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GER Unit 6 > Physio > Flashcards

Physio Flashcards

1
Q

Aa gradient

A

normal difference of 4mmHg between alveoli and artery

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2
Q

absorption curve for CO2 in the blood

A

with increased PCO2, total CO2 increases, pH decreases because Hb is buffering with imidazole group

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3
Q

airflow is dependent on….

A

resistance and pressure gradient (Palv-Patm)

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4
Q

amount of dissolved O2

A

18 ml/min of O2 to tissues, inadequate to meet needs (250-300 ml/min)

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4
Q

alveolar dead space

A

increased Aa gradient with hypoxemia; decreased alveolar ventilation, use O2 therapy to increase blood O2

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5
Q

amount of O2 bound to Hb

A

15 g/100 ml Hb, 1.34 ml O2 bound/Hb→1200ml/min

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5
Q

anemic hypoxia

A

ex. Fe deficiency anemia or congenital hemolytic anemias (e.g., sickle cell)
* normal PaO2 but low CaO2 with normal extraction→low PvO2

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6
Q

ATPS

A

ambient temperature and pressure, saturated (25ºC, 760mmHg, 24mmHg)

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7
Q

factors that induce bronchoconstriction

A
  • histamine via H1 receptors (also causes profound vaso/venodilation, broncho and laryngeal spasm)
  • parasymp via vagus on cholinergic muscarinic receptors
  • **ß2 antagonists **on lung smooth muscle
  • **reflex constriction: **noxious fumes, extreme cold, smoke particles
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7
Q

body plethysmography

A

closed system that measures total air in the lung at FRC

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7
Q

bohr effect

A

deoxyHb is a weaker acid than oxyHb (binds to H+ tighter) so at any given PO2, O2 sat. decreases as PCO2 increases because H+ binding to Hb causes 3D conformation change reducing affinity for O2

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8
Q

BTPS

A

body temperature and pressure, saturated

(37°C, 760mmHg, 47mmHg)

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8
Q

describe the control of breathing by the brainstem

A
  • mainly occurs in the medulla (CPG), modulated by the pons (PRG)
    • ​when cut between pons and medulla: rhythmic breathing but series of gasping
  • medulla: CPG; nuclei work together to generate respiratory rhythm
    • DRG: inspiration
    • VRG: expiration, some inspiration
    • botzinger complex: mostly expiratory
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9
Q

describe the pathophysiology of exercise induced hypoxemia in patients with impaired diffusion capacity

A

cardiac output is increased, transit time in pulmonary capillaries is reduced (normal indviduals can equilibrate; leads to hypoxemia in individuals with diffusion problem)

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10
Q

diffusion problem

A

increased Aa gradient with hypoxemia; O2 therapy (even though you can’t fix diffusion problem you can drive up A PO2 enough to compensate)

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11
Q

dynamic compression

A

forced expiration; partially collapses airways causing equal pressure point to move closer to alveoli with greater expiratory efforts

  • patients with elevated compliance (emphysema) experience greater dynamic compressure during expiration
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12
Q

emphysema

A
  • neutrophils accumulate in lung to remove inhaled smoke particles→release proteases→lung CT digested by proteases→ elevated lung compliance
  • smoke inhibits a1-antitrypsin (normally inhibits proteases and protects lung)
  • *elevated compliance→greater dynamic compression during expiration (epp becomes closer to alveoli); *inspiration is easy but exhalation causes airways to collapse on themselves
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13
Q

eupnea

A

normal quiet breathing; inspiration is active and expiration is passive

  • negative pressure pump because diaphragm contraction→expansive force on intrapleural space→decreases pressure→lungs inflate
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13
Q

factors that induce bronchodilation

A
  • ß2 agonists: (ex. symp→ epi, albuterol) on lung smooth muscle
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14
Q

factors that influence DLCO

A
  • anything that changes area or thickness
  • greater when lying down (more blood to lung, distends capillaries and increases area)
  • increased cardiac output→blood to the lung
  • lung diseases and dysfunction
    • loss of lung tissue
    • ventiliation-perfusion mismatch
    • fibrosis and edema increases diffusion distance (decreases DLCO)
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15
Q

