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Lung physiology Flashcards

1
Q

Differentiating btwn obstructive and restrictive diseases 1

A
  • Use PFTs: spirometry, lung volume, DLCO
  • In obstructive diseases (emphysema, bronchitis) there will be a decreased FEV/FVC ratio (both decreased but FEV is decreased more), FEV/FVC < .7
  • TLC will be normal or slightly elevated (air trapping)
  • There are hyper inflated lungs
  • To distinguish btwn emphysema and chronic bronchitis use DLCO: should be normal in bronchitis and low in emphysema
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2
Q

Differentiating btwn obstructive and restrictive diseases 2

A
  • In restrictive diseases (either intrinsic or extrinsic) the FEV/FVC ratio will be normal (both will be decreased but at equal amount)
  • Main finding: decreased TLC
  • If its an intrinsic restive disease (IPF) the DLCO will be low
  • If its an extrinsic restrictive disease (scoliosis, obesity, neuromuscular) the DLCO will be normal
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3
Q

Lung volumes and capacities

A
  • Vt: tidal volume, the amount of air moment during restful breathing
  • IRV: inspiratory reserve volume, the amount of air that can be breathed in on top of Vt
  • Vt + IRV = IC (inspiratory capacity)
  • ERV: expiratory reserve volume, the amount of air on top of Vt that can be breathed out
  • IC + ERV = VC (vital capacity is amount of air that can be moved overall)
  • RV: reserve volume, amount of air that will stay in lungs all the time and is not able to be moved
  • VC + RV = TLC (or IC + FRC)
  • RV + ERV = FRC (functional reserve volume, volume of air in lungs at end of expiration, the point at which atmospheric pressure is at equilibrium w/ lung pressure)
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4
Q

Importance of lung volumes/capacities

A
  • Lung volumes are related to the height of the individual
  • FRC is very important b/c it tells you the volume in the lungs that generates a pressure exactly equal to atmospheric pressure (end of expiration)
  • FRC is usually around 2,700ml
  • TV is usually around 500ml
  • TLC is usually around 6,700ml (IC of 4,000ml + FRC of 2,700ml)
  • VC is usually around 5,500ml
  • Minute ventilation= Vt x RR
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5
Q

Physiologic purpose of FRC

A
  • Since FRC is the amount of air in lungs after expiration, there is always some accessible air in our lungs for gas exchange
  • This air acts as a buffer during times of apnea (btwn inspiration and expiration, and btwn expiration and inspiration) for gas exchange to continue even though there is no air moving
  • W/o this buffer there would be deoxy blood going from pulm artery to pulm vein during times of apnea
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6
Q

Dead space 1 (!)

A
  • Regions of the respiratory system that contain air but no gas exchange is happening
  • 2 types: alveolar and anatomic
  • Physiologic dead space = alveolar + anatomic
  • Anatomic: airway regions (like bronchioles, bronchi, trachea) that are unable to perform gas exchange
  • Ends at terminal bronchioles, which doesn’t do gas exchange (next segment, respiratory bronchioles, are first site of gas exchange)
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7
Q

Dead space 2 (!)

A
  • Anatomic dead space in mls is equivalent to a persons body weight in lbs (usually about 150ml)
  • At the end of expiration, the air in the anatomic dead space has the same composition as the air in the respiratory zone (where the dead air space came from)
  • At the end of inspiration, the air in the anatomic dead space has the same composition as room air (where the air came from)
  • The only difference btwn respiratory zone air and room air is that ROOM AIR CONTAINS NO CARBON DIOXIDE
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8
Q

Dead space 3 (!)

