55 Cardiopulmonary Exercise Testing in Children with Congenital Heart Disease

Exercise is a common physiologic stress that places demands on multiple organ systems, including skeletal muscle, cardiac muscle, and the pulmonary and systemic circulations. The physiologic response of the heart (to increase cardiac output by increasing heart rate and stroke volume) and lungs (to increase ventilation capacity) to this stress are tightly coupled with the metabolic demands of exercising muscle.

Increased skeletal muscle contraction that occurs with exercise increases the demand for oxygen delivery and for the clearance of important by-products of metabolic work, including CO₂, lactate, and heat (Fig. 55-1). Several processes, including increased oxygen extraction from blood perfusing the active muscles, vasodilation of selected peripheral vascular beds, increased cardiac output, and increased pulmonary blood flow and ventilation, mediate this increased demand. The body’s capacity to deliver and utilize oxygen is determined empirically as maximum oxygen consumption (VO_2max). As defined by the Fick principle, the relationship between oxygen consumption (VO₂), cardiac output (CO), and the arteriovenous oxygen difference (AVO₂ difference) is

Figure 55-1 Physiologic effects of exercise.

AV, atrioventricular; ECG, electrocardiogram; SA, sinoatrial.

By further describing CO as the product of stroke volume (SV) and heart rate (HR), the relationship becomes

Early in exercise, cardiac output is augmented by increases in stroke volume (contractility) and heart rate. Increased venous return and ventricular filling pressure may in part cause increased stroke volume as predicted by the Frank-Starling relationship. Later in exercise, increases in cardiac output are more closely related to increases in heart rate. The heart rate response to exercise is mediated by increased sympathetic tone and decreased parasympathetic (vagal) influence on the heart. Increased heart rate generally parallels increased oxygen uptake and workload and occurs primarily at the expense of diastolic time, which, in some disease states, can result in inadequate ventricular filling time at elevated heart rates. The AVO₂ difference, which normally results in about 23% extraction of oxygen at rest, may increase more than threefold at VO_2max. Arterial oxygen levels remain essentially normal throughout exercise in individuals with normal cardiopulmonary function.

Mean arterial blood pressure is essentially the product of cardiac output and peripheral vascular resistance. The increased cardiac output that occurs with exercise is associated with a marked decrease in peripheral vascular resistance, resulting in a progressive increase in systolic blood pressure and unchanged or mildly decreased diastolic blood pressure. The expected increase in systolic pressure is positively related to body size and age. Attenuated systolic blood pressure responses to exercise may reflect a limitation of cardiac output or an alteration of vascular resistance control.

The ventilatory response to exercise is tightly coupled with production of CO₂. Both tidal volume and respiratory rate increase during progressive exercise to keep pH and PCO₂ (partial pressure of CO₂) constant over a wide range of metabolic work rates. Acidosis occurs only during heavy exercise because of increased blood lactate concentrations. Dyspnea occurring during moderate exercise is due to the increased need for CO₂ release and the tight coupling of minute ventilation to CO₂ production. Further increases in CO₂ production with intense exercise result in a decline in serum sodium bicarbonate, a disproportionate increase in hydrogen ion levels, and consequent acidosis, resulting in a hyperventilatory response.

Normal Responses of Children to Exercise

A complete exercise evaluation includes, at a minimum, the measurement of heart rate and blood pressure and evaluation of the exercising ECG for pathologic changes and for the presence or absence of exercise-induced arrhythmias. In children, the normal response to exercise is for the heart rate to increase due to sinus tachycardia to a maximum of 190 to 200 bpm, with no evidence of atrioventricular block during exercise. The presence of atrial and/or ventricular ectopy, either of which can be stimulated by exercise, is considered an abnormal response. ECG intervals follow characteristic changes; the PR interval generally shortens with exercise and the resultant tachycardia. The QRS duration remains unchanged or shortens slightly. The normal response of the QT interval is to be unchanged or to shorten, but this shortening is often difficult to document because of the merging of the end of the T wave with the following P wave. The interpretation of the ST segment is sometimes difficult because of physiologic J-point depression, but the normal slope of the ST segment at peak exercise is upward instead of flat or downward.

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