Respiratory Resistance and Airway Obstruction Flashcards

1
Q

Elastance

A

Elastance describes the recoil of the lung and chest wall.

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2
Q

Elastance and Compliance

A
  • Elastance = change in pressure /change in volume
  • Compliance = change in volume/ changein pressure

compliance = 1/ Elastance

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3
Q

Resistance

A

Describes the energy lost due to the friction and turbulence (acceleration due to spinning) of gas when there is gas flow

When there is no flow, there is no pressure differenc due to resistance.

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4
Q

Resistance and Ohm’s Law

A

RESISTANCE (cmH2O / L/sec) = ∆PRESSURE (cmH2O) / FLOW (L/sec)

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5
Q

Pulmonary Resistance has…

A

…tissue and airway resistance components (90% of RRS)

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6
Q

Chest Wall…

A

…is a tissue resistance (10% of RRS)

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7
Q

RRS

A

RRS = RL + RCW

  • RRS = Resistance of the respiratory system
  • RL = Resistance of the lung (pulmonary resistance)
  • RCW = Resistance of the tissues of the chest wall
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8
Q

Pulmonary Resistance

A

RL = Raw + Rtis

  • RL = Resistance of the lung
  • Raw = Resistance of the airway (80% of total lung resistance)
  • Rtis = Resistance of the tissues of the lung (20% of total lung resistance)
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9
Q

Laminar Flow

A

Laminar flow occurs in small airways with low gas velocities and is characterized by a streamlined pattern with a parabolic velocity profile.

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10
Q

Ohm’s Law for Laminar Flow

A

The “Ohm’s law” equation for laminar flow is called Poiseuille’s Law and can be written: FLOW = π ∆P r4 / 8 n l

  • π = pi (3.141516)
  • ∆P = driving pressure
  • r = radius of the tube
  • n = viscosity
  • l = length of the tube
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11
Q

Turbulent Flow

A

Turbulent flow occurs in larger, central airways with high gas velocities and at branches in airways. It is characterized by complete disorganization of the streamlines with resultant eddies and swirls.

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12
Q

Turbulence ocurs due to 2 main effects in the airway.

A
  1. Every irregulaity in the airway such as branching of one airway into two causes turbulent airflow.
  2. Velocity plays a large role in determining the occurence and magnitude of turbulent flow.
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13
Q

The two major determinants of gas velocity are […] and […].

A

The two major determinants of gas velocity are the flow (how much gas is moving per second) and the cross-sectional area of the airway (how narrow an airway does the gas have to squeeze through).

Velocity (cm/sec) = Flow (cm3 /Sec)/Cross-Sectional Area (cm2 )

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14
Q

The narrowest cross-sectional area in the airway occurs in the […]. Since all flow goes through this central airway, this is where the […] velocities are seen.

A

The narrowest cross-sectional area in the airway occurs in the subglottic space (below the vocal cords). Since all flow goes through this central airway, this is where the highest velocities are seen.

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15
Q

The greatest total cross-sectional area in the airway is found in the […]. Gas velocity is very […] in these airways and actually approaches zero so that diffusion due to Brownian motion is a relevant cause of gas movement.

A

The greatest total cross-sectional area in the airway is found in the summed areas of the large number of small peripheral airways. Gas velocity is very low in these airways and actually approaches zero so that diffusion due to Brownian motion is a relevant cause of gas movement.

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16
Q

Reynold’s Number

A

Predicts when turbulent flow will predominate. Flow tends to be laminar up until Re > 2000:

Re = 2 r v d n

  • r = tube radius
  • v = average velocity of the gas
  • d = density of the gas
  • n = viscosity of the gas

This equation can be confusing because it appears that a larger radius airway will have a higher Re when one would think it should have lower velocities and thus a lower Re. The equation actually says that for any given velocity of gas, the higher the radius then the higher the Re. Basically, it is easier for the laminar flow to break up into turbulence when the gas flowing in the center of a large airway is far from the friction of the airway wall.

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17
Q

Large central airways with […] gas velocities have […] Re and […] flow predominates.

A

Large central airways with high gas velocities have high Re and turbulent flow predominates.

