PHYSIO Flashcards
physiological functions of the respiratory system regarding the transport of O2 and CO2
CO2 is always being produced in the tissues and even though more of it can be stored in the body compared to O2, they are kept in equilibrium
ventilation
V= f x TV
- f= frequency (breaths/minute)
- TV= Tidal Volume (L/breath)
- analogous to blood flow (same units as CO)
- performed by ventilatory apparatus (conductive and respiratory zones)
branching system of airways
branches 23 times leading to 300,000,000 alveolar sacs
trachea–> bronchi–> bronchioles–> respiratory bronchioles–> alveolar ducts–> alveolar sacs
conductive zone
first 16 branches serving as a transportation route without aiding in oxygen diffusion (trachea- cartilaginous rings for structural support, bronchi, bronchioles-terminal are the smallest airway without gas exchange or alveoli)
*ciliated with mucuous secreted by goblet cells to carry ingested particles to mouth
alveolar, vascular and tissue compartments
?
ideal gas law
PV= nRT (for dry gas)
- a transfusion will increase n so V and P both increase
- closed system- V is indirectly proportional to P
VL= 1.07 Vsp (corrected for lung and spirometer)
*increased volume in lung is due to warmer temperature and water vapor influence
Henry’s law of gas solubility
[cg] = alpha Pi
*the concentration of a dissolved gas at equilibrium is proportional to the partial pressure of the gas about the solution
partial pressure
Pi= niRT/V
- fractional contribution of that gas to the total pressure
- Dalton’s law- sum of the partial pressure of all the gases in the mixture equals the total gas pressure
- when dissolved in a liquid, gas does not exert pressure (dissolved gases do not exert pressure)
fractions of gases in air and in blood
dry gas fraction- Fi= ni/nt
- ni= moles of ith gas, nt= total moles in gas
- air is a mixture of molecules
spirometer
measures ventilation bu collecting expired gas or adding TVs for a minute (N= 7.5 L/min)
*during strenuous exercise, ventilation may increase to 120 L/min as both TV and f increase
ATPS, BTPS, STPD
ATPS (Ambient)= 25 C, 760 mmHg, 24 mmHg (saturated with water vapor
BTPS (Body)= 37 C, 760 mmHg, 47 mmHg (air in lungs always saturated with water vapor)
water vapor pressure is a function of temperature
STPD (Standard)= 0 C, 760 mmHg, 0 mmHg (dry)
4 major components of the respiratory system
- ventilatory apparatus
- pulmonary gas exchanger
- pulmonary circulatory system
- tissue gas exchanger
smoking and mucous
smoking leads to a hypersecretion of mucous by goblet cells which is heavy and thus settles at the bottom of the lung along with carcinogens and microorganisms (leads to smoker’s cough which is trying to help the person get it out)
respiratory zone
last 7 branches which help with exchange between gas and blood (respiratory bronchioles, alveolar ducts- cylindrical and elongated, alveolar sacs- spherical and covered with 1000 pulmonary capillaries each)
- Type I alveolar epithelial cells–> line alveoli
- Type III alveolar cells: sufactant (lipo-protein with DPPC) coating inner alveolar surface to lower surface tension facilitating inhalation and increasing mechanical stability
- Macrophages engulf foreign material
what oxygen must cross to be diffused into the blood:
surfactant-coated alveolar epithelium–> the alveolar interstitial space–> the capillary epithelium–> the plasma–> the RBC membrane–> combines with hemoglobin
pulmonary artery and pulmonary vein
artery: brings mixed venous blood from the right heart
vein: carries oxygenated blood back to the left heart (blood is a mixture of blood that has equilibrated with alveolar gas and a small amount of blood with the composition of mixed venous blood)
alveolar dead space
alveoli that are ventilated but not perfused
trapped volume
gas in the alveoli in which the alveoli may be perfused but not ventilated
respiratory quotient and respiratory exchange ratio
RQ: ratio of tissue metabolic production of CO2 and consumption of O2
RQ= CO2/O2 where CO2 and O2 refer to the TISSUE
RE: measured by analysis of inspired and expired gas at the lung
RE= CO2/O2 where CO2 and O2 refer to the LUNG
capnography
measures CO2 levels (you breathe through it)
*oxygenation vs. ventilation
oxygenation: amount of O2 to lungs, blood and tissues which is measured by pulse oximeter or a needle to the radial artery
ventilation: measured by spirometer (MV (minute ventilation)= RR x TV(tidal volume))
how does asthma affect MV= RR x TV
asthma will decrease TV but still needs to maintain MV so RR increases but eventually the muscles will tire out so eventually MV will decrease
lung as a negative pressure pump
pressure in the intrapleural space is decreased and lung inflates
*can also be inflated by application of positive pressure from a non-invasive positive pressure machine like for sleep apnea (pressure gradient is established)
pneumothorax
pressure in the intrapleural space is normally less than atmospheric but when there is a wound, intrapleural pressure rises up to atmospheric pressure and the lung collapses
*lung collapses inward while chest wall will spring outward
muscles of respiration during eupnea, hyperpnea and strenuous exercise
eupnea (7.5 L/min): inspiration by diaphragm and expiration by passive recoil
hyperpnea (deeper ans faster with active ispiration and expiration- 120 L/min): inspiration by external intercostals (ribs up and out)
strenuous exercise: accessory muscles reduces resistance to airflow; expiration by internal intercostals which depress ribs down and in and the abdominal muscles which expel air out
what keeps the diaphragm alive?