fibrotic lung disease

A
  • caused by inhalation of toxic mineral particles→granulomatous and fibrous tissue (collagen and elastin deposition)→decrease complaince (stiffer lung)
  • inspiration is difficult
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16
Q

functional residual capacity

A

lung volume equilibrium; outward recoil of chest=inward recoil of lungs

  • occurs on graph where P-V curve crosses 0 line
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16
Q

fick’s law for diffusion of gases

A
  • governs diffusion through physical boundary
  • flow of gas across membrane is directly proportional to membrane area and difference in PPgas in alveoli and capillarie; inversely proportional to membrane thickness
    • V=(A/T)D(PA-PC)
  • greater the PP graient the greater flow; single most important factor that governs new flow of as across the membrane
  • DL=DA/T
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16
Q

gradients of intrapleural pressure

A

at top: V/Q ratio >1

  • less Q because of gravity; high compliance because of small lung volume

at middle ratio=1

at base: ratio

  • more Q because of gravity; lower compliance because of larger lung volume
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17
Q

haldane effect

A

*minimizes acidication of venous blood; *deoxyHb is a weaker acid than oxyHb (binds to H+ tighter) so CO2 absorption curve shifts upwards when you deoxygenate the blood, at any given PCO2, total CO2 content in blood is higher than in oxygenated blood

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18
Q

helium dilution

A

measures exchangeable air (FRC) because helium doesn’t get absorbed in alveoli

  • blebs: trapped air that doesn’t communicate with bronchial tree; He underestimates FRC if blebs exist
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19
Q

henderson-hasselbalch equation

A

pH=6.1 + log [HCO3-]/0.03PCO2

  • titration curve for bicarbonate seems like it is not a good buffer for arterial blood because little changes in acid form lead to big changes in pH BUT ventilatory response maintains blood pH (excess CO2 is exhaled; maintains PCO2 at 40mmhg)
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21
Q

henry’s law of gas solubility

A

[cg]=aPi

  • Pi of gas in solution refers only to dissolved gas (NOT gas on Hb)
  • Pi of a gas in solution equals Pi of gas with which the solution has equilibrated
  • Dissolved gases don’t contribute to blood volume or BP
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22
Q

hering-breuer reflex

A

negative feedback during deep inspirations

  • lung inflation→slowly adapting stretch receptors (in smooth muscle of tracheobronchial tree) causes L shift of dissociation curve and inhibits further inflation via vagal afferents and phrenic efferents
  • important when TV increases during periodic deep breaths, exercise, and COPD when patients breathe at high FRC due to increased compliance
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24
Q

historesis

A

P-V relationship during inhalation is different than during exhalation; physiologically advantageous

  • inspiration: slope initially steep but compliance goes down at high lung volumes because lung is more stretched out
  • if you lose water-air interface, you lose historesis
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25
Q

histotoxic hypoxia

A

ex. poisoning of tissue metabolism (e.g., heavy metals, cyanide, toxins)
* normal PaO2 and CaO2 with reduced extraction→elevated PvO2

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26
Q

how are shunts and alveolar dead space exaggerations of physiological conditions?

A
  • shunt: exaggeration of what happens at base of lung→small V/Q ratio, hypoxemia without much hypercapnia
  • alveolar dead space: exaggeration of what happens at top of lung→ventilation without prfusion (e.g., PE) very high V/Q ratio
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27
Q

how do changes in frequency of nerve APs modulate breathing?

A
  • eupnea: some APs generated in abs/internal intercostals but movements are mostly passive due to elastic recoil
  • hyperpnea: phrenic and external intercostal APs intensify, abs/internal intercostal APs increase
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28
Q

how do pH, PCO2, temperature and 2,3 DPG affect the O2 dissociation curve?

A

RIGHT SHIFT when:

  • pH: more acidic
  • PCO2: higher
  • temperature: higher
  • 2,3 DPG: higher
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28
Q

how do peripheral chemoreceptors sense and influence minut rate of ventilation?

A

located in carotid and aortic bodies and activated by low blood PO2, high PCO2 and high [H+]

  • glomus cell: changes to O2, CO2, H+ concentrations→inhibition of K+ channels→reduce ration of K+:Na+ permeability→depolarizes resting membrane potential→opens voltage-sensitive Ca2+ channels→Ca2+ in→NTs released (dopa)→activates CNIX→afferent signal to medulla
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29
Q

how do you measure diffusion capacity?

