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48 Cards in this Set

  • Front
  • Back
Normal Lung Function
maintain normal PaO2, PaCO2 and pH w/out excessive cardiac or pulmonary work
Adequate gas exchange
1. Adequate ventilation
2. Adequate perfusion
3. Distribution of ventilation
4. Diffusion of O2 and CO2 across alveolar cap membrane
Most impt cause of gas exchange abnormalities
Nonuniform distribution of ventilation
Conducting airways (Gen 0-16)

Bronchi

Bronchioles
No gas exchange
Flow is turbulent

Bronchi - lare cartilaginous airways caliber depends on bronchial wall smooth muscle tone

Bronchioles- smaller airways whos caliber depend on lung volume
Function of conducting airways
1. warm and humidify inspired air
2. Distribute inspired air to alveoli for gas exchange
3. remove foreign material from inspired air reaching the alveoli
Respiratory bronchioles (Gen 17-23)
Gas exchange occurs (thinner walled)
Flow is laminar

Respiratory bronchioles receive nutrients from pulmonary circulation
Alveoli
site of gas exchange
Spherical shape
300-500 million alveoli
Total SA 75M2 (90 sq yrds/tennis court)--> impt to distribute entire Cardiac output over a surface one erythrocyte thick

Alveolar- cap membrane 1/2-1 u thick

Pulmonary cap sheets of blood surrounding alveolar airspace not tubular blood vesseles

Airflow in alveoli is by diffusion
O2 and Co2 transport across alveolar-cap membrane by...
Passive diffusion

No active transport
Function of pulmonary circulation
1. bring unoxygenated blood to alveoli
2. serve as a reservoir
3. serve as a filter
4. metabolize (detoxify) substances as they pass through lungs

High compliance, low resistance circuit
Bronchial circulation
perfuses conducting airways and arises from systemic circulation
O2 transport in blood
~5% of O2 carried in blood is dissolved

0.003mL of O2/ dL of blood/ torr of PO2

~95% of O2 carried in blood is bound to hemoglobin

1.34mL O2/ g of 100% saturated Hemoglobin
Saturated O2 to Partial pressure of O2 is non-linear
Oxyhemoglobin dissociation curve to R
Dec hemoglobin affinity for O2 but improve tissue delivery of O2

1. Acidosis
2. Inc P CO2
3. Inc Temp
Oxyhemoglobin dissociation curve to L
Inc hemoglobin affinity for O2 but dec tissue delivery of O2

1. Alkalosis
2. Dec P CO2
3. Dec Temp
CO2 transport in blood
10% is dissolved
30% bound to carbamino compounds in erythrocyte
60% in carbonic acid as HCO3- in plasma

Relationship is linear in physiological range
Bohr effect
CO2 and acidosis dec affinity of hemoglobin for O2
Haldane effect
O2 dec affinity of hemoglobin for CO2
At rest, When is O2 diffusion complete?
before RBC traverse half way thorugh pulmonary cap

PaO2 slightly > PaO2

Normal [PAO2- PaO2]< 10 torr
Alveolar partial pressure - arterial partial pressure
Can O2 diffusion be inc by inc diffusion gradient in normal lung (Inc Fraction inspired O2)?

Person is hypoxic?
NO,


but Inc fraction inspired O2 can inc O2 diffusion in abnormal lungs if person is hypoxic breathi
What limits O2 diffusion?
The inability to carry more O2 in blood

Nearly all oxygen is carried in blood on hemoglobin
Oxyhemoglobin dissociation curve is nonlinear and hemoglobin is 100% saturated with O2 at Pa:O2 100torr

Even if more O2 cannot be carried away by blood

Not, physical barriers like alveolar cap membrane
Inc O2 diffusion by
1. Inc O2 uptake
2. Inc hemoglobin
3. Inc Cardiac output
CO2 is more diffusible than O2
thus PA CO2= Pa CO2
Ventilation/perfusion ratio (V/Q)

What is it in a normal lung?
Determines PA O2 and PA CO2

V/Q=1
PA O2= ~100 torr
PA CO2= 40 torr

PAO2 proportional to V/Q
PA CO2 is inversely proportional to V/Q and to VA
V/Q >1
Partial Alveolar pressure of oxygen PA:O2 is inc (high PA:O2)
close to 1 close PA:O2 --> 100 torr
close to infinite PA:O2 --> 150 torr

Partial alveolar pressure of carbon dioxide PA:CO2 is dec (low PA:CO2)
Closer to 1: PA:CO2--> 40
Closer to infinite: PA:CO2--> 0
V/Q <1
Partial alveolar pressure oxygen (PAO2) is decreased (Low)
Closer V/Q 1 PA:O2-->100
Closer to 0 PA:O2--> lower PA:O2

