Respiratory Physiology Flashcards
Where does tracheal collapse occur during the cycle of respiration?
Inspiratory collapse occurs in the cervical trachea
Expiratory collapse occurs in the intrathoracic trachea
What is the pathophysiologic mechanism of laryngeal collapse in pugs?
Chondromalacia
Explain anatomic dead space
Conducting airways incapable of gas exchange
Describe airflow within the thorax
Air travels 16 generations to get to the alveoli
mainstem bronchi: semicircular cartilage rings similar to the trachea
bronchi in the lungs: irregular cartilate plates
bronchioles: muscular layer intermingled with elastic fibers. outer layer of the wall is made of connective tissue and elastic fibers
Airflow through the large airways is via ______. The size and distribution of the airways occurs based off ________ + ________.
Beginning at the bronchioles, gas flow is determined by ______ instead of bulk flow.
bulk flow
resistance and dead space.
diffusion
What cell types occur in the majority of the respiratory tract?
What replaces goblet cells in the bronchioles?
- Ciliated pseudostratified columnar or cuboidal cells interspersed with mucus-secreting goblet cells
- Club cells
Describe cell types in the alveoli
cuboidal cells become squamous epithelial cells to maximize surface area and minimize the barrier to gas exchange.
Name and describe the two principle cell types in the alveoli
type 1 modified squamous epithelial cells - line 95% of the alveolar surface
type 2 cuboidal alveolar cells - larger, 2x as many, produce surfactant
Name the third alveolar cell type
phagocytic macrophages - patrol the alveolar surface engulfing bacteria and ingesting inhaled particulates
Each alveolus is surrounded by how many pulmonary capillaries?
Approx. 500
What are the pores of Kohn?
Pores that perforate the alveolar septae, which are supported by elastic and connective tissue fibers
They enable interalveolar communication and are a means of collateral ventilation
Collateral ventilation can occur to some extent through these pores enabling pressure equalization in adjvecent alveoli to prevent overdistension and/or collapse
Explain the purpose and mechanisms of collateral ventilation
Without it, alveoli distal to obstructed airways would become atelectatic. interalveolar communications through the Pores of Kohn, between the bronchioles and the alveoli (canals of Lambert), and the interbronchiolar communications of Martin. The relative contribution of these three different types of collateral ventilation is unknown. It is unlikely that any of these pathways are important in health. However, in the patients with lung diseases such as emphysema, there may be substantial collateral ventilation, which may be critical to maintaining oxygenation and ventilation
Explain lung interdependence
The lungs are interdependent on each contiguous unit of connective tissue as well as on the adjacent chest wall.
If during inspiration there is a delay filling a part of the lung then the shape of the
chest wall in that area will be subtly distorted which then decreases pleural pressure in the area over the slowly filling lung. This decrease in pressure is transmitted to the alveoli thereby producing a greater pressure differential between the mouth and the alveoli which then augments or helps to correct flow to the area where it was lagging
Name the components of the chest wall and additional muscles of respiration
Rib cage, external and internal intercostal muscles, parietal pleura, and the diaphragm
Accessory muscles including the rectus abdominis, laryngeal abductor, and sternohyoid and scalenus muscles are recruited to assist the ventilatory pump when the body needs to increase the rate and depth of breathing or when the ventilatory pump is impaired
Name compensatory behaviors to increased work of breathing
patients will straighten the head and neck to reduce airway resistance resulting
from flexion of pharynx and trachea.
they will open their mouth to greatly increase oropharyngeal airway diameter (occurs early in dogs, and late in cats)
most patients will reduce their activity level to minimize oxygen consumption.
later postural adjustments may include a sitting position with forelimbs abducted. recruitment of the accessory muscles will then occur but can be difficult to detect, and hence abduction of the nasal cartilages may be the first indication beyond postural adjustments that respiratory workload has increased.
additional orofacial muscles may also contract with each inspiration, protruding the tongue, depressing the mandible and retracting the lip folds.
recruitment of the abdominal musculature may occur to provide active expiration and to shorten the expiratory time as part of increasing the frequency of breathing
Describe the extrathoracic pressure changes during inspiration
During inspiration, the extrathoracic airways experience a transmural pressure gradient towards the lumen (pressing on the lumen) such that they collapse (low pressure within, high pressure outside). This is what leads to the characteristic inspiratory dyspnea seen in upper airway conditions such as upper airway obstructions, laryngeal paralysis, laryngeal collapse, tracheal collapse, tracheal stenosis and BAS. The reflexive behavior to increase inspiratory effort worsens the transmural pressure gradient
What is transmural pressure
the pressure inside relative to outside of a compartment.
