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What are the functional zones of the pulmonary system?
- 1. Conducting Zone
- 2. Respiratory Zone
Conducting Zone ("Airways")
- conducts air from the atmosphere down into the alveoli
- the trachea, the main stem bronchi & their divisions/branches into secondary/tertiary bronchi, & finally the bronchioles (microscopic part of the airways)
- alveoli (air sacks) themselves where exchange of O2 & CO2 takes place
- a very dense capillary network surrounds and penetrates between each alveoli
- sometimes it's described like each capillary is sitting in a thin layer of blood b/c the capillary network is so dense
What is the combined surface area of where air is in contact with the blood in the body?
- 50–100 m2 (size of a tennis court, all w/in thoracic cavity)
- this is the surface area for gas exchange
- the flow of blood through the lungs
- branches of the pulmonary arteries follow the branching of the airways as far as the terminal bronchioles then split into capillary beds surrounding alveoli
- capillary beds fuse, resulting in alveoli being essentially surrounded by a flowing sheet of blood
- surface area for gas exchange ~100 m2
- capillaries converge ultimately to form venules → 4 pulmonary veins leading to the L Atrium
Path to the Air-blood Barrier
- respiratory bronchiole (smallest bronchiole) opens into an alveolar duct
- an alveolar duct supplies air to individual alveolies
- alveoli is ~partial sphere, w/ alveolar septa that separate one alveoli from another
- 1st: alveolar (squamous) epithelium is the most INNER lining of an alveolus; made up of mostly type I & some type II pneumocytes
- 2nd: basement membrane
- 3rd: Interstitium
- 4th: another basement membrane
- 5th: capillary endothelium
- non-polar gasses in the air are diffusing through a VERY thin layer, less than 0.5 μm thick, from the inner alveolus to the blood stream
Type I Alveolar Cells
- simple squamous epithelial cells that make up 97% of the alveolar surfaces
- most of the cell is flattened into a thin sheet which forms part of the blood-air barrier
- their nucleus & organelles are clustered together in the ‘thick’ part of the cell
Type II Alveolar (Septal) Cells
- cuboidal cells w/ round nuclei found among the type I cells at the ‘corners’ of alveoli
- have mitotic capacity
- are responsible for regeneration/repair of the alveolar surface
- secret pulmonary surfactant packaged in multilamellar bodies (cytosomes) to reduce the surface tension at the air-blood interface
- a mixture of lipids, proteins, and a little carbohydrate
- lipids are mainly phospholipids (dipalmitoyl phosphatidyl-choline
What is the total circulation time through the pulmonary system at rest?
- 4–5 seconds
- pulmonary capillary bed contains ~75 mL of blood & the average erythrocyte takes about 0.75 seconds to pass through the alveolar capillary bed – it's within this time that gasses are exchanged
- (most blood, 60%, is below your waist)
What is the blood flow in the pulmonary circulation?
- the same as that of the systemic circulation, ~5 L/min or 83 mL/s, but in a very different manner
- while the systemic circulatory system is a high pressure system, the pulmonary system is LOW pressure
- lungs have open vessels & low resistance – why we need only a fraction of the pressure (25/7 mmHg) the L ventricle generates to push blood through pulmonary system
What is the average drop of blood pressure from the right ventricle to the left atrium?
- 7 mmHg, the Perfusion Pressure
- the driving force/amount of energy necessary to push blood through the pulmonary system
- the driving force for blood flow in pulmonary system only ~8% of the systemic driving force for same flow (systemic = 93 mmHg)
What is the pulmonary resistance in comparison to that of the systemic resistance?
- less than 10%
- R = ΔP / Q
- Rsyst = 93 mmHg / 83 mL/s = 1.1 PRU
- Rpulm = 7 mmHg / 83 mL/s = 0.08 PRU
- can push the SAME amount of blood through w/ much LESS pressure
Pulmonary Vessel Characteristics
- have larger diameters than comparable systemic vessels (arteries & arterioles stay fairly large)
- are shorter & branch more often
- pulmonary system has MORE arterioles which don't direct flow like those found in the systemic circulation (other factors do that)
- pulmonary arterioles have a lower resting muscle tone therefore lower resistance
- arterioles don't dampen out the pulse in the lungs – even capillaries have a pulse
Pulmonary Arterioles Overall
- much less muscular
- more RAPIDLY dilate (don't have same muscle tone as systemic arterioles)
Pulmonary Vessel Walls
- are thin & have less muscle than systemic vessels – results in high compliance (expand easily)
- have a relatively low pulse pressure (25 - 8 = 17 mmHg)
- vessels can dilate accordingly/easily in response to moderate increases in pulmonary arterial pressure (eg. during exercise)
Is there more blood in the pulmonary system standing up or lying down?
