Heart Rate and Electrocardiogram

Heart rate and rhythm should be monitored continuously using one or more modified chest leads. Standard precordial chest lead configurations (V₁–V₆) allow comparison with resting 12-lead tracings (Criteria for Acceptability 7-1). Twelve-lead monitoring during exercise is practical with electrocardiographs designed for exercise testing. These instruments incorporate filters (digital or analog) that eliminate movement artifact and provide ST-segment monitoring. Limb leads normally must be moved to the torso for ergometer or treadmill testing (modified leads). A resting ECG should be performed to record both the standard and modified leads. Single-lead monitoring allows only for gross arrhythmia detection and HR determination. It may not be adequate for testing patients with known or suspected cardiac disease.

The ECG monitor should allow the assessment of intervals and segments up to the patient’s maximal heart rate (HRmax). Computerized arrhythmia recording or manual “freeze-frame” storage allows the subsequent evaluation of conduction abnormalities while the testing protocol continues (Figure 7-4). Some digital ECG systems generate computerized “median” complexes averaged from a series of beats. These may be helpful in analyzing ST-segment depression. The “raw,” or nondigitized, ECG should also be available. Significant ST-segment changes should be easily identifiable from the tracing up to the predicted HRmax.

HR should be analyzed by visual inspection of the ECG, with manual measurement of the rate rather than by an automatic sensor. Most HR meters average RR intervals over multiple beats. Inaccurate HR measurements may occur with nodal or ventricular arrhythmias or because of motion artifact. Tall P or T waves may be falsely identified as R waves, causing automatic calculation of HR to be incorrect. Accurate measurement of HR is necessary to determine the patient’s maximal HR in comparison with the age-related predicted value.

Motion artifact is the most common cause of unacceptable ECG recordings during exercise. Allowing the patient to practice pedaling on the ergometer or walking on the treadmill permits adequacy of the ECG signal to be checked. Carefully applied electrodes, proper skin preparation, and secured lead wires greatly minimize movement artifact (see Criteria for Acceptability 7-1). Electrodes specifically designed for exercise testing are helpful. Most of these use extra adhesive to ensure electrical contact even when the patient begins perspiring. The skin sites should be carefully prepared. Removal of surface skin cells by gentle abrasion is recommended. Patients with excessive body hair may require shaving of the electrode site to ensure good electrical contact. Lead wires must be securely attached to the electrodes. Devices that limit the movement of the lead wires can greatly reduce motion artifact. Spare electrodes and lead wires should be available to avoid test interruption in the event of an electrode failure.

HR increases linearly with increasing workload, up to an age-related maximum. Several formulas are available for predicting HRmax. For most predicted HRmax values, a variability of ±10–15 beats/min exists in healthy adult patients. Two commonly used equations for predicting HRmax are as follows:

HRmax=220−Age(years) 1

1

HRmax=210−(0.65×Age[years]) 2

2

Equation 1 yields slightly higher predicted values in young adults. Equation 2 produces higher values in older adults. Other methods of predicting HRmax vary, depending on the type of exercise protocol used in deriving the regression data. Specific criteria for terminating an exercise test should include factors based on symptom limitation as well as HR and BP changes (see the section on safety).

HR increases almost linearly with increasing o₂. The increase in CO depends on both HR and stroke volume (SV) according to the following equation:

CO=HR×SV

Increases in stroke volume account for a smaller portion of the increase in CO, primarily at low and moderate workloads (Figure 7-5). While HR increases from 70 beats/min up to 200 beats/min in young healthy upright patients, SV increases from 80 mL to approximately 110 mL. At low workloads, increase in CO depends on the patient’s ability to increase both HR and SV. At high workloads, further increases in CO result almost entirely from the increase in HR.

Deconditioned patients usually have a limited SV. High HR values occur with moderate workloads in deconditioned individuals because it is the primary mechanism for increasing CO. Training (e.g., endurance or aerobic) typically improves SV response. This allows the same cardiac output to be achieved at a lower HR. Training usually results in a lower resting HR as well as a higher tolerable maximum workload. Except in highly trained patients, maximal exercise in healthy individuals is limited by the inability to further increase the CO. Reductions in SV are usually related to the preload or afterload of the left ventricle. Increased HR response, in relation to the workload, implies that SV is compromised.

Reduced HR response may occur in patients who have ischemic heart disease or complete heart block (Interpretive Strategies 7-1). Low HR is also common in patients who have been treated with drugs that block the effects of the sympathetic nervous system (β-blockers, calcium channel blockers). HR response may also be reduced if the autonomic nervous system is impaired or the heart is denervated, as occurs after cardiac transplantation (e.g., chronotropic insufficiency).

In patients who have heart disease (e.g., coronary artery disease, cardiomyopathy), increased HR is typically accompanied by ECG changes such as arrhythmias or ST-segment depression. Deconditioned patients without heart disease show a high HR at lower than maximal workloads but usually without ECG abnormalities. Horizontal or down-sloping ST-segment depression greater than 1 mm (from the resting baseline) for a duration of 0.08 seconds is usually considered evidence of ischemia. ST-segment depression at low workloads that increases with HR and continues into the post-exercise period is usually indicative of multivessel coronary artery disease. ST-segment depression accompanied by exertional hypotension or marked increase in diastolic pressure is usually associated with significant coronary disease. The predictive value of ST-segment changes during exercise must be related to the patient’s clinical history and risk factors for heart disease.

