Intro to Pulm B&B Flashcards
which type of pneumocytes regenerate following injury?
Type 2: produce surfactant, key for regeneration after injury
[Type 1: most common, thin for gas exchange]
what is surfactant made of?
mix of lecithins, esp. dipalmitoylphosphatidylcholine
what changes in fetal alveoli for them to be considered mature?
lungs are considered mature once enough surfactant is present, ~35 weeks
when there is more lecithin than sphingomyelin in the surfactant
what is the use of betamethasone in improving preterm lung function?
betamethasone: steroid that stimulates surfactant production in lungs
(lungs considered mature once enough surfactant is present for alveoli to not collapse)
neonatal respiratory distress syndrome, aka ______, often leads to which congenital heart defect?
neonatal respiratory distress syndrome = hyaline membrane disease, because there is not enough surfactant (so alveoli look clear)
severe hypoxemia due to poor ventilation (surfactant keeps alveoli from collapsing)
complications: patent ductus arteriosus, bronchopulmonary dysplasia, retinopathy (via ROS)
risk factors: maternal diabetes, C-section, prematurity
into which lung is aspiration of a foreign body most likely?
right lung because right bronchus is wider and more vertical than left
if upright - right inferior lobe
if supine - right inferior or right upper
at which vertebral level are the following openings into the diaphragm, and what passes through them?
a. caval opening
b. esophageal hiatus
c. aortic hiatus
a. caval opening (T8): IVC
b. esophageal hiatus (T10): esophagus, vagus nerve
c. aortic hiatus (T12): aorta, thoracic duct, azygous vein
which nerves innervate the diaphragm?
C3, C4, and C5 keep the diaphragm alive!
(C5 = phrenic nerve)
also innervate shoulder, which is why diaphragm irritation (gallbladder disease) can cause referred shoulder pain
also, if a nerve is cut, may seem diaphragm elevation (rather than depression) with inspiration (“sniff test”)
which accessory muscle raise the ribs and sternum, respectively, in exercise breathing?
scalenes - raise ribs
sternocleidomastoids - raise sternum
what is summed to give total lung capacity vs inspiratory capacity vs vital capacity vs functional residual capacity?
total lung capacity = RV + ERV + IRV + TV
inspiratory capacity = TV + IRV
vital capacity = TV + IRV + ERV
functional residual capacity = RV + ERV
how is total lung capacity calculated
sum of all volumes:
RV (residual volume), air that can’t be blown out no matter how hard you try
ERV (expiratory reserve volume), extra air pushed out with force beyond TV
IRV (inspiratory reserve volume), extra air that can be drawn in with force beyond TV
TV (tidal volume), air that moves in/out with each quiet breath
how is vital capacity calculated?
vital capacity = most air you can exhale at max
vital capacity = TV (tidal volume) + IRV (inspiratory reserve volume) + ERV (expiratory reserve volume)
how is functional residual capacity calculated?
functional residual capacity = residual volume after quiet expiration = RV + ERV
basically, the volume of air in the lungs when they are relaxed
chest wall pulling out = lungs pulling in
[remember chest wall has tendency to expand/spring outward, lungs have tendency to collapse/recoil]
anatomic vs physiologic dead space
anatomic dead space: volume of conducting portions of respiratory tract (nose, trachea)
physiologic dead space: anatomic dead space + volume of alveoli that don’t exchange gas well due to insufficient perfusion (mostly in the apex)
*may be increased during disease
when is pressure inside the respiratory system zero?
functional residual capacity: volume where lungs rest after quiet exhalation
chest wall pulling out = lungs pulling in
[remember chest wall has tendency to expand/spring outward, lungs have tendency to collapse/recoil]
how does intrapleural vs alveolar pressure change during inhalation and exhalation? (during quiet breathing)
intrapleural pressure remains negative at all times (always more negative than alveolar)
alveolar pressure becomes negative during inhalation, then positive during exhalation
how does pleural pressure change during forced exhalation?
normally (tidal breathing), pleural pressure is negative at all times
in forced expiration, pleural pressure becomes positive to put pressure on the alveoli, which causes the air to be pushed out
what occurs during the equal pressure point in the lungs?
equal pressure point: pleural pressure = airway pressure, and beyond this point airways collapse (pleural should be more negative than alveoli pressure)
in healthy lungs, this occurs proximally in the cartilaginous airways, which prevents collapse
in disease (bronchitis, emphysema), EPP can move towards alveoli and cause collapse/obstruction
where is resistance to air flow highest in the respiratory system?