Partial pressure of CO2 (PACO2) is increased (High)
Closer to 1 PA:CO2 --> 40
Closer to zero higher PA:CO2 will be
VE = VD + VA
VA= alveolar ventilation (takes part in gas exchange)

VD= wasted ventilation (does not take part)
Calc PA O2 and PA CO2
PACO2 = [VCO2/VA] [PB-47]
PB- barometric pressure

PACO2= 40 [V/Q]^-1

PAO2= PIO2 -[PACO2/0.8]
Lung structure
1. Airways (23 generations /divisions) from trachea to respiratory bronchioles

2. Alveoli
Functional Lung unit
Largest unit where PO2 and PCO2 are uniform

Occurs at level of respiratory bronchiole

~5000 alveoli
Pulmonary artery

Pulmonary vein
Artery- enters lung with airway and lymphatic

Vein- leaves lung separately
PIO2 (partial inspired air)
conster both FIO2 franction inspired oxygen and barometric pressure
Hemoglobin
O2 bound to hemoglobin 1.34 mL of O2 per gram of fully saturated hemoglobin

Relationship of sat hemoglobin to PO2 --> oxyhemoglobin dissociation curve its non linear
P50
Defines the position of the oxyhemoglobin dissociation curve

Where hemoglobin is 50% saturated

Normal P50 for hemoglobin A is 26 torr

Diff types of hemoglobin have diff shaped curves and diff p50 values
Oxyhemoglobin dissociation curve determined by..
1. temperature
2. pH
3. PCO2
Calculate O2 content of Blood (C: O2)
C:O2= 1.34[Hgb][S:O2]+0.003[P:O2]

Normal Sa:O2 is 100%
thus normal Ca:O2= 20.4mL

Normal Sv: O2 is 75%
thus normal Cv:O2=15.2mL
Determinants of C:O2 in arterial blood
1. Lung function (P:O2 and S: O2)
2. Hemoglobin (anemia)
3. Substances interfering with O2 binding to hemoglobin (CO)
RBC through circulation

In the lungs
Lungs:
-Cool Temp causes inc hemoglobin affinity for O2
-Inc O2 affinity on hemoglobin displaces CO2 --> CO2 is exhaled (Haldane effect)
- dec CO2 is alkaline furhter inc affinity for O2

Blood leaving lungs has inc O2 content and dec CO2 content
RBC through circulation

In the tissues
Tissue:
- High temp dec hemoglobin affinity for O2--> enhances tissue deliver of O2
- dec O2 inc hemoglobin affinity for CO2--> CO2 is removed
- Inc CO2 is acidic further dec hemoglobin affinity for O2 (Bohr Effect)

Systemic venous blood is low in O2 and high in CO2
If Ve goes to L and Op goes to R
no gas exchange bc they are not meeting together
O2 concentration in alveolus is proportional to the amt coming in vs amount going out
Amt in is ventiatlation times FI:O2

Minute ventilation (Ve) is measured as amt of exhaled air
Minute ventilation (Ve)
tidal volume (Vt) times respiratory rate

Amt going out is proportional to perfusion (Qp)
Alveolar O2 concentration is an equilibrium determined by
ratio Ventilation to perfusion (V/Q)
Alveolar CO2 concentration is an equilibrium determined by
ratio of amt coming in (proportional to Q) to amoutn going out (V)

Inversely proportional to V/Q
PA:CO2
CO2 produced at constnat rate by body's metabolic rate

CO2 enters alveolus via perfusion and is removed by ventilation

VA (alveolar ventilation is 70% of VE)

Shortcut
PA:CO2=40* V/Q^-1
PA: O2
O2 consumed at a constant rate (VO2) O2 enters alveolus by ventilationa dn O2 enter alveolus is = VA X FIO2

Shortcut:
PA:O2=PI:O2 - [PA:CO2/0.08]
Arterial blood
comes from lungs and reflects lung function

can measure PO2 and PCO2
Venous blood
comes from tissues and reflects tissue metabolism
Cabonic acid
CO2 and acid base status are related by carbonic acid in blood

Thus arterial blood gases assess acid base status as well as oxygenation
Cyanosis
-clinical sign of blue skin coloration
-seen in lips and fingenails
- associated with hypoxia
- when only 5gm/dL of unsaturated hemoglobin

Normal Sv:O2 is 75% for Hgb-14gm/dl only 3.5gm/DL unsat hemoglobin in venous blood --> no cyanosis

Lung disease whos anemic (dec Hgb) may not show cyanosis even if hypoxic

Pts with polycethemia (inc Hgb may show cyanosis even ir normoxic