Respiratory Mechanics I week 5

Question 1

What is Boyle’s Gas Law? What circumstance does it apply to?

Answer 1

PV/T=constant which can be simplified to below equation bc T is constant:

P₁V₁=P₂V₂

Applies to gasses in an enclosed container

Question 2

Why do the parietal and visceral pleura move together during breathing?

Answer 2

Pleural fluid btwn the two pleuras allows them to move together. If the membranes are pulled apart, the presure in the pleural fluid rapidly decreases and pulls the pleura back together again. This is similar to a suction cup on a mirro. When you attempt to pull the suction cup away, the pressure in the air btwn the suction cup and the mirror decreases and pulls the two surfaces together again.

Question 3

How is transmural pressure across the chest wall calculated?

Answer 3

Question 4

pneumothorax

pleural effusion

empyema

Answer 4

pneumothorax: air enters potential space btwn pleura

pleural effusion: fluid enters potential space

empyema: fluid enters potential space in severe infection

Question 5

What is the resting volume of the chest wall? The lungs?

What is the volume of the lungs and chest wall at FRC? What are the alveolar and pleural pressures at FRC and why?

What happens to the pleural pressure in pneumothorax?

Answer 5

The resting volume of the chest wall is 4500 ml. The resting volume of the lungs is 800 ml.

At FRC, the volume of the lungs and chest wall is 2500 ml. This is less than the resting volume of the chest wall and greater than that of the lungs. At FRC (no muscular effort), the inward pull of the lungs exactly balances the outward pull of the chest wall. This creates a negative pleural pressure. Note that at FRC, alveolar pressure (P_A) and atmospheric pressure (P_B) are both 0 so there is no gradient for air to flow. Pleural pressure is less than alveolar pressure at this point and this is true at all times!

The pleura is punctured and this allows for air to flow into this space (bc pleural pressure is negative and air flows from high to low pressure). The lungs collapse due to equlibration of pleural cavity pressure and atmospheric pressure. The individual is unable to expand the chest wall to breathe because the pleura are no longer moving together.

Question 6

Discuss the muscles that contract as well as the pressure and volume changes that occur during inspiration and expiration.

Answer 6

Inspiration:

The most important muscle in inspiration is the diaphragm. Contraction of this dome-shaped muscle forces the abdominal contents downward and forward. The external intercostal muscles upon contraction assist the diaphragm by pulling the ribs upward and outward away from the spinal column. This is known as the “bucket-handle” movement of the ribs, causing the lateral dimension of the thoracic cavity to increase.

Increasing the volume of the thoracic cavity causes the pressure inside the thoracic cavity to decrease. This is explained by Boyle’s Gas Law [Eq. 1: P × V = constant]. If you increase the volume of a closed container, the pressure inside it will decrease. Therefore, when the inspiratory muscles contract, pressure in the lung, P_A, (alveolar pressure) becomes lower than atmospheric pressure (P_B). Air then rushes down its pressure gradient into the lungs, due to negative pressure.
Bottom line: The lungs are inflated by negative pressure through active contraction of muscles. Contract respiratory muscles –> ‘ V of thoracic cavity –> “ PA –> PA < PB –> air flows into lungs.

Expiration:

In contrast, expiration (air leaving the lungs) is usually passive. Relaxing the inspiratory muscles allows the elastic recoil of the lungs to reduce the volume of the thoracic cavity passively. When ventilation is greatly increased, expiration becomes an active process. Then the muscles of expiration (3=internal intercostals) come into play. They pull the ribs downward and inward, opposing the actions of the external intercostals, thereby decreasing the volume of the thoracic cavity.

Bottom line: expiration is passive.

Question 7

What 4 forces must respiratory muscles overcome?

Answer 7

1. Elastic recoil of the lungs
2. Elastic recoil of the chest wall
3. Surface tension
4. Airway resistance

Question 8

What is compliance?

Answer 8

C= change in volume/change in pressure

The volume measured per unit change in pressure. Compliance is the slope of the pressure volume curve.

Note that in the low compliance portion of the curve, the same work is done to increase pressure but a small change in volume is observed.

Question 9

In the attached figure, explain why compliance begins to plateau at high pressures.

Explain the reasons for the compliance curves observed in COPD (obstructive disease) and fibrosis (restrictive disease).

Answer 9

At moderate volumes, near FRC, lung compliance is high. The lung stretchest easily. The lungs are still “unfolding” and can easily increase in volume. At hight lung volumes, the curve is flatter.The tissues have already unfolded and are now being stretched. The compliance of the lung is low at this point. This concept can be thought of as blowing up an air mattress. As you add air (and increase pressure), it is initially easy to blow up the mattress. As pressure increases, it becomes increasingly harder to increase volume. This is also true for the lungs. The alveoli can only expand so much.

