Tmt Seminary

Tmt Seminary

1. Moderator :
Dr. Navneet Agarwal

2. TMT (Tread Mill Test)
PERVIEW
·The exercise test continues to have an integral place in
cardiovascular medicine because of its high yield of diagnostic,
prognostic and functional information.
·In the clinical setting, the major indications for exercise testing
are the diagnosis and prognostication of heart disease.
·The determination of exercise capacity is helpful in quantifying
disability, estimating prognosis and monitoring the disease state
of patients with chronic heart disease and known coronary heart
disease.
·The major emphasis is on the analysis of the electrocardiogram
(ECG) in the majority of clinical tests.

3. ·The reproduction of symptoms such an angina or presyncope is
vital for clinical purposes.
·My seminar reviews the development of exercise ECG, gives a
brief review of the pathophysiologic basis for exercise induced
ST segment depression, provides detailed information on the
performance, interpretation and applications of the exercise
tolerance test and address the controversies and future directions
in exercise ECG.
Exercise is a common physiological stress used to elicit
cardiovascular abnormalities not present at rest and to determine
the ade­quacy of cardiac function. Exercise elec­trocardiography
(ECG) is one of the most frequent noninvasive modalities used
to assess patients with suspected or proven cardiovascular
disease.

4. The test is mainly used to estimate prognosis and to determine
functional capacity, the likelihood and extent of coronary artery
diseases (CAD), and the effects of therapy. Hemodynamic and
ECG measurements combined with ancillary techniques such as
metabolic gas analysis, radionuclide imaging, and echo­
cardiography enhance the information content of exercise testing
in selected patients.
Anticipation of dynamic exercise results in an acceleration of
ventricular rate due to vagal withdrawal, increase in alveolar
ventilation, and increased venous return primarily as a result of
sympathetic veno­constriction. In normal persons, the net effect is
to increase resting cardiac output before the start of exercise. The
magnitude of hemodynamic response during exercise depends on
the severity of the exercise and the amount of muscle mass
involved.

5. In the early phases of exercise in the upright position, cardiac output
is increased by an augmentation in stroke volume mediated through
the use of the Frank­Starling mechanism and heart rate; the increase
in cardiac output in the latter phases of exercise is primarily due to a
sympathetic­mediated increase in ventricular rate. At fixed
submaximal workloads below anaerobic threshold, steady­state
conditions are usually reached after the second minute of exercise,
following which heart rate, cardiac output, blood pressure, and
pulmonary ventilation are maintained at reason­ably constant levels.
During strenuous exertion, sympathetic discharge is maximal and
parasympathetic stimulation is withdrawn, resulting in vaso­
constriction of most circulatory body systems, except for that in
exercising muscle and in the cerebral and coronary circulations.
Venous and arterial nor­epinephrine release from sympathetic
postganglionic nerve endings, as well as plasma renin levels, are
increased; the catecholamine release enhances ven­tricular
contractility.

6. As exercise progresses, skeletal muscle blood flow is increased,
oxygen extraction increases by as much as threefold, total
calculated peripheral resistance decreases, and systolic blood
pressure, mean arterial pressure, and pulse pressure usually
increase. Diastolic blood pressure does not change significantly.
The pulmonary vascular bed can accommodate as much as a
sixfold increase in cardiac output with only modest increases in
pulmonary artery pressure, pulmonary capillary wedge pressure,
and right atrial pressure; in normal individuals, this is not a
limiting determinant of peak exercise capacity.
Cardiac output increases by four­ to sixfold above basal levels
during strenuous exertion in the upright position, depending on
genetic endowment and level of train­ing. The maximum heart
rate and cardiac output are decreased in older individuals, partly
because of decreased beta­adrenergic responsivity.

7. Maximum heart rate can be estimated from the formula 220 ­ age in
years, with a standard deviation of 10 to 12 beats per minute. The
age­predicted maximum heart rate is a useful measure­ment for
safety reasons. However, the wide standard deviation in the various
regression equations used and the impact of drug therapy limit the
usefulness of this param­eter in estimating the exact age­predicted
maximum for an individual patient.
In the postexercise phase, hemodynamics return to baseline within
minutes of termi­nation of exercise. Vagal reactivation is an
important cardiac deceleration mechanism after' exercise and is
accelerated in well­trained athletes but blunted in patients with
chronic heart failure (see also section on heart rate). Intense
physical work or signif­icant cardiorespiratory impairment may
interfere with achievement of a steady state, and an oxygen deficit
occurs during exer­cise. The total oxygen uptake in excess of the
resting oxygen uptake during the recov­ery period is the oxygen
debt.

8. Patient position
At rest, the cardiac output and stroke volume are higher when the
person is in the supine position than when the person is in the
upright position. With exercise in normal supine persons, the eleva­
tion of cardiac output results almost entirely from an increase in
heart rate, with little augmentation of stroke volume. In the upright
posture, the increase in cardiac output in normal individuals results
from a combination of elevations in stroke volume and heart rate. A
change from supine to upright posture causes a decrease in venous
return left ventricular end­diastolic volume and pressure, stroke
volume, and cardiac index. Renin and nor­epinephrine levels are
increased. End­systolic volume and ejection fraction are not
significantly changed. The net effect on exercise performance is an
approximate 10 percent increase in exercise time cardiac index,
heart rate, and rate pressure product at peak exercise in the upright
as compared with the supine position.

9. Cardiopulmonary Exercise Testing
Cardiopulmonary exercise testing involves measurements of
respiratory oxygen uptake (VO
2
), carbon dioxide production
(VCO
2
), and ventilatory parameters during a symptom­limited
exercise test. VO
2
max is the product of maximal arterial­venous
oxygen difference and cardiac output and represents the largest
amount of oxygen a person can use while performing dynamic
exercise involving a large part of total muscle mass. The VO
2
max
decreases with age, is usually less in women than in men, and can
vary among individuals as a result of genetic factors. VO
2
max is
diminished by degree of cardio­vascular impairment and by
physical inactivity.
Peak exercise capacity is decreased when the ratio of measured to
predicted VO2 max is less than 85 to 90 percent.

