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Flashcards in Respiratory 2 Deck (109)
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1
Q

what is pleural space?

A

a relative vacuum

2
Q

what is pleural pressure

A

the negative pressure in the pleural space because lung recoil inwards and chest wall recoils outwards

3
Q

when are the inward and outward forces equal in the pleural space

A

at FRC

4
Q

transpulmonary pressure=

A

alveolar pressure - pleural pressure

5
Q

how much transpulmonary pressure does the first breath of a neonate generate?

A

40-80cmH20

6
Q

Alveolar Pressure

A

is the air pressure in alveoli, its normally = 0cmH20

7
Q

what is the major driving force for air flow into the lungs? during normal quiet inspiration

A

alveolar pressure

8
Q

Pleural Pressures resting=

A

resting -5cmH20

9
Q

Pleural Pressures inspriation=

A

-8cmH20

10
Q

alveolar pressure resting=

A

0cmH20

11
Q

alveolar pressure inspiration=

A

-1cmH20

12
Q

alveolar pressure expiration=

A

+1cmH20

13
Q

at rest what is alveolar pressure equal to? (before inspiration begins)

A

alveolar pressure equal atmospheric pressure and is said to be zero (no flow)

14
Q

how to we measure pleural pressure

A

by a balloon catheter in the esophagus

15
Q

what is FRC

A

functional residual capacity- is lung volume at the end of passive expiration

16
Q

why is pleural pressure negative?

A

the elastic recoil of lungs trying to collapse and the chest wall trying to expand, creates a negative pressure in the intrapleural space.

17
Q

breathing cycle during inspiration

A

inspiratory muscles contract causing the volume of the thorax to increase.

as lung volume increases, alveolar pressure decreases to less than atmospheric pressure (becomes more negative -1cmH20)

the pressure gradient between the atmospheric and alveoli now causes air to flow into the lungs, air flow will continue until the pressure gradient dissipates.

18
Q

during inspiration what happens to pleural pressure

A

it becomes more negative than it was at rest (-5 to -8 cmH20)

19
Q

what is FRC at peak of inspiration

A

lungs volume is the FRC plus one TV

20
Q

during expiration what happens to alveolar pressure

A

alveolar pressure becomes greater (becomes positive +1cmH20) than atmospheric pressure

21
Q

during expiration

A

intra pleural pressure returns to its resting value during a normal passive expiration.

22
Q

what happens during forced expiration

A

intra pleural pressure actually becomes positive. this positive intrapleural pressure compresses the airways and makes expiration more difficult.

23
Q

during expiration and COPD patients. What do we teach them?

A

airway resistance is increased, patient learn to expire slowly with “PURSED LIPS” to prevent the airway collapse that may occur with forced expiration.

24
Q

during expiration what happens to FRC

A

lung volume returns to FRC

25
Q

what does lung compliance show?

A

it shows “distensibility” of lungs and chest wall

26
Q

what is lung compliance inversely related to?

2 things

A

it is inversely related to elastane which depends on the amount of elastic tissue

is inversely related to stiffness

27
Q

lung compliance is the slope of the ?

A

pressure volume curve

28
Q

compliance=

A

change in volume of lung for each unit change in pressure. pressure refers to transpulmonary pressure

29
Q

at high expanding pressure what is compliance?

A

at high expanding pressure, compliance is lowest, the lungs are least distensible, and the curve flattens

30
Q

in middle range of pressure what is compliance

A

compliance is greatest and the lungs are most distensible

31
Q

At FRC what is the collapsing force of the lungs and expanding force of the chest wall considered?

A

equal and opposite. it is at equilibrium

32
Q

as a result of the two opposing forces of the collapsing lungs and expanding chest what is intrapleural pressure

A

Negative (sub atmospheric)

33
Q

Name the condition of air being introduced into the pleural space

A

pneumothorax

34
Q

pneumothorax-

A

intra pleural pressure becomes equal to atmospheric pressure - the lung will collapse (its natural tendency) and chest wall will spring outward (its natural tendency)

35
Q

changes in lung compliance with emphysema

A

lung compliance is increased and the tendency of the lung to collapse is decreased.

36
Q

why do patients with emphysema becomes barrel-shaped.

A

the tendency of the lungs to collapse is less than the tendency of chest wall to expand. the lung-chest wall system will seek a new HIGHER FRC so that the two opposing forces can be balanced the patient then becomes barrel shaped- the patient has increase elastance due to less rubber bands-

37
Q

Fibrosis and lung compliance?

A

lung compliance is decreased and the tendency of lungs to collapse is increased

38
Q

in fibrosis what happens to FRC

A

the tendency of the lungs to collapse is greater than the tendency of the chest wall to expand. the lung chest wall system will seek a new lower FRC so that the two opposing forces can be balanced.

