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Physiology Winter 2012 > Physiology Respiratory Sukoawsi 1 > Flashcards

Physiology Respiratory Sukoawsi 1 Flashcards

1
Q

What are the muscle used for rested inspiration? for forced?

A

Rested- Diaphragm and External Interncostals

Forced- Accessory muscles in teh neck, thorax, and abdominal cavities

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2
Q

What are the muscles used in rested expriration? Foreced?

A

rested- None, passive elastic recoil

Forced: Internal Intercostals, neck, and abdominal muscles

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3
Q

Definition of elastic

A

ability to spring back and resist deformation

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4
Q

Definition of Compliance

A

ability to yeild and be nonresistant (distensibility)

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5
Q

Definition of recoil

A

Ability to rebound or spring back

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6
Q

relation of recoil and compliance

A

The higher the compliance, the lower the recoil (mush ball)- Obstructive disease, emphysema,

The lower the compliance, the higher the recoil (golf ball), Restrictive disease

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7
Q

Examples of Obstructive lung diseases

A

Increased Resistance
Asthma
Bronchitis
Emphysema

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8
Q

Examples of Restrictive lung disease

A

Decreased compliance (higher recoil)
Diffuse Interstitial Fibrosis
Pulmonary Edema

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9
Q

Type A vs Type B COPD

A

Type A- symptoms of Emphysema (man culprit is cigarette smoking, alpha 1 antitrypsin deficiency)

Type B- symptoms of chronic bronchitis

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10
Q

What are clinical features of emphysema

A

HypoxemiaL milkd (PaO2 = ~80)

(A-a) PO2 = 10-15 (normal is

Hypercapnia: None

Acid-base problems: None as long as PaCO2 is normal

Tissue oxygenation: Normal

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11
Q

What is a “pink puffer”

A

Type A COPD

PaO2 - slighly reduced (~80)
PaCO2- normal

Acts like dead space
enough O2 in blood (pink)
needs to breathe more to maintain normal O2 and PaCO2 (puffer)

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12
Q

Chronic Bronchitis

A

Type B COPD
Narrowing of airwasy caused by hypersecretion of mucous and thickening of walls of respiratory tree

Chief culprit is smoking

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13
Q

Clinical Features of Type B COPD (chronic bronchitis)

A

Peristent, productive cough

Hypoxemia : Significatn to severe (PaO2= 40-70)

A-a PO2 ( 20-50)

Hypercapnia: Moderate (PaCo2=~50)

Acid-Base Disorder: mild to moderate acidosis

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14
Q

What is a blue-bloater

A

Decreased arteriolar PO2

Increased PCO2

May show signs of fluid retention with dependent edema

Acts like shunt

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15
Q

What potentiates Hypoxic Vasoconstriction

A

Decreased blood pH

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16
Q

What is the primary diorder in pulmonary blood flow

A

High V/Q ratio

theoretically, hypoxia shouldn’t develop,but often does

Diffusion impairment in areas with high flows

Pulmonary shunts develop

  • Opnieng AV anastomoses
  • blood though areas of hemorrhagic atelectasis
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17
Q

Clinical of Pulonary emoblism

A

PaCO2: Normal or mild hypocapnia

Acid-base disorder: None or mile alkalosis

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18
Q

What is Absorption Atelectasis

A

Occluded airway ,
Nitrogen is poorly soluble in plasma, and thus remains in high concentration in alveolar gas. If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis. This is limited by the sluggish diffusion of Nitrogen. If nitrogen is replaced by another gas, that is if it is actively “washed out” of the lung by either breathing high concentrations of oxygen, or combining oxygen with more soluble nitrous oxide in anesthesia, the process of absorption atelectasis is accelerated. It is important to realize that alveoli in dependent regions, with low V/Q ratios, are particularly vulnerable to collapse.

