resp part2 Flashcards

1
Q

lung compliance

A

Shows “distensibility” of lungs and chest wall
Is inversely related to elastance, which depends on the amount of elastic tissue
Is inversely related to stiffness

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2
Q

In middle range of pressure describe compliance

A

compliance is greatest and the lungs are most distensible

middle range is most compliant

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3
Q

At high expanding pressure describe compliance

A

compliance is lowest, the lungs are least distensible , and the curve flattens.

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4
Q

Compliance=

A

change in volume of lung (change ofV) for each unit change in pressure (change ofP). Pressure refers to transpulmonary pressure

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5
Q

Changes in lung compliance

In patient with emphysema

A

lung compliance is increased and the tendency of the lung to collapse is decreased. Therefore , at original FRC, the tendency of 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’s chest becomes barrel-shaped, reflecting higher volume.

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6
Q

pneumothorax

A

If air is introduced into the pleural space (pneumothorax), the intrapleural pressure becomes equal to atmospheric pressure. The lung will collapse (its natural tendency ) and chest wall will spring outward (its natural tendency)

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7
Q

fibrosis and lung compliance

A

In a patient with fibrosis , lung compliance is decreased and the tendency of lungs to collapse is increased. Therefore, at the original FRC, 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.

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8
Q

Pleural space is a relative

A

vacuum

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9
Q

The negative force always required to keep the lungs open.

A

-5cmH2O

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10
Q

Alveolar Pressure

A

It is the air pressure in alveoli
Normally = 0 cmH2O
decrease in inspiration, increase in expiration
During normal quiet inspiration ,it is the major driving force for air flow into the lungs

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11
Q

Transpulmonary Pressure =?

A

= Alveolar Pressure minus Pleural Pressure

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12
Q

Transpulmonary Pressure -neonates first breath

A

First breath of neonates generates transpulmonary pressure of 40 to 80 cmH2O 

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13
Q

Pleural Pressures

Resting ?
Inspiration?

A

Resting -5 cm H20

Inspiration -8 cm H20

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14
Q

Alveolar Pressure at:
Resting
Inspiration
Expiration

A

Alveolar Pressure at:
Resting 0 cm H20
Inspiration -1 cm H20
Expiration +1 cm H20

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15
Q

Alveolar pressure equals atmospheric pressure and is said to be ?

A

Alveolar pressure equals atmospheric pressure and is said to be zero (no flow)

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16
Q

Pleural pressure ?

A

is always negative

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17
Q

what is lung volume

A

FRC

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18
Q

how do we measure pleural pressure?

A

by a balloon catheter in the esophagus

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19
Q

how does the negative pressure get created in the intrapleural space

A

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

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20
Q

as lung volume increases alveolar pressure becomes what?

A

alveolar pressure decreases to less than atmospheric pressure (becomes negative -1cmh20

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21
Q

during inspiration pleural pressures becomes??

A

more negative than it was at rest -5- -8cmh20

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22
Q

during expiration alveolar pressure

A

alveolar pressure becomes greater becomes positive +1cmh20 than atm pressure.

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23
Q

Intrapleural pressure returns to its resting value during

A

Intrapleural pressure returns to its resting value during a normal (passive ) expiration. However, during a forced expiration, intrapleural pressure actually becomes positive. This positive intrapleural pressure compresses the airways and makes expiration more difficult

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24
Q

SURFACTANT is secreted by?

