Physio Flashcards
1
Q
Aa gradient
A
normal difference of 4mmHg between alveoli and artery
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
3
Q
airflow is dependent on….
A
resistance and pressure gradient (Palv-Patm)
4
Q
amount of dissolved O2
A
18 ml/min of O2 to tissues, inadequate to meet needs (250-300 ml/min)
4
Q
alveolar dead space
A
increased Aa gradient with hypoxemia; decreased alveolar ventilation, use O2 therapy to increase blood O2
5
Q
amount of O2 bound to Hb
A
15 g/100 ml Hb, 1.34 ml O2 bound/Hb→1200ml/min
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
6
Q
ATPS
A
ambient temperature and pressure, saturated (25ºC, 760mmHg, 24mmHg)
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
7
Q
body plethysmography
A
closed system that measures total air in the lung at FRC
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
8
Q
BTPS
A
body temperature and pressure, saturated
(37°C, 760mmHg, 47mmHg)
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
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)
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)
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
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
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
13
Q
factors that induce bronchodilation
A
- ß2 agonists: (ex. symp→ epi, albuterol) on lung smooth muscle
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)
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
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
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
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
17
haldane effect
*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
18
helium dilution
**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
19
henderson-hasselbalch equation
**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)
21
henry's law of gas solubility
[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
22
hering-breuer reflex
*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
24
historesis
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
25
histotoxic hypoxia
ex. poisoning of tissue metabolism (e.g., heavy metals, cyanide, toxins)
* normal PaO2 and CaO2 with reduced extraction→elevated PvO2
26
how are shunts and alveolar dead space exaggerations of physiological conditions?
* **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
27
how do changes in frequency of nerve APs modulate breathing?
* **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
28
how do pH, PCO2, temperature and 2,3 DPG affect the O2 dissociation curve?
**RIGHT SHIFT when:**
* pH: more acidic
* PCO2: higher
* temperature: higher
* 2,3 DPG: higher
28
how do peripheral chemoreceptors sense and influence minut rate of ventilation?
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
29
how do you measure diffusion capacity?
*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
how does CO poisoning affect the O2 dissociation curve\>
**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
how does gravity affect the distribution of pulmonary blood flow?
* **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
how does polycythemia and anemia affect extraction of O2?
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
how to central chemoreceptors sense and inclufluence minute rate of ventilation?
**CO2 crosses blood brain barrier, generates H+** which activate central chemoreceptors in ventrolateral medulla and other brainstem nuclei
33
how to do measure perfusion capacity?
* 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
hyperpnea
active breathing during exercise; inspiration (external intercostals) and expiration are active (internal intercostals)
36
hyperventilation
RR faster than required for oxygenation, leads to alveolar hypocapnea respiratory alkalosis
37
hypoventilation
leads to alveolar hypoxia and hypercapnea respiratory acidemia
38
hypoxic hypoxemia
ex. high altitudes, diffusion problems, hypoventilation
* low PaO2 and low CaO2 with normal extraction→low PVO2
40
ideal gas law
* 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
in what form is most of the CO2 transported in the blood?
**bicarbonate (HCO3-)**
41
inspiratory hypoxia
hypoxemia with normal Aa gradent; give O2
42
negative feedback ventilator response
* 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
Jacobs-Stewart Cycle
* **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
normal anatomical shunt
*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
O2 extraction
CaO2-CvO2=5 vol %; VO2/cardiac output
45
obstructive lung disease
* 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
pathophysiology of hypoxia of altitude
* 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
pathologic shunt
**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
physiological shunt
sum of normal anatomic shunt and pathological shunt (R to L; occurs when airways are blocked→hypoxemia)
49
pulmonary edema
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
pulmonary gas exchanger
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
pulmonary vascular resistance
* 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
restrictive lung disease
* 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
spirometer
floating inverted drum collects expired gas, records movements to measure volume (~7.5L/min)
* can't measure TLC or FRC
56
stagnant hypoxia
ex. sluggish circulation due to low cardiac output (e.g., congestive heart failure)
* normal PaO2 and CaO2, increased O2 extraction→low PvO2
57
static compliance
volume lung and chest wall assume for a given transmural pressure when elastic vessels are at mechnical equilibrium with no air moving
58
STPD
standard temperature and pressure, dry
(0°C, 760mmHg, 0mmHg)
59
surfactant
contains insoluble lipoprotein which ***lowers surface tension of lung and increases compliance***; without it, alveoli are unstable and subject to collapse
61
tachypnea
rapid RR; tidal volume decreases because of increased airway resistance, decreasing dynamic compliance
63
the major of resistance to pulmonary airflow is due to....
airway resistance (80%); majority due to nose and mouth
* 20% due to tissue resistance
64
total compliance
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
transit time for O2 delivery and CO2 uptake
.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
V/Q scans
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
vasoconstrictors
* *hypoxia (locally or globally)*
* low pH
* norepi
* angiotensin II
69
vasodilators
* prostacyclin
* histamine
* Ca2+ channel blockers
* NO
70
ventilation
* flow of air into and out of lungs
* frequency x tidal volume=how much you take in with 1 breath (~0.5L)
72
what are some characteristics of the O2 dissociation curve?
* 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
what are the 2 primary functions of the respiratory system?
1. delivery of O2 from the atmosphere to tissues of the body
2. removal of CO2 produced by metabolism
75
what are the 3 pressures that exist in the pulmonary system?
* 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
what are the 4 major components of the respiratory system?
1. ventilatory apparatus
2. pulmonary gas exchanger
3. pulmonary circulatory system
4. tissue gas exchanger
77
what are the clinical implications of a large difference between FRC measured with helium dilution vs. plethysmography?
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
what are the normal arterial blood gas levels?
* pH ~7
* pCO2 = 40mmHg
* pO2= 93-100mmHg
79
what are the pressures acting on the lung at high lung volumes?
inward elastic recoil of chest wall and lung
80
what are the pressures acting on the lung at very low lung volume?
lung wants to collapse but chest wall wants to expand outwards
81
what contributes to pulmonary compliance?
**tissue elasticity and pulmonary surfactant**
82
what does imparied diffusion lead to hypoxemia before hypercapnia?
CO2 has a higher diffusion coefficient and can overcome diffusion problem
83
what factors influence changes in PVR?
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
what happens to the value of DLCO if patient has polycythemia or anemia?
* 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
when are the two points in the respiratory cycle where there is no pressure gradient?
1. at the end of inspiration
2. at the end of expiration
87
why do the terminal broncioles normally play a small role in overall airway resistance?
even though resistance is inversely related to radius, terminal bronchiole play a small role in overall resistance because they are ***resistors in parallel***
88
why does HbF have a higher affinity than HbA for O2?
HbF does not bind 2,3 DPG as high as HbA
89
would isovolemic anemia cause changes in total CO2 in the blood?
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)**
