heart author" faq
Exercise Test

Exercise testing elicits the body's reaction to measured increases in acute exercise.The changes in heart rate,blood pressure,respiration,and perceived level of exercise provide data that permit quantitative estimation of cardiovascular conditioning and function.Exercise tests provide an opportunity to observe a personduring exercise.By monitoring heart rate and blood pressure and continually observing the ECG, one can detect changes in the hemodynamic response and ischemic type ECG ST segment depression, and can detect and classify disturbances in heart rhythm and conduction associated with exercise.


Exercise can elicit cardiovascular abnormalities not present at rest and can be used to assess function of the cardiovascular system. Isotonic (dynamic) exercise, defined as muscular contraction of large muscle groups resulting in movement, primarily provides a volume load to the left ventricle, and thecardiovascular response is proportional to the degree of the exercise.

Maximum Oxygen Uptake

When dynamic exercise begins, oxygen uptake by the lungs quickly increases. After several minutes,oxygen uptake usually remains relatively stable (steady state) at each intensity of exercise.During the steady state, the heart rate(HR), cardiac output,blood pressure, and pulmonary ventilation are maintained at reasonably constant levels.

Maximal oxygen consumption(Vo2max) is the greatest amount of oxgen a person can utilize while performing dynamic exercise involving large components of total muscle mass and 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 (3.5ml O2 per kilogram of body weight per minute(ml kg-1min-1).Rather than determining each person's true resting oxygen uptake,one MET is designated as this average.resting oxygen uptake.Vo2max is significantly related to age,gender,exercise habits,heredity, and clinicalcardiovascular status

Maximum Vo2 is equal to maximum cardiac output times maximum arteriovenous oxygen(aVo2) difference.Since cardiac output is equal to the product of stroke volume and heart rate(HR),Vo2 is directly related to HR.The maximum aVo2 difference during exercise has a physiological limit of 15 to 17 ml/dl;therefore,if maximum effort is achieved,Vo2max can be used to estimate maximum cardiac output.

Myocardial OxygenUptake

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 HR.Mo2 can be estimated during exercise testing by the product of HR and systolic blood pressure, called rate pressure product.

In general there is a linear relation between Mo2 and coronary blood flow. During exercise,coronary blood flow increases as much as five fold above the resting value. A patient with obstructive coronary disease,however,may not have enough coronary blood flow to supply the metabolic demands of the myocardium during vigorous exercise, and as a consequence,myocardial ischemia occurs.


The response to dynamic exercise consists of a complex series of cardiovascular adjustments to provide active musclec with blood appropriate for metabolic needs,to dissipate heat generated by by active, and to maintain blood supply toessential organs such as thebrain and heart.

As cardiac output increases with dynamic exercise,vasculr resistance decreases in active muscles but increases in tissues that do not function during exercise. Since flow to active muscles increases much more than arterial pressure, there is a significant decrease invascular resistance.

Heart Rate Response

An increase in HR due to a decrease in vagal outflow is an immediate response of the cardiovascular system to exerciseThis is rapidly followed by an increase in sympathetic outflow to the heart and systemic blood vessels, which contribute to the increase in HR

Arterial Blood Pressure Response

Systolic blood pressure increase with dynamic work as a result of increasing cardiac output,while diastlic pressure usually remains about the same or decreases slightly. Paients who develop hypotension during exercise frequently have severe heart disease; patients with aortic valvular disease can also exhibit a drop in systolic pressure.

After maximal exercise, there is normally a decrease in systolic blood pressure,usually reaching resting levels in 6 mins., then often remaining lower than pre-exercise for several hours.In some patients with coronary artery disease(CAD), higher levels of systolic blood pressure, at times even exceeding peak exercise values,may develop in the recovery phase (Figure181). When exercise is terminated abruptly, some healthy persons have precipitous drops in systolic blood pressure due to venous pooling. Figure 181 shows the physiologic response to submaximum and maximum treadmill exercise based on tests of more than 700 apparently healhy men aged 25 t0 54.Maximalrate-pressure product ranges from a 10th percentile value of 25,000 to a 90th percentile of 40,000.

The arterial blood supply to the myocardium and to the other muscles and organs is usually adequate for the maximal perfusion requirement of which the organ is capable. If obstructive disease is present within a coronary artery, only minimal reduction in maximal blood flow will take place until the degree of arterial obstrution becomes quite advanced.The predictive importance of exertional myocardial ischemia is related to the intensity of cardiac activity at which the ischemia became apparent. For example,if there is no evidence of ischemia at 75% of maximum exercise, but there is at 90-100% of maximal exercise, it would likely be associated with a less severe degree of coronary obstruction than if the ischemia had been detectable at only 25-50% of maximal exercise.

