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Respiratory Physiology > Mechanics and Ventilation > Flashcards

Mechanics and Ventilation Flashcards

1
Q

What is Vt?

A

tidal volume, volume inhaled or exhaled with each breath

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2
Q

What is ERV?

A

expiratory reserve volume, volume of air expired during a maximal forced expiration that starts at the end of a normal passive tidal expiration (maximal volume of air expired below FRC)

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3
Q

What is IRV?

A

volume of air that is inhaled during a maximal forced inspiration starting at the end of normal tidal inspiration (maximal volume of air inspired above FRC)

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4
Q

What is IC?

A

volume of air that is inhaled during a maximal inspiratory effort that starts at the end of a normal passive tidal expiration (maximal volume of air inspired above FRC)

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5
Q

What is VC?

A

volume of air expired during a maximal expiratory effort that starts at the end of a maximal inspiratory effort

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6
Q

What are the lung volumes that are measured by direct spirometry?

A

Vt, ERV, IRV, IC, and VC

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7
Q

What is RV?

A

residual volume, volume of air that remains in the lungs after a maximal forced expiration

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8
Q

What is FRC?

A

functional residual volume, volume of air that remains in the lungs at the end of a normal passive expiration

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9
Q

What is TLC?

A

total volume of air in the lungs at the end of a maximal inspiratory effort

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10
Q

What lung volumes are indirectly measured by helium dilution or by plethymsomography?

A

RV, FRC, and TLC

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11
Q

How is the helium dilution calculated?

A

Vapp= volume of apparatus, C1= concentration in apparatus before equilibration, VL= volume of the lung, C2 is concentration after equilibration;
Vapp x C1 = (Vapp +VL) + C2

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12
Q

Which is a more accurate measurement for RV, FRC, and TLV helium dilution or body plethysmography? Why?

A

plethysmography; measures volume of air in lung at FRC including air trapped behind obstructed airways

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13
Q

How do you measure air trapped in the lung?

A

FRC pleth. - FRC helium

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14
Q

What are the passive forces acting on the lung?

A

elastic recoil- potential energy within the walls of an expandable chamber that opposes distension or stretch (recoil force, often called elastic recoil and measured as elastance)

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15
Q

What two major forces in lung tissue act to deflate lungs?

A

interstitial collagen and elastin framework formed by mesenchymal cells (ECM known as parenchyma) and surface tension of H2O lining alveolar wall exposed to air

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16
Q

What two major forces in lung tissue act to inflate lungs?

A

attachment of rib cage to spine by ligaments and cartilage at joints and elasticity (due to elastin and collagen) in relaxed diaphragm muscle

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17
Q

What is equilibrium volume?

A

at the end of quiet expiration, no respiratory muscles are contracting so all forces on the chest cavity are passive, opposing forces establish equilibrium, the volume in the lung at this point is equilibrium or FRC

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18
Q

What is a pneumothorax?

A

opposing recoil forces of lung and thoracic cage cause a vacuum space between the two (pleural space) pleural pressure is negative with respect to atm. if integrity of thoracic cage is breached, pressure equilibrates with atm and lung collapses

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19
Q

What causes the active forces on the lung during inspiration?

A

force generated by respiratory muscles diaphragm and external intercostals that oppose elastic recoil force of the lung

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20
Q

What causes the active forces on the lung during expiration?

A

expiratory muscles abdominal and internal intercostal contract pulling the chest inward below FRC; must oppose passive recoil forces causing the chest wall to expand

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21
Q

When is expiratory work necessary to breath?

A

exercise to increase Vt and if elastic recoil is lost in the lungs due to disease like emphysema and lungs no longer passively deflate even at rest

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22
Q

What is an atelectasis? What are the kinds? Causes?

A

alveoli collapse, pneumothorax if from air, pleural effusion if its fluid in the pleural space, thoracic damage or parenchyma tear

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23
Q

What is the composition of surfactant? Produced where?

A

mostly dipalmitoyl phosphatidylcholine (DPPC), phospholipid produced by alveolar type II cells, small fraction of surfactant is composed of hydrophobic surfactant proteins

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24
Q

What are the 3 functional advantages of surfactant?

A

reduces tremendous surface tension in alveoli, increasing lung compliance to an optimal level, retards alveolar edema, stabilizes alveoli and prevents alveolar collapse (atelectasis) due to Laplace’s law

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25
Q

What is Laplace’s law?

A

P=2T/r; P= pressure in the sphere, T= surface tension of the sphere, r= radius of the sphere

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26
Q

How does surfactant affect alveolar stability?

