Cardiovascular and Pulmonary Physiology

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Chapter 4

Cardiovascular and Pulmonary Physiology

Elizabeth Dean

This chapter reviews basic cardiovascular and pulmonary physiology. A thorough understanding of normal physiology provides a basis for understanding the deficits in cardiovascular and pulmonary function (in the context of limitation of activity and social participation, as well as structure and function) and the adaptations to changing physiological and pathophysiological demands. This knowledge provides the foundation for conducting a thorough assessment and prescribing treatment.1–8

The mechanical activity of the heart is precisely regulated in accordance with the electrical activity of the heart to effect optimal cardiac output to the organs of the body.9,10 The electrical activity of the heart, based on electrocardiography, in both health and pathology, is described in detail in Chapter 12. The electrical and mechanical events of the cardiac cycle and their coupling (electromechanical coupling) are summarized in Figure 4-1. These events include the spread of the wave of electrical excitation throughout the myocardium; the resulting sequence of contraction of the atria and ventricles, followed by dynamic changes in blood pressure and volume in the heart chambers; the heart sounds; and the timing of these events. The cardiac cycle takes 0.8 second in a heart beating at 75 beats per minute. Ventricular systole or ejection takes about one-third of this time. Its onset and termination are marked, respectively, by the closing and opening of the atrioventricular valves (mitral and tricuspid). Diastole, or the period between successive ventricular systoles, in which the ventricles fill with blood, takes two-thirds of the 0.8 second of each cardiac cycle.

Fig. 4-1 Summary of electrical and mechanical events of the heart. A, Atrial systole. B, Isovolumetric contraction. C, Ejection. D, Isovolumetric relaxation. E, Rapid inflow, diastasis, and active rapid filling. Note the relationship between ventricular pressure and volume: a, closure of the atrioventricular valves; b, opening of the semilunar valves; c, closure of the semilunar valves; d, opening of the atrioventricular valves.

Phases of Systole and Diastole

Ventricular systole normally has three phases: the isovolumetric contraction period, the rapid ejection period, and the slower ejection period. Ventricular diastole also has three phases: the passive rapid-filling phase, the slower filling phase (diastasis), and the active rapid-filling phase.

Cardiac Reflexes

The heart behaves automatically and is therefore termed a functional syncytium. Three primary reflexes enable the heart to increase stroke volume and cardiac output with moment-to-moment changes in myocardial demand.

The first reflex is the Starling effect, which refers to the increased force of contraction that occurs with increased venous return (preload). The second reflex, the Anrep effect, refers to the increase in ventricular contractile force as a result of an increase in aortic pressure (afterload). The third reflex, the Bowdich effect, refers to the corresponding increase in heart rate when myocardial contractile force increases. The integrated function of these three reflexes ensures that cardiac output adjusts as demands on the heart change (i.e., in healthy individuals, primarily in response to exercise, body position, and emotional stress).

Volume and Pressure Changes

Changes in the ventricular volume curve and aortic pressure wave reflect changes in atrial and ventricular pressures during systole and diastole. The sequence of events appears in a flow chart in Figure 4-2. Pressure gradients within the heart are responsible for the opening and closing of the valves. Coordinated valve opening and closure are important to promote the forward movement of blood and prevent mechanical inefficiency of the heart pump resulting from valvular regurgitation of blood during ventricular contraction. Regurgitation of blood in the retrograde direction gives rise to heart murmurs that are audible on auscultation of the heart.

Fig. 4-2 The sequence of pressure changes in the heart during the cardiac cycle.

Heart Sounds

The heart sounds are described as a low-pitched, long-duration sound (S₁) followed by a higher pitched, slower duration sound (S₂) that resembles the phonic sounds of LUB-dub. S₁ is associated with the closure of the atrioventricular valves. S₂ is associated with the closure of the semilunar valves. In inspiration, the aortic valve closes several milliseconds before the pulmonic valve, resulting in a splitting of the second heart sound, S₂. During inspiration, intrathoracic pressure becomes more negative, and venous return and right heart volume increase; hence pulmonary ejection is prolonged in this situation, and closure of the pulmonary valve is delayed. Other variations in splitting of S₂ occur with pathology. The presence of a third (S₃) or fourth (S₄) heart sound is usually considered abnormal. S₃ is usually associated with the passive rapid-filling phase and S₄ with the active rapid-filling phase.

