Chapter 12: Exercise Physiology (continued)

from Pulmonary Physiology in Clinical Practice, copyright 1999 by

Lawrence Martin, M.D.

CLINICAL USE OF PHYSIOLOGIC EXERCISE TESTING

Physiologic exercise testing is a useful tool in several clinical situations (see box on p. 250).

Several points should be emphasized about physiologic exercise testing in the clinical setting.

1. Physiologic exercise testing is different from the standard cardiac 'stress test.' Although the two tests can be combined, in practice the cardiac stress test usually looks for evidence only of ECG abnormalities or of coronary insufficiency (chest pain or ST segment depression); it does not ordinarily assess oxygen uptake or make any attempt to diagnose noncardiac causes of dyspnea. Most hospitals maintain a facility for cardiac stress testing, but relatively few also provide for physiologic stress testing.

2. Physiologic exercise testing is only indicated after completion of a full clinical evaluation (history and physical examination, chest xray, hematocrit, resting pulmonary function tests, blood gas analysis, and electrocardiogram), and is used to provide information not otherwise available.

3. Exercise testing is only an adjunct to the clinical evaluation and, like any other test, should be interpreted in light of the full clinical picture. Just as a clinical diagnosis would not be made on the basis of a chest x-ray or blood gas analysis alone, a diagnosis should not be made based on the exercise test alone. Exercise measurements should never substitute for intelligent assessment of the history, physical examination, and other relevant laboratory data. Careful patient observation is also important during the test to gauge the level of cooperation and understanding, as well as for qualitative assessment of the patient's symptoms.

4. Before interpreting exercise test data, one should at least have available the following:

a. Reason for the test (e.g., dyspnea on exertion)

b. Results of physical examination, particularly with regard to heart or lung disease, orthopedic impairment, and neuromuscular problems

c. Results of resting ECG, chest x-ray, hematocrit, and spirometry (including maximal voluntary ventilation)

d. Assessment of the patient's effort during the test. (A physician is always present or close by during the test, but data interpretation may be done by someone who was not present.)

Fig. 12-6. Exercise limitation caused by heart disease. A, Heart rate. B, O2-pulse.

CLINICAL INTERPRETATION OF PHYSIOLOGIC EXERCISE TESTING

All organic causes of dyspnea arise from interference with oxygen delivery to the exercising muscles. The following discussion concentrates on differentiating among cardiac disease, respiratory disease, and poor physical fitness as a cause for exercise limitation. The need to make this distinction is a common reason for physiologic exercise testing.

Cardiac disease. The heart limits exercise when cardiac output cannot meet the body's oxygen needs. This limitation can come about from either inadequate stroke volume (SV) or heart rate (HR). Cardiac output impairment is usually caused by inadequate stroke volume; to compensate for reduced stroke volume, heart rate and oxygen extraction will increase (see Equation 2). Since the heart rate is inappropriately high for the level of oxygen consumption, the O₂-pulse (VO₂/HR) is reduced (Figs. 12-6, A, and 12-6, B). A lower-than expected O₂-pulse is the hallmark of exercise limitation caused by heart disease.

As a result of cardiac limitation to oxygen delivery, the patient experiences an early anaerobic threshold; lactic acid production and hyperventilation (reduced PaCO₂) begin at relatively low level of oxygen uptake. Severe dyspnea ensues, and the patient is unable to reach his maximal exercise capacity.

Respiratory disease. Respiratory impairment can generally limit exercise in one of two ways: (1) decrease in total or minute ventilation (VE); and (2) impairment of gas transfer across the alveolar-capillary membrane.

A decrease in VE is seen in patients with severe restrictive or obstructive lung disease. VE during exercise is a useful measurement, in part because the patient can serve as his own control. The maximal total ventilation is usually measured before exercise testing as the maximal voluntary ventilation (MVV). If MVV is not measured, it can be closely approximated by multiplying the patient's forced expiratory volume, 1 sec (FEV1) by 35. For example, if FEV1 is 3 L, the patient's MVV should be approximately 105 L/min.

With an intact respiratory system, VE is never the limiting factor in exercise. Healthy subjects reach only approximately 60% to 70% of their ventilatory capacity (MVV) at the point of maximal oxygen consumption. A patient who stops exercising (because of dyspnea) when VE is close to his MVV has inadequate ventilatory reserve. Typically, with ventilatory impairment exercise stops well before the anaerobic threshold is reached ( Fig. 12-7). If exercise continues beyond the patient's ventilatory limit, PaCO₂ will likely rise, something that never happens in healthy patients.

Impairment of gas transfer across the alveolar-capillary membrane will cause an abnormal increase in the alveolar-arterial PO₂ difference during exercise. The most common cause of hypoxemia at rest is ventilation/perfusion (V/Q) imbalance (see Chapter 5), but resting V/Q imbalance does not predict hypoxemia during exercise. In many cases V/Q relationships improve during exercise, so the PaO₂ may actually increase (it normally remains unchanged). The change in PaO₂ is a distinguishing point between chronic bronchitis and emphysema; in the former, PaO₂ stays the same or improves with exercise, whereas in emphysema, PaO₂ characteristically falls.

