Normal physiology Flashcards
What is Spirometry? What is it’s usefulness ? What can it mesure ?
- Measures the volume of gas entering or leaving the mouth
- Useful to
- diagnose lung disease in patient
- determine severity of disease
- evaluate evolution of disease
- evaluate treatment effect
- Mesure
- vital capacity (VC)
- tidal volume (VT)
- doesn’t mesure RV (so no TLC, FRC)
What is gas dilution?
- Absolute lung volume cannot be measured by a spirometer because there is no way of expelling the RV into the spirometer (this would require complete collapse of the lungs).
- The subject rebreathes from a bag of volume V1 initially containing helium at concentration C1. After a while, the helium will equilibrate between the bag and the lungs as the helium becomes uniformly mixed throughout the whole closed system. This equilibrium concentration is C2 (and, of course, C1 > C2). However, helium is insoluble and not absorbed to any significant degree by the lungs so the total amount of helium at the end of the manoeuvre is the same as at the start, which is expressed as C1V1=C2V2
-
First bag volume and helium concentration are easily measured. Therefore, the only unknown quantity in this expression is V2, which is the sum of the bag (V1) and lung volume.
- C1V1 = C2(lung volume - V1)
What are the 4 major methods available to mesure lung volume ?
- spirometry
- gas dilution
- plethysmography (body box)
- radiographic techniques (x-ray, CT scan)
On a diagram of airflow and lung volume, where does the curve of obstructive lung disease shifts?
To the left (higher lung volume)
On a diagram of airflow and lung volume, where does the curve of restrictive lung disease shifts?
To the right (lower lung volume)
What is the 2 relations of lung pressure ?
- Ptp = Palv (Pao)-Ppl
- PRS = Palv (Pao)-Patm
What is pulmonary compliance?
The relationship between volume and pressure, a measure of how stiff a lung is (stiff lungs have low compliance)
CL= ∆V
∆P
- compliance is the slope of the P-V curve
In a Volume-Pressure curve, where is the curve of a person with emphysema compared to a person without this disease ?
- Left and up.
- the lung is easier to strech since there’s already air stuck in the alveoli
- The higher TLC is due to the fact that an unstiff lung won’t let you get all the air out
In a Volume-Pressure curve, where is the curve of a person with pulmonary fibrosis compared to a person without this disease ?
- RIght and down
- it takes a lot of pressure to make a big change in your lung volume
What are the determinants of lung volume?
- Pulmonary Compliance
- Chest Wall Compliance
- Respiratory Muscles
By what it influenced pulmonary compliance?
-
Tissue forces
- mesure of the elastin-collagen network
- increase in fibrosis
- decrease in ephysema
- mesure of the elastin-collagen network
-
Surface tension: modified by presence of pulmonary surfactant.
- Two vital properties of pulmonary surfactant
- lowers surface tension to make it easier to inflate and deflate the lungs
- promotes alveolar stability, reducing the chance that alveoli will collapse.
- Two vital properties of pulmonary surfactant
The top and the bottom of the lungs have difference compliance. In the compliance curve, when the lung is at TLC, what part of the lung is more difficult to fill in an upright posture?
BOTH: top and bottom of lungs are at the top portion of the compliance curve, they want to get emptied
The top and the bottom of the lungs have difference compliance. In the compliance curve, when the lung is at FRC, what part of the lung is more difficult to fill in an upright posture?
TOP PART: top is higher in the curve; bottom is in the middle (filled up more easily)
The top and the bottom of the lungs have difference compliance. In the compliance curve, when the lung is at RV, what part of the lung is more difficult to fill in an upright posture?
BOTTOM PART: top part is in the middle (filled up more easily); the bottom part is in the bottom
What are the 2 vital properties of pulmonary surfactant?
- Lowers surface tension to make it easier to inflate and deflate the lungs.
- Promotes alveolar stability, reducing the chance that alveoli will collapse
On what does the flow of the respiratory system depend on?
- Length of the tube
- Diameter of the tube
What are the 2 types of flow ?
- Laminar flow (more energy efficient, smaller airways)
- Turbulent flow (less energy efficient, bigger airways)
The nature of the flow changes as the gas moves from the mouth to the alveoli and back again
How can you change a turbulent flow to a laminar flow?