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18
Q

Small peripheral airways with […] velocities have […] Re and […] flow predominates

A

Small peripheral airways with low velocities have low Re and laminar flow predominates

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19
Q

Turbulent Flow and No Ohm’s Law

A

Under turbulent flow conditions the flow generated is proportional to the square root of the pressure and Ohms law does not describe the pressure/flow relationship:

FLOW ≈ (PRESSURE / CONSTANT)0.5

This is usually written as the pressure generated by turbulent flow:

PRESSURE = K2 (FLOW)2

  • K2 = turbulent flow constant.
  • The constant, K2, varies directly with gas density. Thus the less dense the gas the less energy is lost in turbulence and the lower the pressure drop. That is why we use helium in patients with high airway resistance due to turbulent flow (croup, tracheal tumor)
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20
Q

Transitional Flow

A

In most airways, flow is transitional between turbulent and laminar flow (i.e. it contains flow that is both laminar and turbulent).

21
Q

Transitional Flow and Roher’s Equation

A

PRESSURE = K1 (FLOW) + K2 (FLOW)2

  • K1 = laminar flow constant
  • K2 = turbulent flow constant
22
Q

Dividing Rohrer’s Equation by Flow

A

RESISTANCE = PRESSURE / FLOW

PRESSURE / FLOW = [K1 (FLOW) + K2 (FLOW)2] / FLOW

RESISTANCE = K1 + K2 (FLOW)

•Thus, there is a constant component to resistance (K1) describing laminar flow. This causes the relationship between pressure and flow to be linear and follows Ohm’s law. Resistance also varies with another constant (K2) that is multiplied by flow. This causes the relationship between pressure and flow to vary with flow and is seen in turbulent conditions. At any given time both constants are operating and the above formula best describes this transitional flow regime.

23
Q

Raw

A

Raw is distributed through the airway such that much of the total Raw is in the upper and large central airways. If you do the math then the airway resistance is 80% of the Lung which is 90% of the respiratory system and 80% x 90% = 72% of the respiratory system resistance is due to airway resistance with 28% being due to tissue resistance.

24
Q

Distribution of Airway Resistance

A
  1. Upper Airway Resistance

2, Lower Airway Resistance

25
Q

Upper Airway Resistance

A
  • Mouth, pharynx, and larynx contribute 20-30% of total at rest.
  • The upper airway makes up a significant part of all the airway resistance because of the turbulence in flow through the nose, the pharynx, and the larynx.
  • With high flow rates (exercise) the upper airway resistance may rise to 50% of total resistance. This is due to turbulence in the oral/nasal airways and central conducting airways raising the resistance as flows increase. (Try breathing through only your nose while vigorously exercising and you will appreciate why they are called nasal turbinates.)
26
Q

Lower Airway Resistance

A
  1. Because of large increase in total cross sectional area as the bronchial tree branches there is a dramatic drop of resistance after the 4th to 5thgeneration.
    - It is important to remember that although any given peripheral small airway is quite small, there are a very large number of them and there summed cross-sectional area is quite large. The flow tends to be more laminar in these airways due to the low velocities and thus uses less energy. This is analogous to the cardiovascular system in which the capillaries make up a minimal resistance even though any given capillary is very, very narrow. Their total cross-sectional area is phenomenal. Thus, we have evolved tremendous reserve in our small airways.
  2. Of the total resistance, the small, peripheral airways make up only20%.
    - The small airways have been called the ‘silent zone’ of the lung because they can be significantly damaged before the total resistance to breathing goes up. The table below shows that doubling central resistance results in an 80% increase in the total. In contrast, doubling peripheral resistance only results in a 20% increase in the total.
27
Q

Peripheral Airways

A

Airways < 2 mm in diameter

28
Q

Absolute Resistance

A

Children > Adults

29
Q

Specific Resistance

A

Children = Adults

30
Q

Specific Resistance

A

Specific Resistance = Resistance x Lung Volume

31
Q

Control of Airway Diameter

A
  1. Passive Effects
  2. Active Effects
32
Q

Passive Effects

A

Passive changes in airway diameter are those that occur without the constriction of the airway smooth muscle.

Lung Volume Effects:

  1. Growth
  2. Inspiration

Other:

  1. Conductance
  2. Diseases
33
Q

Growth

A

Larger lungs have larger airways; e.g. an adult has much larger airways than a child and hence lower absolute resistance.

•This is analogous to the situation with compliance where larger lungs are more compliant. Thus, adults use about the same pressures to overcome airway resistance that children do. Similarly, large species have large airways that are proportional to their lung volume.

34
Q

Inspiration

A

When we take a deep breath the airways stretch increasing their diameter. Thus, higher lung volumes are associated with lower resistances as well.

We can correct for this by calculating

SPECIFIC RESISTANCE = RESISTANCE x LUNG VOLUME

•This is very similar to the concept of specific compliance. One difficulty, however, is that within an inspiration from residual volume to total lung capacity the relationship between lung volume and airway resistance is hyperbolic and not linear. For this reason, physiologists have developed the term, conductance.