Reference:Fletcher,G.F.,and Schlant,R.C.,The Exercise Test,Hurst's The Heart,8th Edition,Pp.423-440.


Exercise testing of patients should be conducted only by well-trained personnel with a basic knowledge of exercise physiology. In general, only physicians and other health professionals(especially nurses) familiar with normal and abnormal responses during exercise and qualified in Advanced Cardiac Life Support have the cognitive skills needed to perform exercise tests on patients competently.Equipment,medications ,and personnel trained to provide cardiopulmonary resuscitation(CPR) must be readily available. Although exercise testing of patients is considered safe , there are reports of acute myocardial infarction and death related to the procedure. Several surveys confirm that up to 10 myocardial infarctions or deaths, or both, can be expected per 10,000 tests.The risk is greater in postmyocardial infarction patients and in those being evaluated for malignant ventricular arrhythmias.

Figure 185 lists absolute and relative contraindications to exercise testing

Figure 183 list three classes of complications secondary to exercise tests.

Figure 184 lists the general indications for exercise testing


Good clinical judgement is imperative in determining indications for and contraindications to exercise testing. Whereas absolute contraindications are quite definitive, in select cases with relative contraindications,even submaximal testing may provide valuable information. The physician should be certain that the subject understands the procedure and acknowledges the risks. Good physician-patient communication about testing and its risks is essential.

As stated in the American Heart Association Exercise Standards, exercise testing of patients should be performed under the supervision of a physician who is trained to conduct exercise tests and who is responsible for ensuring that the exercise laboratory is properly equipped and that the testing personnel are appropriately trained.The level or degree of supervision needed during a test is determined by the clinical state of the patient being tested. Supervision must be designated by the physician orphysician's staff, who ask pertinent questions about the patient's medical history,perform a brief physical examination,and review the standard 12-lead ECG performed immediately before testing.The physician should interpret data derived from testing, suggest further evaluation or therapy, and aid in providing effective and timely advanced CPR when necessary. A defibrillator and appropriate medications should be immediately available.

Figure 186 details safety measures for exercise testing.

The degree of supervision of an exercise test can range from assigning monitoring of the test to a properly trained nonphysician(i.e.nurse or exercise specialist) for testing apparently healthy younger persons(less than 40 years old) or assigning patients with stable chest discomfort syndromes to the physician who directly monitors blood pressure and the patient's status throughout execise and recovery.The latter is ideal for testing patients for diagnostic or prognostic purposes and is a requirement for testing all patients at increased risk for an exercise-induced complication.A physician should be immediately available during all exercise tests on patients.

Patient Preparation

Preparatios for exercise testing include the following:

1.The patient should be instructed not to eat or smoke for 2 to 3 h before the test and to dress appropriately for exercise. No strenuouos physical efforts shoulb be performed for at least 12 h before testing.

2.Cessation of medications may,at times, be considered since some drugs interfer with exercise responses,complicating interpretation of execise testing. Most patients are tested on their medications. Specific questioning is important to detrmine which drugs have been taken so that the physician can be aware of possible electrolyte abnormalities and other effects.

3.A brief history and physical examination should be done to rule out contraindications to testing or to detect important clinical signs such as murmurs, gallop sounds, pulmonary bronchospasm, or rales.Patients with a history of increasing or unstable angina or uncontrolled heart failure should not be have exercise testing until their condition stabilizes.A cardiac physical examination should indicate which patients have valvular or congenital heart disease,particularly adult patients with severe aortic stenosis,who generally should not undergo exercise testing.

4.A detailed explanation of the testing procedure should be given,outlining risks and possible complications.The patient should be told how to perform the exercise test, and the testing procedure demonstrated.

5.A standard resting 12-lead ECG should be obtained since it differ from the resting pre-exercise ECG.This is essential,particulaly in patients with known heart disease,since an abnormality or a change may contraindicate testing.Recording the ECG before starting the exercise test and after hypervehtilation at another time may be helpful in detecting false positive(indeterminate)ECG changes,particularly in women.

6.Standing ECG and blood pressure should be recorded to determine vasoregulatory abnormalities, particularly ST depression.


The treadmill and the cycle ergometer remain the most commonly used dynamic exercise testing devices.

Protocols for clinical exercise testing should include an initial low load (warm-up), progressive uninterrupted exercise with an adequate duration in each level, and a recovery period.

The most popular treadmill protocol is the Bruce one.The advantages of the Bruce protocol include a seventh or final stage,which cannot be completed by most individuals, and its use in many published studies,which provides extensive data for comparison.Its disadvantages include large increments in work loads that make estimation of Vo2max less accurate.In addition, the fourth stage can be either run or walked,probably resulting in different oxygen costs.Some subjects are forced to stop prematurely because of musculoskeletal difficulties or inability to toleratethe high work load increments.Regardless of technique used,the optimum exercise testing protocol should last 6 to 12 min and should be adjusted to the type of patient being tested.

