Cardiac Stress Testing Seminar

A treadmill exercise stress test is used to determine the effects of exercise on the heart. Exercise allows doctors to detect abnormal heart rhythms (arrhythmias) and diagnose the presence or absence of coronary artery disease.

This test involves walking in place on a treadmill while monitoring the electrical activity of your heart. Throughout the test, the speed and incline of the treadmill increase. The results show how well your heart responds to the stress of different levels of exercise.

Description
A technologist will explain the test to you, take a brief medical history, and answer any questions you may have. Your blood pressure, heart rate, and electrocardiogram (ECG) will be monitored before, during, and after the test.
You will be asked to sign a consent form. This form is required before the test can proceed.
You will be asked to remove all upper body clothing, and to put on a gown with the opening to the front.
Adhesive electrodes will be put onto your chest to capture an ECG. The sites where the electrodes are placed will be cleaned with alcohol and shaved if necessary. A mild abrasion may also be used to ensure a good quality ECG recording.
Your resting blood pressure, heart rate, and ECG will be recorded.
You will be asked to walk on a treadmill. The walk starts off slowly, then the speed and incline increases at set times. It is very important that you walk as long as possible because the test is effort-dependent.
You will be monitored throughout the test. If a problem occurs, the technologist will stop the test right away. It is very important for you to tell the technologist if you experience any symptoms, such as chest pain, dizziness, unusual shortness of breath, or extreme fatigue.
Following the test, you will be asked to lie down. Your blood pressure, heart rate, and ECG will be monitored for three to five minutes after exercise.
The data will be reviewed by a cardiologist after the test is completed. A report will be sent to the doctor(s) involved in your care.

1. Cardiac Stress Test Presenter: Dr.Arun Vasireddy 18 th 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 Isotonic or Dynamic exercise Isometric or Static exercise Combined exercise PHARMACOLOGICAL Adenosine Dipyridamole Dobutamine Isoproterenol

4. Indications for Non-Invasive Cardiac Stress Testing 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 RESPONSE TO 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 . H eart 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 EXERCISE TESTING 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

20. Contraindications to Exercise Testing

21. Indications for Terminating 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 )

22. 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)

23. 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

24. ECG INTERPRETATION

25. Duke’s Treadmill Score & prognostic Normogram DUKE SCORE = 5 x ST seg deviation – (4 x Treadmill angina Index)

26. 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

27. Pharmacological Stress Testing 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.

28. 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.

29. 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). D irect 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.

30. 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)

31. 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

32. 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

33. Enoximone stress echocardiography D obutamine 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 .

34. 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%)

35. 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

36. 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 Inferior Wall location Abnormal septal motion due to LBBB, Paced Rhythm, post CABG Cardiomyopathy Hypertensive response to stress

37. Myocardial Perfusion Imaging Cardiac Scinitgraphy Techniques utilised : SPECT 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 : After rest After injection of stress stimulating drugs

38. 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 Computed Tomography SPECT images: Myocardial perfusion images (MPI) represent distribution of perfusion throughout myocardium

39. SPECT TOMOGRAPHIC DISPLAY SHORT AXIS

40. SPECT TOMOGRAPHIC DISPLAY VERTICAL LONG AXIS

41. SPECT TOMOGRAPHIC DISPLAY HORIZONTAL LONG AXIS

42. CORONARY BLOOD FLOW RESERVE ABNORMALITIES

43. MPI SPECT REVERSIBLE DEFECTS: ANTETERIOR AND APICAL

44. MPI STRESS TEST 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

45. 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

46. 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

47. 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

48. CARDIAC STRESS Testing Suggested Approach Dx CAD Certain? Risk Prognosis Uncertain ? Assess Rx, Exercise, or disability? Contraindications to Stress? Can Patient Exercise Is Resting EKG Suitable for detecting Ischemia? Do EKG Stress Test High Risk CAD ? Dx Certain? Consider Angiography Pharmacologic Imaging LBBB ? Consider Angiography/Revascularization Consider imaging study or angiography Y Y N N N Y N N Continue/Initiate/Modify Plan N Y Y Y N N Continue/Initiate/Modify Plan N Adenosine SPECT MPI with Exercise Y Adenosine SPECT MPI

49. THANK YOU REFERENCES: BRAUNWALD’S HEART DISEASE 10 TH ED API TEXTBOOK OF MEDICINE 10TH ED AHA JOURNALS