Pulmonary Flashcards
Alveolar Gas equation
PAO2=
PIO2 - (PaCO2/R)
Can be approximated PAO2= 150 - PaCO2/0.8***
A-a gradient
PAO2-PaO2 = 10-15 mmHG
increased indicates underlying lung pathology
Air in the stomach on CXR in an infant be concerned w/
Early warning in the mother?
Trachealoesophageal fistula and esphageal atresa
Polyhydrominos
Most common type of tracheal esophageal fistula
C type w/ esophageal atresia and distal fistula
Type E (or H type) is the just a fistula
Diaphragm is made by the joining of what 4 structures?
Failure leads to?
septum transversum (from the cranial aspect) fuses w/ pueroperitonela folds, abdominal walls, and esophageal mesentery
Failure congenitally leads to herniation and lung hypoplasia (usually the L) polyhydraminos associated
Presentation of congenital diaphragm heniation
polyhydraminos in utero
hypoplastic lung -> cyanosis and inability to breath
flattened stomach
5 structures perforating the diaphragm and at what level?
T8 - IVC
T10 - esophagus
T12 - aorta, azygos vein, thoracic duct
innervation of the diaphragm
Phrenic C3-5
leads to referred pain to the shoulder (spleen and cholecysitis)
Aspiration pneumonia is more likely going to be found in what lobe?
R lobe due to wider and more vertical
Peanut inspiration the same but if lying down will be in the superior portion od the right inferior lobe while standing up it will be inferior portion of R inferior lobe
Importance of bronchopulmonary segments? Contains?
separated by connective tissue - has a bronchus, and 2 arteries per segment, veins are in the periphery
Spepaerates out the right 3 lobes and the L 2 lobes further
Smokers will see what transformation in their trachea
columnar ciliated cells -> stratified squamous through metaplasia
Chronic sinusitis, infertility and situs inversis?
Cause?
Kartagener syndrome
Due to dyenin not functioning leading to cilia defects all over
Important measure of fetal lung maturity
lecithen:Springomyelin ratio being greater than 2.0
See if enough dipalmitolphasphatidylcholine is being made
Product of type II pneumocytes?
dipalmitolphasphatidylcholine
other type II and I pneumocytes during injury
Role of type I pneumocytes?
gas diffusion - very thin
muscles of inspiration
- quiet
- exercise(3)
diaphragm
Sternocleidomastoid, scalenes, external intercostals
muscles of expiration
- quiet
- exercise
quiet is passive
exercise - internal intercostals, transverse abdominus, rectus abdominus, internal and external obliques
TLC is the combination of?
Functional Residual capacity and Inspiratory capacity or
Inspiratory reserve volume and Tidal volume and experatory reserve volume and residual volume
Inspiratory capacity is a combination of?
Tidal volume and inspiratory reserve volume
Vital capacity is a comination of
expiratory reserve capacity, tidal volume and inspiratory reserve capacity
Functional reserve capacity
residual volume and expiratory reserve volume
Determining the physiologic dead space formula
Dead space
= Tidal volume x [(PaCO2 - PeCO2)]/PaCO2
a= arterial
e expired air
Functional residual capacity (FRC) what is the relationship between chest wall and lungs
how does it change in emphysema?
How does it change in fibrosis?
they are balanced in their pull - airway and alveolar pressure are 0 and the intrapleural pressure is negative
in emphasymia there is increased compliance so the FRC is increased. More volume at given pressure
in fibrosis there is decreased compliance so less volume at a given pressure
Diffusion limited gases are?(2)
what does that mean?
CO and O2 (in diseased state: emphysema/fibrosis)
means that the partial pressure of the arterial will not be saturated upon leaving the lung - amount of gas carried limited by the diffusion
Perfusion limited gases(3)
what does that mean?
