The cardiopulmonary system and movement dysfunction.

[Peel C. The cardiopulmonary system and movement dysfunction. Phys Ther. 1996;76:448-455.]

Key Words: Cardiovascular system; Movement disorders; Oxygen transport; Pulmonary, general.

Movement is essential for performance of routine daily tasks and recreational activities and is the direct result of many factors. An individual must have the willingness or motivation to accomplish a task, and the movement must be supported by the musculoskeletal, neuromuscular, and cardiopulmonary systems. As experts in the science of movement dysfunction, physical therapists determine probable causes of problems related to movement and then design programs to improve physical function. Accomplishing this task requires an understanding not only of psychology and the roles of the neuromuscular and musculoskeletal systems in supporting movement but also of the role of the cardiopulmonary system.

The purposes of this introductory article are to describe how the cardiopulmonary system functions to support the increased metabolic needs associated with physical activity and to describe common problems of the cardiovascular and pulmonary systems that produce movement dysfunction. Signs and symptoms that are indicative of potential abnormalities of the cardiopulmonary system also will be discussed.

Cardiopulmonary Function at Rest and During Exercise

The primary purposes of the cardiopulmonary system are to deliver oxygen ([O.sub.2]) to metabolically active tissues and to remove carbon dioxide ([CO.sub.2]) and metabolites. External respiration, or gas exchange between the lungs and atmosphere, is linked to internal cellular respiration by the cardiovascular system.[1] Interactions between skeletal muscle, the heart, and the lungs are characterized in Figure 1. Atmospheric air is brought,, into the lungs where [O.sub.2] moves into pulmonary capillaries and [CO.sub.2] moves from the blood into alveoli for removal in expired air. The heart then PUMPS [O.sub.2]-rich blood to peripheral tissues. At the capillary level, [O.sub.2] moves into tissues and [CO.sub.2] moves into capillary blood. Within the cell, [O.sub.2] moves into mitochondria, allowing adenosine triphosphate generation through aerobic metabolism. The [CO.sub.2] is returned to the lungs via the venous system for removal from the body. Metabolites, such as hydrogen ions (H.sup.+], potassium, adenosine, and lactate, also are removed through the blood system and are either excreted or used for other functions in the body.

During exercise, skeletal muscle activity results in an increase in cellular [O.sub.2] requirements and in the amount of [CO.sub.2] that must be carried to the lungs for removal from the body. To meet the increased [O.sub.2] needs, both ventilation (VE) and cardiac output (CO) must increase in proportion to the increased metabolic rate. Ventilation (in liters per minute) is the product of breathing frequency and tidal volume (VT). Cardiac output (in liters per minute) is the product of heart rate (HR) and stroke volume (SV). In individuals without cardiopulmonary abnormalities, the increases in (VE) and CO are closely matched to the increase in metabolic rate, allowing arterial blood gas and pH levels to remain close to baseline values during exercise.[2] The precision of the system is demonstrated by an appropriate increase in both (VE) and CO as the exercise intensity level ranges from light to very heavy.[3]

An effective system for increasing cardiopulmonary activity in response to various levels of physical activity involves multiple steps. Figure 2 describes the steps involved in the transfer of [O.sub.2] from the atmosphere to skeletal muscle. The initial step is (VE), which is the movement of air in and out of the lungs. Ventilation occurs as a result of respiratory muscle activity. When these muscles contract, a negative pressure within the thorax is created, and air moves inward from the mouth to various parts of the lungs. At rest, the primary muscles of inspiration are the diaphragm, the scalene muscles, and the parasternal intercostal muscles.[4] These muscles function to expand the thorax by producing lower rib cage expansion (diaphragm), elevation of the rib cage (scalenc muscles), and an increase in the anteriorposterior dimension of the rib cage (parasternal muscles).[4] During activity, additional muscles are recruited, including the sternocleidomastoid and external intercostal muscles.[5] The abdominal muscles indirectly assist in inspiration by pushing the diaphragm upward, which increases the length of the diaphragm prior to inspiration.[4]