C3, C4 and C5
alveolar pressure at the end of expiration:
0 cm H2O
what hypoventilation and hyperventilation lead to:
hypoventilation: alveolar hypoxia and hypercapnea respiratory academia due to increased CO2 levels
hyperventilation: alveolar hypocapnea and respiratory alkalosis due to decreased CO2 levels
alveolar, intrapleural and external pressures
alveolar: less than atmospheric pressure during inspiration but greater than atmospheric pressure during expiration; equal to atmospheric pressure when breath is held at any lung volume with no air movement
intrapleural: space outside of the lung but within the chest wall and is fluid-filled (contraction of diaphragm exerts expansive force on intrapleural space decreasing its pressure making it more negative and acting to inflate the lung)
external: constant unless a weight is placed on chest referred to as body surface pressure
transmural pressures
internal minus external pressure (Pt= Pl + Pc= P alv- Patm)
- outwardly directed= positive
- inwardly directed= negative
lung: Pl= Palv- Ppl (pleural space)
chest wall: Pc= Ppl - Patm
pressures at mechanical equilibrium
Pt = 0 Pl= -Pc Patm= o
static compliance and compliance
static compliance: volume the lung and chest wall will assume for a given transmural pressure when the elastic vessels are at mechanical equilibrium with no air moving (muscle activity interferes with its measurement)
compliance: relationship between transmural P and volume of the lung (change in volume/change in transmural pressure or alveolar pressure)
* system consists of two compliances in series–> lung and chest wall in which the transmural pressure across them are additive
why do we separate lung compliance from chest wall compliance?
because decreased total compliance could be due either to the properties of the lung or to chest wall
chest wall compliance
Cc= change in volume/ change in Pc (which is the change in Ppl or simply Ppl-Patm)
*static pulmonary compliance curves
End- expiratory volume (FRC): Pc= -Pl meaning Pt=0 and is at equilibrium (elastic forces exerted by the lung and chest wall are equal and opposite)
End-inspiratory volume: lung is expanded to the mechanical resting position of the chest wall where Pc=0 so only the elastic force of the lung opposes inspiration
what happens to Ppl with larger degrees of inflation?
