Why Do The Pleural Pressure Go Negative

  • April 2020
  • PDF

This document was uploaded by user and they confirmed that they have the permission to share it. If you are author or own the copyright of this book, please report to us by using this DMCA report form. Report DMCA


Overview

Download & View Why Do The Pleural Pressure Go Negative as PDF for free.

More details

  • Words: 2,373
  • Pages: 5
Coop 2010 Physiology - lecture 53 March 12, 2007 9-10am Lecturer: Dr. Forster Writer: Jena Kern Respiratory Structures Dr. Forster started the lecture with a brief review of the anatomical structures involved in respiration. He mentioned that the muscles of inspiration are the diaphragm and the external intercostals, and the muscles of expiration are the internal intercostals and abdominal muscles. These muscles function as a respiratory pump, which creates a change in pressure and allows air to flow. He also mentioned that CNS apnea is where you won’t breath and obstructive apnea is where you can’t breath. 15-20% of Americans have sleep disordered breathing. Respiratory Mechanics 1. How do you define respiratory mechanics? It is a relationship between volume, pressure and flow. 3 main pressures that deal with mechanics: these are important 1. Pleural pressure—pressure between chest wall and lungs (virtual space) 2. Alveolar pressure—pressure within alveoli, is pressure that causes flow (less than atmospheric during inspiration, greater than atmospheric during expiration) 3. Transpulmonary pressure (aka recoil pressure) —difference between alveolar and pleural pressures. PTP=PA-Ppl. Reflects pressure required to overcome lung elasticity since the lungs want to totally collapse. Can’t use pleural and transpulmonary pressures interchangeably, they are different as we will see later. 2. What causes air to flow between atmosphere and alveoli? Keep it simple. Air only flows if there’s a pressure difference. If alveolar pressure is less than atmospheric pressure air will flow in. If it is greater than atmospheric pressure air will flow out. 3. What causes alveolar pressure to change during inspiration? It changes because pleural pressure changes. Part of the change in pleural pressure is transferred to alveoli to give subatmospheric pressure. During eupnea pleural pressure is always slightly negative. Then during inspiration it becomes even more negative, causing alveolar pressure to become negative. 4. What causes pleural pressure to change during inspiration? Due to action of inspiratory pump muscles. The diaphragm and intercostals contract to expand the chest (space increases so pressure decreases). 5. Why during inspiration and expiration does alveolar pressure change less than the change in pleural pressure? (figure is in Guyton, p. 472)

• • •



Lung volume increases and air goes in during inspiration (tidal volume) Pleural pressure goes down during inspiration Alveolar pressure goes down during inspiration (becomes subatmospheric). It does not change as much as pleural pressure because a portion of the change in pleural pressure is needed to overcome elasticity of lungs. The lungs want to totally collapse. Transpulmonary pressure increases during inspiration.

6. What causes alveolar and pleural pressure to change during expiration? The change is passive while resting, no energy is required. The recoil of lungs creates positive alveolar pressure, which causes air to move out. Also, when you exercise, the expiratory muscles contract since need for ventilation is so great and you get a more rapid flow. 7. What is the relationship between pleural pressure and lung volume during inspiration and expiration? (see figure on p. 585) Dr. Forster spent a lot of time on this figure and stated it was very important. He said he would go over it a couple more times throughout his lectures. Pleural pressure goes negative during inspiration, while lung volume increases. So you are basically following the bottom of the oval as you inspire. At end of inspiration, you relax and then air flows out, which is the top part of the oval. Dr. Forster then gave an example of a breath half as large as the breath in the figure and the oval was about half as large (the end of the oval was about half way down the original oval). If you double the tidal volume (volume of each breath), it will get larger. At each reversal point, there is a few milliseconds where there is no air flow so alveolar pressure is zero. This pressure at that point is needed only to overcome the elastic recoil. The slope of the line connecting the beginning of the breath and the reversal point reflects the force necessary to prevent recoil or overcome the elasticity. This is the compliance given by the following equation: C=∆V/∆PTP (he stated the key thing is the transpulmonary pressure) At each reversal point, transpulmonary pressure equals the pleural pressure since flow is zero and alveolar pressure is zero. He said you can get a feel for the recoil if you take a larger than normal inspiration and then at the end of the inspiration, hold your breath, pinch your nose and relax. Your cheeks puff out because the lungs have recoiled and created a positive pressure which normally results in expiration. He then stated that recoil pressure is the same as transpulmonary pressure. Back to the figure. Everything to the left of the diagonal line is the pleural pressure change needed to overcome elasticity. The area to the right of the diagonal is alveolar pressure (pressure needed to overcome the loss of energy due to air molecules bumping against each other and the airway). We can calculate resistance by the following equation: R=∆PA/f (pressure is alveolar pressure, f is flow) (He didn’t say this this year, but its probably good to know)He said that on the test, he could give us a flow and then we would need to obtain the alveolar pressure from the figure by drawing a horizontal line from the diagonal line straight across to the corresponding point where the shaded oval ends. This number or pressure difference is

