(Circulation. 1995;91:580.)
© 1995 American Heart Association, Inc.
Articles |
The purpose of this report is to provide revised standards and guidelines for the exercise testing and training of individuals free from clinical manifestations of cardiovascular disease as well as those with known cardiovascular disease. These guidelines are intended for physicians, nurses, exercise physiologists, specialists, technologists, and other healthcare professionals involved in the regular exercise testing and training of these populations. This report is in accord with the "Statement on Exercise" published by the American Heart Association in Circulation (1992;86:340-344).
These guidelines are a revision of the 1990 standards1 of the AHA that addressed the issues of exercise testing and training. An update of background, scientific rationale, and selected references are provided, and current issues of practical importance in the clinical use of these standards are considered.
Exercise Testing
The Cardiovascular Response to Exercise
Exercise, a common
physiological stress, can elicit cardiovascular
abnormalities not present at rest and can be used to determine the
adequacy of cardiac function. Because exercise is only one of many
stresses to which humans can be exposed, it is more appropriate to call
an exercise test exactly that and not a "stress test." This is
particularly relevant considering the increased use of nonexercise
stress tests.
Types of Exercise
Three types of muscular
contraction or exercise can be applied as
a stress to the cardiovascular system: isometric (static), isotonic
(dynamic or locomotory), and resistive (a combination of isometric and
isotonic).2 3 Isometric exercise, defined as a
muscular
contraction without movement (eg, handgrip), imposes greater pressure
than volume load on the left ventricle in relation to the bodys
ability to supply oxygen. The cardiovascular response to isometric
exercise is difficult to grade. In addition, cardiac output is not
increased as much as in isotonic exercise because increased resistance
in active muscle groups limits blood flow. Isotonic exercise, defined
as muscular contraction resulting in movement, primarily provides a
volume load to the left ventricle, and the cardiovascular response is
proportional to the size of the muscle mass and the intensity of the
exercise. Resistive exercise combines both isometric and isotonic
exercise by using muscular contraction with movement, as in free weight
lifting.
Key Point: Dynamic exercise is preferred for
testing because it puts a volume stress rather than a pressure load on
the heart and because it can be graduated. However, most activities
(especially employment and leisure time activities, such as sports)
usually combine all three types of exercise in varying degrees.
Maximum Oxygen Uptake
When dynamic exercise is
begun or increased, oxygen uptake by the
lungs quickly increases. After the second minute, oxygen uptake usually
remains relatively stable (steady state) at each intensity of exercise.
During steady state, heart rate, cardiac output, blood pressure, and
pulmonary ventilation are maintained at reasonably constant
levels.2
O2max is the
greatest amount of oxygen
a person can use while performing dynamic exercise involving a large
part of total muscle mass.4
O2max represents the amount
of oxygen
transported and used in cellular metabolism. It is convenient to
express oxygen uptake in multiples of sitting, resting requirements.
The metabolic equivalent (MET) is a unit of sitting, resting oxygen
uptake (3.5 mL O2 per kilogram body weight
per minute
[mL · kg-1 · min-1]).
Rather than determining each persons true resting oxygen uptake, a
MET is taken as this average.
O2max is
significantly related
to age, gender, exercise habits, heredity, and cardiovascular clinical
status.
Age: Maximum values of
O2max occur between the
ages of
15 and 30 years, decreasing progressively with age. At age 60, mean
O2max in men is
approximately
three fourths that at age 20. With a sedentary lifestyle, there is a
9% reduction per decade versus less than 5% per decade for an active
lifestyle.
Gender: Through age 12 to 16 years, there is no significant
difference in
O2max among
children, but a decrease is observed in girls between 12 and 14 years
of age. Reduced
O2max in
women
is attributed to smaller muscle mass, lower hemoglobin and blood
volume, and smaller stroke volume as compared with men.
Exercise
habits: Physical activity has an important influence on
O2max. After 3 weeks of bed
rest, there is a 25% decrease in
O2max in healthy men. In
moderately active young men,
O2max is about 12 METs,
whereas
individuals 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).
Heredity:
There is a natural variation in
O2max related to genetic
factors.
Cardiovascular clinical status:
O2max is affected by the
degree
of impairment caused by disease.
It is difficult to accurately predict
O2max from its relation to
exercise habits and age because of considerable scatter and
correlations that are generally low. Table 1
lists key
values of METs that are clinically relevant, and Table 2
depicts normal values for age. The nomogram shown in
Fig 1
expresses the concept of METs by reflecting it
in terms of that expected for age, with 100% being
normal.5
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Maximum
O2 is equal to maximum
cardiac output times maximum arteriovenous oxygen
(a
O2) difference. Since
cardiac
output is equal to the product of stroke volume and heart rate,
O2 is directly related to
heart
rate. The maximum a
O2
difference during exercise has a physiological limit of 15 to 17 vol%
hence, if maximum effort is achieved,
O2max can be used to
estimate
maximum cardiac output.
Myocardial Oxygen Uptake
Myocardial oxygen uptake (MO2) is
determined by intramyocardial wall tension ([left ventricular (LV)
systolic pressure times end-diastolic volume] divided by LV wall
thickness), contractility, and heart rate. Other less important factors
include external work performed by the heart, the energy necessary for
activation, and the basal metabolism of the myocardium (Table
3
).
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Accurate measurement of MO2
requires cardiac
catheterization. MO2 can be estimated during
clinical exercise testing by the product of heart rate and systolic
blood pressure, which is called the double product or
rate-pressure product. There is a linear relation between
MO2 and coronary blood flow. During exercise
coronary blood flow increases as much as fivefold above the resting
value. A subject with obstructive coronary disease often cannot
maintain adequate coronary blood flow to supply the metabolic demands
of the myocardium during exercise and, as a consequence, myocardial
ischemia occurs. Angina pectoris usually occurs at the same double
product rather than at the same external workload. Key
Point: An important basic principle of exercise physiology is that
O2 and
MO2 have distinct determinants and
methods of measurement or estimation (Table 3
).
Although they are directly related, this relation can be altered by
training and cardioactive medications such as ß-blockers.
Response to Dynamic Exercise
The bodys
response to dynamic exercise consists of a complex
series of cardiovascular adjustments to provide active muscles with the
blood supply appropriate for their metabolic needs, to dissipate the
heat generated by active muscles, and to maintain the blood supply to
the brain and the heart.
As cardiac output increases with dynamic exercise, peripheral resistance increases in organ systems and tissues that do not function during exercise and decreases in active muscles.6 Arterial blood pressure increases only mildly; thus, flow can increase as much as fivefold. Since the denominator (flow) increases much more than the numerator (pressure) in the formula for resistance, the result is a decrease in systemic vascular resistance.
Heart Rate
Response
An increase in heart rate due to a decrease in vagal outflow
is an
immediate response of the cardiovascular system to exercise; this
increase is followed by an increase in sympathetic outflow to the heart
and systemic blood vessels. During dynamic exercise, heart rate
increases linearly with workload and
O2. During low levels of
exercise and at a constant work rate, heart rate will reach steady
state within several minutes. As workload increases, the time necessary
for the heart rate to stabilize will progressively lengthen.
Heart rate response is influenced by several factors, including age. There is a decline in mean maximum heart rate with age7 that appears to be related to neural influences. Dynamic exercise increases heart rate more than isometric or resistive exercise. An accentuated heart rate response is observed after bed rest. Other factors that influence heart rate include body position, certain physical conditions, state of health, blood volume, and environment.
Key Point: Heart rate response to maximum dynamic exercise depends on numerous factors, particularly age and health. It appears that the reduction in heart rate averages 5 to 7 beats per minute per decade.
Arterial Blood Pressure
Response
Systolic blood pressure rises with increasing dynamic work as
a
result of increasing cardiac output, whereas diastolic pressure usually
remains about the same or may be heard to zero in some normal subjects.
Normal values of maximum systolic blood pressure for men have been
defined and are directly related to age.
An inadequate rise in systolic blood pressure (less than 20 to 30 mm Hg) can result from aortic outflow obstruction, LV dysfunction, or myocardial ischemia. Changes of blood pressure reflect more than the contractile function of the LV since they also depend on peripheral resistance. Subjects who develop hypotension during exercise frequently have severe heart disease; subjects with valvular or myocardial disease can also exhibit a drop in systolic blood pressure. A drop in systolic pressure below standing rest is of great concern during the actual test or during follow-up.
After maximum exercise there is usually a decline
in systolic blood
pressure, which normally reaches resting levels in 6 minutes, then
often remains lower than preexercise levels for several hours. In some
subjects with coronary artery disease (CAD), higher levels of systolic
blood pressure exceeding peak exercise values have been observed during
the recovery phase. When exercise is terminated abruptly, some healthy
persons have precipitous drops in systolic blood pressure due to venous
pooling. Fig 2
shows the physiological response to
submaximum and maximum treadmill exercise based on tests of more than
700 apparently healthy men aged 25 to 54 years. Maximum double product
(heart rate times systolic blood pressure) ranges from a tenth
percentile value of 25 000 to a 90th percentile value of 40 000.
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Testing Procedures
The Physicians Role
Exercise testing should be conducted only by well-trained
personnel with a basic knowledge of exercise physiology. Only
technicians and physicians familiar with normal and abnormal responses
during exercise can recognize or prevent untoward events. Equipment,
medications, and personnel trained to provide cardiopulmonary
resuscitation (CPR) must be readily available.
Although exercise
testing is considered a safe procedure, there are
reports of acute myocardial infarctions (MIs) and deaths. Multiple
surveys confirm that up to 10 MIs or deaths or both can be expected per
10 000 tests.8 However, the relative risk of an adverse
event during an exercise test versus during usual activity of subjects
with CAD is estimated to be 60- to 100-fold. Risk is greater in the
post-MI subject and in those being evaluated for malignant ventricular
arrhythmias. A recent review summarizing eight studies of estimates of
sudden cardiac death during exercise testing revealed rates from 0.0
(four studies) to 5 per 100 000 tests.8 Table 4
lists three classes of complications secondary to
exercise tests.
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Good clinical judgment should be foremost in deciding
indications and
contraindications for exercise testing.9 Whereas absolute
contraindications are definitive, in selected cases with relative
contraindications even submaximum testing can provide valuable
information. Table 5
lists absolute and relative
contraindications to exercise testing.
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In any procedure with a risk of complications, the physician should be certain that the subject understands the situation and acknowledges the risks. Some physicians believe that informing subjects of possible risks may cause them to become anxious or discourage them from undergoing a test. This possibility and the fact that a signed consent form does not protect a physician from legal action have recently led to less insistence on obtaining written consent. However, if consent is not initially obtained, a physician may be held responsible for a major adverse event, even if the test is carefully performed. The argument can be made that the subject would not have undergone the procedure if he or she had been aware of the risks associated with the test. Good physician-subject communication about testing is mandatory.
Exercise testing should be performed under the supervision of a physician who is appropriately trained to conduct exercise tests. The physician should be responsible for ensuring that the exercise laboratory is properly equipped and that exercise testing personnel are appropriately trained. The degree of subject supervision needed during a test can be determined by the clinical status of the subject being tested. This determination is made by the physician or physicians designated staff member, who asks pertinent questions about the subjects medical history, performs a brief physical examination, and reviews the standard 12-lead ECG performed immediately before testing. The physician should interpret data derived from testing, suggest further evaluation or therapy, and help deliver effective and timely advanced CPR when necessary. The physician or senior medical professional conducting the test must be trained in advanced CPR. A defibrillator and appropriate medications should also be immediately available.
The degree of supervision can range from assigning direct monitoring of the test to a properly trained nonphysician (ie, a nurse or exercise physiologist or specialist) for testing apparently healthy younger persons (less than 40 years old) and those with stable chest pain syndromes to the physician who directly monitors the subjects blood pressure and status throughout exercise and recovery. The latter is the ideal for testing subjects for diagnostic or prognostic purposes and is certainly a requirement for testing all subjects at increased risk for exercise-induced complications. A physician should be immediately available during all exercise tests.
Subject Preparation
Preparations for exercise testing include the following:
The subject should be instructed not to eat or smoke for 3 hours before the test and to dress appropriately for exercise, especially with regard to footwear. No unusual physical efforts should be performed for at least 12 hours before testing.
A brief history and physical examination should be performed to rule out contraindications to testing or to detect important clinical signs such as a cardiac murmur, gallop sounds, pulmonary bronchospasm, or rales. Subjects with a history of increasing or unstable angina or heart failure should not undergo exercise testing until their condition stabilizes. A cardiac physical examination should indicate which subjects have valvular or congenital heart disease. Because hemodynamic responses to exercise may be abnormal in such subjects, they always warrant careful monitoring, and at times they may be excluded from testing.
When exercise testing is performed for diagnostic purposes, withdrawal of medications may be considered since some drugs interfere with exercise responses and complicate the test interpretation. There are no formal guidelines for tapering medications, but rebound phenomena may occur with discontinuance of ß-blockers. Therefore, most subjects are tested while taking their usual medications. Specific questioning is important to determine which drugs have been taken so that the physician can be aware of possible electrolyte abnormalities and other effects.
If the reason for the exercise test is not clear, the subject should be questioned and the referring physician contacted.
A resting 12-lead ECG should be obtained since it may differ from the resting preexercise ECG. This is essential, particularly in subjects with known heart disease, since an abnormality or a change may contraindicate testing. Recording the ECG before starting the exercise test and after hyperventilation at another time may be helpful in confirming a false-positive (or indeterminate) ECG change.
Standing ECG and blood pressure should be recorded to determine vasoregulatory abnormalities, particularly ST depression.
A detailed explanation of the testing procedure should be given that outlines risks and possible complications. The subject should be told how to perform the exercise test, and the testing procedure should be demonstrated.
Electrocardiographic
Recording
Skin preparation. The most critical point of
the
electrode-amplifier-recording system is the interface between electrode
and skin. Removal of the superficial layer of skin significantly lowers
its resistance, thus decreasing 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 a fine sandpaper or rough material.
With these procedures, skin resistance should be reduced to 5000
or
less.
Electrodes and cables. Many electrodes are available for performing exercise testing. Silver plate or silver chloride crystal pellets are preferred because they have the lowest offset voltage. The electrodes should be constructed with a metal interface that is sunken, creating a column to be filled with either an electrolyte solution or a saturated sponge. When using fluid column electrodes, direct metal-to-skin contact should be avoided in order to decrease motion artifact.
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. Cables generally have a life span of a year or so, depending on use. They eventually become a source of both electrical interference and discontinuity and must be replaced.
Lead systems. Bipolar leads. Bipolar
lead systems were
the first to be used to detect ECG changes during exercise. The
relatively short placement time, freedom from motion artifacts, and the
ease with which noise problems can be located are factors that favor
their use. The usual positive reference is an electrode placed in the
same position as the positive reference for V5 (the fifth intercostal
space at the midclavicular line). The negative reference for V5 is
Wilsons central terminal. Fig 3
illustrates negative
electrode placement for most bipolar lead systems. CM5 is
the most sensitive for ST segment changes. CC5 excludes the
vertical component included in CM5 and decreases the
influence of atrial repolarization (Ta), thus reducing false-positive
responses.10 Key Point: Electrode
placement affects ST segment slope and amplitude. The various
placements do not result in comparable waveforms for analysis. For
comparison of the resting 12-lead recording, arm and leg electrodes
should be moved to the wrists and ankles, with the subject in the
supine position.
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Multiple leads. Since a standard 12-lead ECG with electrodes placed on the limbs cannot be obtained during exercise, other electrode placements have been used. Differences can be minimized by placing the arm electrodes as close to the shoulders as possible and the leg electrodes below the umbilicus and by recording the resting ECG with the subject supine. Any modification of lead placement should be recorded on the tracing.
Relative sensitivity of leads. The lateral precordial leads (V4 through V6) are capable of detecting 90% of all ST depression observed in multiple lead systems. Other reports indicate that using other leads in addition to V5 will increase the yield of abnormal responses by about 10%. However, the specificity of an abnormal response in other leads is lower. Key Point: Complete 12-lead tracings during exercise are not needed in many individuals with normal resting ECGs. However, they are necessary in subjects with arrhythmias, Q waves consistent with myocardial damage, or symptoms suggestive of coronary spasm and when evaluating severity of disease in subjects with known CAD.
Recorders. There are many good recorders designed to capture high-quality ECG data during exercise. Many use microprocessors to generate average waveforms and make ECG measurements. The physician must compare the raw analog data with computer-generated output to validate its accuracy. Computer processing is not completely reliable because of software limitations in handling noise and inadequacy of the available algorithms.
Equipment and Protocols
Fig
4
illustrates the relation of METs to stages
in the common testing protocols. Numerous devices have been used in the
past to provide dynamic exercise for testing, including steps,
escalators, and ladder mills. However, the treadmill and cycle
ergometer are now the most commonly used dynamic exercise testing
devices.
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Cycle. Mechanical or electrically braked
cycles vary the force
to the pedaling speed (rate-independent ergometers), permitting better
power output control since it is common for uncooperative or fatigued
subjects to decrease their pedaling speed. The highest values of
O2 and heart rate are
obtained
with pedaling speeds of 50 to 80 rpm. Cycles are calibrated in
kiloponds (kp) or watts; 1 W is equivalent to approximately 6
kilopond-meters per minute (kpm/min). Since exercise on a cycle
ergometer is nonweight bearing, kiloponds or watts can be converted
to oxygen uptake in milliliters per minute. METs are obtained by
dividing
O2 in milliliters
per
minute by the product of body weightx3.5.
The cycle ergometer is usually less expensive, occupies less space, and makes less noise than a treadmill. Upper body motion is usually reduced, making it easier to obtain blood pressure measurements and to record the ECG. Care must be taken to prevent isometric or resistive exercise of the arms.
There is a marked difference between the
bodys response to acute
exercise in the supine and upright positions. In healthy persons,
stroke volume and end-diastolic volume change little during supine
cycle exercise from volumes obtained at rest, whereas in the upright
position, these values increase and then plateau during mild work. In
subjects with cardiac abnormalities, LV filling pressure is more likely
to increase during exercise in the supine position than in the upright
position. When subjects with angina perform identical submaximum cycle
work in the supine and upright positions, heart rate is higher in the
supine position, maximum work performed is lower, and angina develops
at a lower double product. ST segment depression is usually greater in
the supine position because of the greater LV volume. A major
limitation to cycle ergometer testing is the discomfort and fatigue of
the quadriceps muscles. Usually leg fatigue of an inexperienced
"cyclist" causes subjects to stop before reaching a true
O2max. Thus,
O2max is 10% to 15% lower
in
cycle versus treadmill testing in those not accustomed to cycling.
Treadmill. The treadmill should have front and/or side
rails
for subjects to steady themselves; some subjects may also require the
assistance of the person administering the test. Subjects should not
tightly grasp the front or side rails since this decreases
O2 and increases exercise
time
and muscle artifact. Most subjects can walk without the aid of hand
rails, but older subjects may need such support. It is helpful if
subjects take their hands off the rails, close their fists, and place
one finger on the rails to maintain balance after they are accustomed
to walking on the treadmill. The treadmill should have both variable
speed and grade capability and must be accurately calibrated.
Protocols. Protocols for clinical exercise testing include an initial warm-up (low load), progressive uninterrupted exercise with increasing loads and an adequate duration in each level, and a recovery period. For cycle ergometry, the initial power output is usually 10 or 25 W (150 kpm/min), usually followed by increases of 25 W every 2 or 3 minutes until end points are reached. If arm ergometry is substituted for cycle ergometry, a similar protocol may be used, except that initial power output and incremental increases are lower. Two-minute stages are most popular with arm ergometry.11 12
Several different treadmill protocols are in use. The advantages of the
Bruce protocol include a seventh or final stage that cannot be
completed by most individuals as well as its use in many published
studies. Its disadvantages include large increments in work that make
estimation of
O2max less
accurate. The fourth stage can be either run or walked, resulting in
different oxygen costs. Some subjects are forced to stop exercising
prematurely because of musculoskeletal discomfort or an inability to
tolerate the high workload increments. An initial zero and one-half
stages (1.7 mph at 0% and 5% grades) can be used for subjects with
compromised exercise capacities. Many exercise testing laboratories
currently use Balke-type protocols (Stanford, McHenry, and the
frequently used Naughton) with even MET level increments for stage
advances. The optimum protocol should last 6 to 12 minutes and should
be adjusted to the subject.
Exercise protocols should be individualized according to the type of subject being tested. Three-minute stages are not necessary to achieve steady state at a low workload. Performance can be estimated with the oxygen cost of maximum workload or power output achieved rather than by total treadmill time if subjects do not use hand rails, allowing comparison of performance in different protocols. A 9-minute targeted Ramp protocol that increases in small steps has many advantages, including more accurate estimates of MET level. Key Point:It is important to adjust or select the treadmill or cycle ergometer protocol to the subject being tested. The optimum protocol is 6 to 12 minutes. Exercise capacity should be reported in METs rather than minutes.