The next step involves gas exchange between the alveoli and pulmonary capillary blood. To accomplish this task, the alveoli that receive fresh air must be perfused with blood. The blood must have a sufficiently long transit time in the pulmonary capillary to allow time for diffusion of gases. The time needed for [CO.sub.2] to move into the alveoli and for [O.sub.2] to move into capillary blood is approximately 0.25 seconds6 (Fig. 3). Another critical factor is that the alveoli that are well ventilated also must be well perfused. Because of regional differences in the distributions of both (VE) and perfusion,[6] the possibility exists to have areas of the lung that are well ventilated but underperfused, or vice versa. During exercise, there is an increase in both perfusion and (VE), which facilitates the matching of (VE) and perfusion.

From the lungs, oxygenated blood enters the left-side of the heart. The heart then must be able to generate a force great enough to propel blood to various parts of the body. During diastole, when blood moves into the left ventricle, the myocardium is relaxed and compliant. A high degree of compliance is important to facilitate the movement of blood into the left ventricle. Compliance can decrease with myocardial ischemia and left ventricular hypertrophy. In these conditions, the ability to adequately fill the left ventricle may be impaired, and patients may experience dyspnea or signs and symptoms of decreased CO. During systole, the myocardium contracts. As the pressure in the left ventricle exceeds the pressure in the aorta, the aortic valve opens and blood moves into the arterial system.

Cardiac output is determined by SV and HR, and varies depending on the body's [O.sub.2] requirements. Increased activity of the sympathetic nervous system (SNS) produces an increase in CO, which results from increases in both the rate of contraction and the strength of contraction. Cardiac output also can be increased by greater venous return reaching the left ventricle, as during exercise.[7] The increased volume, or preload, stretches the ventricular muscle. A stronger contraction is produced because of a more advantageous length-tension relationship. During exercise, CO is increased because of increases in both SV and HR, with SV reaching its maximal level at approximately 40% of maximal oxygen consumption ([[VO.sub.2]max).[8] Consequently, for moderate-to-heavy exercise (levels greater than 40% of [VO.sub.2]max), increases in CO result from increases in HR.

As the blood leaves the heart, adjustments in the vascular system direct blood proportionally to the tissues with the highest metabolic needs. Contraction and relaxation of smooth muscle in the walls of arteries and arterioles produce changes in the size of these vessels. Increasing the size of a vessel's lumen, or vasodilation, allows greater blood flow to the area of the body supplied by those vessels. During activity, CO is directed to active skeletal muscles and to the skin to allow dissipation of heat, with vasoconstriction occurring in inactive muscles and visceral organs. The degree of vasodilation versus constriction is controlled centrally by the SNS and locally by cellular metabolites. As muscles become more active, there is an increase in the local concentration of metabolites, such as [CO.sub.2] and [H.sup.+], which produces vasodilation.[9] The increase in temperature also facilitates vasodilation. This local mechanism allows blood to be shunted to muscles with the greatest metabolic activity. Having reached the tissue level, [O.sub.2] moves from capillaries into muscle cells, with [CO.sub.2] Moving in the opposite direction.

Another important factor for an adequate [O.sub.2] delivery system is the [O.sub.2]-carrying capacity of the blood. The [O.sub.2] content of the blood is determined by the amount of hemoglobin in the blood and by the partial pressure of oxygen ([PO.sub.2]) in the blood.[6] The oxyhemoglobin dissociation curve, as demonstrated in Figure 4, describes the relationship between the [PO.sub.2] and the saturation of hemoglobin. Factors that alter the oxyhemoglobin dissociation curve will affect [O.sub.2] delivery to skeletal muscle. A shift of the curve to the left impairs the amount of [O.sub.2] extracted by muscle, whereas a shift to the right facilitates the unloading of [O.sub.2] from hemoglobin.6 Increased concentration of carboxyhemoglobin, which occurs with smoking, produces a leftward shift of the curve, impairing [O.sub.2] delivery. Acidosis and increased body temperature, which occur with exercise, facilitate the unloading of [O.sub.2] from hemoglobin and the diffusion of [O.sub.2] from capillaries to muscle cells.