A
  • Alveolar dead space is the amount of air in alveoli that isn’t receiving any blood so no gas exchange is occurring
  • Alveolar dead space CANNOT be measured, but anatomic dead space can be (estimated)
  • Alveolar ventilation: VA = (500-150)xRR
  • The anatomic dead space (150) is subtracted from the Vt (500) b/c of the inhaled 500ml, 150 of it doesn’t reach the alveoli and instead is left in the anatomic dead space
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9
Q

Muscles of respiration

A
  • Inspiration is an active process, the major respiratory muscle (diaphragm) and muscle of the chest wall all for expansion of the thoracic cavity
  • Expiration is a passive process, under resting conditions
  • Simply relaxing the respiratory muscles will allow partial collapse of the thoracic cavity
  • Expiration can be active such as during exercise
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10
Q

Physiology of respiration 1

A
  • The pleural space is of negative pressure (most negative at apices, least negative at base, average is -5)
  • This means that its the act of expanding that allows air to flow into lungs
  • Increasing the volume in the chest leads to a decreased pressure (less than ATM), thus air flows into lungs (boyle’s law)
  • Upon relaxation of respiratory muscles, the elastic recoil and slightly higher than ATM pressure causes the air to flow out
  • In some pathologies, the pleural pressure is positive (pleural effusion, pneumothorax)
  • Positive pleural pressure act to collapse the lung
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11
Q

Physiology of respiration 2

A
  • As lungs enlarge recoil increases, and as lungs collapse recoil decreases (recoil always works to collapse lungs)
  • Lungs expand when: intrapleural pressure is a greater force than recoil
  • Lung volume decreases when: recoil force is greater than the intrapleural pressure
  • If these two forces perfectly balance, the lung volume will not change
  • Intrapleural pressure changes based on the size of the chest cavity (as chest expands, the pleural pressure becomes more negative)
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12
Q

Differences in alveolar size in the lung regions

A
  • Alveoli are more distended in the apices than in the base, even at rest (due to gravity and more negative pleural pressure at apex)
  • That means the alveoli in base have a greater capacity to fill since their normal tone is small (high compliance)
  • Thus, alveoli in the base get more air flow
  • But the alveoli in the apices are over ventilated
  • Apical alveoli distended all the time, base alveoli compressed w/ high compliance
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13
Q

Transpulmonary pressure

A
  • The pressure difference across the lungs (alveolar pressure minus pleural pressure)
  • Determines whether the lung will inflate or deflate
  • If transpulmonary pressure is positive the lung will inflate, and if its negative the lungs will collapse
  • Normally always positive since the pleural pressure is large and negative and the alveolar pressure is small and changes slightly based on respiratory cycle phase
  • Thus our lungs don’t collapse
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14
Q

Overview of respiratory cycle (!)

A
  • Start at FRC, as chest expands the intrapleural pressure becomes more negative
  • This increases lung volume, slightly decreases alveolar pressure, and air flows into lungs
  • During expiration the muscle relax, recoil dominates, and intrapleural pressure begins to increase back to FRC state
  • Recoil causes lung volume to decrease, which makes alveolar pressure slightly higher than ATM and thus there is flow out of the alveoli
  • Back to start once at FRC
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15
Q

Cardiovascular changes w/ respiration 1

A
  • When placing a catheter into a pulmonary artery, want to put it in an artery thats in the base of the lung and want to measure pressure at end of expiration (alveoli least distended)
  • This is because the distended alveoli in the apices will compress the pulmonary arteries there and falsely increase the blood pressure
  • The pulmonary vascular resistance changes based on the respiratory cycle, since when the alveoli are more distended and filled with air there is more compression of arteries and thus more resistance
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16
Q

Cardiovascular changes w/ respiration 2

A
  • Pulm vascular resistance is lowest during FRC (alveoli most collapsed)
  • (Lower) Airway resistance is lowest at end of inspiration (TLC) since inspiration causes lower airways to widen (expiration causes them to close)
  • Upper airways react the opposite way: they close during inspiration and open during expiration
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17
Q

