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Resp I > Michels Phys > Flashcards

Michels Phys Flashcards

1
Q

Tidal volume

A

(VT): amount of air that enter or leaves the lung in a single cycle ~500 ml (normal breath)

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2
Q

Functional residual capacity

A

(FRC): volume of gas that remains in the lung at then end of a passive expiration (equilibrium point for lung)

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3
Q

Inspiratory capacity

A

(IC): maximal volume of air that can be inhaled from FRC

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4
Q

Inspiratory reserve volume

A

(IRV): volume of air that can be inhaled after a normal inspiration

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5
Q

Expiratory reserve volume

A

(ERV): volume that can be exhaled after a normal expiration

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6
Q

Residual volume

A

(RV): volume of air that remains in the lungs after maximal expiration (cannot be measured by spirometry)

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7
Q

Vital capacity

A

(VC): maximal volume that can be expired after maximal inspiration

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8
Q

Total lung capacity

A

(TLC): amount of air in the lung after maximal inspiration

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9
Q

PIgas

A

Fgas(Patm-Ph20)

For PIO2=150mmHg

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10
Q

Method to determine FRC

A

Helium Dilution
- helium allowed to diffuse into lungs once valve is open
Body Plethysmography
- airtight box, subject inside,close mouthpiece valve at FRC
- subject tries to inhale against closed valve, changing lung by changing volume and box by - changing volume and lowering/raising pressure in lung box

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11
Q

Anatomical dead space

A

volume of conducting airways (about 150ml)

- define conducting airways

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12
Q

Alveolar dead space

A

alveoli containing air but not participating in gas exchange

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13
Q

Physiologic dead space

A

total dead space for the system (1/3 total)

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14
Q

alveolar ventilation

A

room air delivered to the respiratory zone per minute
VA = (VT – VD)f

VT = tidal volume		VD = dead space
f   = respiratory rate
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15
Q

total ventilation is

A

tidal volume x respiratory frequency

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16
Q

How can alveolar ventilation be increased

A

by increasing tidal volume or respiratory volume

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17
Q

Where is expired CO2 derived from

A

all expired CO2 derives from the alveolar space and none from the dead space.

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18
Q

What is the relationship between CO2 concentration and alveolar ventilation

A

CO2 concentration is inversely related to alveolar ventilation

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19
Q

Where is ventilation highest

A

Ventilation is highest at the base of the lung due to gravitational effects.

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20
Q

What factors influence diffusion rate

A

Pressure gradient
Thickness or diffusion distance
Area of barrier
Diffusion constant

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21
Q

Perfusion limited

A

: amount of gas transported is limited by blood flow (partial pressure gradient is not maintained)

O2 is perfusion limited

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22
Q

Diffusion limited

A

: amount of gas that is transported depends on the diffusion process (diffusion will continue as long as the partial pressure gradient is maintained

CO is diffusion limited

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23
Q

Normal uptake of O2 in the Pulmonary Capillary

A

PVO2 = 40 mm Hg

Under normal conditions, the PaO2 nearly equals the PAO2 by the time the RBC is 1/3 through the capillary bed

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24
Q

Abnormal uptake of O2 in Pulmonary Capillary

A

Decreasing the PIO2 will result in increased time to equilibrate PAO2 and PaO2 (diffusion equilibrium)

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25
Q

CO2 Transfer

A

The diffusion for CO2 is approximately 20X higher than O2.
However, the concentration gradient for CO2 is lower than O2 and the reaction of CO2 with blood is complex.
Generally, hypercapnia is rare but there is a potential for elevated levels of CO2 due to thickening of the blood-gas barrier.

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26
Q

Diffusion Capacity

A

Diffusing capacity of the lung includes the distance that a gas travels across membranes into the blood and the time it takes to react with hemoglobin
Diffusing capacity is measured by the uptake of CO in the lung measured in mL•min-1•mm Hg-1 (assays lung structural features)
Normal diffusing capacity for CO is 25 mL•min-1•mm Hg-1

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27
Q

Pathological Changes that Reduce DL

A 
Diffuse interstitial pulmonary fibrosis
- Thickening of the interstitium, alveolar wall and destruction of capillaries
Chronic obstructive pulmonary disease
- Loss of lung elastic tissue and pulmonary capillaries (decreases surface area and total Hb content)
Loss of functional lung tissue
- Decreases surface area and Hb content
Anemia
- Fall in Hb content
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28
Q

Diffusion of gas across a barrier

A

is proportional to the area of the barrier and the partial pressure difference, and inversely proportional to the thickness

29
Q

Muscles of Inspiration

A

Diaphragm
External intercostals
Accessory muscles of inspiration include the scalenus and sternomastoids and the pectoralis

30
Q

Muscles of Expiration

A

Passive during rest

Forced expiration can involve the internal intercostals and abdominal muscles

31
Q

Transmural pressure

A

Transmural pressure is the pressure measured from inside to out.