- LYING DOWN
- the large compliance of pulmonary vessel walls allows vessels to expand & accept large amounts of blood that shift from the lower limbs to lungs when a person changes from standing to recumbent (lying down)
What happens to pulmonary vascular resistance as mean pulmonary arterial pressure rises?
- it DECREASES
- vessels dilate easily in response to greater flow (high pressure) b/c of their high elastic/low-ish smooth muscle composition
What happens when there is an increases cardiac output, such as during exercise?
- pulmonary arterial or venous pressure increases
- vessels dilate
- in dilated vessels, resistance decreases
- → an increase in blood flow
- as mean pulmonary arterial pressure increases, SO does pulmonary blood flow
What are the 2 ways in which the pulmonary system can accommodate increasing flow but NOT increasing resistance or pressure (eg. during physical activity)?
- 1. Recruitment
- 2. Distension
- previously collapsed vessels OPEN UP
- in an upright resting individual not all of the capillaries are being perfused (esp. in upper part, apex, of lung)
- vessels that weren't previously being perfused now WILL BE (spec. APICAL part of lung)
- individual capillary segments INCREASE their RADII (can expand) → increases blood flow
- the arterioles leading into the capillaries can do so as well
What else does the high compliance of pulmonary vessels allow for?
- makes them susceptible to deformation by external forces
- external forces may CRUSH or PULL vessels open
- different effects from these forces are seen in alveolar vs. extra-alveolar vessels
What are the two general kinds of vessels in the lung?
- Alveolar & Extra-alveolar
- alveolar includes capillaries + some slightly larger vessels that are themselves surrounded by alveoli
- their resistance depends upon transmural pressure, PTm
- pressure across the vessel wall
- PTm = Piv – PA
- Piv = intravascular pressure
- PA = pressure in the alveoli
- aka = the differences between the intravascular pressure & the pressure in the alveoli (open to the atmosphere - will expand & contract w/ breathing)
- intravascular pressure also changes b/c capillaries are pulsatile
High v. Low Piv & PA
High PA, Low Piv: vessel would be squeezed, ↓ vessel diameter & blood flow
High Piv, Low PA: vessel would expand, ↑ blood flow (alveolus squeezed)
What causes variations in Piv (intravascular pressure)?
- 1. cardiac cycle variations
- 2. the vertical position of the vessel relative to the heart
How does Piv vary w/ the cardiac cycle?
- flow in pulmonary capillaries is pulsatile b/c there are NO high resistance arterioles to dampen the pulse (like there are in systemic capillaries)
- every time the heart beats, Piv goes up
- Piv goes down during diastole
How does Piv vary w/ vertical position of the vessel relative to the heart?
- the Higher the VESSEL, the LOWER Piv
- there's a position dependent change:
- the pressure drops considerably (b/c it's so low to start w/ from the R ventricle) when blood is pumped from the pulmonary artery to the apex (top) of the lung
- flow at the upper part of the lung when you're upright is decreased
- when you're pumping blood down the the base (lower part) of the lung, the effect of gravity increases the pressure
Experiment: Effect of Gravity on Pulmonary Blood Flow
- give small dose of radio-labeled gas
- person breaths gas in → passes through their pulmonary system
- devise that counts radiation shows maximum radiation at bottom of lung
- as you move up the lung, radiation count FALLS
What causes variations in PA (alveolar pressure)?
respiratory cycle variations
How does PA vary w/ the respiratory cycle?
- if there's no airflow (when breathing stops), PA = Patm (~760 mmHg)
- during inspiration PA decreases (expanding the alveoli causes a pressure DROP [Boyle's law])
- during expiration PA rises above atmospheric pressure (Patm) [alveoli are SQUEEZED → pressure increases]
What combination of intravascular & alveolar pressures dilates vessels & decreases resistance?