Ppl becomes more positive
*occurs when muscles are relaxed and weight is placed onto the spirometer
*increasing volume during inspiration will cause P around the lung to increase (since inspiration is propagated by a negative intrapleural P) but the curve is not linear and will level off since the lung gets stiffer the more inflated it is and thus increasing P around lung will not increase V in lung as drastically
*emphysema
increased lung compliance making it difficult to exhale
*increased C= increased FRC and TLC
*since an inhibitor of an inhibitor is present leading to the destruction of alveolar septae, merging of adjacent alveoli and the formation of large blebs with overall loss of alveolar surface area and elastic recoil
fibrosis
decreased lung compliance making it difficult to inspire
*decreased C= decreased FRC and TLC
*lungs have become stiff due to pneumonconioses induced by inhalation of dust, asbestos, coal, silica and other toxic mineral particles leading to formation of granulomatous and fibrous tissue so volume in lung does not change as much with increasing pressure
*emphysema mechanism
- smoking leads to increased neutrophil production in attempts to remove inhaled particles
- proteases are released by neutrophils
- proteases are normally inhibited by alpha 1-antitrypsin but SMOKING INHIBITS THE INHIBITOR ALPHA 1-ANTITRYPSIN
- uninhibited proteases digest connective tissue (elastin and collagen) of lung
- increased lung compliance
air-filled and saline-filled lung compliance
saline inflation: less recoil P since air-liquid interface is eliminated, abolishing recoil P due to surface tension (increased compliance traps air making it harder to exhale)
air inflation without surfactant: higher recoil pressure so compliance is decreased due to inwardly directed surface tension forces at the air-water interface
surfactant and result of its deficiency
made of insoluble lipoprotein and dipalmitoyl lecithin which lowers the surface tension of the lung and increased compliance
- deficiency would increase surface tension and increased elastic recoil of alveoli leading to deflation of lung (seen in respiratory distress syndrome in which babies are unable to keep their lungs inflated)
- also leads to emptying of smaller alveoli into one (unstable)
atelectasis
partial collapse of the lung but prevented by surfactant’s ability to stabilize alveoli
Laplace’s law
if two bubbles have the same surface tension, the smaller bubble will have a larger internal pressure
p= 2T/r
- alveoli of different sizes would have different transmural pressures
- HOWEVER< the surface tension of alveoli with surfactant increases with increasing inflation volumes to stabilize alveolar structure
FRC and RV
FRC- where lung and chest wall are at equilibrium (Pt=0 and Pc = -Pl)
RV- little bit of air in lungs even after expiration
duration of inspiration and expiration
inspiration= 1/3 of time expiration= 2/3 of time
when does maximum flow occur?
minimum Palv at mid-inspiration and maximum Palv at mid-expiration
intrapleural pressure during the measurement of chest wall compliance
swings positive even though it is negative during inspiration
- intrapleural pressure becomes positive when muscles are relaxes and weight is placed onto spirometer
- with larger degrees of inflation, Ppl becomes more positive
small airway disease and its effect on dynamic compliance
mucous plugs or inflammatory swelling will increase resistance causing dynamic compliance to decrease and have a greater discrepancy from static compliance (less flow for a given pressure change–> less air inhaled per breath–> decreased Cdyn at higher breathing rates)
*compliance is actually more of a measure of resistance since it measures tissue elastic properties
small airway disease and its effect on TV and RR
increased R will cause decreased TV at higher RR
turbulent and laminar flow in the airways
laminar: in trachea (Re 3000)
frictional resistance to flow/breathing
20% due to tissue resistance (motion of the lung and chest wall tissue)
80% due to airway resistance (due to the motion of the air)
airway resistance as you proceed down the bronchial tree
- first 3 divisions- cross sectional area decreases by 20% so velocity increases by 20%
- small bronchi down there is a large sudden increase in total cross sectional area decreasing the velocity (decreasing the total resistance)
- resistance also falls as the lung volume increased during inflation
- main resistance is in the beginning of the system serving the functions of humidifying, warming, filtering and cleansing the air before it is accelerated to the lung
*epi’s effect on airway resistance in flight or fight
- epi binds to B2 receptors
- increase in cAMP
- cAMP stimulates PKA
- PKA phosphorylates MLCK
- decrease in sensitivity of MLCK for Ca-Calmodulin
- binding of myosin cross bridges to actin is inhibited
- resistance is reduced
- bronchi and bronchioles are dilated enhancing breathing