10. Oximetry, performed noninvasively, can be used to monitor arterial
oxygen saturation, and the value normally does not decrease by
more than 5 percent during exercise. Estimates of oxygen
saturation during strenuous exercise using pulse oximetry can be
unreliable in some patients.
ANAEROBIC THRESHOLD
·Anaerobic threshold is a theoretical point during dynamic
exercise when muscle tissue switches over to anaerobic
metabolism as an additional energy source. Lactic acid begins to
accumulate when a healthy untrained subject reaches about 50 to
60 percent of the maximal capac­ity for aerobic metabolism.
Above the anaerobic threshold, carbon dioxide is produced in
excess of oxygen consumption.

11. ·The anaerobic threshold is a useful parameter because work
below this level encompasses most activities of daily living.
Anaerobic threshold is often reduced in patients with significant
car­diovascular disease.
·Changes in anaerobic threshold and peak VO­
2
with repeat testing
can be used to assess disease progression, response to medical
therapy, and improvement in cardiovascular fitness with training.
VENTILATORY PARAMETERS
The respiratory exchange ratio represents the amount of carbon
dioxide produced divided by the amount of oxygen consumed.
The respiratory exchange ratio ranges from 0.7 to 0.85 at rest and
is partly dependent on the pre­dominant fuel used for cellular
metabolism (e.g., the respira­tory exchange rate for predominant
carbohydrate use is 1.0, whereas the respiratory exchange ratio
for predominant fatty acid use is 0.7).

12. At high exercise levels, carbon dioxide pro­duction exceeds VO
2
,
and a respiratory exchange ratio greater than 1.1 often indicates that
the subject has performed at maximal effort.
METABOLIC EQUIVALENT
In current use, the term metabolic equivalent (MET) refers to a unit
of oxygen uptake in a sitting, resting person; 1 MET is equivalent to
3.5 ml 02/kg/min of body weight. Measured VO
2
in ml 02/min/kg
divided by 3.5 ml 02/kg/min determines the number of METs
associated with activity. Work activities can be calculated in
multiples of METs; this measurement is useful to determine
exercise prescriptions, assess disability, and standardize the
reporting of submaximal and peak exercise workloads when
different protocols are used.

13. The measurements obtained with cardiopulmonary exercise testing
are useful in under­standing an individual patient’s response to
exercise and can be useful in the diagnostic evaluation of a patient
with dyspnea.
METHODS
General concerns prior to performing an exercise test include –
•Safety precautions and equipments needs.
•Patient preparation
•Choosing a test type
•Choosing a test protocol
•Patient monitoring
•Reasons to terminate a test
•Post test monitoring

14. SAFETY PRECAUTIONS AND EQUIPMENT
·The safety precautions outlined by the American Heart
Association are very explicit in regard to the requirements for
exercise testing.
·Everything necessary for cardiopulmonary resuscitation must be
available and regular drills should be performed to ascertain that
both personnel and equipments are ready for a cardiac
emergency.
·Room temperature should be between 64° and 72°F (18° to 22°C)
and humidity less than 60%.
·The first survey of clinical exercise facilities by Rochmis and
Blackburn showed exercise testing to be a safe procedure and
approximately 1 death and 5 non fatal complications per 10000
tests.

15. ·Besides emergency equipment, the safety and accuracy of testing
equipment should be considered.
·The treadmill should have front and side rails for subjects to
steady themselves.
·It should be calibrated monthly.
·An emergency stop button should be readily available to the staff
only.
·A small plateform or stepping area at the level of belt is advisable
so that the subject can start the test by “pedaling” the belt with
one foot prior to stepping on.
·Although numerous clever devices have been developed to
automate blood pressure measurement during exercise, none can
be recommended. The time proven method of holding the
subject’s arm with a stethoscope placed over the brachial artery
remains most reliable.

16. ·Exercise test should be performed under the supervision of a
physician who has been trained to conduct exercise tests. An
ACC/AHA clinical competence statement in exercise testing
published in 2000 describes a “majority opinion” of its authors
that supervising physician should participate in at least 50
exercise test procedure during training and perform at least 25
exercise test per year”.
·The degree of supervision required is primarily dependent on the
type of patient being tested and can range from direct
performance of the test for patients who are at higher risk of
complications (e.g. those who have unstable angina after
stabilization, who have congestive heart failure or who have high
risk of arrhythmias) to assigning the performance of the test to an
appropriately trained exercise physiologist or a specialist in
patients at lower risk. In all cases a physician should be
immediately available during the exercise test.

17. Emergency stop button

18. TMT Room

19. Tread Mill

20. PRETEST PREPARATION
·During the pretest evaluation, the physician should establish and
understanding of any patterns of cardiopulmonary compromise
associated with exercise and the patient’s usual level of exercise
tolerance.
·The patient should be asked whether he or she has ever become
light headed or fainted while exercising and whether anyone in the
family has died suddenly during exercise.
·The physician should also ask about family history and general
medical history, making note of any considerations that may
increase the risk of sudden death.
·A brief physical examination should always be performed prior to
testing to rule out significant outflow obstruction.
·If abnormal findings occur at levels of exercise that the patient
usually performs, then it may not be necessary to stop the test
because of them.

21. Preparation for exercise testing include the following –
•The subject should be instructed not to eat or smoke atleast 2 hours
prior to the test and to come in loose fitting clothes.
•Unusual physical exertion should be avoided before testing.
•A brief history physical examination (particularly noting systolic
murmurs) should be accomplished to rule out any
contraindications to testing.
•Specific questioning should determine which drugs are being
taken, and potential electrolyte abnormalities should be
considered. The labeled medication bottles should be brought
along so that medications can be identified and recorded. Because
of a greater potential for cardiac events with the sudden cessation
of b­blockers , they should not be automatically stopped prior to
testing but done so gradually under physician guidance, only after
consideration of the purpose of the test. Many post infarct patients
referred for exercise testing have been prescribed beta­adrenergic
blocking agents and angiotensin converting enzyme inhibitors.

