To detect presence of myocardial infarction secondary to CAD To predict the prognosis
TMT Exercising muscles need energy to contract and relax. Energy is derived from oxidative metabolism to generate ATP. Energy requirement at rest or active state can be estimated from measurement of TOTAL BODY O2 UPTAKE = Vo2
TMT Fick equation demonstrates that Vo2 = CO x Perip . O2 extractn (A-V o2difference) Vo2 expressed in multiples of resting o2 requirements ( Metabolic equivalents METs ) 1 MET = basal resting energy expenditure = 3.5mL o2 / kg body wt / mt
Eg . 5 MET activity requires 5 times the energy required at rest. Vo2 max = peak o2 uptake achieved during highest level of exercise . Dep on age, sex, heridity , exercise habits, cvs status
During exercise, CO increases 4-6 times the resting levels HR- 2to 3 fold increase. SV plateaus at 50-60% of vo2 max O2 extraction at periphery can increase 3 fold Max A-V o2 difference has a physiologic limit 15-17mlo2 / 100ml blood
Vo2 Peak During tmt , pts are prompted to exercise not until they reach vo2 max but rather to the vo2 that is attained during symptom limited , maximum tolerated exercise – this level is termed as vo2 peak
Myocardial ischemia = demand supply mismatch of o2 blood Many factors influence this delicate balance TMT is performed to stress these relationships and observe the physiologic responses To assess the devolepment of ischemia And to evaluate at what level of myocardial o2 demand and physical activity ( work rate ) ischaemia occurs.
Myocardial Oxygen Demand Indirectly measured as the Double Product or rate pressure product “Double Product” = HR x SBP Reliable index of myocardial o2 demand Increases to more than 20,000 on exercise
Isometric (Static) -weight-lifting -pressure work for heart, limited cardiac output Isotonic (Dynamic) -walking, running, swimming, cycling -Flow work for heart - ↑CO,↓ TPR Mixed
Isotonic exercise(cardiac output) Early phase- SV+HR Late phase-HR
Post Exercise Vagal reactivation ↑in well trained athletes Blunted in CCF
ENERGY REQ ACTIVITY 1 MET TAKING CARE OF SELF WALKING INDOORS WALK AT 2-3 mph 4 METS LIGHT WORK AROUND THE HOUSE WALKING AT 3-4 mph >4-<10 METS CLIMB 1 FLIGHT OF STAIRS/UP HILL WALK>4 mph, SHORT RUNNING SCRUBBING FLOOR,MOVING FURNITURE >10 METS RUNNING> 6-7 mph HEAVY LABOUR SWIMMING,FOOTBALL
Calculation of METs on the Treadmill METs = Speed x [0.1 + (Grade x 1.8)] + 3.5 3.5 Calculated automatically by Device
Patient Assessment Withhold cardiac medications on the day of study to better assess ischemic response If taking medications , to evaluate the effects on HR, BP, Symptoms and ischemia during exercise If ICD ; Peak HR < 10 beats/min below the programmed heart rate threshold for antitachycardia pacing & defibrillation
Contraindications to Exercise Testing Absolute A/c MI (< 2 d) High-risk unstable angina Uncontrolled cardiac arrhythmias causing symptoms with hemodynamic compromise Symptomatic severe AS Decompensated heart failure Acute pulmonary embolus or infarction A/c myocarditis or pericarditis Physical disability
Contraindications to Exercise Testing Relative LMCA stenosis Mod- AS + symptoms CHB Tachyarrhythmias with FVR HOCM with sev . Resting gradient Mental or physical impairment leading to inability to exercise adequately
Rate of major complications (MI/ hospitaliation ) <1-5 per 10,000 tests Recent MI, low EF, exertion induced myocard ischemia & serious ventric . Arrythmias = Highest risk Death < 0.5 per 10,000 tests
Pretest Probability Based on the pat's h/o ( age, gender, chest pain ), phy ex and initial testing, and the clinician's experience. Typical or definite angina →pretest probability high
The Bruce protocol 1949 by Robert A. Bruce, considered the “father of exercise physiology”. Published as a standardized protocol in 1963. gold-standard for detection of myocardial ischemia when risk stratification is necessary.