innervation on bronchial smooth muscle and other factors affecting airway resistance
innervation:
sympathetic–> epi–> B2 receptors = dilation
parasympathetic–> vagus nerve–> muscarinic receptors = constriction
other factors:
swelling of mucosa increases airway resistance (Raw)
positive end-expiratory pressure decreases Raw
histamine- bronchoconstrictor but vasodilator
*low lung volumes
increased resistance to expiration (in which the intrapleural and intraalveolar pressures are high)
- increasing the driving pressures leads to a maximal flow rate and that the maximal flow rate increases with increasing lung volumes
- low conductance
*conductance
1/R in which is if higher at greater lung volumes
anatomic dead space
volume of air not participating in gas exchange
*measured by single-breath analysis and Bohr method
alveolar ventilation and CO2 levels
increased alveolar ventilation will lead to decreased CO2 levels where as decreased alveolar ventilation will lead to increased CO2 levels since CO2 is still being made but it cannot get out due to decreased ventilation function
what causes constriction
histamine, cholinergic agents and beta 2 antagonists
*obstructive vs. restrictive lung diseases
obstructive: increased compliance, harder to exhale, decreased FEV1, decreased FEV1/FVC, increased TLC(examples: COPD, asthma)
restrictive: decreased compliance, harder to inhale, decreased FEV1, normal FEV1/FVC and normal to low TLC (example: interstitial lung disease)
* normal TLC= 5.1-8.4)
normal partial pressures for CO2 and O2
CO2- 40
O2- 90-100
*only suggestions/treatments that can be given by physicians
smoking cessation, supplemental O2, bronchodilator (anticholinergic or beta2 agonist) or non-invasive positive ventilation
MEFV curves
- Maximal Expiratory Flow-Volume
- shows the maximal flow that can be attained at each lung volume without the use of an esophageal balloon or body plethysmograph to assess obstructive and restrictive lung diseases with the help of a spirometer
- effort-independent where as IVPF and FEV1 tests are effort-dependent
- exhale to the RV with a maximal force of expiration
- will be low if the lung elastic recoil P is low or if the airway dimensions are restricted abnormally
*peak flow is effort-dependent while mid-expiratory flow is independent of effort
normal MEFV loop values
normal VC (vital capacity)= 4.75 L
peak expiratory flow occurs at–> 75% VC
100% of VC exhaled at–> 1 second
*peak flow is effort-dependent while mid-expiratory flow is independent of effort
parameters of flow volume loop
FVC= forced vital capacity
FEV1= forced expired volume in 1 sec
PEF= peak expiratory flow
FEF 25-75= forced expired flow between 25% and 75% of expired volume
FEV1/FVC= FEV1 as a fraction of FVC (80% in normal lungs and 50% if obstruction is present such as in COPD)
characteristics of MEPV curves for emphysema, bronchitis, fibrosis, COPD
emphysema (obstructive): increased time for expiration, peak expiratory flow is normal, at low lung volumes the increased compliance results in abnormally low mid-expiratory flows
bronchitis (obstructive): increased time for expiration
fibrosis (restrictive): decreased VC
COPD (obstructive): increased RV, peak expiratory flow is decreased and overall flow is decreased
effect of compliance on FRC
increasing age leads to increased compliance which increased FRC (equilibrium)
3 methods to measure FRC
- open-circuit nitrogen washout
- closed-circuit helium dilution
- body plethysmograph
- FRC in He dilution or Ni washing will not measure volume of lungs in blebs (only measures exchangeable air)
- body plethysmograph= FRC
- combining measurements will give amount of air trapped
body plethysmograph
a way to measure total amount of gas in lung at FRC in a “body box” the acts as a closed system in order to be able to utilize Boyle’s law
Box- P1V1 = P2 (V1 - change in V)
Lung- P3 FRC = P4 (FRC + change in V)
- gas tight chamber in which breathing line is closed when lung is at FRC
- subject makes expiratory effort against a P transducer (records P of lung)
- this compresses the V of the lung and raises the P by [change in P]
- chamber will expand by [change in V] which is equal t the compression of air in the lungs (records decrease in P of box)
lung volumes and capacities
TLC- total lung capacity: max lungs can contain
VT- tidal volume: in and out in one breath
IRV- inspiratory reserve volume: max inhaled from end-tidal inspiratory position
ERV- expiratory reserve volume: volume that can be exhaled from end-tidal expiratory position
RV- residual volume: gas contained after max expiration
VC- vital capacity: max that can be exhaled after max inspiration
IC- inspiratory reserve capacity: max that can be inhaled from resting expiratory position
FRC- functional residual capacity: mechanical equilibrium (includes RV)
VC = IRV + VT + ERV = TLC - RV IC = VT + IRV = TLC = FRC
open-circuit nitrogen washout
wash out all of the N2 from the lung and expired gas is collected
*conservation of mass
closed-circuit helium dilution