A final critical factor is the need for a method of regulation that prevents large fluctuations in arterial blood gases and pH. It is well known that changes in the partial pressure of oxygen in arterial blood (Pa[O.sub.2]), the partial pressure of carbon dioxide in arterial blood (Pa[CO.sub.2]), and [H.sup.+] concentration stimulate the respiratory system and produce changes in (VE) that serve to return blood gas values to normal.[7] The increase in metabolism with exercise results in an increase in [CO.sub.2] production so that arterial blood gases and pH remain close to baseline during mild and moderate exercise.[2] The exact mechanism of control is unknown and may involve the rate of [CO.sub.2] flow to the lungs or the central nervous system.[10,11]

In summary, the cardiopulmonary system plays a critical role in delivering [O.sub.2] to skeletal muscles to support movement. Consequently, problems involving either the cardiopulmonary system or the musculoskeletal system can adversely affect a person's ability to perform routine functional activities. Because of the multiple steps that are involved in the transfer of [O.sub.2] from the atmosphere to skeletal muscles, there are a variety of problems that can have an adverse effect.

Respiratory Muscle Dysfunction and Chest Wall Deformities

Respiratory muscle dysfunction and chest wall deformities limit the ability of the thorax to expand, and therefore pulmonary ventilation is compromised. Respiratory muscle dysfunction can be caused by paralysis or partial paralysis of the respiratory muscles and often occurs with cervical spinal cord injuries and Guillain-Barre syndrome.[12,13] Progressive muscular diseases, such as muscular dystrophy and amyotrophic lateral sclerosis, can cause myopathy of respiratory muscles.[13] Chest wall deformities occur with ankylosing spondylitis, kyphosis, and Scoliosis.[14] A noncompliant or rigid chest wall also can limit thoracic expansion, a condition that occurs with aging.[15] If the condition is severe, VT at rest may be decreased, requiring an increased breathing frequency for adequate (VE). With less severe conditions, individuals may be limited in their ability to increase (VT) or breathing frequency during exercise, resulting in a decrease in maximal exercise capacity.

Ventilation-Perfusion (V/Q) Mismatching

In conditions in which parts of the lung are perfused but not ventilated, or ventilated with poor perfusion, effective gas exchange cannot occur. The term "ventilation-perfusion (V/Q) mismatching" is used to describe inequalities between areas of (VE) and perfusion. This condition can occur with the obstructive lung diseases of emphysema and chronic bronchitis because (VE) is not evenly distributed to parts of the lungs and blood flow is affected by destruction of portions of the capillary bed.[16] The result is a decrease in Pa[O.sub.2] or an increase in Pac[O.sub.2]. Perfusion of parts of the lungs could be decreased because of vascular abnormalities such as pulmonary emboli. The result of this condition is an increase in alveolar dead space, or "wasted" (VE). Alveolar dead space is the volume of gas in alveoli that are ventilated, but poorly perfused or underperfused.[17] This condition occurs when blood flow is blocked by a pulmonary embolus. The opposite condition occurs with pulmonary fibrosis, where selected alveoli are replaced with scar tissue, decreasing (VE) to areas with normal perfusion.[18] Adequate perfusion without (VE) is referred to as a shunt.

Diffusion Abnormalities

Movement of gases across the alveolar-capillary membrane may be limited because of abnormalities in the membranes or because of an accumulation of fluid in the alveoli or interstitial space. Pulmonary diseases that result in thickening of the alveolar capillary membrane cause an impairment in diffusion. A common example is idiopathic pulmonary fibrosis.[19] In pulmonary edema or congestive heart failure, fluid fills the space between the capillaries and alveoli. Both of these conditions result in impaired diffusion of [O.sub.2] from the alveoli to the capillary blood, resulting in an abnormally low Pa[O.sub.2]. The condition worsens with activity because blood moves faster through the pulmonary capillaries and there is less time for diffusion. In Figure 3, the effect of exercise on [O.sub.2] transfer in the pulmonary capillary is illustrated.