Submaximum Versus Maximum Exercise Testing
In some cases, testing is terminated when subjects reach 85% to
90% of predicted maximum heart rate for their age and level of
training. Unfortunately, there is a wide spread of maximum heart rate
around the regression line, declining with age (SD, 12 beats per
minute). Thus, the target heart rate is maximal for some subjects,
beyond the limit of others, and submaximal for still others. A test is
considered maximal when the subject appears to give a true maximum
effort (point of bodily exhaustion) or when other clinical end points
are reached. Paradoxically, when using an age-predicted heart
ratetargeted submaximum test, the most vulnerable subjects are
stressed to a relatively greater extent, whereas the less impaired are
limited by the submaximum target heart rate.
Perceived exertion. The subjective rating of the
intensity of
exertion perceived by the person exercising is generally a sound
indicator of relative fatigue. Rather than using heart rate alone to
clinically determine intensity of exercise, the 6 to 20 Borg scale of
perceived exertion13 is useful (Table 6
).
Special verbal and written explanations about the rating of perceived
exertion are available for subjects. Although there is some variation
among subjects in their actual rating of fatigue, they seem to rate
consistently from test to test. Thus, the Borg scale can assist the
clinician in judging degree of fatigue reached from one test to another
or to correlate the level of fatigue during testing with that
experienced during daily activities.
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Indications for terminating exercise testing. Indications for interruption of an exercise test have been derived from clinical experience.
Absolute indications
Drop in systolic blood pressure (persistently below baseline) despite an increase in workload
Increasing anginal pain
Central nervous system symptoms (eg, ataxia, dizziness, or near syncope)
Signs of poor perfusion (cyanosis or pallor)
Serious arrhythmias (ie, high-grade ventricular arrhythmias such as multiform complexes, triplets, and runs)
Technical difficulties monitoring the ECG or systolic blood pressure
Subjects request to stop
Relative indications
ST or QRS changes such as excessive ST displacement, extreme junctional depression, or marked axis shift
Fatigue, shortness of breath, wheezing, leg cramps, or claudication
General appearance (see below)
Less serious arrhythmias, including supraventricular tachycardias
Development of bundle branch block that cannot be distinguished from ventricular tachycardia
Postexercise Period
Some abnormal responses occur only in recovery after exercise. If
maximum sensitivity is to be achieved with an exercise test, subjects
should be supine in the postexercise period; however, for subject
comfort, many physicians prefer the sitting position. A cooldown walk
after the test can delay or eliminate the appearance of ST segment
depression; however, the cooldown may be indicated in some subjects.
Monitoring should continue for 6 to 8 minutes after exercise or until
changes stabilize, and heart rate and ECG are close to baseline. In the
supine position, 4 to 5 minutes into recovery, approximately 85% of
subjects with abnormal responses are abnormal at this time only or in
addition to any other time. An abnormal ECG response occurring only in
the recovery period is not unusual, nor is it more likely to be
false-positive. Mechanical dysfunction and electrophysiological
abnormalities in the ischemic ventricle after exercise can persist from
minutes to hours. Monitoring of blood pressure should continue during
recovery, as abnormal responses may occur.
Interpretation
Clinical Responses
Symptoms. Ischemic chest pain induced by the exercise
test is
strongly predictive of CAD and is even more predictive with ST
depression. It is important to obtain a careful description of the pain
from the subject to ascertain that it is typical angina rather than
nonischemic chest pain.
Subjects appearance. The subjects general appearance is helpful in clinical assessment. A drop in skin temperature, cool and light perspiration, and peripheral cyanosis during exercise can indicate poor tissue perfusion due to inadequate cardiac output with secondary vasoconstriction. Such subjects should not be encouraged to attempt higher workloads. Neurological manifestations such as light-headedness or vertigo can also indicate inadequate cardiac output.
Physical examination. Cardiac auscultation immediately after exercise can provide information about ischemia-induced LV dysfunction. Gallop sounds or a precordial bulge can result from LV dysfunction. A new mitral regurgitant murmur suggests papillary muscle dysfunction, which may be related to transitory ischemia. It is preferable to have subjects lie supine after exercise testing and allow those who develop orthopnea to sit up. In addition, severe angina or ominous arrhythmias after exercise may be lessened by allowing the subject to sit up, since ischemia may be decreased. Key Point: Symptoms and signs of ischemia induced by exercise testing are clinically important, and their combinations influence interpretation.
Exercise
or Functional Capacity
O2max is a measure
of the
functional limit of the cardiovascular system and the best index of
exercise capacity. As previously discussed,
O2max depends on many
factors
(training, age, and gender) and is an indirect estimate of maximum
cardiac output. A decline in maximum cardiac output, which is the major
hemodynamic consequence of symptomatic CAD, usually causes a decrease
in exercise capacity. Although many subjects may stop exercising
because of anginal pain, acute reduction in LV performance resulting in
decreased stroke volume and heart rate and increasing pulmonary artery
pressure appear to be the mechanisms limiting cardiac output. In normal
women as opposed to normal men, LV ejection fraction (LVEF)
"plateaus" and may decrease with maximal
exercise.14
A mean exercise capacity of 10 METs has been observed in nonathletic middle-aged healthy men. If subjects with CAD reach 13 METs, their prognosis is good, regardless of other exercise test responses that may occur and medical or surgical treatment. Mortality is higher in subjects with an exercise capacity of 5 METs or less compared with subjects whose exercise capacities are higher.
A normal exercise capacity does not exclude severe cardiac impairment. Mechanisms proposed to explain a normal work performance in these subjects include increased peripheral oxygen extraction, preservation of systolic volume and chronotropic reserve, ability to tolerate elevated pulmonary wedge pressures without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Many subjects with decreased ejection fractions at rest can perform relatively normal levels of exercise, some without side effects, whereas others report increased fatigue for some time after the test. Key Point: An exercise capacity of 5 METs or less is associated with a poor prognosis in subjects less than 65 years old. An exercise capacity of 13 METs indicates a good prognosis despite abnormal exercise test responses. Resting LVEF does not correlate well with exercise capacity.
Hemodynamic Responses
Blood Pressure During Exercise
Blood pressure is dependent on cardiac output and peripheral
resistance. Systolic blood pressure at maximum exertion or at immediate
cessation of exertion is considered a clinically useful first
approximation of the hearts inotropic capacity. An inadequate rise or
a fall in systolic blood pressure during exercise can occur. Although
some normal subjects have a transient drop in systolic blood pressure
at maximum exercise, this finding is frequently associated with severe
CAD and ischemic dysfunction of the myocardium. Exercise-induced
hypotension also identifies subjects at increased risk for ventricular
fibrillation in the exercise laboratory. Key Point: A
drop in systolic blood pressure below standing rest during exercise is
associated with increased risk in subjects with a prior MI or
myocardial ischemia.
Heart Rate During Exercise
Relatively rapid heart rate during submaximum exercise or recovery
could be due to deconditioning, a condition that decreases vascular
volume or peripheral resistance, prolonged bed rest, anemia, or
metabolic disorders. This finding is relatively frequent soon after MI
and coronary artery surgery. Relatively low heart rate at any point
during submaximum exercise could be due to exercise training, enhanced
stroke volume, or drugs. The common use of ß-blockers, which lower
heart rate, has complicated interpretation of the heart rate response
to exercise. Conditions that affect the sinus node can attenuate the
normal response of heart rate during exercise testing. Key
Point: Abnormalities of exercise capacity, systolic blood
pressure, and heart rate response to exercise can be due to either LV
dysfunction, ischemia, cardioactive drugs, or autonomic dysfunction.
Responses in Subjects With Normal Resting ECGs
Normal responses. P wave. During exercise, P vectors
become more vertical, and P wave magnitude increases significantly in
inferior leads. There are no significant changes in P wave duration.
PR segment. The PR segment shortens and slopes downward in the inferior leads during exercise. The decreasing slope has been attributed to atrial repolarization (the Ta wave) and can cause false-positive ST depression in the inferior leads.
QRS complex. The Q wave shows very small changes from the resting values; however, it does become slightly more negative at maximum exercise. Changes in median R wave amplitude are noted near maximum effort. A sharp decrease in the R wave is observed in the lateral leads (V5) at maximum exercise and into the first minute of recovery. In the lateral and vertical leads (V5 and aVF), the S wave becomes greater in depth (more negative), showing a greater deflection at maximum exercise, and then gradually returns to resting values in recovery. As the R wave decreases in amplitude, the S wave increases in depth.
J-junction depression. The J-junction is depressed in lateral leads to a maximum depression at maximum exercise, then gradually returns toward preexercise values in recovery. A dramatic increase in J-junctional depression is observed in all leads and is greatest at 1 minute into recovery. Subjects with resting J-junction elevation may develop an isoelectric J-junction with exercise; this is a normal finding. These changes return toward pretest values later in recovery. The normal ST segment vector response both to tachycardia and exercise is a shift rightward and upward. There appears to be considerable biological variation in the degree of this shift.
T wave. A gradual decrease in T wave amplitude is observed in all leads during early exercise. At maximum exercise the T wave begins to increase, and at 1 minute into recovery the amplitude is equivalent to resting values in the lateral leads.
U wave. No significant changes are noted with exercise; however, U waves may be difficult to identify because of the close approximation of the T and P waves with the increased heart rate of exercise.
Abnormal responses. ST segment changes. The ST level is measured relative to the PR segment since the UP segment disappears during exercise. ST elevation is measured as the deviation from the baseline ST level. ST depression is measured from the isoelectric PR level since the normal response is a downward shift from early repolarization. If the baseline ST segment is depressed, the deviation from that level to the level during exercise or recovery is considered. The point for measuring the ST level is the J-junction. Points beyond this (60 or 80 milliseconds) should only be used if the ST segment slope is horizontal or downsloping. Considering ST depression that is rapidly upsloping to be abnormal increases sensitivity but decreases specificity. Many ST scores to quantify ischemia have been recommended, but none have been validated as superior to standard measurements. Exercise-induced myocardial ischemia can result in one of three ST segment manifestations on the surface ECG: depression, elevation, and normalization.
ST segment depression. ST segment depression is
the most
common manifestation of exercise-induced myocardial ischemia. It
represents subendocardial ischemia, with direction determined largely
by the placement of the heart in the chest. The standard criterion for
this abnormal response is horizontal or downsloping ST segment
depression of 0.10 mV or more for 80 milliseconds. However, as shown in
Fig 5
, other criteria have been considered.
Downsloping ST segment depression is a more significant change than
horizontal depression. In the presence of baseline abnormalities,
exercise-induced ST segment depression is less specific for ischemia.
Other factors related to the probability and severity of CAD include
the amount, time of appearance, duration, and number of leads with ST
segment depression.
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Severity of CAD is also related to the time of appearance of ischemic shifts. The lower the workload and double product at which it occurs, the worse the prognosis and the more likely the presence of multivessel disease. The persistence of ST depression in the recovery phase is also related to the severity of CAD. Key Point: The probability and severity of CAD are directly related to the amount of J-junction depression and are inversely related to the slope of ST segment (ie, the greater the depression and the downslope, the more likely and more severe the CAD).
ST segment elevation. ST elevation must be classified by whether it occurs over Q waves of an MI or in an ECG area without Q waves. The mechanisms and implications are markedly different. ST segment elevation has been more frequently observed in anterior leads (V1 and V2) with Q waves.15
ST segment elevation over Q waves of prior MI. Prior MI is the most frequent cause of ST segment elevation during exercise and appears to be related to the presence of dyskinetic areas or ventricular aneurysms. Approximately 50% of subjects with anterior MI and 15% of subjects with inferior MI exhibit this finding during exercise. Subjects with elevation usually have a lower ejection fraction than those without elevation over Q waves. These changes can result in reciprocal ST depression that simulates ischemia in other leads. ST segment elevation and depression during the same test may indicate multivessel CAD. The underlying extent of Q waves or myocardial damage actually determines the amount of ST elevation rather than independently reflecting the amount of dysfunction.
ST segment elevation without Q waves. In subjects without previous MI (absence of Q waves on the resting ECG), ST segment elevation during exercise frequently pinpoints the site of severe transient ischemia resulting from significant proximal disease or spasm. Key Point: Severe transmural ischemia is the mechanism for ST segment elevation during exercise in subjects without prior MI or diagnostic Q waves on the resting ECG. It locates the site of ischemia, in contrast to ST depression, which does not.16
In subjects with variant angina, ST segment elevation occurs during spontaneous anginal episodes, frequently at rest. During exercise, ST segment elevation has been reported in about 30% of these subjects. A reversible thallium-201 perfusion defect usually corresponds to the site of ST elevation. Many subjects with ST elevation have coexistent ST segment depression in other leads. Ventricular arrhythmias also appear to be more frequent in subjects with ST elevation.
ST segment normalization or absence of change. Another manifestation of ischemia may be normalization of or no change in the ST segment related to cancellation effects, but this is nonspecific. ECG abnormalities at rest, including T wave inversion and ST segment depression, reportedly return to normal during attacks of angina and during exercise in some subjects with ischemic heart disease, but they can also be observed in subjects with a persistent juvenile pattern on the resting ECG. This cancellation effect is rare but should be considered.
Diagnostic value of R wave changes. Many within-subject estimates of the variability of R wave amplitude changes during exercise in normal subjects have been reported. However, the average response in normal subjects is an increase in R wave amplitude during submaximum exercise, with a drop at maximum exercise. Exercise-induced changes in R wave amplitude have not improved diagnostic accuracy despite use of several lead systems, clinical subsets of subjects, and different criteria for an abnormal response. Key Point: A multitude of factors affect the R wave amplitude response to exercise, and the response does not have diagnostic significance.
T wave changes. In normal subjects, a gradual decrease in T wave amplitude is observed in all leads during early exercise. At maximum exercise the T wave begins to increase, and 1 minute into recovery amplitude is equivalent to resting values in lateral leads.
U wave changes. U wave inversion is associated with LV hypertrophy, CAD, and aortic and mitral regurgitation. These conditions are associated with abnormal LV distensibility. Exercise-induced U wave inversion in subjects with a normal resting ECG appears to be a marker of myocardial ischemia and suggests left anterior descending CAD.
ST/HR index and slope. Although research and clinical data are available on this methodology in exercise testing, the ST/HR index is not recommended because of problems with validation. A meta-analysis revealed that positive results with this method were obtained only by centers that were also responsible for over half the published reports.17
Other Studies
Exercise
tests can be performed with radionuclear techniques to
further evaluate myocardial perfusion and function. As an example,
thallium, an isotope that behaves like potassium, is taken up by
perfused, viable myocardium when injected at maximum exercise. Imaging
performed immediately after exercise can reveal defects. If defective
areas fill in during resting scans, they are usually due to ischemia;
if such areas do not fill in, the defects can be due to scarring or
severe ischemia. Technetium can be tagged to red blood cells and can
provide an image of the LV cavity blood volume during exercise. Changes
in ejection fraction, wall motion, and ventricular volume can be
assessed.
Echocardiographic images and Doppler flow measurements can be made during and after exercise. Ejection fraction, wall motion, and valvular function can be assessed with this technique.
More recently, thallium single-photon emission computerized tomography has been used in exercise evaluation. Such evaluation should be delayed 10 to 15 minutes after exercise to avoid artifacts secondary to heart position and respiratory rate immediately after exercise.18 As further sophistication of imaging evolves, positron emission tomography will likely become a clinically applicable tool in exercise evaluation. This technique offers the opportunity to quantify regional function in the heart spanning blood flow, biochemical reaction rates, substrate fluxes, and receptors.19 Pharmacologic stress is available for subjects who are unable to exercise. Dipyridamole infusion as a coronary vasodilator causes an increase in myocardial blood flow that is altered in the presence of diseased coronary arteries.18 Adenosine infusion, which also causes vasodilation, can be used similarly to dipyridamole in pharmacological testing,18 and dobutamine, with its chronotropic and inotropic effects, can be used with thallium scintigraphy or echocardiography to delineate regional ischemia and wall motion abnormalities.18
Magnetic resonance imaging is a relatively new technology that may serve as an excellent tool for studying the effects of exercise in both the normal and failing heart. These methods are well-suited to study the myocardial effects of chronic exercise.20
Diagnostic Value of the Exercise Test
Sensitivity and
Specificity
Sensitivity and specificity define how effectively a test
separates subjects with disease from healthy individuals, ie, how well
a test diagnoses disease. Sensitivity is the percentage of those
individuals with a disease who will have abnormal tests. Specificity is
the percentage of those without the disease who will have normal test
results; specificity may be affected by drugs such as digoxin, baseline
ECG patterns, LV hypertrophy, and gender.
Sensitivity and specificity are inversely related; when sensitivity is the highest, specificity is lowest and vice versa. All tests have a range of inversely related sensitivities and specificities that can be selected by specifying a discriminate or diagnostic cut point.
The choice of a discriminate value is further complicated by the fact that some exercise test responses do not have established values that separate normal subjects from those with disease. Once a discriminate value that determines a tests specificity and sensitivity is chosen, the population tested must be considered. If the population is skewed toward individuals with a greater severity of disease, the test will have a higher sensitivity. For instance, the exercise test has a higher sensitivity in individuals with triple-vessel disease than in those with single-vessel disease. A test can also have a lower specificity if it is used in individuals who are more likely to give false-positive results. For instance, the exercise test has a lower specificity in women and in individuals with mitral valve prolapse.
Sensitivity and specificity of exercise-induced ST segment depression can be demonstrated by comparing the results of exercise testing and coronary angiography.21 From these studies, it can be seen that the exercise test cut point of 0.1 mV horizontal or downsloping ST segment depression has approximately 84% specificity for angiographically significant CAD; ie, 84% of those without significant angiographic disease had a normal exercise test. These studies had a mean 66% sensitivity of exercise testing for significant angiographic CAD, with a range of 40% for one-vessel disease to 90% for three-vessel disease. Key Point: Sensitivity and specificity are inversely related, affected by the population tested, and determined by the choice of a cut point or discriminate value.
Relative Risk and Predictive Value
Relative risk
and predictive value help define the
diagnostic value of a test. Table 7
shows how
sensitivity, specificity, relative risk, and predictive value are
calculated.
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Prognostic Use of the Exercise Test
Rationale
There are two principal reasons for estimating prognosis. The
first is to provide accurate answers to a subjects questions about
the probable outcome of his or her illness. Although discussion of
prognosis is inherently delicate and probability statements can be
misunderstood, most subjects find this information useful in planning
their work, recreational activities, personal estates, and finances.
The second reason for determining prognosis is to identify subjects in
whom cardiovascular interventions might improve outcome.
Pathophysiology of CAD
The basic pathophysiological
features of CAD include arrhythmic
risk, myocardial damage (reflected by LV function), and the degree of
myocardium in jeopardy. Arrhythmic risk does not appear to be
independently predicted by exercise testing since the prognosis of
arrhythmias is closely related to LV abnormalities. (Twenty-four hour
ambulatory ECG recording provides more information about arrhythmias
except for those that are clearly related to exercise.) Exercise test
responses due to myocardial ischemia include angina, ST segment
depression, and ST segment elevation over ECG areas without Q waves.
Predicting the amount of ischemia (ie, the amount of myocardium in
jeopardy) is difficult. It is inversely related to the double product
at the onset of signs or symptoms of ischemia. Responses related to
ischemia or LV dysfunction include chronotropic incompetence, drops in
systolic blood pressure, and poor exercise capacity.
Exercise capacity correlates poorly with LV function in subjects without signs or symptoms of heart failure, nor is exercise testing helpful in identifying subjects with moderate LV dysfunction. LV dysfunction is better recognized by a history of heart failure, physical examination, resting ECG, echocardiogram, or radionuclide ventriculogram. Several subject groups have been studied to determine prognosis with exercise testing, including post-MI subjects, subjects with stable CAD (including silent ischemia), subjects after coronary artery bypass surgery (CABS), subjects after percutaneous transluminal coronary angioplasty (PTCA), and asymptomatic individuals.
Post-MI Subjects. Purpose. Table 8
lists reasons for performing an exercise test in post-MI subjects.
Exercise testing may expedite and optimize discharge from the hospital
of subjects recovering from an MI. Ventricular arrhythmias not present
at rest can be provoked during exercise. The subjects reaction to
exercise, work capacity, and limiting factors at the time of discharge
from the hospital can be assessed. An exercise test before discharge is
important for providing guidelines for exercise at home, reassurance of
physical status, and determination of risk of complications. It also
provides a safe basis for advising the subject to resume or increase
his or her activity level and return to work. The test can demonstrate
to the subject, family, and employer the effect of MI on capacity for
physical performance. Psychologically, it may improve self-confidence
by decreasing the subjects anxiety about daily physical activities.
The test also reassures spouses of subjects physical capabilities.