32
Q

Movement of Lung and Chest wall as result of pneumothrax

A

When intrapleural pressure is equal to atmospheric:

lung wants to recoil and chest wall wants to expand

33
Q

Lung compliance

A

Relates to transmural pressure change required to achieve a given change in volume.

34
Q

How is compliance determined

A

Compliance is determined by elastic recoil and surface tension.

  • elastic recoil of the lung is determined by elastic tissue (elastin and collagen - geometry of meshwork conveys elasticity)
  • surface tension is reduced by surfactants
35
Q

What changes compliance

A

Obstructive (problems with exhalation) increases compliance.

Restrictive (problems with inhalation, ie fibrosis) reduces compliance.

36
Q

What are the functions of surfactants

A
  1. Lowers surface tension
  2. Increases alveolar stability
  3. Keeps alveoli dry
37
Q

What happens in a diseased state where surfactant is absent

A
  • Compliance is reduced
  • Collapsed region of lungs
  • Wet regions
38
Q

Characteristic of lung apex during ventilation

A

Intrapleural pressure more negative
Greater transmural pressure gradient
Alveoli larger, less compliant
Less ventilation

39
Q

Characteristics of lung base during ventilation

A

Intrapleural pressure less negative
Smaller transmural pressure gradient
Alveoli smaller, more compliant
More ventilation

40
Q

Driving pressure

A

Is the pressure change from one end of the tube to the other: P = flow x resistance
For the same flow, pressure of laminar flow > turbulent

41
Q

Laminar flow

A

resistance is constant irrespective of flow

42
Q

Turbulent flow

A

resistance increases w/flow rate

43
Q

Velocity of gas in the lung

A

Increase airway in parallel with increase cross sectional area as move down tree
- resistance drops
Increasing velocity as move up tree to maintain flow
- turbulent pattern

44
Q

Types of resistance in lung

A

Airway and Tissue
Tissue resistance must be overcome for lung to inflate
Over 85% of total resistance is airway

45
Q

Factors that determine cross-sectional area of airways

A
  1. Lung volume - holds airways open
  2. Lung elasticity - contributes to tethering effect
  3. Bronchial smooth muscle tone
46
Q

Airway resistance and lung volume

A

As lung volume increases, resistance decreases.

Patients with obstructive disease breathe at higher lung volumes to decrease airway resistance

47
Q

Chemical factors that Affect Airway Resistance

A

All act by affecting smooth muscle tone of bronchioles (medium sized airways). Smooth muscle tone is the greatest determinant of resistance of the medium-sized airways.

48
Q

Bronchoconstrictors

A

Cause constriction of SM.
Parasymp nervous system (acetylcholine and methacholine).
histamine
irritants (i.e. cigarette smoke)

49
Q

Bronchodilators

A

Cause relaxation of SM.
Symp nervous system (NE via B2 receptors).
Agonsists for B2 receptors (i.e. isoproteronol, albuterol).
Increases PCO2 in bronchioles

50
Q

Transmural pressure during quiet respiration

A

transmural pressure remains positive during exhalation

51
Q

Transmural pressure during forced expiration

A

Engagement of expiratory respiratory muscles raises intrapleural pressure which is often positive

  • If intrapleural pressure exceeds airway pressure the transmural pressure becomes negative and the airway will collapse unless supported by SM or cart
  • Where ad if airway collapse during a forced expiration depends on the loss of pressure along the airway.
    • Pressure lost as resistance is overcome
    • Pressure is lost as velocity increases and flow becomes turbulent
52
Q

Dynamic Airway Compression Upon Forced Expiration

A

Loss of pressure occurs as gas moves from the alveolus to the mouth

  • Increase resistance
  • Increase velocity
  • Transition from laminar to turbulent flow
53
Q

Elastic Forces and Airway Compression

A

Quiet resp: driving force is diff btwn alveolar and mouth pressure.
Airway compression: driving force is diff btwn alveolar pressure and pleural pressure.
Elastic recoil pressure is the diff btwn alveolar and pleural pressure.

