A cardiac stress test assesses a heart's response to stress and can help diagnose coronary artery disease. Dr. Arun Vasireddy's seminar discussed the types and indications for stress testing, including exercise tests and pharmacological tests. Stress tests evaluate coronary blood flow, cardiac function, and the development of ischemia through changes in EKG readings, imaging, and symptoms. Interpreting stress test results involves analyzing changes in heart rate, blood pressure, perfusion imaging, wall motion, and other metrics during rest and stress conditions. Stress echocardiography and myocardial perfusion imaging are important non-invasive tests to evaluate cardiac function and identify ischemic areas of the heart muscle.

1. CARDIAC STRESSTEST
Presenter: Dr.ArunVasireddy
18th January 2016
SEMINAR

2. INTRODUCTION
■ A cardiac stress test helps measure a heart's ability to respond to
external stress in a controlled clinical environment.
■ Aim is to assess the Coronary flow system, Perfusion & Cardiac function.
■ Stress response is induced by drugs or exercise under clinical supervision

3. Types of Stress testing
■ EXERCISE
a. Isotonic or Dynamic exercise
b. Isometric or Static exercise
c. Combined exercise
■ PHARMACOLOGICAL
a. Adenosine
b. Dipyridamole
c. Dobutamine
d. Isoproterenol

4. Indications for Non-Invasive Cardiac
StressTesting
I. Diagnosis of Obstructive Coronary Artery Disease
II. Risk Assessment and Prognosis in Patients with Symptoms or a
Prior History of Coronary Artery Disease
III. Post MI Risk Assessment and Prognosis
IV. Special Groups
Asymptomatic Patients
Post Revascularization Patients
Rhythm Disorders
Women

5. EXERCISE PHYSIOLOGY
– Adaptation to the increasing intensity of exercise by increasing the
metabolic rate by 20 times the BMR.
– Increase in CO from 5 lt/min to 25 lt/min
– Increased Heart rate
– Increased SBP (maintained Diastolic)
– Fall in Peripheral vascular resistance

6. METABOLIC EQUIVALENTS
1 MET Resting
2 METs Level walking at 2 mph
4 METs Level walking at 4 mph
<5 METs Poor prognosis; peak cost of basic activities of daily living
10 METs Prognosis with medical therapy as good as coronary artery
bypass surgery; unlikely to exhibit significant nuclear perfusion
defect
13 METs Excellent prognosis regardless of other exercise responses
18 METs Elite endurance athletes
20 METs World-class athletes
MET, metabolic equivalent, or a unit of sitting resting oxygen uptake; 1 MET = 3.5 mL/kg/min oxygen uptake

7. ACUTE CARDIOPULMONARY RESPONSETO
EXERCISE
 Active muscles receive blood supply appropriate to their metabolic needs.
 Heat generated by the muscles is dissipated.
 Blood supply to the brain and heart is maintained.
■ This response requires a major redistribution of cardiac output along with a number of local
metabolic changes.
■ Thus, the limits of the cardiopulmonary system are defined by Total body oxygen consumption
(VO2max), which can be expressed by the Fick principle.
VO2max = maximal cardiac output × maximal arteriovenous oxygen difference

8. The cardiopulmonary limits (VO2max) are defined by the following:
• A central component (cardiac output) describes the capacity of the heart
to function as a pump.
• Peripheral factors (arteriovenous oxygen difference) describe the capacity
of the lung to oxygenate the blood delivered to it as well as the capacity of
the working muscle to extract this oxygen from the blood.

9. Central determinants of maximal oxygen
uptake
■ Heart Rate:
- First response by sympathetic and parasympathetic nervous system
- Vagal withdrawal is responsible for the initial 10 to 30 beats/ min change,
later largely caused by increased sympathetic outflow.
- Heart rate increases linearly with workload and oxygen uptake.
■ Heart rate response to exercise is influenced by age, type of activity, body position,
fitness, the presence of heart disease, medication use, blood volume, and
environment.
■ Of these, the most important factor is age; a significant decline in maximal heart
rate occurs with increasing age.

10. ■ Stroke Volume:
– product of stroke volume (the volume of blood ejected per heartbeat) and
heart rate determines cardiac output.
– It is equal to the difference between end-diastolic and end-systolic volume.
Thus, a greater diastolic filling (preload) will increase stroke volume.
– During exercise, stroke volume increases up to approximately 50% to 60% of
maximal exercise capacity, after which increased cardiac output is caused by
further increase in heart rate.