A

use CO to measure because affinity of Hb for CO is 210x that for O2, prevent equilibrium (Hb is a sink for diffused CO); DLO2=1.23DLCO

  • O2 can reach equilibrium because you breath enough to saturate Hb
  • could impact if you increase area or decrease thickness of capillary
29
Q

how does CO poisoning affect the O2 dissociation curve>

A

L SHIFT; results in substitution of CO for O2 bound to Hb (P50=0.12mmHg)

  • decreases O2 in blood and also increases O2 affinity for Hb so it isn’t released
30
Q

how does gravity affect the distribution of pulmonary blood flow?

A
  • ​zone 1: **not present in healthy lung (loss of blood or low cardiac output), Papex < Palv→capillaries collapse→region is ventilated but not perfused
  • zone 2: **PV has no influence on magnitude of flow, Palv>PPV→partial collapse of capillaries on low pressure side but maintenance of flow determined by PPA-Palv(PPA increases down the lung)
  • zone 3: PV exceeds Palv→capillaries wide open and flow is determined by PPA-PPV: driving pressure remains constant but because vessels are more disteded at base, rsistance diecreases and flow increases as you go down
31
Q

how does polycythemia and anemia affect extraction of O2?

A

curve looks the same whether you have a lot or a little Hb because affinity does not change (saturation does not change, content curve will)

32
Q

how to central chemoreceptors sense and inclufluence minute rate of ventilation?

A

CO2 crosses blood brain barrier, generates H+ which activate central chemoreceptors in ventrolateral medulla and other brainstem nuclei

33
Q

how to do measure perfusion capacity?

A
  • use N2O to measure* because diffusion across alveolar-capillary membrane is rapid BUT does not bind to Hb (remains physically dissolved)
  • flow through capillaries limits amount of N2O and O2 that can be taken up
34
Q

hyperpnea

A

active breathing during exercise; inspiration (external intercostals) and expiration are active (internal intercostals)

36
Q

hyperventilation

A

RR faster than required for oxygenation, leads to alveolar hypocapnea respiratory alkalosis

37
Q

hypoventilation

A

leads to alveolar hypoxia and hypercapnea respiratory acidemia

38
Q

hypoxic hypoxemia

A

ex. high altitudes, diffusion problems, hypoventilation
* low PaO2 and low CaO2 with normal extraction→low PVO2

40
Q

ideal gas law

A
  • PV=nRT (for dry gas)
  • VL=1.07Vsp
  • water vapor does not follow ideal gas law so you have to subtract water vapor pressure from total pressure
41
Q

in what form is most of the CO2 transported in the blood?

A

bicarbonate (HCO3-)

41
Q

inspiratory hypoxia

A

hypoxemia with normal Aa gradent; give O2

42
Q

negative feedback ventilator response

A
  • respiratory rate and depth is controlled by blood gas concentrations and lung stretch receptors
    • set point established by higher CNS
    • e.x. apnea after hyperventilation because CO2 levels are below normal
  • sensitivity of alveolar ventilation to PaCO2 is increased by hypoxia
    • pH stimulates ventilation and shifts the CO2 sensitivity curve upwards
    • body is sensitive to PO2 but not normoxia
42
Q

Jacobs-Stewart Cycle

A
  • isohydric shift: CO2 combine with carbonic acid→bicarb and H+; H+ is taken out of reaction by Hb (imidazole buffer: histidine on Hb binds H+)
  • chloride shift: transporter proton moves bicarb outside of RBC and cloves Cl- in (water follows→RBC swells)
  • REACTION TAKES PLACE BACKWARDS IN LUNG
    • O2 diffuses into blood→binds to Hb→H+ leaves RBC
43
Q

normal anatomical shunt

A

L to R shunt of bronchial circulation at base of aorta perfuses large airways→drains into bronchial vein→pulmonary vein

  • responsible for slight drop of
  • arterial pressure is thus a little less than alveolar pressure
44
Q