Peripheral Circulation

The purpose of the peripheral circulation, including the microcirculation at the tissue level, is to provide saturated oxygenated blood and remove partially desaturated blood. The microcirculation within each organ regulates the blood flow both exogenously, via the neurological system, and endogenously, via the humoral system, commensurate with the metabolic needs of that tissue bed (see Chapter 3). The four principal factors that determine the movement of fluid in the microcirculation are the following:

1. The capillary hydrostatic pressure from the blood pressure, which tends to move blood across the capillary membrane and out of the circulation into the interstitium

2. The capillary oncotic pressure from the proteins within the blood vessels, which tends to retain fluid in the circulation

3. The interstitial hydrostatic pressure, which tends to move fluid back into the circulation

4. The interstitial oncotic pressure, which tends to draw fluid out of the circulation and into the interstitium

The net forces acting on the capillary fluid are nearly in equilibrium, with a slight tendency for fluid to be filtered out of the systemic circulation into the interstitium. Box 4-1 illustrates the mean pressures that determine normal fluid dynamics across capillary membranes.

Box 4-1 Balance of Forces Moving Fluid into and out of the Capillary

Mean Forces Moving Fluid out of the Capillary

Mean capillary pressure	17.0 mm Hg
Negative interstitial pressure	6.3 mm Hg
Oncotic interstitial pressure	5.0 mm Hg
Total outward pressure	28.3 mm Hg

Mean Forces Moving Fluid into the Capillary

Plasma oncotic pressure	28.0 mm Hg
Total inward pressure	28.0 mm Hg

Net Outward Pressure

28.3 (outward pressure) − 28.0 (inward pressure) = 0.3 mm Hg

Transport of Oxygen

Once oxygen reaches the blood, it rapidly combines with hemoglobin to form oxyhemoglobin. A small proportion of oxygen is dissolved in the plasma. The use of the hemoglobin molecule as an oxygen carrier allows for greater availability and efficiency of oxygen delivery to the tissues in response to metabolic demand. Saturation of the oxygen-carrying sites on the hemoglobin molecule is curvilinearly related to the partial pressure of oxygen in the tissues. This relationship is called the oxyhemoglobin dissociation curve and is a sigmoid, or S-shaped, curve (Fig. 4-3). The hemoglobin of arterial blood is 99%, or almost completely saturated with oxygen. Under normal circumstances, arterial blood is mixed with a small proportion of venous blood from the coronary and pulmonary circulation, resulting in arterial saturation slightly less than 100%. The graph shows a range of partial pressures of oxygen that may exist in the tissues. At relatively high arterial oxygen pressures, the oxygen saturation is high. This reflects high association or low dissociation between oxygen and hemoglobin. Saturation does not fall significantly until the partial pressure of oxygen falls below 80 mm Hg. Even at PO₂ levels of 40 to 50 mm Hg, arterial saturation is still 75%. This suggests that the oxyhemoglobin dissociation system has an enormous capacity to meet the varying needs of different tissues without severely compromising arterial saturation. A PO₂ of less than 50%, for example, has a profound effect on arterial saturation. This demonstrates an adaptive response of hemoglobin dissociation to respond to low oxygen tissue pressures by greater dissociation of oxygen from hemoglobin as the need arises. As PO₂ improves with increased supply of oxygen or decreased demand, the affinity between oxygen and hemoglobin increases, and arterial saturation increases. Thus oxygen is not released unless there is a need for greater oxygen delivery to the tissues.

Fig. 4-3 The oxyhemoglobin dissociation curve.

Various conditions can increase or decrease hemoglobin’s affinity for oxygen and thereby cause a shift in the oxyhemoglobin dissociation curve (see Fig. 4-3). A shift to the right results in decreased oxygen affinity and greater dissociation of oxygen and hemoglobin. In this instance, for any given partial pressure of oxygen, there is a lower saturation than normal. This means that there is more oxygen available to the tissues. Shifts in the curve to the right occur with increasing concentration of hydrogen ions (i.e., decreasing pH), increasing PCO₂, increasing temperatures, and increasing levels of 2,3-DPG (diphosphoglycerate), a byproduct of red blood cell metabolism. West suggests that “a simple way to remember these shifts is that an exercising muscle (increased metabolic demand), is acid, hypercapnic and hot, and it benefits from increased unloading of oxygen from its capillaries.”⁸

A shift of the curve to the left results in increased oxygen affinity. Thus for any given partial pressure of oxygen, there is a higher saturation than normal. This means that there is less oxygen available to the tissues. This occurs in alkalemia, hypothermia, and decreased 2,3-DPG.