medium bronchi, due to turbulent flow
resistance lowers in terminal bronchioles, slowing laminar flow
how is 2,3 BPG generated?
created from diverted 1,3 BPG, which is a substrate of glycolysis
sacrifices ATP from glycolysis in RBC (which have no mitochondria, so can only use glycolysis for energy), but worth it for more O2 delivery
how do the following affect the O2 saturation curve?
a. 2,3 BPG
b. H+
c. low CO2
left shift = higher O2 affinity
right shift = lower O2 affinity
a. 2,3 BPG —> R shift
b. H+ —> R shift
c. low CO2 —> L shift
how does carbon monoxide affect the oxygen saturation curve?
CO binds iron in heme with MUCH higher affinity than O2 —> blocked O2 binding sites = less O2 absorbed
shifts O2 sat curve to LEFT (higher affinity) and pulls the max % saturation DOWN (less carrying capacity because of less binding sites)
what state is iron in methemoglobin and what is the treatment for methemoglobinemia?
methemoglobin: oxidized iron (Fe3+, instead of Fe2+)
Fe3+ cannot bind oxygen
treatment: methylene blue
what is the effect of cyanide poisoning on the respiratory system?
blocks electron transport chain in mitochondria
aerobic metabolism stops —> functional hypoxia, especially for brain and heart
anaerobic metabolism occurs —> lactic acidosis
PaO2, CaO2, and SaO2 will all be normal, but oxygen in mixed venous blood will be INCREASED because cyanide is preventing oxygen USE
how can the following be used as treatment for cyanide poisoning?
a. nitrates
b. hydroxocobalamin
c. thiosulfate
a. nitrates: generate methemoglobin (Fe3+), which cyanide binds, pulling it away from mitochondria (where it disrupts ETC)
b. hydroxocobalamin: precursor of Vit. B12, binds CN and forms cyanocobalamin, which is readily excreted
c. thiosulfate: transforms CN to thiocyanate, which is readily excreted
how does systemic vs pulmonary circulation respond to low oxygen levels?
system - vasodilation
pulmonary - hypoxic vasoconstriction, in order to shunt blood away from poorly ventilated areas (important in fetal circulation)
what 3 parameters influence the rate of diffusion from air to blood?
- pressure difference between air and blood
- area of alveoli for diffusion
- thickness of alveolar tissue
how is O2 uptake limited in healthy vs disease-state patients? (what is the limiting factor)
healthy: O2 uptake is perfusion limited - more blood flow in capillaries alongside alveoli = more O2 uptake
disease (fibrosis, emphysema): O2 uptake is diffusion limited - thickened alveolar walls limit how much O2 can be taken up
how does primary pulmonary hypertension classically present?
rare disease, classically affects young women
increased endothelin (vasoconstrictor), decreased NO
associated with BMPR2 gene mutation —> abnormal endothelial and vascular smooth muscle proliferation
how are each of the following drugs used to lower pulmonary vascular resistance?
a. Epoprostenol
b. Bosentan
c. Sildenafil
a. Epoprostenol: prostacyclin (IV)
b. Bosentan: antagonize endothelin-1 receptors (PO)
c. Sildenafil: inhibits PDE5 in smooth muscle of lungs (PO)
what 3 parameters determine O2 content in the blood?
- O2 binding capacity (determined by hemoglobin)
- % saturation (of hemoglobin)
- dissolved O2
O2 content = (O2 binding capacity)x(% Sat) + (dissolved O2)
do the following primarily cause hypoxemia or hypoxia?
a. heart failure
b. anemia
a. heart failure: low CO —> hypoxia (low O2 delivery to tissues)
b. anemia: low O2 carrying capacity —> hypoxemia (low O2 content in blood)
how will the following causes of hypoxia affect O2 content and PaO2 (partial pressure of O2 in the blood, reflecting amount of dissolved O2), respectively?
a. hypoxemia
b. heart failure
c. anemia
d. carbon monoxide
a. hypoxemia (low O2 content): LOW O2 content, LOW PaO2
b. heart failure (low CO): NORMAL O2 content, NORMAL PaO2
c. anemia (low O2 carrying capacity): LOW O2 content, NORMAL PaO2
d. carbon monoxide (“functional anemia”): LOW O2 content, NORMAL PaO2
what would be the cause of hypoxemia with a normal vs high A-a gradient? (Alveolar to arterial O2 partial pressure)
hypoxemia with normal A-a gradient: alveoli are working, but not enough O2 is being inhaled - hypoventilation, high altitude
hypoxemia with high A-a gradient: alveoli are not working - most lung diseases (fibrosis, shunt, V/Q mismatch)
[V/Q = ventilation/perfusion]
what does a V/Q ratio < 1 indicate?