22. Although beta­adrenergic blocking drugs may attenuate the
ischemic, they do not interfere with poor functional capacity as a
marker of adverse prognosis and should be continued in patients
referred for testing. (BRAUNDWALD PAGE 167).
2.Pretest standard 12 lead ECG are necessary in both the supine and
standing positions.
3.Good skin preparations must cause some discomfort but is
necessary for good conductance and to avoid artifacts.
4.Patients should continue antihypertensive drug therapy on the day
of testing.
5.Hyperventilation is not necessary prior to testing. Subjects both
with or without disease may or may not exhibit ST segment
changes with hyperventilation, the value of this procedure in
lessening the number of false positive responders is no longer
considered useful. (HURST PAGE 462)

23. DURING THE TEST
·Most problems can be avoided by having an experienced physician
standing next to the subject, measuring blood pressure and assessing
appearance during the test.
·Subjects should be reminded not to grasp the front or side rails
because this decreases the work performed and create noise in the
ECG. Hanging on increases exercise time resulting in an over
estimation of exercise capacity.
Contraindications
·The AHA published standards for performance of exercise testing in
2001 which define absolute and relative contraindications to
exercise testing, these recommendations were slightly modified in
ACC/AHA guidelines published in 2002.
Relative contraindications are those that can be superseded if
clinicians believe that the benefits of testing outweigh the risk of
exercise.

25. Exercise Protocols
The main types of exercise are isotonic or dynamic exercise,
isometric or static exercise, and resistive (combined isometric and
isotonic) exercise. Dynamic protocols most frequently are used to
assess cardiovascular reserve, and those suitable for clinical testing
should include a low intensity warm­up phase. In general, 6 to 12
minutes of con­tinuous progressive exercise during which the
myocardial oxygen demand is elevated to the patient's maximal level
is optimal for diagnostic and prognostic purposes. The protocol
should include a suitable recovery or cool­down period. If the
protocol is too strenuous for an individual patient, the test must be
terminated early, and there is no opportunity to observe clinically
important responses. If the exercise protocol is too easy for an
individual patient, the prolonged procedure tests endurance and not
aerobic capacity.

26. Thus, exercise protocols should be individualized to accommodate a
patient’s limitations. Protocols may be set up at a fixed duration of
exercise for a certain intensity to meet minimal qualifications for
certain industrial tasks or sports programs.
TREADMILL PROTOCOL
The treadmill protocol should be consistent with the patient’s
physical capacity and the purpose of the test. In healthy individuals,
the standard Bruce protocol is popular, and a large diagnostic and
prognostic data base has been published using this protocol. The
Bruce multistage maximal treadmill protocol has 3­minute periods
to allow achievement of a steady state before work­load is increased.
In older individuals or those whose exercise capacity is limited by
cardiac disease, the protocol can be modified by two 3­minute warm
­up stages at 1.7 mph and 0 percent grade and 1.7 mph and 5 percent
grade.

27. A limitation of the Bruce protocol is the rela­tively large increase in
VO
2
between stages and the additional energy cost of running as
compared with walking at stages in excess of Bruce’s stage III.
It is important to encourage patients not to grasp the handrails of the
treadmill during exercise, particularly the front handrails. Functional
capacity can be overestimated by as much as 20 percent in tests in
which handrail support is permitted, and VO
2
is decreased. Because
the degree of handrail support is difficult to quantify from one test to
another, more consistent results can be obtained during serial testing
when handrail support is not permitted.
The 6-Minute Walk Test
The 6­minute walk test can be used for patients who have marked
left ventricular dysfunc­tion or peripheral arterial occlusive disease
and who cannot perform bicycle or treadmill exercise.

28. Patients are instructed to walk down a 100­foot corridor at their own
pace, attempt­ing to cover as much ground as possible in 6 minutes.
At the end of the 6­minute interval, the total distance walked is
determined and the symptoms experienced by the patient are
recorded. The 6­minute walk test as a clinical measure of
ambulatory function requires highly skilled personnel fol­lowing a
rigid protocol to elicit reproducible and reliable results. The
coefficient of variation for distance walked during two 6­minute
walk tests was 10 percent in one series of patients with peripheral
arterial occlusive disease.

29. Estimated oxygen cost of bicycle ergometer and selected treadmill protocols. The standard Bruce
protocol starts at 1.7 mph and 10 percent grade (5 METs), with a larger increment between stages
than protocols such as the Naughton, ACIP, and Weber, which start at less than 2 METs at 2mph and
increase by 1­ to 1.5­MET increments between stages. The Bruce protocol can be modified by two 3­
minute warm­up stages at 1.7mph and 0 percent grade and 1.7mph and 5 percent grade. METs =
metabolic equivalents. (Adapted from Fletcher GF, Balady G, Amsterdam EA, et al: Exercise
Standards for Testing and Training. A statement for healthcare professionals from the American
Heart Association. Circulation 104:1694, 2001.

30. Electrocardiographic Measurements
LEAD SYSTEMS. The Mason­Likar modification of the standard
12­lead ECG requires that the extremity electrodes be moved to the
torso to reduce motion artifact. The arm elec­trodes should be
located in the most lateral aspects of the infraclavicular fossae, and
the leg electrodes should be in a stable position above the anterior
iliac crest and below the rib cage. The Mason­Likar modification
results in a right­axis shift and increased voltage in the inferior
leads and may produce a loss of inferior Q waves and the
development of new Q waves in lead aV
1
. Thus, the body torso limb
lead posi­tions cannot be used to interpret a diagnostic resting
12­1ead ECG. The more cephalad the leg electrodes are placed, the
greater is the degree of change and the greater is the aug­mentation
of R wave amplitude.

32. Types of ST Segment Displacement
In normal persons, the PR, QRS, and QT intervals shorten as
heart rate increases. P amplitude increases, and the PR
segment becomes progressively more downsloping in the
inferior leads. J point, or junctional, depression is a normal
finding during exercise.

33. J point depression of 2 to 3 mm in leads V
4
to V
6
with rapid upsloping ST segments
depressed approximately 1mm 80msec after the J point. The ST segment slope in leads
V
4
and V
5
is 3.0mV/sec. This response should not be considered abnormal.

34. In patients with myocar­dial ischemia, however, the ST segment
usually becomes more horizontal (flattens) as the severity of the
ischemic response worsens. With progressive exercise, the
depth of ST segment depression may increase, involving more
ECG leads, and the patient may develop angina. In the
immediate post re­covery phase, the ST segment displacement
may persist, with downsloping ST segments and T wave
inversion, gradually returning to baseline after 5 to 10 minutes.

