pulmonary Flashcards
Increase Capillary permeability (Kf, σ)
- Oxygen toxicity: too much O2 is bad for the lungs.
- Acute respiratory distress syndrome
- Inhaled or circulating toxins
Alveolar plateau of closing volume test [6]
This test is not usually done because it doesn’t work very well for the patients with high airways resistance.
shunt equation
-Ratio of shunted flow (mixed venous flow that goes directly to the left side of circulation) divided by (over) the total cardiac output (total blood flow) is = to (end capillary O2 content – arterial O2 content) divided by (over) the (end capillary O2 – mixed venous O2 content)
, the person has alveolar dead space.
If arterial pCO2 > end tidal pCO2 ,
Causes of Increased Alveolar-Arterial Oxygen Partial Pressure Gradient [17]
- The arterial oxygen difference can also be measured.
- Alveolar pO2 is calculated using the alveolar air equation, which provides an ideal alveolar pO2 value.
- Situations that increase the difference between alveolar and arterial pO2:
- Increased shunting (venous blood flowing to arterial side without picking up oxygen) will increase the difference between alveolar pO2 and arterial pO2.
- Both abnormal anatomic shunts and intrapulmonary shunts can increase this difference.
- Some level of V ̇/Q ̇ mismatch.
Everyone has some level of V ̇/Q ̇ mismatch, but larger mismatches can affect the alveolar-arterial O¬¬2 partial pressure gradient.
-Impaired diffusion due to fluid in lower portions of the lung. Interstitial fluid collects (especially in the lower parts of the lung) until it is removed by the lymph system.
- Increased inspired partial pressure of O2
- Decreased mixed venous partial pressure of O2
- Shift of oxyhemoglobin dissociation curve
Increased Capillary hydrostatic pressure (Pc)
Increased left atrial pressure resulting from left ventricular infarction or mitral stenosis.
Over-administration of intravenous fluids.
Decreased interstitial hydrostatic pressure (PIS)
Too rapid evacuation of pneumothorax or hemothorax.
Decreased oncotic pressure (π_pl)
- Protein starvation/dilution of blood proteins by intravenous solutions.
- Renal problems resulting in urinary protein loss (proteinuria).
C. Carbamino Compounds [28]
CO2 can bind to a terminal amine group in a protein in the blood to form a carbamino compound, but a hydrogen ion gets released in the process
Most carbamino compounds form with Hb, but some can form with other trace proteins and albumin, etc.
- Bohr Effect
a. Deoxyhemoglobin is a base, so it is willing to pick up the hydrogen ion, shifting the reaction forward, forming the carbamino compound.
b. Oxyhemoglobin is an acid, so it gives up that extra hydrogen or the CO2, and makes reaction go in the other direction
c. Much more CO2 will be carried as carbamino compounds in venous blood where there is more deoxyhemoglobin than in arterial blood
COPD (case 1) o Smoking history o Prolonged expiratory phase o Resonant chest, hyperinflation of lungs (Chest X-ray) o FEV1 = 0.55 low (13% predicted) o FVC = decreased FEV1:FVC ratio= decreased
Pulmonary Fibrosis (case 2)
o 5 year history of worsening dyspnea
o Nonproductive cough
o Rheumatoid arthritis autoimmune, causes pulmonary fibrosis in lungs
o Low RR
o Crackles and rails at bases of lungs, chest X-ray with white shit in lungs
o FVC = 55% low
o FEV1 = 52% low
o FEV1/FVC > 70%= normal (
o Increased resistive work (on expiration)
work to inflate and deflate the lungs (fat people- have to move a lot of tissue to breathe, and NO resistive work)
o Exercise = increased airway resistance, more trapped hair so FVR is increased with exercise compromising FVC
o Pulmonary function tests “sagging and wide” due to dynamic airway compression;
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o All volumes low = restrictive disorder
o Diffusing capacity= doesn’t measure diffusion
measures uptake of carbon monoxide (CO
) CO comes into body and goes to Hb
forms carboxyhemoglobin. Can calculate how much CO is taken up. Binds to Hb in capillaries
measures effective capillary volume (which affects the diffusion capacity (anemia, or things that destroy pulmonary capillaries (fibrosis))
o Increases elastic work (stiff lungs= harder to inflate) – elastic recoil is high, no resistance (leather balloon), low compliance
o(elastic work-takes place when theres stiffness in the lungs or the chest wall)
Stiff lungs decreased compliance= pulmonary fibrosis
increased elastic work of breathing
Giving O2 will not help
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o Increase alveolar dead space = ventilation but not perfused
o High V/Q – increases with exercise (ventilation increases without recruitment of vessels)
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Negative intrapleural pressures during inspiration
Moving fluid also exerts less pressure
Cartilage prevents collapse with inspiration normally- but his trachea is damaged, allowing collapse
o Resistive work of breathing (on inspiration)
************** She’s just nervous tell her that there’s no disease or reason that she is getting SOB. She just needs to work on her exercise
o To see what it is, do a PFT with exercise! Brings out abnormal physiology that affects a disease process
o Pulmonary Function with Exercise Testing = abnormal
MVV – maximal amount of air you can breathe in and out in a min.