subject is connected to spirometer containing initial dry gas fraction (Fi) of helium and the subject breathes until the final He mole fraction (Ff) is uniform
*conservation of mass
total ventilation calculation
total ventilation equals dead space ventilation plus alveolar ventilation
Ve = Vd + Va
*anatomic dead space (in mL) is approximately equal to the subject’s weight (in lbs)
hypoventilation and hyperventilation in terms of the partial pressures of CO2 and O2
hypoventilation= hypercapnea (increased CO2) and hypoxia (decreased O2)
hyperventilation= hypocapnea (decreased CO2) and hyperoxia (increased O2)
oxygen consumption and partial pressure effects on alveolar oxygen
increased oxygen consumption decreases alveolar oxygen
increased partial pressure of oxygen in the inspired gas increases alveolar oxygen
*alveolar gas consumption does not change much with each breath
gas exchange at capillaries
due to the P gradient between the venous blood of the capillaries (PvO2= 40, PvCO2= 46) and the alveolar air (PaO2= 100, PaCO2= 40) in which oxygen will diffuse down its gradient from the alveoli to the blood and CO2 will diffuse down its gradient from the blood to the alveoli
*diffusion through 2 cell types and interstitial membrane in between (0.2-0.5 microns thick)
*Henry’s Law of Solubility
- at equilibrium, gases in solution have partial pressures; the partial pressure of these gases in H2O is equal to the partial pressures at the gaseous phase
- in blood, all dissolved gases have partial pressures but won’t contribute to the BP
- some gases don’t always remain as gases (such as O2 that binds to hemoglobin) which then won’t contribute to the partial pressure since are bound
*increased partial pressure = increased [gas]
*increased partial pressure = increased solubility
([gas] = solubility coefficient x partial pressure of gas)
*since gases have different solubilities, their content in a solution at the same partial pressure will be different
difference between Henry’s law and Fick’s law
Henry’s: equilibrium between gaseous and liquid phases
Fick’s: rate of movement of gas between 2 compartments containing gases of differing partial pressures
*Fick’s law
Dl = DA/T
(Dl= diffusion capacity of the lung)
(A and T are area and thickness)
(D- diffusion coefficient is proportional to solubility and inversely proportional to the square root of its molecular weight)
the greater the partial pressure gradient, the greater the flow of gas across membrane from higher chemical potential to lower chemical potential as a result of random movement of molecules
diffusion coefficients of O2 and CO2
O2= 0.42
CO2= 8.59 (very high- diffusing 20x more rapidly than O2)
*diffusion problem will produce hypoxemia WITHOUT hypercapnea since CO2 has a higher diffusion capacity and can overcome the problem
transit time
the time to diffuse t=V/Q
t= volume of blood in pulmonary capillaries (75 mL) / cardiac output (100 mL/sec)
t= 0.75 sec
*perfusion vs. diffusion limited
perfusion limited: N2O (remains dissolved- nothing to bind so it reaches equilibrium quickly) and O2 (reaches equilibrium before transit time is over and there’s a lot more than CO so even though a few will bind to hemoglobin, there is enough left to contribute to the partial pressure)
*uptake of N2O can be increased by increasing cardiac output and reducing the amount of time the blood stays in the capillaries after equilibrium
diffusion limited: CO (most will bind to its sink- hemoglobin due to its high affinity for it so those that bind will not contribute to partial pressure)
CO2 diffusion along pulmonary capillary
abnormal levels of CO2 from bicarbonate will cause a longer transit time
*slows down the rate of equilibration
exercise and transit time
exercise will reduce the transit time in pulmonary capillaries but a normal individual can still equilibrate the pulmonary capillary blood with alveolar gas
*in individuals with a diffusion problem–> exercise-induced hypoxemia
inspiratory hypoxia of altitude
high altitudes cause the partial pressure of inspired oxygen to be reduced, decreasing the partial pressure of oxygen in the alveolar gas
- normal individual- equilibrate resulting in hypoxic-hypoxemia
- individual with diffusion problems- even more hypoxemic
measuring diffusion capacity with the diffusion capacity of CO
DL O2 = 1.23 DL CO
- get DL CO from influx=efflux assumption
- mass conservation (indirect measurement of how much is in alveolar compartment)
*factors that influence DL CO
- exercise will increase DL CO so more blood goes to the lung
- increases with supine as compared to upright
- anything changing area or thickness will affect diffusion
- lung diseases and dysfunction will decrease it (loss of tissue, emphysema destruction of alveoli, mismatch of ventilation to perfusion like in obstruction, fibrosis and pulmonary hypertension with edema)
what is unique about pulmonary circulation compared to circulation through other organs in the blood?
