Los valores y la educación

1.0 Introduction

2.0 Intended Learning Outcomes (ILOs) 3.0 Main Content

3.1 The Mechanism of breathing

3.2 The Application of Boyle’s law in the pulmonary system 4.0 Conclusion

5.0 Summary

6.0 Tutor-Marked Assignment 7.0 References/Further Reading

1.0 INTRODUCTION

This unit describes the mechanism of breathing in Pulmonary system.

2.0 INTENDED LEARNING OUTCOMES (ILOS)

By the end of this Unit, you will be able to;

• Define breathing

• State the factors responsible in the mechanism of breathing in the pulmonary system.

3.0 MAIN CONTENT

3.1 The Mechanism of breathing

The movement of air into the lungs from the atmosphere depends on two factors: pressure gradient (ΔP) and resistance (R).

A pressure gradient is simply the difference between two pressures.

Difference is represented by the Greek capital letter delta: Δ. The larger the differences in pressure, the larger the pressure gradient is. Gases—in this case, air which is a mixture of gases—move from areas of high pressure to areas of low pressure. Resistance is the sum of the forces opposing the flow of the gases. About 20% of resistance to airflow is caused by tissue friction as the lungs move during inspiration and expiration. The remaining 80% is due to the friction between the gas molecules and the walls of the airway (airway resistance) and the internal friction between the gas molecules themselves (viscosity). Airway resistance is determined by the size of the airway and the smoothness or turbulence of the airflow.

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In order for air to flow, the pressure gradient must be greater than the resistance to the flow. Thus, for inspiration to take place, pressure must be higher in the atmosphere than in the lungs; for expiration, pressure in the alveoli of the lungs must be higher than in the atmosphere. It shows how the inspiratory pressure gradient is created.

3.2 Boyle’s Law and Mechanism of breathing

Boyle’s law states that the pressure of a gas is inversely related to its volume (or vice versa) under conditions of constant temperature: low pressure is associated with large volume, and high pressure is associated with small volume. For pulmonary ventilation, an increase in chest cavity volume is accomplished by muscle contraction for inspiration. This increase in volume leads to an internal lung pressure decrease according to Boyle’s law. As a result, a negative pressure exists in the chest cavity relative to the atmosphere outside the body. Thus, a pressure gradient has been created. Air flows into the chest cavity in an attempt to equalize this pressure difference. The volume change per unit of pressure is called compliance (West, 2005).

The main inspiratory muscle is the dome-shaped diaphragm. With neural stimulation, the diaphragm contracts and moves downward, elongating the chest cavity (Figure 9.3B). In normal resting breathing, the diaphragm moves about 1 cm; in heavy or forced breathing, it may move as much as 10 cm (West, 2005).

During exercise, the chest cavity is further enlarged by the action of the external intercostal muscles and others, known collectively as the accessory muscles, which elevate the rib cage and cause expansion both laterally (side-to-side) and anteroposteriorly (front-to-back). The extent of accessory muscle activity and the resultant drop in pressure depends on the depth of the inspiration. These changes in the chest cavity volume transfer themselves to the lungs through the pleura. Pleurae are thin, double-layered membranes that line both the chest cavity (the inner surfaces of the thorax, sternum, ribs, vertebrae, and diaphragm) and the external lung surfaces. The portion covering the chest cavity is called the parietal pleura; the portion covering the external lung surfaces is called the visceral or pulmonary pleura. A fluid secreted by the pleura fills the space between the pleurae (the intrapleural space), allowing the lungs to glide smoothly over the chest cavity walls. It also causes the parietal and the pulmonary pleurae to adhere to each other in the same way that two pieces of glasses are held together by a thin film of water. Because of this adhesion, the lungs themselves move when muscle actions move the chest cavity (Guyton and Hall, 2006; Martin et al., 1979).

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During normal resting conditions, expiration occurs simply because the diaphragm and other inspiratory muscles relax. When these muscles relax, both the lungs and the muscles, which are highly elastic, recoil to their original positions. This elastic recoil decreases lung volume and thus creates a pressure inside the chest cavity that is higher than the atmospheric pressure. As the chest cavity volume decreases, the intrathoracic pressure increases slightly above that of the atmosphere. The result is that the air moves out of the lungs into the atmosphere. The pressures equalize again, and the cycle repeats with the next inspiration.

A complete respiratory cycle includes both inspiration and expiration.

During heavy breathing, as in exercise, expiration is an active process.