The response to exercise testing reassures and encourages many subjects
to increase their activities.
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Some investigators use symptoms or sign-limited end points 2 or 3 weeks after MI. However, a submaximum limited test using predetermined end points seems more clinically appropriate. A heart rate limit of 140 beats per minute and a MET level of 7 is arbitrarily used for subjects under the age of 40 years; a heart rate limit of 130 beats per minute and a MET level of 5 is used for subjects over 40. A Borg perceived exertion level in the range of 13 to 15 can be used as a test end point, particularly for subjects receiving ß-blockers. A symptom-limited maximum test is probably most appropriate more than 3 weeks after MI, when the subject is ready to resume full activities.
Safety. A review of numerous subjects with predischarge and post-MI exercise tests reports few serious complications: two cases of recurrent MI and two cases of ventricular fibrillation, one fatal. These findings represent 0.05% morbidity and 0.02% mortality.22
Meta-analysis reveals that only an abnormal systolic blood pressure response or a low exercise capacity is significantly associated with poor outcome in post-MI subjects. Submaximum testing resulted in the highest proportion of positive associations and the highest risk ratios. Abnormal responses at higher workloads are not as predictive as those at lower workloads.22 Key Point: In post-MI subjects, clinical judgment identifies subjects at highest risk, and exercise-induced ST displacement is not as predictive as an abnormal systolic blood pressure response (drop of 20 mm Hg or more or flat response for duration of the test) or poor exercise capacity. However, exercise-induced ST segment depression appears to be associated with increased risk in subjects without diagnostic Q waves (ie, subendocardial MI).23
Subjects with stable CAD. Studies using exercise testing of subjects with stable CAD have attempted to predict angiographic findings, cardiac events in subjects with silent ischemia, or improved survival with CABS.
Angiographic findings. Numerous studies have been devised to predict left main or triple-vessel disease or both.24 Different criteria have been used with varying results. Predictive value refers to the percentage of those with abnormal criteria who actually have left main or triple-vessel disease.
Exertional hypotension. In most studies, exercise-induced hypotension predicts a poor prognosis, with a positive predictive value of 50% for left main or triple-vessel disease.25 Exercise-induced hypotension is also associated with cardiac complications during exercise testing, appears to be alleviated by CABS, and can occur in subjects with CAD, valvular heart disease, or cardiomyopathy. Occasionally, subjects without clinically significant heart disease will exhibit exercise-induced hypotension during exercise related to dehydration, antihypertensive therapy, or prolonged strenuous exercise. Key Point: The definition of exercise-induced hypotension is of crucial importance in evaluating the exercise test response. A drop in systolic blood pressure below preexercise values is the most ominous criterion; a drop of 20 mm Hg or more after a rise is reason to stop a test if accompanied by serious ventricular arrhythmias or ischemia.
Cardiac events in subjects with silent ischemia. In the presence of unstable angina, asymptomatic (silent) ischemia detected by ambulatory ECG (Holter) recording appears to confer an adverse prognosis. The prognostic implication of asymptomatic ischemia detected during exercise testing is controversial. Subjects with silent ischemia may be at greater risk for cardiac death because they do not have an intact "warning system." However, in three large population studies of subjects with a high prevalence of CAD who underwent exercise testing, those with ST segment depression with or without angina during testing had similar prognoses.26 Ischemia is silent in approximately 60% of subjects with ischemic ST segment depression. Silent ischemia occurring with treadmill testing does not confer an increased risk for death relative to subjects experiencing angina. Thus, therapy should not be more intense for silent ischemia than for subjects with angina and ST depression.
Exercise-induced ventricular arrhythmias. In subjects with CAD, exercise-induced ventricular arrhythmias do not usually represent an independent risk factor for subsequent mortality or coronary events. However, recent data suggest that these arrhythmias add independent prognostic information to thallium-201, ST segment, and heart rate changes,27 28 and they are associated with severe CAD and wall motion abnormalities. Exercise testing may be of considerable value in the evaluation of drug therapy for ventricular arrhythmias, particularly in subjects with CAD.
Prognostic scores. Scores
based on the coefficients from Cox
Hazzard Survival models appear to be the optimal way of estimating
cardiovascular mortality. The Duke score represented in Fig 6
as a nomogram is the best validated and has been
shown to function in a wide range of populations, including women.
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Improved survival after CABS. One study suggests that subjects with cardiomegaly, exercise capacity of less than 5 METs, or a maximum systolic blood pressure of less than 130 mm Hg would have a better outcome if treated with surgery.29 In one surgery trial, subjects who had an exercise test response of 1.5 mm of ST segment depression showed enhanced survival with surgery. Improved survival also extended to those with baseline ST segment depression and those with claudication.30 In another trial31 the surgical benefit to mortality was greatest in subjects with 1 mm ST segment depression at less than 5 METs. There was no difference in mortality in subjects who exceeded exercise capacity of 10 METs, and in this group, the prognosis is generally quite good. Key Point: In subjects with stable CAD, studies comparing angiographic findings, cardiac events, and the differential outcome of CABS compared with medical therapy have shown the exercise test to have prognostic power. These studies indicate that subjects with marked degrees of ST segment depression (ie, greater than 2 mm, in multiple leads, and prolonged into recovery) accompanied by poor exercise capacity, exertional hypotension, ectopic ventricular contractions, angina, or all of the above are at increased risk of having triple-vessel or left main disease and a poor prognosis.
Subjects who become symptomatic after CABS. Because more than 300 000 Americans undergo CABS each year, predicting prognosis of subjects who become symptomatic after this procedure is an important issue. Several studies have evaluated graft occlusion and recurrence of symptoms; however, exercise-induced ST depression does not predict prognosis after CABS. An exercise capacity of 9 METs or more indicates a good prognosis, regardless of other responses.32
Subjects who have undergone PTCA. More than 250 000 PTCAs are performed annually,33 with an expected angiographic restenosis rate of 30% to 40%34 within the subsequent first 6 months. Several studies have assessed the value of exercise testing in the detection of restenosis and/or in the prediction of adverse cardiac events after PTCA.34 35 36 37 38 39 40 41 Interpretation of these studies is limited because of their variability in subject populations and study design, with regard to the number of vessels diseased, the adequacy of revascularization after PTCA, the timing of the exercise test, and the definition of restenosis. Several general conclusions, however, can be drawn from these studies. Exercise electrocardiography early after PTCA is more often positive for an ischemic response among subjects with multivessel coronary disease and those who have incomplete revascularization.35 36 37 The sensitivity of exercise electrocardiography in the detection of angiographic restenosis has been reported to range widely, from 24% to 60%.38 39 40 Moreover, among asymptomatic subjects with single vessel CAD, the detection of restenosis and the utility of the exercise test to predict subsequent cardiac events is particularly low.36 38 39
In summary, the sensitivity, specificity, and predictive value of exercise testing after PTCA is sufficiently low to preclude its routine use as a screening test for restenosis and the assessment of subsequent prognosis, particularly in asymptomatic subjects. Such testing appears to have the highest yield among symptomatic subjects with multivessel coronary disease and in those with incomplete revascularization. As such, exercise testing after PTCA, if done, should be performed and interpreted with regard to the timing of the test after PTCA, assessment of clinical symptoms, and assessment of coronary anatomy at the time of PTCA.
High risk coronary profile. Exercise testing in subjects with coronary risk factors such as hypercholesterolemia and high blood pressure may be beneficial, particularly if there are symptoms suggesting CAD. The detection of myocardial ischemia or other abnormal end points can lead to further diagnostic studies and appropriate management strategies.
Apparently healthy individuals. Silent ischemia induced by exercise testing in apparently healthy men is not as predictive of a poor outcome as once thought. Use of the exercise test for screening is even more misleading than previously appreciated because of the higher false-positive rate. Approximately 19 of 20 abnormal ST responses will be false-positives. Earlier superior results can be explained by inclusion of angina pectoris as an end point, which could be caused by cardiac concerns resulting from an abnormal exercise test.42 43 Key Point: The nonselective use of exercise testing for screening apparently healthy individuals should be discouraged because of the poor predictive value of minimum (1 mm) ST segment depression. Unfortunately, this abnormal response may lead to psychological and vocational disability as well as unnecessary medical expense and risk. In these individuals, the test is helpful for motivational purposes and for designating exercise prescriptions. Only combinations of other abnormal responses and at least 2 mm or more ST depression should be considered predictors of increased risk of cardiovascular events in asymptomatic men.
There is substantial evidence to support the use of exercise testing as the first noninvasive step after the history, physical examination, and resting ECG in prognostic evaluation of subjects with CAD. Exercise testing accomplishes both purposes of prognostic testing: it provides information about the subjects status and is helpful when making recommendations for optimum management. Some studies show that the value of exercise testing for risk stratification is enhanced by the addition of radionuclide imaging, particularly with submaximum testing after an uncomplicated MI. Exercise test results enhance selection of subjects who should undergo further evaluation such as coronary angiography. Since the exercise test can be performed in the physicians office and provides valuable information about activity levels, response to therapy, and disability, it is the reasonable first choice for prognostic assessment. Because of its widespread use, the exercise test can have an enormous impact on the cost-effective delivery of cardiovascular care.
Other Uses of the Exercise Test
Assessment of Valvular
Heart Disease
Exercise testing has been used in subjects with valvular
heart
disease to quantify disability, to reproduce exercise-induced symptoms,
and to evaluate responses to medical and surgical
interventions.44 The exercise test has also been used to
identify concurrent CAD, but there is a high prevalence of
false-positive responses (ST depression not due to ischemia) because of
frequent baseline ECG abnormalities and LV hypertrophy. Some physicians
use exercise testing to determine when surgery is indicated. Exercise
testing has been used most frequently in subjects with aortic
stenosis.
Aortic stenosis. Effort syncope in subjects with aortic stenosis45 46 is an important and well-appreciated symptom. Most guidelines for exercise testing list moderate to severe aortic stenosis as a relative contraindication for testing because of concern about syncope and cardiac arrest. Four proposed mechanisms for exercise-induced syncope in subjects with aortic stenosis include carotid hyperactivity, LV failure, arrhythmia, and LV baroreceptor stimulation. Exercise testing is relatively safe in both the pediatric and adult subject when performed appropriately. Attention should focus on the subjects symptoms, minute-by-minute response of blood pressure, slowing heart rate, and ventricular and atrial arrhythmias. In the presence of an abnormal blood pressure response, the subject with aortic stenosis should take at least a 2-minute cooldown walk at a lower stage of exertion to avoid acute LV volume overload, which may occur when the subject lies down.
Exercise plays an important role in the objective assessment of symptoms, hemodynamic response, and functional capacity. Whether ST segment depression indicates significant CAD remains unclear. The benefits of surgery and baseline impairment can be quantified by performing an exercise test before and after the operation. Exercise testing offers the opportunity to objectively evaluate disparities between history and clinical findings, eg, in the elderly asymptomatic subject with physical and/or Doppler findings of severe aortic stenosis. Echocardiographic studies are often inadequate in such subjects, particularly in smokers. When Doppler echocardiography reveals a significant gradient in the asymptomatic subject with normal exercise capacity, progress should be monitored until symptoms develop. Surgery appears to be indicated in subjects with an inadequate systolic blood pressure response to exercise or a fall in systolic blood pressure from the resting value when symptoms occur.
Aortic regurgitation. Subjects with aortic
regurgitation47 usually maintain a normal exercise
capacity for a longer time than those with aortic stenosis. Volume
workload of the myocardium requires less oxygen than pressure work.
During exercise, the decreases in diastolic duration and regurgitation
volume favor forward output. As the myocardium fails, heart rate tends
to slow, and ejection fraction and stroke volume decrease. There is an
increase in ventricular diameter and metabolic requirements. Exercise
testing is useful for monitoring subjects with aortic regurgitation,
using onset of ST segment depression, a reduction of heart rate
response to each workload, and decrease in peak
O2 as markers for worsening
LV
function.
Mitral stenosis. Subjects with mitral stenosis48 may show either a normal or excessive increase in heart rate during exercise. Since stroke volume cannot be increased, the normal rise of cardiac output is attenuated and may eventually fall during exercise, frequently accompanied by exercise-induced hypotension. A rise in pulmonary resistance results in increases in myocardial oxygen demands. In subjects with mitral stenosis, chest pain and ST segment depression during exercise may occur as a consequence of reduction in coronary perfusion or because of pulmonary hypertension. ST depression is attributed to a decrease in coronary perfusion as a consequence of a fall in cardiac output and increased myocardial oxygen demand secondary to right ventricular overload. Shortening of diastole associated with tachycardia and increased pulmonary blood flow during exercise increases effects of preexistent mitral stenosis and may cause pulmonary congestion.
Mitral regurgitation. Subjects with mild to moderate mitral regurgitation49 maintain normal cardiac output during exercise. Blood pressure, heart rate, and ECG responses are usually normal. When mitral regurgitation occurs suddenly during exercise as a result of ischemic papillary muscle dysfunction, a flat response in systolic blood pressure can occur. Subjects with severe mitral regurgitation usually show a decreased cardiac output and limited exercise capacity. ST segment depression is infrequent in these subjects since there is no significant increase in myocardial oxygen consumption with mitral regurgitation. However, a hypotensive response can develop, and arrhythmias frequently occur.
Mitral valve prolapse. Several mechanisms have been suggested to explain ST depression in subjects with mitral valve prolapse,50 including regional ischemia of the papillary muscle, abnormalities of the coronary arteries, compression of the anterior descending artery, coronary spasm, and primary cardiomyopathy. Angiography and scintigraphy studies in these subjects have been normal. ECG changes can be normalized by propranolol or other nonselective ß-blockers, which will improve the specificity of the exercise test.
Evaluation of an Exercise Program
An
exercise test is often used to evaluate the safety of an
exercise training program and is useful in formulating an exercise
prescription. In general, a sedentary individual who at the age of 40
years decides to enter an exercise program of a higher intensity than
walking at 50% to 60% of maximum heart rate reserve should undergo an
exercise test. Testing should also be recommended for younger
individuals with coronary risk factors or a strong family history of
CAD. Because of the wide scatter of maximum heart rate when plotted
against age, determining an individuals maximum heart rate during
exercise in order to assign a target for training is preferable to
giving a predicted value. It is advantageous in certain individuals to
objectively evaluate the response to exercise in a monitored setting
before an exercise program is begun. An exercise test can be used in
adult exercise or cardiac rehabilitation programs to safely advance an
individual to a higher intensity of effort. Test-demonstrated
improvement in exercise capacity can also be an effective incentive to
continue the program and encourage risk factor modification. (Further
information may be found in the section titled "Exercise
Training.")
Functional Classification of Disability
Exercise testing is used to determine the degree of
disability of subjects with various forms of heart disease. Subjects
who exaggerate their symptoms or who have a psychological impairment
can often be identified. Exercise testing is a more accurate measure of
the degree of cardiac impairment than a physicians assessment of
exercise capacity.
O2max is
the
best noninvasive measurement of the exercise capacity of the
cardiovascular system. Inability to reach 5 METs (below 18
mL · kg-1 · min-1) without
signs or
symptoms is a criterion of disability used by the Social
Security Administration. Determination of a subjects exercise
capacity affords an objective measurement of the degree of cardiac
impairment and can be useful in treatment.51
Evaluation of Risk for Surgery
Results of exercise
testing do not appear to substantially add to
the risk stratification provided by the resting ECG in subjects without
known CAD who are candidates for major elective noncardiac
surgery.52 Therefore, exercise testing is not recommended
as a routine procedure before major elective noncardiac surgery under
general anesthesia. Exercise testing has been used in subjects with
intermittent claudication to evaluate results of iliofemoral bypass.
Assessment of Special Populations
Subjects before and after revascularization. The
efficacy of a
revascularization intervention can be noninvasively assessed by
exercise testing since signs and symptoms of ischemia can be
demonstrated and exercise capacity can be measured.53
The elderly. Exercise testing can be effectively performed in older individuals. Attention must focus on musculoskeletal stability, and often testing protocols must be modified. The expected lesser heart rate response (even in the absence of medications) and higher systolic pressure response must be interpreted appropriately for higher age ranges.
Subjects with heart failure. Testing protocols are usually modified in degree of graded work for those subjects with heart failure. Closer medical supervision is indicated, and care must be taken in assessing blood pressure response and ventricular arrhythmias. Auscultation after exercise may detect cardiac "gallop" rhythm, pulmonary rales, and bronchospasm.
The physically disabled. Special protocols are available for testing54 musculoskeletally disabled subjects, especially those with hemiplegia or paresis after stroke or those with lower limb amputation or spinal cord injury. Many testing protocols use arm cycle ergometry with the subject sitting to optimize the exercise load, but some protocols consist of arm-leg or leg cycle ergometry. Effective testing can be performed by most of these subjects.
Cardiac transplantation recipients. These subjects often have exercise testing for prescription formulation for "reconditioning" in a supervised exercise program. Heart rate and blood pressure responses in these individuals are often quite modest, and other end points such as perceived exertion are best used as end points in exercise training. Exercise test protocols should be selected to provide slow increases in intensity of workload to allow time for the denervated heart to respond to circulating catecholamines.
Drugs and Exercise Testing
ß-Blockers
Subjects with angina who receive ß-blockers may achieve a higher
exercise capacity with less ST segment depression and less angina if
the drugs prevent their reaching the ischemic double product. Maximum
heart rate and systolic blood pressure product may be profoundly
reduced. The time of ingesting medications before testing should be
recorded.
Vasodilators
These agents can increase
exercise capacity in subjects with
angina or heart failure or both.55 There has been no
scientific validation that long-acting nitrates increase exercise
capacity in subjects with angina when they are tested after chronic
administration. Hydralazine decreases peripheral resistance and
arterial blood pressure. There is often an increase in heart rate
(reflex tachycardia) that tends to increase cardiac output. This agent
is useful in treatment of heart failure by decreasing afterload and
increasing exercise capacity.
Angiotensin-Converting Enzyme
Inhibitors
These agents decrease blood pressure at rest and during
exercise
through decreases in plasma levels of angiotensin II and aldosterone.
They increase exercise capacity in subjects with chronic heart failure
and enhance their survival rates.
Calcium Antagonists
Calcium antagonists (slow channel-blocking agents) have multiple
hemodynamic effects. They can delay time to ischemia and improve
exercise capacity. ST segment depression is usually delayed until
higher workloads. Heart rate and systolic blood pressure are decreased
for a given level of exercise.
Digitalis
ST segment
depression can be induced or accentuated during
exercise in individuals who are taking digitalis, including both normal
subjects and subjects with CAD.56 Profound ST segment
depression (more than 2 mm above baseline) almost always indicates
ischemia, even in subjects who are taking digitalis. A normal QT
interval is associated with digitalis-induced ST changes, whereas
prolonged QT intervals occur with ischemia, other drugs, electrolyte
imbalance, and other medical problems. Exercise-induced ST segment
depression is said to persist for 2 weeks after digitalis is
discontinued.
Antiarrhythmic Agents
Quinidine can
cause prolongation of phase 2 of the ventricular
action potential, decreasing the repolarization gradient during the ST
segment and thus diminishing the magnitude of ST depression. However,
quinidine does not change the ST segment, heart rate, or
O2max in normal subjects or
subjects with CAD.
A decrease of 20 beats per minute in maximum exercise heart rate has been reported in subjects taking amiodarone. Amiodarone also increases duration of the QRS complex during exercise.
Diuretics
Most diuretics have little influence on heart rate and cardiac
performance but do decrease plasma volume, peripheral resistance, and
blood pressure. Diuretics can cause hypokalemia, which results in
muscle fatigue, ventricular ectopy, and, rarely, ST segment
depression.
Special Cases of Exercise Testing Interpretation
Exercise Testing in Women
The difference in the
predictive accuracy of exercise testing
between men and women can be explained in part by the difference in
prevalence of CAD.57 However, because specificity is also
intrinsically lower in women, two factors merit attention. First,
careful characterization of chest pain is especially important; second,
ST segment depression in the presence of typical angina is highly
predictive of disease compared with atypical or no pain. Several
mechanisms have been suggested to explain the high false-positive rate
of ST depression in women, including medications (digitalis) and
resting ST-T abnormalities. Because estrogens have a similar chemical
structure to digitalis, they may be partially responsible for the high
prevalence of false-positive exercise test results in women.
Hypertension
Exercise testing has been proposed as
a means of detecting labile
hypertensive subjects or individuals who will eventually become
hypertensive, but there is a lack of support for this
theory.58 59 In addition, subjects whose hypertension
is
poorly controlled (ie, those on therapy) may be identified by
abnormally high pressure responses with exercise. Hypertensive subjects
frequently have ECG abnormalities (LV hypertrophy with strain) and
myocardial hypertrophy, both of which make false-positive ST responses
more likely.