Anemia (reduced red blood cell count and hemoglobin) and polycythemia (excess red blood cell count and hemoglobin) produce changes in the oxygen content of the blood, as well as in its saturation. Anemia shifts the curve to the right and lowers the maximal saturation achievable. Polycythemia has the opposite effect. The curve is shifted to the left, and maximal saturation approaches 100%.

Transport of Carbon Dioxide

Carbon dioxide (CO₂) is an acid produced by cells as a result of cell metabolism. It is carried in various forms by venous blood to the lungs, where it is eliminated. Most of the CO₂ added to plasma diffuses into the red blood cells, where it is buffered and returned to the plasma to be carried to the lungs. The buffering mechanism is so effective that large changes in dissolved CO₂ can occur with small changes in blood pH.

The transport of CO₂ has an important role in the acid-base status of the blood and maintenance of normal homeostasis. The lung excretes 10,000 mEq of carbonic acid per day. (Carbonic acid is broken down into water and CO₂. The CO₂ is buffered and eliminated through the lungs.) The kidney can excrete only 100 mEq of acid per day. Therefore alterations in alveolar ventilation can have profound effects on the body’s acid-base status. A decrease in the lung’s ability to ventilate causes a sharp rise in PCO₂ and a drop in pH. This causes acute respiratory acidosis. If this change occurs gradually, the pH will remain within normal limits while the PCO₂ is elevated. This is known as a compensated respiratory acidosis. Hyperventilation or excessive ventilation causes rapid elimination of CO₂ from the blood. This results in a decreased PCO₂ and an increased pH and is known as acute respiratory alkalosis. Again, if the change occurs gradually, the pH remains within normal limits, even though the PCO₂ is decreased. This is a compensated respiratory alkalosis.

Cardiopulmonary Physiology

Ventilation

Ventilation is the process by which air moves into the lungs. The volume of air inhaled can be measured with a spirometer. The various lung capacities and volumes are defined in Chapter 9.

Regional differences in ventilation exist throughout the lung. Studies using radioactive inert gas with a radiation counter over the chest wall have shown that when the gas is inhaled by an individual in the seated position and measurements are taken, radiation counts are greatest in the lower lung fields, intermediate in the midlung fields, and lowest in the upper lung fields. This effect is position or gravity dependent. In the supine position, the apices and bases are ventilated comparably, and the lowermost lung fields are better ventilated than the uppermost lung fields. Similarly, in the lateral, or side-lying, position, the lower lung fields are preferentially ventilated compared with the upper lung fields (see Chapter 19).

The causes of regional differences in ventilation can be explained in terms of the anatomy of the lung and the mechanics of breathing. An intrapleural pressure gradient exists down the lung. In the upright position, intrapleural pressure tends to be more negative at the top of the lung and becomes progressively less negative toward the bottom of the lung. This pressure gradient is thought to reflect the weight of the suspended lung. The more negative intrapleural pressure at the top of the lung results in relatively greater expansion of that area and a larger resting alveolar volume. The expanding pressure in the bottom of the lung, however, is relatively small, so there is a smaller resting alveolar volume in the bottom. This distinction between the upper and lower lung fields is fundamental to understanding differences in regional ventilation. Regional differences in resting alveolar volume should not be confused with regional differences in ventilation volume. Ventilation refers to volume change as a function of resting volume. The relatively higher resting volume in the upper lung fields renders them stiffer, or less compliant, than the lower lung fields, where there are low lung volumes and greater compliance. The lower lung fields, therefore, exhibit a greater volume change in relation to resting volume, and that effects greater overall ventilation, compared with the upper lung fields. Ventilation is favored in the lowermost lung fields, regardless of body position.