V/Q ratio = ventilation (V) to perfusion (Q) ratio
low V/Q ratio indicates reduced ventilation relative to perfusion - blood going where not enough O2 is present in the lungs (such as physiologic dead space)
if V/Q = 0 —> shunting (venous blood to arterial system without oxygenation)
explain physiologic shunting as caused by atelectasis
atelectasis = collapsed airway (alveoli)
physiologic shunting: blood perfuses alveoli that doesn’t work, so venous blood is shunted to arterial system without oxygenation —> hypoxemia
what does a V/Q ratio > 1 indicate?
V/Q ratio = ventilation (V) to perfusion (Q) ratio
high V/Q ratio indicates reduced perfusion relative to ventilation - gas is going in where there is insufficient blood flow
extreme example: anatomic or physiologic dead space
Inadequate gas exchange can be caused by shunting, V/Q mismatch, or dead space. Which of these will NOT respond to 100% O2 administration?
shunting (venous blood to arterial system without picking up O2) won’t correct with 100% O2 because functional alveoli are already extracting max O2
dead space and V/Q mismatch will be corrected with 100% O2, because increasing O2 content in alveoli will increase PaO2
Inadequate gas exchange can be caused by shunting, V/Q mismatch, or dead space. Which of these will present with hypercapnia (high PaCO2)?
dead space: classic cause of hypercapnia, due to perfusion problem and ventilation is wasted
shunting and V/Q mismatch rarely cause increase in PaCO2 (increased ventilation resolves hypercapnia)
describe the Bohr effect
CO2 + H2O <> HCO3- + H+
via carbonic anhydrase
H+ can bind to hemoglobin and convert Hgb to tense form which releases O2
this shifts O2 saturation curve to the right —> more O2 offload for a given PO2
explain why RBC have a high Cl- content in venous blood
RBC convert CO2 to HCO3- via carbonic anhydrase
HCO3- inside RBC leave cell to plasma, and Cl- enters to maintain electrical neutrality
describe the Haldane effect and how it works in synergy with the Bohr effect
in low O2 environments, hemoglobin is more likely to bind CO2, such as in the tissues
low O2 and high CO2 in tissues favors O2 unloading (Bohr effect) and CO2 loading (Haldane effect),
while high O2 and low CO2 in lungs favors O2 loading (Bohr effect) and CO2 unloading (Haldane effect)
explain why high altitude causes alkalosis
high altitude = lower pO2
hypoxia —> hyperventilation —> decrease pCO2 —> respiratory alkalosis (leftward shift)
after 24-48h, renal excretion of HCO3- causes pH to fall back to normal
2,3 BPG production will also increase, shifting curve back to normal
how does exercise affect O2 and CO2 levels in veins vs arteries?
exercise —> increase ventilation and blood flow
more O2 consumed/ CO2 produced by muscle
veins: O2 falls, CO2 rises
arteries: NORMAL O2 and CO2
what is the major stimulus for breathing, and where are the central vs peripheral chemoreceptors?
PaCO2 is major stimulus for breathing
central chemoreceptors in medulla most important, some input from peripheral chemoreceptors in carotid and aortic bodies (these are more sensitive to O2)
high PaCO2 —> increase respiration
what do rales indicate on physical exam?
rales = crackles
heard when small airways pop open after collapse
classic causes: pulmonary edema, pneumonia, interstitial fibrosis
what do wheezes indicate on physical exam?
wheezes = air flow through narrowed bronchi
classically caused by asthma, can also be caused by heart failure (cardiac asthma), chronic bronchitis, or obstruction (tumor - localized wheeze)
what is the classic cause of rhonchi being heard on physical exam?
rhonchi = course breath sounds due to secretions in large airways
classically caused by COPD
what does stridor indicate on physical exam?
stridor = wheeze that is almost entirely inspiratory, usually heard loudest over neck
indicates partial obstruction of larynx or trachea
classic causes: laryngotracheitis (croup), epiglottitis (Hib virus in children), retropharyngeal abscess, diphtheria (pseudomembrane)