By changing the gas density (Reynold’s number)
What is the formula of resistance?
Resistance is the energy cost of flow. To calculate it:
V̇ = ∆P or R = ∆P
R V̇
True or false: the harder a person forces air out of their lungs, the faster gas will come out.
FALSE: Not in the effort-independant phase of expiration. Surprisingly, once flow reaches a certain level, no matter how hard the expiratory muscles push, flow will not increase any further. This phenomenon is called flow limitation.
there’s an effort-independant region in the flow curves
- As expiration proceeds the airways become narrowed at different sites creating choke points : at this point, the more you make an effort to expire, the more you squeeze the tubes and the more flow is limited.
What are the 2 large categories of lung disease?
- Obstructive: emphysema and brochitis
- Restrictive: pulmonary fibrosis and chest wall disease
On what depends maximum expiratory flow?
- Airway resistance
- Elastic recoil of the lungs
- Expiratory muscle strength
What is the index of obstruction? What does it means when it’s low ?
FEV1/FVC (>0.7 when normal) in expiratory spirometry
- when low, it indicates that it’s taking longer than usual to get air out.
What is dead space?
The total dead space, also refered to as physiological dead space, is the volume of inspired gas hat doesn’t exchange CO2
- Anatomic dead space (about 150 ml of inspired gas that get lost in the conducting zone)
- Alveolar dead space
- VD (physiological dead space) = anatomical dead space + alveolar dead space
What is the pressure of O2 in the alveols? What’s its air fraction ?
100 mmHg compared to 159 mmHg (21% of air fraction)
What is the pressure of CO2 in the alveols?
40 mmHg compared to 0 in the ambient air
What is the pressure of H20 in the alveols?
47 mmHg compared to 0 in the ambient air
What are the 2 CO2 ventilation problems?
- Hypoventilation : alveolar ventilation too low = Increased PACO2 = Respiratory Acidosis (H+ in the blood)
- Hyperventilation : alveolar ventilation too high = Decreased PACO2= Respiratory Alkalosis (less H+ in the blood)
When the respiratory system is unable to keep up and cannot accomplish its job of exchanging O2 and CO2 the patient is said to exhibit respiratory failure. What are the 2 types of respiratory failure?
- Type I: Decreased PaO2: various causes
- Type II: Increased PaCO2 : because of inadequate alveolar ventilation (CO2 then accumulates)
What are the major categories of problems leading to respiratory failure?
- Abnormal lungs with impaired gas exchange
- Stiff lungs or stiff chest wall (low compliance)
- Obstructed airways (high resistance and low compliance)
- Impaired muscle function (ex. Hyperinflation leads to inspiratory muscle dysfunction –> flat diaphragm)
- Suppression of respiratory drive (drugs)
Describe pulmonary circulation
True or flase: The systemic pressure and resistance is higher than the pulmonary pressure and resistance.
True. The arteries of the lungs are also thin and don’t have much resistance.
- the walls of the right ventricule are less muscular than those of the left ventricule because the pulmonary circulation is a relatively low pressure system
- the size of the pulmonary arteries can change depending on the pressure inside relative to outside of the pulmonary artery wall. So it can expend with high pressure and contract with low pressure to accomodate flow without posing a lot of problem
True are false: The pulmonary and system circulations carry the same flow (cardiac output) at any one time
True.
True or false: lung volume changes have opposite effects on the diameter of alveolar vessels compared to extra-alveolar vessels
True. Changes in lung volume alters the resistance of the pulmonary vessels:
- Alveolar vessels get smaller with increasing lung volume (they get squiched, increased alveolar pressure compresses septal capillaries)
- Extra-alveolar vessels get larger with increasing lung volume (as you increase lung volume, because they have attachment to the wall they also get bigger)
What are West’s zones of the lung?
- Pulmonary Alveolar pressure decreases from zone 1 to 3.
- Pulmonary arterial pressure increases from zone 1 to 2.
- Pulmonary venous pressure increases from zone 2 o 3.
What are the 3 determinants of regional flow in the lung?