Diffusion

Once air has reached the alveoli, it must cross the alveolar-capillary (A-C) membrane (Fig. 4-4). Gases, specifically oxygen entering the lungs and carbon dioxide leaving the lungs, must cross through the surfactant lining, the alveolar epithelial membrane, and the capillary endothelial membrane. Oxygen then has to travel through a layer of plasma, the erythrocyte membrane, and intracellular fluid in the erythrocyte, until it encounters a hemoglobin molecule. This distance is actually small in normal lungs, but in disease states it may increase. The alveolar wall and the capillary membrane often become thickened. Fluid, edema, or exudate may separate the two membranes. These conditions are often first detected when arterial PO₂ becomes chronically lower than normal. Oxygen diffuses slowly through the A-C membrane in comparison to CO₂ diffusion. As a result, patients with diffusion problems frequently have hypoxemia with a normal PCO₂. Sarcoidosis, asbestosis, scleroderma, and pulmonary edema are conditions that decrease the diffusing capacity of the gases. The capacity may also decrease in emphysema because of a decrease in total surface area for gas exchange.

Fig. 4-4 The transfer of carbon monoxide and oxygen molecules across the alveolar-capillary membrane, through plasma, and across the red blood cell membrane. Also represented is the reaction with hemoglobin. *(From Mason RJ, Broaddus VC, Martin T, et al*: Murray and Nadel’s textbook of respiratory medicine, *ed 5, Philadelphia, 2011, Saunders.)*

Perfusion

Perfusion of the lungs refers to the blood flow of the pulmonary circulation available for gas exchange. The pulmonary circulation operates at relatively low pressures compared with the systemic circulation. For this reason, the walls of the blood vessels in the pulmonary circulation are thinner than comparable vessels in the systemic circulation. Compared with the systemic circulation, the lungs have little requirement for marked regional differences in perfusion.

Hydrostatic pressure has a significant effect on the perfusion of the lower lobes. Hydrostatic pressure reflects the effect of gravity on the blood and tends to favor perfusion of the lower lung fields. This fact has been substantiated using radioactive tracers in the pulmonary circulation and measuring radiation counts over the lung fields. The nonuniformity of perfusion reflects the interaction of alveolar, arterial, and venous pressures down the lung. Normally blood flow is determined by the arteriovenous pressure gradient. In the lungs there are regional differences in alveolar pressure that can exert an effect on the arteriovenous pressure gradient. For example, in the upper lung fields, alveolar pressure approximates atmospheric pressure, which overrides the arterial pressure and effectively closes the pulmonary capillaries. In the lower lung fields, the opposite occurs. The relatively low volume of air in the alveoli is overridden by the greater capillary hydrostatic pressure. Thus the capillary pressure effectively overcomes the alveolar pressure.

Pulmonary blood vessels constrict in response to low arterial pressures of oxygen. This is termed hypoxic vasoconstriction. Hypoxic vasoconstriction in the lung is believed to serve as an adaptive mechanism for diverting blood away from underventilated or poorly oxygenated lung areas. Although hypoxic vasoconstriction may have an important role in improving the efficiency of the lungs as a gas exchanger, it may be potentially deleterious to a patient who has reduced arterial oxygen pressure secondary to pulmonary pathology.

The acid-base balance of the blood also affects pulmonary blood flow. A low blood pH, or acidemia, for example, potentiates pulmonary vasoconstriction. Thus, impaired ventilatory function can disturb blood-gas composition and, in turn, acid-base balance. This effect can be amplified because of the cyclical reaction of pH on pulmonary vasoconstriction. Consideration of these basic physiological mechanisms is paramount to optimize physical therapy intervention.

Ventilation and Perfusion Matching

As discussed previously, gravity tends to pull blood into the dependent positions of the lung (Fig. 4-5). In erect humans, therefore, there is greater blood flow at the bases of the lung. In places, the arterial blood pressure exceeds the alveolar pressure and causes compression or collapse of the airways (Fig. 4-6). Blood flow to the apices is decreased because of gravity. Alveoli in this region are more fully expanded as a result of high transmural pressures and may further decrease blood flow by compressing blood vessels. It follows that the areas of optimal gas exchange occur where there is the greatest amount of perfusion and ventilation. This occurs toward the base of the lungs in erect humans. Changes in posture cause changes in perfusion and ventilation. Generally, greater air exchange occurs toward the gravity-dependent areas. In side-lying, there is greater gas exchange in the dependent lung (Fig. 4-7).

Fig. 4-5 The perfusion of the lungs is dependent on posture. In the upright position, three areas can be seen. Zone III has perfusion in excess of ventilation. In zone II, perfusion and ventilation are fairly equal. In zone I, ventilation occurs in excess of perfusion.