11. ■ End-Systolic Volume:
– depends on two factors: contractility and afterload.
– Contractility describes the force of the heart’s contraction. (ejection fraction)
– Increasing contractility reduces end-systolic volume, which results in a greater stroke
volume and thus greater cardiac output.
– Afterload is a measure of the force resisting the ejection of blood by the heart.
Increased afterload results in a reduced ejection fraction and increased end-diastolic
and end-systolic volumes.
– During dynamic exercise, the force resisting ejection in the periphery is reduced by
vasodilation, owing to the effect of local metabolites on the skeletal muscle vasculature.
Thus, despite even a five-fold increase in cardiac output among normal subjects during
exercise, mean arterial pressure increases only moderately.

12. PERIPHERAL FACTORS

13. AUTONOMIC CONTROL
NEURAL CONTROL MECHANISMS
■ Central command — neural impulses, arising from the central nervous system,
recruit motor units, excite medullary and spinal neuronal circuits, and cause the
cardiovascular changes during exercise.
■ Muscle afferents — muscle contraction stimulates afferent endings within the
skeletal muscle, which in turn reflexively evoke the cardiovascular changes.
■ Exercise pressor reflex, comprises all of the cardiovascular changes reflexly
induced from contracting skeletal muscle that cause changes in the efferent
sympathetic and parasympathetic outputs to the cardiovascular system that
are in turn responsible for increases in arterial blood pressure, heart rate,
myocardial contractility, cardiac output, and blood flow distribution.

14. GUIDELINES FOR PROPER SELECTION OF
PATIENTS
• Pretest Probability of Coronary Artery Disease by Symptoms, Gender, and Age

15. METHODOLOGY OF EXERCISETESTING
■ Commonly used is Dynamic/isotonic Exercise – defined as rhythmic
muscular activity resulting in movement, initiates a more appropriate
increase in cardiac output and oxygen exchange.
■ Involves greater muscle mass - Higher level of O2 uptake.
■ Bruce Protocol is commonly used.

16. Patient Assessment for Exercise
Testing
History
■ Medical diagnoses and past medical history—a variety of diagnoses should be reviewed, including
CVD, arrhythmias, syncope, or presyncope; pulmonary disease, including asthma, emphysema, and
bronchitis or recent pulmonary embolism; cerebrovascular disease, including stroke; PAD; current
pregnancy; musculoskeletal, neuromuscular, and joint disease
■ Symptoms—angina; chest, jaw, or arm discomfort; shortness of breath; palpitations, especially if
associated with physical activity, eating a large meal, emotional upset, or exposure to cold
■ Risk factors for atherosclerotic disease—hypertension, diabetes, obesity, dyslipidemia, smoking; if
the patient is without known CAD, determine the pretest probability of CAD
■ Recent illness, hospitalization, or surgical procedure
■ Medication dose and schedule
■ Ability to perform physical activity

17. Physical Examination
■ Pulse rate and regularity
■ Resting blood pressure while sitting and standing
■ Auscultation of the lungs, with speci c attention to uniformity
of breath sounds in all areas, particularly in patients with
shortness of breath or a history of heart failure or pulmonary
disease
■ Auscultation of the heart, particularly in patients with heart
failure or valvular disease
■ Examination related to orthopedic, neurologic, or other
medical
■ conditions that might limit exercise

18. Bruce Protocol

19. Hemodynamics during exercise

21. Contraindications to ExerciseTesting

22. Indications forTerminating Exercise
Testing
■ Drop in systolic blood pressure (SBP) despite an increase in workload
■ Moderate-to-severe angina
■ Increasing neurological symptoms (eg, ataxia, dizziness, near-syncope)
■ Signs of poor perfusion (cyanosis or pallor)
■ Subject’s desire to stop
■ Sustained ventricular tachycardia
■ ST elevation (> 1 mm) in leads (other than V 1 or aVR)

23. Safety and risks in exercise testing
■ Nonselected patient population: Mortality < 0.01%
■ Within 4 weeks of MI:
Mortality = 0.03% and
Morbidity = 0.09% (reinfarction, cardiac arrest)

24. Decreased
Myocardial
Perfusion
resulting in the
onset of Ischemia
Regional
Wall Motion
Changes
ST Segment
Changes
Development of
Angina
Start
Exercise
Timeline of Events During Exercise Stress
Time
The Ischemic Cascade