35
Q

Conductance

A

CONDUCTANCE is the inverse of resistance.

Conductance has units of Flow per Pressure; i.e. (L/sec) / cmH2O. It is a description of how conductive the airways are. It tells us how much flow we will get for a given driving pressure. It is sort of analogous to compliance where compliance tells us how much volume change we will get for a change in pressure.

CONDUCTANCE = 1 / RESISTANCE

36
Q

Diseases

A

Diseases like emphysema that decrease lung recoil also decrease the recoil pulling the airways open, and thus, cause an increase in airway resistance.

37
Q

Emphysema

A
  • Emphysema is a lung disease that destroys the alveolar walls. There are less healthy alveoli and the lung recoil is decreased. Thus, the airways will be at a lower diameter for any lung volume because they do not have the alveoli holding them open.
  • This is particularly important near FRC. Patients with emphysema may have complete airway closure at relatively high lung volumes. Thus, they cannot exhale to a normal RV.
  • This ‘gas trapping’ causes an increase in the RV and an increase in the RV/TLC ratio. Assuming TLC is only minimally increased, then if RV increases, VC will decrease.
  • Patients with emphysema get ‘barrel chests’ and despite apparently large lungs, they can only exhale small volumes because of the airway closure and gas trapping.
38
Q

Active Effects

A

Active change in airway diameter is commonly due to smooth muscle contraction (bronchoconstriction). Further, if the airways are inflamed then mucus production and mucosal edema will also actively narrow the airways.

  1. Stimuli
  2. Chemicals released from mast cells.
39
Q

Stimuli

A

Airway smooth muscle tone responds with constriction to many stimuli.

40
Q

Neural Stimuli: […] causes contraction and […] causes relaxation.

A

Cholinergic causes contraction and Adrenergic (Beta2) causes relaxation.

41
Q

Neurohumoral Stimuli: […] causes contraction and […] causes relaxation.

A

Acetylchloine causes contraction and Norepinephrine causes relaxation.

42
Q

Chemical Stimuli: […] cause contraction, [..] cause relaxation.

A

Histamine and Leukotrienes cause contraction, Prostaglandin 2 causes relaxation.

43
Q

Physical Stimuli: […] cause contraction.

A

Smoke, cold air, SO2 cause contraction.

44
Q

Chemicals

A

Chemicals released from mast cells in response to an allergic reaction or infection (histamines, bradykinins, leukotrienes) also cause airway mucosal edema and mucus production.

•We commonly use albuterol (a selective Beta2 receptor agonist) to acutely bronchodilate patients with asthma attacks. However, asthma is an inflammatory disease and we need to use inhaled corticosteroids or leukotriene receptor antagonists to reduce the inflammation. The bronchodilators really only treat asthma symptoms where the anti-inflammatories treat the basic inflammatory disease.

45
Q

A good approach to any obstructed tube in the body is to realize that there are only three ways in which it can be obstructed:

A
  1. In the lumen.
  2. Due to alterations in the wall.
  3. From compression by structures outside the wall or failure to hold the wall open.
46
Q

In the Lumen

A

a. Foreign body (peanuts, sunflower seeds, toys, pen tops etc)
b. Mucus or mucopurulent material
c. Blood clots in pulmonary hemorrhage
d. Tumor

47
Q

Alterations in the Wall

A

a. Inflammation (asthma, bronchiolitis, chronic bronchitis, cystic fibrosis, acute bronchitis, aspiration of stomach content/acid, inhalation of chemicals/gases, crouplaryngotracheobronchitis)
b. Bronchospasm (asthma, aspiration of stomach content/acid, inhalation of chemicals/gases)
c. Vascular congestion (cardiac asthma)
d. Tracheobronchomalacia (floppy airways with loss or failure to develop cartilaginous structures)
e. Tumor
f. Cysts (particularly the upper airway)
g. Vocal cord paralysis
h. Fibrosis/scarring (post lung transplant/airway surgery, sub-glottic stenosis after airway trauma from intubation)

48
Q

Compression

A

a. Lymph nodes at the hilum (tumor such as lymphoma, infection such as coccidiodomycosis or tuberculosis)
b. Mediastinal mass (reduplication of the esophagus, tumors, bronchogeniccysts)
c. Vascular sling or ring (aberrant subclavian, pulmonary sling, double aortic arch, right sided aortic arch)
d. Cardiac enlargement (especially left lower lobe)
e. Neck mass (infection, cystic hygroma, tumor)
f. Failure of elastic recoil to maintain patency of the small airways (emphysema)