Cardiomyopathies
Exercise testing has
been used in subjects with dilated
cardiomyopathy to determine exercise capacity, assess pulmonary
response to LV dysfunction, determine the grade of ventricular ectopy,
and evaluate the effectiveness of treatment.60 Subjects
with LV dysfunction may have reduced exercise capacity and develop
signs and symptoms of pulmonary and right ventricular involvement.
There is an inadequate increase in cardiac output during exercise,
which limits
O2max and
exercise
tolerance. Subjects with severe LV dysfunction can often double cardiac
output only with upright exercise. Stroke volume may increase normally
during upright exercise despite a decrease in LVEF. Ventricular
dilation facilitates use of the Starling mechanism but may reduce
chronotropic reserve. With increasing exercise, stroke volume and
cardiac output cannot continue to meet the increased demands, and
exertional hypotension is often observed.
Certain subjects may have normal exercise tolerance despite severe LV dysfunction. Several compensatory mechanisms have been proposed to explain the poor correlation between LV function and exercise capacity. This is especially so for those with a resistance to right-sided impairment (ie, pulmonary congestion). Exercise may increase the frequency of ventricular ectopy or induce other more serious arrhythmias. Even supraventricular arrhythmias can lead to ventricular tachycardia.
Hypertrophic Obstructive Cardiomyopathy
Exercise can be related to sudden death due to arrhythmias in this
condition.61 62 Chest pain, an abnormal resting ECG,
and
exercise-induced ST segment depression are frequent. Exercise testing
under careful supervision may be especially helpful to demonstrate the
level at which significant events occur, such as the presence or
severity of arrhythmias, myocardial ischemia, murmurs indicating
obstruction in LV outflow, and presyncopal manifestations. Ventricular
arrhythmias are often observed during exercise.
Intracardiac Conduction Blocks
Intraventricular blocks. Intracardiac conduction
blocks can
exist before exercise or develop or disappear during exercise.
Rate-dependent intraventricular blocks that develop during exercise
often precede the appearance of chronic blocks that are present at
rest.63 64 65 Diagnosis of ischemia from
the exercise ECG is
impossible when left bundle branch block is present. There can be a
marked degree of exercise ST segment depression in addition to that
found at rest in normal subjects with left bundle branch block. There
is no difference in ST segment response to exercise between those with
and those without ischemia. Left bundle branch block that occurs with a
heart rate below 125 beats per minute in subjects with typical angina
is frequently associated with CAD, whereas left bundle branch block
occurring at a heart rate above 125 beats per minute occurs more
frequently in subjects with normal coronary arteries. The presence of
intraventricular blocks and their disappearance during exercise are
rare. Subjects with left bundle branch block who develop a normal QRS
pattern during exercise have been reported.
Right bundle branch block. Preexisting right bundle branch block66 67 68 69 70 does not influence interpretation of the exercise test except in the anterior precordial leads (V1, V2), where ST depression is frequent. However, overall sensitivity of exercise testing in these subjects is uncertain.
Intraventricular blocks during exercise. In addition to left or right bundle branch block, left anterior or posterior hemiblock and bifascicular block (a combination of right bundle branch block and left anterior or posterior hemiblock) may be induced with exercise. The presence of such blocks is primarily a rate-related phenomenon that occurs during exercise as the sinus rate increases beyond a critical point. Intraventricular blocks are difficult to distinguish from ventricular tachycardia.
Conduction abnormalities. Atrioventricular (AV) conduction disturbance. Shortening of the PR interval (as much as 0.10 or 0.11 second) during exercise as the sinus rate increases is common, probably because of increased sympathetic tone, such as usually occurs in young, healthy individuals.
First-degree AV block. First-degree AV block occurs occasionally at the end of exercise or during the recovery phase. Medications or conditions that may produce prolonged AV conduction time (eg, digitalis, propranolol, myocarditis) predispose the individual to lengthening of the PR interval.
Second-degree AV block. The occurrence of Wenckebach Mobitz type I AV block during exercise is rare. The clinical significance of exercise-induced Mobitz type II AV block is not known, but the type II block may also be a rate-related phenomenon that appears as the sinus rate is accelerated beyond a critical level. It may, however, reflect more critical underlying conduction system disease, and if second-degree AV block develops with testing, the test should be terminated.
Complete AV block. Acquired complete AV block at rest is a relative contraindication to exercise testing. Exercise testing can be conducted in subjects with congenital complete AV block if there are no coexisting significant congenital anomalies.
Sinus arrest. Rarely, subjects develop long periods of sinus arrest immediately after exercise. Sinus arrest usually occurs in subjects with severe ischemic heart disease.
Preexitation syndromes. Exercise may provoke, abolish, or not interfere with anomalous AV conduction in individuals with known Wolff-Parkinson-White (WPW) syndrome.71 Exercise usually does not abolish anomalous AV conduction, but when it does, these individuals are thought to be in less danger of exercise-induced ventricular tachycardia. When exercise does not interfere with preexisting anomalous AV conduction, significant ST depression can be observed during exercise testing. In the presence of WPW syndrome, the ST depression may not be due to ischemia but may instead be a false-positive (indeterminate) occurrence. Although exercise has been considered a predisposing factor to initiate tachyarrhythmia in WPW syndrome, there is a low prevalence of tachyarrhythmias during or after exercise in WPW subjects. Approximately half of WPW subjects develop normal conduction during the test.
Cardiac Arrhythmias
Exercise may induce cardiac arrhythmias under several conditions,
including diuretic and digitalis
therapy,72 73 74 and recent
ingestion of alcohol or caffeine may exacerbate arrhythmias. Since
exercise increases myocardial oxygen demand, in the presence of CAD,
myocardial ischemia could predispose the subject to ectopic activity
during exercise. It appears that subendocardial ischemia (ST
depression) is not as arrhythmogenic as transmural ischemia (ST
elevation). Exercise-induced arrhythmias are generated by enhanced
sympathetic tone, increased myocardial oxygen demand, or both. The
immediate postexercise period is particularly dangerous because of the
high catecholamine levels that are associated with a generalized
vasodilation. Peripheral arteriolar dilation induced by exercise and
reduced cardiac output resulting from diminished venous return
secondary to sudden termination of muscular activity may lead to a
reduction in coronary perfusion while the heart rate is still elevated.
The increased sympathetic tone in the myocardium may stimulate ectopic
Purkinje pacemaker activity by accelerating phase 4 of the action
potential, which provokes spontaneous discharge and leads to increased
automaticity.
Exercise can suppress cardiac arrhythmias present at rest. This phenomenon has been attributed to the overdrive suppression of the ectopic impulse formation by sinus tachycardia that is caused by exercise-induced vagal withdrawal and increased sympathetic stimulation. Exercise-induced sinus tachycardia may inhibit automaticity of an ectopic focus because it reduces automaticity of the Purkinje tissue.
Ectopic ventricular contractions are the most frequent cardiac arrhythmia during exercise, followed by supraventricular arrhythmias and fusion beats. Their prevalence is directly related to age and cardiac abnormalities. In general, ectopic ventricular contractions are of concern in subjects with a family history of sudden death or a personal history of cardiomyopathy, valvular heart disease, or severe ischemia.
Sinus arrhythmias with periods of sinus bradycardia and wandering atrial pacemaker are relatively common during exercise and the immediate recovery phase. Atrial ectopic contractions and atrial "group" beats can occur in either normal or diseased hearts. Exercise-induced transient atrial fibrillation and flutter occur in less than 1% of individuals who undergo exercise testing.75 These arrhythmias may be induced by exercise in healthy individuals or subjects with rheumatic heart disease, hyperthyroidism, WPW syndrome, or cardiomyopathy. Paroxysmal AV junctional tachycardia is observed during exercise only rarely. Exercise-induced supraventricular arrhythmias alone are not related to CAD but are more often related to pulmonary disease, recent alcohol ingestion, or excessive caffeine intake.
Obtaining Informed Consent for Exercise Testing
Although obtaining written consent from a subject does not protect a physician from legal action, a signed consent form is nonetheless desirable because a physician may be held responsible for a major adverse event, even if the test is carefully administered and monitored.
Informed Consent for Exercise Testing
To determine my cardiovascular response to exercise, I voluntarily agree to engage in an exercise test. The information obtained about my heart and circulation will be used to help my doctor advise me about activities in which I may engage.
I have been told that before I undergo the test, I will be interviewed and examined by a physician in an attempt to determine if I have a condition indicating that I should not engage in this test.
I am told that the test I will undergo will be performed on a
(description), with gradually increasing effort until symptoms such as fatigue, shortness of breath, or chest discomfort may appear, indicating to me that I should stop. I have been told certain changes may occur during the test, including abnormal blood pressure, fainting, abnormal ECG showing heart "strain," disorders of heart beat (too rapid, too low, or ineffective), and, possibly, heart attack and death.
I agree that the information obtained may be used and published for statistical or scientific purposes.
I have read the above and understand it, and my questions have been answered to my satisfaction.
Subject
Physician supervising the test
Witness
Date
Exercise Training
Care must be taken to ensure that apparently healthy individuals who are beginning an exercise program do not have detectable disease and that subjects with known disease are stable with no evidence of new or changing symptoms. Medical clearance should be obtained before entry into exercise training programs unless the anticipated activity is low level (less than 50% of maximum capacity, eg, moderate walking). Exercise testing is helpful in establishing guidelines for exercise training in apparently healthy adults and is mandatory for subjects with known or suspected cardiovascular disease. Care should be taken to exclude from training subjects with evidence of unstable heart disease such as angina, uncontrolled heart failure, or arrhythmia. Training programs for subjects with cardiovascular disease should be medically supervised until safe levels of activity have been established. Physician presence is discussed under the section titled "Types of Supervised Programs."
Exercise Training of Apparently Healthy Individuals
Risks of Exercise
Exercise has both risks and benefits,
and the challenge to the
physician is to provide guidelines that minimize risks and maximize
benefits. Screening procedures are not perfect for identifying the rare
individual who is at risk, but risks can be decreased by proper
screening precautions.
Many factors affect risk of exercise. Three of
the most important are
age, presence of heart disease, and intensity of exercise. Sudden
cardiac death is rare in apparently healthy individuals. In individuals
under the age of 35 years, sudden cardiac death is usually attributed
to congenital heart disease, whereas CAD is a more likely cause for
those over 35. The results of selected studies reporting risks of
sudden cardiac arrest during exercise training are summarized in Table
9
.
|
These studies indicate that in the general population, risk of sudden cardiac death during vigorous exercise is very low. Since these studies were not randomized controlled trials, the contribution of all potential variables to sudden cardiac arrest or death cannot be determined. However, it is generally believed that the benefits of exercise exceed the risks, and individuals should be encouraged to exercise prudently.
It is recommended that anyone who plans to begin an exercise program more vigorous than walking should have a current (within 6 to 12 months) physical examination. Individuals under the age of 40 years who have no symptoms of cardiovascular disease, no major coronary risk factors, and no physical findings (including murmurs and hypertension) can be considered free of disease, do not need an exercise test, and should not be restricted in their exercise program.
Individuals 40 years of age or older or those with symptoms such as chest pain, abnormal physical examinations suggesting heart disease, or two or more major coronary risk factors should have a symptom-limited, maximum exercise test (unless otherwise contraindicated) if they plan to participate in vigorous exercise (such as jogging or running). If an exercise test is not done or is abnormal, these individuals should restrict their activities to moderate intensities. Key Point: The risks of serious complications of physical activity are highest during vigorous exercise and in individuals with heart disease. Hence, screening should ensure that cardiovascular disease is not present, that physical activity is limited to low or moderate intensities (walking or the equivalent), or that activity is medically supervised.
Physiological Changes
Physical
conditioning can be measured as changes in
O2max, exercise test time,
submaximal heart rate response, or ability to perform a standard amount
of exercise.
Maximal oxygen uptake.
O2max
is the peak oxygen
uptake achieved by muscular exercise. By strictest definition,
O2max cannot be exceeded
despite an increase in power output. Although demonstration of the
O2 plateau against work
rate is
certainly a valid demonstration of
O2max, subjects often
cannot
achieve the plateau because of leg fatigue, lack of necessary
motivation, and general discomfort. Hence, it is customary 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. Data presenting
O2max equivalents for
exercise test work stages are presented in Fig 4
.
Increased
O2max
after training
is associated with an increase in the capacity of the cardiovascular
system to deliver oxygen and of the muscles to use that oxygen (greater
arteriovenous oxygen
[a
O2]
difference and use). Higher cardiac output after training is achieved
solely by an increase in stroke volume, since maximal heart rate is not
usually increased after training in normal individuals.87
O2 is the product of
cardiac
output and systemic a
O2 difference.
Some of
the increase in
O2max is
the
result of widening of the
a
O2
difference as well as an increase in maximal cardiac
output.87 Based on data in healthy
subjects,88 a training effect can be achieved in a subject
in the presence of selective or nonselective ß-adrenergic blockade.
However, such changes may be attenuated89 and/or may not
be detected by metabolic studies (ie,
O2max) until after the drug
is
withdrawn88 ("unmasking"). Key
Point: The increase in
O2max as a result of
training
in normal individuals is due to a higher maximum cardiac output and to
greater extraction of oxygen from the systemic circulation, reflecting
both central and peripheral adjustments.
Central hemodynamic changes. Although a higher maximal
cardiac output can be achieved after training, submaximum values are
usually unchanged.90 Submaximal heart rate is reduced
after training, with a concomitant increase in stroke
volume.87 90 The mechanism of these changes is not
known.
Exercise training has resulted in an increase in myocardial
contractility in animals.91 Participation in a home
exercise training group (compared with a control group) by physically
disabled men with CAD significantly improved peak exercise LVEF and
fractional shortening between baseline and 6 months.54
Early results of another study revealed that in men with CAD, rest to
peak LVEF improved with 1 year of training only in those doing
high-intensity (85%
O2max)
compared with low-intensity (50%
O2max) training. This
improvement occurred in subjects with both depressed (<50%) as well
as those with normal (>50%) LVEF. The increase in stroke volume that
occurs with short-term training is probably largely related to
augmentation of blood volume and hence ventricular
preload.92 Fig 7
depicts relations of
heart rate and stroke volume before and after training. Key
Point: Submaximal heart rate is reduced after training in normal
individuals, but because stroke volume is increased, cardiac output
remains unchanged.
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Autonomic nervous system changes. Blood and urinary catecholamine levels are lower at rest and during submaximal exercise after training,93 presumably because of less sympathetic nervous system activity. Parasympathetic tone may also be increased and, with sympathetic adjustments, may account for the slower heart rate and lower arterial blood pressures seen after training.
Peripheral changes. Skeletal muscle changes after exercise training include increases in oxidative enzyme concentration, capillary density, myoglobin concentration, adaptation of muscle fiber type to a higher percentage of red (slow twitch) fibers, and muscle glycogen. All potentially contribute to greater capacity to use oxygen and to better endurance.94 Key Point: Greater oxidative potential in the skeletal muscles after training contributes to more endurance.
Submaximal endurance capacity. Endurance training enhances the individuals ability to perform exercise at both submaximal and maximal intensities,95 as demonstrated either by the ability to exercise longer at a similar work intensity or by doing more exercise in a given time. Improvements in endurance may be due to several factors, including greater availability of oxygen to the exercising muscles, greater use of aerobic processes (the most efficient energy sources), lower blood lactate levels, and/or greater anaerobic capacity. Adaptation to submaximal exercise is associated with a lower rate-pressure product (systolic blood pressure multiplied by heart rate) for a standard exercise task.
Changes in the skeletal muscles tend to improve accessibility to oxygen from the blood because of the higher myoglobin concentration and the greater capillary density, both of which enhance oxygen transport.
A greater concentration of oxidative enzymes allows muscles to obtain a larger share of their energy from aerobic rather than anaerobic sources. In so doing, the amount of high-energy phosphates generated from each mole of substrate metabolized is much greater, resulting in increased efficiency of substrate use. Lactate accumulation is also decreased, and the metabolic anaerobic threshold is increased.
Available muscle glycogen is a determinant of endurance time at higher submaximal work intensities. Since muscle glycogen is higher after training, the time required to deplete it would be expected to increase, which has been shown to augment endurance.96 Key Point: Submaximal endurance is increased with training due to changes in the muscle cells that allow more aerobic activity and provide more glycogen for anaerobic energy.
Preventive Value of Exercise Conditioning
Habitual exercise eliminates one of the risk markers associated
with a higher incidence of CAD. Physical inactivity has also been
designated by the AHA as a major modifiable coronary risk factor, along
with cigarette smoking, hypertension, and
hyperlipidemia.97 Other risk factors include age, gender,
obesity, diabetes mellitus, and family history. Of these, hypertension,
hyperlipidemia, obesity, and diabetes mellitus may be favorably
affected by proper physical exercise. The Centers for Disease Control
and Prevention have also proclaimed that inactivity is a major risk
factor, with an overall weight for preventive value similar to high
total cholesterol, cigarette smoking, and high blood
pressure.98 Some of the preventive value of exercise is
related to associated improvements in other risk factors, but exercise
exerts an independent effect as well.
Specific changes that accompany exercise training include the following:
Decrease in blood pressure
Increase in high-density lipoprotein cholesterol level
Decrease in triglyceride level
Augmentation of weight reduction efforts
Beneficial psychological effects Less depression Reduced anxiety
Improved glucose tolerance
Although no randomized, controlled studies have been performed, several prospective population studies have reported lower heart attack and death rates in active, apparently healthy populations compared with their sedentary counterparts. This association has been observed during leisure activity,99 100 total daily activity,101 and occupational activity.102 One significant longitudinal study103 followed up 10 224 men and 3120 women for 8 years after a baseline exercise evaluation. Those who demonstrated a low functional capacity had the greatest subsequent mortality. Age-adjusted relative risks for low- compared with high-conditioning level were approximately 9 in women and 8 in men. Some of this protection is no doubt due to modification of risk factors, but some is an independent effect of exercise. The mechanism of the independent effect is not known. Whatever the mechanism, the benefits of exercise appear to outweigh the risks of even vigorous exercise.104 Key Point: Sedentary lifestyle is a key independent risk factor for developing CAD.
Exercise Needed for an Optimum Effect
Any activity
performed for training should be assessed in terms of
intensity, frequency, duration, mode, and progression. The intensity of
activity needed to improve physical conditioning varies among
individuals and may be as little as 50% of
O2max for 20 minutes three
times per week. An exercise intensity-duration relation is likely, so
low-intensity exercise requires more time to increase functional
capacity than higher intensity exercise. From a health and conditioning
standpoint, the major advantage of moderate- and low-intensity exercise
is less likelihood of complications, whereas vigorous exercise has the
advantage of accomplishing the goal in less time.
Total work performed
is usually expressed as kilocalories.
Experience with normal populations suggests that activity equal to or
greater than 700 kcal (2940 kJ) per week is associated with higher
maximal working capacities. Morbidity and mortality from heart attacks
may also be related to amount of exercise. One group concluded that
individuals whose activity score was 28 or less had a higher incidence
of CAD (MIs, angina pectoris, and sudden death) than those whose score
was higher.101 Activity score in this study was determined
by weighting activity by intensity and time so that 1 unit of score
approximated 1 hour multiplied by 1 MET. Studies of college alumni
whose jobs were sedentary concluded that mortality and morbidity were
lowest in those whose activities required an average of 2000 or more
kcal (8400 kJ) per week.100 More recent studies have shown
advantages of physical activities conducted at 35% to 40% of
O2max but with greater
frequency and duration.105 Table 10
lists the energy requirements of various activities.
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Activities that
are 60% of
O2max are generally
categorized
as moderate. Body weight must be used to calculate calories since METs
are corrected for weight. The following conversion formula is used:
calories per minutex(METsx3.5xbody weight in kilograms)/200.
A threshold of intensity is probably required to achieve benefit, although the exact value is not known and may vary from one person to another. Although a threshold cannot be defined from available information, much of the exercise described in published reports and associated with good health is moderate in intensity, such as walking. Thus, exercise likely need not be of high intensity to be beneficial; the total amount of activity is more important for health than high-intensity exercise.
Vigorous exercise such as jogging and running also seems beneficial. In one study,104 individuals who regularly performed vigorous exercise had an overall lessened likelihood of sudden death. More orthopedic injuries and higher dropout rates are associated with high-intensity exercise compared with low- to moderate-intensity programs. However, this does not mean that better guidelines could not reduce the risk of vigorous exercise further, providing an even greater overall benefit. Hence, these recommendations are directed toward minimizing risk and maximizing benefit.
Occupational
Activity
Early studies of longshoremen suggest that occupational
activity
can provide protection from CAD.102 Occupational activity
was also considered a part of overall activity in another
study.100 The level of physical effort required of
longshoremen was heavy and is rarely duplicated in the United States
today because of widely available mechanical devices.