CO2, O2, N20
it means that the amount of gas that leaves the lung, the amount of gas carried is limited by the perfusion of the lung, equilibrates very quickly
How does COPD lead to Cor pulmonale
Cor pulmonale is heart failure due to lung disease. In COPD there is less oxygen perfusing the pulmonary vasculature leading to vasoconstriction and increased pressure. This increased pressure feeds back on the R heart leading to failure
-normally vessels expand w/ decreased O2, lungs shunt away
Pulmonary hypertension is defined as?
> 25mmHg in rest
35 mmHg exercising
Normally 10-15 mmHg
Pressure is equal to?
How does radius affect the system?
∆P = Q x R
R = (8 x length x viscosity)/(pi x r^4)
IN pulmonary resistance, what can change? What can’t generally?
radius of the tube
viscosity of the fluid
can’t really change the length
R = (8 x length x viscosity)/(pi x r^4)
Adding He to Oxygen does what
decreases the viscosity of the air and thus leads to less pressure
R = (8 x length x viscosity)/(pi x r^4) ∆P = Q x R
Primary pulmonary hypertension is due to
BMPR2 mutation -> increased smooth muscle proliferation
Loss of function mutation where normally BMPR2 regulates growth and lose radius
Causes of secondary pulmonary hypertension (6)
COPD/fibrosis (vasoconstriction w/ low alveolar oxygen) Mitral stenosis(feeds back)
Autoimmune (infammation -> intimal fibrosis)
sleep apnea/ high altitude
thromboembolic events
Left to right shunt (increased circulation)
Rx for pulmonary hypertension (4)
bosentan/ambriasentan
prostaglandin analogs
Sildenafil - phosphodiesterase inhibitors
Dihydropyradine CCB - nifedipine
Adult Hemoglobin is normally made out of?
How does it compare to fetal hemoglobin?
4 globin molecules (2 alpha 2 beta)
w/ 4 heme molecules
Fetal hemaglobin(2 alpha 2 gamma) has a higher preference for oxygen by being less affinity high 2,3 BPG, allows acquiring of oxygen from
2 types of states hemoglobin can be in and what favors each state
Taut - favors tissue and unloading
- in the presence of high: H, temp, 2,3 BPG, CO2
relaxed form favors O2 binding
-in the presence of low CO2, how H concentration and temp and 2,3 BPG
Hard working muscles leads to what type of hemoglobin state?
taught form and unloading of oxygen
lactic acidosis, low CO2, increased temp and metabolites of oxidation (2,3 BPG)
Methoglobin is what?
Ferric form (Fe 3+), oxidized iron in the hemoglobin instead of ferrous (Fe+2) form
Toxic for it favors cyanide more readily and does not favor O2 as much
Nitrates indue this and is Useful Rx cyanide poisoning w/ thiosulfate to excrete the thiocyante
Rx for methomoglobinemia (2)
methylene blue and Vitamin C
Also can give cimetidine over longer time
Agents known to cause methoglobin(6)
Methelglobin is the oxidized form of hemoglobin (Fe +3)
Nitrates/nitrities Antimalarials - chloroquine/primaquine Dapsone sulfonamide local anesthetics - lidocaine metoclopramide
Carboxyhemaglobin is?
Complications associated w?
hemoglobin bound to CO, see cherry red lips
- have decreased oxygen unloading in the tissues as a result
Causes a L shift in the graph due to readily binding of CO to the hemoglobin and thus not able to carry as much oxygen
(thus why pulse ox still shows high % sat because cannot differentiate what the hemoglobin is saturated w)
CO causes what kind of shift in the oxygen hemoglobin curve
Left shift
Causes a L shift in the graph due to readily binding of CO to the hemoglobin and thus not able to carry as much oxygen
(thus why pulse ox still shows high % sat because cannot differentiate what the hemoglobin is saturated w)
that causes a right shift in the hemoglobin oxygen curve and what does that mean from a oxygen unloading stanpoint
increased: CO2, [H] (low pH), temp and 2,3 BPG causes a right shift. Meaning there is left hemoglobin saturation at a given partial pressure of oxygen favoring unloading into the tissue(taut form)
The opposite is true for low CO2, [H], temp and 2,3 BPG and CO-> fairs Hg saturation at lower arterial pressure
Anemia leads to what changes in the the following lab results:
PaO2
Total oxygen content
O2 saturation
PaO2 normal
total oxygen content decreased
O2 saturation normal
COPD leads to what changes in the the following lab results:
PaO2
Total oxygen content
O2 saturation
PaO2 decreased
Total oxygen content down
O2 Saturation decreased
Physiologic shunt moves oxygen away from healthy tissue
Exercise leads to what changes in the the following labs
PaO2
venous O2
PaO2 normal
venous O2 is lower
-due to increased metabolites -> right shift on the hemoglobin oxygenation curve
Normal A-a gradient?