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19
Q

How do you treat Absorption Atelectasis

A

Problem can be minimezed by regularly hyperinflating lungs during anesthesia (a sigh) or by PEEP (positive and expiratory pressure)

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20
Q

What are static characteristics of respiration

A

Compliance and Recoil

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21
Q

What is equation of compliance

A

Change in volumepressure

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22
Q

What are two factors of recoil

A
  1. Recoil due to surface tension (major part of recoil force of lung)
    - reduced by surfactant but not elimated (80%)
  2. Recoil due to tissue elastic elements (Elastin, collagen, etc) 20%
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23
Q

What are the dynamic characterisitcs of respiration

A
  1. Resistance to airflow due to airway resistance (AWR) - 80%
  2. Resistance to airflow due to tissue frictional or viscour resistance (20%)
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24
Q

What detemrines airlow/ AWR

A
  1. flow rate
  2. flow pattern (diameter of airways and branching)
  3. Density
  4. Viscosity
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25
Q

What determines Flow rate?

A
  1. recoil pressure (determined by lung volume and compliance)
  2. AWR
26
Q

What are factors that increase compliance (easier to inflate)

A

Emphysema

Asthma

Age

Asthma

27
Q

Decreased Compliance (harder to inflate)

A

Fibrosis

Edema

High pulmonary venous pressure

Lack of surfactant

Increased recoil

28
Q

Definition of Ventilation

A

Movement of flow of air form outside through air passages to terminal respiratory units (alveoli)

29
Q

What determines the amt of ventilation (

A
  1. Distensibility of lungs (compliance)
  2. Factors that govern air movement
    - Muscular effort required to enlarge thorax and lungs, thereby generating a pressure differnce to drive air flow

AWR impedes air flow

30
Q

What par tof lung receives greatest ventilation? Why?

A

Bottom of lung receives the greates ventialtion when one spires from FRC

  1. diferent IP P vertically, with top alveoli experiecning a more negative pressure holding them open before inspritation . Top alveoli has less reserve to enlarge
  2. Weight of lung compresses lower alveoli. With inspriationa nd lowering dipahram, elastic componens of lung reduces this effect
  3. Sum of all factors places lower lugn ona more favorable segment of the compliance curve at FRC
31
Q

What is surface tension

A

at he air-liquid interphase inside the lung; tends to collapse the lung to a smaller volume

32
Q

What is LaPlace’s Law

A

Pressure (inside) = (2xST) / Radius

33
Q

What is responsible fo tissue elastic recoil?

A

Geometric arrangement of elastin and collagen fibers

COnsider effects on compliance of lung fibrosis or elastin changes seen with aging

34
Q

Are alveoli bigger at base or apex of lung? WHy

A

At apex (top) they are bigger. The alveoli are smaller at the base b/c of gravity

The Bottom of the lung has a higher negative pressure (more positive) than top of lung

35
Q

Where d you meaures P-V bevavior in a pateint

A

in teh esophagus!

Place small balloon in esophagus and measure pressure

36
Q

What is the normal compliance of the lung

A

1000/5 = 200 ml/cm H20

37
Q

What needs to happen to intrapleural pressure in ordr for lungs to expand?

A

Intrapleural pressure needs to decerase so lungs can expand

38
Q

Which alveoli are more compliant, larger or smaller alveoli?

A

Smaller alveoli at the bottom! Using LaPlace’s Law , where Presssure is lower with smaller radius (smaller alveoli)

39
Q

What is responsible for elasticity/ compliance of lung?

A
  1. geometry of fibers

2. Surface tension

40
Q

In a closed thorax, what is responsible for negative IP pressure at FRC

A

elastic recoil of chest wall outward

Lung recoil inweard

41
Q

What happens to IP Pressure duing forced expiration? Forced inspriaton?

A

Forced expiration- IP more positive at FRC

Forced inspiration- IP more negative at FRC

42
Q

What is the units of measurement used for ST

A

Dynes/cm

43
Q

What do pressure-volue curves describe

A

lugn compliance at different lung volumes and show HYSTERESIS

44
Q

What does difference in compliance depnd on

A

level in lung at any one lung volume at FRC (after normal expiration)

45
Q

what happens to small airways athe base of lung at !0% Vital Capcity or less?