- high Piv
- low PA
- means you have GREATER FLOW
What combination of intravascular & alveolar pressures tends to crush the vessels & increase resistance?
- low Piv
- high PA
- means you have LESS FLOW
- larger vessels NOT surrounded by alveoli but by lung parenchymal tissue (CT)
- adventitia of these vessels are attached to the lung tissue
- when lungs expanded during inspiration, extra-alveolar vessels are pulled OPEN by expansion of the surrounding tissue
- (their diameter ↓ during exhalation)
What happens to alveolar vessels at high lung volumes?
- they are COMPRESSED by expanded alveoli
- this increases resistance
- this same expansion (high volume) pulls open extra-alveolar vessels by the expansion of attached parenchymal tissue
- there, resistance is decreased
- NET RESULT: a drop in total resistance followed by an rise
Summary: Lung Volume Effects on Resistance
- breath in: resistance ↓ initially b/c extra-alveolar vessels are pulled open
- as lung volume is increased, resistance ↑ due to alveolar expansion, which compresses capillaries
What happens to pulmonary vessels when oxygen pressure is LOW (eg. blocked airways)?
- pulmonary vessels CONSTRICT
- when PAO2 < 60 mmHg
- called Hypoxic Vasoconstriction
- in CONTRAST to systemic vessels which DILATE in response to local hypoxia (opposite happens in pulmonary system)
- is a local action on the vascular smooth muscle that possibly works by inhibiting a voltage-gated K+ channel → leading to influx of Ca2+ → smooth muscle contraction
- doesn't involve Nervous or Hormonal signaling (happens in isolated excised pieces of lung tissue)
Effects of Hypoxic Vasoconstriction
- flow is diverted AWAY from poorly ventilated
- alveoli → alveoli that are WELL ventilated
- ensures maximum exchange of O2
- between alveoli & blood
- low alveolar PO2 (PAO2) = LOW blood flow in corresponding capillaries
What other agents affect pulmonary vascular resistance?
- ↑ PACO2, ↓ pH: constriction (weaker than hypoxia)
- Nitric Oxide (NO): vasodilation (made by pulmonary endothelial cells; regulates pulmonary vascular tone)
- Atrial Natriuretic Factor: vasodilation (released by heart to relax pulmonary smooth muscle when there's high blood volume)
- Prostaglandin I2, Platelet Activating Factor: ↓ vascular tone
Relationship between Alveolar, arterial, & venous Pressure
- top (Apex) of lung: minimal flow
- PA > Pa > Pv
- heart (Middle) level: intermittent flow
- Pa > PA > Pv
- base of lung: open, complete flow
- Pa > Pv > PA
- *can change
Where will an upside-down person have highest perfusion in the lung?
- in the APEX
- b/c hydrostatic effects are dependent on gravity the above relationships will change when a person’s position changes from standing or sitting to lying down
How will lung perfusion change with exercise?
- increasing pulmonary artery pressure will exceed Alveolar pressure at all lung levels
- Pa > PA
- pulmonary flow will become more uniform through recruitment & distension
How is pulmonary vascular pressure measured?
- using a catheter w/ a pressure transducer at its tip threaded into a vessel or chamber in the heart
- is used for direct measurements of right atrial, ventricular, & pulmonary artery pressures
Pulmonary Capillary Wedge Pressure (PCWP)
- ~equal to Left atrial pressure
- a balloon-tipped (Swan-Ganz) catheter is inserted into a pulmonary arteriole as far as possible
- ballon inflation occludes arteriole & the catheter tip measures the “wedge pressure” which approximates Left atrial pressure (~7-8 mmHg)
What defines the rate of fluid flux out of the pulmonary capillaries into the interstitium (JV)?
