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Exercise Standards for Testing and Training

2013; Lippincott Williams & Wilkins; Volume: 128; Issue: 8 Linguagem: Inglês

10.1161/cir.0b013e31829b5b44

1524-4539

Gerald F. Fletcher, Philip A. Ades, Paul Kligfield, Ross Arena, Gary Balady, Vera Bittner, Lola A. Coke, Jerome L. Fleg, Daniel E. Forman, Thomas C. Gerber, Martha Gulati, Kushal Madan, Jonathan Rhodes, Paul M. Thompson, Mark A. Williams,

Cardiovascular Function and Risk Factors

HomeCirculationVol. 128, No. 8Exercise Standards for Testing and Training Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBExercise Standards for Testing and TrainingA Scientific Statement From the American Heart Association Gerald F. Fletcher, MD, FAHA, Chair, Philip A. Ades, MD, Co-Chair, Paul Kligfield, MD, FAHA, Co-Chair, Ross Arena, PhD, PT, FAHA, Gary J. Balady, MD, FAHA, Vera A. Bittner, MD, MSPH, FAHA, Lola A. Coke, PhD, ACNS, FAHA, Jerome L. Fleg, MD, Daniel E. Forman, MD, FAHA, Thomas C. Gerber, MD, PhD, FAHA, Martha Gulati, MD, MS, FAHA, Kushal Madan, PhD, PT, Jonathan Rhodes, MD, Paul D. Thompson, MD and Mark A. Williams, PhDon behalf of the American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee of the Council on Clinical Cardiology, Council on Nutrition, Physical Activity and Metabolism, Council on Cardiovascular and Stroke Nursing, and Council on Epidemiology and Prevention Gerald F. FletcherGerald F. Fletcher Search for more papers by this author , Philip A. AdesPhilip A. Ades Search for more papers by this author , Paul KligfieldPaul Kligfield Search for more papers by this author , Ross ArenaRoss Arena Search for more papers by this author , Gary J. BaladyGary J. Balady Search for more papers by this author , Vera A. BittnerVera A. Bittner Search for more papers by this author , Lola A. CokeLola A. Coke Search for more papers by this author , Jerome L. FlegJerome L. Fleg Search for more papers by this author , Daniel E. FormanDaniel E. Forman Search for more papers by this author , Thomas C. GerberThomas C. Gerber Search for more papers by this author , Martha GulatiMartha Gulati Search for more papers by this author , Kushal MadanKushal Madan Search for more papers by this author , Jonathan RhodesJonathan Rhodes Search for more papers by this author , Paul D. ThompsonPaul D. Thompson Search for more papers by this author and Mark A. WilliamsMark A. Williams Search for more papers by this author and on behalf of the American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee of the Council on Clinical Cardiology, Council on Nutrition, Physical Activity and Metabolism, Council on Cardiovascular and Stroke Nursing, and Council on Epidemiology and Prevention Originally published22 Jul 2013https://doi.org/10.1161/CIR.0b013e31829b5b44Circulation. 2013;128:873–934Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2013: Previous Version 1 Table of ContentsExercise Testing 874 Purposes of Exercise Testing 874 Physiology of Exercise Testing 874 Types of Exercise 874 Cardiovascular Responses to Exercise in Normal Subjects 874 Exercise Testing Procedures 876 Clinical and Cardiopulmonary Responses During Exercise 882 The ECG During Exercise 883 Stress Imaging Modalities and Exercise Testing 889 Prognosis and Diagnosis 890 Additional Uses of Exercise Testing 893 Interpretation of the Exercise Test in Specific Populations and Settings 893 Drugs and Electrolytes in Exercise Testing 902 The Exercise Electrocardiographic Test Report 903Exercise Training 903 Exercise and Health 903 Exercise Prescription for Apparently Healthy Individuals 907 Exercise Training Techniques 908 Behavioral Aspects of Initiating and Sustaining an Exercise Program 911 Evaluation and Exercise Prescription in Patients With CVD 912 Effects of Exercise Training in Patients With CVD 914 Prognostic Benefits of Exercise in Patients With CVD 914 Targeting Exercise Prescription to Relevant Outcomes 915References 920The 2001 version of the exercise standards statement1 has served effectively to reflect the basic fundamentals of ECG–monitored exercise testing and training of both healthy subjects and patients with cardiovascular disease (CVD) and other disease states. These exercise standards are intended for use by physicians, nurses, exercise physiologists and specialists, technologists, and other healthcare professionals involved in exercise testing and training of these populations. Because of an abundance of new research in recent years, a revision of these exercise standards is appropriate. The revision deals with basic fundamentals of testing and training, with no attempt to duplicate or replace current clinical practice guidelines issued by the American Heart Association (AHA), the American College of Cardiology Foundation (ACCF), and other professional societies.It is acknowledged that the published evidence for some recommendations made herein is limited, but the depth of knowledge and experience of the writing group is believed to