O2 extraction

A

CaO2-CvO2=5 vol %; VO2/cardiac output

45
Q

obstructive lung disease

A
  • ex. emphysema/COPD, asthma (reversible)
  • high lung compliance (low pressure to inhale but difficult to exhale)
  • high TLC (barrel chest)
  • low FEV1
    • pursed lip breathing reverses dynamic hyperinflation through increase intraluminal pressure→shift of EPP from distal to proximal airways, prolongation of exhalation, and prevention/attenuation of dynamic airway collapse
  • IVPF curve shows concavity (increase in resistance due to dynamic airway compression, restricts expiratory flow)
46
Q

pathophysiology of hypoxia of altitude

A
  • PPO2 is reduced, decreasing PPO2 in alveoli AND takes longer for O2 to equilibrate because of hypoxic vasoconstriction
  • normal individuals will equilibrate end-capillary blood with alveolar gas→hypoxic hypoxemia
    • individuals with a diffusion problem will be even more hypoxemic
  • give O2
46
Q

pathologic shunt

A

R to L shunt: blood returning to heart bypasses lung and mixes with oxygenated blood OR blockage of airway (blood flow is maintained BUT is going through regions where airflow is blocked)

  • asthma is a false shunt (O2 therapy helps)
  • venous side has reduced O2 and lowers O2 content when it mixes with oxygenated blood; pulmonary vein→L heart→hypoxemia
  • increased Aa gradient leads to hypoxemia but O2 therapy does not help because normal Aa gradient at the functional alveolar compartment
  • more hypoxemia than hypercapnia in arterial blood (similar to diffusion issue)
48
Q

physiological shunt

A

sum of normal anatomic shunt and pathological shunt (R to L; occurs when airways are blocked→hypoxemia)

49
Q

pulmonary edema

A

mean pulmonary BP of >25→fluid out of capillaries and into alveolar air space

  • CO2 can dffuse through edematous fluid but O2 cannot→hypoxia without hypercapnia
  • causes: toxins→leaky capillaries, pulm. hypertension, decrease in plasmas colloid osmotic pressure (nephrotic disease or protein starvation)
51
Q

pulmonary gas exchanger

A

diffusion of gas between lung and blood; large surface area available for diffusion permits equilibration of alveolar gas with blood

  • achieved with partial pressure of a gas is the same in alveolar gas and in pulmonary capillary blood
53
Q

pulmonary vascular resistance

A
  • pulmonary BP is low and dissipated along vasculature
  • PPA 20/7, mean = 11mmHg (vs. 93mmHg in aorta)
    • mean >20=pumonary hypertension
  • measure with Swan-ganz catheter: jugular, brachial, or femoral vein→pumonary artery
    • pulmonary wedge pressure estimates PLA: advance catheter until it blocks P in one of the arteries in pulmonary ciruclation and occludes flow; pressure must be the same in the beginning and end of artery (otherwise there would be flow)
54
Q

restrictive lung disease

A
  • ex. interstitial lung disease
  • low lung compiance (high pressure to inhale)
  • low FEV1 but normal FEV1/FVC
  • normal to low TLC
  • IVPF curve is compressed
55
Q

spirometer

A

floating inverted drum collects expired gas, records movements to measure volume (~7.5L/min)

  • can’t measure TLC or FRC
56
Q

stagnant hypoxia

A

ex. sluggish circulation due to low cardiac output (e.g., congestive heart failure)
* normal PaO2 and CaO2, increased O2 extraction→low PvO2

57
Q

static compliance

A

volume lung and chest wall assume for a given transmural pressure when elastic vessels are at mechnical equilibrium with no air moving

58
Q

STPD

A

standard temperature and pressure, dry

(0°C, 760mmHg, 0mmHg)

59
Q

surfactant

A

contains insoluble lipoprotein which lowers surface tension of lung and increases compliance; without it, alveoli are unstable and subject to collapse

61
Q

tachypnea

A

rapid RR; tidal volume decreases because of increased airway resistance, decreasing dynamic compliance

63
Q

the major of resistance to pulmonary airflow is due to….