- what does it mean
what may raise A-a gradient
15-10 mmHg
means the difference in the O2 content in the alveoli - the O2 content in the arterial
elevated gradient may mean hypoxemia
- V-Q mismatch
- older age
- elevated FiO2 (giving O2)
- fibrosis
If PaCO2 increases and all else is the the same, what happens to PAO2?
It decreases
PAO2 =150 - (PaCO2/0.8)
What may change the PI02 in the alveolar gas equation
normally PAO2 = PIO2 (PaO2/R)
-> PAO2= 150 - (PaCO2/0.8)
PI O2 varries w/ atmospheric pressure and FiO2( the % oxygen content)
high altitude lowers PAO2
A-a ratio
PaO2/FiO2
normally equals 300mmHg
<200 = severe hypoxemia
What may cause normal A-a gradient hypoxeima?(2)
Elevated ?(4)
normal ( low O2 in alveoli -> low O2 in blood)
- elevated altitude
- hypoventilation
Elevated (not transfering)
- fibrosis
- VQ mismatch
- R to L Shunt
What is ischemia and what are some causes?(2)
lack of blood FLOW
Obstruction - MI/stroke
Venous blockage - traffick jam
What is hypoxia and some causes? (4)
hypoxia is lack of O2 in the tissue
heart failure, low CO output
anemia
hypoxemia
CO poisoning
V/Q ratio at the base of the lungs?
is < 1
due to gravity there is excess perfusion to the amount of ventillation
V/Q ratio at the apex of the lungs
> 1
due to blood falling down, there is excess ventilation ( why TB loves it here)
With exercise the ratio approaches 1 w/ capillary recruitment of the apex
V/Q in pulmonary edmea
approaches 0 and is known as a shunt
airway obstruction limits the ventilation no mater how much blood flows through
Which of the following circumstances benefits from O2 High V/Q or low V/Q
Higher ventilation to perfusion would benefit more because of capillary recruitment
low V/Q or ~ 0 would be a shunt and no mater how much O2 you give it will not make it
V/Q ratio in a PE
Blood obstruction leads to V/Q ratio approaching infinity
The small flow can be increased w/ other capillaries being recruited with the ventilation
-assuming less than 100% deadspace
CO2 is carried in the blood how (3)
- dissolve in blood
- Bicarb
- carried on the N terminal of the glob in (NOT heme group) as carbaminohemoglobin
- -binding encourages taut form (O2 release)
Exercise has what effect on the following?
V/Q ratio pulmonary blood flow pH PaO2 PaCo2 Venous O2 Venous Co2
V/Q-> 1 pulmonary blood flow increases w/ CO pH drops w/ lactic acidosis Pa O2 - No∆ Pa Co2 - no ∆ Venous O2 - decreases Venous CO2 - increases
How does hematocrit and Hemoglobin change in high altitude
Increases
40%-> 60% hematocrit
15 g/dL -> 20 g/dL
Responses of the bode to high altitude(5)
Increase in ventilation
Increase in EPO -> (increased Hct and Hbg)
Increased bicarb excretion (renal comp for Resp alkalosis)
Increase in 2,3 BPG -> right curve shift
Increase in mitcochondria
How does acetazolamide help with acute mountain sickness
acetazolimide augments the loss of bicarb already being losses to help with respiratory alkalosis due less alveolar oxygen pressure -> hypoxemia