Inadequate Cardiac Output

Cardiac abnormalities have the potential to impair cardiac output either at rest or during activity. Common problems involving the heart include myocardial ischemia, heart failure, valvular abnormalities, and cardiac dysrhythmias. Myocardial ischemia can result from either atherosclerosis or vasospasm of coronary arteries.[20] Chronic heart failure involves impaired contractile function of cardiac muscle and can occur as a result of many causes including coronary artery disease, myocarditis, hypertension, and some systemic diseases.[21] Valvular abnormalities prevent the normal flow of blood through the heart and result from a variety of causes including rheumatic fever, myocardial infarction, and congenital abnormalities.[22] Of the many types of cardiac arrhythmias, those that have the greatest potential to limit CO include ventricular dysrhythmias and heart blocks.[23] If any of these conditions is severe, CO at rest may not be sufficient to meet the needs of the body. With less severe conditions, CO may be adequate at rest but inadequate during the stress of physical activity. Consequently, [O.sub.2] delivery to active skeletal muscles is impaired, requiring an increase in energy generation using anaerobic metabolic pathways. Blood levels of lactic acid increase, producing metabolic acidosis, which can be manifested as fatigue, dyspnea, or limited exercise tolerance. Other signs and symptoms of inadequate CO include skin color changes such as pallor or cyanosis, light-headedness or dizziness, and weakness.

Limitations in Peripheral Blood Flow

If the ability to either vasodilate or vasoconstrict in parts of the circulation is impaired, then [O.sub.2] delivery to active skeletal muscle may be impaired. In persons with atherosclerosis involving peripheral arteries, blood flow may be decreased by the atherosclerotic lesion or by the inability of sclerotic vessels to vasodilate.[24] Ischemia, producing pain and limiting physical activity, results when muscles become active and require additional [O.sub.2].

In persons with spinal cord injuries, normal SNS control of peripheral blood vessels' may not be present. Without sympathetic control, the reflex vasoconstriction in inactive skeletal muscle and in visceral organs that normally occurs with activity will not occur.[25] Consequently, blood flow to skeletal muscle may be limited because blood is not being diverted from other tissues. The inability to vasoconstrict in appropriate parts of the vascular system also can affect skin blood flow and limit heat dissipation. Without adequate [O.sub.2], active skeletal muscles must increase their use of anaerobic energy generating pathways. The outcome is fatigue and dyspnea because of increased lactic acid and metabolic acidosis.

Low Oxygen-Carrying Capacity

The most common condition producing a decrease in 2-Carrying capacity is anemia. In persons with anemia, as the blood moves through the circulatory system, the [PO.sub.2] drops faster than usual as [O.sub.2] leaves the limited amount of hemoglobin.[1] As the blood reaches skeletal muscle, the low [PO.sub.2] levels may not provide a sufficient gradient for diffusion of [O.sub.2] from blood to skeletal muscle. Consequently, lactic acid increases, and metabolic acidosis and fatigue result. A common compensatory mechanism is tachycardia, which assist in increasing CO. A potential consequence is an exaggerated increase in HR in response to low-intensity activities.

Signs and Symptoms of Cardiovascular or Pulmonary Abnormalities

When the cardiovascular or pulmonary system cannot respond appropriately to the increased demand of exercise, abnormal physiological responses or symptoms of activity intolerance occur. The abnormalities provide clues to the underlying pathology. Problems often become symptomatic first during activity when the cardiopulmonary system is stressed. As the condition becomes more severe, signs and symptoms also may occur at rest. BY carefully observing symptoms and documenting responses during activity, early detection of cardiopulmonary problems is possible. A summary of common signs and symptoms is presented in the Table.