- Starling’s law:
- JV = K[(Pc - Pt) + σ(πt - πc)]
- K: capillary membrane permeability coefficient
- Pc: pulmonary capillary hydrostatic pressure (~10 mmHg)
- Pt: pulmonary interstitial hydrostatic pressure (<3 mmhg)
- σ: reflection coefficient of the membrane
- πt: lung interstium oncotic pressure (~20 mmHg)
- πc = plasma oncotic pressure (~ 26 mmHg)
How is fluid in the interstitium removed? (3)
- 1. vaporization in the alveoli
- 2. reabsorption into venules
- 3. taken up by lung lymphatics
- several hundred mL of fluid leave the capillaries & enter the interstitium per day
How is Pulmonary Hypertension defined?
if a patient has a mean pulmonary (arterial) pressure greater than 25 mmHg (normal = 15 mmHg) at rest, or 35 mmHg during exercise
Primary determinants of pulmonary arterial pressure (Ppa):
- Left atrial pressure, Pla
- pulmonary blood flow, Q
- pulmonary vascular resistance, Rp
- ΔP = Q * R
- Ppa - Pla = (Q * Rp) or
- Ppa = (Q * Rp) + Pla
Ppa = (Q * Rp) + Pla
- pulmonary hypertension is defined as when Ppa > 25 mmHg
- this would happen w/ an increase in all 3 of those other variables
Causes of Pulmonary Hypertension
- ↑ Q: left to right shunts (eg. ventricular & atrial septal defects, patent ductus arteriosus) increase pulmonary flow relative to systemic flow (when it's 1.5 : 1 = pulm HTN)
- ↑ Rp: from hypoxic vasoconstriction, clot, tumor, inflammation
- ↑ Pla: from Left ventricular cardiomyopathies & valvular disease (eg. mitral stenosis, mitral regurgitation - pressure backs up into pulm system)
- occurs when pulmonary CAPILLARY pressure > 25 mmHg
- fluid flux out of the capillary exceeds capacity of lymphatics to drain interstitium
- defined as excessive fluid in the interstitial tissue or alveoli
Progression of Pulmonary Edema
- 1. flooding of peri-capillary interstitial spaces
- 2. crescentic filling of alveoli
- 3. flooding of individual alveoli w/ loss of gas exchange (hear as 'crackles')
How can pulmonary edema occur WITHOUT a capillary pressure > 25 mmHg (i.e. a normal capillary pressure)?
- with increased capillary permeability*
- due to damage by toxins, bacteria, or inflammation
- can lead to ARDS (adult respiratory distress syndrome)
Symptoms of Pulmonary Edema
- Dyspnea (shortness of breath), worse when supine (orthopnea - lying down)
- Increased respiratory rate: can't breathe as deeply b/c when there's water in lungs, elasticity ↓ - need to take more breaths to compensate
- Hypoxemia (PO2 < 80 mmHg): blood oxygen drops below normal b/c fewer alveoli are participating in gas exchange
What circulation that passes through the lungs DOESN'T come from the Right heart?
- the bronchial vessels - are part of the Systemic circulation
- they are branches of the aorta that carry oxygenated blood to the larger conducting airways
- ~1/2 drains into (O2-ated) pulmonary veins; is a small right to left shunt that minimally reduces amount of O2-ated blood that enters the L heart
- the rest drain into the azygos vein then to the Right heart
What is there none of in the fetus?
- there is no gas exchange
- therefore pulmonary perfusion is only 3-10% of the cardiac output
- blood is diverted into systemic circulation through the ductus arteriosus & foramen ovale
- fetal pulmonary vessels remain vasoconstricted b/c their pulmonary PO2 is low (17-20 mmHg)
- pathway (anastamoses) from the R ventricle to the Aorta
- most of the blood in the R heart is shunted into the L heart through this & the foramen ovale
- shunt where blood from the R atrium passes directly into the L atrium in the fetus
- b/c most blood doesn't pass through vasoconstricted lungs, a very high pressure system
What happens to the pulmonary circulation at BIRTH?
- it changes from a high to a LOW pressure system in response to the rise in PO2 & vascular mediators of vasodilation (PGI2 & PAF) that activate as the first breaths are taken
- the reduction in R atrial pressure decreases flow through the foramen ovale which closes & seals typically within MONTHS
- ductus arteriosus closes by constriction of its muscular walls within HOURS after birth (vasospasm)
Besides breathing, what metabolic functions does the pulmonary system have?
- angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II; affects blood pressure & kidney function
- vasoactive amines & peptides are INactivated during passage through the lungs (eg. NE, serotonin, bradykinin) as are enkephalins, prostaglandins, & histamine
- endothelial cells make PGI2, PAF, & NO, vasoDILATORS in the lung
- damage to endothelium → pulmonary vasoconstriction + damaged endothelial cells release pro-inflammatory & coagulant substances; can ↑ pulmonary resistance