Since there is strong evidence that the level of exercise required to produce ischemia is the most important part of the exercise test result,the question arises of how the exercise test work load shall be selected.There is overwhelming agreement on use of a progressive increasing protocol beginning with a stage low enough to be tolerated by the" weakest" candidate for testing and ending with a stage sufficiently difficult to challenge "the fittest" candidate.Each stage should be long enough in duration for the subject to reach or closely approach steady state, and the the work increments from one stage to the next should be small enough topermit the desired degree of precision in estimating work capacity.The Bruce treadmill protocol is widely used(figure 187).Typical work output requirements for each stage in terms of oxygen consumption have been determined, and the range of stages is adequate both for sedendary individuals and athletes.To increase applicability, two easier stages may be added below Stage1 in order to accommodate virtually all ambulatory individuals. In order for measurements of of treadmill performance exercise time, or rate-pressure response to be directly related to the actual cardiac work involved, the subject must have reached or closely approached "steady state". This implies that if the subject continued to exercise at this intensity,cardiac output,HR,and other indices would stay essentially the same until the point of fatigue. Steady state attainment requires at least 3 min, and perhaps longer on the treadmill, and exercise times shorter than this will not yield a reliable reflection of cardiovascular capacity.

Rather than assign a certain stage of exercise protocol as a goal for an individual,it is preferable to require the sibject to exercise progressively through the protocol until it becomes excessively uncomfortable or impossible to continue,i.e.,to an end-point of exhaustion unless other terminating end-points occur. Failure to attain an exercise tachycardia reasonably close to a predicted maximum may not provide an adequate indication of the degree of effort (figure 188).


Insomecases,testing is terminated when the patient reaches 90% of predicted maximum HR for age and level of training.The designated target HR, however, may be maximal for some subjects ,beyond the limit of others, but submaximal for others. A test is considered maximal when the patient appears to give a true maximal effort(point of bodily exhaustion) or when other clinical end-points are reached.

Indications for Terminating Exercise Testing

Indications for discontinuing an exercise test include absolute and relative indications (figure 189).

Some abnormal responses occur only in recovery after exercise. For maximum sensitivity, patients should be supine in the postexercise period. Monitoring of Blood pressure and ECG should continue for at least 6 to 8min after exercise. An abnormal ECG response occurring only in the recovery period is not unusual;these responses are likely not false positive unless the occur late in recovery. Mechanicaldysfunction andelectrophysiological abnormalities in the ischemic ventricle after exercise can persist from minutes to hours.


Clinical Responses

Classic ischemic chest discomfort induced by the exercise test is strongly predictive of CAD and is even more predictive in the presence of ST depression. The patient's general appearance is also helpful.A decrease in skin temperature,cool perspiration, and peripheral cyanosis during exercise may indicate poor tissue perfusion due to inadequate cardiac output with secondary vasoconstriction, and higher work loads are not encouraged.Neurological signs such as light-headedness or vertigo can also indicate inadequate cardiac output.

Physical examination

Cardiacexamination immediately after exercise canprovide information about ventricular functio.A percordial bulge or gallop rhythm can result from left ventricular dysfunction.A mitral regurgitant murmur suggests papillary muscle dysfunction related to transient ischemia.

Exercise or Functional Capacity

The maximal oxygen consumption (V o2max) is the best index of maximal exercise capacity. A decrease in maximum cardiac output may be a consequence of CAD, and exercise may be limited by either anginal pain or an acute reduction in LV output. An increase in LV diastolic filling pressure and increasing pulmonary artery pressure will also limit exercise. A mean exercise capacity of 10 MET's has been observed in nonathletic middle-aged healthy men. If patients with CAD reach 13 MET's, their prognosis is good, regardless of other exercise test responses. As expected, patients with an exercise capacity of less than 5 MET's have a higher mortality during follow-up than patients with higher capacities.

A normal exercise capacity does not exclude severe cardiac impairment. Mechanisms proposed to explain a normal exercise performance in such patients include increased peripheral oxygen extraction, preservation of chronotropic reserve, ability to tolerate elevated pulmonary wedge pressure without dyspnea, and increased levels of plasma norepinephrine at rest and during exercise.


Blood pressure is a function of cardiac output and peripheral resistance, 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 patients at increased risk for ventricular fibrillation in the exercise laboratory.

Figure 190 illustrates normal and abnormal systolic blood pressure responses to exercise tests.