A

type II alveolar cells

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25
surfactant is composed of?
phospholipid, proteins, and ca++
26
how does surfactant work
Lines the alveoli, act as surface tension ‘reducer’ by 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
27
surfactant Synthesis starts week
24 week of gestation | Almost always present at week 35
28
how do we check to see if surfactant is present for fetal lung maturity.
Lecithin-to- Sphingomyelin (L/S) ratio of > 2:1 in amniotic fluid is indicative of fetal lung maturity
29
Neonatal respiratory distress syndrome: S&S?
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  V/Q
30
neonatal treatment for prematurity
Treatment Maternal steroid shots before birth. This speeds up formation of surfactant in the fetus. Artificial surfactant to infants by inhalation
31
airflow equation
q=change p/R q=airflow change p= pressure gradient r= air way resistant
32
resistance to flow
R= resistance = viscosity of the inspired gas l = length of airway r = radius of airway Notice the powerful inverse fourth-power relationship between resistance and size ( radius) of airways. 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 R= 8nl/PIEr4
33
Contraction and relaxation of bronchial smooth muscles | Parasympathetic stimulation
irritants, slow reacting substance of anaphylaxis-A (asthma) constrict the airways,  the radius and  the resistance to airflow
34
Contraction and relaxation of bronchial smooth muscles | Sympathetic stimulation
and sympathetic agonist dilate the airways , increase radius and decrease resistance to airflow via 2 receptor
35
Low lung volumes
are associated with less radial traction and increased airway resistance
36
High lung volumes
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.
37
Site of airway resistance
The major site of airway resistance in the medium-sized bronchi. The smallest airways would seems to offer the highest resistance, but they do not, because of their parallel arrangement.
38
“Work” of Breathing
During normal quiet condition, respiratory muscles ‘work’ only during inspiration and NOT during expiration.
39
Work of inspiration: | 3 things
Compliance work Tissue Resistance Work Airway Resistance Work
40
Tidal Volume:
Tidal Volume: is the volume inspired or expired with each normal breath
41
Inspiratory Reserve Volume
Inspiratory Reserve Volume: is the volume that can be inspired over and above the tidal volume. It is used during exercise
42
Expiratory Reserve Volume
Expiratory Reserve Volume: is the volume that can be expired after the expiration of tidal volume
43
Residual Volume
is the volume that remains in the lungs after a maximum expiration. It cannot be measured by spirometry
44
Helium Dilution Method.
Pulmonary Volumes are recorded by Spirometer except Residual Volume which is measured by Helium Dilution Method.
45
Vital Capacity (VC)
Is the sum of TV, IRV and ERV.
46
How is pulmonary capacity determined
Pulmonary Capacity is combination of two or more pulmonary volumes
47
Inspiratory Capacity
TV+IRV
48
Functional Residual Capacity
ERV+ Residual Volume | Volume remaining in the lungs after a tidal volume is expired
49
Total Lung Capacity
Is the sum of all four volumes. It is the volume in lungs after a maximum inspiration “Vital Capacity is everything but the residual volume”
50
Functional Residual Capacity - FRC
Volume of air remaining in lung after normal tidal exhalation Acts as RESERVIOR for O2 during airways obstruction or apnea Prevents large SWINGS of PO2 by acting as buffer
51
FRC=?
ERV+RV
52
FRC is reduced by
Supine position Obesity Pregnancy Anesthesia
53
decreased from what 4 things will decrease FRC and predispose a patient to what?
Therefore, all these things predispose to HYPOXEMIA
54
Implication: preoxygenation/denitorgenation does what to FRC?
PREOXYGENATION / DENITORGENATION 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.
55
FRC Increases by:
PEEP , CPAP | Increase airway resistant – asthma
56
Forced vital capacity (FVC)
Is the volume of air that can be forcibly expired as hard and as rapid possible, after taking maximum inspiration
57
FORCED EXPIRATORY VOLUME IN 1ST SECOND ( FEV1)
Is the volume of air that can be expired in the first second of a forced maximal expiration as hard and as rapid possible Is normally 80% of the forced vital capacity (FVC) FEV1/FVC ratio = 4/5= 0.80 (80%) FEV1 is low in both obstructive and restrictive diseases (trouble is blowing air out
58
obstructive lung diseases what happens in FVC and FEV
In obstructive lung diseases such as asthma and COPD, FEV1 is reduced more than FVC so that FEV1/FVC is decreased (hallmark)
59
restrictive lung disease what happens to FVC and FEV
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
60
Forced expiratory flow (FEF 25-75) or Midmaximal expiratory flow
Is best of accessing small airway disease
61
Obstructive Lung Disease ‘increase resistance to flow’
Obstruction of air flow, resulting in air trapping in the lung. Emptying impaired-high RV , low VC FEV1/FVC ratio decreases (hallmark)
62
4 Types of Obstructive lung disease :
Bronchiectasis Chronic Bronchitis Emphysema Asthma
63
Restrictive Lung Disease ‘stiff lungs, decrease expansion’
Restricted lung expansion causes decreased all lung volumes ( VC and TLC), PFTs: FEV1/FVC ratio >80%
64
Poor breathing mechanics (extrapulmonary)
Poor muscular effort: polio, M gravis | Poor apparatus: scoliosis
65
Poor lung expansion (pulmonary)
Lungs are restricted; cannot expand Defective alveolar filling: pneumonia, ARDS, pulmonary edema Interstitial fibrosis: causes increased recoil (decrease 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
66
slide 47
slide 48
67
PCWP
is an indirect measure of ‘left atrial pressure’ | normally 10mmhg
68
how do we measure right sided heart catheterization
Measure by Right Sided Heart Catheterization (SWAN-GANZ)
69
PWP
is used in CHF to study pressure changes in left atrium decrease BP decrease PCWP = Hypovolemic shock, give fluid decrease BP increase PCWP = Failing heart, give inotrops
70
Right atrium pressure
<5mmhg
71
Right ventricle pressure
<25/<5mmhg
72
Left atrium pressure
< 12mmhg
73
Left ventricle pressure
<150/10mmhg
74
Pulmonary trunk pressure
<25/10mmhg
75
Aorta pressure
<150/90mmhg
76
PCWP pressure
<12mmhg
77
What is PCWP measuring?
PCWP (mmHg) is a good approximation of left atrial pressure. Measured with Swan
78
Pulmonary artery Pressures
``` Systolic= 25 mmHg Diastolic= 8 mmHg Mean= 15 mmHg Capillary= 7 mmHg ```
79
Pressure and Cardiac output in the pulmonary circulation | Pressure
Are much lower in pulmonary circulation (15mmHg) than in the systemic circulation (100mmHg)
80
Pressure and Cardiac output in the pulmonary circulation | Compliance
Is much higher
81
Pressure and Cardiac output in the pulmonary circulation | Resistance
is much lower
82
Pressure and Cardiac output in the pulmonary circulation | Cardiac output of the right ventricle
Is pulmonary blood flow | Is equal to CO of the left ventricle
83
In lungs, alveolar hypoxia causes
In lungs, alveolar hypoxia causes vasoconstriction
84
This diverts blood away from poorly ventilated, hypoxic regions towards well-ventilated regions of lung leads to?
decrease shunting of blood (protective)
85
Fetal pulmonary vascular resistance is very high due to hypoxic vasoconstriction
decrease blood flow
86
Oxygenation with first breath decreases pulmonary vascular resistance
increase blood flow
87
Global hypoxia (breathing in thin air at high altitude)
vasoconstriction of entire lungs leads to pulmonary HTN leads to RVF
88
Pulmonary vascular resistance (PVR)
PVR= P pul artery-P l atrium/C0 x 80
89
SVR
SVR= MAP-CVP/CO x 80 normal value 900-1200