• Ventilation on exercise (VE) = 65% MVV (low)
• Ventilatory reserve (MVV – VE)
CO = normally limiting factor to exercise
OSA
- Collapse of the upper airway during normal inspiration is normally prevented by contraction of the pharyngeal dilator reflex
- Upper airway obstructions during sleep cause alveolar hypoxia and hypercapnia
- HPV occurs in response to the hypoxia and hypercapnia and increase PVR
- Repeated episode of pulmonary HTN may lead to vascular remodeling resulting in chronic pulmonary HTN
- Chronic alveolar hypoxia during the episodes of upper airway obstruction leads to hypoxemia,causing renal release of erythropoietin
The increased PAP and increased blood viscosity chronically increase the afterload of the RV, producing RV hypertrophy, which can be seen as right axis deviation in ECG
This could lead to cor pulmonale, RV failure secondary to pulmonary HTN
- Arterial hypoxemia and hypercapnia during episodes of upper airway obstruction cause increased cerebral BF, caused by dilation of cerebral blood vessels—-this repeated occurance causes HA
- increased RVEDP and volume lead to increased RA volume, which increases the secretion of atrial natriuretic peptide from atrial myocytes, increasing sodium excretion. The increased atrial volume also stretches receptors that suppress ADH secretion from the posterior pituitary gland and increases urine volume
physiologic dead space
is approximately equal to the anatomic deadspace in healthy lungs
minute volume is expressed as follows:
MV= VT X Breaths/min
Alveolar Ventilation is expressed as follows:
Alveolar ventillation= (VT-dead space) X Breaths/min
FEV1-
Obstructive d/o:
Restrictive lung d/o
A decreased FEV1= large airway problem
FEV1/FVC ratio is decreased
FEV1/FEC ratio is either normal or increased
Emphesema
increased lung compliance = decrease tendency of the lungs to collapse
at the original FRC, the tendency for the lungs to collapse is less than the tendency of the CW to expand
think exhale…so outward cw recoil is > inward recoil of the lung!!!!!
the opposing forces will seek a new higher FRC so that they will be balanced….barrel chest…shift to the left
Fibrosis
decrease lung compliance = increased tendency for the lungs to collapse…..
think inhale….inward recoil of the lungs is increased and > than outward recoil of the CW
A new lower FRC will occur to balance the opposing forces…a shift to the Right happens
Laplace’s law with alveolus
LaPlace’s law creates a collapsing pressure that is = to surface tension and inversely proportional to alveolar radius
ex:small alveolus have high collapsing pressures
large alveolus have low collapsing pressures
Air flow is……. to airway resistance?????
Who’s law describes resistance of the airways and what is the formula???
inversely proportional
Q=change in pressure/R
Poiseuille’s law
R= 8nl/ pie r4
resistance= viscosity of the inspired gas and the length of the airway
and inversely proportional to the radius to the 4th power
small airways do not offer a lot of resistance because they are in parallel
medium size bronchi actually offer the most resistance
Breathing cycle:
@ rest
inspiration
expiration
@ rest: intraplueral = atm
inspiration: alveolar pressure < atm
- lung volumes increase, alveolar pressure decrease, intrapleural pressure decreases, transmural pressure increases
expiration: alveolar pressure> atm
- lung volumes decrease, alveolar pressure increases, intralpleural pressure increases, and transmural pressure decreases
changes in oxyhemaglobin dissacciation curve:
shifts to the right:
shift to the right:
-when P50 is increased and unloading of O2 from arterial blood to the tissues is facilitated
-for any level of Po2, the % saturation of Hb is decreased
Hypoxemia produces……
hyperventilation by a direct effect on the carotid and aortic body chemoreceptors
type of chemoreceptors:
central- medulla….. low pH….high PCO2
arterial- carotid and aortic….low pH, low PO2, high CO2
In CSF
Co2 combines with H20 to produce H and HCO3
the resulting H acts directly on the central chemoreceptors
central chemoreceptors are in the medulla.
they are sensitive to the pH of the CSF
a decrease in the pH of the CSF produces and increase in breathing rate
H does not cross the BBB, but CO2 does
Co2 diffuses from arterial blood into the CSF because CO2 is lipid soluble and readily crosses the BBB
Increase to PaCo2
the response of the arterial chemoreceptor to Co2 is < important than the response of the central chemoreceptor to CO2 or H
If an area of the lungs is not ventilated secondary to bronchial obstruction, the pulmonary capillary blood serving that area will have a PO2 that is……
equal to mixed venous PO2
In the transport of Co2 from the tissues to the lungs…what occurs in the venous blood?