- alveolar pressure (Palv)
- pulmonary artery pressure (Pa)
- pulmonary venous pressure (Pv)
What is Henry’s law?
It is the Partial pressure at equilibrium law.
At a constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid: P = kC. This applies to the O2 in the blood, which
How can you calculate O2 in the blood?
- Total blood oxygen content = oxygen bound to hemoglobin + dissolved oxygen
- Oxygen bound to hemoglobin : [Hgb] X O2 saturation X binding capacity
- binding capacity is a constant = 1,39 ml/g for O2
- Dissolved oxygen : PO2 X solubility
- solubility for O2 is 0,003
- Oxygen bound to hemoglobin : [Hgb] X O2 saturation X binding capacity
FORMULA:
TOTAL BLOOD OXYGEN CONTENT : [Hgb] X O2 saturation X binding capacity + PO2 X solubility
Interpret the O2 dissociation curve for hemoglobin
- Arterial blood leaving the lungs has nearly the same PO2 as the alveolar gas
- -> The flat shape of the curve means that wide variations in PO2 have little effect on O2 content - The steep part of the curve means that small changes in tissue demand result in big shifts of O2 from the blood to the tissues
- -> small changes in tissue demand (i.e. changes in tissue PO2) result in large amounts of O2 being released from the blood to the tissues
Why is CO poisonous? How can you treat it ?
- Because is has the same Hb binding sites as for O2 (competitive binding) but much higher affinity (>200X).
- It alters binding affinity of Hb for O2, resulting in impaired release to tissues
- Treatment can be made with high PO2 that will slowly eliminates CO from the blood
What are the 3 ways the body transports CO2? What’s the relation between total CO2 content in blood and CO2 partial pressure ?
- About 70-80% of CO2 is transported as HCO3- (bicarbonate)
Made within the RBC, HCO3- then enters the plasma in exchange of bicarbonate for chloride ions. This exchange across the membrane is called the “chloride shift”
- 5% – 10% is dissolved in the plasma
- 5% – 10% is bound to hemoglobin as carbamino compounds
Total CO2 content in blood is roughly linear to the CO2 partial pressure
What is the main interactions between O2 and CO2 transport?
Changes in CO2 lead to shifts in the O2Hb dissociation curve
- Shifts right: Increased CO2 (Bohr effect), increased temp, increased 2,3 DPG (occur in chronic hypoxia, like in high altitude), decreased pH
- facilitates unloading of O2 to peripheral tissues at given PO2 in a tissue
- Shifts left: Decreased CO2, decreased temp, decreased 2,3 DPG, increased pH
What is the The Haldane effect?
-
Increased loading of CO2 on deoxygenated Hb (increased CO2 carrying capacity of deoxygenated blood). When the PO2 of blood is reduced (after giving it to the tissus) the CO2 dissociation curve is shifted upwards (venous curve). This allows more CO2 to be taken up by blood at a given PCO2, and increases the efficiency of CO2 transport.
- Under venous conditions CO2 content is higher for any given partial pressure of CO2
What is Fick’s law of diffusion?
- Diffusion is proportional to surface area and inversely proportional to thickness
- (A/T)
- Diffusion is proportional to partial pressure difference (movement of gases from regions of higher partial pressures, to lower partial pressures)
- (P1-P2)
- Diffusion is proportional to the solubility of the gas in the tissue, but inversely proportional to the square root of molecular weight (diffusion constant)
- D
Vgas (diffusion rate) = A/T x D x (P1-P2).
It’s a passive process
Define diffusion limitation versus perfusion limitation in the context of O2 and CO2 diffusion
-
O2 taken up depends on blood flow (perfusion) and not diffusion properties of blood gas barrier
* if you want to get more oxygen to your tissue, you could just accelerate the blood flow* - Transfer of CO is limited by the diffusion properties of blood gas barrier
* since you can take up as much CO as the time you spend in the pulmonary capillaries (no back-pressure from the blood because out CO pressure in the arterial blood is 0)*
On what depends diffusion resistance?
- Diffusion through the blood-gas barrier (includes diffusion through plasma and into red cell interior) and
- Reaction of O2 with hemoglobin. Sum of these two resistances (in series)
How is diffusion capacity measured clinicaly in a patient ?