An operational definition of heavy occupational activity is a job that requires lifting loads of 20 pounds or more at least once an hour throughout the day or constantly moving loads of any size from one place to another without mechanized transportation. In the longshoremen and other studies, frequent walking or standing had no protective value, although other studies suggest that individuals who walk for long periods of time (such as postal employees) obtain protection. It is likely that unless individuals walk for 1 hour or more each day (low to moderate intensity), they should supplement that activity with leisure-time exercise.
Exercise Recommendations for Men and
Women
Gender is an important factor in formulating risk for CAD, and
much additional research is needed to define the exercise needs of
women. Women require approximately the same intensity, frequency, and
duration of exercise as men to increase
O2max.106 Most
reported studies of heart disease prevention have focused on men
because of the higher incidence of CAD in men; nevertheless, CAD is a
major cause of mortality and morbidity in women. The requirements and
recommendations for the prevention of heart disease in women may differ
somewhat from those developed from data collected on men, but until
more research is complete, the same guidelines for exercise must be
recommended for both men and women.
Recommendations for
Maintenance of Cardiovascular Health
Occupational activity. Unless an individuals
occupation
meets minimum requirements of heavy exercise, a leisure-time exercise
program should be followed. Occupational activity is defined as heavy
(and adequate) if it requires continual climbing of stairs or inclines,
lifting loads of 20 pounds or more each hour, or carrying loads of any
size continuously throughout the day. Because of automation and the use
of mechanized lift devices, very few jobs require such energy
expenditure today.
Leisure-time activity. Leisure-time activity for minimum conditioning and health benefits should consume a minimum total of 700 kcal/wk; the necessary activity should be performed on three or more nonconsecutive days (the amount associated with improved conditioning). Individuals should be encouraged to engage in activities requiring up to 2000 kcal/wk for maximum health benefits. Walking 20 miles each week is one way to accomplish this goal. Key Point: Regular physical activity is important for health maintenance. Walking appears to be as beneficial as more vigorous activities. Some benefit is apparently derived from as little as 20 minutes of low-intensity exercise performed three times per week. However, incremental benefits appear to accrue from up to 2000 kcal/wk (20 miles of walking or jogging). There is no evidence of a health benefit at more than 2000 kcal/wk. Occupational activity provides adequate health benefits only when a job requires sustained heavy activities. The same recommendations are made for men as women, but more research is needed for women.
Exercise Training Techniques
Activities
that cause the greatest increase in
O2max have certain
characteristics that, when present, are said to qualify the exercise as
endurance or cardiovascular. These characteristics include dynamic
exercise, alternately contracting and relaxing the muscles (as opposed
to isometric or resistive exercise), and large muscle group activities
such as walking or running. Exercise must be performed at least three
times per week for a minimum of 30 minutes per session at a minimum
intensity of 50% to 60%
O2max. In addition to
walking
and running, other examples of endurance or cardiovascular activities
are swimming, cycling, stair-stepping, and cross-country skiing. Such
activities of higher intensity should be done with care by subjects
with cardiovascular disease.
Exercising at a low intensity for 5 to 10 minutes before (warm-up) and after (cooldown) the training session is a routine recommendation. Such activities help stretch and warm up muscles and ligaments in preparation for the activity session. The cooldown period also prevents hypotension, which may occur with sudden cessation of exercise.107
Properly selected resistance exercises (calisthenics and weights) are helpful for promoting muscle strength and flexibility, which are important components of physical conditioning.
Resistance exercise involves activities that use low or moderate repetition movements against a resistance, generating a rise in muscle tension that ultimately yields increases in muscular strength. Weight lifting is the prototype resistance exercise. The increased muscle tension during such exercise leads to both a restriction in muscle blood flow during contraction due to compression of arterioles and capillaries that perfuse the muscle bed108 and a centrally mediated pressor response. The blood pressure and heart rate responses during resistance exercise are proportional to the relative intensity of muscular contraction (ie, the percent of maximal voluntary contraction), the size or mass of the muscle groups involved, and the duration of the contraction.109 Unlike dynamic (aerobic) exercise, which can lead to changes in skeletal muscle aerobic capacity via changes in mitochondrial number and in the enzymes necessary for glycogen and fat metabolism,110 the effects of long-term resistance exercise on the skeletal muscle appear limited to muscle cell hypertrophy via the synthesis of increased contractile protein and the thickening of connective tissue.111 Subsequent increases in muscle strength (or maximal voluntary contraction) after training will lead to an attenuated heart rate and blood pressure response to a given load because that load now represents a lower percentage of the maximal voluntary contraction.112 Importantly, the heart rateblood pressure product during maximal upper body resistance exercise is lower than that observed during maximal dynamic effort,113 primarily due to a lower peak heart rate response.
Several reports documenting the safe attainment of improved muscle strength after a resistance training program in subjects with cardiac disease114 115 116 117 118 have alleviated previously unsubstantiated concerns about weight training in such subjects. Strength gains of 22% to 29%114 115 116 117 118 as well as increases in the number of repetitions in a given submaximal load118 have been achieved by cardiac subjects. No adverse outcomes have been reported in subjects participating in supervised light to moderate intensity resistance training in cardiac rehabilitation.
As such, resistance training is encouraged as part of the overall exercise program for most subjects with cardiac disease. Such training can be performed using a wide variety of equipment, including free weights and dumbbells, wall-mounted pulleys, or exercise machines equipped with weight stacks. Resistance exercise can and should be performed in a variety of body positions, both to isolate specific muscle groups and to ensure maximum orthopedic stability. To avoid the additive cardiovascular responses of the Valsalva maneuver, subjects should be trained to exhale during the contraction phase of the movement. Resistance training should include 8 to 10 exercises that train the major muscle groups of the body, ie, arms, shoulders, chest, abdominals, back/trunk, hips, and legs. The intensity of each weight training exercise can be adjusted by alterations in any of the following factors: weight load, number of repetitions per set, number of sets, and rest period between sets. Generally, for subjects with cardiovascular disease, 2 to 3 days per week of resistance training using one set of 10 to 15 repetitions to moderate fatigue is recommended. Once 15 repetitions can be completed, the weight can be increased an additional 5%. Initial weight training activities are usually introduced during the first 2 weeks of an outpatient program. They include the use of light calisthenics and 3- to 5-lb dumbbell weights. Later in the program, if subjects are medically stable, they can be cleared for regular weight training activities using barbells and weight machines. This sequence of range of motion exercise and strength training has been shown to be safe for use with both MI and CABS patients.119 During this early period, resistance training should only employ light weights. Clinical experience has shown that less than 5% of CABS subjects have any contraindications to this exercise. Key Point: Physical activity should consist of cardiovascular exercise preceded by a warm-up period and followed by a cooldown period. Calisthenics and resistance training are useful for promoting strength and flexibility but probably do not significantly contribute to cardiovascular health.
Medical
Clearance for Physical Activity in Apparently Healthy
Populations
Medical history. Of particular interest
are data in the
history that indicate unsupervised exercise may be hazardous, including
CAD, significant valvular heart disease, cardiomyopathy, and congenital
heart disease. If any of these heart conditions are present, the
individual should follow the guidelines for individuals with heart
disease in the next section. Persons taking cardiovascular medications
should also follow the guidelines found in the next section. Obesity
and neuromuscular disease tend to increase the risk of orthopedic
injury; thus lower intensity, low-impact exercise of longer duration in
such persons is preferred.
Symptoms. Symptoms suggesting cardiovascular or pulmonary disease should be evaluated to exclude the presence of such disease. They include chest discomfort, shortness of breath (after climbing one flight of stairs or less), and leg discomfort consistent with claudication.
Physical examination. Hypertension requires assessment and management. Murmurs suggesting significant valvular heart disease or other signs of cardiac disease (eg, heart failure, ischemia) should be regarded as indicating the presence of cardiovascular disease until proven otherwise.
Detection of occult disease. One of the most difficult tasks a physician may undertake is detection of occult disease. It is well known that individuals can have significant CAD in the complete absence of symptoms or signs and in the presence of a normal ECG and a normal exercise test. However, the exercise test is the best method for detecting significant occult CAD.
Medical Clearance Strata
1. A recent medical history and physical examination should be
done.
a. If the history or physical examination indicates significant cardiovascular disease, the person should be treated as noted in the section "Guidelines for Exercise Training of Individuals With Cardiovascular Disease." Examples of cardiovascular disease include previous MI, CABS, angina pectoris, valvular heart disease (except most cases of mitral valve prolapse), and cardiomyopathy.
b. If the individual knows of no cardiovascular disease but has symptoms or signs that suggest the presence of significant disease or major coronary risk factors, an exercise test is needed to evaluate for the presence of a high-risk condition. If an exercise test cannot be performed, activity should be limited as outlined in the next section. Examples include intracardiac lesions of uncertain severity (septal defects, valve abnormalities), symptoms suggesting angina, and certain murmurs.
2. Age should be considered.
a. If the individual is younger than 40 years, no further workup is needed and he or she can be cleared for any activity if No. 1 above is normal.
b. If the individual is 40 years of age or older:
(1) An exercise test should be recommended if vigorous exercise is planned. If the test is normal, no further restrictions are needed. If the test is abnormal, the individual should be treated as if he or she has CAD.
(2) If the individual chooses not to undergo an exercise test, he or she should follow the activity guidelines outlined in the next section. Key Point: The medical clearance stratification enables physicians to classify individuals by activity and to give advice and options for physical activity programs.
If the medical clearance strata outlined above are used, all subjects may be placed in one of the following categories.
Activity classification. After the medical clearance stratification is complete, subjects can be classified by risk based on their characteristics. The following classifications are recommended, and subsequent ECG monitoring is advised based on this classification.
Class A: Apparently healthy. There is no evidence of increased cardiovascular risk for exercise. This classification includes (1) individuals under age 40 years who have no symptoms of or known presence of heart disease or major coronary risk factors and (2) individuals of any age without known heart disease or major risk factors and who have a normal exercise test.
Activity guidelines: No restrictions other than basic guidelines
ECG and blood pressure monitoring: Not required
Supervision required: None
Class B: Presence of known, stable cardiovascular disease with low risk for vigorous exercise but slightly greater than for apparently healthy individuals. Moderate activity is not believed to be associated with increased risk in this group. This classification includes individuals with (1) CAD (MI, CABS, PTCA, angina pectoris, abnormal exercise test, and abnormal coronary angiograms) whose condition is stable and who have the clinical characteristics outlined below; (2) valvular heart disease; (3) congenital heart disease; (4) cardiomyopathy; and (5) exercise test abnormalities that do not meet the criteria outlined in class C below.
Clinical characteristics: (1) New York Heart Association (NYHA) class 1 or 2; (2) exercise capacity over 6 METs; (3) no evidence of heart failure; (4) free of ischemia or angina at rest or on the exercise test at or below 6 METs; (5) appropriate rise in systolic blood pressure during exercise; (6) no sequential ectopic ventricular contractions; and (7) ability to satisfactorily self-monitor intensity of activity.
Activity guidelines: Activity should be individualized with exercise prescription by qualified personnel trained in basic CPR or with electronic monitoring at home.
ECG and blood pressure monitoring: Only during the early prescription phase of training, usually six to 12 sessions
Supervision required: Medical supervision during prescription sessions and nonmedical supervision for other exercise sessions until the individual understands how to monitor his or her activity.
Class C: Those at moderate to high risk for cardiac complications during exercise and/or unable to self-regulate activity or to understand recommended activity level. This classification includes individuals with (1) CAD with the clinical characteristics outlined below; (2) cardiomyopathy; (3) valvular heart disease; (4) exercise test abnormalities not directly related to ischemia; (5) previous episode of ventricular fibrillation or cardiac arrest that did not occur in the presence of an acute ischemic event or cardiac procedure; (6) complex ventricular arrhythmias that are uncontrolled at mild to moderate work intensities with medication; (7) three-vessel disease or left main disease; and (8) low ejection fractions (less than 30%).
Clinical characteristics: (1) Two or more MIs; (2) NYHA class 3 or greater; (3) exercise capacity less than 6 METs; (4) ischemic horizontal or downsloping ST depression of 4 mm or more or angina during exercise; (5) fall in systolic blood pressure with exercise; (6) a medical problem that the physician believes may be life-threatening; (7) previous episode of primary cardiac arrest; and (8) ventricular tachycardia at a workload of less than 6 METs.
Activity guidelines: Activity should be individualized with exercise prescription by qualified personnel.
ECG and blood pressure monitoring: Continuous during exercise sessions until safety is established, usually in six to 12 sessions or more.
Supervision: Medical supervision during all exercise sessions until safety is established.
Class D: Unstable disease with activity restriction. This classification includes individuals with (1) unstable ischemia; (2) heart failure that is not compensated; (3) uncontrolled arrhythmias; (4) severe and symptomatic aortic stenosis; and (5) other conditions that could be aggravated by exercise.
Activity guidelines: No activity is recommended for conditioning purposes. Attention should be directed to treating the subject and restoring him or her to class C or higher. Daily activities must be prescribed based on individual assessment by the subjects personal physician.
The above classifications are presented as a means of beginning exercise with the lowest possible risk. They do not consider accompanying morbidities (eg, insulin-dependent diabetes mellitus, morbid obesity, severe pulmonary disease, or debilitating neurological or orthopedic conditions) that may necessitate closer supervision during training sessions. As the individual gains experience, the decision may be made to place the subject in another category. In most cases, as the safety of exercise and improvement in working capacity are demonstrated, graduation to classes nearer A and B is appropriate. Key Point: An activity classification is offered to help the physician decide on the activity guidelines, monitoring, and supervision required for various conditions.
Exercise Prescription
Exercise for individuals with
cardiovascular disease should be
prescribed as outlined in the section "Guidelines for Exercise
Training of Individuals With Cardiovascular Disease." Guidelines for
physical activity for apparently healthy individuals are recommended
below.
A useful approach to activity prescription is to identify the
desirable rating of perceived exertion and ask individuals to adhere to
that intensity. A suggested rating of perceived exertion for most
healthy individuals is 12 to 16 (moderate to heavy) on a Borg
scale of 6 to 20, an approach that is both effective and
acceptable.120 See Table 6
for more details on
rating of
perceived exertion.121
Individual Guidelines for Cardiovascular Exercise
1. Exercise
only when feeling well.
Wait until symptoms and signs of a cold or the flu (including fever) have been absent 2 days or more before resuming activity.
2. Do not exercise vigorously soon after eating. Wait at least 2 hours. Eating increases the blood flow requirements of the intestinal tract. During vigorous exercise, the demand of the muscles for blood may exceed the ability of the circulation to supply both the bowel and the muscles, depriving organs of blood, resulting in cramps, nausea, or faintness.
3. Adjust exercise to the weather.
Exercise should be adjusted to environmental conditions. Special precautions are necessary when exercising in hot weather. It is difficult to define when it is too hot to exercise since air temperature is greatly influenced by humidity and air movement (wind), which are not easy to measure. The following guidelines are recommended for a noncompetitive workout: if air temperature is over 70°F, slow the pace, be alert for signs of heat injury, and drink adequate fluids to maintain hydration. A good rule to follow is to exercise at the usual workout pace (rating of perceived exertion, 12 to 16), which may be a slower pace or lower work intensity because of environmental conditions.
Acclimatization to moderate levels of heat is gradual, requiring 12 to 14 days. Accommodation to extreme heat never occurs. Signs of heat injury may be varied at the onset; hence, any symptom should be regarded as evidence of heat overload. The following indications of heat stress are particularly likely to occur: headache, dizziness, faintness, nausea, coolness, cramps, and palpitations. If any of these symptoms are present, stop exercising immediately and go to a cooler environment. If the air temperature is over 80°F, exercise in the early morning or late afternoon to avoid the heat. Air-conditioned shopping malls are popular for walking. Exercise is tolerated better if humidity is low and a breeze is present. Exercise in the heat causes excessive fluid loss, so adequate fluid intake is important before, during, and after each session.
4. Slow down for hills.
Watch for hills. When ascending hills, decrease speed to avoid overexertion. Again, a useful guide is to maintain the same rating of perceived exertion as in a usual workout.
5. Wear proper clothing and shoes.
Dress in loose-fitting, comfortable clothes made of porous material appropriate for the weather. Use sweat suits only for warmth. Never use exercise clothing made of rubberized, nonporous material. In direct sunlight, wear light-colored clothing and a cap. Wear shoes designed for exercise (eg, walking or jogging shoes).
6. Understand personal limitations.
Everyone should have periodic medical examinations. When under a physicians care, ask if there are limitations.
7. Select appropriate exercises.
Cardiovascular (aerobic) exercises should be a major component of activities. However, flexibility and strengthening exercises should also be considered for a well-rounded program.
8. Be alert for symptoms.
If the following symptoms occur, contact a physician before continuing exercise. Although any symptom should be clarified, these are particularly important:
a. Discomfort in the upper body, including the chest, arm, neck, or jaw, during exercise. The discomfort may be of any intensity and may be present as an aching, burning, tightness, or sensation of fullness.
b. Faintness accompanying the exercise. Sometimes brief light-headedness may follow unusually vigorous exercise or a limited cooldown period. This condition does not usually indicate heart disease and may be managed by exercising at a lower intensity with a gradual cooldown at the end of the session. If a "fainting spell" or feeling of faintness occurs during exercise, discontinue the activity until after evaluation by a physician.
c. Shortness of breath during exercise. During exercise, rate and depth of breathing should increase but should not be uncomfortable. A useful rule is that breathing should not be so difficult that an ordinary conversation is an effort, wheezing develops, or more than 5 minutes are required for recovery.
d. Discomfort in bones and joints either during or after exercise. There may be slight muscle soreness when beginning exercise, but if back or joint pain develops, discontinue exercise until after evaluation by a physician.
9. Watch for the following signs of overexercising:
a. Inability to finish. Training sessions should be completed with reserve.
b. Inability to converse during the activity. Breathing normally increases during exercise but should not be uncomfortable. When a conversation cannot be conducted during exercise because of difficulty breathing, the conditioning activity is too intense.
c. Faintness or nausea after exercise. A feeling of faintness after exercise may occur if the activity is too intense or has been stopped too abruptly. In any event, decrease the intensity of the workout and prolong the cooldown period.
d. Chronic fatigue. During the remainder of the day or evening after exercise, an individual should feel stimulated, not tired. If fatigue persists during the day, intensity and/or duration of the workout should be decreased.
e. Sleeplessness. If unable to sleep well despite feelings of fatigue, the amount of activity should be decreased until symptoms subside. Insomnia is particularly likely during distance training. A proper training program should make it easier, not more difficult, to have a good nights rest.
f. Aches and pains in the joints. Although there may be some muscle discomfort, joints should not hurt or feel stiff. Check exercise procedures, particularly stretching and warm-up exercises, to ensure that you are using the correct technique. Muscle cramping and back discomfort may also indicate poor technique. If symptoms persist, check with a physician before continuing.
10. Start slowly and progress gradually. Allow time to adapt. Key Point: General guidelines can provide an activity prescription for apparently well individuals. The benefits of exercise outweigh the risks when such an approach is used.
Noncardiovascular Injuries
Musculoskeletal injuries are
common and include direct injuries
such as bruises, sprains, and strains, and indirect problems such as
arthritis and back pain. The traumatic impact of exercise is usually
classified as low and high impact. Low-impact exercises (walking,
cycling, and swimming) cause little stress on bones and joints, whereas
high-impact exercises (running and aerobic dancing) cause repeated
impact on the knees, ankles, and feet.
Studies of injuries during
exercise show that two important factors in
determining the frequency of injuries during exercise are age and the
impact nature of exercise. (See Table 11
.)
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Therefore,
it is recommended that any individual older than 40 should
take special care to avoid high-impact
activities.122 123
If such activities are chosen, they should be initiated at low levels
and increased slowly. A day of rest between exercise periods permits
the body to gradually adapt to stresses and strains. More attention
should also be given to warm-up and cooldown periods with stretching,
low-level calisthenics, and low-level aerobic exercises. In general,
fast walking is a well-tolerated, low-impact exercise that provides
excellent results. Swimming, stair climbing, rowing, and stationary
cycling may also be appropriate. Several popular forms of exercise are
classified by musculoskeletal impact in Table 12
.
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Guidelines for Exercise Training of Individuals With Cardiovascular
Disease
Types of Cardiovascular Disease
Exercise
training is obviously useful in treatment of CAD subjects
because the physiological changes that occur lessen ischemia at rest
and during submaximal exercise. Physical activity is also associated
with protection from development or
progression124 125 126 of
CAD. Certain precautions are necessary to avoid injury. In this
section, the principles of surveillance for safety and expectations for
improvement are largely intended for subjects with CAD but may also
apply to other subjects with a variety of noncoronary cardiac,
vascular, and pulmonary diseases.