Fig. 4-6 The relationship between the size of the airways and the amount of perfusion in the area when lungs are in the upright position. A, Perfusion is decreased in the apices because of gravity. This enables the alveoli to expand fully. This expansion may compress blood vessels and thereby further decrease blood flow. B, Perfusion is increased in the bases of the lungs because of gravity. The enlarged vessels prevent full expansion of alveoli and may, in fact, compress them to a smaller size.

Fig. 4-7 The effect of positioning on the perfusion of the lung. Note that gravity-dependent segments have the greatest amount of perfusion.

In normal lungs there is an optimal ratio, or matching of gas and blood. This ratio of ventilation to perfusion (V/Q) is 0.8 to maintain normal blood gas values of PO₂ and PCO₂. Therefore the lungs must be able to supply four parts ventilation to about five parts perfusion. When the ratio is not uniform throughout the lung, the arterial blood cannot contain normal blood-gas values. Regions with low ratios (perfusion in excess of ventilation) act as shunts, whereas regions with high ratios (ventilation in excess of perfusion) act as dead space (Fig. 4-8). Hypoxemia results if regions of abnormal V/Q predominate. An elevation in arterial PCO₂ may also occur unless the patient increases ventilation.

Fig. 4-8 A, The oxygen–carbon dioxide diagram. The diagonal line represents all possible PaO₂-PaCO₂ combinations from absolute shunt to absolute dead space in a single alveolus. The diagonal line also represents end-capillary PO₂ and PCO₂ values. represents mixed venous blood composition; ∞ represents inspired gas composition; I represents inspired tracheal gas composition. B, The shunt–dead-space continuum. *(From Beachey W:* Respiratory Care Anatomy and Physiology: Foundations for Clinical Practice, ed 2. Philadelphia, 2008, Mosby.)

Physical therapists who are positioning patients with cardiovascular and pulmonary pathology may find that their patients experience greater distress when placed in certain positions. Such position-dependent distress can be explained by ventilation-perfusion inequalities that cause poor gas exchange in the dependent lung.

The relationship of ventilation and perfusion in the lung is summarized in the following figures. Figure 4-9 shows increases in ventilation and perfusion down the upright lung. When optimal ventilation and perfusion match, V/Q occurs in the midlung zones. In the upright position, ventilation is in excess of perfusion in the apices, and perfusion is in excess of ventilation in the bases. Figure 4-10 illustrates the effects of shunt and physiological dead space on V/Q matching in the upright lung and shows their effect on alveolar gas. Specifically, Figure 4-10 shows a schematic representation of regional differences in ventilation and perfusion in the upper, middle, and lower zones of the upright lung. These gradients are reflected in the alveolar Po₂ and Pco₂ levels associated with alveolar dead space in the apices, appropriate V/Q matching in the midlung, and shunt in the bases.

Fig. 4-9 The effect of gravity on ventilation, perfusion, and ventilation-perfusion matching (V/Q ratio).

Fig. 4-10 Schemata showing the effect of gravity on ventilation and perfusion down the upright lung.

Pulmonary Physiology

Reflexes

Hering-Breuer Reflex

In the late 1800s, Hering and Breuer noted that distention of anesthetized animal lungs caused a decrease in the frequency of inspiration and an increase in expiratory time. Receptors for this reflex are thought to lie in the smooth muscle of airways from the trachea to the bronchioles. More than 800 mL of lung volume above functional residual capacity are needed to activate the reflex and delay the next breath.

Cough Reflex

Mechanical or chemical stimuli to the larynx, trachea, carina, and lower bronchi result in a reflex cough and bronchoconstriction. The high velocity created by the cough sweeps mucus and other irritants up toward the pharynx (see Chapter 23).

Stretch Reflex

The intercostal muscles and the diaphragm contain sensory muscle spindles that respond to elongation. A signal is sent to the spinal cord and anterior horn motor neurons. These neurons signal more muscle fibers to contract (recruitment) and thus increase the strength of the contraction. Theoretically, such a stretch reflex may be useful when there is an increase in airway resistance or a decrease in lung compliance. Stretching the ribs and the diaphragm may activate the stretch reflex and help the patient take a deep breath. The fundamental pathways of the stretch reflex are shown in Figure 4-12. Research is needed, however, to establish the therapeutic role of proprioceptive neurofacilitation techniques based on stretch reflex theory in altering pulmonary function.