A

lowers T of alveolar walls at low lung volumes, consequently trans-pulmonary pressure of large and small communicating airspaces; w/o surfactant surface tension remains constant as lung volume changes, recoil pressure of small airspaces exceeds that of large ones causing small alveoli empty into large ones

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27
Q

What two factors counteract alveolar collapse?

A

surfactant, and interdependence- alveoli tethered to one another because they share common septal walls

28
Q

What is elastance?

A

one measure of the ability of a substance to maintain its original shape, commonly think of this as stiffness

29
Q

What is compliance?

A

used to measure elastance of pulmonary and cardiovascular vessels, it is inverse of elastance and its measure of the ease with which an object is distended, distensibility; CL= delta VL/ delta PL; delta V is change in lung volume, delta P is change in trans-pulmonary pressure

30
Q

How does movement of lungs effect surfactant?

A

alveoli deflate- surfactant is pushed into adjoining and reabsorbed or eliminated, Type II cell also reabsorb surfactant, 1/2 life variable (longer in infants), surfactant is secreted when stretched; overnight decreased O2 so decreased Vt so decreased surfactant, sighs are to make up

31
Q

What factors decrease lung compliance below normal?

A

scar tissue from pulmonary fibrosis, IRDS (insufficient secretion of surfactant from type II cells), destruction of type II cell due to prolonged hypoxemia or inhalation of toxins ARDS often results in atelectasis and ultimately death; excessive accumulation of H2O in alveolar space due to edema; and prolonged quiet breathing

32
Q

What factors increase lung compliance above normal?

A

destruction of lung tissue by protease and collagenase enzymes formed by chronic inflammation (emphysema) and excessive secretion of surfactant (rare)

33
Q

What are the consequences to lungs with decreased compliance?

A

TLC and VC reduced because a stiff lung cannot be expanded, work of breathing increases for a stiff lung; work of breathing increases because inspiratory muscles must generate more force to expand it

34
Q

What are the consequences to lungs with increased compliance?

A

TLC increased but due to dynamic compression of airways during expiration VC decreases; highly compliant lung has little recoil force for deflation during expiration, expiratory muscles must be used to help deflate the lung, increasing work of breathing

35
Q

What is Ohms law? how does it relate to the lung?

A

V=PA-Pao/Raw V=airflow, PA= alveolar pressure, Pao= pressure at airway opening, Raw= airway resistance; laminar flow obeys the derivative of Ohms law

36
Q

What aspect of lung function follows the derivative of Poiseulle’s law? What is it?

A

resistance to laminar airflow; Raw=8nl/Pi r ^4; n= viscosity , l= length of airway, r= radius of airway

37
Q

What is reynold’s number? What part of lung function is proportional to Reynolds number?

A

Re= 2rvd/n; v= velocity of flow, d= gas density; resistance to turbulent flow is proportional to Reynolds number

38
Q

What are the major sites of resistance to airflow?

A

larger airways, upper airways: nose, mouth, larynx and trachea; and in medium sized lobar segmental and subsegmental bronchi; dues to Re, cross sectional area much larger causing greater velocity

39
Q

what factors determine airway resistance?

A

laminar resistance: airway smooth muscle contraction, secretion of mucus, swelling of airway mucosa, lung volume; and turbulent resistance: density and air velocity

40
Q

What is dynamic compression? what effect does it have?

A

during forced expiration, small bronchiole collapse due to increased pleural pressure, deflate lung rapidly; it increases resistance to airflow during expiration, add expiratory work breathing; rarely occurs during normal quiet breathing in healthy subjects and can be exhibited only by large forced expiration

41
Q

What effect does restrictive lung disease have on lung mechanics?

A

decreased lung compliance, decreased IC, increase in elastic recoil will pull chest wall inward at rest resulting in decreased FRC, TLC decreased bcuz inspiratory muscles less capable of overcoming increased elastic recoil, VC decreased

42
Q

what are general complications of restrictive lung disease?

A

respiratory failure- muscles fatigue and fail, atelectasis- alveoli collapse due to high recoil, and impaired VC- ventilation limitation

43
Q

What are the different types of restrictive lung disease?

A

ILD (pulmonary fibrosis), Respiratory Distress and Syndrome (ARDS or IRDS)

44
Q

What are the effects of Obstructive disease with overly compliant lungs on lung mechanisms?

A

decrease in elastic recoil allows chest wall to pull lung outward at rest which increases FRC and TLC, VC is decreased in obstructive disease bcuz air is trapped in lung due to dynamic compression of airways, increase in FRC means less inspiratory capacity; lung must be actively expired below FRC to sustain Vt (abdominal breathing)

45
Q

What are general complications of obstructive lung disease?

A

respiratory failure- increased work of expiratory muscle, lung hyperinflation- trapping air in lungs due to dynamic compression, Impaired VC- limiting ventilation

46
Q

What is the major type of obstructive lung disease? causes?