Fig. 12-7. Exercise limitation caused by ventilatory impairment.

The PaO₂ usually falls during exercise when there is diffusion impairment. Normally, as cardiac output speeds through the pulmonary capillaries, the large reserve for diffusion assures that end-capillary PO₂ is maintained at a normal level. Diffusion impairment causes a fall in end-capillary and arterial PO₂ during exercise (Fig. 12-8, p. 254). This fall in PaO₂ is seen in emphysema (loss of capillary vascular bed) and interstitial lung disease (thickening of alveolar capillary membrane).

Poor physical fitness. Exercise limitation from poor physical fitness can usually be appreciated from the pattern of ventilatory and cardiac response in relation to the work load and oxygen uptake. Commonly the subject ''poops out" well before anaerobic threshold, although the heart rate and VE have increased appropriately for the level of exercise. Occasionally the heart rate or VE will rise more than expected for the level of work because of anxiety or early (and inappropriate) hyperventilation, respectively. Nonetheless, by carefully analyzing the exercise data in light of the total resting evaluation, poor fitness can usually be distinguished from cardiac and respiratory limitation.

Based on the previous discussion, exercise test interpretation can be approached systematically. This approach is based on testing that includes Group 1, 2, and 3 measurements (see Table 12-1).

1. Determine if anaerobic threshold is reached. Generally, AT is determined from analysis of respiratory quotient, end-tidal partial pressure of carbon dioxide (PetCO₂), and ratio of slope of VE to the slope of oxygen consumption (VO₂) (see Fig. 12-4 and box on p. 246). Normally, anaerobic threshold (AT) should occur at an oxygen consumption near 20 ml/min/kg; for a 50-kg person, this is a VO₂ of 1 L/min.

2. Determine if ventilatory limit has been reached by comparing the patient's exercise minute ventilation to his resting maximal voluntary ventilation (MVV). If MVV was not measured before the exercise test, use 35 x FEV1 to estimate MVV.

3. If blood gas analysis is available, check for fall in PaO₂ and calculate the alveolar-arterial oxygen pressure difference (P(A-a)O₂) (see Chapter 5). Check for an early fall in Paco,; a decrease in PaCO₂ before AT may indicate hyperventilation from anxiety. Any increase in PaCO₂ during exercise is abnormal and indicates severe ventilatory limitation.

The following cases illustrate this approach.

Fig. 12-8. Exercise limitation caused by diffusion impairment. PaO2 falls in the presence of diffusion impairment.

SUMMARY

During exercise much more oxygen and carbon dioxide are exchanged than at rest. This single metabolic fact accounts for the changes in cardiac, pulmonary, and circulatory physiology during exercise. When the cardiopulmonary system can no longer deliver enough oxygen for the increase in metabolism during exercise, the body turns to anaerobic metabolism to furnish energy. Whereas aerobic exercise can continue indefinitely, anaerobic metabolism leads to buildup of lactic acid and results in early dyspnea and fatigue.

Mild-to-moderate exercise, i.e., exercise done before anaerobic threshold is reached, does not lead to hyperventilation. Alveolar ventilation rises to meet the increase in carbon dioxide production so that PaCO₂ stays fairly constant. At the point where anaerobic threshold begins, lactic acid increases and PaCO₂ falls.

Many measurements can be made during exercise. Exercise measurements can be grouped according to the equipment required and range from totally noninvasive (no mouthpiece or needles) to highly invasive (right-sided heart catheter). The pattern of changes in heart rate, minute ventilation, expired gases, and many other measurements can be helpful in some clinical situations. Indications for physiologic exercise testing include dyspnea during exertion that is unexplained by resting studies and the need for evaluation of exercise-induced asthma.

Two common limitations to exercise are heart disease and lung disease. In heart disease, the heart rate often rises higher than predicted for the level of exercise; in lung disease, minute ventilation may not rise to the expected value for a given level of exercise. Diffusion impairment can also limit exercise. Although diffusion impairment does not generally lead to reduced PaO₂ at rest, it can cause a fall in PaO₂ during mild-to-moderate exercise.

REVIEW QUESTIONS

State whether each of the following is true or false.

1.Both oxygen uptake and carbon dioxide production increase during exercise.

2.Hyperventilation (reduction in PaCO₂) during exercise usually begins when pulse rate and respiratory rate rise by 20% to 25% above resting levels.

3.Anaerobic threshold can be identified by a rise in minute ventilation out of proportion to the rise in oxygen uptake.

4.Diffusion barrier that does not cause hypoxemia at rest will not lead to hypoxemia during exercise.

5.In the healthy individual, alveolar ventilation will always rise to meet any increase in carbon dioxide production so that hypercapnia never occurs during exercise.

6.Given a patient with chronic obstructive pulmonary disease, a fall in exercise PaO₂ is more characteristic of emphysema than of chronic bronchitis.

7.With increasing amounts of exercise, the level of oxygen uptake also rises and never reaches a plateau.

8.One measure of fitness is the level of oxygen uptake for a given amount of exercise.

9.Daily aerobic exercise leads to improved air flow rates as measured by spirometry.

10.Daily aerobic exercise leads to a reduction of resting heart rate.

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