Under static conditions, the transmural pressure is equal to the elastic recoil pressure of the compartment.
The transmural pressure of the lungs is also called transpulmonary
pressure .
What is paradoxical abdominal movement
When the abdominal wall moves in during inspiration.
It has just a few differentials – URT obstruction, pleural effusion, reduced pulmonary compliance (stiff lungs) and diaphragmatic rupture or paralysis
Describe the intrathoracic pressure changes during inspiration
During inspiration, sub-atmospheric pressure is transferred from the intrathoracic space to the airways (-> air moves from the outside world (atmosphere) into the alveoli via pressure gradient). This pressure gradient is created through the concerted action of the respiratory muscles, most especially the diaphragm. The transmural pressure gradient created by the increase in intrathoracic volume expands the alveoli.
Explain how the intrathoracic transmural/transpulmonary pressure is formed and the WOB
the respiratory muscles perform the work of breathing to generate the intrathoracic transmural pressure gradient by overcoming the elastic recoil of the lung tissue and chest wall. Some of this work is stored as elastic recoil energy in the lung tissues and
chest wall, enabling passive exhalation. The other major component of the work of breathing (WOB) is overcoming airway resistance, which is very small in normal lungs
- Since the WOB must overcome a combination of airway resistance and lung elastic recoil, any disease process which significantly increases either airway resistance or increases the tendency of the lungs to recoil / makes the lungs less compliant will increase the work of breathing. The phenomenon of an increased WOB is a very significant contributor to respiratory failure in patients with severe pulmonary disease. It is also the most difficult to objectively quantify. It has been estimated that the metabolic cost of breathing for patients with severe lung disease may increase from the normal 2% of total VO2 to between 25-50%. As a result, the increased oxygen content that can be obtained from this increased WOB is offset in large part by the increased oxygen consumption required to obtain it. The increased work of breathing also increases heat production and animals may become hyperthermic as a result, further increasing
respiratory drive.
Describe what occurs at the end of inspiration
At the end of inspiration, there is potential energy stored in the elastic tissues of the lung, which during normal quiet expiration, returns the lung to its original volume.
The chest wall is elastic like the lung, but normally tends to expand
such that at the functional residual capacity, the inward recoil of the lung and the outward recoil of the chest wall are balanced.
Describe functional residual capacity
the volume of gas in the lungs at the end of a passive exhalation. It is not the minimum volume of gas in the lungs (the residual volume), since an active expiratory effort can push additional air out of the lungs (the expiratory reserve volume).
Describe what happens at FRC (the end of passive exhalation)
At the FRC, intrapleural pressure is sub-atmospheric (negative) because the pleural liquid is between the opposing forces of the inward recoil of the lungs and the outward
recoil of the chest wall. The lungs are above their resting volume while the thorax is below its resting volume. This potential space does not fill with gas from capillary blood because the partial pressure of the gasses dissolved in capillary blood is 706 (PH2O 47 + PCO2 46 + PN2 573 + PO2 40), which remains < atmospheric pressure of 760mmHg,
The natural sub-atmospheric intrapleural pressure is also the reason that air from a pneumothorax is absorbed if the communication between the alveoli and the pleural space closes.
Describe pressure changes during forced expiration
During forced expiration, intrapleural pressure becomes positive causing a transmural closing pressure that drives gas out of the alveoli and collapses small airways. This dynamic compression of the airways during forced expiration results in flow that is effort-independent. = alveolar pressure minus intrapleural pressure
- this is why lower airway disease leads to expiratory dyspnea! In lower airway disease, inflamed and thickened intima and reduction of airway lumen by mucus leads to collapse of the lower airways as the transmural gradient is applied. In severe disease, air trapping occurs and requires some degree of active exhalation. A compensatory forced exhalation occurs which increases transmural pressure, exacerbates lower airway collapse and manifests as expiratory effort.
