Treadmill and Pharmacologic Stress Testing

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

Feil and Seigel first noticed the significance of cardiovascular exercise stress testing in 1928; they reported ST and T changes following exercise in 3 patients with chronic stable angina.1 The following year, Master and Oppenheimer introduced a standardized exercise protocol to assess functional capacity and hemodynamic response.

Continued research into causal mechanisms of ST displacement, refinement of exercise protocols, and determination of diagnostic and prognostic exercise variables in clinical patient subsets have continued to evolve since 1929.

After the establishment of coronary angiography as a diagnostic tool, the limitation of exercise-induced ST-segment depression as a diagnostic marker for obstructive CAD in patient populations with a low disease prevalence became apparent.

Introduction

Exercise testing is a cardiovascular stress test using treadmill bicycle exercise with 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, and echocardiography, can provide further information that may be needed in selected patients, such as those with moderate or prior risk.

Exercise physiology

The initiation of dynamic exercise results in increases in the ventricular heart rate, stroke volume, and cardiac output due to vagal withdrawal and sympathetic stimulation. Also, alveolar ventilation and venous return increase as a result 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).

Venous and arterial norepinephrine release from sympathetic postganglionic nerve endings is increased, and epinephrine levels are increased at peak exertion, resulting in an increase 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.

The maximum heart rate and cardiac output are decreased in older individuals, related in part to decreased beta-adrenergic responsiveness. Maximum heart rate can be calculated by subtracting the patient's age (y) from 220 (has a standard deviation of 10-12 beats per minute [bpm]). The age-predicted maximum heart rate is a useful measurement for safety reasons and as an estimate of 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 of discontinuing exercise. The return of vagal stimulation is an important cardiac deceleration mechanism after exercise and is more pronounced in well-trained athletes but 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.