- Diffusion capacity is measured using inhaled carbon monoxide (CO) since it’s diffusion limited.
- single-breath method : once breathing a little bit of CO, you mesure how much CO they breath out and know the diffusion rate (how much CO has diffused through the membrane)
- the normal diffusing capacity is about 25 ml/min/mmHg
- The DLCO (diffusion limitation of CO) has 2 component : the diffusion through the blood-gas barrier (Dm) and the reaction of O2 with hemoglobin (theta x Vc). Hence, a lot of conditions can lead to a drop or increased DLCO.
On what depends the rate of O2 delivery to the alveoli?
- Ventilation
- Inspired PO2
On what depends the O2 uptake into blood ?
The needs of the tissues and the perfusion (more blood flow = more Hb/unit of time = more O2 to the tissues
How do you calculate PAO2 ? (see if the patient has hypoxemia)
- PAO2 = [FiO2 x (Pbaro - 47)] - (PACO2 / R)
- R = 0,85
- Pbaro = 760
What determines the PO2 and PCO2 levels in the alveolus?
The ventilation-perfusion ratio
True or false: When blood with low O2 content mixes with blood with high O2 content, the PO2 of the resulting mixture is proportionately pulled down by the blood that has low PO2.
FALSE. When blood with low O2 content mixes with blood with high O2 content, the PO2 of the resulting mixture is disproportionately pulled down by the blood that has low PO2
What is a pulmonary shunt?
- Shunt is an extreme where there is no ventilation but still perfusion (VQ = 0)
- PaO2 = mixed venous PvO2 and PaCO2 = PvCO2.
- TYPES OF SHUNT
- Pulmonary (extreme form of V/Q mismatch) :a region of the lung receives blood flow, but is not ventilated. The blood flowing from this region constitutes a pulmonary shunt
-
Extra-pulmonary : blood bypasses the pulmonary circulation altogether (trou dedans le coeur)
- i.e. : a portion of the bronchial veins drains into the pulmonary vein instead of the vena cava
What is a pulmonary dead space? How can you calculate it ?
- Dead space is an extreme where there is no perfusion but still ventilation (VQ = infinity).
- Dead space is NOT a primary cause of hypoxemia
- it increases the PaCO2 content
- Dead space can be measured by the Bohr method.
- Similar to model used to calculate the shunt fraction, think of the lung as having two compartments: one perfused, and one unperfused (dead space). Expired gas is collected in a bag over a period of minutes, and it represents a mix of gas from normally perfused compartment and dead space
- So the bigger your deadspace, the more dilute that final CO2 is since the quantity of CO2 in mixed gaz = quantity of CO2 in eliminated gaz
What happends if you give oxygen therapy to a patient who is hypoxemic because of a pure shunt?
- There will be no response because all the O2 is going to the good compartment where the Hb is fully saturated.
- you will still have a really small change in the overall arterial blood O2 content because the «good alveoli» will be able to change the dissolved oxygen a little bit)
- Oxygen therapy works with low V/Q.
What are the 5 causes of hypoxemia?
- Decreased PiO2 (decreased barometric pressure, ex. Mount Everest)
- Hypoventilation (you’re not bringing fresh gaz to the alveolus)
- V/Q mismatch (LOW V/Q, ventilation and perfusion not always equal, influenced by gravity, MOST COMMON cause of hypoxemia)
- Shunt: alveoli with no ventilation but still perfusion, extreme low V/Q mismatch
- Diffusion limitation (rare, elite athlete)
Is pulmonary dead space a cause of hypoxemia?
NO YOU DUMB BITCH
What is the main sensor of CO2? How is it percieved ?
- Central chemoreceptors are specialized groups of cells located on the ventrolateral surface of the medulla-the H+ (CO2) sensors. Main locus of CO2 sensitivity is now known to be the retrotrapezoid nucleus (RTN) (also called the “Parafacial Respiratory Group”) in the ventral medulla.
- This is intimately related to the pre-Botzinger complex/Ventral Respiratory Group
- the brain senses the increase of CO2 in the blood via an increase in H+
What is the main sensor of O2? Composition ?