the conversion of Co2 and H20 to H and HCO3 in the RBC occurs in the venous blood
Transport of CO2 as HCO3
CO2 is generated in the tissues (low O2, high CO2) and diffuses freely into the venous plasma and then into the RBCs
In the RBC, CO2 combines with H20 to form H2CO3, a reaction that is catalyzed by (carbonic anhydrase)
H2CO3 Dissociates as H and HCO3
High pH, low PaO2, low PaCO2
low PaO2 causes hyperventilation via the arterial chemoreceptors. PaO2 must be < than 60mmhg for this to occur
low PCO2 results from hyperventilation and causes a high pH, which inhibits breathing via the peripheral and central chemoreceptors
High altitudes
- decreases PAO2 b/c of low barometric pressure
- this causes low PaO2 and hypoxemia occurs
- this causes hyperventilation via arterial chemo receptors (resp alkalosis)
- 2,3 DPG increase b/c of the hypoxia
- they bind to Hb and cause a shift to the right to improve unloading of O2 in the tissues
- the pulmonary vasculature constricts (HPV) in response to Alveolar hypoxia
- which causes an increase in PAP
- which causes hypertrophy of the RV
why is venous blood slightly more acidic than arterial blood?
- In venous blood, CO2 combines with H20
- H2CO3 is formed to make H and HCO3
- the resulting H is buffered via deoxyhemoglobin
- which makes venous blood a bit more acidic
What is VC?
the volume expired in a forced maximal expiation
Supplemental O2 will be helpful in which V/Q mismatch?
- Supplemental O2 is most helpful in tx of hypoxemia associated with a V/Q defect if it is low V/Q
- Regions of low V/Q have the highest BF
- breathing high PO2 air will raise the PO2 of a large volume of blood and have the > influence on the total BF leaving the lungs
Variable and fixed upper airway
-extrathoracic (above the thorax) V/Q= >1 (OSA)
–intrathoracic: V/Q= < 1
:
during the early portion of forced expiration when lung volume is still high:
the effective pressure gradient for airflow is > @ higher lung volumes than @ low lung volumes
alveolar elastic recoil is greater at high lung volumes because the transmural pressure is high and because high volumes help oppose dynamic compression and decrease airway resistance by traction on small airway
during a forced expiration, as soon as dynamic compression occurs the effective driving pressure for airflow becomes transmural pressure instead of alveolar pressure minus atmospheric pressure
why is alveolar ventilation less than the minute volume?
because the last part of each expiration remains in the conducting airways and does not reach the alveoli
the Bohr equation
permits the determination of the sum of the anatomic and the alveolar dead space
the anatomic dead space plus the alveolar dead space is know as the physiologic dead space
physiologic dead space = anatomic dead space + alveolar dead space
the bohr equation makes use of the simple concept:
any measurable volume of CO2 found in the mixed expired gas must come from alveoli that are both ventilated and perfused because there are negligible amounts of CO2 in inspired air
Inspired air remaining in the anatomic dead space or entering unperfused alveoli will leave the body as it entered (except for having been heated to body temperature and humidified), contributing little or no CO2 to the mixed expired air
In healthy people, alveolar PCO2 is in equilibrium with PaCO2…so if alveolar ventilation is doubled and CO2 production unchanged, then….
the PACO2 and PaCO2 are reduced by 1/2
At constant Co2 production, alveolar PCO2 is….
approximately inversely proportional to alveolar ventilation
alveolar PO2 must be calculated with the alveolar air equation
what is the effect on each of the following standard lung volumes and capacities of changing from a supine to an upright position? FRC- RV- ERV- TLC VT IRV IC VC
-as a person stands up, the effects of gravity alter the mechanics of breathing (and also decrease VR)
-The contents of the abdomen are pulled away from the diaphragm, thus increasing the outward elastic recoil of the chest wall.
-the inward recoil of the lungs is not affected, and so the
FRC-increased
RV- doesn’t change
ERV- increase because the FRC increased and the RV is relatively unchanged
TLC- may slightly increase because of the slight decrease of inward elastic recoil of the chest wall at high lung volumes because abdominal contents are pulled away from diaphram
VT- no change
IRV- decrease because the FRC, TLC and VT are higher
IC- decrease
VC- unchanged, although it may be slightly increased because of the slight increase in TLC and the decreased intrathoracic blood volume
How would the predicted values for the standard lung volumes and capacities and the closing capacity of a healthy elderly person differ from those of a young healthy person? FRC- RV- ERV- TLC VT IRV IC VC
Assuming general good health and normal weight, the main changes seen with age are a loss of pulmonary elastic recoil and a slight increase of the elastic recoil of the CW, especially at higher volumes.
-the loss of pulmonary elastic recoil has the secondary effect of increasing airway closure in dependent areas of the lung at the lower lung volumes
FRC- increased RV- increased ERV- decreased because the increase in RV due to airway closure is > than the increase in FRC TLC- decreased VT- unchanged or may be either slightly increased or decreased, depending on whether the increased lung compliance, increased airways resistance, decreased chest wall compliance predominates. IRV- decreased IC- decreased VC-decreased closing volume is also increased