What is Ohm’s law
Pressure = V (flow) x R
Define pulmonary resistance and Poiseuille’s law
resistance = Change in pressure/ the flow (V)
resistance in the airways (Raw) = P alveolus - P mouth / V (flow)
Raw = 8 η l / π r4
where n = viscosity, l = length and r = radius
meaning the greater the radius of the tubular airway, the lower the resistance ( inversely proportional to the radius to the 4th power)
medium sized bronchi have the greatest resistance in the lower airways (apart from the nose and upper airway)
Describe the levels of resistance along the airway
the nose has the single largest fraction of resistance constituting 0.5-0.66 of the
total resistance at low flow rates. Mouth, pharynx, larynx, and trachea provide 20-30% of the airway resistance. Most of the remainder of the airway resistance is associated with bronchi with diameters >2mm
nasal resistance increases disproportionately with increasing flow rates such that
during exercise, or when respiratory distress occurs, there is a switch from nasal breathing to mouth breathing.
Describe nervous system control of the bronchioles
Bronchial smooth muscle is under control of the autonomic nervous system whereby parasympathetic stimulation causes bronchoconstriction and sympathetic stimulation causes bronchodilation. Contraction of the bronchial smooth muscles narrows their airway lumen and leads to increased resistance.
- This is why Stimulation of the irritant receptors in the tracheobronchial tree induces bronchoconstriction reflexively via the vagal parasympathetic fibers. In patients with lung disease, mucosal edema, hypertrophy and hyperplasia of mucous glands, increased production of mucus, and hypertrophy of the bronchial smooth muscle all tend to decrease airway caliber and contribute to airway resistance. Administration of beta-adrenergic or methylxanthine bronchodilators or antiinflammatory corticosteroids to patients with airway diseases such as asthma leads to a significant decrease in the
airway resistance and reductions in respiratory distress
Describe compliance and elastic recoil
change in volume divided by the change in pressure C = ΔV/ΔP
C = V2-V1 / P2-P1
Highly compliant lungs: small increase in pressure causes a large increase in volume. These lungs would have a steep slope on their pressure-volume curve.
Less compliant lungs require a large distending pressure to effect a small change in volume. These lungs would have a shallow slope on their pressure-volume curve.
- If a 20kg dog has normal lungs and a 2 cmH2O inspiratory pressure change causes a volume change of 200 mL then its pulmonary compliance is 100 mL/cmH2O. What if the same took in a normal 10mL/kg tidal volume and then decided to sniff in some more air? If the dog generated an additional 2 cmH2O of inspiratory pressure once the lungs were
already distended by 200 mL of tidal volume there would not be a further increase in lung volume of 200 mL. The dog would need to generate a greater inspiratory pressure to achieve this. In other words, alveoli are more compliant (with less elastic recoil) at low volumes and are less compliant (with more elastic recoil) at high volumes
Define hysteresis
At any given volume, the pressure is lower on expiration than inspiration meaning there is a loss of energy, which is mostly heat, and is described as hysteresis.
For any given pressure, the volume of the lung is greater in expiration than inspiration. For the same change in pressure, the change in volume on inspiration is greater than the change in volume on expiration, meaning expiratory compliance is worse (less).
List the five determinants of hysteresis
- elastic recoil & surface tension
- the pressure generated by elastic recoil on expiration is always less than the distending transmural pressure gradient required to inflate the lung
- surfactant reduces surface tension and thus elastic recoil, which then improves compliance. When the lung is inflated, liquid molecules along the air-liquid interface are spread apart and the pull to one another, or the surface tension (the pressure causing elastic recoil, with the addition of lung connective tissue), is greater, thus the lung is less compliant than when it is deflated. Once the lung is fully inflated, the initial stages of the deflation curve have lower compliance or a lower change in volume over substantial changes in pressure - alveolar recruitment on inspiration and derecruitment on expiration
- collapsed alveoli require greater pressure to open them up (change their volume) - gas absorption during measurement
- not really a property of the lung parenchyma itself but rather an artifact of measurement. As mentioned above, measurement of static lung compliance has a certain built-in pause in every step, which allows some of the gas to become absorbed in living systems, leading to an apparent change in volume and pressure - relaxation of lung tissue: refers to the loss of energy in the lung parenchyma which occurs with stretch. This resembles the classical definition of hysteresis, as the quantity of unrecovered energy which results from something being imperfectly elastic. The imperfect lung stretches, consumes energy, and then wastes it on changing the shape of its collagen and elastin fibres instead of storing it for later release
- differences in expiratory and inspiratory air flow (for dynamic compliance)
What is surfactant
Complex liquid made by type II pneumocytes, consisting of 65%
dipalmitoyl phosphatidylcholine, 20% phosphatidyl glycerol and 15% surfactant proteins SP-A, -B, -C and -D.