A relatively rapid HR during submaximum exercise or recovery could be due to vasoregulatory asthenia, decreased vascular volume or peripheral resistance, prolonged bed rest, anemia, or metabolic disorders and, therefore, may not reflect intrinsic cardiac disease. This finding is also relatively frequent in patients soon after myocardial infarction or coronary artery surgery. A relatively low HR at any point during submaximum exercise may due to lack of training or drugs such as beta blockers. Conditions that affect the sinus node can also attenutate the normal response of HR during exercise testing.
Figure 191 shows predicted exercise HR in normals.


ECG Responses in Subjects with Normal Resting Electrocardiograms

During exercise, the P-wave vector tends to become more vertical and the P wave magnitude increases in the inferior leads. The PR segments (intervals) shortens and slopes downward in the inferior leads. The change, which has been attributed to atrial repolarization (Ta wave), may cause false-positive or indeterminate ST depression in the inferior leads. Changes in R-wave amplitude are noted near maximum effort with a decrease in the R wave in the lateral leads (V5) at maximum exercise and 1 min into recovery. In the lateral and veritical leads (V5 and and VF), the S wave becomes greater in depth, showing a greater deflection at maximum exercise, and then gradually returning to resting values in recovery.

The J-Junction is depressed in the lateral leads at maximum exercise, then gradually returns to pre-exercise values in recovery. A dramatic increase in J-junctional depression may be observed in all leads and may be greatest at 1 min into recovery. Subjects with resting J-junction elevation may develop an isoelectric J-junction with exercise as normal finding. These changes revert in recovery. The normal ST segment vector response to both tachycardia and exercise is a shift rightward and upward in the frontal plane; however, there appears to be considerable biological variation in the degree of this shift. 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-min recovery the amplitude is equivalent to resting values in the lateral leads.

Abnormal Response

The ST-segment level is measured relative to the PR segment since the U-P segment usually is unclear during exercise. ST elevation is measured as the deviation from the base-line ST level. If the base-line ST segment is depressed, the deviation from that level to the level during exercise or recovery is measured. The point for measuring the ST level is the J-junction; points 60 to 80 ms beyond this are usually used when the ST-segment slope is horizontal or downsloping. Considering a rapidly upsloping ST depression to be abnormal increases test sensivity but decreases specificity. Various ST scores have been recommended, but none have been validated as superior to standard "visual" measurements, Exercise induced myocardial ischemia can result in one of three ST-segment changes on the surface ECG; depression, elevation, and normalization.

ST-segment depression is the most common manifestation of exercise-induced myocardial ischemia. It usually reflects diffuse subendocaridal ischemia, with vector direction determined largely by the area of ischemia and the placement of the heart in the thoracic cavity. The standard criterion for this abnormal reponse is horizontal or downsloping ST-segment depression of 0.10 mV (1.0 mm) or more for 80ms, at least, three consecutive "isoelectric" or level complexes.
As shown in figure 192, however, other criteria have been considered.

Downsloping (divergent) ST-segment depression usually reflects more ischemia than horizontal depression. In the presence of base-line abnormalities (especially in patients on digitialis), exercise-induced ST-segment depression is less specific for ischemia. Factors related to the probablity and severity of CAD included the degree, time of appearance, duration, persistence in recovery, and number of leads with ST segment depression. The lower the work load and the double product at which the ST change occurs, the worse the prognosis and the more likely the presence of multivessel CAD.

ST elevation must be judged by whether or not it occurs in the presence of Q waves from a previous myocardial infarction. ST-segment elevation is more frequently observed in anterior leads (V1 and V2) with Q waves.

Previous myocardial infarction is the most frequent cause of ST-segment elevation during exercise and seems to be related to dyskinetic areas or ventricular aneurysms. Approximately 50 percent of patients with recent anterior and 15 percent with inferior myocardial infarction exhibit this finding during exercise. Patients with elevation usually have a lower left ventricular ejection fraction (LVEF) than those without such ST-segment elevation in leads with abnormal Q waves from prior myocardial infarction. These changes may result in reciprocal ST depression simulating ischemia in other leads. The development of both ST-segment elevation and depression during the same test may indicated multivessel coronary artery disease (CAD).

In patients without previous myocardial infarction (absence of Q waves on the resting ECG), ST-segment elevation during exercise frequently reflects severe transient ischemia resulting from significant proximal CAD or spasm.

In patients with variant angina, ST-segment elevation usually occur during spontaneous anginal episodes, frequently at rest. During exercise, ST-segment elevation had been reporte in about 30 percent of these patients and a reversible thallium-201 perfusion defect usually corresponds to the site of ST elevation. Another manifestation of ischemia may be the normalization of an ST segment. ECG abnormalities at test, including T-wave inversion and ST-segment depression, may return to normal during attacks of angina and during exercise in some patients with myocardial ischemia. This can also be observed in subjects with a "persistent juvenille pattern" on the resting ECG.

The R-wave amplitude may increase during exericse in certain subjects with cardiac disease; however, exercise-induced changes in R-wave amplituded have not improved diagnostic accuracy despite use of several lead systems, clinical subsets of patients, and different criteria for an abnormal response.