Pulsus paradoxus 1

A
  • During inspiration the HR increases in response to a decrease in BP
  • BP is decreased in one of 3 ways: physiologic, positive pressure ventilation, pathologic
  • Physiologic: normally during inspiration, RA return is increased, but LA filling is decreased due to higher resistance in pulm vasculature (thus less flow back to LA)
  • The decreased LA filling leads to decreased SV, CO, and BP and thus compensatory increase in HR
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18
Q

Pulsus paradoxus 2

A
  • During positive pressure ventilation (PPV) there is a decrease in return to both the R and L sides (due to increased intrathoracic pressure)
  • Decreased venous return to L side leads to decreased BP
  • During some pathologies (cardiac tamponade), there is decreased VR on both sides of heart (due to high pressure around the heart) and thus a decreased BP
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19
Q

Cardiac reflex due to inspiration

A
  • HR increases as BP drops due to low pressure baroreceptors
  • Low pressure receptors are stretch receptors in the RA (and large pulm vessels/systemic veins) that sense the volume in RA
  • On inspiration the RA volume increases, causing the receptors to fire and thus the HR is increased due to the reflex (bain bridge reflex)
  • High pressure baroreceptors will increase HR when BP is decreased and will decrease HR when BP is increased
  • In this sense, the high pressure and low pressure baroreceptors are antagonizing one another
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20
Q

PEEP

A
  • Positive end expiratory pressure
  • Anytime there is positive pressure (ventilator) there will be pulses paradoxus (decrease in BP and increase in HR)
  • W/ PEEP there is increased inspiration volume and decreased expiration volume, thus the intrathoracic pressure is even greater and CO/BP decreases even further
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21
Q

Pneumothorax

A
  • Puncture in one of the pleural layers (usually visceral)
  • This allows the intrapleural pressure to equilibrate w/ atm pressure
  • Pleural pressure goes from -5mmHg to 760mmHg, thus compressing the lung (lung collapse), expanding the chest wall, and shifting the mediastinum away from the affected side
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22
Q

Lung recoil

A
  • 2 components: collagen/elastin of the lung and the surface tension forces along the alveoli
  • Surface tension is the greatest component of lung recoil, and is opposed by surfactant
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23
Q

Law of laplace and surfactant

A
  • Pressure and radius are inversely related, such that smaller alveoli have greater pressures and large alveoli have smaller pressures
  • This is why small alveoli are more prone to collapse, since their high pressures means the air might flow to larger alveoli (lower pressure) causing the small ones to collapse (atelactasis)
  • Surfactant does 3 things, one of them is stabilizes small alveoli so they don’t collapse
  • Surfactant lowers surface tension, thus reducing recoil and increasing compliance
  • Surfactant also reduces capillary filtration to prevent pulmonary edema
24
Q

FEV1

A
  • The amount of air someone can exhale in 1 sec after being at TLC
  • Should be about 80% of VC
25
Q

Obstructive pulmonary diseases

A
  • Chronic bronchitis, asthma, bronchiectasis, alpha-1 AT deficiency, emphysema
  • There is an increased airway resistance during expiration
  • Results in an increased TLC and RV (air trapping) w/ hyper inflated lungs
  • FEV1/FVC ratio decreased (<.7)
  • Markedly decreased FEV1, FVC also decreased
  • Spirometry is not good for detecting early COPD b/c there must be significant damage to distal airways to see changes in spirometry
26
Q

Restrictive pulmonary diseases

A
  • Decrease in lung compliance, measured as a decrease in all lung volumes w/ a FEV/FVC ratio being normal to high
  • Can be intrinsic or extrinsic (use DLCO to distinguish)
  • All lung values decreased, but TLC markedly decreased and FEV/FVC normal to high
27
Q

COPD etiology example

A
  • Tobacco smoke and free radicals in actives anti-protease nzs (alpha1 anti trypsin), allowing protease nzs (elastases) to breakdown alveoli and the elastic tissue of small airways
  • This leads to collapse of these airways during expiration (loss of radial traction)
  • Since the airways collapse during expiration the air cannot leave and is trapped
  • This increases the TLC and RV
28
Q