Decreases surface tension and thus keeps alveoli from becoming atelectic
A number of factors may modulate surfactant secretion, including glucocorticoids, epidermal growth factor, cyclic adenosine monophosphate (cAMP), and lung distention.
Explain what happens in premature neonatal hypoxia
Premature neonates have inadequately developed surfactant production. As a result their lungs are unstable and have very low compliance. This instability leads to complete atelectasis of many alveoli, producing a right-to-left shunt and profound hypoxemia. The decreased compliance and atelectatic alveoli lead to alveolar hypoventilation. Surfactant production can be augmented by the administration of corticoids to the mother prenatally, which results in a decreased incidence of the syndrome.
A lung unit with normal compliance and resistance will fill within a
normal length of time and with a normal volume. Lung units with normal resistance but low compliance fill rapidly (fast lung unit / short time constant). Lung units with normal compliance but high resistance fill slowly (slow lung unit / long time constant). Flow applied to these two distinct lung units for the same amount of time will result in a difference in volume, or in other words to fill each unit equally requires different amounts of time. These units have different time
constants.
- Decisions regarding how best to ventilate an individual patient should be based on an assessment of the time constant of the majority of the lung and on how the patient responds to therapy. In patients with airway disease or abnormal compliance there can be transient gas movements out of some alveoli and into others as a result of lung units with different time constants, even when bulk flow has ceased at the mouth. Filling of a lung region with a partially obstructed airway will lag behind the rest of the lung such that it may continue to fill even when the rest of the lung has begun to empty with gas moving into from adjoining lung units. This phenomenon is called the pendelluft effect. As the breathing frequency is increased, the proportion of the tidal volume that goes to this partially obstructed region becomes smaller and smaller. Thus, less and less of the lung is participating in the tidal volume changes, and therefore the lung appears to become less compliant.
See above
Differentiate static from dynamic compliance
Static compliance is a measure of the lung’s true compliance after flow has stopped (after any inspiratory hold)
Dynamic compliance occurs during a state of flow (measured using peak inspiratory pressure) and takes into account airway resistance
Static compliance is always greater than dynamic compliance
Define alveolar ventilation
Alveolar ventilation is the volume of fresh gas entering the respiratory zone per minute
and is = to CO2 output divided by the concentration of CO2 in the expired gas.
The concentration of CO2 in arterial blood and hence its partial
pressure in alveolar gas is inversely related to alveolar ventilation.
PaCO2 ∝ V̇ CO2 / V̇ A
Differentiate physiologic from anatomic dead space
The physiologic dead space is the sum of the anatomic dead space and the alveolar dead space.
Anatomic dead space is the amount of air remaining in the conducting airways at the end of inspiration that doesn’t participate in gas exchange
Alveolar dead space is the alveoli that are ventilated but not perfused and thus do not pick up CO2
Alveolar ventilation = minute ventilation – anatomic dead space ventilation
V̇ A = V̇ T - V̇ D(Anatomic)
Explain the PaCo2 vs EtCo2 gradient
If expired air originates from the alveolus, and all of the alveoli are able to participate in gas exchange, then the pCO2 of arterial blood and expired gas are the same. Because of alveolar dead space, however, the alveolar/EtCO2 are always lower than arterial as ventilated/inspired alveoli without perfusion (alveolar dead space) has the same pCO2 of inspired air, the EtCo2 is diluted and leads to a typical gradient of 2-5mmHg in healthy lungs.
Give the equation for alveolar dead space
VD(Alveolar)/VT = (PaCO2 – PETCO2)/ PaCO2
Things that increase anatomic dead space include
- Increasing body size
- Increasing age
- Increasing lung volume
- Sat posture
- Hypoxia (bronchoconstriction)
- Lung disease (emphysema)
- Endotracheal intubation
Define physiologic dead space and list things that increase it
Physiologic dead space is the sum of the anatomic and alveolar dead spaces
• Increasing age
• Decreased pulmonary artery pressure (Increase in Zone 1)
• IPPV (increased PVR, decreased pulmonary blood flow, short Ti causing maldistribution)
• Increasing tidal volume
• Hyperoxic vasodilatation
• Anesthetic gases
• Lung diseases (ALI/ARDS, PTE, atelectasis etc.)