At RV (after forced expiration)

A

small airways at the base of lung CLOSE b/c of the POSITIV PRESSSURE (intraplural), trapping air in teh distal alveoli

This CLOSING VOLUME increases with age and disease

46
Q

What is the PRIMARY factor that causes static recoil of lungs?

A

Surface Tension

47
Q

What kind of cells produce surfactant

A

Type II alveolar Cells

48
Q

What does Surfactant do to surface tension? What molecule?

A

Reduces ST and stabilizes lung alveoli

Surfactant contains DPP , detegent synthesized by FFAs and other

These cause HYSTERESIS seen in compliance curves

49
Q

What does impedence of blood flow to a region do to surfactant synthesis

A

It prevents surfactant synthesis

50
Q

What are the functions of Surfactant (3)

A
  1. Increases Compliance (makes it easier to inflate lungs)
  2. Surfacatant keeps lung dry/reduces tendency of alveolar edema (reduces forces that “pull” fluid out of capillary”
  3. Increases Alveolar stability (less likely that smaller alveoli empty into larger alveoli)
51
Q

How does surfactant reduce tendency of alveolar edema

A

B/c without surfactant, alveoli with lining layer –> alveolus contracts due to high ST Pressure –> reduces pressure around capillaries of alvelar wall –> edema moves out

Interdependence also increases alveolar stability and eeps pressure low around large BV and airways as sthe lung epands. This ist eh site of early edema

52
Q

Loss of surfacatnat results in (3)

A
  1. Stiff lungs (elevated surface tenson)
  2. Areas of atelectasis
    3 Alveoli filled iwth fluid
53
Q

How does surfactatn keep lungs dry? Whawt happens without surfactant?

A

Lack of surfactant increases ST of the alveolus, drawing the alveolar walls inward (recoil)

This causes greater negative interstitial space, overcoming colloid osmotic pressure (COP) of blood, resulting in more fluid filtering out of capillaries into interstiial space and into alveoli

54
Q

What happens to surfactant in premature inants

A

Lack of surfactatn resuts in infant respiratory distress syndrome

Similar condition exists in adutls nad is called Adult Respiratory Distress Syndrom (ARDS)

55
Q

What are factors that increase compliance (easier to inflate)

A

Emphysema

Age

Asthma

56
Q

Decreased Compliance (harder to inflate)

A

Fibrosis

Edema

High pulmonary venous pressure

Lack of surfactant

57
Q

Definition of Ventilation

A

Movement of flow of air form outside through air passages to terminal respiratory units (alveoli)

58
Q

What determines the amt of ventilation (

A
  1. Distensibility of lungs (compliance)
  2. Factors that govern air movement
    - Muscular effort required to enlarge thorax and lungs, thereby generating a pressure differnce to drive air flow

AWR impedes air flow

59
Q

What par tof lung receives greatest ventilation at FRC? Why?

A

Bottom of lung receives the greates ventialtion when one spires from FRC

  1. diferent IP P vertically, with top alveoli experiecning a more negative pressure holding them open before inspritation . Top alveoli has less reserve to enlarge
  2. Weight of lung compresses lower alveoli. With inspriationa nd lowering dipahram, elastic componens of lung reduces this effect
  3. Sum of all factors places lower lugn ona more favorable segment of the compliance curve at FRC
60
Q

Which lung gets more ventialtion at RV? Why?

A

Upper lungs receive greateest venitaltion intiially!

Small airways (Respiratory bronchioles) in teh bottom of lung close as one exhales and approacehs RV

Restuls in air trapping in lower lunga nd greater precetnatge of expired air coming from uper protions of lung at eh end of a forced expiration to RV

With age, lugns more compliant, closure of small aiways occurs at higher lung ovluems (even at FRC)

61
Q

Chest wall and lungs- relaxation curve

A

Chest wall and lungs each attempt to recoil to their lowest free energy equilibrium position

62
Q

What is chest walla and lungs at FRC

A

outwards at FRC for chest wall

Inward at FRC for lungs

FRC is determined when the two reocil forces balane each other

Physiology Winter 2012 (10 decks)

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