provide justification for certain consensus recommendations based on expert opinion.With regard to a literature search for this revision, no specific strategy or formal data quality assessment was used. Each of the 15 members of the writing group has specific expertise in ≥1 sections of the document. Accordingly, references were selected by the group on the basis of personal experience or readily available publications and databases. The cited references represent a consensus of the writing group.Exercise TestingPurposes of Exercise TestingExercise testing has been used for the provocation and identification of myocardial ischemia for >6 decades,2 and during this time additional purposes for testing have evolved. Exercise testing now is used widely for the following:Detection of coronary artery disease (CAD) in patients with chest pain (chest discomfort) syndromes or potential symptom equivalentsEvaluation of the anatomic and functional severity of CADPrediction of cardiovascular events and all-cause deathEvaluation of physical capacity and effort toleranceEvaluation of exercise-related symptomsAssessment of chronotropic competence, arrhythmias, and response to implanted device therapyAssessment of the response to medical interventionsUnderstanding the purpose of the individual exercise test allows the test supervisor to determine appropriate methodology and to select test end points that maximize test safety and obtain needed diagnostic and prognostic information. During the past several decades, exercise testing has been focused increasingly on assessment of cardiovascular risk, not simply detection of coronary obstruction.3 Ultimately, improved clinical outcome is a major goal of exercise testing.Physiology of Exercise TestingAerobic exercise, progressively increasing to maximal tolerance, is a common physiological stress that can elicit cardiovascular or pulmonary abnormalities not present at rest, while aiding in the determination of the adequacy of cardiac function. However, in addition to exercise, the cardiovascular response to physiological stress is also commonly evaluated through the use of pharmacological stress agents. Thus, whereas “stress testing” traditionally has referred to “exercise,” this term no longer remains precise. The following section will focus specifically on exercise as a means to provoke cardiovascular and pulmonary stress.Types of ExerciseExercise involves muscle activity that has both mechanical (dynamic, static) and metabolic (aerobic, anaerobic) properties. Dynamic (isotonic) exercise, which causes movement of the limb, is also further classified as either concentric (shortening of the muscle fibers, which is the most common type of muscle action) or eccentric (lengthening of the muscle fibers, such as might occur when a weight is lowered against gravity). Static (isometric) exercise results in no movement of the limb. The metabolic classification refers primarily to the availability of oxygen for the contraction process and includes aerobic (oxygen available) or anaerobic (without oxygen) processes. Most exercise involves both dynamic and static contractions as well as aerobic and anaerobic metabolism, and depending on the contribution of each, the physiological responses can be significantly different. Current clinical exercise testing procedures manifest a predominant dynamic–aerobic (endurance) component.Cardiovascular Responses to Exercise in Normal SubjectsAs exercise is initiated and as its intensity increases, there is increasing oxygen demand from the body in general, but primarily from the working muscles.4 To meet these requirements, cardiac output is increased by an augmentation in stroke volume (mediated through the Frank-Starling mechanism) and heart rate (HR), as well as an increasing peripheral arteriovenous oxygen difference. However, at moderate- to high-intensity exercise, the continued rise in cardiac output is primarily attributable to an increase in HR, as stroke volume typically reaches a plateau at 50% to 60% of maximal oxygen uptake (o2max) except in elite athletes. Thus, maximal cardiac output during exercise is the product of augmentation of both stroke volume and HR. o2max is equal to the product of maximum cardiac output and maximum arteriovenous oxygen difference, and even in the absence or minimization of change in cardiac output, an important increase in o2max during exercise can result from increased oxygen extraction. Maximum arteriovenous oxygen difference has a physiological limit of 15 to 17 mL O2 per 100 mL blood. As a consequence, if maximum effort is achieved, o2max can be used to estimate maximum cardiac output.At fixed, mild-to-moderate submaximal workloads below anaerobic threshold (the point during progressive exercise beyond which muscles cannot derive all required energy from oxygen utilization), steady-state conditions usually are reached within 3 to 5 minutes after the onset of exercise, and subsequently, HR, cardiac output, blood