Define Fick’s law of diffusion
Diffusion of the gas (V gas diffusing per minute) = (As x D × ∆P)/ T
As = Membrane surface area
D = Diffusion coefficient of the gas
ΔP = Partial pressure gradient across the barrier between the pulmonary capillary and the alveoli
T = Membrane thickness
The volume of gas diffusion is inversely proportional to its thickness
The surface area and membrane thickness can be altered by changes in the pulmonary capillary blood volume, the cardiac output or the pulmonary artery pressure, or by changes in lung volume.
Describe diffusion-limited gases and give an example
In a diffusion-limited gas, the partial pressure of the gas in the pulmonary capillary equilibrates fully with the partial pressure of the gas in the alveoli during the time that the blood spends adjacent to the alveolus. The properties of the barrier and the diffusability of the gas limit its transfer across the barrier.
Carbon monoxide
Increasing the available surface area for diffusion can increase its uptake.
Describe perfusion-limited gases and given an example
diffuse extremely rapidly and therefore the alveolar pressures of these gases
equilibrates completely with the mixed venous blood before the blood has left the alveolar-capillary unit.
nitrous oxide
Additional diffusion of these gases is only possible once new mixed venous blood arrives at the alveolus.
Under normal conditions the transfer of both oxygen and carbon dioxide are perfusion-limited but some diffusion limitation may occur under some conditions, including intense exercise, thickening of the blood-gas barrier, and alveolar hypoxia.
Carbon dioxide is inherently much more diffusible than oxygen, however the alveolar-mixed venous gradient for CO2 is much lower than that for O2 (60 mmHg versus 5 mmHg), which offsets this inherent difference.
List the 5 causes of hypoxemia
Hypoventilation
Ventilation/Perfusion mismatch
Shunting (right to left) whereby there is no ventilation at all
Diffusion impairment
- processes that thicken the barrier including interstitial or alveolar edema and interstitial or alveolar fibrosis
- processes that decrease surface area including low cardiac output, tumors, or emphysema
- processes that decrease erythrocyte uptake including anemia and low pulmonary capillary blood volumes
Low inspired oxygen
Explain how alveolar hypoventilation contributes to hypoxemia
Hypoventilation leads to an increase in the arterial partial pressure of Co2 which inevitably decreases the partial pressure of oxygen because it is more readily diffusible frm the arterial blood into the alveolus than oxygen is and because maximal alveolar pressure cannot exceed that of atmospheric pressure (760mmHg). This means the alveolar partial pressure of oxygen is capped by 760 - (partial pressure of nitrogen + water + CO2).
Define the alveolar oxygen equation and its use with the alveolar-arterial oxygen gradient
The alveolar oxygen equation = [Fi02 x (Patm - PH20)] - pCO2/0.8
= 0.21 x (760-47) - pCO2/R (R=0.8)
PH20 is the partial pressure of water or water vapor pressure
0.8 is the respiratory quotient which depends on the diet and metabolic state of the patient. the quotient = the amount of CO2 produced / the amount of O2 consumed. It is 0.8 for the standard human, carinovirous diet. As the proportion of carbohydrates increases, the quotient becomes closer to 1.
The A-a gradient helps determine the effect of hypoventilation
Increasing Fi02 has a substantial effect on increasing alveolar oxygen even in the face of increased pCO2 concentrations as it displaces nitrogen
An elevated A-a gradient is caused by a normal shunt, VQ mismatch, and/or diffusion limitation
Describe the P:F ratio and it’s utility
This is the index of the partial pressure of paO2 and the Fi02. Normal P:F ratio is 500 whereby patient’s breathing 21% oxygen have a paO2 of 100, 100% oxygen have a paO2 of 500
PAO2/FiO2 <300 = ALI
and <200 = severe ARDS
Describe pulmonary blood flow
Receives 2% of blood from the bronchial circulation and 98% of blood from the pulmonary circulation
Describe pulmonary circulation to the lungs
The lungs receive the entire cardiac output of the right ventricle via pulmonary arteries. This blood is mixed venous blood and is pumped under low pressure to the lungs for gas exchange. Pulmonary vasculature is also a low pressure system with thin walls and minimal smooth muscle making it easily distensible and compressible. Gravity, body position, lung volume, alveolar and intrapleural pressures, intravascular pressures, and right ventricular cardiac output all impact pulmonary vascular resistance. In the pulmonary circulation, capillaries are the main capacitance vessels whereas the veins are in the systemic circulation.