The most common arrhythmia that occurs during exercise testing is the premature ventricular contraction (PVC) (see Figure 7-4). Exercise-induced PVCs occurring at a rate of more than 10 per minute are often found in ischemic heart disease. Increased PVCs during exercise may also be seen in mitral valve prolapse. Coupled PVCs (couplets) often precede ventricular tachycardia or ventricular fibrillation. Occurrence of couplets or frequent PVCs may be an indication for terminating the exercise evaluation. Some patients with PVCs at rest or at low workloads may have these ectopic beats suppressed as exercise intensity increases. The most serious ventricular arrhythmias are sometimes seen in the immediate post-exercise phase.

Shortness of breath (SOB) brought on by exertion is perhaps the most widespread indication for cardiopulmonary exercise evaluation. The combination of cardiovascular parameters (e.g., HR, SV) with data obtained from the analysis of exhaled gas (i.e., o₂) permits the assessment of dyspnea on exertion. Table 7-5 generalizes some of the basic relationships between cardiovascular and pulmonary exercise responses. These relationships help delineate whether exertional dyspnea is a result of cardiac or pulmonary disease, or whether the patient is simply deconditioned. In some instances, poor effort may mimic exertional dyspnea. Comparison of data from cardiovascular and exhaled gas variables can confirm inadequate patient effort.

Table 7-5

Exercise Variables and Dyspnea*

	Cardiac	Ventilatory	Deconditioned	Poor Effort
o2max	Less than 80% of predicted	Less than 80% of predicted	Less than 80% of predicted	Less than 80% of predicted
Emax	Less than 70% of MVV	Greater than 90% of MVV; Emax less than 15 L	Less than 70% of MVV	Variable
Anaerobic threshold	Achieved at low o2	Usually not achieved	Achieved at low o2	Not achieved
HR	Greater than 85% of predicted	Less than 85% of predicted	Greater than 85% of predicted	Less than 85% of predicted
ECG/signs of ischemia	ST changes, arrhythmias, chest pain	Usually normal	Normal	Normal
Sao2	Greater than 90%	Often less than 90%, hypoxemia	Greater than 90%	Greater than 90%

MVV, Maximal voluntary ventilation; SaO₂, arterial oxygen saturation.

^*This table compares the usual findings for the exercise variables listed in subjects with dyspnea caused by cardiac disease, pulmonary disease, or deconditioning. Some subjects may have dyspnea because of a combination of causes. Poor effort during exercise may result from improper instruction, lack of understanding by the subject, or lack of motivation by the subject.

Blood Pressure

Systemic BP may be monitored intermittently with the standard cuff method. Automated noninvasive cuff devices for monitoring BP are also available. Although these methods work well at rest and at low workloads, they may be difficult to implement during high levels of exercise. However, recent advances in automated systems that pair sophisticated Korotkoff sound detection with QRS complex activation have improved the ability to measure exercise BP more accurately with these devices. BP sounds may be difficult to detect because of treadmill noise or patient movement. It is important to monitor the pattern of BP response at low and moderate workloads to establish that both systolic and diastolic pressures respond as anticipated.

Continuous monitoring of the BP may be accomplished by the connection of a pressure transducer to an indwelling arterial catheter (Figure 7-6). An indwelling line allows the continuous display and recording of systolic, diastolic, and mean arterial pressures. In addition, the catheter provides ready access for arterial blood sampling. Arterial catheterization may be easily accomplished using either the radial or the brachial site. The catheter must be adequately secured to prevent loss of patency during vigorous exercise. Insertion of arterial catheters presents some risk of blood splashing or spills. Adequate protection for the individual inserting the catheter, as well as for those withdrawing specimens, is essential. See Chapter 6 for specific recommendations regarding arterial sampling via catheters.

Systolic BP increases in healthy patients during exercise from 120 mm Hg up to approximately 200–250 mm Hg (see Figure 7-5). Diastolic pressure normally rises only slightly (10–15 mm Hg) or not at all. The mean arterial pressure rises from approximately 90 mm Hg to approximately 110 mm Hg, depending on the changes in systolic and diastolic pressures. The increase in systolic pressure is caused almost completely by increased CO and mostly by the SV. Even though CO may increase fivefold, (e.g., from 5–25 L/min), the systolic pressure only increases twofold. Systolic pressure only doubles because of the tremendous decrease in peripheral vascular resistance. Most of this decrease in resistance results from vasodilatation in exercising muscles. Increased systolic pressure (>250–300 mm Hg) should be considered an indication for terminating the exercise evaluation (Box 7-2). Similarly, if the systolic pressure fails to rise with increasing workload, the exercise test should be terminated and the patient’s condition stabilized. Variations in BP during exercise are often caused by the patient’s respiratory effort. Phasic changes with respiration are particularly common in patients who have large transpulmonary pressures because of lung disease (i.e., pulsus paradoxus). Differences of as much as 30 mm Hg between inspiration and expiration may be seen during the continuous monitoring of arterial pressure.