lungs= only vascular bed to receive the entire cardiac output in order for gas exchange to take place (increasing cross sectional areas) while maintaining a low relative pressure
*metabolic and synthesizes NO and prostaglandins
where does autoregulation occur?
in systemic vessels but NOT in pulmonary vessels which distend passively with increased pressure or flow
PVR compared to TPR
PVR= pulmonary vascular resistance TPR= total peripheral resistance
PVR is 10 times less than TPR (thus the pulmonary circulation is known as the lesser circulation)
PVR x 10 = TPR
pulmonary circulation R x 10 = systemic circulation R
RV and LV afterloads
RV afterload (pulmonary) < LV afterload (systemic)
*left heart does more work
bronchial circulation and lymphatic system of vessels in a normal anatomic left-to-left shunt
bronchial circulation: (main bronchial artery originates at the base of the aorta) 1-2% of the CO but can increase to 20% during chronic pulmonary vascular obstruction; contributes to small difference measured between the outputs of the RV and LV
lymphatic system: drains excess fluid from the interstitial space returning it to the circulation via the caudal mediastinal lymph node and the thoracic ducts (valves are regulated by intrinsic propulsion, mechanical pumping during breathing and sympathetic activity)
physiological shunt and what it causes
the sum of the normal anatomic shunt and pathological right-to-left shunts when airway is blocked
*could lead to hypoxemia
pulmonary vessels
- thin-walled (thinner than systemic) and highly distensible
- gas-exchanging vessels are smaller (maximizes SA to V ratio)
- no distinct arterioles
- degradation of musculature
pulmonary blood pressure
-dissipates along vasculature measured by Swan Ganz cardiac catheter (measures pulmonary artery P and LA P by creating a wedge)
-mean pulmonary artery pressure= 12 mmHg (systolic) and 5 mmHg (diastolic)
>20 = pulmonary hypertension
>25 = pulmonary edema –> diffusion problem
*be careful when measuring pulmonary artery P since it is low thus errors an have significant false implications
Swan Ganz cardiac catheter
long catheter inserted into peripheral vein and advanced into pulmonary artery to measure BP using balloon at the tip and can measure LA pressure by creating a wedge through inflation of the balloon occluding the vessel
PVR formula
PVR = (P pa - P la) / CO
Q= change in P / PVR
autoregulation
altering the flow of blood to meet oxygen demands
*pulmonary vasculature is incapable of this so PVR will decrease as flow or P increase whereas R in a systemic vascular bed increases as a compensation to increased perfusion P
pulmonary blood volume
approximately 200-300 mL but can increase 2-3x during exercise
decrease of PVR during exercise:
due to passive distension of perfused regions as well as by recruitment of additional capillaries (local effects in the vasculature)
*P doesn’t change much since vessel C is high
alveolar blood vessels response to inflation
stretched and become narrower until closure since they are thin and can distend or collapse
- influenced by alveolar pressure
- in series with extra-alveolar blood vessels
extra-alveolar blood vessels response to inflation
expand due to the more negative intrapleural P and will never collapse since they are larger and protected by elastic forces of surrounding parenchyma/tissue
- influenced by intrapleural pressure
- in series with alveolar blood vessels
when can we observe a minimum PVR?
near FRC
*will increase as transpulmonary pressure increases or decreases due to alveolar and extra-alveolar vessels which are arranged in series (resistances are additive)
what happens to P pa during mechanical ventilation?
highly increased alveolar P–> increased R of capillaries–> increased P pa–> increased RV afterload
how do pathological conditions lead to increased PVR?