Safety is the major reason for establishing special guidelines for subjects with cardiovascular disease. These recommendations should be considered appropriate for any condition associated with a higher than normal risk for sudden cardiac arrest or MI during exercise, but if carefully followed, they could benefit the individual by increasing his or her physical working capacity. With the following conditions physical working capacity increases with regular exercise conditioning and surveillance is recommended:
Abnormal exercise test indicating ischemia
Angina pectoris
MI
CABS
PTCA
Heart transplant
Cardiomyopathies (including heart failure)
Valvular heart disease
Hypertension
Pacemakers Key Point: Regular physical activity is beneficial in the presence of cardiovascular disease if prudent guidelines are followed.
The Elderly
Special
considerations must be addressed when prescribing exercise
for the elderly. In these subjects maximal end-diastolic volume
increases, while maximal heart rate, LVEF, and cardiac output all
decrease. In the presence of disease, these factors may affect the
cardiac response to a given exercise prescription. In addition,
exercise-induced arrhythmias increase in frequency in older individuals
and may be of concern in cardiac rehabilitation
programs.127
Heart Failure
Medically
stable subjects with compensated heart failure may
participate in exercise training programs. Benefits that accrue from
conditioning of the musculoskeletal system include increased skeletal
muscle vascular conductance and oxygen extraction and decreased
skeletal muscle lactate production.128
Risk of
Sudden Death
Individuals with cardiac disease seem to have higher
risks for
sudden cardiac arrest during vigorous exercise (such as jogging) than
do healthy individuals. However, with judicious programs, activity is
clearly beneficial. The most compelling argument for exercise training
in cardiac subjects is that randomized controlled trials show a lower
death rate in groups that exercised compared with sedentary
groups,124 125 126 indicating that
exercise is safe and
beneficial. However, those studies were performed under strictly
controlled conditions, and similar results can be expected only if
careful guidelines are followed. The random incidence of sudden cardiac
arrest in populations with CAD has been estimated to be 1 in 80 000 to
160 000 man-hours.129 The type and intensity of activity
and the use of monitoring apparently affect incidence of sudden cardiac
arrest; Table 9
shows that in cardiac subjects, incidence is
lowest
during activities that are largely controlled, such as walking,
cycling, or treadmill walking. Table 9
also suggests that
continuously
ECG-monitored activities have the lowest rates of sudden cardiac arrest
compared with those that are unmonitored or only intermittently
monitored.
Obviously, these studies cannot answer the questions regarding the relative contributions of each of the potential variables to sudden cardiac arrest. However, they strongly suggest that the incidence of sudden cardiac arrest in all mixed activities is similar to that expected by chance alone. This, in turn, suggests that jogging increases the incidence of sudden cardiac arrest.
The higher incidence
of sudden cardiac arrest during jogging in
subjects with heart disease is probably related to intensity. Jogging
at even the slowest pace generates a
O2 that is from 80% to 100%
of maximum for most untrained individuals. If individuals with cardiac
disease jog, they should do so under medical supervision.
Monitoring is
important because it helps the individual establish an
appropriate exercise pace, which is about 60% to 70% of
O2max. This pace can best
be
learned during monitored sessions. Key Point: The risks
of exercise for sudden cardiac arrest and MI are higher in individuals
with known heart disease who engage in vigorous physical activity such
as jogging. Hence, individuals with heart disease should
either exercise under medical supervision or restrict their activity to
a moderate-intensity activity such as walking. Monitoring during
exercise is recommended for all individuals with heart disease until
the subjects tolerance for the activity and its safety have been
demonstrated.
Physiological Changes
Although
physical working capacity increases with training when
heart disease is present, reported physiological changes have differed
somewhat from those reported in apparently healthy individuals and are
outlined below.
Maximal oxygen uptake. Subjects with
CAD have an increase in
O2max with training. The
magnitude of the change is less in subjects with heart disease than
observed in apparently healthy individuals, but the increase is
noteworthy, and maximal heart rate may be the same or slightly greater
after training in those with heart disease.83 The smallest
increments in
O2max are
seen in
individuals with heart failure, but even in those subjects the
improvement is of great rehabilitative value for restoring ability to
perform daily activities.
Cardiac output. The increase
in maximal cardiac output is due
to an increase in both stroke volume and maximal heart rate, which
differs from normal subjects, whose maximal heart rate usually does not
change. In subjects with cardiac disease, the submaximal cardiac output
may be lower, with maintenance of
O2 by widening the
a
O2 difference after
training.130 Such a result suggests improved overall
efficiency for delivery of oxygen to the tissues.
Decreased myocardial oxygen uptake. Exercise training has special significance for individuals with CAD because the changes promote lower myocardial oxygen uptake (MO2). Changes associated with lower MO2 are lower heart rate, lower systolic blood pressure, and lower circulating catecholamines.
The benefits of these adjustments can be demonstrated
by the greater
amount of work that can be done before angina orECG-determined ST depression
occurs.131 Fig 8
reflects the positive effects of
conditioning
exercise on angina.
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Collateral formation. Present knowledge does not support the concept that collateral circulation is likely to develop in the coronary arterial distribution of humans as a result of exercise conditioning. Improvement of ischemia is believed most likely to occur by reducing MO2 rather than by increasing supply.
Improved myocardial function. Although animal studies have shown increased contractility and resistance to hypoxia with exercise training, human data have not consistently shown improved myocardial performance.132 However, as mentioned previously, recent studies54 have revealed increases in LVEF in subjects with CAD after exercise training. Key Point: Individuals with heart disease increase their working capacities in much the same way as healthy subjects. A major beneficial adjustment in subjects with CAD is the lowering of MO2 demand, which in turn lessens ischemia. Collateral formation in the coronary arterial distribution and improved myocardial performance may occur with exercise in some cases but not with regularity.
Secondary
Prevention
Coronary risk profile. Exercise training
induces improvement
in coronary risk profile. Reductions in blood pressure, triglycerides,
and body fat, improved glucose tolerance, increase in high-density
lipoprotein cholesterol, and favorable changes in blood coagulation
seem to occur in individuals with CAD, especially in those who can
perform large amounts of exercise.
Exercise is also associated with an improved mental outlook. Specifically, standard psychological tests have documented less depression and anxiety.133 Lessening of depression is particularly important in post-MI subjects, who tend to be clinically depressed. Although postinfarction depression is self-limited, regular exercise probably hastens improvement.
Morbidity and mortality. The large number of subjects required and the need for careful follow-up of those subjects for long periods of time have precluded a definitive, randomized, controlled trial of cardiac rehabilitation. Several studies have been conducted, and although most show a beneficial trend, none are large enough to draw definitive conclusions. A meta-analysis of the randomized, controlled trials that examined the influence of cardiac rehabilitation on outcome has shown a distinct benefit that seems largely the result of exercise.124 125 126 The significant benefit is a reduction in overall cardiovascular mortality and of sudden cardiac death; no significant reduction in reinfarction could be demonstrated.
Although exercise was an integral part of the programs of all these studies, they were multifactorial in nature. In addition, all exercise was supervised and moderate in intensity.
Return to work. The use of exercise early after infarction has also been evaluated and compared with bed rest. In many studies, physical activity soon after MI promotes earlier discharge from the hospital and a greater likelihood of the subjects returning to usual activities.134 Key Point: Although no reduction in frequency of MI has been shown, regular physical activity is associated with improved survival when combined with other interventions such as diet. Other benefits include earlier discharge from the hospital and greater likelihood of returning to work after MI.
Procedures and Techniques for Exercise in Cardiac
Rehabilitation
Precautions. All individuals must be
carefully screened for
medical status before beginning an exercise program. They must also
have adequate instruction and follow-up to lessen the likelihood of
complications. If exercise might aggravate an existing cardiac
condition, it should be avoided.
Systemic infections. Acute systemic infections can be adversely affected by activity. Even individuals with chronic infections may benefit more from rest than exercise. However, as the infection responds to treatment, exercise can begin. For example, in the treatment of bronchitis, moderate exercise can begin when the individual has normal temperature, white blood cell count, and cultures. Local infections are probably not affected by exercise as long as the activity does not irritate the lesion.
Thromboembolic disease. Thrombophlebitis, arterial embolism, or pulmonary embolism should be treated with rest, even though factors that cause clot dislodgment are not clearly defined. Low-level walking or range-of-motion exercise is probably safe as soon as the individual is in a stable treatment program and has had no recurrence of symptoms. A moderate exercise program can be started when anticoagulants have been discontinued or 6 weeks of anticoagulant therapy have passed since the last symptoms or signs of thromboembolism.
Endocarditis. Individuals with vegetative endocarditis should avoid exercise until the disease is stable. The contribution of physical activity to emboli is not known for certain, but low-to-moderate activity levels seem prudent until the course of antibiotics is completed.
Neuromuscular diseases. Neuromuscular inflammation and injuries should be evaluated by a qualified rheumatologist, orthopedist, or physiatrist to assess the desirability of physical activity and to determine the types of activities that are suitable.
Cardiovascular disease complications. HEART FAILURE. Low-to-moderate physical activity is usually beneficial to subjects with stable cardiovascular disease. In contrast, individuals with uncompensated heart failure have developed fulminant pulmonary edema with exercise. Therefore, exercise is not recommended if the subjects condition is unstable.
MYOCARDITIS. As with any infection, activity should be maintained at low levels until the individual has no signs of active infection. When the infection has subsided, there is no evidence of harm if exercise is prescribed prudently.
ACUTE ISCHEMIA. Individuals with unstable myocardial ischemia as judged by anginal symptoms or a changing pattern in the ECG should not exercise.
ARRHYTHMIAS. Although there is some evidence that regular physical activity may be helpful for subjects with arrhythmias, most studies have focused on benign arrhythmias. The occurrence of exercise-induced high-grade ventricular ectopy (three or more sequential ventricular premature beats) may be hazardous, and vigorous exercise should be avoided. The usual strategy is to prescribe activity that generates a lower heart rate than that associated with abnormalities. In general, individuals with arrhythmias other than high-grade ventricular ectopy may exercise if they are asymptomatic and remain hemodynamically stable. Monitoring during rehabilitative sessions may be helpful for adjusting drug treatment for arrhythmias.
ELECTRONIC PACEMAKERS. If performance during an exercise test is satisfactory, individuals with pacemakers are no more prone to problems than other cardiac subjects. Although the paced rate of some pacemakers can be accelerated during exercise, many cannot. Physical activity intensities in fixed-rate pacemakers must be gauged by a method other than pulse counting, such as defining specific work- loads that are about 60% to 70% of peak working capacity on the exercise test and by using the rating of perceived exertion.
SURGICAL INCISION AFTER CABS. The extent of healing of surgical incisions from CABS is the most limiting factor. Hence, the decision to start activity is often deferred to the surgeons. Low-level activities are usually acceptable 24 to 48 hours after surgery. Chest and leg wounds usually require 4 to 8 weeks for complete healing. Upper body exercises that cause sternal tension should be avoided until healing is complete. The same precautions should be exerted for CABS subjects as for post-MI subjects.
PTCA. Subjects may begin or resume exercise 24 to 48 hours after PTCA. Care must be taken to assure that anginal symptoms are recorded and properly evaluated. Exercise testing may be of considerable value in assessing new or different symptoms.
Prescribed physical activity. Prescribed physical
activity is beneficial and safe because it helps subjects restrict
intensities to low-risk levels. Moderate activity actually means
exercise that is about 60% to 80% of
O2max. That intensity is
effective for increasing
O2max if performed on a
regular basis, and it is associated with a low incidence of sudden
cardiac arrest.
Exercise tests. Exercise tests are an important part of the rehabilitative process. They provide initial levels of working capacity, specific precautions, and heart rates used to prescribe activity. Tests are also useful for assigning risk stratification. Exercise tests should be performed to write the exercise prescription for post-MI subjects or subjects with chronic CAD who enter cardiac rehabilitation programs. The exercise test should be repeated annually.
Rehabilitation sessions. Rehabilitation sessions are serial sessions in which the subject is taught good health behaviors, including proper diet and lifestyle modifications such as smoking cessation and exercise. Rehabilitation sessions are conducted to teach exercise techniques of intensity, duration, frequency, mode, and progression. Activity is monitored during these sessions to ensure safety. The number of monitored sessions needed depends on the clinical circumstances. In some cases, only one or two sessions may be needed, but in others, three or four sessions per week over several months are necessary.
Monitoring of activity. Symptoms. CHEST DISCOMFORT suggesting ischemia may present as chest tightness, fullness, pressure, or dull pain in the anterior precordium and may radiate to the neck or arm.
SHORTNESS OF BREATH may suggest pulmonary congestion, and appropriate assessment for pulmonary edema is needed. Some shortness of breath and fatigue may occur because of the deconditioning effect of bed rest after a cardiovascular event or surgery. Edema on the chest x-ray film, rales, or a third heart sound on examination will clarify the presence of significant pulmonary edema.
FAINTNESS (or light-headedness) is common after a period of inactivity. This symptom does not necessarily have cardiac implications since it is often due to a contracted blood volume or loss of postural reflexes caused by inactivity or surgery. Even so, individuals who become faint usually have a fall in blood pressure that could be hazardous if unattended.
WEAKNESS is a common symptom after a confining illness and need not be a concern. The sensation of fatigue will usually improve with time and conditioning. Weakness after cardiac surgery is particularly likely to occur because of low hemoglobin and may persist, interfering with the early phases of cardiac rehabilitation. Restitution of hemoglobin to normal requires several weeks unless transfusions are administered.
Heart rate. A target heart rate should be considered when exercise is prescribed. The target heart rate is usually determined from the exercise test, but if an exercise test has not been done, a useful goal is to avoid increases of more than 20 beats per minute over the resting heart rate.
Blood pressure. Blood pressure should be under control at the start of an exercise program. Specific guidelines for resting levels are difficult to set, but in general, activity should be restrained until the clinician is satisfied with resting levels. A slight increase in systolic pressure may precede exercise training sessions due to anticipation and is not a cause for concern.
Increments in systolic blood pressure during exercise are normal. However, if systolic blood pressure falls, the reason must be determined, and therapy should be initiated before proceeding.
Physical activity after MI, CABS, or PTCA. Early exercise. Walking is recommended as the major mode of exercise for these subjects unless the individual can attend classes where other monitored activities can be provided. Walking near the bedside and to the bathroom are permitted initially. If symptoms develop, he or she can quickly return to bed. Encouraging the individual to sit up is an important part of this phase. Walking should start slowly and gradually increase as tolerated until 5 to 10 minutes of continuous movement has been achieved. Active but nonresistive range of motion of upper extremities is also well tolerated early after MI or CABS, as long as the activities do not stress or impair healing of the sternal incision.
Initial activities should be monitored, and symptoms, rating of perceived exertion, heart rate, and blood pressure should be recorded. When tolerance is documented, the activity can be performed without supervision.
The emphasis of exercise within the first 2 weeks after MI
should be to
avoid or offset the effects of bed rest. When the individual is stable
as measured by ECG, vital signs, and symptomatic standards, he or she
can begin walking. Although this activity is well tolerated and safe,
certain precautions are recommended as outlined in Table 13
.
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Late exercise. A symptom-limited exercise test is performed after the individual is stable and is walking without difficulty (as early as 2 to 6 weeks after hospital discharge). If more studies such as angiography are not indicated, a regular conditioning program can be initiated. Careful activity prescription is recommended.
General principles of conditioning activity. For conditioning purposes, large-muscle group activities should be performed for at least 20 minutes, preceded by warm-up and followed by cooldown, at least three times per week. The intensity of exercise should be gauged by exercise prescription.
Follow-up supervised group sessions are recommended to enhance the educational process, to ensure that the participant is tolerating the program, to confirm that progress is occurring, and to provide medical supervision in high-risk situations.
A long-term follow-up should be encouraged at infrequent intervals (every 1 to 3 months) to encourage long-term compliance and to ensure that the program is being followed properly.
General
Principles of Exercise Prescription
Prescription in the absence of ischemia or significant arrhythmias.Exercise
intensity should approximate 50% to 80% of
O2max, which can be
ascertained
by an exercise test. (If a test is not done initially, the measurement
of 20 beats per minute above resting heart rate is adequate until
testing is performed.) The steps in this process are as follows:
1. The target heart rate may be considered as 50% to 75% of heart rate reserve ([maximal heart rate-resting heart rate] x50% to 75%) plus resting heart rate. That heart rate can be used for the prescription of many types of dynamic leg exercise.
2. Activities can be prescribed as the target work intensity that achieves the training heart rate after 5 to 10 minutes at that workload (steady state). It may be expressed as watts on an ergometer, speed on a treadmill, or in METs.
3. If an individual wants to exercise but cannot assess intensity, then heart rate counting (manually or with a cardiotachometer) is useful. Heart rate counters are widely available and are generally fairly accurate for low to moderate intensity exercise.
4. If an individual intends to walk on a level surface, activity can be prescribed as the step rate found on a treadmill to generate the desirable heart rate.135 The usual procedure is to determine the step rate on a treadmill and prescribe it. Step rate can be easily measured as it requires less skill than counting heart rate. If this approach is used, individuals should be cautioned about avoiding hills. Walking in shopping malls or gyms allows subjects to avoid inclement weather. Exercise should be monitored for the first few sessions while the individual begins activity. Monitoring assures that the instructions are understood and that the activity is well tolerated.
5. Individuals can also judge the intensity of exercise as
the rating
of perceived exertion, which can be equated to desirable heart rate
during laboratory exercise and to their activities. The original scale
is a 15-grade category scale ranging from 6 to 20, with a verbal
description at every odd number. (See Tables 6
and
14
.)
|
The following rating of perceived exertion values should be followed: <12 light, 40% to 60% of maximal
12-13 somewhat hard (moderate), 60% to 75% of maximal
14-16 hard (heavy), 75% to 90% of maximal
6. Activities can progress as tolerance is demonstrated. The
appropriate initial intensity of training is 50% to 60% of
O2max or a rating of
perceived
exertion of 12 to 13 on a scale of 6 to 20. After safe activity levels
have been established, duration is increased in 5-minute increments
each week. Later, intensities can be increased as heart rate response
to exercise decreases with conditioning.
Prescription in the presence of ischemia or arrhythmias. An exercise test is essential for this type of prescription. The manifestations of arrhythmias or ischemia that require such precautions can vary but usually include ventricular ectopic beats in sequence, an arrhythmia that is symptomatic or hemodynamically unstable, chest discomfort believed to be angina, ST depression of 2 mm or more, or a fall in systolic blood pressure of 20 mm Hg or more from baseline.
The exercise test is performed in the usual fashion, but the conditioning work intensity is derived from the heart rate associated with the abnormality. If the exercise test continues to a high level of effort, the heart rate at 50% to 60% of heart rate maximum can be used if it falls at least 10 beats per minute below the abnormal level. Otherwise, the recommended training heart rate is 10 beats per minute less than that associated with the abnormality.
Guidelines
for Electrocardiographic Monitoring
Role in exercise training. Various recommendations
exist
regarding the number of ECG-monitored sessions that are necessary and
reasonable in an exercise training program. Some programs use as few as
six sessions, with progression in mode and intensity of the exercise
during these periods.136 Others have used as many as 36
sessions of ECG monitoring. The fewest possible sessions should be
used, and it is recommended that the classification suggested here be
used as a guideline for the number of follow-ups required. (See Table
15
.)
|
Individuals who are class A (apparently healthy) do not require ECG-monitored sessions, as the general guidelines are adequate. Class B individuals should be monitored and supervised until they understand their desirable activity levels (usually 6 to 12 sessions). Class C individuals should be medically supervised with ECG monitoring until they understand the level of activity that is safe and the medical team determines that the exercise is safe and effective. Usually six to 12 sessions or more are needed.
Monitored cardiac rehabilitation. Monitoring sessions should ideally be performed with continuous ECG monitoring by either hardwired apparatus or telemetry. The sessions should be conducted by personnel who understand the exercise principles involved and have a basic knowledge of electrocardiography. The sessions should also be supervised by either a physician or a nurse trained in emergency CPR, preferably with previous experience in intensive cardiac care. CPR capability can be demonstrated by completion of an AHA-sponsored course in advanced cardiac life support. Standing orders for management of a complication should be immediately available.
Monitored sessions should also include symptom assessment by the staff, systolic blood pressure recording, the subjects rating of perceived exertion, and instructions to subjects about selection and proper use of exercise equipment. ECG-monitored sessions should include instruction for different modes and progressions of exercise.
Home-monitored programs. The use of transtelephonic ECG monitoring at home has been suggested as a substitute for outpatient visits to the clinic.137 138 Such programs have the disadvantage of lacking emergency medical care, but the advantage of requiring no clinic visit. These programs may be particularly useful in following subjects in the event clinics are not readily available.
Unmonitored home programs. In the first 1 or 2 weeks after discharge from the hospital after MI, individuals may walk at a slow, regular pace with increasing duration, starting with 10-minute periods and working up to 1 hour. Such activity need not be supervised.