35. Bruce protocol. lead V
4
, the exercise
electrocardiographic (ECG) result is
abnormal early in the test, reaching
0.3mV (3mm) of horizontal ST
segment depression at the end of
exercise. The ischemic changes persist
for at least 1 minute and 30 seconds
into the recovery phase. The right
panel provides a continuous plot of the
J point, ST slope, and ST segment
displacement at 80msec after the J
point (ST level) during exercise and in
the recovery phase. Exercise ends at
the vertical line at 4.5 minutes (red
arrow). The computer trends permit a
more precise identification of initial
onset and offset of ischemic ST
segment depression. This type of ECG
pattern, with early onset of ischemic
ST segment depression, reaching more
than 3mm of horizontal ST segment
displacement and persisting several
minutes into the recovery phase, is
consistent with a severe ischemic
response.

36. Bruce protocol. In this type of
ischemic pattern, the J point at peak
exertion is depressed 2.5mm, the
ST segment slope is 1.5mV/sec,
and the ST segment level at 80msec
after the J point is depressed
1.6mm. This “ slow upsloping” ST
segment at peak exercise indicates
an ischemic pattern in patients with
a high pretest prevalence of
coronary disease. A typical
ischemic pattern is seen at 3
minutes of the recovery phase when
the ST segment is horizontal and 5
minutes after exertion when the ST
segment is downsloping. Exercise
is discontinued at the vertical line
in the right panels at 7.5 minutes.

37. Ischemic ST segment displacement may be seen only during
exercise, emphasizing the importance of adequate skin preparation
and electrode placement to capture high~ quality recordings during
maximum exertion. In about 10 percent of patients, the ischemic
response may appear only in the recovery phase. This is a relevant
finding, and the prevalence of reversible perfusion defects by
single­photon emission computed tomography criteria are compa­
rable to those observed when the ischemic ST segment response
occurs both during and after exercise. Patients should not leave the
exercise laboratory area until the post­exercise ECG has returned to
baseline.

38. Bruce protocol. The exercise
electrocardiographic (ECG)
result is not yet abnormal at
8:50 minutes but becomes
abnormal at 9:30 minutes
(horizontal arrows, right) of a
12-minute exercise test and
resolves in the immediate
recovery phase. This ECG
pattern in which the ST
segment becomes abnormal
only at high exercise
workloads and returns to
baseline in the immediate
recovery phase may indicate a
false-positive result in an
asymptomatic individual
without atherosclerotic risk
factors. Exercise myocardial
imaging would provide more
diagnostic and prognostic
information if this were an
older person with several
atherosclerotic risk factors.
Vertical arrow indicates
termination of exercise.

39. Illustration of eight typical exercise electrocardiographic (ECG) patterns at
rest and at peak exertion. The computer­processed incrementally averaged
beat corresponds with the raw data taken at the same time point during
exercise and is illustrated in the last column. The patterns represent
worsening ECG responses during exercise. In the column of computer­
averaged beats, ST 80 displacement (top number) indicates the magnitude of
ST segment displacement 80 msec after the J point relative to the PQ junction
or E point. ST segment slope measurement (bottom number) indicates the ST
segment slope at a fixed time point after the J point to the ST 80
measurement. At least three noncomputer average complexes with a stable
baseline should meet criteria for abnormality before the exercise ECG result
can be considered abnormal (see Fig. 10­9). The normal and rapid upsloping
ST segment responses are normal responses to exercise. J point depression
with rapid upsloping ST segments is a common response in an older,
apparently healthy population. Minor ST depression can occur occasionally at
submaximal workloads in patients with coronary disease; in this illustration,
the ST segment is depressed 0.09mV (0.9mm) 80msec after the J point. The
slow upsloping ST segment pattern often demonstrates an ischemic response
in patients with known coronary disease or those with a high pretest clinical
risk of coronary disease. Criteria for slow upsloping ST segment depression
include J point and ST 80 depression of 0.15mV or more and ST segment
slope of more than 1.0mV/sec. Classic criteria for myocardial ischemia
include horizontal ST segment depression observed when both the J point and
ST 80 depression are 0.1mV or more and ST segment slope is within the
range of 1.0mV/sec. Downsloping ST segment depression occurs when the J
point and ST 80 depression are 0.1mV and ST segment slope is − 1.0mV/sec.
ST segment elevation in a non­Q wave noninfarct lead occurs when the J
point and ST 60 are 1.0mV or greater and represents a severe ischemic
response. ST segment elevation in an infarct territory (Q wave lead) indicates
a severe wall motion abnormality and in most cases is not considered an
ischemic response.

40. Measurement of ST Segment Displacement
For purposes of interpretation, the PQ junction is usually chosen as
the isoelectric point. The TP segment represents a true isoelectric
point but is an impractical choice for most routine clinical
measurements.
The development of 0.10 mV (1 mm) or greater of J point
depression measured from the PQ junction, with a relatively flat ST
segment slope (e.g., <0.7 to 1 mV/sec), depressed 0.10 mV or more
80 msec after the J point (ST 80) in three consecutive beats with a
stable base­line is considered to be an abnormal response. When the
ST 80 measurement is difficult to determine at rapid heart rates
(e.g., >130 beats/min), the ST 60 measure­ment should be used. The
ST segment at rest may occasion­ally be depressed. When this
occurs, the J point and ST 60 or ST 80 measurements should be
depressed an additional 0.10 mV or greater to be considered
abnormal.

41. Magnified ischemic exercise–
induced electrocardiographic
pattern. Three consecutive
complexes with a relatively stable
baseline are selected. The PQ
junction (1) and J point (2) are
determined; the ST 80 (3) is
determined at 80 msec after the J
point. In this example, average J
point displacement is 0.2mV (2mm)
and ST 80 is 0.24mV (24mm). The
average slope measurement from the
J point to ST 80 is −1.1 mV/sec.