Describe bronchial circulation to the lungs
In addition to the mixed venous blood supplied to the lungs via the pulmonary circulation via the pulmonary “arteries,” lungs also receive arterial blood from the left heart via the bronchial circulation.
Describe vascular drainage of the lungs
The venous drainage of the bronchial circulation is split between the azygos vein (which drains the bronchoesophageal veins, intercostal muscles, and dorsal body wall before draining into the cranial vena cava as it enters the right atrium) and the pulmonary veins which enters the left atrium. As such the bronchial venous blood entering the pulmonary venous blood is part of the normal anatomic right-to-left shunt.
Describe how PVR changes during phases of respiration
PVR is high at the residual volume (maximal forceful expiration), is low around FRC (end of passive expiration), and increases again during a normal inspiration towards TLC (total lung capacity) which is at the end of maximal inspiration
Describe the changes in PVR during PPV (mechanical ventilation) and PEEP
During PPV, alveolar pressure and intrapleural pressure (ie intrathoracic pressures) are both positive during inspiration. As lung volume increases, alveolar and extra-alveolar vessels are compressed and PVR increases in addition to a decrease in venous return, right ventricular output, and pulmonary blood flow. This is even greater when there is PEEP as alveolar pressure and intrapleural pressure are positive during both inspiration and expiration. PEEP also increases RV workload and decreases venous return by increasing CVP and compressing intrathoracic vessels such as the vena cava.
In healthy lungs with normal compliance, only 25% of PEEP is transmitted to the central veins. However this number increases with worsening compliance and is even more exacerbated with hypovolemia whereby substantial reductions in cardiac output, stroke volume, and pulse pressure variation can occur.
Describe the effect of PEEP in the setting of CHF
In the setting of CHF where intravascular volume is increased by sodium and water retention, and preload is enhanced with sympathetically driven arteriolar constriction, PEEP decreases the work load of the heart by decreasing left and right ventricular preload.
Additionally, PEEP decreases left ventricular afterload, which is = to the pressure generated by the myocardium + the pressure added to it by PEEP, or the transmural pressure (which is reduced in the setting of CHF and PEEP) and SVR. By reducing the transmural pressure, PEEP reduces afterload and assists left ventricular systolic function. The presence of PEEP in the setting of CHF pushes it into a more efficient part of the Frank-Starling curve.
Explain the Frank Starling Curve
The heart is obligated to push out the volume which is delivered to it, or basically how ventricular preload affects stroke volume. The heart’s ability to pump changes in response to the amount of venous return delivered to it.
The x axis contains the left ventricular end diastolic pressure (LVEDP, mmHg) and the y axis represents stroke volume (SV, mLs)
Explain how mean pulmonary artery pressure is maintained in the face of increasing cardiac output.
At normal cardiac output, not all pulmonary capillaries are perfused due to gavirty induced hydrostatic effects and variations in critical opening pressures. Thus once cardiac output is increased and pulmonary arterial blood flow increases, additional pulmonary capillaries are recruited and also distended. As the perfusion pressure increases, the transmural pressure gradient of the pulmonary blood vessels increases, distending vessels and reducing resistance.
Derecruitment caused by low right ventricular output or high alveolar pressures decreases the surface area for gas exchange and may increase alveolar (physiologic) dead space.
Explain hypoxic pulmonary vasoconstriction
When sections of alveoli are hypoxic or atelectic, there is compensatory vasoconstriction to shunt blood away from these poorly ventilated regions to well ventilated areas. The mechanism is poorly understood but is believed to be secondary to local vasoconstriction of hypoxia on pulmonary vascular smooth muscle at a pa02 of 20-100mmHg. Hypoxia inhibits an outward potassium current, depolarizing cells and allowing calcium entry, enabling contraction. Oxidation of the potassium channel opens it.
High pulmonary artery pressures and alkalosis interfere with the response. When global hypoxia is encountered such as at altitude, whole-lung hypoxic pulmonary vasoconstriction can occur, greatly increasing pulmonary hydrostatic pressure and the workload on the right ventricle and may lead to high altitude pulmonary edema
Hypercapnia also causes hpvc however the mechanism is in question.