Unmonitored exercise139 can also be used for conditioning
after the individual has recovered from the MI (2 weeks or more after
hospital discharge) or in other cases of stable CAD, although medically
supervised and monitored exercise is preferred. If cardiac
rehabilitation facilities are not available, activity guidelines can
still be provided to cardiac subjects, and they should be encouraged to
exercise. Activity should be restricted to walking (ordinary walking,
not race walking) or equivalent activities. If individuals carefully
watch for signs of intolerance and are attentive to heart rate and
rating of perceived exertion, this activity level is considered safe.
Walking is a safe, low-impact, controllable exercise that in the
majority of cases generates an intensity that is 50% to 70% of
O2max.
It is recommended that activity be monitored if possible and prescribed from the exercise test results. However, if monitoring is not available, an activity other than walking (ie, cycle ergometry) can be prescribed, provided the intensity is similar to walking and that it is dynamic (as opposed to static). Range-of-motion exercises and light calisthenics can be performed in an unmonitored setting.
Activities are
considered safe and appropriate if they meet the
criterion of moderate intensity as perceived by the physician or judged
by an exercise test. A useful guide to moderate (or less) activity is
found in Table 14
.
Individuals can participate in physical training classes if they carefully follow recommended guidelines for unmonitored exercise. In some cases, classes are desirable because of the camaraderie.
Types of Supervised Programs
Medically supervised group (moderate- to high-risk subjects).These
activity programs are needed to provide close medical
supervision for individuals who are at particularly high risk for a
complication associated with vigorous physical activity. Such
individuals are largely from class C.
These classes require careful
medical supervision and surveillance to
ensure that the activity is well tolerated. A physician should be
readily available for these classes, although the presence of a
properly trained nurse in the exercise room is sufficient if a
physician is not available. The qualifications of the physician may
vary, but experience in internal medicine and cardiovascular disease
and in treatment of subjects with heart disease is recommended.
Training programs should be medically supervised until the low risk of
the prescribed activity has been established. All individuals entering
these programs should be screened as described in Table 16
.
|
The program should provide staff, space, equipment, and facilities.
(See Table 17
.)
|
Medically supervised group (low-risk subjects). Low-risk
subjects (class B) benefit from medically supervised programs because
vigorous exercise can be conducted more safely and group dynamics often
help subjects comply with good health behaviors. Immediate medical
supervision of low-risk subjects can be provided by a well-trained
nurse working under a physicians standard orders. If medical
supervision by a physician cannot be provided, the supervisor should
have successfully completed an AHA-sponsored course in advanced cardiac
life support and should be able to administer emergency medications.
Well-trained cardiovascular nurses usually meet these criteria. All
individuals entering these programs should be screened as outlined in
Table 18
. The program should provide the same basic
requirements detailed for high-risk subjects in Table 17
.
|
Nonmedically supervised group (low-risk subjects). These programs consist of activities for subjects who do not require medical supervision. They are desirable because group dynamics are helpful and because exercise professionals can assist the subjects.
Records. Cardiac rehabilitation instructors should maintain evaluation forms, records of progress in problem areas, daily logs, and careful documentation of complications in much the same way as clinic and hospital charts.
Regular exercise testing. Exercise testing is important in all programs and should be performed at regular intervals, regardless of location or type of rehabilitation program. Once a year is adequate, although more frequent tests may be necessary if the subjects condition is uncertain. Key Point: Precautions and procedures for activity programs are outlined. Symptoms and signs, types of activity, techniques of activity prescription, guidelines for ECG monitoring, types of supervised programs, and requirements for exercise testing must all be considered. Activities and precautions are geared to the severity of the illness.
Social Service and
Vocational Rehabilitation
Helping the individual return to activities
and a lifestyle that
is as normal as possible is the focus of rehabilitation and requires
close cooperation between the subject, physician, employer, and social
service agencies. Decisions about long-term goals must be made early.
These goals include issues of personal safety, an acceptable standard
of living for the subject, and productivity for the employer.
Since few jobs require jogging, it is difficult to know how occupational activity relates in terms of risk. The general concept of lifting no more than 20 pounds is poorly supported by facts, but it is thought that lifting may be hazardous because of the risk of acute increase in afterload on the heart. Measuring heart rate and blood pressure response is helpful but is seldom possible because of the type of work involved.
One of the most difficult tasks facing a physician is advising the subject to return to work. Heavy labor can increase afterload, increasing the risk of sudden cardiac arrest accordingly. It also poses a problem for employers who are liable for workers compensation if a complication of heart disease occurs on the job. Conversely, loss of employment increases feelings of anxiety.
If the subject is in a low-risk activity category (class B) and exerts reasonable precautions, the probability of a complication is very small. Hence, such subjects should be encouraged and helped to return to work. If the subject is in a high-risk category (class C), the case must be judged on its individual merits. Even so, many of these subjects can return to work if the following guidelines are followed.
The subject should participate in an organized, medically supervised cardiac rehabilitation program to enhance strength and endurance and to provide surveillance and education during return to activity.
Assist devices should be used to limit the amount of lifting performed.
Good cardiovascular health should be maintained through risk factor reduction, including weight control, and regular medical follow-up.
If the subject is required to perform lifting or "carrying" activities or lift more than 20 pounds per load, lifting should be infrequent, take place in optimum environmental conditions, and be spaced with rest periods to avoid cumulative effects. Arm or resistance training in cardiac rehabilitation programs may be particularly useful for individuals in this group. Key Point: Assessing the subjects ability to return to work should include his or her illness and conditions of employment. Most subjects can return to work with few precautions. Cooperation with the employer is essential for optimum return to work.
The Importance of Risk Factors
It
is important to encourage smoking cessation, stress
management, and nutrition guidelines and good health behavior
counseling as needed for individuals undergoing cardiac
rehabilitation.97 Physical activity should be regarded as
a part but not the whole of cardiac rehabilitation.
Sexual
Activity
Sexual activity is similar to moderate-intensity exercise for
most
individuals with CAD. Heart rates rarely achieve 120 beats per minute,
systolic blood pressure is under 170 mm Hg, and metabolic requirements
are between 5 and 7 METs.140 There appears to be no
particular benefit in altering positions or sexual customs. Exercise
training can, however, lessen the hemodynamic stress of sexual
activity.
The use of ß-blockers and other drugs may impair sexual performance. The subject should be cautioned about such adverse reactions before leaving the hospital and encouraged to report them.
An exercise test within 3 weeks after MI, CABS, or PTCA may reassure both subject and spouse as well as provide guidelines.
Sexual activity should be resumed at the same time as other activities are resumed. In general, sexual activity should be deferred until activities such as walking and driving are resumed, usually about 2 to 4 weeks after returning home.
Obtaining Informed Consent for Exercise Training
Obtaining informed signed consent before initiating an exercise training program helps to clarify the responsibilities and goals of both the physician and the subject.
Informed Consent for Exercise Training
I want to participate in the
exercise training program to improve my cardiovascular function. This program was recommended by my physician,
Dr .
I will have a clinical evaluation before I enter this exercise program. This evaluation will include a medical history and physical examination consisting of but not limited to ECG at rest and, in some instances, with effort, and measurements of heart rate and blood pressure. The purpose of this evaluation is to determine the safety of my participation in this exercise training program.
The program will follow an exercise prescription prepared by
Dr .
I understand that activities are designed to place a gradually increasing workload on the circulation in an attempt to improve its function. The reaction of the cardiovascular system to such activities cannot be predicted with complete accuracy. Certain changes may occur during or after exercise, including abnormalities of blood pressure or heart rate, ineffective heart function, and, possibly, in some instances, heart attacks or cardiac arrest.
I realize that it is necessary for me to promptly report symptoms or signs indicating any abnormality or distress to the exercise supervisor. I consent to administration of immediate resuscitation measures deemed advisable by the exercise supervisor.
I have read the above and I understand it. My questions have been answered to my satisfaction.
Subject
Physician
Witness
Date
Acknowledgments
The authors are greatly indebted to Philip Ades, MD (University of Vermont) for his special review and critique of this statement.
Footnotes
Requests for reprints should be sent to the Office of Scientific Affairs, American Heart Association, 7272 Greenville Ave, Dallas, TX 75231.
Appendix
Glossary
Testing
Arrhythmia-Dysrhythmia or abnormal heart rhythm
a
O2-Arteriovenous
oxygen difference
Balke-type protocol-Constant speed (2.0-3.0 mph) variable grade treadmill exercise test
Bruce-type protocol-Variable speed and grade treadmill exercise test (incremental speed and grade increase every 3 minutes)
CAD-Coronary artery disease: coronary heart disease, myocardial infarction, coronary artery bypass surgery, coronary angioplasty, and ischemia
Calories-Kilocalorie: amount of energy required to raise temperature of 1 kg water by 1°C
Calories/minuteMETsx3.5xbody weight in kilograms/200
Exercise capacity-Functional capacity, training or conditioning level, level of fitness
Isometric-Static exercise: Muscle contraction with no movement (see "Resistive" below)
Isotonic-Dynamic exercise: Muscle contraction producing movement
J-junctional depression-Depression of beginning of ST segment
Kg-Kilogram: 1000 g
Kpm-Kilopond- or kilogram-meter of work: 1 J (10 ergs)
MET-Metabolic equivalent (3.5 mL · kg-1 · min-1 of oxygen uptake)
MO2-Myocardial oxygen uptake
0.1 Mv-1 mm (provided calibration is set at 10 mm/Mv)
Predictive value-Percentage of those with or without disease who are identified correctly
PTCA-Percutaneous transluminal coronary angioplasty
Rating of perceived exertion-Borg scale of 6 to 20 or 1 to 10
Resistive-Muscle contraction with limited movement
Sensitivity-Percentage of persons who are unhealthy who will have a positive test
Specificity-Percentage of persons who are healthy who will have a negative test
ST depression-Horizontal or downsloping (0.10 Mv for msec), measured from isoelectric PR level
Training-Physical activity, conditioning, leading to fitness
O2-Oxygen
uptake
O2max-Maximal
oxygen
uptake Training
Aerobic-Exercise in which energy needed is provided by using oxygen inspired to combust metabolites
Anaerobic-Exercise in which energy needed exceeds oxidative processes and nonaerobic metabolism begins
Cardiac output-Volume of blood ejected from heart in liters per minute. Normal: 6 L/min at rest
Cardiovascular exercise-Predominantly dynamic exercise us ing large muscle groups
Ejection fraction-Ratio of left ventricular stroke volume to end-diastolic volume (or percentage of end-diastolic volume ejected with each cardiac contraction). Normal: 60% to 75%
Flexibility activity-Activity designed to enhance range of motion of joints
Medical supervision-Physician readily available (the presence of a properly trained nurse in the exercise room is acceptable if physician is not available in the exercise room).
NYHA-New York Heart Association classification:
Class 1: Heart disease without symptoms
Class 2: Heart disease with symptoms during ordinary activity
Class 3: Heart disease with symptoms during less than
ordinary activity
Class 4: Heart disease with symptoms at rest
Occupational activity-On-the-job activity such as a job requiring lifting of loads of 20 pounds or more at least hourly throughout the day or constantly moving any size load from place to place without mechanized aid
Strength activity-Muscular contraction against resistance
designed to increase skeletal muscle strength
Stroke volume-Amount of blood ejection from heart with each contraction. Normal: 80 to 90 mL at rest
References
1. Fletcher GF, Froelicher VF, Hartley LH, Haskell WL, Pollock ML. Exercise standards: a statement for health professionals from the American Heart Association. Circulation.. 1990;82:2288-2322.
2. Rowell LB. Human Circulation. Regulation During Physical Stress. New York, NY: Oxford University Press; 1986.
3. MacDougall JD. Blood pressure responses to resistive static and dynamic exercise. In: Fletcher GF, ed. Cardiovascular Response to Exercise. Mount Kisco, NY: Futura Publishing Co Inc; 1994:155-173.
4. Cohn JN, ed. Quantitative exercise testing for the cardiac patient: the value of monitoring gas exchange: introduction. Circulation. 1987;76(suppl VI):VI-1-VI-2.
5. Morris CK, Myers J, Froelicher VF, Kawaguchi T, Ueshima K, Hideg A. Nomogram based on metabolic equivalents and age for assessing aerobic exercise capacity in men. J Am Coll Cardiol. 1993;22:175-182. [Abstract]
6. Higginbotham MB. Cardiac performance during submaximal and maximal exercise in healthy persons. Heart Failure. 1988;4:68-76.
7. Londeree BR, Moeschberger ML. Influence of age and other factors on maximal heart rate. J Cardiac Rehabil. 1984;4:44-49.
8. Gordon NF, Kohl HW. Exercise testing and sudden cardiac death. J Cardiopulmonary Rehabil. 1993;13:381-386.
9. Guidelines for exercise testing. A report of the Joint American College of Cardiology/American Heart Association Task Force on Assessment of Cardiovascular Procedures (Subcommittee on Exercise Testing): Schlant RC, Blomqvist CG, Brandenburg RO, DeBusk R, Ellestad MH, Fletcher GF, Froelicher VF Jr, Hall RJ, McCallister BD, McHenry PL, Ryan TJ, Sheffield LT. Special report. Circulation.. 1986;74:653A-667A.
10. Becker RC, Alpert JS. Electrocardiographic ST segment depression in coronary heart disease. Am Heart J.. 1988;115:862-868. [Medline] [Order article via Infotrieve]
11. Franklin BA. Exercise testing, training and arm ergometry. Sports Med. 1985;2:100-119. [Medline] [Order article via Infotrieve]
12. Balady GJ, Weiner DA, McCabe CH, Ryan TJ. Value of arm exercise testing in detecting coronary artery disease. Am J Cardiol. 1985;55:37-39. [Medline] [Order article via Infotrieve]
13. Borg G. Psycho-physical bases of perceived exertion. Med Sci Sports Exerc.. 1982;14:377-381.
14. Bonow RO. Left ventricular response to exercise. In: Fletcher GF, ed. Cardiovascular Response to Exercise. Mount Kisco, NY: Futura Publishing Co Inc; 1994;31-47.
15.
Bruce RA, Fisher LD, Pettinger M, Weiner DA, Chaitman BR. ST
segment elevation with exercise: a marker for poor ventricular function
and poor prognosis. Circulation.. 1988;77:897-905.
16. Mark DB, Hlatky MA, Lee KL, Harrell FE Jr, Califf RM, Pryor DB. Localizing coronary artery obstructions with the exercise treadmill test. Ann Intern Med. 1987;106:53-55.
17. Bobbio M, Detrano R, Schmid JJ, Janosi A, Righetti A, Pfisterer M, Steinbrunn W, Guppy KH, Abi-Mansour P, Deckers JW, et al. Exercise-induced ST depression and ST/heart rate index to predict triple-vessel or left main coronary disease: a multicenter analysis. J Am Coll Cardiol. 1992;19:11-18. [Abstract]
18. Johnson LL, Pohost GM. Nuclear cardiology. In: Schlant RC, Alexander RW, eds. The Heart. 8th ed. New York, NY: McGraw-Hill Inc; 1994;2281-2323.
19. Schelbert HR. Positron emission tomography. In: Schlant RC, Alexander RW, eds. The Heart. 8th ed. New York, NY: McGraw-Hill Inc; 1994;2361-2377.
20. Blackwell GG, Dell Italia LJ, Pohost GM. Magnetic resonance methods to assess physiological exercise of the cardiac vascular system. In: Fletcher GF, ed. Cardiovascular Response to Exercise. Mount Kisco, NY: Futura Publishing Co Inc; 1994;377-385.
21. Gianrossi R, Detrano R, Mulvihill D, Lehmann K, Dubach P, Colombo A, McArthur D, Froelicher V. Exercise-induced ST depression in the diagnosis of coronary artery disease: a meta-analysis. Circulation. 1989;80:87-98.
22. Froelicher VF, Perdue S, Pewen W, Risch M. Application of meta-analysis using an electronic spread sheet to exercise testing in patients after myocardial infarction. Am J Med. 1987;83:1045-1054. [Medline] [Order article via Infotrieve]
23. Klein J, Froelicher VF, Detrano R, Dubach P, Yen R. Does the resting electrocardiogram after myocardial infarction determine the predictive value of exercise-induced ST depression? A 2 year follow-up study in a veteran population. J Am Coll Cardiol.1989;14:305-311.
24. Lee TH, Cook EF, Goldman L. Prospective evaluation of a clinical and exercise-test model for the prediction of left main coronary artery disease. Med Decis Making. 1986;6:136-144.
25. Dubach P, Froelicher VF, Klein J, Oakes D, Grover-McKay M, Friis R. Exercise-induced hypotension in a male population: criteria, causes, and prognosis. Circulation. 1988;78:1380-1387.
26. Dagenais GR, Rouleau JR, Hochart P, Magrina J, Cantin B, Dumesnil JG. Survival with painless strongly positive exercise electrocardiogram. Am J Cardiol. 1988;62:892-895. [Medline] [Order article via Infotrieve]
27.
Kaul S, Lilly DR, Gascho JA, Watson DD, Gibson RS, Oliner
CA, Ryan JM, Beller GA. Prognostic utility of the exercise thallium-201
test in ambulatory patients with chest pain: comparison with cardiac
catheterization. Circulation.. 1988;77:745-758.
28. Marieb M, Beller G, Gibson R, Lerman B, Sanjiv K. Clinical relevancy of exercise-induced ventricular arrhythmias in suspected coronary artery disease. Am J Cardiol.. 1990;66:172-178. [Medline] [Order article via Infotrieve]
29. Bruce RA, Fisher LD, Hossack KF. Validation of exercise-enhanced risk assessment of coronary heart disease events: longitudinal changes in incidence in Seattle community practice. J Am Coll Cardiol. 1985;5:875-881. [Abstract]
30. European Coronary Surgery Study Group. Long-term results of prospective randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet. 1982;2:1173-1180. [Medline] [Order article via Infotrieve]
31. Weiner DA, Ryan TJ, McCabe CH, Chaitman BR, Sheffield LT, Fisher LD, Tristani F. The role of exercise testing in identifying patients with improved survival after coronary bypass surgery. J Am Coll Cardiol. 1986;8:741-748. [Abstract]
32. Dubach P, Froelicher V, Klein J, Detrano R. Use of the exercise test to predict prognosis after coronary artery bypass grafting. Am J Cardiol. 1989;63:530-533.
33. Heart and Stroke Facts. Dallas, Tex: American Heart Association; 1994.
34. Califf RM, Fortin DF, Frid DJ, Harlan WR III, Ohman EM, Bengtson JR, Nelson CL, Tcheng JE, Mark DB, Stack RS. Restenosis after coronary angioplasty: an overview. J Am Coll Cardiol. 1991;17(suppl B):2B-13B.
35. Thomas ES, Most AS, Williams DO. Objective assessment of coronary angioplasty for multivessel disease: results of exercise stress testing. J Am Coll Cardiol. 1988;11:217-222. [Abstract]
36. Deligonul U, Vandormael MG, Shah Y, Galan K, Kern MJ, Chaitman BR. Prognostic value of early exercise stress testing after successful coronary angioplasty: importance of the degree of revascularization. Am Heart J. 1989;117:509-514. [Medline] [Order article via Infotrieve]
37. Balady GJ, Leitschuh ML, Jacobs AK, Merrell D, Weiner DA, Ryan TJ. Safety and clinical use of exercise testing one to three days after percutaneous transluminal coronary angioplasty. Am J Cardiol. 1992;69:1259-1264. [Medline] [Order article via Infotrieve]
38. Laarman G, Luijten HE, van Zeyl LG, Beatt KJ, Tijssen JG, Serruys PW, de Feyter J. Assessment of silent restenosis and long-term follow-up after successful angioplasty in single vessel coronary artery disease: the value of quantitative exercise electrocardiography and quantitative coronary angiography. J Am Coll Cardiol. 1990;16:578-585. [Abstract]
39. Wijns W, Serruys PW, Reiber JH, de Feyter PJ, van den Brand M, Simoons ML, Hugenholtz PG. Early detection of restenosis after successful percutaneous transluminal coronary angioplasty by exercise-redistribution thallium scintigraphy. Am J Cardiol.. 1985;55:357-361. [Medline] [Order article via Infotrieve]
40. Bengtson JR, Mark DB, Honan MB, Rendall DS, Hinohara T, Stack RS, Hlatky MA, Califf RM, Lee KL, Pryor DB. Detection of restenosis after elective percutaneous transluminal coronary angioplasty using the exercise treadmill test. Am J Cardiol.. 1990;65:28-34. [Medline] [Order article via Infotrieve]
41.
Manyari DE, Knudtson M, Kloiber R, Roth D. Sequential
thallium-201 myocardial perfusion studies after successful percutaneous
transluminal coronary artery angioplasty: delayed resolution of
exercise-induced scintigraphic abnormalities. Circulation.. 1988;77:86-95.
42.
