Physiology Flashcards
How is oxygen moved between alveoli and pulmonary arteries?
Diffusion* -Pressure difference (pO2) pIO2 is 150 mmHg pAO2 is 100mmHg PaO2 is 40mmHg (venous)
CO2 is moved from blood to the air
pICO2 is 0
pACO2 is 40mmHg
paCO2 is 46mmHg
Parameters for diffusion?
Cross sectional area
Thickness
Permeability
Pressure difference
Anatomic dead space
When does it increase?
Conducting airways - trachea to terminal bronchioles (NOT respiratory bronchioles)
Anatomic dead space is NOT involve in gas exchange
Increases in a giraffe or when ventilating someone** must increase tidal volume
What causes expansion of thoracic cavity during inspiration? On exhalation?
Diaphragm contracts and moves down
Intercostals contract to raise ribs
Exhalation is passive - elastic recoil
Where would dust settle in the lungs if inhaled?
In terminal bronchioles - it cannot move past there due to the alveoli septa
What happens to lung compliance and effort to breath in pts with restrictive lung disease? Examples?
Lung compliance decreases, takes more force.
Normal: 7% of energy used
COPD: 20% of energy used - they are always tired
Pulmonary fibrosis
What reduces surface tension of alveoli?
Surfactant - produced by type II pneumocytes
If not surfactant the smaller alveoli would collapse.
Tidal Volume
Vital Capacity
Residual Volume
Amount of air inspired and expired in routine breathing (500 ml)
Max volume of air that can be exhaled after a maximum inspiration
Amount of air left after maximal expiration
Total lung capacity
Vital capacity plus residual volume
Reduced in pneumothorax**
What does COPD do to residual volume?
Increases it**
Barrel chest
What do restrictive lung diseases do to lung volumes?
Decrease all of them.
Physioligic Dead space
What increases it?
Calculated by taking faction of CO2 in expired gas and comparing to alveolar gas…
PE increases physiologic dead space - it blocks flow so there are alveoli in the lungs the do not get any O2 exchange from blood
What increases alveolar ventilation?
Exercise
Functional residual capacity
Amount of air remaining in lungs after a normal breath
What determines diffusion across the blood-gas barrier?
Pressure difference**
Surface area
1/thickness
1/(molecular weight of gas) how fast it goes through - smaller faster
Solubility of gas (how fast/easy it goes through)
What changes pressure difference in blood-gas barrier?
Decreased at altitude
Increased in supplemental O2
What changes surface area of blood-gas barrier?
Emphysema lessens it
COPD lessens it
Pneumothorax lessens
Atelectasis lessens
What changes the thickness of the blood-gas barrier?
Fibrosis, pneumonia, heart failure
Do solubility and weights of gas change?
What is more soluble, CO2 or O2?
NO
But CO2 is MUCH more soluble than O2 (20X)
Perfusion limited gases?
O2 and CO2 are not as soluble in blood - i.e. don’t bind to RBC as well as a non perfusion limited gas like CO. The pO2 and pCO2 will rise when O2 or CO2 are added (unlike CO).
N2O is also perfusion limited but it does not bind to RBC..all goes into blood.
Diffusion limited gases?
CO is diffusion limited. CO binds immediately to RBC so it does NOT increase the pCO of blood.
When is O2 a diffusion limited disease?
Pulmonary diseases that increase the blood-gas barrier thickness or decrease the pressure difference
- Pneumonia, fibrosis
- Very high altitudes
- COPD, HF - they can’t walk very far-pO2 drops very quickly
- PE also
Diffusion barrier resistance
Defined as partial pressure difference / volume of gas transferred
R = P/F
Lung pressures
Normally 25/8
Increased by HF, valve stenosis/regurgitation
Resistence = P2-P1/Q
R = Mean(10) - left atrial (5) / 5L/min (CO) = 2mmHg/L/min
Much lower than systemic
Pulmonary vessels are pulled open during? and compressed during?
What causes the pressure to change in the vessels?
Pulled open during inspiration (negative, sub atmospheric), and compressed (couple mmHg) during expiration
Tension pnemothorax
Positive pressure ventilation
What decreases pulmonary artery resistance?
