Respiration 4 Flashcards
Identify static lung volume and capacities on a spirogram. Given lung volumes calcluate lung capacities. Draw the Static lung volumes curve.
As you breath, a rotating drum allows you to calculate howw much, the breath moves a pen without losing any air. It can measure TLC but some air is left in your lungs and therefor can’t measure ALL lung volumes.
Static lung volume.
At this card go see static lung volumes
Tidal volume: what you breath normally tV (1/2 litre)
IRV: inspiratory reserve volume
IC: inspiratory capacity (tV plus IRV)
Vital capacity: maximum inspiration to maximum expiration.
- Largest tidal volume that you can generate.
TLC: total lung capacity: VC +Residual volume (RV)
FRC: Functional residual capacity at end of a normal breath
Inspiratory reserve volume: what you can still breath in
IRV + TV = Inspiratory capacity.
ERV: what you can still breath out (expiratory reserve volume)
RV: residual volume (what you can’t breath out)
Functional residual capacity (erv + rv)
outline 3 factors that effect lung volumes
Height
Gender
Age: lung volume increases with age, then stops at 25, when you get older RV and FRC and increases and VC decreases resulting in gas trapping. Due to stiffening of the chest wall.
Ethnicity: body build/length/chest wall size.
describe and compare effect of obstructive and restrictive respiratory diseases on FEV1 (volume after 1 second) to FVC (total volume) ratio
Normal: Fev1/FVC= 75% or more
Obstructive <70% takes a long time to empty lungs.
Restrictive >70% or normal, but don’t get enough IN. but can get it out quickly.
Distinguish between minute, alveolar and dead space ventilation and calcuate them given didal volume, breathing frequency and anatomic dead space. How does breathing affect ventilation?
** not done properly find lecture 4 and rewrite.
Volume that you expire is 500ml.
- 150 ml goes into conducting airways
- 350 goes into the alveoli (respiratory zone)
You already have FRC, so with each breath you dilute the FRC by 350 ml.
Some of it participates in gas exchange, some remains in dead space.
Minute ventilation
Alveolar gas exchange: 350mL 4.2 L/min
Remaining of breathing: deadspace ventilation: 1.8L /min
tV and breathing frequency gives us different alveolar ventilation and dead space ventilation.
Gas exchange in alveoli.
O2, removal of c02 is important in gas exchange.
Panting: reduced tidal volume, more breaths, very low volume high frequency, very LOW GAS EXHANGE.
Deep and slow: more volume but slower, more gas exchange.
ALVEOLAR AND DEAD SPACE ARE DEPENDANT ON VOLUME!! (I.E. VENTILATORS CAN’T BE PROGRAMMED TO 500ML
Need alveolar gas exhange!!
Alveolar Dead space: air reaches alveoli but can’t do gas exhange because not enough perfusion. (not an issue in healthy lungs but when there is a blood clot this is problematic.
Compare partial pressures of gases in an ideal alveolus to extreme mismatch.
Key to gas exchange is with alveolar and capillary.
- in steady state (breathing normally)
- partial pressure of a gas (co2 or o2) by the time gas exhange happens at end of capillary the partial pressures become the same.
When gas exhange is done, the end of capillary and the alveolus will be the same
100 o2
40 for 02
Blood that going past,
When the blood flows past, the exhange is complete
- lose carbon dixide until its at equilibrium with the co2 in the alveoli.
- rate that you breath in must match the rate that the blood goes past.
- if flow is blocked, no blood going past, over time, partial pressures will match what is inspired. (no blood to swap with) alveolar 02 will go high and co2 will go low.
- best that it can do is match the partal pressures.
Theoretical infinity.
Rate of blood flow vs rate of alveolar ventilation
(ventilation/perfusion) is key to gas exchange.
Alviolar ventilation: breathing that reaches alveoli
At steady state this is the same as p02 and pco2
Alveolar perfusion: what’s coming back. Relative rates.
Describe homeostatic mechanisms in place for matching of ventilation and perfusion at alveolar level.
View lecture 4 for an image. Makes way more sense that way.
Deadspace ventilation
- Good ventilation - Not enough blood flow
Co2 will contract the local airways
- On smooth muscle airwys - It will constrict it - Increase airway resistance, reduce airflow
Elevated 02 in the airway will relax smooth muscle
- Dilate local blood vessel - Decrease resistance - Increase blood flow.
Same thing happens for ventilation perfusion
Same thing happens in the airway (mucus plug in the airway)
- The blood going past will just bypass it, the alveolar gasses will match the mixed blood.
Small airflow, large bloodflow
- Regulation of local airway of smooth muscle
- Local airway of vessels
- Homeostatic mechanism that reverses the situation.
Airflow increases (high c02 relaxes airway muscle, dilating it and reducing resistance) Bloodflow decreases (low o2, contracting artial smooth muscle, constriction, increase vascular resistance, decrease bloodflow)
What is the first step in diagnosing respiraotry diseases?
Forced vital capacity maneuver. Restrictive diseases make inspiration hard due to
- pulmonary fibrosis (140 causes, idiopathic, occupational, asbestosis, silicosis, farmers lung (moldy hay), bird breeders’s lung (excreta)or
- stiff chest wall. (ankylosing spondylitis, kyphoscoliosis)-can’t expand chest wall.
Obstructive diseases make breathing OUT hard. due to crhonic obsructive pulmonary disase (COPD), asthma, bronchitis, emphysema.
What are some mechanisms behind obstructive disease and narrowing.
Causes behind airway narrowing
already mentioned.
1. Smooth muscles (bronchoconstriction) COPD, asthma
2. Inflammation (copd, asthma, bronchitis
3. Increase mucous production (asthma, bronchitic, cystic fibrosis
4. Reduced alveolar elastic recoil (emphysema)- arent’ pulling each other apart, so therefor they are narrowed.
1-3 airway narrowed, flow limiting.
4: recoiling inwards: keeping it open. But when recoil is reduced in emphysema (cause airway walls destroyed, greater compliance, not opening airway of interest as much cause they aren’t pulling towards each other as much) THAT MAKES MUCH MORE SENSE (LECTURE 4 34.00)
Negative intrapleural pressure
Expiration is positive intrapleural pressure.
How do you quantify breathing?
Ve: minute ventilation. VE= volume x breathing frequency. 500 ml for normal quiet breath or 6lmmin