In normal, a gradual decrease in T wave amplitude is observed in all leads during early exercise although the T wave begins to increase with maximum exercise. At 1-min recovery, T-wave amplitude usually returns to resting values. U-wave inversion may be associated with LV hypertrophy, CAD, and aortic and mitral regurgitation. Exercise-induced U wave inversion in patients with a normal resting ECG appears to be a maker of myocardial ischemia and suggests left anterior descending CAD. U-wave changes may, however, be diffucult to assess during exercise, which increases HR and increases the proximity of the T and P waves.

Plasma potassium increases with maximal exercise testing and increases more after training in subjects on atenolol and propanolol therapy. In addition (in sedentary individuals), both plasma potassium and magnesium increase significantly with maximal exercise, and these increase are unaffected by atenolol and propranolol blockade. To the contrary, propranolol, but not atenolol and placebo, prolongs the time of return to base line of potassium (compared to magnesium) after the acute exercise. Such changes must be considered with exercise testing because of electrolyte effects on ST, T, and U waves.

Exercise tests can be performed with radionuclide imaging to further evaluate myocardial perfusion. Echocardiographic images and Doppler flow measurements can also be made during and after exercise, and LV EF, wall motion, and valvular function can be assessed with these techniques.


Sensitivity and Specificity

The sensitivity and specificity are terms used to define how effectively a test detects disease. Sensitivity is the percentage of those with a disease who will have an abnormal test. Specificity is the percentage of those without the disease who will have a normal test. This may be affected by drugs, baseline E C G patterns, and whether a test is submaximal or maximal. Sensitivity and specificity are inversely related ;when the sensitivity is the highest, the specificity is the lowest and vice versa.

If the population studied has a greater prevalence of disease, the test will have a higher sensitivity. For instance, the exercise test has a higher sensitivity in individuals with triple vessel CAD than 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 (indeterminate) results such as women or 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. In these studies the exercise tests with 0.1 mV horizontal or down sloping ST depression has approximately 84 percent specificity for angiographically significant CAD; that is 84 percent of those without significant angiographic disease had a normal exercise test.These studies had a mean 66 percent sensitivity of exercise testing for significant angiographic CAD , with the range from 40 percent for one vessel disease to 90 percent for three- vessel disease


The two major reasons for determining prognosis are to provide reliable answers about the probable outcome of the cardiovascular illness and to identify patients in whom interventions might improve the eventual outcome.

Figure 193 lists indications for performing an exercise tests in patiens after myocardial infarction.

Exercise testing may be appropriate and expedite hospital discharge of patients recovering from a myocardial infarction. Ventricular arrhythmias not present at rest may be provoked during exercise and the patient's reaction to exercise at the time of discharge from the hospital can be assessed. An exercise test before discharge is important for providing guidelines for activity at home, reassurance of physical status, determination of risk of complications, and to provide a basis for advising the patient to resume or increase activity level and return to work.

Some investigators perform exercise tests using symptom-or sign- limited end points two to the three weeks after myocardial infarction. In many, the submaximal limited test is quite appropriate. The heart rate limit of 130 to140 beats per minute and a MET of five to seven is arbitrarily used, and a Borg perceived exertion level in the range of thirteen to fifteen can be used as an end point, particularly for patients receiving beta blockers. The maximal test is probably more appropriate three of more weeks after myocardial infarction, when the patiens is more often ready to assume full activities.

One review of numerous predischarge and postmyocardial infarction exercise tests reported a few serious complications: two cases of recurrent infarction and two cases of ventricular fibrillation, one fatal,representing 0.05% morbidity and 0.0 2% mortality. In studies of exercise testing after myocardial infarction with a follow-up for cardiac end-points, tested patients consistently had a lower risk, regardless of criteria used for testing. Of the usual general criteria, only an abnormal systolic blood pressure response or a low exercise capacity were significantly associated with poor outcome. When thestudies were subgrouped by whether testing was done before or after discharge from the hospital, a high proportion of the predischarge test results indicated poor outcome. Submaximal testing resulted in the highest proportion of positive associations and the highest risk ratios, and abnormal response at higher workloads were not as predictive as those at lower workloads.

Studies using exercise testing of the patiens with stable CAD have provided data to predict angiographic findings, cardiac events and those with silent ischemia, or improved survival with coronary artery bypass surgery(CABS) .

Exercise testing has been used to predict left main or triple vessel coronary artery disease, or both, with varying results.

Exertional Hypotension

In most studies, exercise- induced hypotension indicates a poor prognosis, and has a predictive value of up 50 percent for left main/triple vessel disease. Exercise induced hypotension can occur in patients with CAD, valvular heart disease, or cardiomyopathy. Occasionally, however, subjects without clinically significant heart disease will exhibit exercise induced hypotension during exercise related to antihypertensive therapy or prolonged strenuous exercise.