Joint and Muscle Receptors

Peripheral joints and muscles of the limbs are believed to have receptors that respond to movement and enhance ventilation in preparation for activity. Ventilation has also been shown to be stimulated by a similar reflex in humans and anesthetized animals in response to passive movement of the limbs. The precise pathways for these reflexes have not been well established.

Mechanoreceptors

Changes in systemic blood pressure cause corresponding changes in pressure receptors in the carotid and aortic sinuses. Increase in blood pressure causes mechanical distortion of the receptors in these sinuses, producing reflex hypoventilation. Conversely, a reduction in blood pressure can result in hyperventilation.

Mechanical Factors in Breathing

The flow of air into the lungs is a result of pressure differences between the lungs and the atmosphere. In normal breathing, inspiration occurs when alveolar pressure is less than atmospheric pressure. Muscular contraction of the respiratory muscles lowers alveolar pressure and enlarges the thorax. The decreased pressure causes air to flow from the atmosphere into the lungs. Patients who are unable to create adequate negative pressure may have to be mechanically ventilated. The ventilators create a positive pressure (greater than atmospheric pressure) that forces air into the lungs, where there is atmospheric pressure. The iron lung used during the poliomyelitis epidemic of the 1950s assisted ventilation by using cycles of negative pressure to inflate the lungs.

Exhalation occurs when alveolar pressure is greater than atmospheric pressure. At the cessation of inspiration, the respiratory muscles return passively to their resting positions. The diaphragm rises, compressing the lungs and thereby increasing alveolar pressure. As the intercostals relax, the ribs resume their preinspiratory position, further compressing the lungs and increasing alveolar pressure. The increased alveolar pressure contributes to air flowing from the lungs. Normally, expiration is a passive process reflecting the elastic recoil of the lung parenchyma.

Resistance to Breathing

Compliance

The inner wall of the thorax, which is lined with parietal pleura, and the parenchyma of the lung, which is enclosed in visceral pleura, lie close to each another. The pleurae are separated by a potential space containing a small amount of pleural fluid. Muscular contraction of the intercostals and the diaphragm mechanically enlarges the thorax. The lungs are enlarged at this time because of their close proximity to the thorax. The healthy lung resists this enlargement and tries to pull away from the chest wall. The ease with which the lungs are inflated during inspiration is known as compliance and is defined as the volume change per unit of pressure change. Normal lungs are very distensible or compliant. They can become more rigid and less compliant as a result of diseases that cause alveolar, interstitial, or pleural fibrosis, or alveolar edema. Compliance increases with age and in emphysema, because of the loss of elastin.

The elastic recoil or compliance of the lung is also dependent on a surface fluid called surfactant, which lines the alveoli. This fluid increases alveolar compliance by lowering the surface tension, thereby reducing the muscular effort necessary to ventilate the lungs and keep them expanded. It is a complex lipoprotein that is produced in type II alveolar cells (see Chapters 2 and 4). A decrease in surfactant causes the alveoli to collapse. Reexpanding these alveoli requires a tremendous amount of work on the part of the patient. The patient may become fatigued and need mechanical ventilation. This occurs in respiratory distress syndrome in premature infants (previously called hyaline membrane disease) and in acute respiratory distress syndrome in adults. In another disease, alveolar proteinosis, there is excessive accumulation of protein in the alveolar spaces. This may be because of excessive production of surfactant or deficient removal of surfactant by alveolar macrophages.

The elastic properties of the lungs tend to collapse them if not counterbalanced by external forces. The tissues of the thoracic wall also have elastic recoil, which causes them to expand considerably if unopposed. These two forces oppose each other, keeping the lungs expanded and the thoracic cage in a neutral position. If these forces are interrupted (as in pneumothorax), the lung collapses and the thoracic wall expands (Fig. 4-13). Similarly, the overinflated, barrel-shaped chest of a patient with chronic obstructive pulmonary disease (COPD) is caused by the elastic tension of the chest wall being unopposed by the usual elastic forces of the lungs, which have been damaged by disease.