54
Q

FEV/FVC

A

Normally around 80%
Obstructive (increased airflow resistance): drops as FEV decreases
Restrictive (increase elastic resistance): increases as both FEV and FVC decrease disproportionately

55
Q

Pulmonary pressure

A

Can be altered by
1. Recruitment
2. Distension
Recall pulmonary arteries contain relatively little smooth muscle- ensures arteries are highly compliant

56
Q

Behavior of Alveolar and Extra-alveolar Vessels

A

Pulmonary capillaries- exposed to alveolar pressures and have the propensity to collapse when alveolar pressure exceeds capillary pressure
Extra-alveolar vessels- Include pulmonary arteries and veins; diameter increases when lung tissue expands
Do contain some smooth muscle- tone can be effected by pharmacologic agents
Vasodilation of pulmonary capillaries- acetylcholine, isoproterenol, NO, prostacyclins
Vasoconstriction of pulmonary capillaires- serotonin, histamine, norepinephrine

57
Q

Pulmonary Vascular Resistance (PRV)

A

Pulmonary Vascular Resistance- normally very low

  1. Recruitment and distension of pulmonary capillaries can lower the pulmonary vascular resistance
    • Exercise
    • Increased pressure
    • gravity
  2. PVR Increases at high and low lung volumes
  3. Increases with alveolar hypoxia due to hypoxic pulmonary vasoconstriction
58
Q

Chemicals and PRV

A

nitric oxide (NO) and prostacyclins cause vasodilation

Viagra: a selective inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5)

59
Q

Capillary recruitment and distension

A

Recruit in parallel
Distension increases capillary diameter
Both recruitment and distension usually occur at the same time

60
Q

Changes in pulmonary resistance with changes in lung volume

A

Resistance increases at high lung volumes due to increased alveolar pressure, and stretching of the capillary wall.
Diameter increases with expanding lung tissue and decreases at low lung volume.

61
Q

Hypoxic Vasoconstriction

A

Note it is alveolar PO2 that controls hypoxic vasoconstriction.
An example of hypoxic vasoconstriction is travel to high altitude where the PIO2 is less.

62
Q

Mechanical influences that increase PVR

A 
Increased lung volume (above FRC)
- lengthening and compression of pulmonary caps
Decreasing lung volume
- compression and loss of traction of extra-alveolar
  vessels
Increased interstitial pressure
- compression of vessels
Increased blood viscosity
- increased resistance
63
Q

Mechanical influences that decrease PVR

A

Increased pulmonary artery pressure, left atrial pressure, pulmonary blood volume, cardiac output
- recruitment and distension
Gravity
- recruitment and distension due to hydrostatic effects

64
Q

Positive-Pressure Ventilation

A 
Impact on PVR: Increases PVR
Increased alveolar pressure
- compression of alveolar vessels
Positive intrapleural pressure
- compression of extra-alveolar vessels; decreased in pulmonary blood flow
65
Q

Endogenous Chemicals and Effects on Vascular SM (Extra-alveolar vessels)

A

Vasoconstrictors→ serotonin, histamine, norepinephrine
- Increases vascular resistance
Vasodilators→ acetylcholine
- Decreases vascular resistance

66
Q

Causes of pulmonary edema

A

Increased cap hydrostatic pressure
- MI, mitral stenosis, fluid overload, pulmonary veno-
occlusive disease
Increased cap permeability
- Inhaled or circulating toxins,sepsis, radiation, O2
toxicity; ARDS
Reduced lymph drainage
- Increased central venous pressure, lymphangitis
carcinoma
Decreased interstitial pressure
- Rapid removal of pleural effusion or pneumothorax,
hyperinflation
Decreased colloid osmotic pressure
- Overtransfusion, hypoalbuminemia, renal disease
Uncertain etiology
- high altitude, neurogenic, overinflation, heroin

67
Q

Control of circulation

A
  • Hypoxic vasoconstriction limits pulmonary blood flow with PIO2 is reduced (hypoxic vasoconstriction limits pulmonary blood flow in fetuses which is quickly reversed upon delivery)
  • Nitric oxide (NO) is an endothelium-derived factor that relaxes pulmonary vessels and capillaries
    Endothelins are endothelium-derived factors that constrict pulmonary vessels and capillaries.
  • Sympathetic stimulation (ex. Norepinephrine) acts as a vasoconstrictor.
68
Q

Metabolic functions of Pulmonary Circulation

A
  • Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) found on the surface of capillary endothelial cells
  • Bradykinin is inactivated by ACE in the lung
    Serotonin is inactivated by uptake and storage in the lung
  • Prostaglandins E1, E2, and F2α are inactivated in the lung
  • Norepinephrine is partly taken up by the lung
  • Other substances such as epinephrine, prostaglandins A1 and A2, angiotensin II, and vasopressin are not metabolized by the lung

Resp I (2 decks)

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