25. ECG INTERPRETATION

28. Duke’sTreadmill Score & prognostic Normogram
DUKE SCORE = 5 x ST seg deviation – (4 xTreadmill angina Index)

29. Advantages of the Standard Exercise EKG Stress Test
• Low Cost, Availability, Acceptability, Convenience
• Exercise tolerance determined
• Provides independent prognostic information
• Correlate symptoms with activity
• Assess rhythm, rate, BP, response to activity
Disadvantages of the Standard Exercise EKG Stress Test
• Limited Sensitivity and Specificity
• Does not localize ischemia
• No Estimate of LV Function
• Requires Cooperation and Ability to Walk

30. Pharmacological StressTesting
■ Planned only after ETT, is a diagnostic procedure in which cardiovascular stress
induced by pharmacologic agents is demonstrated in patients with decreased
functional capacity or in patients who cannot exercise.
■ Pharmacologic stress testing is used in combination with imaging modalities such
as radionuclide imaging and echocardiography.
■ Adenosine, dipyridamole, and dobutamine are the most widely available
pharmacologic agents for stress testing.
■ Regadenoson, an adenosine analog, has a longer half-life than adenosine, and
therefore a bolus versus continuous administration.

31. General indications:
■ Elderly patients with decreased functional capacity and possible CAD
■ Patients with chronic debilitation and possible CAD
■ Younger patients with functional impairment due to injury, arthritis, orthopedic problems,
peripheral neuropathy, myopathies, or peripheral vascular disease, in which a maximal heart rate is
not easily achieved with routine exercise stress testing, usually because of an early onset of fatigue
due to musculoskeletal, neurologic, or vascular problems rather than cardiac ischemia
■ Other cases, including patients taking beta-blockers or other negative chronotropic agents that
would inhibit the ability to achieve an adequate heart response to exercise
■ Patients with LBBB or ventricular pacemaker should undergo pharmacologic vasodilator stress
because exercise stress often produces a false-positive perfusion defect in the interventricular
septum.

32. Adenosine
■ Adenosine is a naturally occurring substance found throughout the body in various tissues. It
functions to regulate blood flow in many vascular beds, including the myocardium.
■ Dose - 0.14 mg/kg/min IV for 6 minutes (total cumulative dose of 0.84 mg/kg).
■ Direct coronary artery vasodilation induced by adenosine is attenuated in diseased coronary
arteries, which have a reduced coronary flow reserve and cannot further dilate in response to
adenosine.
■ In cases of severe vessel stenosis or total occlusions with compensatory collateral circulation, a
decrease in coronary blood flow may occur in the diseased coronary artery, thus inducing ischemia
via a coronary steal phenomenon.
■ This regional flow abnormality also induces a perfusion defect during radionuclide imaging.

33. ContraIndications for using cardiac
Vasodilators
■ active bronchospasm
■ Patients with more than first-degree heart block (without a ventricular-demand pacemaker)
■ Patients with an SBP less than 90 mm Hg
■ Patients using dipyridamole or methylxanthines (eg, caffeine and aminophylline)

34. Dipyridamole
■ Dipyridamole is an indirect coronary vasodilator that works by increasing intravascular adenosine
levels.
■ This occurs by the inhibition of intracellular reuptake and deamination of adenosine.
■ However, the increase in coronary blood flow induced by dipyridamole is less predictable than that of
adenosine.
■ Dose - Infused at a rate of 0.142 mg/kg/min IV for 4 minutes (not to exceed a cumulative dose of 0.57
mg/kg).
■ Contraindicated in Pts with active bronchospasm, more than first-degree heart block, SBP less than 90
mm Hg, using dipyridamole or methylxanthines

35. Dobutamine
■ Dobutamine is a synthetic catecholamine, which directly stimulates both beta-1 and beta-2 receptors.
■ A dose-related increase in heart rate, blood pressure, and myocardial contractility occurs.
■ As with physical exertion, dobutamine increases regional myocardial blood flow based on physiological
principles of coronary flow reserve.
■ A similar dose-related increase in subepicardial and subendocardial blood flow occurs within vascular
beds supplied by significantly stenosed arteries, with most of the increase occurring within the
subepicardium rather than the subendocardium.Thus, perfusion abnormalities are induced by the
development of regional myocardial ischemia.
■ Contraindicated in Patients with recent (1 wk) MI; unstable angina; significant aortic stenosis or
obstructive cardiomyopathy; atrial tachyarrhythmias with uncontrolled ventricular response; history of
ventricular tachycardia, uncontrolled HTN, or thoracic aortic aneurysm; or LBBB

36. Enoximone stress echocardiography
■ Dobutamine may sometimes induce ischemia in patients with a critical coronary stenosis,
which might mask hibernation by preventing the improvement in wall motion.
■ Another approach is the use of an imidazole phosphodiesterase inhibitor such as enoximone or
milrinone, drugs that are relatively unaffected by concurrent use of a beta-blocker and are used
for inotropic support in congestive heart failure.
■ Enoximone stress echocardiography as an additional stress testing modality was evaluated in
one study of 45 patients with chronic coronary artery disease and left ventricular dysfunction
who underwent echocardiography with both dobutamine and enoximone.
■ Both increased heart rate, but enoximone did not cause a significant change in systolic blood
pressure.The positive predictive value and specificity were similar between enoximone and
dobutamine.