Fig. 4-13 Various relationships between the lungs and the thorax. *A₁,* The size the lungs would assume if they were not acted on by the elastic recoil of the thoracic wall. *A₂,* The normal size of lungs within the thorax. *B₁,* The size the thorax would assume if it were not acted on by the elastic recoil of the lungs. *B₂,* The normal position of the chest wall when acted on by the elastic recoil of the lungs. C, The normal relationship of lungs to thorax. D, The positions assumed by the lungs and thorax in a tension pneumothorax.

Pressure-Volume Relationships

Pressure-volume curves help define the elastic properties of the chest wall and lungs. The elasticity of the respiratory system as a whole is the sum of its two major components, the lungs and the chest wall. The so-called relaxation pressure curve is shown in Figure 4-14. The curve illustrates the static pressure of the lungs and chest wall and the combination of the two measured at given lung volumes. Functional residual capacity (FRC) reflects the balance of elastic forces exerted by the chest wall and the lungs and has significant implications for the clinical presentation and management of patients with cardiovascular and pulmonary dysfunction.

Fig. 4-14 The relaxation pressure curve. The pressure in the lungs at any volume reflects the elastic forces of the lungs and chest wall.

The relaxation pressure curve represents static pressure measurements. This means that the respiratory muscles are inactive, and the volume in the lungs at a given point in the respiratory cycle is determined by the balance of forces between the chest wall and the lungs. The chest wall and lungs exert elastic forces that oppose each other. The chest wall attempts to pull the lung out, and the lungs attempt to recoil and pull the chest wall in. The curves labeled “lung” and “chest wall” (see Fig. 4-14) are theoretical and illustrate the elastic force exerted by each when it is permitted to act unopposed by the other. Normally these two forces are exerted together, producing the pressure-volume relaxation curve. At FRC, these forces are in equilibrium; therefore this capacity constitutes the resting volume of the respiratory system.

In lung disease, the balance between chest wall and lung forces is disrupted.¹¹ More work and energy are required to sustain the respiratory effort.¹² The patient is less able to rely on normal elastic recoil of the chest wall, lungs, or both. Therefore the patient must expend more energy to effect equivalent respiration. The limits of respiratory excursion are determined by both elastic and muscular forces. At total lung capacity, the elastic forces of the respiratory system are balanced by the inspiratory muscle force. At residual volume, the elastic forces of the chest wall are balanced by the maximum expiratory muscle force. This volume excursion from total lung capacity to residual volume reflects vital capacity.

Although the curves representing the elastic forces of the lungs and chest wall are theoretical, they are helpful in understanding the effect of lung dysfunction on pulmonary function and on the clinical presentation of the patient.¹¹ For example, in individuals with COPD, the characteristic barrel chest reflects the unopposed elastic forces of the chest wall as it succeeds in increasing the excursion of the chest as a result of reduced elastic recoil of the lungs. At the other extreme is the effect on the chest wall of a puncture wound, which disrupts the intrapleural pressure gradient that normally keeps the lung expanded and the chest wall contained. The result of such a puncture is to produce a pneumothorax in which the lung collapses down to the hilum and the chest wall springs outward (see Fig. 4-13).

Airway Resistance

The flow of air into the lungs depends on pressure differences and on the resistance to flow in the airways. Resistance is defined as the pressure difference required for one unit flow change. The air passages are divided into upper and lower airways (see Chapter 3). The upper airways are responsible for 45% of airway resistance. The resistance to airflow by the lower airways depends on many factors and is therefore difficult to predict. The branching of the lower airways is irregular, and the diameter of the lumen may vary because of external pressures and because of the contraction or relaxation of bronchial or bronchiolar smooth muscle. The lumen diameter may also decrease as a result of edema or mucus. Any of these changes in the airway diameter may cause an increase in airway resistance. Flow of air through these airways can be either laminar or turbulent (Fig. 4-15). Laminar flow is a streamlined flow in which resistance occurs mainly between the sides of the tubes and the air molecules. It tends to be cone shaped, with the molecules in contact with the walls of the tubes moving more slowly than the molecules in the middle of the tube. Turbulent flow occurs when there are frequent molecular collisions in addition to the resistance of the sides of the tubes. This type of flow occurs at high flow rates and in airways where there are irregularities caused by mucus, exudate, tumor, or other obstructions. In normal lungs, airflow is a combination of laminar and turbulent flow and is known as tracheobronchial flow.