- Carotid body (at the base of the carotid to make sure oxygen levels going to the brain are well regulated)
- composed of
- Type I : glomerus cells (O2 sensing)
- Type II : sustentacular cells (supporting)
What are the causes of hyperventilation?
- Metabolic (acidosis, liver disease, hyperthyroidism)
- Drugs (progesterone, theophylline, acetazoloamide)
- Central nervous system (infection, tumour, stroke)
- Lung disease (asthma, fibrosis, pulmonary edema, pulmonary embolism)
- Psychogenic
What are the causes of hypoventilation?
- Metabolic (alkalosis, hypothyroidism)
- Drugs (opioids, benzodiazepines, alcohol)
- Central nervous system (stroke, tumour, degenerative such as Congenital Central Hypoventilation Syndrome: Ondine’s Curse)
- Respiratory pump
- Chest wall abnormalities (ex. Scoliose)
- Neuromuscular disease
- Parenchymal lung disease
What is hyperventilation?
reduced PaCO2
What is hypoventilation?
Increased PaCO2
True or false: an old patient presents with COPD exacerbation in the ER. You have to give him uncontrolled 100% O2.
Why ?
- FALSE: HE WILL DIE BECAUSE OF YOU. We don’t give uncontrolled O2 to patients with chronic hypoventilation (worsening of PaCO2 by administration of high FiO2: mechanisms). You give max 93% controlled O2.
- do not give O2 to a chronic hypercapnic
-
Why ?
- hyperoxia will reduce ventilatory drive, leading in increase in PaCO2
- hyperoxia will also overcome hypoxic vasoconstriction in poorly ventilated lung units (increase perfusion of poorly ventilated units and reduced perfusion of well-ventilated units leads to increased PaCO2
identify the hidden components
- Inspiration reserve volume (IRV)
- Tidal volume (TV)
- Expiratory reserve volume (ERV)
- Residual volume
- Funtional Residual Capacity (FRC)
- Vital capacity (VC)
- Total lung capacity (TLC)
VC + RV = ?
TLC (total lung capacity)
IC + ERV = ?
IC (inspirational capacity) + ERV (expiratory residual volume) = VC (vital capacity)
What are the different respiratory muscles ?
- diaphragm (primary)
- inspiratory intercostal muscle (external and parasternal intercostal)
- accessory muscle (scalenes, mastoid process, trapezius) : backup system for the primary respiratory muscles
Expiratory muscles ?
- expiration is normally passive, driven by the elastic recoil of the lung
- during exercise, expiration is aided by
- abdominal muscle (obliques, transverse abdominis, etc.)
- thoracic muscle (internal intercostal muscle)
What are do those spirometry terms mean ?
- FEV1
- FVC
- FEV1/FVC
- PEF
- FEV1: volume of air that can be forcibly expelled from maximum inspiration in the first second
- FVC: volume of air that can be forcibly expelled from maximum inspiration to maximum expiration
- FEV1/FVC: ratio (ratio goes down with age and diseases)
- PEF: maximum flow attained during a forced expiratory manoeuvre (what’s the most that comes out in terms of liters/seconds)
What are the key points in a spirometry test when the patient has an obstructive lung disease ?
- FEV1 and PEF are decrease
- FVC is decrease or unchanged (could decrease because the RV is going up, like in COPD)
- FEV1/FVC is decreased (hallmark of obstructive lung disease)restr
What are the key points in a spirometry test when the patient has an restrictive lung disease ?
- FEV1 decrease
- FEV1/FVC normal or elevated
Why would we use the plethysmography technique to mesure lung volume ?
Because using the gas dillution technique, you have to assume that the He is going everywhere in your lungs at the same time, but it doesn’t happen in certain conditions where the gas won’t go as well to every part of the body = underestimation of the lung volume by He
- the body box technique can measure trapped air volume not accessile by gas dilution
how do you make a P-V curve in order to mesure pulmonary compliance ?