A

emphysema; old age, inflammatory, genetic alpha 1 antitrypsin deficiency

47
Q

What are the effects of obstructive disease with increased airway resistance due to lung compliance?

A

obstructive because they obstruct airflow due to effects on the airways, not lung compliance; lung volumes usually are not greatly affected, unless so great it retards expansion of lung reducing TLC or trap air increasing RV and TLC

48
Q

What are the different types of obstructive disease from increased airway resistance?

A

asthma- hypersensitivity bronchoconstriction, chronic bronchitis- bronchoconstriction, airway inflammation, mucus over-secretion; and cystic fibrosis- secretion of thick mucus

49
Q

What lung volumes change of PFTs with lung disease?

A

TLC and FRC always decreased in restrictive but not always increased in obstructive lung disease, TLC and FRC are increased with emphysema/COPD but not usually asthma alone

50
Q

What changes on spirometer is impaired in both restrictive and obstructive lung disease?

A

VC impaired in both

51
Q

What is FEV1.0?

A

volume forcefully exhaled in 1st second after a maximal inspiration to TLC. Its proportional to expired airflow and is reduced in obstructive but not restrictive disease unless vital capacity is so compromised that limits total amount of air exhaled in 1 sec.

52
Q

What is FVC?

A

total volume expelled in maneuver. it is decreased in restrictive diseases, less affected in obstructive diseases but often reduced simply because air is trapped in lungs due to dynamic compressions and obstructions

53
Q

What is FEV/FVC%

A

ratio of two measures, value typically depressed in obstructive disease and normal or elevated in restrictive disease; provides best differential diagnosis

54
Q

What is the metabolic cost of breathing?

A

amount of respired O2 required to produce energy for work of breathing, normally small <5% resting, can increase as much as 50% in severe lung disease

55
Q

What are the physiological consequences of positive pressure ventilation?

A

impedes venous return into thorax and reduces cardiac output; aggravates V/Q mismatch, positive pressure in alveoli tends to impede capillary blood flow, particularly in upper regions of the lung, alveolar pressure prevents alveolar capillary flow which increases zone 1; increased risk of overinflating the lungs or hypo or hyperventilating patient

56
Q

What is VE? How is it calculated?

A

expired volume per minute, VE= Vt (f); f= breaths per minute, Vt= tidal volume

57
Q

What is VA? How is it calculated?

A

alveolar ventilation, volume of fresh air that enters the functioning gas exchange regions of the lung per minute; VA= (Vt - VD) f; VD is volume of dead space

58
Q

How is VA regulated?

A

VA must be proportional to O2 consumption and CO2 production; so during exercise VA must increase in proportion to the increased metabolic demands in order to ensure adequate delivery of O2 and CO2 removal from tissue; regulated by respiratory centers in the brain stem that control respiratory muscles which alters depth of inspiration VT and f so VA remains proportional to VO2 and VCO2

59
Q

What is fowler’s method?

A

determining anatomical dead space using nitrogen washout

60
Q

How is physiological dead space? How is it determined?

A

= anatomical dead space + alveolar dead space; using the Bohr eqtn; VD= PACO2-PECO2/PACO2 x Vt; PECO2= partial pressure of CO2 in mixed expired air

61
Q

What is VW?

A

wasted ventilation; VW=VD (f); volume of air per minute used to ventilate the physiological dead space

62
Q

What is VD/Vt? What is it normally? How can it be decreased? Example. Increased? Example.

A

wasted fraction of each breath; normally 25-35%, increasing tidal volume decreases wasted fraction; exercise normally 10-15%, increase in alveolar dead space increases VD/Vt significantly

63
Q

What factors promote alveolar dead space and wasted ventilation? Examples.

A

suppressed pulmonary blood flow: heart failure, hemorrhage, shock, pulmonary emboli, positive pressure ventilation, generalized hypoxic pulmonary vasoconstriction due to inspiring hypoxic air as at high altitude; impaired diffusion across respiratory membrane: pulmonary interstitial edema, pulmonary fibrosis; gravity and posture- not normally but can aggravate

64
Q

How does gravity effect ventilation?

A

pills lung mass downward stretching out upper alveoli to a greater extent than lower alveoli making the compliance less in the upper alveoli; alveoli in lower are distended with greater ease and accept more inspired air; so VA is greater at the bottom of lungs at the top; when Vt increases alveoli in top portions are recruited

65
Q

What is closing capacity?

A

aka closing volume; increased with small airways disease such as emphysema that facilitate dynamic compression,, also increases slightly with age due to natural deterioration of lung tissue

Respiratory Physiology (6 decks)

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