Approach to hyperemic pt

A
  • Look at A-a gradient
  • Response to supp O2
  • DLCO
29
Q

Diffusion factors

A
  • Structural: surface area (increased SA = increased diffusion) and thickness (increased thickness = decreased diffusion)
  • Physiologic: pressure difference (greater difference = increased diffusion), solubility (CO2>O2>N2)
30
Q

A-a gradient

A
  • Difference btwn alveolar O2 (PAO2, or PO2) and arterial O2 (PaO2)
  • PaO2 is measured via ABG
  • PAO2 = (Patm-Ph2o)x(FiO2) - (PaCO2/.8)
  • This all simplifies to PAO2 = 150- (PaCO2.8)
  • Patm is 760, Ph20 is 47 and FiO2 is .21 (21% O2 at room air)
  • A-a gradient should be roughly around: (age+4)/4
31
Q

Widening of A-a gradient examples: diffusion limited

A
  • Seen in hypoxemia
  • Can be due to problems w/ alveoli (decreased SA as seen in emphysema, leading to decreased diffusion)
  • Decreased diffusion widens the A-a gradient
  • Problems in interstitium, as seen in IPF (increases thickness of interstitium, decreasing diffusion
  • Problem in capillary (pulm HTN, scleroderma), leading to increased thickness of capillaries and decreased diffusion
  • If there is a widened A-a gradient, the problem is usually V/Q mismatch (blood and air are not getting anatomically matched together)
32
Q

Changes in PAO2

A
  • Can lead to a widened A-a gradient if PAO2 is increased enough
  • Decreased atm pressure (high altitude) will decrease PAO2
  • Increased % O2 inhaled (FiO2) such as giving 100% O2 will increase PAO2
  • Minute ventilation: hyperventilation will increase PAO2 and hypoventilation will decrease PAO2
33
Q

Factors that affect PCO2

A
  • Metabolic rate and alveolar ventilation
  • Hypoventilation: PaCO2 increase
  • Tylenol (antipyretic): slows down metabolism and decreases CO2 generation
34
Q

O2 delivery

A
  • O2 is primarily delivered by Hb, and PaO2 is simply a force that acts to keep O2 bound to Hb
  • Most important factor in O2 delivery: cardiac output (!)
  • This binding depends on PaO2, and on Hb affinity for O2
  • Things that make Hb have a higher O2 affinity shift the O2 sat curve to the left
  • These include: low temp, low PaCO2, alkalosis (low H+), low 2,3 BPG, metHb (Fe3+, oxizided Hb due to nitrates, lidocaine, G6PD def)
  • Things that decrease Hb affinity for O2 shift the curve to the right: high temp, high PaCO2 (Bohr effect), high 2,3 BPG, acidosis (high H+)
  • Shifting it to the left: easier for Hb to pick up O2, but more difficult for tissues to take O2 from Hb
  • Shifting to the right: more difficult for Hb to pick up O2, but easier for tissues to take O2 from Hb
35
Q

Moving O2 sat curve up and down (!)

A
  • Moving it up: increase in RBCs (polycythemia, EPO dependent)
  • In polycythemia there is normal PaO2, but an increased Hb concentration (w/ normal O2 sat), and an increase in O2 content overall (due to high Hb)
  • Moving it down: anemias of any kind
  • In anemia, there is normal PaO2, but decreased Hb concentration (w/ normal O2 sat), and a decrease in O2 content overall due to decreased Hb
  • In CO poisoning, there is normal PaO2, normal Hb concentration, but decreased O2 sat (CO pushes O2 off Hb due to higher affinity) and thus a decreased O2 content (from decreased O2 sat)
36
Q