The primary expiratory muscles are the abdominals and the internal intercostals. The abdominals (rectus abdominus, the obliques, and the transverse abdominus) push the abdominal organs—and hence the diaphragm—upward; the internal intercostals pull the ribs inward and down. This decrease in chest volume increases intrathoracic pressure more quickly than passive elastic recoil alone, and the air is forced out of the lungs faster. The pleurae also serve a purpose during expiration.

Pressure in the intrapleural space fluctuates with breathing in a way that parallels pressure within the lungs. However, the intrapleural pressure is always negative (24–28 mmHg) relative to the intrapulmonary (lung) pressure. This negative pressure protects the lungs from collapsing. If the intrapleural pressure were equal to the atmospheric pressure, the lungs would collapse at the end of expiration because of the elastic recoil.

Because muscle activity is involved during the respiratory cycle of inhalation and exhalation, energy is consumed. During rest, however, this energy consumption (restricted to inspiratory muscles) amounts to only 1–2% of the total body energy expenditure in nonsmokers (Pardy et al., 1984).

SELF-ASSESSMENT EXERCISE

i. Describe the structure of the pulmonary system

ii. Differentiate between Conducive and Respiratory zone.

4.0 CONCLUSION

Having read this course and successfully completed the assessment and self-assessment test, it is assumed that you have attained understanding of the introductory knowledge on mechanism of breathing.

5.0 SUMMARY

This Unit has successfully summarized the mechanism behind every form of breathing.

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6.0 TUTOR-MARKED ASSIGNMENT

7.0 REFERENCES/FURTHER READING

Adams, W. C., E. M. Bernauer, D. B. Dill, & J. B. Bomar: Effects of equivalent sea-level and altitude training on V.O2max and running performance. Journal of Applied Physiology.39(2):262–266 (1975).

Andrew, G. M., M. R. Becklake, J. S. Guleria, & D. V. Bates:Heart and lung functions in swimmers and nonathletes during growth.

Journal of Applied Physiology. 32(2):245–251 (1972).

Aguilaniu, B., P. Flore, J. Maitre, J. Ochier, J. R. Lacour, & H. Perrault:

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men. Journal of Applied Physiology. 92(5):1879–1894 (2002).

Amann, M., A. W. Subudhi, & C. Foster. Predictive validity of ventilatory and lactate thresholds for cycling time trial performance.

Scandinavian Journal of Medicine & Science in Sports. 16:27–34 (2006).

Armstrong, L. E.: Performance in Extreme Environments. Champaign, IL: Human Kinetics (2000). Ashley, F., W. B. Kannel, P. D. Sorlie,

& R. Masson: Pulmonary function: Relation to aging, cigarette habit and mortality; the Framingham Study. Annals of Internal Medicine. 82:739–745(1975).

Asmussen, E.: Similarities and dissimilarities between static and dynamic exercise. Circulation Research. 48(6 Suppl. I):I-3–I-10 (1981).

Åstrand, P.-O.: Experimental Studies of Physical Working Capacity in Relation to Sex and Age. Copenhagen: Munksgaard (1952).

Åstrand, I.: Aerobic work capacity in men and women with special reference to age. Acta Physiologica Scandinavica.

49(Suppl.169):1–92 (1960).

Åstrand, P.-O., T. E. Cuddy, B. Saltin, & J. Stenberg: Cardiac output during submaximal and maximal work. Journal of Applied Physiology. 19(2):268–274 (1964).

Åstrand, P.-O., L. Engstrom, B. O. Eriksson, P. Karlberg, I. Nylander, B.

Saltin, & C. Thoren: Girl swimmers: With special reference to

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respiratory and circulatory adaption and gynecological and psychiatric aspects. Acta Paediatrica. 147(Suppl.):1–73 (1963).

Bachman, J. C., & S. M. Horvath: Pulmonary function changes which accompany athletic conditioning programs. Research Quarterly.

39(2):235–239 (1968).

Bar-Or, O.: Pediatric Sports Medicine for the Practitioner: From Physiological Principles to Clinical Applications. New York, NY:Springer-Verlag, 1–65 (1983).

Bechbache, R. R., & J. Duffi n: The entrainment of breathing frequency by exercise rhythm. Journal of Physiology. 272:553–561 (1977).

Becklake, M. R., H. Frank, G. R. Dagenais, G. L. Ostiguy, & C. A.

Guzman: Infl uence of age and sex on exercise cardiac output.

Journal of Applied Physiology. 20(5):938–947 (1965).

Bell, H. J.: Respiratory control at exercise onset: An integrated systems perspective. Respiratory Physiology and Neurobiology. 152(1):1–

15 (2006).

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UNIT 3 RESPIRATORY CIRCULATION