A

airway resistance (80%); majority due to nose and mouth

  • 20% due to tissue resistance
64
Q

total compliance

A

inverse slope of pressure-volume curve for L+C

  • CT=∆V/∆PT=∆V/∆PALV
  • measure chest and lung compliance separately to assess cause of decreased total compliance
66
Q

transit time for O2 delivery and CO2 uptake

A

.75s; CO2 has greater diffusion capacity than O2 but it takes the same time to equilibrate because in blood CO2→bicarb (reaction takes time)

67
Q

V/Q scans

A

breathe mixture of gases then exhale; gases differ in solubilities→histogram shows amount o ventilation with a certain V/Q ratio and amount of blood flow with a certain V/Q ratio

68
Q

vasoconstrictors

A
  • hypoxia (locally or globally)
  • low pH
  • norepi
  • angiotensin II
69
Q

vasodilators

A
  • prostacyclin
  • histamine
  • Ca2+ channel blockers
  • NO
70
Q

ventilation

A
  • flow of air into and out of lungs
  • frequency x tidal volume=how much you take in with 1 breath (~0.5L)
72
Q

what are some characteristics of the O2 dissociation curve?

A
  • sigmoid shape facilitates unload of O2 in tissues
    • steep in capillaries: small drop in PO2→release of large amounts of O2
  • plateau permits toleration of hypoxemia
73
Q

what are the 2 primary functions of the respiratory system?

A
  1. delivery of O2 from the atmosphere to tissues of the body
  2. removal of CO2 produced by metabolism
75
Q

what are the 3 pressures that exist in the pulmonary system?

A
  • external (Patm): outside chest
  • pleural (PPl): outside lung/inside chest
  • alveolar (Palv): varies during breathing
  • pressure gradients across these structures (transmural perssures) assess degree of chest wall inflation
76
Q

what are the 4 major components of the respiratory system?

A
  1. ventilatory apparatus
  2. pulmonary gas exchanger
  3. pulmonary circulatory system
  4. tissue gas exchanger
77
Q

what are the clinical implications of a large difference between FRC measured with helium dilution vs. plethysmography?

A

suggests existance of blebs in lungs, puts person at mechanical disadvantage because lungs can’t contract as well

  • treat with lung reduction volume surgery
78
Q

what are the normal arterial blood gas levels?

A
  • pH ~7
  • pCO2 = 40mmHg
  • pO2= 93-100mmHg
79
Q

what are the pressures acting on the lung at high lung volumes?

A

inward elastic recoil of chest wall and lung

80
Q

what are the pressures acting on the lung at very low lung volume?

A

lung wants to collapse but chest wall wants to expand outwards

81
Q

what contributes to pulmonary compliance?

A

tissue elasticity and pulmonary surfactant

82
Q

what does imparied diffusion lead to hypoxemia before hypercapnia?

A

CO2 has a higher diffusion coefficient and can overcome diffusion problem

83
Q

what factors influence changes in PVR?

A

changes in PVR are mostly passive, allows large increases in cardiac output to be accomodated without great increase in PPA;

  • flow depends on vessel radius: when you breath, alveoli expand, capillaries on top get narrower (R increases), extra-alveolar vessels inflate like lungs when intrapleural pressure gets negative and transmural pressure increases (R decreases)
  • PVR is minimum at FRC
85
Q

what happens to the value of DLCO if patient has polycythemia or anemia?

A
  • doesn’t change the diffusion capacity of the lung
  • Hb concentration affects DLCO by changing the number of available Hb binding sites
    • polycythemia causes an increase
    • anemia causes a decrease
86
Q

when are the two points in the respiratory cycle where there is no pressure gradient?

A
  1. at the end of inspiration
  2. at the end of expiration
87
Q

why do the terminal broncioles normally play a small role in overall airway resistance?

A

even though resistance is inversely related to radius, terminal bronchiole play a small role in overall resistance because they are resistors in parallel

88
Q

why does HbF have a higher affinity than HbA for O2?

A

HbF does not bind 2,3 DPG as high as HbA

89
Q

would isovolemic anemia cause changes in total CO2 in the blood?

A

less Hb means less ability to carry CO2 BUT less Hb also leads to further deoxygenation, allowing more CO2 to be carried in the blood (haldane effect, compensates)

GER Unit 6 (5 decks)

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