- using a esophageal balloon catheter, you mesure the pleural pressure (Ppl)
- once you have the Ppl, you can find the transpulmonary pressure and do a curve using the relation : Ptp = Pao - Ppl
Explain the relationship between the prevention of alveoli collapse using Laplace’s law
P = 2T/r
- The smaller the size of the alveoli, the greater the pressure
- Since air flows from high pressure to low pressure environment, the small alveoli will have a tendency to empty into the large one and collapse completely (which would make it super hard to refill on the next breath)
- Surfactant promote the stability of alveoli so that it doesn’t flow from smaller to biger alveoli = improve compliance
What determines your TLC (lung volume)
- Lung and chest wall recoil inward (both want to recoil)
What determines your FRC (lung volume)
- lung recoils inward, chest outward = balance
- there’s a balance between the inward recoil of the lungs and the outward recoil of the chest wall. That’s when we stop breathing normally (it’s easy to reinflate the lungs since we are on the linear slope of the pressure/volume curve)
What determines your RV (lung volume)
Lung recoild inward, chest wall outward plus effect of age and muscle strength
- this is how it works in youth
- In old people, the limit on emptying the lung is more defined by the notion of closing volume
- your airway is close a little early, so even if the chest wall wanted to push out more air, if the airways were closed it couldn’t
- could also be limited by the expiratory force
- if your too weak, you can’t blow
why is there regional differences in compliance inside a same lung ?
- Because of gravity, you have larger alveoli at the top of the lungs than at the bottom.
- the intrapleural pressure is less negative at the bottom compared to the apex
- So depending on where you are in the lung, it takes more or less pressure to have a change in volume
- bottom of the lung has a smaller resting volume and expands better during inspiration compared to the apex
What are the caracteristic of the laminar flow? How can you calculate the driving pressure needed to generate a given amount of flow? How do you call a perfectly laminar flow ? When is it more likely to happen ?
- the flow rate (V̇) is directly proportional to the driving pressure (∆P)
- The ∆P needed to generate a given amount of flow through the tube varies directly with the tube lenght and inversely with the fourth power of the tube radius
- When a flow is perfectly laminar, a special minimum-energy and highly efficient kind of flow occurs called poiseuille flow
- Key point :
- most likely to occur when the flow rate is low and the tube diameter is small
What are the caracteristic of the turbulent flow ? How can you calculate the driving pressure needed to generate a given amount of flow? When is it more likely to happen ?
- the ∆P needed to maintain a given V̇ varies with the square root of the flow
- less energetically efficient
- Key point :
- turbulent flow is most likely to occur when the flow rate is high and when the tube diameter is large
On what depend the total resistance of multiple tubes ?
- On their geometrical arragement
- tubes in series have greater total resistance that tubes in parallel
- key point
- the dichotomous branching arrangement of the airways (tubes connected in parallel) allows for a lower total airways resistance despite the fact that the individual airways are getting smaller)
- As you get deeper in the airway tubes, you compensate the airways’ smaller diameter by the fact that it’s now laminar flow and tubes are in parallel
for poiseuille flow, R is determined by ?
Inversly proportional to the 4th power of the tube radius
what happens with the overall airway’s resistance when you get from the mouth to the alveoli ?
Although each individual airway gets smaller, the total cross-sectional area of all the airways taken together actually increases, and this reduces the overall resistance.
On what depend the total pulmonary resistance ?
- airway resistance (A BIG EFFECT) : loss of energy as air flows through the airways
- tissue resistance(A small effect) : loss of energy as lung tissue changes lenght and volume (elastic energy). Energy is dissipated as fibres and molecules move past each other.
What happens with the normal flow-volume loops in emphysema, fibrosis and chest wall disease ?
- Emphysema (blue)- flow is reduced with decreased FEV1/FVC ratio
- Fibrosis (green)- flow is preserved with increased FEV1/FVC ratio
- Chest wall disease (purple)- flow is reduced with variable FEV1/FVC
how many generations of airways (tubes) are they ? What are the different zones ?
- 23 generations
- first 16 : conducting zone
- last 7 : respiratory zone
what is minute ventilation ?
total volume of fresh gas drawn into the lungs each minute
- it’s the sum of alveolar ventilation and dead space ventilation
When is there pulmonary vasoconstriction ? What about Pulmonary vasodilatation ?