pressure, and pulmonary ventilation are maintained at reasonably constant levels.5 As the exercise intensity surpasses anaerobic threshold and progresses toward a maximum level, sympathetic discharge becomes maximal and parasympathetic stimulation is inhibited, resulting in vasoconstriction in most circulatory body systems, except in exercising muscle and in the cerebral and coronary circulations. As exercise progresses, skeletal muscle blood flow and oxygen extraction increase, the latter as much as 3-fold. Total calculated peripheral resistance decreases, while systolic blood pressure, mean arterial pressure, and pulse pressure usually increase. Diastolic blood pressure can remain unchanged or decrease to a small degree, each of which is considered a normal response. The pulmonary vascular bed can accommodate as much as a 6-fold increase in cardiac output without a significant increase in transpulmonary gradient. In normal subjects, this is not a limiting determinant of peak exercise capacity. Cardiac output can increase as much as 4- to 6-fold above basal levels during strenuous exertion in the upright position, depending on genetic endowment and level of training.HR ResponseThe immediate response of the cardiovascular system to exercise is an increase in HR that is attributable to a decrease in vagal tone, followed by an increase in sympathetic outflow.5 During dynamic exercise, HR in sinus rhythm increases linearly with workload and oxygen demand. In subjects not prescribed a β-blocking agent, the maximal HR achieved during exercise is influenced heavily by age and age-related neural influences; the expected value can be predicted from one of several available equations, some of which are derived separately for men and women.6–8 For one of the commonly used equations (maximum predicted HR=220–age in years), a high degree of variability exists among subjects of identical age (±12 beats per minute [bpm]). Accordingly, the practice of using achievement of 85% of age-predicted maximal HR to define sufficient effort during exercise testing is limited and should not be used in isolation as a termination criterion.9Dynamic exercise increases HR more than either isometric or resistance exercise. A normal increase in HR during exercise is ≈10 bpm per metabolic equivalent (MET). Moreover, the HR response is generally continuous with increasing workload. An accelerated HR response to standardized submaximal workloads is observed after prolonged bed rest, indicating that physical conditioning also plays a role in the HR response, which also can change in response to anemia, metabolic disorders, variable vascular volume or peripheral resistance, or ventricular dysfunction. These conditions themselves do not appear to affect maximal HR unless capacity for exercise intensity becomes limited. Conversely, a lower-than-expected incremental rise in HR during a progressive exercise test could be attributed to an enhanced level of fitness and left ventricular (LV) function. As will be discussed in detail, inadequate HR response to exercise can be a marker not only for sinus node dysfunction but also for prognostically important cardiac disease and has been defined as chronotropic incompetence. The use of a β-blocking drug lowers both the incremental rise in HR and maximal HR obtained during exercise, thus limiting the physiological interpretation of the cardiac response to exercise. Other factors that can influence HR include body position, type of dynamic exercise, certain physical conditions, state of health, blood volume, sinus node function, medications, and the environment.The change in HR immediately after termination of the exercise test, termed HR recovery, has received an increasing amount of attention in recent years. The decline of HR after exercise generally exhibits a rapid fall during the first 30 seconds after exercise, followed by a slower return to the preexercise level.10 The rapid decline in HR is likely the manifestation of vagal reactivation.11 Abnormality of HR recovery has consistently demonstrated prognostic value.12–17Arterial Blood Pressure ResponseBlood pressure is dependent on cardiac output and peripheral vascular resistance. Systolic blood pressure rises with increasing dynamic work as a result of increasing cardiac output, whereas diastolic pressure usually remains about the same or is moderately decreased because of vasodilatation of the vascular bed. On occasion, diastolic blood pressure sounds can be heard down to 0 mm Hg in some normal subjects. A normal systolic blood pressure response to progressive exercise is dependent on both sex (higher in males) and age (higher with advancing age).5 The average rise in systolic blood pressure during a progressive exercise test is about 10 mm Hg/MET.After maximum exercise, systolic blood pressure usually declines because of the rapid decrease in cardiac output, normally reaching resting levels or lower within 6 minutes, and even remaining lower than preexercise