Recruitment of more vessels
Relaxation of arteries
Expansion of lung (sub atmospheric pressure)
Acetylcholine, PROSTACYCLIN** (COX2 inhibitor lawsuit)
It is less than systemic due to larger radius and shorter length.
What increases pulmonary artery pressure?
Exhalation
Norepinepherine
Serotonin
HISTAMINE*** (normally a vasodilator but in lungs its a vasoconstrictor)
Where in the lung as alveolar pressure greatest and also blood flow?
In the base
Where in the lung is air flow greatest (most oxygen) and least blood flow?
Apex.
Hypoxia in the lungs causes ________ to the vessels?
VASOCONTSTRICTION
Mechanism of hypoxia induced vasoconstriction in pulmonary vessels?
Inhibition of voltage gated K channels, thus DEPOLARIZING the RMP - this causes an increase of Ca leading to vasoconstriction.
What is a mechanism to keep the lungs dry? i.e. not edematous?
Conditions that cause pulmonary edema?
Lower hydrostatic pressure (less resistance) of pulmonary arteries compared to systemic*
Heart failure
What causes a cough with administration of ACE inhibitors?
ACE (angiotensin converting enzyme) is primarily in the lungs. Another function of ACE is to INactivate bradykinin, therefore while on an ACEinh bradykinin is active and causes vasoconstriction of pulmonary vessels causing a cough.
What is function of the lungs in terms of prostaglandins and leukotrienes?
The lungs synthesize both! They are both bronchoconstricors**
What is an important role of PGE infetal life? Maintaining the ductus arteriosis.
Where in the lung is the physiologic dead space?
Zone 1 - where pA is greater than pa is greater than pv… (the vessels will collapse)
What is the alveolar gas equation?
pAO2 = pIO2 - (pACO2/R)
R is the respiratory quotient, usually .8 with fatty acid oxidation (rest) and 1 with pure glucose metabolism (extreme exercise)
What does the A-a gradient determine?
If A-a gradient is near zero it means it is NOT a lung problem, if it is over 5 or so it is pulmonary pathology.
What is a pulmonary shunt?
An area of lung vasculature or alveoli that is collapsed causing deoxygenated blood to be added to oxygenated blood. The O2 sat % can never get to 100%.
Congenital defects, PE
What is the major cause of hypoxemia in lung disease?
Mismatch of ventilation & perfusion**
If no perfusion to an area of lung but alveoli are still inflated there is no gas exchange (alveoli will be 150mmHg O2 and 0mmHg CO2). Example?
PE
Increased ventilation/perfusion ratio
Right side of graph (high O2, no CO2)
If there is perfusion to a section of alveoli but the there is no flow to the alveoli there is no gas exchange (alveoli will reach values of venous blood, pO2 40, pCO2 46)
Pneumothorax
Decreased ventilation/perfusion ratio
Left side of graph low O2 and high CO2
Does the apex of the lung have a high or low ventilation/perfusion ratio?
High ratio - high ventilation, low perfusion
Lower CO2
High O2
Does the base of the lung have a high or low ventilation/perfusion ratio?
Low ratio - low ventilation, high perfusion
Higher CO2
Low O2
No matter how high you raise pO2 of the arterial blood you can only get to ______ saturation?
100% - Hbg is fully saturated
at paO2 of 40mmHg we are 75% saturated… at paO2 of 100 we are 100% saturated.
What happens to pCO2 in lung disease?
What will a high paCO2 do to breathing?
It is close to normal.. alterations in CO2 change breathing rapidly**
A high CO2 will INCREASE breathing.
Example of ventilation perfusion abnormality:
paO2 measured: 50
paCO2 measured: 60
Assume resp quotient of .8, so pAO2 = pIO2 - (paCO2/.8)
pAO2 should be the same as paO2 (60 in this case) : A-a gradient of zero.
BUT pAO2 = 150 - (60/.8) = 75mmHg… so A-a gradient is 75-60 = 15… this is bad. Means its a primary lung pathology of ventilation perfusion mismatch.