- Vasoconstriction : hypoxia and accentuated by low pH (they constrict to send the blood somewhere else where they’ll be able to pick up oxygen)
- Vasodilatation : nitric oxyde (causes smooth muscles relaxation)
what is the total atmospheric pressure at sea level ?
760 mmHg
What is the alveolar air equation for CO2 ? PACO2 is thus determined by what ?
- PACO2 = V̇CO2 / V̇A
- the partial pressure of CO2 in the alveolus is proportional to the amount of CO2 that is produced and excrete and inversly proportional to the amount of ventilation that occurs
- PACO2 is thus determined by the ratio of CO2 production and alveolar ventilation
Is the blood oxygenated or not in the bronchial veins ? What about the bronchial arteries ?
Where does the bronchial veins drain (and what does is cause) ?
- bronchial arteries : arise from the aorta to supply the bronchial tissues and therefore carry oxygenated blood
- bronchial veins : carry partially de-oxygenated blood
- The bronchial veins drain into the pulmonary veins and thence into the left atrium (bypass the vena cava)
- deoxygenated blood mixes with oxygenated blood
- this creates a small shunt
Caracteristics of West’s Zones III
- Pa>Pv>PA
- the arterial pressure is pretty high because it’s below the ventricule (++ gravity)
- Flow depends on arterio-venous pressure difference rather than arterial-alveolar pressure difference (normally what occurs in systemic circulation)
Why is PVR lower at higher flows ?
Increases in flow change the mechanics of the pulmonary vasculature through 2 mechanisms
- Vascular distension : increased diameter of open vessels
- Vascular recruitment : opening of previously closed vessels
Caracteristics of West’s Zones I
- PA>Pa>Pv
- pulmonary capillary pressure is so low at the top that the pressure in the alveolus is actually higher than the pressure inside the capillary = squish those capillaries
- An healthy lung has really little zone I
Caracteristics of West’s Zones II
- Pa>PA>Pv
- at this point, flow depends on the difference between Pa and PA (waterfall condition)
What are the 2 pressures helping the alveolar surface «dry» for optimal gas exchange ? Is there leakeage usually ?
- 2 pressure influencing the kfc (capillary filtration coefficient)
- Hydrostatic pressure : pressure inside the capillaries that generate a little bit of leaking
- Oncotic pressure : protein in the bloodstream that try to conterbalance that hydrostatic pressure to keep the fluid from leaving the vessels
- Usually, there’s a very small gradient of pressure (about 1 mmHg) moving fluid of the capillaries into the interstitial space
- most of this fluid is carries away by the lymphatics to prevent accumulation
What are the 2 kinds of pulmonary edema ?
Both are causes when the capacity of the lymphatics vessels to handle this fluid
- Insterstitial pulmonary edema : at the start, edema restricted to the interstitial space
- Alveolar pulmonary edema : When the pressure in too high in the interstitial space (positive), the alveolar epithelial membrane ruptures and the alveolai flood = airspace disease
what happens on the diffusion limitation of O2 in case of a disease of the blood-gas barrier ?
It becomes diffusion limited (like with fibrosis)
why is it useful to calculate the A-a gradient ? Is a gradient normal ?
- To determine the efficiency of gas exchange in a given lung
- To help determine the cause of hypoxemia
If PAO2 = PaO2, the lung is operating at its highest efficiency as a gas exchanger. However, we all have a small shunt and a difference of 10 mmHg in A-a gradient is normal.
what is hypoxemia ? How is it different form hypoxia ?
It’s an abnormal low PO2 in arterial blood (i.e. low PaO2), while hypoxia is when a tissue miss oxygen
MSN
tissue : salut kd9 ?
oxygen : k
tissue: ça va ?? je m’ennuie
tissue : wizz
wizz
wizzz
oxygen : kk i’m out, TTYN
How can you calculate the content in oxygen of blood leaving the lungs in a 2 alveolar model of v/q mismatch on 1 alveoli ?
Why not just add the saturations ?
- The final content O2 in the blood leaving the lungs (ml/dl) = (PO2 of low V/Q alveoli x % of cardiac output of low V/Q alveoli) + (PO2 of perfect V/Q alveoli x % of cardiac output of perfect alveoli)
- we don’t just add the saturations because of the shape of the dissociation curve !