What determines V/Q and alveolar PO2 and PCO2. What is the normal VQ.
Well ventilated alveoli deliver O2 and take up CO2 as well perfused pulmonary capillaries deliver CO2 and take up O2.
For a given lung unit, normal V/Q is 0.8-1.2
If V/Q increases for a given unit, alveolar pO2 will increase as pCO2 decreases
If V/Q falls then oxygen delivery and carbon dioxide removal decreases, thus alveolar p02 will decrease and pCO2 will increase
Explain normal inspired pO2 and pCO2 concentrations among alveoli and pulmonary capillaries under normal V/Q conditions
Inspired air entering the alveolus has a pO2 of 150mmHg and a pCO2 of 0 where as mixed venous blood entering pulmonary caillaries as a pO2 of 40 and pCO2 of 45mmHg. Following equilibration of both gases, the alveolar pAO2 is 100mHg and the pACO2 is 40. The gradient for the diffusion of oxygen into capillaries is thus 60 while the gradient for diffusion of CO2 into alveolar gas is about 5. These gradients are what make oxygen and carbon dioxide perfusion limited despite CO2 being 20x more soluble than oxygen.
Describe what happens in a right to left shunt
No fresh inspired air enters that alveolus as it is not ventilated. The alveolar CO2 and O2 concentrations match new mixed venous blood that enters as a result of normal perfusion . Blood perfusing this alveolus leaves exactly as it entered and joins circulation in the pulmonary venous system going to the left side of the heart however the CO2 concentration is greater and the O2 concentration is lower.
Describe what happens when V/Q and what this means
When V/Q is infinite, blood flow is completely occluded. None of the available oxygen can enter the pulmonary capillary blood and no carbon dioxide can enter the alveolus. Thus the gas composition of this unperfused alveolus is the same as inspired air. This is alveolar dead space.
Each individual alveolar-capillary unit can exist anywhere on the continuum between infinite V̇ /Q̇ and zero V̇ /Q̇ . Units with low V̇ /Q̇ have low PO2 and high PCO2 while units with high V̇ /Q̇ have high PO2 and low PCO2.
List ways V/Q mismatch can be calculated
calculating physiologic shunt, the physiologic dead space and differences
between the alveolar and arterial PO2 and PCO2 values.
Describe right-to-left shunts
when mixed venous blood enters the left side of the heart (arterial circulation) without having been (fully) oxygenated.
shunts can be anatomic, absolute (true) intrapulmonary shunts, or shunt-like states (Small areas of low V/Q)
Physiologic anatomic shunts include systemic venous blood entering the left ventricle without having traversed pulmonary vasculature and accounts for 1-2% of cardiac output
- bronchial veins, thesbian veins, and pleural veins.
Pathologic anatomic shunts include right to left intra-cardiac shunt such as tetralogy of fallot (pulmonic stenosis, VSD, right ventricular hypertrophy, and overriding aorta; clinical signs include cyanosis and polycythemia)
True (intrapulmonary) shunts occur when mixed venous pulmonary blood that traverses along unventilated or collapsed alveoli. Shunt like states are just smaller regions of this
Calculate shunt fraction
Shunt fraction = Qs/Qt = (CcO2 - CaO2)/ (CcO2 - CvO2)
Qs = shunt flow
Qt = total cardiac output
CcO2 = calculated pulmonary capillary blood oxygen content
= ([Hb (g/L)] x 1.34 (hufner’s factor, a constant (1.34-1.39), maximum oxygen carrying capacity of blood in ml O2/g Hb) x SaO2 (% saturation of hemoglobin)) + (0.003 (oxygens water solubility at 37*C 0.03 ml/L/mmHg) x pa02 (partial pressure of arterial oxygen))
CaO2 = arterial oxygen content
CvO2 = mixed venous oxygen content
venous admixture is the resulting amount of shunt flow that enters arterial flow
to assess for the presence of shunt, calculate this at room air or slightly increased Fi02 levels then again after a few minutes on 100% oxygen. After a few minutes, the areas of low V/Q should have enough pa02 values to fully saturate the hemoglobin perfusing them to leave you with a shunt fraction that is representative of true/absolute shunts.
Describe oxygen solubility in plasma
At 37°C, 1 mL of normal arterial blood
with a PaO2 of ~100 mmHg contains ~0.003 mL O2, thus most of the oxygen within the bloodstream is combined with hemoglobin
