Physio Perfusion (25)

Card Set Information

Physio Perfusion (25)
2014-03-25 19:14:38
MBS Physiology
Exam 3
Show Answers:

  1. What are the functional zones of the pulmonary system?
    • 1. Conducting Zone
    • 2. Respiratory Zone
  2. 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)
  3. Respiratory Zone
    • 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
  4. 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
  5. Perfusion
    • 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
  6. 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
  7. Air-blood Barrier
    • 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
  8. 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
  9. 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
  10. Surfactant
    • a mixture of lipids, proteins, and a little carbohydrate
    • lipids are mainly phospholipids (dipalmitoyl phosphatidyl-choline
  11. 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)
  12. 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
  13. 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)
  14. 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
  15. 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
  16. Pulmonary Arterioles Overall
    • much less muscular
    • more RAPIDLY dilate (don't have same muscle tone as systemic arterioles)
  17. 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)
  18. Is there more blood in the pulmonary system standing up or 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)
  19. 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
  20. 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
  21. 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
  22. Recruitment
    • 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)
  23. Distension
    • individual capillary segments INCREASE their RADII (can expand) → increases blood flow
    • the arterioles leading into the capillaries can do so as well
  24. 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
  25. 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
  26. Transmural Pressure
    • 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
  27. 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)
  28. What causes variations in Piv (intravascular pressure)?
    • 1. cardiac cycle variations
    • 2. the vertical position of the vessel relative to the heart
  29. 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
  30. 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
  31. 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
  32. What causes variations in PA (alveolar pressure)?
    respiratory cycle variations
  33. 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]
  34. What combination of intravascular & alveolar pressures dilates vessels & decreases resistance?
    • high Piv
    • low PA
    • means you have GREATER FLOW
  35. What combination of intravascular & alveolar pressures tends to crush the vessels & increase resistance?
    • low Piv
    • high PA
    • means you have LESS FLOW
  36. Extra-alveolar Vessels
    • 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)
  37. 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
  38. 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
  39. 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)
  40. Hypoxic Vasoconstriction
    • 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)
  41. 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
  42. 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
  43. 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
  44. 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
  45. 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
  46. 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
  47. 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)
  48. 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)
  49. 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
  50. 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
  51. 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
    • [Poiseuille’s]
  52. 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
  53. 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)
  54. Pulmonary Edema
    • 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
  55. 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')
  56. 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)
  57. 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
  58. 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
  59. 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)
  60. Ductus Arteriosus
    • 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
  61. 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
  62. 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)
  63. 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