levels for several hours.18 When exercise is terminated abruptly, some healthy people have precipitous drops in systolic blood pressure because of venous pooling (particularly in the upright position) and a delayed immediate postexercise increase in systemic vascular resistance to match the reduction in cardiac output. This postexercise hemodynamic response highlights the importance of an active cool-down period when possible.Myocardial Oxygen UptakeMyocardial oxygen uptake is determined primarily by intramyocardial wall stress (ie, the product of LV pressure and volume, divided by LV wall thickness), contractility, and HR.1,4 Accurate measurement of myocardial oxygen uptake requires cardiac catheterization to obtain coronary arterial and venous oxygen content. However, myocardial oxygen uptake can be estimated during clinical exercise testing by the product of HR and systolic blood pressure (double product or rate–pressure product) and ranges from the 10th percentile value of 25 000 to a 90th percentile value of 40 000 at peak exercise. A linear relationship exists between myocardial oxygen uptake and coronary blood flow. During exercise, coronary blood flow increases as much as 5-fold above the resting value. A subject with obstructive CAD often cannot provide adequate coronary blood flow to the affected myocardial tissue to meet the metabolic demands of the myocardium during exercise; consequently, myocardial ischemia occurs. Myocardial ischemia usually occurs at the same rate–pressure product rather than at the same external workload (eg, exercise test stage).19Oxygen Uptake and the Ventilatory Thresholdo2max is the peak oxygen uptake achieved during the performance of dynamic exercise involving a large part of total muscle mass. It is considered the best measure of cardiovascular fitness and exercise capacity.5 By strictest definition, o2max cannot be exceeded, despite an increase in work output. Although demonstration of the o2 plateau against work rate is a valid demonstration of o2max, patients often cannot achieve the plateau because of leg fatigue; lack of necessary motivation; general discomfort; or the presence of heart disease, LV dysfunction, myocardial ischemia, and associated symptomatology. Hence, it is common to refer to o2max as the peak o2 attained during volitional incremental exercise. In clinical practice, o2max is not usually measured during an exercise tolerance test but is estimated from the peak work intensity achieved.In contrast, submaximal oxygen uptake is the general designation for any level of oxygen uptake between maximal and resting levels. Submaximal oxygen uptake is most frequently described in terms of a percentage of o2max (eg, 60%, 70%, or 80% of o2max) in designating exercise workload or intensity. To meet the metabolic demand of dynamic exercise, oxygen uptake quickly increases, achieving steady state, as previously described, when exercise intensity is of light or moderate intensity and is below the ventilatory threshold. The ventilatory threshold is another measure of relative work effort and represents the point at which ventilation abruptly increases in response to increasing carbon dioxide production (co2) associated with increased work rate, despite increasing oxygen uptake. In most cases, the ventilatory threshold is highly reproducible, although it might not be achieved or readily identified in some patients, particularly those with very poor exercise capacity.4It is convenient to express oxygen uptake in multiples of resting oxygen requirements—that is, METs, whereby a unit of sitting/resting oxygen uptake (1 MET) is defined as ≈3.5 mL O2 per kilogram of body weight per minute (mL kg−1 min−1). For example, an oxygen uptake expressed as a 7-MET level would equal 24.5 mL kg−1 min−1. o2max is influenced by age, sex, exercise habits, heredity, and cardiovascular clinical status.V.o2max is equal to the product of maximum cardiac output and maximum arteriovenous oxygen difference. o2max divided by the HR at peak exercise (a quantity defined as the oxygen pulse) is therefore equal to the forward stroke volume (ie, cardiac output divided by HR) at peak exercise times the arteriovenous oxygen difference at peak exercise. Because the arteriovenous oxygen difference at peak exercise reaches a physiological limit and usually varies little across a wide spectrum of cardiovascular function, most of the clinical variation in the oxygen pulse at peak exercise is therefore attributable to variation in the forward stroke volume at peak exercise. Valid inferences about a patient’s forward stroke volume at peak exercise therefore can be made from determinations of the oxygen pulse at peak exercise. Normal values for the oxygen pulse (and stroke volume) at peak exercise are dependent on a patient’s age, size, and sex. Predicted values can be calculated easily, however, by dividing the patient’s predicted o2max (in milliliters per minute) by the predicted peak HR.20 The oxygen pulse also