Why do we say that the lung isn’t ideal regarding the V/Q mismatch ?
-
GRAVITY
- ventilation : it’s lower at the top of the lung than the bottom
- perfusion : blood flow is greater at the bottom of the lungs
Both ventilation and perfusion vary according to vertical gravity-dependant gradients, but the rate of increase in perfusion from apez to base is steeper than that for ventilation, hence the existence of vertical V/Q inequality (greater ventilation/perfusion at the bottom of the lungs, but not to the same extent, the gradient of perfusion is greater than the ventilation one**)
what is the shunt fraction ?
what proportion of cardiac output is going to that pure shunt compartment to account for how hypoxemic my patient is (what fraction of the pulmonary blood flow appears to be passing through a compartment with no ventilation)
Know that it exists, and what is represents, but you will NOT be asked to calculate the shunt fraction
how can hypoxemia be caused by diffusion limitation ?
it can be observed in elite athletes since they increase their perfusion so much that the PaO2 is now diffusion limited instead of perfusion limited (they don’t spend the 0,25 second necessary for them to exchange Hb to be fully oxygenated.
In this case, the A-a gradient is normal since it’s not a problem in gaz exchange
What’s the clinically relevant way to approch hypoxemia ?
How do you calculate an A-a gradient ?
- Calculate the PAO2 (assuming R= 0,85 and PAC02 = PaCO2)
- PAO2-PaO2 = > 10 = problem with the lungs
What are the causes of hypercapnia ?
- Increase CO2 production
- Reduced minute-ventilation
- Increased dead space
- cause 2 and 3 result in reduced ALVEOLAR ventilation
- Remember ! PACO2 = VCO2/VA
Explain briefly the respiratory control system
- The main respiratory generator is the medulla
- In the rostral medulla, you have those nuclei that generate the respiratory rythm
- nucleus tractus solitarius : receive feedback from the body and modulates the respiratory response
- preBötzinger complex : the respiratory pacemaker for the inspiration
- Bötzinger complex : modulates expiratory rythm
- Nucleus paraambigualis and retroambigualis : the output of the pattern generator is modulated by those structures (both inspiration and expiration)
Activity of the central controller is modulated by inputs from the respiratory system including : (and what feedback do they provide ?
- chemoreceptors
- oxygen sensing (carotid body)
- CO2 sensing (RTN)
- lung parenchymal & airway afferents (vagus)
- provides feedback regarding lung inflation and terminate inspiratory drive (no controller, the inspiratory time will increase)
- chest wall (respiratory muscles, rib cage)
- muscle action
- upper airways
- provide feedback concerning pressure, flow to the central controller
What’s the model of O2 sensing/response in the carotid body ? What does it do in the case of hypoxia ?
- In hypoxia, you have a inhibition of the production of HO-2 which allows accumulation of CSE activity leading to an overproduction of H2S (hydrogen sulfide) that then leads to the opening of the Ca2+ channel and augmentation of nerve impulse to the brain stem = augmentation of ventilation
what are the ventilatory pattern response to hypoxia and hypercapnia ?
- Hypoxia:
- Rapid,shallow (ie relatively greater increase in frequency than tidal volume)
- Minimizes O2 cost of breathing (curvilinear pressure-volume relationship of lung inflation)
- doubling tidal volume requires more than double the work of breathing
- under hypoxic condition, you have a restriction in your oxygen supply so you want to reduce the amount of work of breathing as you increase ventilation.
- Hypercapnia:
- Deep,slow (ie relatively greater increase in tidal volume than frequency)
- Minimizes dead space ventilation (VD/VT) to optimize CO2 elimination
what ion informs you of the ventilation status ?
CO2 !!!!!!!!!!!!!!!!!!!!!!!!!
what is Ondine’s curse ?
- A congenital central hypoventilation syndrome leading to hypoventilation from early life
- impaired CO2 chemosensitivity
- sleep hypoventilation
- extention wakefulness
- shown to be due to polyalanine repeat mutations in Phox2b
How do you treat hypoventilation ?
- Reverse underlying cause
- Non-invasive positive pressure ventilation
- Ventilatory stimulants
- Diaphragmatic pacing