Cardiac Events in Patients with the Silent Ischemia

The prognostic implication of asymptomatic(" silent") ischemia detected during exercise testing is controversial. It has been suggested that those with silent ischemia are at greater risk of cardiac death; however, in three large studies of patients with a high prevalence of CAD who underwent exercise testing, those with ST-segment depression, with or without angina during testing,had similar prognoses. Ischemia is asymptomatic in approximately 60 percent of patients with CAD and ischemic ST-segment depression and silent ischemia occurring with treadmill testing does not appear to confer an increased risk for death relative to patients experiencing angina with signs of ischemia.

Figure 194 itemizes exercise testing findings associated with a poor prognosis in patients with CAD

and figure 195 shows data from eight studies in the prediction of cardiac events.

In patients with CAD, exercise-induced ventricular arrhythmias are not an independent risk factor for subsequent mortality or coronary events.Some studies, however ,suggests that these arrhythmias may add independent prognostic information to thallium-201, ST-segment, and heart rate changes and are associated with severe CAD and wall motion abnormalities. In selected subjects with CAD, exercise testing may be of considerable value in the evaluation of drug therapy of ventricular arrhythmias.

One study suggests that patients with multi- vessel CAD, cardiomegaly, exercise capacity of less than 5 METS,or a maximum systolic blood pressure of less than 130 mmHG.do better with surgery.In another trial,patients who had an exercise test response of 1.5 mm of ST-segment depression or claudication.In another study. the benefit of surgery was greatest in patients with 1 mm ST-segment depression at less than 5 METS.

In several studies that evaluated graft occlusion and reoccurrence of symptoms, exercise- induced ST depression did not predict prognosis after coronary artery bypass surgery. An exercise capacity of nine mets or more, however, indicates a good prognosis, regardless of other responses.

Exercise testing may be of value in the routine( six to twelve month) follow up with patients who have undergone percutaneous coronary angioplasty, especially in evaluation of chest discomfort and detection of restenosis. Testing is ofparticular benefit in patients in cardiac rehabilitation programs. It may be especially helpful in the patient with symptoms suggested of ischemia or the patient whose progress in rehabilitation is limited.

There is substantial support for the use of exercise testing as the first noninvasive procedure after the history, physical examination, and resting ECG in the prognostic evaluation of patients with coronary artery disease. Exercise testing accomplishes both purposes of prognostic testing by providing information about the patient's clinical status and in helping provide recommendations for proper management. Exercise testing also helps select patients who should undergo further evaluation such as radionuclear studies and coronary angiography. Since the exercise test can be performed as an outpatient patient procedure and provides valuable information about activity levels, response to therapy,and disability , it is a reasonable first choice for prognostic assessment. Because of its widespread availability ,the exercise test can have an enormous impact on cost- effectiveness delivery of cardiovascular care. The exercise test is not usually recommended for screening apparently healthy persons without risk factors since it has a high rate of false positive results.


Exercise testing has been used in patients with a valvular heart disease to evaluate exercise- induced symptoms to quantitative disability, and to evaluate the response to medical and surgical therapy. It has also been used to identify a concurrent coronary artery disease; however, there is a high prevalence of false positive responses because of frequently seen baseline ECG abnormalities and left ventricular hypertrophy .

In selected patients with valvular heart disease exercise, testing may be useful to determine when surgery indicated .Effort syncope in patients with aortic stenosis is an important symptom. Most guidelines for exercise testing list moderate to severe aortic stenosis as a contrindication for testing because of concerns about syncope. and cardiac arrest. Therefore, exercise testing of patients with the aortic stenosis should be restricted to patients with mild to moderate gradients. Four proposed mechanisms for exercise- induced syncope in patients with the aortic stenosis include carotid hypersensitivity, left ventricular failure,arrhythmias, and left ventricular Baroreceptor stimulation. Exercise testing ,however, is relatively safe in both the pediatric and adult patient with mild to moderate aorticstenosis when performed very carefully and with experienced supervision. Attention should focus on the patient's symptoms, minute by minute response of blood pressure, slowing heart rate, and both ventricular and atrial arrhythmias.In the presence of an abnormal blood pressure response, the patient with a aortic stenosis should take at least a two minute cool- down walk at a lower stage of exertion to avoid acute left ventricular volume overload, which may occur when the patient assumes the supine position

Patients with aortic regurgitation usually maintain a normal exercise capacity for a longer period of time than those with the aortic stenosis, as volume workload of the myocardial requires less oxygen and pressure work. During exercise, there is a decrease in the diastolic duration and regurgitant volume and a decrease in vascular peripheral resistance, favoring forward output. As the myocardium fails,both the left ventricular ejection fraction and stroke volume decrease with an increase in both end-diastolic and and end-systolic ventricular diameter. Exercise testing is usable for monitoring selected patients with aortic regurgitation, using the appearance of the ST- segment depression, a reduction in heart rate response to each workload ,and a decrease in Vo2 max as markers for decreasing left ventricular function.