Table.
Signs and Symptoms Associated With Abnormalities of the
Cardiovascular and Pulmonary Systems

Condition                 Signs/Symptoms
Respiratory distress   Difficulty breathing as demonstrated by
                        shortness of breath, increased breathing
                        rate, use of accessory muscles, and nasal
                        flaring
                      Chronic coughing
                      Changes in skin color (pallor or cyanosis)
Cardiac dysfunction   Abnormal responses to activity such an
                       excessively high or low heart rate,
                       decreasing systolic blood pressure,
                       increased diastolic blood pressure,
                       changes in electrocardiographic activity
                       or heart sounds, excessive fatigue
                     Chest pain
                     Dyspnea
Peripheral vascular  Intermittent claudication
  disease            Decreased or absent peripheral pulses
                     Changes in the appearance of involved
                      extremities, which may include dry or
                      cool skin, hair loss, or muscular atrophy

Signs and Symptoms of Respiratory Distress

One of the most common symptoms of respiratory distress is dyspnea, or the sensation of difficult or labored breathing. Having difficulty breathing, or being out of breath," is expected when working at or near maximal capacity but not when working at low or moderate levels of effort. Dyspnea also can occur at rest and is easily detected because patients cannot complete a full sentence without stopping to breathe. Another symptom of a problem involving the respiratory system is a chronic cough. Whether the cough is productive or not, characteristics of sputum such as consistency, color, and smell are important to identifying the problem.[26]

A rapid breathing rate, or tachypnea, also may indicate distress. Persons who are unable to increase (VE) by increasing VT or depth of breathing rely on their ability to increase the breathing rate. Increasing the breathing rate, rather than VT, is a less efficient strategy of increasing (VE) because there is a relative increase in dead-space (VE). A change in the regularity of breathing also may indicate abnormal function. Normal breathing involves regular inspiration and expiration, with a deep breath or sigh interspersed periodically. An example of an abnormal breathing pattern is Cheyne-Stokes respiration, which involves increasing and decreasing the depth of breathing, with periods of apnea interspersed.[27] This pattern often occurs in patients with heart failure or cerebrovascular disease.[28]

Other signs of respiratory distress include use of accessory breathing muscles, changes in skin color, behavioral changes, and nasal flaring. Increased use of neck muscles for inspiration or abdominal muscles for expiration is abnormal when resting or performing low levels of exercise. Cyanosis or pallor is an indication of abnormal oxygenation, or hypoxemia. Behavioral changes, such as confusion or agitation, also can indicate hypoxemia. Nasal flaring is a sign of severe distress and occurs when individuals exert increased effort during inspiration.

Signs and Symptoms of Cardiac Dysfunction

One of the most common symptoms of a cardiac problem is angina, or chest pain. Angina may be described by patients as a feeling of heaviness, pressure, or burning rather than as a painful sensation. The discomfort associated with angina may occur in areas other than the chest, such as the arms, cervical region, jaw, or upper back. The term exedional angina is used if the pain occurs during activity and is relieved when the individual stops the activity. Exertional angina is thought to result from myocardial ischemia due to an increase in myocardial [O.sub.2] demand that cannot be met because atherosclerosis limits an increase in blood flow to the heart. Chest pain that occurs at rest can indicate a coronary artery spasm or an impending myocardial infarction.[29] Chest pain also can result from other causes, including pericarditis, pleural effusion, or a musculoskeletal injury. Differentiating angina from other problems associated with chest pain is an important part of the clinical assessment.[30]

Other symptoms of cardiac dysfunction include dyspnea, light-headedness or dizziness, and fatigue. Dyspnea, typically associated with pulmonary dysfunction, often occurs with myocardial ischemia and heart failure. Dyspnea also can occur in patients with left ventricular hypertrophy, which often is caused by hypertension or aortic valve disease and results in impaired ventricular relaxation. Light-headedness or dizziness is associated with heart failure or myocardial ischemia, and also with hypotension. Fatigtie that results from routine activities, or that occurs with low-intensity exercise, is associated with heart failure.

Signs of cardiac dysfunction include abnormal responses to exercise. An HR that is either excessively high or exceptionally low during exercise may indicate heart disease. The amount of increase in HR with activity is related to the intensity of the activity, age of the individual, medications, and ambient temperature.[31] Heart rate responses that are either higher or lower than would be expected based on these factors could indicate an abnormality. Abnormal blood pressure responses include either a systolic blood pressure that does not rise progressively as work level increases or a systolic blood pressure that falls during exercise. An increase in diastolic blood pressure during exercise that is greater than 15 to 20 mm Hg also is considered abnormal.[32] Other signs include electrocardiographic changes such as dysrhythmias or St-segment depression and changes in heart sounds.