42. When the degree of resting ST segment depression is 0.1 mV or
greater, the exercise ECG becomes less specific, and myocardial
imaging modalities should be considered.
In patients with early repolarization and resting ST segment
elevation, return to the PQ junction is normal. Therefore, the
magnitude of exercise­induced ST segment depression in a patient
with early repolarization should be determined from the PQ junction
and not from the elevated position of the J point before exercise.
Exercise­induced ST segment depres­sion does not localize the site
of myocardial ischemia, nor does it provide a clue about which
coronary artery is involved. For example, it is not unusual for
patients with isolated right CAD to exhibit exercise­induced ST
segment depression only in leads V
4
to V
6
, nor is it unusual for
patients with disease of the left anterior descending coronary artery
to exhibit exercise­induced ST segment displacements in leads II,
III, and aVf,

43. Exercise­induced ST segment elevation is relatively specific for the
territory of myocardial ischemia and the coronary artery involved.
UPSLOPING ST SEGMENTS. Junctional or J point depression is
a normal finding during maximal exercise, and a rapid upsloping ST
segment (>1 mV/sec) depressed less than 0.15 mV (1.5 mm) after
the J point should be considered to be normal.
Occasionally, however, the ST segment is depressed 0.15 mV (1.5
mm) or greater at 80 msec after the J point. This type of slow
upsloping ST segment may be the only ECG finding in patients with
well­defined obstructive CAD and may depend on the lead set used.
In patient subsets with a high CAD prevalence, a slow upsloping ST
segment depressed 0.15 mV or greater at 80 msec after the J point
should be considered abnormal. The importance of this finding in
asymptomatic individuals or those with a low CAD prevalence is
less certain.

44. Increasing the degree of ST segment depression at 80 msec after the
J point to 0.20 mV (2.0 mm) or greater in patients with a slow
upsloping ST segment increases speci­ficity but decreases
sensitivity.
ST SEGMENT ELEVATION. Exercise­induced ST seg­ment
elevation may occur in an infarct territory where Q waves are
present or in a noninfarct territory. The develop­ment of 0.10 mV (1
mm) or greater of J point elevation, per­sistently elevated greater
than 0.10 mV at 60 msec after the J point in three consecutive beats
with a stable baseline, is con­sidered an abnormal response. This
finding occurs in approximately 30 percent of patients with anterior
myocardial infarctions and 15 percent of those with inferior ones
tested early (within 2 weeks) after the index event and decreases in
frequency by 6 weeks.

45. As a group, postinfarct patients with exercise­induced ST segment
elevation have a lower ejection fraction than those without, a greater
severity of resting wall motion abnormalities, and a worse
prognosis. Exercise­induced ST segment elevation in leads with
abnor­mal Q waves is not a marker of more extensive CAD and
rarely indicates myocardial ischemia. Exercise­induced ST segment
elevation may occasionally occur in a patient who has regenerated
embryonic R waves after an acute myocardial infarction; the clinical
significance of this finding is similar to that observed when Q waves
are present.
When ST segment elevation develops during exercise in a non­Q
wave lead in a patient without a previous myocardial infarction, the
finding should be considered as likely evi­dence of transmural
myocardial ischemia caused by coronary vasospasm or a high­grade
coronary narrowing. This finding is relatively uncommon, occurring
in approxi­mately 1 percent of patients with obstructive CAD.

46. The ECG site of ST segment elevation is relatively specific for the
coro­nary artery involved, and myocardial perfusion scintigraphy
usually reveals a defect in the territory involved.

47. A 48­year­old man with several
atherosclerotic risk factors and a normal
resting electrocardiographic (ECG)
result developed marked ST segment
elevation (4 mm [arrows]) in leads V
2
and V
3
with lesser degrees of ST
segment elevation in leads V
1
and V
4
and J point depression with upsloping
ST segments in lead II, associated with
angina. This type of ECG pattern is
usually associated with a full­thickness,
reversible myocardial perfusion defect
in the corresponding left ventricular
myocardial segments and high­grade
intraluminal narrowing at coronary
angiography. Rarely, coronary
vasospasm produces this result in the
absence of significant intraluminal
atherosclerotic narrowing. HR = heart
rate; METs = metabolic equivalents;
SBP = systolic blood pressure.

48. T WAVE CHANGES. The morphology of the T wave is
influenced by body position, respiration, hyperventilation, drug
therapy, and myocardial ischemia/necrosis. In patient
populations with a low CAD prevalence, pseudonormaliza­tion
of T waves (inverted at rest and becoming upright with exercise)
is a nondiagnostic finding. In rare instances, this finding may be
a marker for myocardial ischemia in a patient with documented
CAD, although it would need to be substantiated by an ancillary
technique, such as the concomitant finding of a reversible
myocardial perfusion defect.

49. Pseudonormalization of T waves in a 49­year­
old man referred for exercise testing. The
patient had previously been seen for typical
angina. The resting electrocardiogram in this
patient with coronary artery disease shows
inferior and anterolateral T wave inversion, an
adverse long­term prognosticator. The patient
exercised to 8 METs, reaching a peak heart
rate of 142 beats/min and a peak systolic blood
pressure of 248 mm Hg. At that point, the test
was stopped because of hypertension. During
exercise, pseudonormalization of T waves
occurs, and it returns to baseline (inverted T
wave) in the postexercise phase. The patient
denied chest discomfort, and no arrhythmia or
ST segment displacement was noted. Transient
conversion of a negative T wave at rest to a
positive T wave during exercise is a
nonspecific finding in patients without prior
myocardial infarction and does not enhance the
diagnostic or prognostic content of the test;
however, the ability to exercise to 8 METs
without ischemic changes in the ST segment
places this patient into a subset of lower risk.
HR = heart rate; METs = metabolic
equivalents; SBP = systolic blood pressure.

50. OTHER ELECTROCARDIOGRAPHIC MARKERS.
Changes in R wave amplitude during exercise are relatively
nonspecific and are related to the level of exercise performed. When
the R wave amplitude meets voltage criteria for left ventricular
hypertrophy, the ST segment response cannot be used reliably to
diagnose CAD, even in the absence of a left ventricular strain
pattern. U wave inversion can occasionally be seen in the precordial
leads at heart rates of 120 beats/min. Although this finding is
relatively specific for CAD, it is relatively insensitive.
COMPUTER-ASSISTED ANALYSIS
When the raw ECG data are of high quality, the computer can filter
and average or select median complexes from which the degree of J
point displacement, ST segment slope, and ST displacement 60 to
80 msec after the J point (ST 60 to 80) can be measured. The
selection of ST 60 or ST 80 depends on the heart rate response.