Patients with mitral stenosis may have either a normal or excessive increase in heart rate during exercise. As stroke volume cannot be increased, the usual increase in cardiac output is less and may eventually fall during exercise, frequently accompanied by exercise- induced hypotension. The increase in heart rate and right ventricular pressure results in an increase in right ventricular myocardial oxygen demand. In patients with mitral stenosis chest discomfort and ST- segment depression during exercise may occur either due to coronary artery disease or secondary to pulmonary hypertension.ST depression during exercise is attributed both to a decrease incoronary perfusion secondary to tachycardia and a fall in cardiac output and to an increase in myocardial oxygen demand secondary to right ventricular overload. The shortening of diastole associated with tachycardia and the increase in pulmonary blood flow associated with exercise increase left atrial pressureand may cause pulmonary congestion.

Patients with mild to moderate mitral regurgitation maintain normal cardiac output during exercise. Blood pressure, heart rate, and ECG responses are usually also normal. When transient mitral regurgitation occurs suddenly during exercise as a result of ischemic papillary muscle dysfunction, however, a flat response in systolic pressure can occur. Patients with severe mitrall regurgitation usually have decreased cardiac output and limited exercise capacity. ST-segment depression during exercise is infrequent in these patients; however, a hypotensive response can develop, and arrhythmias arefrequent.

Several mechanisms have been suggested to explain the ST depression noted in some patients with mitral valve prolapse including regional ischemia of the papillary muscle, coronary artery disease, compression of the anterior descending artery, coronary spasm, and primary cardiomyopathy.ECG ST changes can be normalized by propranolol or other nonselective beta blockers, improving the specificity of the exercise test.

An exercise test is often used to evaluate the safety of an exercise training program and to formulate an exercise prescription. In general, an exercise test is useful for a sedentary individual who at the age of 40 decides to enter an exercise program of a higher intensity than walking at 50 to 60 percent of maximum heart rate reserve. Testing should also be done in younger individuals with coronary risk factors or a strong family history of coronary artery disease. It is preferable to determine an individual's maximum heart rate rather than give a predicted value for maximal heart rate to be attained during training, because of the wide scatter of maximum heart rate when plotted against age An exercise test can be used in adult exercise or cardiac rehabilitation programs to safely advance an individual to a higher intensity. An improvement in exercise capacity on an exercise test can also be an effective incentive to continue the program and to encourage risk factor modification.

Exercise testing is used to determine the degree of impairment and disability of patients with various forms of heart disease. Patients who "exaggerate" their symptoms who have a psychological impairment can often be identified.Vo2max is the best none invasive measurement of exercise capacity of the cardiovascular system. Inability to reach five METS without symptoms or signs is a criteria of disability used by the social security administration. The determination of the patient's exercise capacity affords an objective measurement of the degree of cardiac impairment

The results of exercise testing do not add significantly to the risk stratification provided by the resting the ECG in patients without known coronary artery disease or candidates for major elective noncardiac surgery. Therefore, exercise testing is not routinely recommended before elective noncardiac surgery under general anesthesia.The efficacy of angioplasty or surgery for peripheral vascular disease can be assessed by exercise testing.

Fletcher,G.F.,M.D. and Schlant,R.C.,The Exercise Test,Hurst's The Heart,8th Edition,P.423-440.


Beta Blockers

Maximun heart rateand systolic blood pressure product during exercise may be reduced by beta blockers. Patients with angina who receive beta blockers may have a greater exercise capacity with less ST-segment depression and less ischemia if the drug prevent their reaching the ischemic rate product.In some patients, however, angina disappears, but the ST depression occurs if th e ischemic product can still be reached.


Vasodilators can increase exercise capacity in patients with angina or heart failure, or both. To date, however, there's no good data that long acting nitrates increase exercise capacity in patients with angina when they are tested after chronic administration.

Angiotensin converting enzyme inhibitors

Angiotensin converting enzyme inhibitors decrease the blood pressure both at rest and duringI exercise and can increase exercise capacity in patients with chronic heart failure.

Calcium Antagonists

Calcium antagonists have multiple hemodynamic effects.. They can delay time to ischemia,improve exercise capacity, delay ST-segment depression until higher work loads.Heart rate and systolic blood pressure are decreased for a given level ofexercise.