39
Q

name the 4 causes of decreased Lung compliance

A

high expanding pressures
increase Pulmonary venous pressure
fibrosis (deposition of collagen)
lack of surfactant.

40
Q

name the two causes of increase lung compliance

A

emphysema (destruction of elastic fibers)

old age

41
Q

tell me about collapsing pressure and small alveoli

A

have high collapsing pressure and are more difficult to keep open In the absence of surfactant the small alveoli have a tendency to collapse (atelectasis)

42
Q

tell me about collapsing pressure and larger alveoli

A

have low collapsing pressure and are easy to keep open

43
Q

p=?

A

2T/r

p= collapsing pressure on alveolus (or pressure required to keep alveolus open)
T=surface tension
R=radius of alveolus

44
Q

what type of cells secrete surfactant

A

type 2 alveolar cells

45
Q

what is surfactant composed of?

A

composed of phospholipid, proteins, and calcium

46
Q

What week gestation does synthesis of surfactant start at?

when is it almost always present?

A

24 weeks

week 35

47
Q

what is the mechanism of action for surfactant

A

lines the alveoli- surface tension reducer- disrupting the intermolecular forces(hydrogen bond) between the water molecules of liquid-act like detergent.
this reduction in surface tension prevents small alveoli from collapsing and increases compliance, decrease work of inspiration allowing the lungs to inflate much more easily

48
Q

neonatal respiratory distress syndrome

A

Occurs in premature infants because of lack of surfactant. The infant shows atelectasis (lung collapse), difficulty reinflatting the lungs( as a result of decreased compliance) and hypoxemia because of decreased V/Q

49
Q

Treatment for Neonatal respiratory distress syndrome

A

Treatment
Maternal steroid shots before birth. This speeds up formation of surfactant in the fetus.
Artificial surfactant to infants by inhalation

50
Q

slide 27 ground glass appearance of the lung

A

These findings correlate clinically with moderate to severe retractions and oxygen dependence in premature infants with RDS.

51
Q

Q=
Change P=
R=

A

air flow
pressure gradient
airway resistance

52
Q

Q=

A

change P/R

53
Q

R=
n=
l=
r=

A

resistance
viscosity of the inspired gas
length of airway
radius of airway

54
Q

Notice the powerful inverse fourth-power relationship between resistance and size ( radius) of airways.

A

If airway radius decreases by a factor of 4, then resistance will increase by a factor of 256(44) and air flow will decrease by a factor of 256

55
Q

Contraction and relaxation of bronchial smooth muscles

Parasympathetic stimulation

A

irritants, slow reacting substance of anaphylaxis-A (asthma) constrict the airways, decrease the radius and increase the resistance to airflow

56
Q

Contraction and relaxation of bronchial smooth muscles

Sympathetic stimulation

A

and sympathetic agonist dilate the airways , increase radius and decrease resistance to airflow via B2 receptor

57
Q

Low lung volumes

A

are associated with less radial traction and increased airway resistance

58
Q

High lung volumes

A

are associated with greater radial traction and decrease airway resistance. In asthma, pt “learn” to breath at higher lung volumes to offset the high airway resistance associated with their disease.

59
Q

Site of airway resistance

where is the major site of airway resistance

A

the medium sized bronchi

60
Q

do the smallest airways offer the highest resistance???

A

no they do not because of their parrallel arrangement

61
Q

when do respiratory muscles work?

A

during normal quiet condition, respiratory muscles work only during inspiration and not during expiration

62
Q

Tidal Volume:

A

is the volume inspired or expired with each normal breath

63
Q

Inspiratory Reserve Volume

A

is the volume that can be inspired over and above the tidal volume. It is used during exercise

64
Q

Expiratory Reserve Volume

A

is the volume that can be expired after the expiration of tidal volume

65
Q

what type of pulmonary volume is seen with exercise

A

inspiratory reserve volume

66
Q

Residual Volume

A

is the volume that remains in the lungs after a maximum expiration. It cannot be measured by spirometry

67
Q

pulmonary volumes are recorded by

A

spirometer

68
Q

residual volume is measured by

A

helium dilution method

69
Q
Vital Capacity (VC) 
is the sum of?
A

TV, IRV, and ERV

everything but residual volume

70
Q

Inspiratory Capacity=

A

TV+IRV

71
Q

Functional Residual Capacity

A

ERV+ Residual Volume
Volume remaining in the lungs after a tidal volume is expired
Acts as RESERVIOR for O2 during airways obstruction or apnea
Prevents large SWINGS of PO2 by acting as buffer

72
Q

Total Lung Capacity

A

Is the sum of all four volumes.