3 forms of CO2

A
  • PaCO2
  • CO2 bound to Hb (binds to site separate from O2 binding sites)
  • Bicarbonate (majority), via carbonic anhydrase (in RBCs) converting CO2+H2O to HCO3- + H+
  • At tissues bicarb leaves RBCs (after CO2 enters) and to balance the movement of negative charge a Cl- enters the RBCs
  • In the lung bicarb enters RBC (so that CO2 can leave and be breathed out), and to balance this Cl- moves out of the RBC
37
Q

5 causes of hypoxemia

A
  • V/Q MM
  • Hypoventilation
  • Anatomical shunt (intracardiac shunting)
  • High altitude
  • Diffusion limited
38
Q

V/Q MM

A
  • There is a mismatch btwn where blood in lungs are going and where air in lungs are going
  • If ventilation is problem (V) then there is shunt defect (there is perfusion but no air around the blood)
  • If perfusion is problem (Q) then there is dead space defect (there is air in alveoli but no blood there)
39
Q

Hypoventilation

A
  • Due to drugs (narcotics, BZDs, barbiturates, alcohol), neuromuscular
  • Problem is in nervous system not initiating proper muscle control to breathe
  • Thus the A-a will be normal, since the problem is not in lungs (all the air getting to the lungs gets to the blood normally)
  • These pts will respond to supp O2, since the higher O2 pressure gradient means they can get more O2 into the blood w/ each breath
40
Q

R-L cardiac shunt

A
  • There is mixing of oxy blood and deoxy blood going into systemic circulation
  • This means that A-a will be widened since PAO2 is normal, but PaO2 is low due to mixing w/ deoxy blood
  • Pts will not respond at all to supp O2 b/c the increased O2 gradient in lungs does nothing to solve the mixing problem
41
Q

Diffusion limited

A
  • Ex: IPF
  • Widened A-a (due to poor diffusion) and O2 supp does correct (increases diffusion by increasing pressure gradient)
  • Looks like V/Q MM
42
Q

DLCO

A
  • Separates bronchitis from emphysema
  • Separates intrinsic from extrinsic restrictive diseases
  • Will be high during pulm hemorrhage
43
Q

Regulation of alveolar ventilation

A
  • Central chemoreceptors located in medulla are sensitive to both CO2 and H+, will induce hyperventilation
  • Since H+ can’t cross BBB, it must be generated in CNS: infections
  • Peripheral chemoreceptors (carotid body, aortic arch) sense both O2 and CO2 levels, but are most sensitive to CO2
  • A small increase in PaCO2 will cause hyperventilation
44
Q

Giving a COPD pt supp O2 and how it changes PaCO2 1

A
  • It does not cause them to stop breathing
  • PaCO2 will increase in these pts when they are given supp O2 b/c giving O2 will worsen the V/Q matching
  • This is b/c under normal conditions the alveoli receiving little O2 have constricted capillaries, and the functional alveoli have dilated capillaries
  • Giving O2 will remove this matching of blood to O2, since all alveoli will be receiving O2 even if they can’t perform gas exchange
45
Q

Giving a COPD pt supp O2 and how it changes PaCO2 2

A
  • Therefore the functional alveoli where gas exchange can occur lose blood flow, since blood is shunted to non-functional alveoli
  • Since there is less blood in the functional alveoli there is less CO2 exchange and the PaCO2 will increase
  • Other less important reasons: increase O2 will push off more CO2 from Hb and raise the PaCO2 (haldane effect)
46
Q

Central respiratory centers

A
  • Apneustic center in pons generates a constant stimulus to promote inspiration
  • Is inhibited by pulmonary stretch receptor input to prevent over inflation of lungs (Hering-breuer reflex)
  • Pneumotaxic center, also in pons, cyclically inhibits apneustic center to cease inspiration
  • Regulates the amount of air a person can take in w/ each breath
47
Q

Central respiratory centers

A
  • Apneustic center in pons generates a constant stimulus to promote inspiration
  • Is inhibited by pulmonary stretch receptor input to prevent over inflation of lungs (Hering-breuer reflex)
  • Pneumotaxic center, also in pons, cyclically inhibits apneustic center to cease inspiration
  • Regulates the amount of air a person can take in w/ each breath
  • Limitation to holding breath: PaCO2 levels
48
Q

High altitude acclimatization (!)