the ∆PA. We could then calculate airway resistance from these numbers. Dr. Forster said we need to know how to use this graph to obtain transpulmonary pressure to calculate compliance and alveolar pressure to calculate resistance. His main point was that we have to extract alveolar pressure and transpulmonary pressure from pleural pressure as described above. 8. What is the relationship between transpulmonary pressure and lung volume? (The figure on pg 586 is lung at three different volumes, x-axis is transpulmonary pressure or how much lungs want to recoil) RV (residual volume)--lowest volume we can reach in lungs (about 20% of lung capacity). We will still have air in lungs even after we forcefully expire and lungs will want to recoil. VC (vital capacity) is maximal amount of air we can inhale. As you move up the curve, there is a greater tendency for lungs to want to recoil. So there is a greater pressure required to maintain a larger volume. This is the compliance curve, so there is a direct relationship between PTP and VC that is not linear since it levels off at higher lung volumes. What is lung compliance? Lung compliance is the relationship between change in volume and change in transpulmonary pressure reflecting the elasticity of lung. What is difference between static and dynamic lung compliance? The difference is only in how compliance is measured. Dynamic compliance is measured during normal breathing and the two endpoints are taken to measure PTP. Static is measured by holding breath (a purposefully stop) at each reversal point. They both give the same value in normal individuals, but in disease states, static compliance is more useful. 9. How does relationship between volume and pressure differ between an air filled and a saline filled lung? We will create these graphs in lab. The major difference in curves is it takes more pressure to fill a lung with air than it does with saline. With saline, the entire elastic force is due to tissue itself. With air filled, there is an added contribution of surface tension. Surface tension is due to the liquid molecules attracting each other on an air-liquid interface, which acts as an elastic component. Here is the equation for surface tension: P=2T/r (T is surface tension of a specific liquid and r is radius of airway) This is reduced in alveoli due to surfactant production from type II pneumocytes. From the equation, one can see that the collapsing pressure created would be greater for a small alveoli than for a large alveoli. The concentration of surfactant is higher at low lung volumes than at high lung volumes so because of this, as lung volume increases, surface tension actually increases thereby minimizing small alveoli emptying into large alveoli (figure at bottom of page sort of helps to explain this). Another way to describe this relationship is as lung volume increases surface tension increases because the density of surfactant molecules on the surface becomes less. If we didn’t have surfactant we would need to work harder to overcome elasticity. The next page (p. 588) shows compliance curves for normal and diseased individuals. Emphysema patients have a very high compliance because they have lost elasticity. They have had a destruction of elastic tissue and it’s easier to fill the airways. The fibrosis curve shows low compliance because the lung is stiff due to environmental