In obstructive diseases such as COPD, compliance is high becasue there is a loss of alveolar tissue. This makes it easy to increase volume with changes in pressure. In restrictive diseases such as fibrosis, the tissue resists expansion and compliance decreases. With maximal inspiratory effort, the pt’s lung volume does not increase as much as a pt with no lung disease.

Question 10

What is the principal feature of pulmonary fibrosis? Discuss the cellular changes that occur.

Answer 10

The principle feature of diffuse interstitial pulmonary fibrosis is thickening of the interstitium of the alveolar wall. There is infiltration with lymphocytes and plasma cells, followed by fibroblasts, which lay down thick collagen bundles. The alveolar capillary in the attached figure is surrounded by collagen.

Question 11

What is the definition of COPD? What is emphysema characterized by?

Answer 11

“COPD is an ill-defined term that is often applied to patients who have emphysema, chronic bronchitis, or a mixture of the two” (West, 1998). We sometimes use the terms “COPD” and “emphysema” interchangeably. The American Thoracic Society defines COPD as “the presence of airflow obstruction due to chronic bronchitis or emphysema…” Note that chronic bronchitis is NOT the same as emphysema, although they are both categorized as COPD. Emphysema is characterized anatomically by enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.

Question 12

What effect does alveolar edema have on lung compliance?

What effect does increased pulmonary venous pressure have on lung compliance.

Answer 12

1. Edema makes it harder to inflate alveoli-reduces compliance
2. Increased pulmonary venous pressure causes the lung to become engorged with blood which decreases compliance.

Question 13

We have already established that at all physiologically attainable lung volumes, pleural pressure is less than alveolar pressure. Explain why.

Answer 13

Due to elastic recoil of both lungs (inward) and chest wall (outwards), the pleural pressure P_pl is usually negative. At all physiologically attainable lung volumes, the elastic recoil of the lung pulls inward, Ppl < P_A. This is always true.

Why is Ppl always less than PA? No matter what volume the lungs occupy, their elastic recoil is inward {in a living person without pneumothorax}. Regardless of the pressure inside the lungs (P_A), their elastic recoil will pull toward smaller volumes. This recoil will compress the air inside the lungs, thus increasing its pressure above whatever Ppl is.

Question 14

Describe the attached figure. Be sure to explain the resting volumes of the chest wall and lungs as well as what occurs at FRC.

Answer 14

The chest wall is relaxed at 80 percent of TLC. At any smaller volume, the chest wall pulls out. To get it down to a smaller volume, one must compress it (which is hard because compliance decreases with decreasing volume). In other words, the chest wall pulls out over most physiological range of volumes.

The lung is completely at rest at minimal volume. This volume is less than 1 L and is also less than residual volume. This means it takes positive pressure to inflate the lungs over the entire range of volumes that are possible in a human. The elastic recoil of lungs is always pulling inwards. This is the reason alveolar pressure is always greater than pleural pressure.

At very high volumes near 100% of VC, the elastic recoil of both the chest wall and the lungs pulls inwards, so the respiratory muscles have to work hard to inflate the lungs to TLC.

It is important to note that the lung and chest wall curves never come together. This means that at all volumes, the luns is always pulling away from the chest wall and pleural pressure is always lower than alveolar pressure.

Note that the compliance of the system is less than that of the lung or chest wall alone.

At FRC, the elastic recoils of the chest wall and lungs are equal and opposite. Compliance is the greatest at this point. Compliance is highest in middle range (curve is flatter at top and bottom ends). This is the point at which we start breathing- where compliance is highest. this minimizes the amount of work it takes to breathe.

Question 15

What is surface tension? Why is there surface tension in the lung? What effect does surface tension have on alveoli?

Answer 15

Surface tension is a force that acts in the plane of an interface btwn two phases (air/water, oil//water). In the lung, surface tension exists bc of the attractive forces btwn liquid molecules lining the alveoli. Surface tension acts to minimize the surface area of the interfaces. Thus surface tension tends to collapse alveoli.

Bubbles experiment: bubbles form in air because this reduces the the surface area that is in contact with air.

Question 16

Explain this graph. (open dots are inflation, closed dots are deflation). Discuss why inflation and deflation of the lungs follow different curves.

Answer 16

Surface tension increases the work to inflate and deflate the lungs.

Saline inflation: lungs are inflated with saline easily bc this procedure eliminates the air-water interface and therefor surface tension.

Air inflation: lungs inflated with air require 3-4x more work that saline inflation bc surface tension resists expansion of the lungs.

Note that inflation and deflation of the lungs with air follow different curves and this is called hysteresis. Hysteresis is partly due to pulmonary surfactant that lines the air/water interface.