The patients's age, medications, and corresponding symptoms must be considered when interpreting abnormal responses to exercise. A single abnormal finding in a patient who is asymptomatic may not be indicative of a problem, whereas multiple abnormal findings in a patient who is symptomatic provide support for a cardiac abnormality. An example is a rapid HR, a falling blood pressure response, and the appearance of a third heart sound, a combinafion of abnormal findings that suggests heart failure.

Signs and Symptoms of inadequate Peripheral Blood Flow

Intermittent claudication is one of the most common symptoms of inadequate peripheral blood flow. Pain rcsulting from ischemia occurs when [O.sub.2] delivery cannot meet the increased [O.sub.2] requirements of active skeletal muscle. Discomfort typically occurs during walking and is relieved when the individual stops to rest. Pain also may occur when the lower extrcmitics are elevated, with relief occurring when the extremities are moved to a dependent position.

Chronic deprivation of [O.sub.2] often produces trophic changes, which include muscle atrophy, hair loss, and dry skin.[33] The skin may feel cool, and peripheral pulses in corresponding arteries may be weak or absent. Changes in skin color with clevation of the involved extremities also may occur. Typically, there is blanching of the skin with elevation, followed by redness when the extremity is returned to the dependent position. The timing of the changes in skin color can be used to estimate the severity of the condition.[34]

Summary

The cardiovascular and pulmonary systems are essential to normal movement because of their role in delivering [O.sub.2] from the atmosphere to active skeletal muscle. There are multiple steps involved in the transfer of [O.sub.2] from the air to blood and in the delivery of [O.sub.2]-rich blood to metabolically active tissues. An impairment in any of the steps can result tin inadequate [O.sub.2] delivery. By understanding and identifying the mechanism involved when [O.sub.2] delivery is iiiadequate, therapists can. determine optimal methods of patient management.

In the early stages of cardiovascular and pulmonarv diseascs, the signs and symptoms may be subtle. Careful observation and monitoring of responses during and after physical activity is important to be able to identifn' potential problems. Because of their role in physical rehabilitation, physical therapists are in a position to identify problems. Early identification of problems may lead to treatment that may arrest or slow the progression of the disease.

[Figures 1 to 4 ILLUSTRATION OMITTED]