is influenced by hemoglobin levels and the arterial oxygen saturation. Proper interpretation of oxygen pulse data therefore should take into account abnormalities in these indices.AgeMaximum values of o2max occur between the ages of 15 and 30 years and decrease progressively with age. At age 60 years, mean o2max in men is approximately two thirds of that at 20 years.1 A longitudinal decline in peak o2max was observed in each of 6 age decades in both sexes; however, the rate of decline accelerated from 3% to 6% per 10 years in individuals in their 20s and 30s to >20% per 10 years in individuals in their 70s and beyond,21 as seen in Figure 1.Download figureDownload PowerPointFigure 1. Progressive and accelerating decline in peak o2 according to age decades in clinically healthy men and in women. Reprinted from Fleg JL et al.21 Copyright © 2005, the American Heart Association, Inc.SexWomen demonstrate a lower o2max than that of men.22 This lower o2max in women is attributed to their smaller muscle mass, lower hemoglobin and blood volume, and smaller stroke volume relative to men.1 The rate of decline for each decade is larger in men than in women from the fourth decade onward.21Exercise HabitsPhysical activity has an important influence on o2max. In moderately active young men, o2max is ≈12 METs, whereas young men performing aerobic training such as distance running can have a o2max as high as 18 to 24 METs (60 to 85 mL kg−1 min−1).1 A similar relationship was found in active versus sedentary women.22Cardiovascular Clinical Statuso2max is affected by the degree of impairment caused by disease. In particular, preexisting LV dysfunction or the development of such with exercise-induced myocardial ischemia can greatly affect o2max. In addition, the development of signs or symptoms associated with the need for exercise test termination, such as angina pectoris, hypertension, or cardiac dysrhythmia, can greatly impact o2max. Thus, it is difficult to accurately predict o2max from its relation to exercise habits and age alone because of considerable scatter because of underlying disease. However, achieved values for o2max can be compared with average normal values by age and sex.1Exercise Testing ProceduresAbsolute and Relative Contraindications to Exercise TestingAbsolute and relative contraindications to exercise testing balance the risk of the test with the potential benefit of the information derived from the test. Assessment of this balance requires knowledge of the purpose of the test for the individual subject or patient and what symptom or sign end points will be for the individual test.Absolute ContraindicationsAcute myocardial infarction (MI), within 2 daysOngoing unstable anginaUncontrolled cardiac arrhythmia with hemodynamic compromiseActive endocarditisSymptomatic severe aortic stenosisDecompensated heart failureAcute pulmonary embolism, pulmonary infarction, or deep vein thrombosisAcute myocarditis or pericarditisAcute aortic dissectionPhysical disability that precludes safe and adequate testingRelative ContraindicationsKnown obstructive left main coronary artery stenosisModerate to severe aortic stenosis with uncertain relation to symptomsTachyarrhythmias with uncontrolled ventricular ratesAcquired advanced or complete heart blockHypertrophic obstructive cardiomyopathy with severe resting gradientRecent stroke or transient ischemic attackMental impairment with limited ability to cooperateResting hypertension with systolic or diastolic blood pressures >200/110 mm HgUncorrected medical conditions, such as significant anemia, important electrolyte imbalance, and hyperthyroidismSubject PreparationPreparations for exercise testing include the following:The purpose of the test should be clear in advance to maximize diagnostic value and to ensure safety. If the indication for the test is not clear, the referring provider should be contacted for further information.The subject or patient should not eat for 3 hours before the test. Routine medications may be taken with small amounts of water. Subjects should dress in comfortable clothing and wear comfortable walking shoes or sneakers.The subject or patient should receive a detailed explanation of the testing procedure and purpose of the test, including the nature of the progressive exercise, symptom and sign end points, and possible complications.When exercise testing is performed for the diagnosis of ischemia, routine medications may be held because some drugs (especially β-blockers) attenuate the HR and blood pressure responses to exercise. If ischemia does not occur, the diagnostic value of the test for detection of CAD is limited. No formal guidelines for tapering or holding medications exist, but 24 hours or more could be required for sustained-release preparations, and the patient should be instructed to resume medication if rebound phenomena occur. Many exercise test evaluations occur while patients are taking usual medications, which should be recorded for correlation