Question 17

atelectasis

Answer 17

collapse of alveoli

Question 18

The tendency of alveoli to collapse is determined by 2 properties, as determined by LaPlace’s Law. What is LaPlace’s Law? What are these 2 properties?

Answer 18

We know that surface tension makes it harder to expand collapsed lungs and that surface tension tends to cause alveolar collapse (atelectasis). LaPlace’s law describes surface tension as a function of radius:

P = 2T/r

P= pressure in a thin-walled sphere, T=tension, r=radius of the sphere

The tendency of alveoli to collapse is determined by 2 properties:

1. size of the alveoli (r): as an alveolus is inflated, the pressure required to overcome surface tension decreases at higher volumes. larger alveoli remain open bc they have large radii –> small collapsing P. smaller alveoli collapse mroe easily because they have small radii –> large collapsing P. in the balloon experiment, air went from the smaller to the larger balloon because there was higher pressure in the smaller balloon (smaller radius)
2. surface tension (T)

Question 19

Surface tension makes it harder to reinflate a collapsed alveolus. Describe why using the attached graph.

Answer 19

Pressure due to surface tension is maximal at small volumes (small r). When an alveolus is collapsed, you have to exert large pressure to open it due to surface tension. It takes 10x more pressure to open alveolus as it does to open it when breathing air in and out.

B is the critical opening pressure which we know occurs due to surface tension (T). Once get past this, alveoli begin to operate at normal pressures.

The elastic recoil of an alveolus is stronger/exerts more pressure at higher volumes. This is the behavior one expects intuitively. At very large volumes, the compliance decreases - it becomes very hard to inflate further. Counterintuitively, surface tension exerts the greatest effect at lower volumes. When the effects of surface tension are combined with elastic recoil, there is a non-monotonic relationship (dashed curve). To inflate a collapsed alveolus requires a large increase in pressure to get beyond the ‘hump’ or “critical opening pressure” that is due mainly to surface tension at low volumes. This is like blowing up a balloon-it is hard to get it started, but then becomes much easier.

Question 20

What 2 factors is atelectasis opposed by?

Answer 20

1. Interconnectedness of lung tissues: when one alveolus begins to collapse, it must pull on surrounding alveoli. The surrounding alveoli pull back because they have elastic recoil.
2. Pulmonary surfactant

Question 21

What is the primary component of pulmonary surfactant? How does it work to reduce surface tension?

What are two other benefits of pulmonary surfactant?

What alveolar cells produce and secrete pulmonary surfactant?

Answer 21

The primary component of pulmonary surfactant is dipalmitoylphosphatidylcholine (DPPC). It is an amiphilic organic compound that forms a monolayer at the alveolar subphase (thin layer of fluid that lines the alveolus). Surfactant reduces surface tension exerted on the alveolus by opposing the intermolecular attractive forces btwn the liquid molecules that line the alveoli. The hydrophobic side of the compound is oriented toward the air and the hydrophilic side is oriented toward water. Pulmonary surfactant increases stability of the alveoli and reduces the work of breathing.

Surfactant is secreted and stored in lamellar bodies of Type II alveolar epithelial cells.

Question 22

Where are type II cells physically located in alveoli?

Answer 22

Question 23

When do Type II cells appear in gestation? When do they begin to secrete pulmonary surfactant?

What is the leading cause of death of premature infants? Why?

Answer 23

• Type II cells first appear at ~6 months gestation.
• They start to produce surfactant at 7-8 months.
• Premature infants are at risk of inadequate surfactant production. Infants’ lungs exibit atelectasis which causes hypoxemia.
• Leading cause of death in premature infants is IRDS (Infant Respiratory Distress Syndrome) which is caused by inadequate surfactant.
• BTW, this shows that surface tension plays an important role in the lung!

Question 24

In what situations is surfactant reduced in?

In what situations in surfactant increased in?

Answer 24

Situations exist in which abnormal levels of surfactant are present.
• Surfactant is reduced in:
o Oxygen related abnormalities
ƒ Hypoxia (low oxygen), anoxia (extreme hypoxia)
ƒ O2 toxicity (too much O2)
o Acidosis
o Atelectasis (localized lung collapse)
o IRDS (Infant Respiratory Distress Syndrome)
o ARDS (Adult Respiratory Distress Syndrome)
o Pulmonary embolus-(prevents “food” getting to type II cells, decreasing production)
o Shock
o Drowning, lavage (same mechanism) - lavage liquid exhibits surfactant properties (lavage is therapeutic rinsing of an organ or part)
o Smoking
o abdominal surgery

• Surfactant is increased as a result of:
o Secretagogues (E-adrenergic agonists, experimental agents)
o Mechanical stretch (yawn)
o Birth (due to hormonal effects)