pathologic conditions–> vasculature remodeling–> release of mediators–> increase in PVR
blood flow at apex vs. base of lungs
- increased transmural P (by 10 mmHg)
- decreased R to flow
- increased flow (6x more)
- more distended
three zone model for pulmonary blood flow
zone 1: not normally present in a healthy lung and occurs if the pressure at the top of the lung calls below P alv and the capillaries collapse stopping flow (ventilation but no perfusion)
zone 2: flow depends on (P pa and P alv difference) alveolar pressure which is exceeded by intravascular P resulting in recruitment and opening of capillaries with an increase in blood flow (alveolar P remains greater than the P in the veins leading to partial collapse of the capillaries but with maintenance of flow)
zone 3: flow increases due to gravity and passive distension (flow is determined by the difference in P pa = P pv and driving P remains constant but because the vessels are more distended near the base, the R decreases and the flow increases going down this zone)
discrepancy in 3 zone model
pattern of flow is actually different in which there is a decrease of flow in the base due to the small lung volume and extravasation of edematous fluid
*leads to increased PVR and decreased flow despite high intravascular hydrostatic P
pulmonary edema treatment
targeting at lowering P with diuretics, vasodilators, morphine, inotropic agents and a high alveolar P to keep alveoli clear
dissolved oxygen
(provides 18 mL) inadequate to meet the oxygen consumption needs of the body (250-300 mL) which is why hemoglobin is used
dissolved O2 = alpha O2 (solubility which increases with decreasing temperature) x PO2
*extraction of dissolved oxygen from the blood to tissues
oxygen consumption by the tissues (VO2)
related to cardiac output and the A-V oxygen concentration difference:
VO2 = Q (CaO2 - CvO2)
oxygen content and saturation at PO2 of 100 mmHg and 40 mmHg
PO2 100 mmHg: oxygen content is 20 mL/dL, 97.5% sat
PO2 40 mmHg: oxygen content is 15 mL/dL, 75% sat
oxygen dissociation curve right shift
reduction of binding affinity
why is the oxygen dissociation curve sigmoidal in shape?
it permits the unloading of O2 so that PaO2 is maintained high favoring the diffusion of O2 to the tissues where PO2 is low
normal hemoglobin content
concentration of hemoglobin is 12-14 g Hb/100mL blood
- 10% higher in males than in females
- binding capacity of Hb for oxygen is 1.34 mL O2/g Hb
what does the oxygen dissociation curve plateau signify?
toleration of hypoxemia
*practically constant oxygen content
polycythemia and anemia oxygen content
polycythemia: excessive production of RBCs in which the hematocrit is 60% (N= 35 mL cells / 100 mL blood)–> elevated concentration of O2 in vol%
anemia: increased RBC destruction leading to low Hb content–> concentration of O2 in vol% is decreased
what does erythropoietin promote?
differentiation of proerythroblasts into erythrocytes to help O2 reach tissues
hypoxia–> increased hypoxia-inducible factor 1alpha–(renal fibroblasts)–> increased EPO mRNA–> increased EPO synthesis–> increased proerythroblasts–> increased erythrocytes
4 factors that regulate the oxygen dissociation curve
a right shifted P50 of the oxygen dissociation curve suggests facilitate release of O2 from Hb (at a specific PO2, Hb will be less saturated) which can be the result of:
decreased pH
increased temperature
increased PCO2
increased 2-3 DPG (takes several days)
amount of O2 in arterial blood
about 20 vol% or 20 mL O2 per 100 mL blood
- only 0.3 vol% is “dissolved oxygen”
- major fraction of O2 is bound reversibly to Hb
PAO2 = PaO2 (according to Henry’s law)
*dissolved O2 equilibrates with the binding sites on Hb
hypoxic hypoxia
low PaO2 and low CaO2 with normal extraction and therefore low PvO2 (due to hypoventilation, high altitude and diffusion problems)
stagnant hypoxia
normal PaO2 and CaO2, increased extraction and therefore low PvO2 (due to sluggish circulation due to low cardiac output like in congestive heart failure)
histotoxic hypoxia
normal PaO2 and CaO2 with reduced extraction and elevated PvO2 (due to poisoning of tissue metabolism by heavy metals, cyanide or other toxins)
anemia hypoxemia
normal PaO2 but low CaO2 with normal extraction and low PvO2 (due to iron deficiency anemia or congenital hemolytic anemias such as sickle cell anemia)
carbon monoxide poisoning
results in substitution of CO for O2 bound to Hb since Hb has a 240x higher affinity for CO than O2 causing the oxygen binding capacity of Hb to be reduced
- left-shift of the oxygen dissociation curve facilitating oxygen retention by Hb
- cigarette smoke contains 4% CO which results in a 5-10% reduction in oxygen transport capacity
P50 for O2 and CO
CO–> 0.12 mmHg
O2–> 26 mmHg