References

[1] Wasserman K, Hansen JE, Suc DY, Whipp BJ. Principles of Exercise Testing and Interlyretation. Philadelphia, Pa: Lea & Febiger; 1987. [2] Astrand PO, Rodahl K. Textbook of Work Physiolog. New York, NY: McGraw-Hill Book Co; 1986. [3] Saltin B, Aslrand PO. Maximal oxygen uptake in athletes. J Appl Physiol 1967;23:353-358. [4] Reid WD, Dechman G. Considerations when testing and training the respiratory muscles. Phys Ther. 1995;75:971-982. [5] Taylor A. The contribution of the intercostal muscles to the effort of respiration in man. J Physiol (Lond). 1960; 151:390-402. [6] West JB. Respiratory Physiolog. Baltimore, Md: Williams & Wilkins; 1979. [7] Guyton AC. Textbook of Medical Physiology. Philadelphia, Pa: WB Saunders Co; 1991. [8] Poliner LR, Dehnier G , Lewis SE, et al. Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and stipine positions. Circulation. 1980;62:528-534. [9] Olsson RA. Local factors regulating cardiac and skeletal muscle blood flow. Annu Rev Physiol. 1981;43:385-395. [10] Wasserman K, Whipp BJ, Casaburi R. Respiratory control during exercise. In: Cherniack N, Widdicombe JG, eds. Handbook of Physiology Volume 2. Bethesda, Md: American Physiological Society; 1986:595-619. [11] Eldridge FL, Millhorn DE, Aaldrop TG. Exercise hyperpnea and locomotion: parallel activation from the hypothalamus. Science. 1981; 211:844-846. [12] Wetzel JL, Lunsford BR, Perterson MJ, Alvarez SE. Respiratory rehabilitation of the patient with a spinal cord injury. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:579-603. [13] Prakash UBS. Netirologic diseases. In: Baum GL, Wolinsky E, eds. Textbook of Pulmonary Diseases. Boston, Mass: Little, Brown and Coinpany Inc; 1989:1409-1436. [14] Prakash UBS. Skeletal diseases. In: Baum GL, Wolinsky E, eds. Textbook of Pulmonary Diseases. Boston, Mass: Little, Brown and Company Inc; 1989:1437-1446. [15] Mittman C, Edelman NH, Norris AH, Shock NW. Relationship between chest wall and pulmonary compliance and age. J Appl Physiol. 1965;20:1211-1216. [16] West JB. Pulmonary Pathophysioloay. 2nd ed. Baltimore, Md: Williams & Wilkins; 1987. [17] Shaffer TH, Wolfson MR, Gault JH. Respiratory physiology. In: Invin S, Tecklin JS, eds. Cardiopulmonaty Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:237-264. [18] Tecklin JS. Common pulmonary diseases. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:26.9-291. [19] Clough P. Restrictive lung dysfunction. In: Hillegas EA, Sadowsky HS, eds. Essentials ofcardiopulmonaty Physical Therapy, Philadelphia, Pa: WB Saunders Co; 1994:189-255. [20] McColgan G. Ischcmic cardiac conditions. In: Hillegas F-A, Sadowsky HS, eds. Essentials of Cardiopulmonary Physical Therapy. Philadelphia, Pa: WB Saunders Co; 1994:99-121. [21] Braunwald E. Clinical manifestations of heart failure. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, Volume 1. Philadelphia, Pa: WB Saunders Co; 1988:471-484. [22] Braunwald E. Valvular heart disease. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, Volume 1. Philadelphia, Pa; WB Saunders Co; 1988:1023-1092. [23] Brown KR, Jacobson S. Mastering Dysrhythmias. Philadelphia, Pa:FA Davis Co; 1988. [24] Barker NAT. Peripheral Arterial Disease. 2nd ed. Philadelphia, Pa: WB Saunders Co, 1975. [25] Glaser RM. Pxercise and Locomotion for the Spinal Cord Injured. New York, NY: Macmillan Publishing Co; 1985:263-303. [26] Fishman AP. Pulmonaty Diseases and Disorders. New York, NY: McGraw-Hill Book Co; 1980. [27] Comroe JH. Physioloay of Respiration. 2nd ed. Chicago, Ill: Year Book Medical Publishers; 1974. [28] Cherniack NS. The regulation of ventilation. In: Fishman AP, ed. Pulmonary Diseases. New York, NY: McGraw-Hill Book Co; 1980:317-330. [29] Hurst JW. The recognition and treatment of four Lypes of angina pectoris and angina equivalents. In: Hurst JW, Schlant RC, Rackley CE, et al, eds. The Heati. New York, NY: McGraw-Hill Information Services Co; 1990:1046-1052. [30] Invin S, Blessey RL. Patient evaluation. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:106-141. [31] Irwin S. Abnormal exercise physiology. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:92-105. [32] Sheps DS, Ernst JC, Briese FW, Myerburg RJ. Exercise-induced increase in diastolic pressure: indicator of severe coronary artery disease. Am J Cardiol. 1979;43:708-712. [33] Eisenhardt Jr. Evaluation and physical treatment of the patient with peripheral vascular disorders. In: Irwin S, Tecklin JS, eds. Cardiopulmonary Physical Therapy. 3rd ed. St Louis, Mo: Mosby-Year Book Inc; 1995:215-233. [34] Winsor T, Hyman C. A Pyimer ofpmpherat Vascular Diseases. Philadelphia, Pa: Lea & Febiger; 1965.

C. Peel, PhD, PT, is Associate Professor, Department of Physical Therapy, School of Pharmacy and Allied Health Professions, Creighton University, Omaha, NE 68178 (USA) ([e-mail]).