Stress Testing By Treadmill

Published Date: January 1st, 2013

Exercise testing is a cardiovascular stress test that uses treadmill bicycle exercise with electrocardiography (ECG) and blood pressure monitoring. Pharmacologic stress testing, established after exercise testing, is a diagnostic procedure in which cardiovascular stress induced by pharmacologic agents is demonstrated in patients with decreased functional capacity or in patients who cannot exercise. Pharmacologic stress testing is used in combination with imaging modalities such as radionuclide imaging and echocardiography.

Exercise stress testing, which is now widely available at a relatively low cost, is currently used most frequently to estimate prognosis and determine functional capacity, to assess the probability and extent of coronary disease, and to assess the effects of therapy. Ancillary techniques, such as metabolic gas analysis, radionuclide imaging (see the images below), and echocardiography, can provide further information that may be needed in selected patients, such as those with moderate or prior risk.

Normal radionuclide uptake (dipyridamole-Cardiolit
Normal radionuclide uptake (dipyridamole-Cardiolite).
Normal wall motion with radionuclide uptake.
Normal wall motion with radionuclide uptake.

Cardiovascular exercise stress testing in conjunction with ECG has been established as one of the focal points in the diagnosis and prognosis of cardiovascular disease, specifically coronary artery disease (CAD).

Exercise physiology

The initiation of dynamic exercise results in increases in ventricular heart rate, stroke volume, and cardiac output as a result of vagal withdrawal and sympathetic stimulation. Alveolar ventilation and venous return also increase as a consequence of sympathetic vasoconstriction. The overall hemodynamic response depends on the amount of muscle mass involved, exercise efficiency, conditioning, and exercise intensity.

In the initial phases of exercise in the upright position, cardiac output is increased by an augmentation in stroke volume mediated through the use of the Frank-Starling mechanism and heart rate. The increase in cardiac output in the later phases of exercise is due primarily to an increase in ventricular rate.

During strenuous exertion, sympathetic discharge is maximal and parasympathetic stimulation is withdrawn, resulting in autoregulation with generalized vasoconstriction, except in the vital organs (cerebral and coronary circulations).

Release of venous and arterial norepinephrine from sympathetic postganglionic nerve endings is increased, and epinephrine levels are increased at peak exertion, resulting in a rise in ventricular contractility. As exercise progresses, skeletal muscle blood flow increases; oxygen extraction increases as much as 3-fold; peripheral resistance decreases; and systolic blood pressure (SBP), mean arterial pressure, and pulse pressure usually increase. Diastolic blood pressure (DBP) remains unchanged or may increase or decrease by approximately 10 mm Hg.

The pulmonary vascular bed can accommodate as much as a 6-fold increase in cardiac output, with only modest increases in pulmonary arterial pressure, pulmonary capillary wedge pressure, and right atrial pressure; this is not a limiting determinant of peak exercise capacity in healthy subjects.

Maximum heart rate and cardiac output are decreased in older individuals, in part because of decreased beta-adrenergic responsiveness. Maximum heart rate can be calculated by subtracting the patient’s age (in years) from 220 (standard deviation, 10-12 beats/min).

The age-predicted maximum heart rate is a useful measurement for safety purposes and for estimating the adequacy of the stress to evoke inducible ischemia. A patient who reaches 80% of the age-predicted maximum is considered to have a good test result, and an age-predicted maximum of 90% or better is considered excellent.

In the postexercise phase, hemodynamics return to baseline within minutes after exercise is discontinued. The return of vagal stimulation is an important cardiac deceleration mechanism after exercise; it is more pronounced in well-trained athletes but is blunted in patients with chronic congestive heart failure.

Intense physical work or important cardiorespiratory impairment may interfere with achievement of a steady state, and an oxygen deficit occurs during exercise. The oxygen debt is the total oxygen uptake in excess of the resting oxygen uptake during the recovery period.


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