ST-segment depression can be induced or accentuated during exercise in individuals are taking digitalis, including normalsubjects and patients with CAD.Profound ST-segment depression(Greater than2mm more) compared to baseline usually indicates ischemia, even in patients who are taking digitalis.The exercise induced ST-segment depression related to digitalis has been said to persist for 2 or more weeks after digoxin is discontinued.

Other drugs

Quinidine can cause prolongation of phase 2 of the ventricular action potential, decreasing the repolarization gradient during the ST segment and thus decreasing the magnitude of the ST depression. A decrease of twenty beats per minute in maximum exercise heart rate has been reported in patients taking amiodarone .Amiodarone also increases duration of QRScomplex during exercise. Diuretics can cause hypokalemia,producing muscle fqtigue ventricular ectopy ,and rarely ST segment depression with exercise.

Fletcher,G.F.,M.D. and Schlant,R.C.,The Exercise Test,Hurst's The Heart,8th Edition,P.423-440.


A relatively low heart rate at any point during submaximal exercise may be due to lack of training or drugs such as beta blockers.

Conditions that affect the sinus node can also attenuate the normal response of heart rate during exercise.First-degree atrioventricular(AV)block occasionally occurs at end of exercise or during recovery phase.Medications or conditions that may produce prolonged AV conduction time (e.digitalis, propanolol, myocarditis) may also predispose the individual to lengthing of the PR interval. Second degreeAV block-Wenckeback(Mobitz 1) during exercise is rare.Mobitz type-2 AV block has been seen in patients with CAD.

Exercise may induce cardiac arrhythmias under several conditions,especially diuretic and digitalis therapy.The recent ingestion of alcohol or caffeine may also exacerbate exercise-induce arrhythmias.CAD(coronary artery disease) can predispose some patients to arrhythmias during exercise.

Ecotopic ventricular beats(PVC's) are the most frequent typed cardiac arrhythmia that develop during exercise, followed by supraventricular arrhythmias.Their prevalence is directly related to age and cardiac abnormalities.In general,ectopic ventricular contractions are of concern in patients with a family history of cardiomyopathy, valvular heart disease or known severe ischemia.

Sinus arrhythmias with periods of sinus bradycardia and a wandering atrial pacemaker are relatively common during exercise and the immediate recovery phase.Atrial ectopy can occur in normal or diseased hearts.Exercise-induced transient atrila fibrillation and flutter occur in less than1% of individuals who undergo exercise testing.These arrhythmias may be induced by exercise in both healthy individuls and patients with rheumatic heart disease, hyperthyroidism,WPW syndrome,or cardiomyopahty.Exercise induced supraventricular arrhythmias alone are usually not related to CAD, but are more often related to pulmonary disease ,recent alcohol ingestion, or excessive caffeine.

Fletcher,G.F.,M.D. and Schlant,R.C.,The Exercise Test,Hurst's The Heart,8th Edition,P.423-440.

Blood Pressure Response

Systolic blood pressure should rise with increasing treadmill workload, whereas diastolic blood pressure usually remains about the same (Fig.181 ). A rising diastolic blood pressure can be associated with coronary heart disease: however, it ismore likely a marker for labile hypertension, which leads to coronary disease. A drop in systolic blood pressure below preexercise values is the most ominous criterion, whereas a drop of 20 mmHg or more without a fall below preexercise values appears to have less predictive value. Exercise-induced hypoten-sion (EIH) can be due to either left ventricular dysfunction (as reflected by myocardial infarction status), ischemia, or outflow obstruction. When EIH occurs without association with either of these two factors, EIH appears to be benign.
The highest systolic blood pressure should be achieved at maximal workload. When exercise is stopped, approximately 10 percent of people tested will abruptly drop their systolic blood pressure owing to peripheral pooling. To avoid fainting, patients should not be left standing on the treadmill. The systolic blood pressure usually normalizes on resuming the supine position during recovery but may remain below normal for several hours after the test. Irving et al. examined variations in clinical noninvasive systolic pressure at the point of symptom-limited exercise on a treadmill. Lower maximal systolic pressures often were associated with two- or three-vessel disease or reduced ejection fraction or both. The annual rate of sudden cardiac death decreased from 98 per 1000 men to 25 and 7 per 1000 men as the range of maximal systolic pressure increased from less than 140 to 140 to 199 to 200 mmHg or more, respectively.
The 3-min systolic blood pressure ratio is a useful and readily obtainable measure that can be applied in all patients who are undergoing exercise testing for the evaluation of known or suspected ischemic heart disease . The ratio is calculated by dividing the systolic blood pressure 3 min into the recovery phase of a treadmill exercise test by the systolic blood pressure at peak exercise. A 3-min systolic blood pressure ratio greater than 0.90 is considered abnormal. Higher values for the ratio are associated with more extensive coronary artery disease, as well as an adverse prognosis after myocardial infarction.