with test findings.A brief history and physical examination are required to rule out contraindications to testing and to detect important clinical signs, such as cardiac murmur, gallop sounds, pulmonary wheezing, or rales. Subjects with a history of worsening unstable angina or decompensated heart failure should not undergo exercise testing until their condition stabilizes. Physical examination should screen for valvular or congenital heart disease, and abnormal hemodynamic responses to exercise in these patients could require early termination of testing.A resting supine standard 12-lead ECG should be obtained before exercise to compare to previously obtained standard ECGs to determine if changes have occurred over time. Subsequently, supine and standing (sitting if cycle ergometry is used) “torso” ECGs (with the limb electrodes on the trunk of the body to minimize motion and muscle artifact during exercise) should be recorded because these could differ importantly from the preexercise standard ECG. The torso ECG is not equivalent to a standard ECG because the torso ECG can shift the frontal plane axis to the right, increasing voltage in the inferior leads.23,24 This could cause a disappearance of Q waves in a patient with a documented previous Q-wave inferior MI or could produce lead placement–dependent artifactual Q waves in some normal subjects. Most of the change between supine limb-lead standard electrocardiographic recordings and upright torso electrocardiographic recordings is attributable to electrode position and not to the positional change.25Standing control torso-lead ECGs should be recorded before testing to allow direct comparison with exercise tracings. If torso-lead tracings will be taken in the supine position during recovery, a supine torso-lead tracing also should be obtained in the control period. Blood pressures in the upright position should be recorded before beginning exercise. Hyperventilation at rest could produce nonspecific ST-segment changes in some otherwise normal subjects, and these also might occur during exercise as false-positive responses for the identification of ischemia.26–28 Hyperventilation before testing has been suggested to decrease test specificity, and its routine use has been criticized in a recent guideline.29 When electrocardiographic changes occur with hyperventilation, this should be acknowledged in the test interpretation.Electrocardiographic RecordingSkin PreparationAn important factor governing the recording quality of an exercise ECG is the interface between electrode and skin. Removal of the superficial oils and layer of skin by gentle abrasion significantly lowers resistance, thus improving the signal-to-noise ratio. The areas for electrode application are first shaved and then rubbed with alcohol-saturated gauze. After the skin dries, it is marked with a felt-tipped pen and rubbed with fine sandpaper or other rough material. With these procedures, skin resistance can be reduced to 5000 Ω or less.Electrodes and CablesDisposable electrodes used in exercise testing are generally silver–silver chloride combinations with adherent gel. Contact between electrodes and the skin generally improves with several minutes of application time and with the moisture that occurs with sweating during exercise, although excess sweating can result in loosening of the contact between electrode and skin. Wrapping the torso with a 6-inch elastic bandage or with a fitted torso net can reduce noise produced by electrode and cable movement, especially in obese patients. Electrode placement for signal stability in large-breasted women can be difficult, sometimes requiring tradeoff of variable location and motion artifact.Hard-wired connecting cables between the electrodes and recorder should be light, flexible, and properly shielded. Most available commercial exercise cables are constructed to lessen motion artifact by digitizing the electrocardiographic waveform at the cable box proximal to the attachment to the electrocardiograph recorder itself. Cables generally have a life span of about 1 year and eventually must be replaced to reduce acquired electrical interference and discontinuity. It is increasingly popular to use digital conversion boxes that wirelessly transmit to the recording electrocardiograph.Electrocardiographic Leads for Exercise TestingBecause a high-quality standard 12-lead ECG with electrodes placed on the limbs cannot be obtained during exercise, electrode placement on the torso is standard for routine testing. Multiple leads improve test sensitivity.30 As noted, varied electrode placement results in varied waveforms.23 Although these do alter QRS and T-wave morphology, they are nonetheless valid for interpretation of heart rhythm and are generally similar to the standard ECG for detecting ST-segment deviation.24,31,32 Torso electrodes generally are applied under the lateral clavicles (for the arm leads) and high under the ribcage (for the leg leads), as shown