pollutants or in respiratory distress syndrome. The lung becomes less distensible and compliance and elasticity is increased. 10. What are the elastic characteristics of the chest wall? The chest wall has elastic characteristics. The lungs want to go to zero (this is their equilibrium position). The chest wall's equilibrium position is about 60% vital capacity. To go either below or above this, you need work or energy. 11. At the end of a normal expiration (FRC), the lungs remain partially filled. Why? (Graph is pressure vs. vital capacity) The lung and the chest wall act as a unit and this graph reflects their opposing tendencies. The lines show the lung wanting to go to zero and the chest wall wanting to go to sixty. When you put the two together, the lungs want to suck the chest in, the chest wall wants to pull the lungs out. So in a completely relaxed position, you end up somewhere in between, which is the functional residual capacity (FRC). This value is about 40% total lung capacity in a normal individual. In emphysema, FRC increases due to loss of lung recoil. In fibrosis, the opposite occurs. The answer to the question above is because it reflects the balance between the chest wall and lungs going toward their own equilibrium position. 12. What factors determine airway resistance? • Length of airway • Diameter of airway--major determinant (and the one you can change) • Density of gas molecules (helium gives a decrease in resistance) 13. What is the importance of lung elastic tissue on airway diameter? Elastic tissue of the alveoli exerts attraction to help keep airway open. First graph is airway resistance vs. volume. This shows that resistance is much higher at low volumes than high volumes. At high volumes the elastic tissue acts as a tether, or “tugs” to hold airways open. This does not occur at low volumes. In emphysema, you have less elasticity so less tethering action resulting in smaller airways and increased resistance. The second graph is resistance vs. airway generation. The table on the next page goes along with this graph. Over the first four generations, the total cross sectional area decreases resulting in an increase in resistance. Afterward, the total cross sectional area increases even though diameter of each individual airway will decrease. This is due to an increase in the number of airways. So, overall resistance is lesser deep in the lungs than it is in the upper airway. The greatest resistance to airflow occurs in the upper airway. *From last year’s co-op… Dr. Forster then mentioned four diseases of increased airway resistance due to narrowing. They are: -emphysema—increased resistance due to reduced tethering -chronic bronchitis--due to increased mucus production -asthma—due to constriction of airway smooth muscle -loss of dilation in larynx and pharynx (obstructive sleep apnea and snoring)

14. What is the relationship between maximum expiratory flow and lung volume? The graph at the top of the page shows relationship between flow and lung volume. Curve A shows a maximal effort. Flow decreases even though you are pushing as hard as you can throughout. Why does flow go down even though you are maintaining same effort throughout? This happens for two reasons. The first is that the driving alveolar pressure for flow will decrease as lungs reach lower volumes (recoil pressure becomes less so driving pressure is less while pleural pressure remains at it’s max). The second reason is because the resistance will increase because the tethering action of the elastic tissue on the airways becomes less so airways become smaller. Curves B and C shows exerting 50 and 25% max effort. The peak flow decreases because pleural pressure is less. At low volumes flow or expiration becomes independent of effort. The reason you reach the same point on all three curves is depicted on the next figure. The drawing on the left shows airway and alveolar pressure before an inspiration, which are both the same (0) so there is no flow. Pleural pressure is slightly negative to offset the tendency of alveoli to collapse, keeping the airway open. The top drawing shows the beginning of inspiration. The pleural and alveolar pressures become more negative so air flows in. The difference between the inside and outside of the airway is now +6 instead of +5 so that will have a dilating effect on the airway. The right drawing is at the end of inspiration. This is the reversal point so alveolar and airway pressure are equal and there is no flow. The pleural pressure is more negative to hold it at the higher volume, so the transpulmonary pressure has increased from -5 to +10 overall. The pleural pressure has a huge dilating effect on airways. The bottom is the forced expiration. The muscles create a very positive pleural pressure which is transferred to alveoli and contributes to driving pressure for flow. In addition, there is a recoil pressure so alveolar pressure is greater than pleural pressure. As you go down airway, pressure decreases due to air molecules bumping into each other and the wall. Eventually you reach a point where the pressure inside of the airway is less than outside of the airway and the airway collapses. At this point, the increase in driving pressure is offset by the collapsing pressure so you get the same flow irrespective of effort. Dr. Forster stopped here for today.

Related Documents