51. At ventricular rates greater than 130 beats/min, the ST 80
measurement may fall on the upslope of the T wave, and the ST 60
measurement should be used instead. In some computerized
systems, the PQ junction or isoelectric interval is detected by
scanning before the R wave for the 10­msec inter­val with the least
slope. J point, ST slope, and ST levels are determined; the ST
integral can be calculated from the area below the isoelectric line
from the J point to ST 60 or ST 80.
ST/HEART RATE SLOPE MEASUREMENTS.
Heart rate adjustment of ST segment depression appears to improve
the sensitivity of the exer­cise test, particularly the prediction of
multivessel CAD. The ST/heart rate slope depends on the type of
exercise performed, number and loca­tion of monitoring electrodes,
method of measuring ST segment depres­sion, and clinical
characteristics of the study population.

52. Calculation of maximal 5ST/heart rate slope in mV/beats/min is
performed by linear regression analysis relating the measured amount
of ST segment depres­sion in individual leads to the heart rate at the
end of each stage of exercise, starting at the end of exercise. An
ST/heart rate slope of 2.4 mV/beats/min is considered abnormal, and
values that exceed 6 mV/beats/min are suggestive evidence of three­
vessel CAD. The use of this measurement requires modification of
the exercise protocol such that increments in heart rate are gradual, as
in the Cornell protocol, as opposed to more abrupt increases in heart
rate between stages, as in the Bruce or Ellestad protocols, which limit
the ability to calculate statistically valid ST segment heart rate slopes.
The measurement is not accurate in the early postinfarction phase. A
modification of the ST segment/heart rate slope method is the ST
segment/heart rate index calculation, which represents the average
change of ST segment depres­sion with heart rate throughout the
course of the exercise test.

53. The ST/heart rate index measurements are less than the ST/heart rate
slope measurements, and a ST/heart rate index of 1.6 is defined as
abnormal.
Mechanism of ST Segment Displacement
PATHOPHYSIOLOGY OF THE MYOCARDIAL ISCHE-MIC
RESPONSE. Myocardial oxygen consumption (MO
2
) is determined
by heart rate, systolic blood pressure, left ven­tricular end­diastolic
volume, wall thickness, and contractility. The rate­pressure or double
product (heart rate × systolic blood pressure) increases progressively
with increasing work and can be used to estimate the myo­cardial
perfusion requirement in normal persons and in many patients with
coronary artery disease. The heart is an aerobic organ with little
capacity to generate energy through anaerobic metabolism. Oxygen
extraction in the coronary circulation is nearly maximal at rest.

54. The only significant mechanism available to the heart to increase
oxygen con­sumption is to increase perfusion, and there is a direct
linear relationship between MO
2
and coronary blood flow in normal
individuals. The principal mechanism for increasing coronary blood
flow during exercise is to decrease resistance at the coronary
arteriolar level. In patients with progressive ath­erosclerotic
narrowing of the epicardial vessels, an ischemic threshold occurs, and
exercise beyond this threshold can produce abnormalities in diastolic
and systolic ventricular function, ECG changes, and chest pain. The
subendocardium is more susceptible to myocardial ischemia than the
subepi­cardium because of increased wall tension; causing a relative
increase in myocardial oxygen demand in the subendo­cardium.

55. Dynamic changes in coronary artery tone at the site of an
atherosclerotic plaque may result in diminished coronary flow during
static or dynamic exercise instead of the expected increase that
normally occurs from coronary vasodilation in a normal vessel; that
is, perfusion pressure distal to the stenotic plaque actually falls as
during exercise, resulting in reduced subendocardial blood flow.
Thus, regional left ventricular myocardial ischemia may result not
only from an increase in myocardial oxygen demand during exercise
but also from a limitation of coronary flow as a result of coronary
vasoconstriction, or inability of vessels to suffi­ciently vasodilate at
or near the site of an atherosclerotic plaque.
Increased myocardial oxygen demand associated with a­ failure to
increase or an actual decrease in regional coronary blood flow usually
causes ST segment depression; ST segment elevation may
occasionally occur in patients with more severe coronary flow
reduction.

56. NON ELECTROCARDIOGRAPHIC OBSERVATIONS
·The ECG is only one part of the exercise response and abnormal
hemodynamics or functional capacity is just as important as, if not
more important then ST segment displacement.
1) Blood pressure
·The normal exercise response is to increase systolic blood pressure
progressively with increasing workloads to a peak response ranging
from 160 to 200mmHg with the higher range of the scale in older
patients with less compliant vascular systems.
·Failure to increase systolic blood pressure beyond 120mmHg, a
sustained decrease greater than 10mmHg repeatable within 15
seconds or a fall in systolic blood pressure below standing resting
values during progressive exercise.

57. when the blood pressure has otherwise been increasing
appropriately is abnormal and reflects either inadequate elevation of
cardiac output because of left ventricular systolic pump dysfunction
or an excessive reduction in systemic vascular resistance.
·Exertional hypotension ranges from 3 to 9 percent and is higher in
patients with three vessel or left main CAD.
·Conditions other than myocardial ischemia that have been
associated with a failure to increase or an actual decrease in systolic
blood pressures during progressive exercise are cardiomyopathy,
cardiac arrythmias, vasovagal reaction. Left ventricular outflow
tract obstruction, ingestion of antihypertensive drugs, hypovolumia
and prolonged vigorous exercise.
·An abnormal hypertensive blood pressure response in patients with
a high prevalence of CAD is associated with more extensive CAD
and more extensive myocardial perfusion defects.

58. •In normal persons, the diastolic blood pressure does not usually
change significantly.
(2) MAXIMAL WORK CAPACITY
·Maximal work capacity in normal individuals is influenced by
familiarization with exercise test equipment, level of training, and
environmental conditions at the time of testing.
·In patients with known or suspected CAD, a limited exercise capacity
is associated with an increased risk of cardiac events and in general
the more severe the limitation, the worse the CAD extent and
prognoses.
·In estimating functional capacity the amount of work performed (or
exercise stage achieved) expressed in METs and not the number of
minutes of exercise, should be the parameter measured.
·Major reduction in exercise capacity indicates significant worsening
of cardiovascular status.

59. (3) SUBMAXIMAL EXERCISE
·The interpretation of exercise tests results for diagnostic and
prognostic purposes requires consideration of maximal work
capacity.
·When a patient is unable to complete moderate levels of
exercise or reach at least 85 to 90% of age predicted maximum,
the level of exercise performed may be inadequate to test
cardiac reserve. Thus ischemic ECG, scientigraphic, or
ventriculographic abnormalities may not be evoked and the test
may be non diagnostic.
·Non diagnostic test results are more common in patients with
peripheral vascular disease, orthopedic limitation or
neurological impairment and in patients with poor motivation.
Pharmacological stress imaging studies should be considered in
this settings.