McHenry PL, ODonnell J, Morris SN, Jordan JJ. The abnormal
exercise electrocardiogram in apparently healthy men: a predictor of
angina pectoris as an initial coronary event during long-term
follow-up. Circulation.. 1984;70:547-551.
43. Sox HC Jr, Littenberg B, Garber AM. The role of exercise testing in screening for coronary artery disease [see comments]. Ann Intern Med. 1989:110:456-469.
44. Hochreiter C, Borer JS. Exercise testing in patients with aortic and mitral valve disease: current applications. Cardiovasc Clin.. 1983;13:291-300. [Medline] [Order article via Infotrieve]
45. Areskog NH. Exercise testing in the evaluation of patients with valvular aortic stenosis. Clin Physiol. 1984;4:201-208.
46. Atwood JE, Kawanishi S, Myers J, Froelicher VF. Exercise testing in patients with aortic stenosis. Chest.1988;93:1083-1087.
47. Misra M, Thakur R, Bhandari K, Puri VK. Value of the treadmill exercise test in asymptomatic and minimally symptomatic patients with chronic severe aortic regurgitation. Int J Cardiol.. 1987;15:309-316. [Medline] [Order article via Infotrieve]
48. Vacek JL, Valentin-Stone P, Wolfe M, Davis WR. The value of standardized exercise testing in the noninvasive evaluation of mitral stenosis. Am J Med Sci.. 1986;292:335-343. [Medline] [Order article via Infotrieve]
49. Weber KT, Janicki JS, McElroy PA. Cardio-pulmonary exercise testing in the evaluation of mitral and aortic valve incompetence. Herz. 1986;11:88-96.
50. Broustet JP, Douard H, Mora B. Exercise testing in arrhythmias of idiopathic mitral valve prolapse. Eur Heart J. 1987;8(suppl D):37-42.
51. Lee TH, Shammash JB, Ribeiro JP, Hartley LH, Sherwood J, Goldman L. Estimation of maximum oxygen uptake from clinical data: performance of the Specific Activity Scale. Am Heart J.. 1988;115:203-204. [Medline] [Order article via Infotrieve]
52. Carliner NH, Fisher ML, Plotnick GD, Garbart H, Rapoport A, Kelemen MH, Moran GW, Gadacz T, Peters RW. Routine preoperative exercise testing in patients undergoing major noncardiac surgery. Am J Cardiol.. 1985;56:51-58. [Medline] [Order article via Infotrieve]
53. McPhail N, Calvin JE, Shariatmadar A, Barber GG, Scobie TK. The use of preoperative exercise testing to predict cardiac complications after arterial reconstruction. J Vasc Surg. 1988;7:60-68. [Medline] [Order article via Infotrieve]
54. Fletcher BJ, Dunbar SB, Felner JM, Jensen BE, Almon L, Cotsonis G, Fletcher GF. Exercise testing and training in physically disabled men with clinical evidence of coronary artery disease. Am J Cardiol. 1994;73:170-174.
55. Sullivan M, Savvides M, Abouantoun S, Madsen EB, Froelicher V. Failure of transdermal nitroglycerin to improve exercise capacity in patients with angina pectoris. J Am Coll Cardiol. 1985;5:1220-1223. [Abstract]
56. Sullivan M, Atwood JE, Myers J, Feuer J, Hall P, Kellerman B, Forbes S, Froelicher V. Increased exercise capacity after digoxin administration in patients with heart failures. J Am Coll Cardiol.. 1989;13:1138-1143. [Abstract]
57.
Guiteras P, Chaitman BR, Waters DD, Bourassa MG, Scholl JM,
Ferguson RJ, Wagniart P. Diagnostic accuracy of exercise ECG lead
systems in clinical subsets of women. Circulation.. 1982;65:1465-1474.
58. Exercise hypertension: a symposium issue. Herz. 1987;12:76-149.
59. Liao Y, Emidy LA, Gosch FC, Stamler R, Stamler J. Cardiovascular responses to exercise of participants in a trial on the primary prevention of hypertension. J Hypertens.. 1987;5:317-321. [Medline] [Order article via Infotrieve]
60. Wilson JR, Fink LI, Ferraro N, Dunkman WB, Jones RA. Use of maximal bicycle performance in patients with congestive heart failure secondary to coronary artery disease or to idiopathic dilated cardiomyopathy. Am J Cardiol. 1986;15:601-606.
61. Losse B, Kuhn H, Loogen F, Schulte HD. Exercise performance in hypertrophic cardiomyopathies. Eur Heart J. 1983;4(suppl F): 197-208.
62. Savage DD, Seides SF, Maron BJ, Myers DJ, Epstein SE. Prevalence of arrhythmias during 24-hour electrocardiographic monitoring and exercise testing in patients with obstructive and nonobstructive hypertrophic cardiomyopathy. Circulation.1979;59:866-875.
63. Heinsimer JA, Irwin JM, Basnight LL. Influence of underlying coronary artery disease on the natural history and prognosis of exercise-induced left bundle branch block. Am J Cardiol.. 1987;60:1065-1067. [Medline] [Order article via Infotrieve]
64. Vasey C, ODonnell J, Morris SN, McHenry P. Exercise-induced left bundle branch block and its relation to coronary artery disease. Am J Cardiol. 1985;56:892-895.
65. Whinnery JE, Froelicher VF Jr, Stewart AJ, Longo MR Jr, Triebwasser JH, Lancaster MC. The electrocardiographic response to maximal treadmill exercise in asymptomatic men with left bundle branch block. Am Heart J. 1977;94:316-324. [Medline] [Order article via Infotrieve]
66. Williams MA, Esterbrooks DJ, Nair CK, Sailors MM, Sketch MH. Clinical significance of exercise-induced bundle branch block. Am J Cardiol. 1988;61:346-348. [Medline] [Order article via Infotrieve]
67. Wayne VS, Bishop RL, Cook L, Spodick D. Exercise-induced bundle branch block. Am J Cardiol. 1983;52:283-286.
68. Whinnery JE, Froelicher VF. Exercise testing in right bundle-branch block. Chest. 1977;72:684-685. Letter.
69. Whinnery JE, Froelicher VF Jr, Longo MR Jr, Triebwasser JH. The electrocardiographic response to maximal treadmill exercise of asymptomatic men with right bundle branch block. Chest.1977;71:335-340.
70. Whinnery JE, Froelicher VF. Acquired bundle branch block and its response to exercise testing in asymptomatic aircrewmen: a review with case reports. Aviat Space Environ Med.1976;46:69-78.
71. Sharma AD, Yee R, Guiraudon G, Klein GJ. Sensitivity and specificity of invasive and noninvasive testing for risk of sudden death in Wolff-Parkinson-White syndrome. J Am Coll Cardiol.. 1987;10:373-381. [Abstract]
72. Allen BJ, Casey TP, Brodsky MA, Luckett CR, Henry WL. Exercise testing in patients with life-threatening ventricular tachyarrhythmias: results and correlation with clinical and arrhythmia factors. Am Heart J. 1988;116:997-1002.
73. Ryan M, Lown B, Horn H. Comparison of ventricular ectopic activity during 24-hour monitoring and exercise testing in patients with coronary heart disease. N Engl J Med.. 1975;292:224-229.[Abstract]
74. Sami M, Chaitman B, Fisher L, Holmes D, Fray D, Alderman E. Significance of exercise-induced ventricular arrhythmia in stable coronary artery disease: a coronary artery surgery study project.Am J Cardiol. 1984;54:1182-1188.
75. Atwood JE, Myers J, Sullivan M, Forbes S, Friis R, Pewen W, Callaham P, Hall P, Froelicher V. Maximal exercise testing and gas exchange in patients with chronic atrial fibrillation. J Am Coll Cardiol.. 1988;11:508-513. [Abstract]
76. Vuori I, Makarainen , Jaaskelainen A. Sudden death and physical activity. Cardiology. 1978;63:287-304.
77.
Gibbons LW, Cooper KH, Meyer BM, Ellison RC. The acute
cardiac risk of strenuous exercise. JAMA. 1980;244:1799-1801.
78. Thompson PD, Funk EJ, Carleton RA, Sturner WQ. Incidence of death during jogging in Rhode Island from 1975 through 1980. JAMA. 1982;247:2535-2538.
79. Vander L. Cardiovascular complications of recreational physical activity. Physic Sports Med.. 1982;10:89-98.
80.
Fletcher GF, Cantwell JD. Ventricular fibrillation in a
medically supervised cardiac exercise program: clinical, angiographic,
and surgical correlations. JAMA.. 1977;238:2627-2629.
81. Leach CN Jr, Sands MJ Jr, Lachman AS, Skinner W. Cardiac arrest during exercise training after myocardial infarction. Conn Med.. 1982;46:239-243. [Medline] [Order article via Infotrieve]
82.
Mead WF, Pyfer HR, Thrombold JC, Frederick RC. Successful
resuscitation of two near simultaneous cases of cardiac arrest with a
review of fifteen cases occurring during supervised exercise.
Circulation.. 1976;53:187-189.
83. Hartley LH. Exercise and cardiac rehabilitation. Proc N Engl Cardiovasc Soc.. 1976;28:37-40.
84. Hossack KF, Hartwig R. Cardiac arrest associated with supervised cardiac rehabilitation. J Cardiac Rehabil. 1982;2:402-408.
85.
Haskell WL. Cardiovascular complications during exercise
training of cardiac patients. Circulation.. 1978;57:920-924.
86.
Van Camp SP, Peterson RA. Cardiovascular complications of
outpatient cardiac rehabilitation programs. JAMA.. 1986;256:1160-1163.
87. Hartley LH, Grimby G, Kilbom A, Nilsson NJ, Astrand I, Bjure J, Ekblom B, Saltin B. Physical training in sedentary middle-aged and older men: 3. Cardiac output and gas exchange during submaximal and maximal exercise. Scand J Clin Lab Invest. 1969;24:335-344. [Medline] [Order article via Infotrieve]
88. Sweeney ME, Fletcher BJ, Fletcher GF. Exercise testing and training with beta-adrenergic blockade: role of the drug washout period in unmasking a training effect. Am Heart J. 1989;118(pt 1):941-946.
89. Pollock ML, Lowenthal DT, Foster C, Pels AE III, Rod J, Stoiber J, Schmidt DH. Acute and chronic responses to exercise in patients treated with beta blockers. J Cardiopulmonary Rehabil. 1991;11:132-144.
90. Saltin B, Blomqvist G, Mitchell JH, Johnson RL Jr, Wildenthal K, Chapman CB. Response to exercise after bed rest and after training. Circulation. 1968;38(suppl 7):1-78.
91.
Scheur J. Physical training and intrinsic cardiac
adaptations. Circulation.. 1973;47:677-680. Editorial.
92. Rerych SK, Scholz PM, Sabiston DC Jr, Jones RH. Effects of exercise training on left ventricular function in normal subjects: a longitudinal study by radionuclide angiography. Am J Cardiol.. 1980;45:244-252. [Medline] [Order article via Infotrieve]
93.
Hartley LH, Mason JW, Hogan RP, Jones LG, Kotchen TA, Mougey
EH, Wherry FE, Pennington LL, Ricketts PT. Multiple hormonal responses
to prolonged exercise in relation to physical training. J Appl
Physiol. 1972;33:607-610.
94.
Holloszy JO. Biochemical adaptations in muscle: effects of
exercise on mitochondrial oxygen uptake and respiratory enzyme activity
in skeletal muscle. J Biol Chem.. 1967;242:2278-2282.
95.
Gleser MA, Vogel JA. Endurance exercise: the effect of
work-rest schedules and repeated testing. J Appl Physiol.. 1971;31:735-739.
96. Hultman E. Studies on muscle metabolism of glycogen and active phosphate in man with special reference to exercise and diet. Scand J Clin Lab Invest. 1967;19(suppl 94):1-63.
97.
Fletcher GF, Blair SN, Blumenthal J, Caspersen C, Chaitman
B, Epstein S, Falls H, Froelicher ES, Froelicher VF, Pina IL. Statement
on exercise: benefits and recommendations for physical activity
programs for all Americans: a statement for health professionals by the
Committee on Exercise and Cardiac Rehabilitation of the Council on
Clinical Cardiology, American Heart Association.
Circulation.. 1992;86:340-344.
98. Protective effect of physical activity on coronary heart disease. MMWR. 1987;36:426-430. [Medline] [Order article via Infotrieve]
99. Morris JN, Everitt MG, Pollard R, Chave SP, Semmence AM. Vigorous exercise in leisure-time: protection against coronary heart disease. Lancet. 1980;2:1207-1210.
100.
Paffenbarger RS Jr, Wing AL, Hude RT. Physical activity as an
index of heart attack risk in college alumni. Am J
Epidemiol. 1978;108:161-175.
101. Kannel WB, Gordon T, Sorlie P, McNamara PM. Physical activity and coronary vulnerability: the Framingham Study. Cardiol Dig.. 1971;6:28.
102. Paffenbarger RS, Hale WE. Work activity and coronary heart mortality. N Engl J Med. 1975;292:545-550. [Abstract]
103.
Blair SN, Kohl HW III, Paffenbarger RS Jr, Clark GA, Cooper
KH, Gibbons LW. Physical fitness and all-cause mortality: a prospective
study of healthy men and women. JAMA.. 1989;262:2395-2401.
104. Siscovick DS, Weiss NS, Fletcher RH, Lasky T. The incidence of primary cardiac arrest during vigorous exercise. N Engl J Med.. 1984;311:874-877. [Abstract]
105.
Leon AS, Connett J, Jacobs DR Jr, Rauramaa R. Leisure-time
physical activity levels and risk of coronary heart disease and death:
the Multiple Risk Factor Intervention Trial. JAMA. 1987;258:2388-2395.
106. Kilbom A. Physical training in women. Scand J Clin Lab Invest. 1971;119:1-34.
107.
Dimsdale JE, Hartley LH, Guiney T, Ruskin JN, Greenblatt D.
Postexercise peril. Plasma catecholamines and exercise.
JAMA. 1984;251:630-632.
108. Asmussen E. Similarities and dissimilarities between static and dynamic exercise. Circ Res. 1981;48(pt 2):I-3-I-10.
109.
Seals DR, Washburn RA, Hanson PG, Painter PL, Nagle FJ.
Increased cardiovascular response to static contraction of large muscle
groups. J Appl Physiol.. 1983;54:434-437.
110.
Holloszy JO, Coyle EF. Adaptations of skeletal muscle to
endurance exercise and their metabolic consequences. J Appl
Physiol.. 1984;56:831-838.
111. Sharkey B. Specificity of exercise. In: Blair SN, et al, eds. Resource Manual for Guidelines for Exercise Testing and Prescription. Philadelphia, Pa: Lea & Febiger; 1988:5.
112. Franklin BA, Bonzheim K, Gordon S, Timmis GC. Resistance training in cardiac rehabilitation. J Cardiopulmonary Rehabil. 1991;11:99-106.
113.
DeBusk RF, Valdez R, Houston N, Haskell W. Cardiovascular
responses to dynamic and static effort soon after myocardial
infarction: application to occupational work assessment.
Circulation.. 1978;58:368-375.
114. Kelemen MH, Stewart KJ, Gillilan RE, Ewart CK, Valenti SA, Manley JD, Kelemen MD. Circuit weight training in cardiac patients. J Am Coll Cardiol. 1986;7:38-42. [Abstract]
115. Stewart KJ, Manson M, Kelemen MH. Three-year participation in circuit weight training improves muscular strength and self efficacy in cardiac patients. J Cardiopulmonary Rehabil. 1988;8:292-296.
116. Ghilarducci LE, Holly RG, Amsterdam EA. Effects of high resistance training in coronary artery disease. Am J Cardiol.. 1989;64:866-870. [Medline] [Order article via Infotrieve]
117. Sparling PB, Cantwell JD, Dolan CM, Neiderman RK. Strength training in a cardiac rehabilitation program: a six-month follow-up. Arch Phys Med Rehabil.. 1990;71:148-152. [Medline] [Order article via Infotrieve]
118. McCartney N, McKelvie RS, Haslam DR, Jones NL. Usefulness of weightlifting training in improving strength and maximal power output in coronary artery disease. Am J Cardiol.. 1991;67:939-945. [Medline] [Order article via Infotrieve]
119. Sennett SM, Pollock ML, Pels AE III, Foster C, Dolatowski R, Laughlin J, Patel S, Schmidt DH. Medical problems of patients in an outpatient cardiac rehabilitation program. J Cardiopulmonary Rehabil.. 1987;7:458-465.
120. Pollock ML, Wilmore JH, eds. Exercise in Health and Disease: Evaluation and Prescription for Prevention and Rehabilitation.Ed 2. Philadelphia, Pa: WB Saunders Co; 1990.
121. Carroll JF, Pollock ML, Graves JE, Leggett SH, Spitler DL, Lowenthal DT. Incidence of injury during moderate- and high-intensity walking training in the elderly. J Gerontol.. 1992;47:M61-M66. [Abstract]
122. Kilbom A, Hartley LH, Slatin B, Bjure J, Grimby G, Astrand I. Medical evaluation of the effect of physical conditioning in middle-aged men. Scand J Clin Lab Invest. 1969;24:315-323. [Medline] [Order article via Infotrieve]
123. Pollock ML, Carroll JF, Graves JE, Leggett SH, Braith RW, Limacher M, Hagberg JM. Injuries and adherence to walk/jog and resistance training programs in the elderly. Med Sci Sports Exerc.. 1991;23:1194-1200. [Medline] [Order article via Infotrieve]
124.
Oldridge NB, Guyatt GH, Fischer ME, Rimm AA. Cardiac
rehabilitation after myocardial infarction: combined experience of
randomized clinical trials. JAMA. 1988;260:945-950.
125.
OConnor GT, Buring JE, Yusuf S, Goldhaber SZ, Olmstead
EM,
Paffenbarger RS Jr, Hennekens CH. An overview of randomized trials of
rehabilitation with exercise after myocardial infarction.
Circulation.. 1989;80:234-244.
126.
Berlin JA, Colditz GA. A meta-analysis of physical activity
in the prevention of coronary heart disease. Am J Epidemiol.. 1990;132:612-628.
127. Fleg JL. Effects of aging on the cardiovascular response to exercise. In: Fletcher GF, ed. Cardiovascular Response to Exercise. Mount Kisco, NY: Futura Publishing Co Inc; 1994:387-404.
128. Sullivan MJ. Role of exercise conditioning in patients with severe left ventricular dysfunction. In: Fletcher GF, ed. Cardiovascular Response to Exercise. Mount Kisco, NY; Futura Publishing Co Inc; 1994:359-376.
129. Cobb LA, Weaver WD. Exercise: a risk for sudden death in patients with coronary heart disease. J Am Coll Cardiol. 1986;7:215-219. [Abstract]
130.
Detry JM, Rousseau M, Vandenbroucke G, Kusumi F, Brasseur LA,
Bruce RA. Increased arteriovenous oxygen differences after physical
training in coronary heart disease. Circulation.. 1971;44:109-118.
131. Redwood DR, Rosing DR, Epstein SE. Circulatory and symptomatic effects of physical training in patients with coronary-artery disease and angina pectoris. N Engl J Med.. 1972;286:959-965.
132. Sim DN, Neill WA. Investigation of the physiological basis for increased exercise threshold for angina pectoris after physical conditioning. J Clin Invest. 1974;54:763-770.
133. Hellerstein HK. Exercise therapy in coronary disease. Bull NY Acad Med. 1984;44:1028.
134. Bloch A, Maeder JP, Haissly JC, Felix J, Blackburn H. Early mobilization after myocardial infarction: a controlled study. Am J Cardiol. 1974;34:152-157.
135. Ekblom B, Day WC, Hartley LH, et al. Reproducibility of exercise prescribed by pace description. Scand J Sports Sci. 1979;1:16-19.
136. Fletcher BJ, Thiel J, Fletcher GF. Phase II intensive monitored cardiac rehabilitation for coronary artery disease and coronary risk factors: a six-session protocol. Am J Cardiol. 1986;751-756.
137.
Fletcher GF, Chiaramida AJ, LeMay MR, Johnston BL, Thiel JE,
Spratlin MC. Telephonically-monitored home exercise early after
coronary artery bypass surgery. Chest.. 1984;86:198-202.
138. DeBusk RF, Haskell WL, Miller NH, Berra K, Taylor CB, Berger WE III, Lew H. Medically directed at-home rehabilitation soon after clinically uncomplicated acute myocardial infarction: a new model of patient care. Am J Cardiol.. 1985;55:251-257. [Medline] [Order article via Infotrieve]
139. Fletcher BJ, Lloyd A, Fletcher GF. Outpatient rehabilitative training in patients with cardiovascular disease: emphasis on training method. Heart Lung. 1988;17:199-205. [Medline] [Order article via Infotrieve]
140.
Hellerstein HK, Friedman EH. Sexual activity and the
postcoronary patient. Arch Intern Med. 1970;125:987-990.
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