37. STRESS ECHOCARDIOGRAPHY
■ 2D Echo imaging before, during and after cardiovascular stress
■ Cost effective means to assess CP
■ Stress  ETT, Bicycle ergometer, Dobut
■ Compare wall motion at rest to stress can identify inducible ischemic
dysfx and assign a specific coronary territory
■ Sensitivity~88% (74-97): Specificity~84% (62-93%)

38. Stress Echocardiography
Advantages
Comprehensive – Ischemia,
EF, Valvular function
Widely available
Relatively low cost
Disadvantages
Limited by echocardiographic
windows and body habitus
Highly technician dependent
Steep technician learning
curve
Interpreting physician
dependent

39. FACTORS AFFECTING STRESS
ECHOCARDIOGRAPHY
False Negatives False Positives
■ Inadequate stress
■ Antianginal therapy
■ Left Circumflex disease
■ Poor image quality
■ Delayed image acquisition
■ Interpreter bias (“over-call”)
■ Basal InferiorWall location
■ Abnormal septal motion due to
LBBB, Paced Rhythm, post
CABG
■ Cardiomyopathy
■ Hypertensive response to stress

40. Myocardial Perfusion Imaging
Cardiac ScinitgraphyTechniques utilised:
1) SPECT
2) PET
■ a radiotracer (Tc-99 mibi, thallium-201 or 99Tc-Tetrofosmin) is injected
■ scans are acquired with a gamma camera to capture images of the blood
flow.
■ Usually done on two separate days OR between 3-4 hrs:
1. After rest
2. After injection of stress stimulating drugs

41. MPI : SPECT Perfusion
■ Injected isotope extracted by viable myocytes
■ Photons emitted from myocardium in proportion to uptake, which is
related to perfusion
■ Gamma camera captures gamma photons and converts to digital data
representing magnitude and location of uptake
■ Single Photon Emission ComputedTomography SPECT images: Myocardial
perfusion images (MPI) represent distribution of perfusion throughout
myocardium

42. SPECTTOMOGRAPHIC DISPLAY SHORT AXIS

43. SPECTTOMOGRAPHIC DISPLAYVERTICAL LONGAXIS

44. SPECTTOMOGRAPHIC DISPLAY HORIZONTAL LONG
AXIS

45. CORONARY BLOOD FLOW RESERVE ABNORMALITIES

46. MPI SPECT REVERSIBLE DEFECTS: ANTETERIOR AND APICAL

47. MPI STRESSTEST REPORTING
■ Normal
■ Fixed defect  implies Myocardial Infarction
■ Reversible defect  implies obstructive CAD/ischemia
■ Mixed defect  implies “partial thickness infarct” with ischemia in
remaining, viable myocardium

48. Myocardial Perfusion Imaging
Advantages
Applicable to almost all patients
Incremental value - prognosis,
guidance to therapy
Assessment of LV function
Disadvantages
Detects coronary
heterogeneity as a surrogate
for ischemia
Relatively Expensive
Artifacts
Isotope availability
Radiation exposure

49. Echocardiographic vs. Scinitigraphic Methods for the Detection of Occlusive
Coronary Artery Disease
SUMMARY
• Both techniques have comparable sensitivity and sensitivity
• Echocardiography is highly dependent on technician expertise
• Echocardiography is less costly
• Scintigraphy can be applied to almost all patients

50. PROGNOSIS
Provides useful Info on prognosis for
■ Pts with CAD who suffered a cardiac event or have underwent cardiac intervention
■ Patients with valvular heart disease
■ Pts with CHF
■ Adverse prognosis:
– Duration of symptom limited exercise of <5 METs
– Poor chronotropic heart response
– Failure of SBP rise above 120mmhg or persistent BP fall >10 mmHG during exercise
– Exercise induced ST elevation
– Clinical angina at low workloads
– Sustained VT during stress test

51. THANKYOU
REFERENCES:
• BRAUNWALD’S HEART DISEASE 10TH ED
• APITEXTBOOK OF MEDICINE 10TH ED
• AHA JOURNALS