60. (4) HEART RATE RESPONSE
·The sinus rate increases progressively with exercise mediated in
part through sympathetic innervation of SA node and circulating
catecholamine.
·An inappropriate increase in heart rate at low exercise
workloads may occur in patients who are in atrial fibrillation,
physically disconditioned, hypovolumic or anaemic or who have
marginal left ventricular function, this increase may persist for
several minutes in recovery phase.
·In some patients, heart rate (HR) fails to increase appropriately
with exercise and is associated with an adverse prognosis.

61. ·Chronotropic incompetence is determined by decreased heart
rate sensitivity to the normal increase in sympathetic tone during
exercise and is defined as inability to increase hart rate to atleast
85 percent of age predicted maximum or as an abnormal heart
rate reserve.
·Heart rate reserve is calculated as follows –
% HRR used = (HR
peak
­ HR
res
) / (220­age­HR
res
)
·Abnormal heart rate recovery refers to a relatively slow
deceleration of heart rate following exercise cessation. This type
of response reflects decreased vagal tone and is associated with
increased mortality.

62. (5) RATE PRESSURE PRODUCT
·The heart rate systolic blood pressure product an indirect measure
of myocardial oxygen demand, increases progressively with
exercise and the peak rate pressure product can be used to
characterize cardiovascular performance.
·Most normal individuals develop a peak rate pressure product of 20
to 35mmHg×beats/min×10
­3
.
(6) CHEST DISCOMFORT
·Characterization of chest pain during exercise can be useful
diagnostic finding, particularly when the symptom complex is
compatible with typical angina pectoris.
·In some patients, however chest discomfort may be the only signal
that obstructive CAD is present.
·The new development of an S
3
, holosystolic apical murmur or
basilar rales in the early recovery phase of exercise enhances the
diagnostic accuracy of test.

63. TERMINATION OF EXERCISE
·Termination of exercise should be determined in part by the
patients recent activity level.
·The rate of perceived patient exertion can be estimated by the
borg scale. The scale is linear, with values of –
9 – for very light
11 –fairly light
13 –somewhat hard
15 –hard
17 –very hard
19 –very­very hard
·Borg readings of 14 to 16 approximate anaerobic threshold and
readings of 18 or greater approximate a patient’s maximum
exercise capacity.

64. ·It is helpful to grade exercise induced chest discomfort on a 1 to
4 scale, with 1 indicating initial onset of chest discomfort and 4
of the most severe chest pain the patient has ever experienced.
·The physician should note the onset of grade 1 chest discomfort
on the work sheet and the test should be stopped when the
patient reports grade 3 chest pain.
·In the absence of symptoms, it is prudent to stop exercise when
a patient demonstrates 0.3mvV (3mm) or greater of ischemic
ST segment depression or 0.1mV (1mm) or greater of ST
segment elevation in a non­infarct lead without an abnormal Q­
wave.
·Significant worsening of ambient ventricular ectopy during
exercise or the unsuspected appearance of VT is an indication
to terminate exercise.

65. ·A progressive, reproducible decrease in systolic blood pressure
of 10mmHg or more may indicate transient left ventricular
dysfunction or an inappropriate decrease in systemic vascular
resistance and is an indication to terminate exercise.
·The test should be stopped if the arterial blood pressure is
250­270/120 to 130 mmHg or higher.
·Relative indications for termination of testing are those that can
be supersided when the clinician considers the benefit of
continued exercise to exceed the risk.

67. Indications of TMT
Clearly indicated
Diagnosis of CAD in men with atypical symptoms.
Patient has known CAD; assess prognosis and functional capacity
Symptomatic, recurrent, exercise­induced arrhythmias
Patient has experienced an uncomplicated myocardial infarction;
evaluate prognosis and functional capacity
Patient has undergone coronary artery revascularization; evaluation
recommended
Possibly indicated
Diagnosis of CAD in woman with typical or atypical angina
Diagnosis of CAD in patient taking digitalis
Diagnosis of CAD in patient with complete right bundle
branch block

68. Patient has CAD or heart failure; evaluate functional capacity
and response to therapy
Patient has variant angina; evaluation recommended.
Patient has known CAD; serial evaluation recommended
Asymptomatic man who is older than 40 yr and in a high­risk
occupation, who has­two or more risk factors for CAD, or who
is sedentary and plans to begin a vigoi'ous exercise program;
evaluation recommended
Asymptomatic patient after coronary revascularization; annual
evaluation recommended Selected patients with valvular heart
disease; evaluate functional capacity
Probably not indicated
Asymptomatic patient with isolated ventricular ectopy;
evaluation recommended

69. Patient is enrolled in a cardiac rehabilitation program; serial
evaluation recommended Diagnosis of CAD in patient with left
bundle branch block or ventricular preexcitation (Wolff­
Parkinson­White) syndrome on resting electrocardiography
Asymptomatic man or woman; evaluation recommended
Man or woman with chest pain of noncardiac etiology;
evaluation recommended
Diagnostic Use of Exercise Testing
Approximately 75 to 80 percent of the diagnostic information on
exercise­induced ST segment depression in patients with a normal
resting ECG is contained in leads V
4
to V
6
Exercise ECG is less
specific when patients in whom false­positive results are more
common are included, such as those with valvular heart disease, left
ventricular hypertrophy, marked resting ST segment depression, or
digitalis therapy.

70. Exercise Testing in Determining Prognosis
Exercise testing provides not only diagnostic information but also,
more importantly, prognostic data. The value of exercise testing to
estimate prognosis must be considered in light of what is already
known about a patient’s risk status. Left ventricular dysfunction,
CAD extent, electrical instability, and noncoronary comorbid
conditions must be taken into consideration when estimating long­
term outcome.
ASYMPTOMATIC POPULATION. The prevalence of an
abnormal exercise ECG result in middle­aged asymptomatic men
ranges from 5 to 12 percent.
The future risk of cardiac events is greatest if the test result is
strongly pos­itive or if an asymptomatic subject has atherosclerotic
risk factors such as diabetes, hypertension, hypercholesterolemia,
smoking history, or familial history of premature coronary disease.