It is the volume in lungs after a maximum inspiration

73
Q

what reduces FRC (4)

A

Supine position
Obesity
Pregnancy
Anesthesia

74
Q

Implication: PREOXYGENATION / DENITORGENATION

A

before anesthetic induction is very important providing reservoir of O2, as this “fills” the FRC with 100% O2, allowing more time (upto10 min.) for airways manipulation, breath holding episodes etc.

75
Q

FRC Increases by:

A

PEEP , CPAP

Increase airway resistant – asthma

76
Q

Forced vital capacity (FVC)

tell me about the ratio?

A

Is the volume of air that can be forcibly expired as hard and as rapid possible, after taking maximum inspiration

Is normally 80% of the forced vital capacity (FVC)
FEV1/FVC ratio = 4/5= 0.80 (80%)

77
Q

FORCED EXPIRATORY VOLUME IN 1ST SECOND ( FEV1)

A

Is the volume of air that can be expired in the first second of a forced maximal expiration as hard and as rapid possible

78
Q

what two conditions are FEV1 low in?

A

both obstructive and restrictive diseases (trouble is blowing air out )

79
Q

what do you find for FEV1 and FVC with obstructive lung diseases?

A

In obstructive lung diseases such as asthma and COPD, FEV1 is reduced more than FVC so that FEV1/FVC is decreased (hallmark)

80
Q

what do you find for FEV1/FVC for restrictive lung diseases?

A

In restrictive lung disease such as pulmonary fibrosis, pneumothorax, scoliosis, myasthenia gravis or ALS, both FEV1 and FVC are reduced and FEV1/FVC is either normal or is increased

81
Q

Forced expiratory flow (FEF 25-75) or Midmaximal expiratory flow
what does it access?

A

Is best of accessing small airway disease

82
Q

obstructive lung disease

what is the FEV1/FVC ratio?

A

increases resistance to flow. resulting in air trapping in the lung.

emptying impaired leads to high RV low VC

FEV1/FVC ratio decreases (hallmark sign)

83
Q

4 types of obstructive lung disease

A

bronchiectasis
chronic bronchitis
emphysema
asthma

84
Q

Restricted lung disease- LUNG VOLUMES?

A

causes decreased all lung volumes. decrease vital capacity decrease TLC. PFT, FEV1/FVC ratio >80%

85
Q

restrictive lung disease poor breathing mechanics

A

extra pulmonary

Poor muscular effort: polio, M gravis
Poor apparatus: scoliosis

86
Q

restrictive lung disease Poor lung expansion

A

pulmonary

Lungs are restricted; cannot expand
Defective alveolar filling: pneumonia, ARDS, pulmonary edema
Interstitial fibrosis: causes increased recoil (compliance), thereby limiting alveolar expansion. Complications include cor pulmonale. Can be seen in diffuse interstitial pulmonary fibrosis and bleomycin toxicity. Symptoms include gradual progressive dyspnea and cough

87
Q

PCWP

A

is an indirect measure of ‘left atrial pressure’
Normally ~ 10mmHg
Measure by Right Sided Heart Catheterization

88
Q

when is pwp used?

A

CHF to study pressure changes in left atrium

89
Q

hypovolemic shock

A

decrease wedge decreased BP

90
Q

failing heart

A

decreased BP increased Wedge

91
Q

right atrium pressure

A

<5

92
Q

right ventricle pressure

A

<25/<5

93
Q

left atrium pressure

A

<12

94
Q

left ventricle pressure

A

<150/10

95
Q

pulmonary trunk pressure

A

<25/10

96
Q

aorta pressure

A

<150/90

97
Q

wedge pressure

A

<12

98
Q

Pressure pulmonary circulation

A

Are much lower in pulmonary circulation (15mmHg) than in the systemic circulation (100mmHg)

99
Q

compliance pulmonary circulation

A

is much higher

100
Q

resistance pulmonary circulation

A

is much lower

101
Q

cardiac output of the right ventricle

A

Is pulmonary blood flow

Is equal to CO of the left ventricle

102
Q

what does alveolar hypoxia cause

A

vasoconstriction

103
Q

explain vasoconstriction during hypoxia

A

This diverts blood away from poorly ventilated, hypoxic regions towards well-ventilated regions of lung leads to decrease shunting of blood (protective)

104
Q

SVR=

A

MAP-CVP/Cardiac output x80

105
Q

normal svr

A

900-1200

106
Q

fetal pulmonary vascular resistance is very high due to hypoxic vasoconstriction which leads to?

A

decreased blood flow

107
Q

oxygenation with first breath decreases pulmonary vascular resistance

A

increases blood flow

108
Q

global hypoxia breathing in thin air at high altitude leads to vasoconstriction of entire lungs leads to

A

pulmonary HTN leads to RVF

109
Q

PVR=

A

Pul Art-Pul L atrium/ cardiac outputx80