A
  • In high altitude the main stimulus for hyperventilation changes from high CO2 to low O2
  • Acute changes in high altitude (days): decreased PaCO2, PACO2, PaO2, and PAO2, alkalosis, no Hb change, decreased Hb O2 sat, decreased systemic O2 content
  • Acclimatization (years): decreased PaCO2, PACO2, PaO2, and PAO2, normal or acidic pH (due to met acidosis from renal compensation), increased Hb content (polycythemia), Hb O2 sat decreased, systemic O2 content normal or increased
49
Q

Diving (high pressure)

A
  • Nitrogen is normally not diffused into the blood b/c its insoluble (just breathed out)
  • Under high pressures it diffuses into the blood and if divers resurface too quickly the N2 will precipitate out of solution as bubbles and can embolize
  • Use hyperbaric chambers to Rx
50
Q

V/Q MM in various parts of lung 1

A
  • Normally, the base of the lung is under ventilated compared to the perfusion it receives (Q>V-> shunt problem)
  • This is b/c there is less resting tone of the alveoli at base, and theres more blood flow to base due to gravity/lower resistance (compressed alveoli)
  • At the apex of the lung there is under perfusion compared to the ventilation the alveoli receive (Q dead space problem)
51
Q

V/Q MM in various parts of lung 2

A
  • Alveoli at the apex are over ventilated b/c they have a larger resting tone and there is less blood to apex due to gravity/higher resistance (distended alveoli)
  • Lungs that have better V/Q matching (V/Q = .8) will have lower PaCO2, higher PaO2, and higher pH at end of capillaries
  • V/Q > .8 is over ventilated
  • V/Q < .8 is under ventilated
52
Q

ARDS

A
  • Adult respiratory distress syndrome
  • Defined as acute lung injury: PaO2/FiO2 <200
  • Causes: aspiration, PNA, inhalation injuries, sepsis, pancreatitis, trauma
  • Characterized by increased permeability of the alveolar-capillary membrane
  • Causes pulm edema, hypoxemia, decreased pulm compliance
  • This is a shunt pathology, there is no problem w/ perfusion but there is a problem w/ ventilation
53
Q

Rx ARDS

A
  • Use ventilator, but to prevent ventilator-induced lung injury want to use low tidal volume (protects intact alveoli)
  • To improve shunt physiology want to pop open closed alveoli, to do this use PEEP
  • Can also put pt in lateral DQ w/ good lung down (more blood to good lung-> better V/Q matching)
  • Low Vt will result in high PaCO2, but will be compensated for by kidneys (pts will have low pH and high PaCO2- respiratory acidosis compensated by metabolic alkalosis)
  • Lower Vt also means less compliance and O2 (can lead to atelectasis), but giving PEEP will help expand alveoli and increase PaO2
  • If there is hemoptysis put bleeding lung down to minimize asphyxiation
54
Q

Pulmonary and hemodynamic effects of ventilation 1

A
  • Ventilation will increase physiologic dead space and decrease physiologic shunting
  • Filling alveoli w/ air collapses the capillaries and thus reduces perfusion to well ventilated areas (increases dead space)
  • However in regions of atelectasis the positive pressure can open up these airways and minimize shunting
55
Q

Pulmonary and hemodynamic effects of ventilation 2

A
  • The positive pressure will decrease venous return to both sides of the heart and thus decrease CO
  • However in pts w/ LV failure the increased intrathoracic pressure is beneficial, as decreasing VR helps to minimize preload and the increased thoracic pressure also decreases after load
  • If measuring pressure in pulm circulation want to measure at end of expiration so the alveoli aren’t distended and don’t falsely elevate the pressure

Pulm (30 decks)

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