flow
Vd
Volume of dead space gas
Va
Volume of alveolar gas
R
Respiratory exchange ratio
Ppl
Pleural pressure
Palv
Alveolar pressure
Pb
Atmospheric pressure
DL O2
Diffusing capacity of lungs for O2
Vi
Inspired volume of ventilation per minute
Vs
Shunt flow
VO2
Rate of O2 uptake per minute
Minute respiratory volume
- New air into airway per minute
- TV x respiratory rate
- 500 x 12 = 6000 mls/min
- respiratory rate can go as high as 40-50 bpm but not long
Alveolar ventilation
- new air into alveoli per minute
- (TV-dead space) x resp rate
- (500-150) x 12 = 4200 mls/min
- determines pO2 and pCO2
- increase pulm rate…increase O2 and decrease CO2
Anatomical dead space
- all space in resp system other than alveoli
- where no gas exchange occurs
- increases with age
Physiological dead space
- anatomical dead space + not functioning alveoli w/ no blood flow
- normally just equal to anatomical dead space
- in diseased can be up to 10x larger than anatomical dead space
Bronchial circulation
- high pressure, low flow
- arterial blood to lung tissue (1-2% of CO)
- arises from thoracic aorta
- returns venous blood to pulmonary veins
- deoxy blood merges with oxy blood
Pulmonary circulation
- low pressure, high flow
- deoxy blood to pulmonary capillaries (gas exchange)
- oxy blood to LA
Pulmonary Artery
- divides into R and L main pulmonary arteries
- thin (1/3 of aorta) and distensible (7 mls/mmHg)
- short
- deoxy blood (75% O2 vs 99%)
Bronchial arteries
- 1-2 % of CO
- carry O2 blood
- supplies tissues of lungs
- empty into pulmonary veins and enters LA (like a shunt)
- so SV of LV is 1-2% greater than that of RV
Lymphatics in the lungs
Jobs:
- remove particulate matter entering alveoli (also coughing)
- collect plasma proteins leaked from pulmonary caps (no edema)
- empty into right thoracic lymphatic duct
RV diastolic / RA pressure
0-1 mmHg
RV systolic / PA pressure
25 mmHg
Mean Pulmonary pressure
15 mmHg
Left atrial pressure
2 mmHg
- what we are trying to measure (filling pressure)
PCWP
5 mmHg
-ca use as LA indicator…just a little higher (due to more resistance)
Pulmonary capillary pressure
7 mmHg
PA diastolic pressure
8 mmHg
Blood volume in lungs
- 9% of total blood volume
- 450 mls (arts + caps + veins)
- 70 mls in caps (alveolar SA is 770 - 1075 ft^2)
Changes in pulmonary blood volume
- can go from 1/2 to 2x normal
- hard expulsion of air can move 250 mls blood out
- L heart failure / mitral valve probs can increase resistance to flow out
- can cause 100% increase (2x normal) in volume and pressure
- drops gas exchange
Compliance of pulmonary vessels
- very high….unlike aorta
- minimizes high pressure risk for RV (want to keep low)
Low O2 in alveoli
- if pO2 < 73 mmHg…vessels constrict
- stops flow to alveoli because poor gas exchange will happen
- opposite of systemic caps
- directs blood to better gas exchange areas away from dead space
Hydrostatic pressure gradient
- pressure under surface of water/air interface
- pressure increases 1 mmHg / 13.6 mm depth
- due to gravity / weight of water above
Hydrostatic pressure gradient in body
- RA: 0 mmHg (heart pumps excess blood)
- Brain: 10 mmHg lower
- Feet: 90 mmHg higher
Hydrostatic gradient in lungs
- top: 15 mmHg lower than level of heart
- bottom: 8 mmHg higher than level of heart
- total pressure difference = 23 from top to bottom
- note that even though pressure changes at different levels…pressure gradient that drives movement through vessels stays same
- flow at bottom of lungs would be higher than top if R stays same
Pulmonary cap pressure depends on:
- driving pressure from RV
- effect of hydrostatic pressure
- alveolar pressure in surrounding tissue
Zone 1
- top of lungs
- no flow ever
- alveolar pressure > pulm cap pressure
- no zone 1 under normal conditions
- will if low MAP or high alveolar pressure
Zone 2
- intermittent flow
- pulm cap pressure > alveolar pressure …in systole only
- little to no flow in diastole….opposite relationship
- apex of lung
Zone 3
- continuous blood flow
- pulm cap pressure > alveolar pressure
- all of lung except apex (zone 2)
- during exercise, blood flow increases…all areas become zone 3
Ventilation vs perfusion
- If only perfusion… only venous blood
- pO2 and pCO2 will equilibrate
- If only ventilation… alveoli constantly refreshed
- pO2 and pCO2 max and min out…150 and 0
- Normal Va/Q values = 104 and 40 (pO2 and pCO2)
How lungs handle increase in CO
- Exercise can increase CO 4-7x
- Want to keep pulm pressures down…RV can’t handle
- More caps open up (3x)
- Distending open caps more (x2)
- Increasing pulm art pressure
- Increase in pulm pressure small compared to CO increase
- prevents edema formation
Pulmonary response to high LA pressure
- Never above 6 mmHg
- Pulmonary veins dilate in response to increase in pressure
- In L side failure, LA can get to 40-50!
- Increases right heart workload
- above 25-30 mmHg causes pulmonary edema (dead < 30 min)
Normal CO speed of blood in pulmonary caps
0.8 secs
- As low as 0.3 with high CO
- More caps open in high CO to prevent any lower than 0.3 secs
Pulmonary capillary hydrostatic pressure vs systemic
- Lower
- 7 vs 17 mmHg
- force pushing out of cap
Pulmonary interstitial hydrostatic vs systemic
- Lower
- -5 to -8 vs -3
- force pulling out
Pulmonary interstitial oncotic vs systemic
- higher
- 14 vs 8 mmHg
- leaky pulmonary caps
- force pulling out
Pulmonary plasma oncotic vs systemic
- same
- 28 mmHg
- biggest one we affect
- After all pressures added up….1 mmHg total outward force
- Lymph ducts carry away excess fluid and also evaporation
Acute pulmonary edema
- occurs if increase rate of filtration
- occurs if decrease rate of lymph removal
- Causes:
- L heart failure / mitral valve disease (increase LA pressure)
- damage to cap membrane / pneumonia , toxic gases (pulm oncotic pressure decreases)
Chronic pulmonary edema
- lungs compensate if pulm cap pressure high for 2 weeks
- lymph vessels expand…carry 10x normal
- pressure of 40 mmHg and can still live
- this needs to happen gradually over time
Pleural fluid
- few mls
- kept at minimum by lymphatics
- provides -4 mmHg to keep lungs expanded to normal size
Pleural effusion
- excess fluid in cavity
Causes: - blockage of lymph vessels
- heart failure w/ high pulm pressures
- increased fluid/protein into pleural space
- reduced plasma colloid pressure (perfusionist fault)
- infection/inflammation of pleural membrane