71. Serial change of a negative exercise ECG result to a positive one in
an asymptomatic person carries the same prognostic importance as
an initially abnormal test result. However, when an asymptomatic
indi­vidual with an initially abnormal test result has significant
worsening of the ECG abnormalities at lower exercise work­loads,
this finding may indicate significant CAD progression and warrants
a more aggressive diagnostic work­up.
In general, the prognostic value of an ST segment shift in women
is less than in men.
SYMPTOMATIC PATIENTS. Exercise testing should be
routinely performed (unless this is not feasible or unless there are
contraindications) before coronary angiography in patients with
chronic ischemic heart disease. Patients who have excellent exercise
tolerance (e.g., >10 METs) usually have an excellent prognosis
regardless of the anatomical extent of CAD.

72. Mark and colleagues developed a treadmill score based on 2842
consecutive patients with chest pain in the Duke data bank; these
patients underwent treadmill testing using the Bruce protocol and
cardiac catheterization. Patients with left bundle branch block
(LBBB) or those with exercise ­induced ST elevation in a Q wave
lead were excluded. The treadmill (TM) score is calculated as
follows:
TM score = exercise time - (5 × ST deviation) -- (4 × treadmill
angina index)
Angina index was assigned a value of 0 if angina was absent, 1 if
typical angina occurred during exercise, and 2 if angina was the
reason the patient stopped exercising.
ST deviation was defined as the largest net ST displacement in any
lead.

73. The 13 percent of patients with a treadmill score of ­11 or less had a
5­year survival rate of 72 percent, as compared with a 97 percent
survival rate among the 34 percent of patients at low risk with a
treadmill score of +5 or greater. The score worked equally well in
men and women, although women had a lower overall risk than men
for similar scores.
SILENT MYOCARDIAL ISCHEMIA In patients with
documented CAD, the presence of exercise­induced ischemic ST
segment depression confers increased risk of subsequent cardiac
events regardless of whether angina occurs during the test.
ACUTE CORONARY SYNDROMES
The prognostic risk assess­ment after an acute coronary syndrome
should incorporate findings from the history, physical examination,
resting 12­lead ECG, and level of serum markers to optimize
mortality and morbidity estimates and to categorize patients into
low­ intermediate, and high­risk groups.

74. Exercise testing should be considered in the outpatient evaluation of
low­risk patients with unstable angina (biomarker negative) who are
free of active ischemic symptoms for a minimum of 8 to 12 hours,
and in hospitalized low­ to intermediate­risk ambulatory patients
who are free of angina or heart failure symptoms for at least 48
hours. In many intermediate or high­risk patients, coronary
angiography will have been performed during the acute phase of the
illness; coronary disease extent, left ven­tricular function, and
degree of coronary revascularization, if performed, should then be
incorporated with the exercise test data to determine the overall
predischarge prognostic risk estimate.

75. MYOCARDIAL INFARCTION
Exercise testing after myocardial infarction (both non­ST and ST
eleva­tion) is useful to determine (1) risk stratification and
assessment of prog­nosis, (2) functional capacity for activity
prescription after hospital discharge, and (3) assessment of
adequacy of medical therapy and need to use supplemental
diagnostic or treatment options. A low­level exercise test
(achievement of 5 to 6 METs or 70 to 80 percent of age­predicted
maximum) is frequently per­formed before hospital discharge to
establish the hemodynamic response and functional capacity. The
ability to complete 5 to 6 METs of exer­cise or 70 to 80 percent of
age­predicted maximum in the absence of abnormal ECG or blood
pressure is associated with a I­year mortality rate of 1 to 2 percent
and may help guide the timing of early hospital discharge.

76. Parameters associated with increased risk include inability to
perform or complete the low­level predischarge exercise test, poor
exercise capacity, inability to increase or a decrease in exercise
systolic blood pressure, and angina or exercise­induced ST segment
depression at low workloads.
Many postinfarct patients referred for exercise testing have been
prescribed beta­adrenergic blocking agents and angiotensin­
converting enzyme inhibitors. Although beta­adrenergic blocking
drugs may attenuate the ischemic response, they do not interfere
with poor functional capacity as a marker of adverse prognosis and
should be con­tinued in patients referred for testing.
The relative prognostic value of a 3­ to 6­week postdischarge
exercise test is minimal once clinical variables and the results of the
low­level predischarge test are adjusted for.

77. For this reason, the timing of the exercise test after the infarct event
favors pre­discharge exercise testing to allow implementation of a
definitive treat­ment plan in patients in whom coronary anatomy is
known as well as risk stratification of patients in whom coronary
anatomy has not yet been determined.
There is a trend toward early predischarge exercise testing (within 3
to 5 days) in uncomplicated cases after acute myocardial infarc­
tion. A 3 to 6­week test is useful in clearing patients to return to
work in occupations involving physical labor in which the MET
expenditure is likely to be greater than that performed on a
predischarge test.
In patients with negative T waves after infarction, stress­induced
normalization of the T waves may also indicate higher coronary
flow reserve than in patients unable to normalize their T waves.

78. Nomogram of prognostic relations using the Duke treadmill score, which incorporates
duration of exercise (in minutes) – (5 × maximal ST segment deviation during or after
exercise) (in mm)–(4 × treadmill angina index). Treadmill angina index is 0 for no
angina, 1 for nonlimiting angina, and 2 for exercise­limiting angina. The nomogram can
be used to assess the prognosis of ambulatory outpatients referred for exercise testing.
In this example, the observed amount of exercise­induced ST segment deviation (minus
resting changes) is marked on the line for ST segment deviation during exercise (1).
The degree of angina during exercise is plotted (2), and the points are connected. The
point of intersection on the ischemic reading line is noted (3). The number of METs (or
minutes of exercise if the Bruce protocol is used) is marked on the exercise duration
line (4). The marks on the ischemia reading line and duration of exercise line are
connected, and the intersection on the prognosis line determines 5­year survival rate and
average annual mortality for patients with these selected specific variables. In this
example, the 5­year prognosis is estimated at 78 percent in this patient with exercise­
induced 2­mm ST depression, nonlimiting exercise angina, and peak exercise workload
of 5 METs. MET = metabolic equivalent.