Normal Response to Stress Testing Heart rate increases Blood pressure increases Cardiac output increases Total peripheral resistance decreases Dysrhythmias – isolated unifocal PVC’s and PAC’s (suppressed at increased heart rate) Oxygen consumption increases
Exercise capacity Strong predictor of mortality & Non fatal cardiovascular outcome in both men & women with or without CAD Predicted METS = 18-(0.15x age) Predicted METS = 14.7- (0.13x age)
MHR HR max = 220 – age HR max = 208 – (0.7 x age) HR max = 206 – (0.88 x age) HR max = 164 – (0.7 x age)
Abnormal Response to Stress Testing Heart rate fails to rise above 120 or unable to attain THR of 85% of max SBP shows a drop Physically unable to complete test Marked hypertension, > 260/115 Chest Pain and/or unusual shortness of breath
Chronotropic incompetence inability of the heart to increase its rate to meet the demand placed on it Independent predictor of mortality < 85 % of age predicted MHR = incomplete study Chronotopic index [(HR max- HR rest )x 100 ]/[(220-age)- HR rest] < 80 % = CI <62 % = CI (B blocker)
HR recovery < 12beats / min after 1 min with post exercise cool down < 18 beats / min after 1 min with complete cessation of movement < 45 beats / min after 2 min. Associated with increase in mortality indepently , in both asymptomatic and in ppl with established heart disease
Exaggerated systolic pressure response > 210 mm hg ; > 190 mm hg Not an indication to terminate the test May indicate future development of hypertension or adverse cardiac events
Excercise induced hypotension Systolic pressure during exercise < resting pressure 20 mm hg fall in BP after an initial rise Reason to terminate the test More predictive of poor prognosis & multiple vessel CAD Cardiomyopathy, LVOT obstruction, hypovolumia , hypertensive medications
Low systolic peak Rise in BP to 140mm hg Overall rise less than 10 mm hg Severe CAD Worse cardiovascular outcome in persons with and without CAD
Normal Response of ECG to Stress Testing ECG Changes QRS complex ↓ in size PR,QRS,QT shorten J point ↓ , resulting in up sloping of ST segment ST segment returns to baseline by 80 milliseconds PR segment may down slope( Inf leads– baseline PQ junction) R amplitude may decr at rates > 130 P ampl ↑ T wave decreases
The Electrocardiographic Response
1 = Iso-electric 2 = J point 3 = J + 80 msec The Exercise ECG
ST 60 -- HR > 130/min ST 80 -- HR ≤ 130/min
ST-Segment Changes on the Exercise ECG ST DEPRESSION: Measurements made on 3 consecutive ECG complexes ST level is measured rel to the P-Q junction When J-point is depressed rel to P-Q junction at baseline : Net diff from the rest J junction - amount of deviation When the J-point is ↑ rel to P-Q junction at baseline and becomes ↓ isoel with exercise : Mag of ST dep - P-Q junction and not the resting J point
Abnormal and Borderline ST-Segment Depression ABNORMAL: 1.0 mm or > horizontal or downsloping ST dep at 80 msec after J point on 3 consecutive ECG complexes BORDERLINE: 0.5 to 1.0 mm horizontal or downsloping ST dep at 80 msec after J point on 3 consecutive ECG complexes 1.5 mm or > upsloping ST dep at 80 msec after J point on 3 consecutive ECG complexes
ECG changes during stress test
Normal Rapid Upsloping Minor ST Depression Slow Upsloping
ECG Patterns Indicative of Myocardial Ischaemia ECG Patterns Not Indicative of Myocardial Ischaemia
In lead V4 , the exercise ECG result is abnormal early in the test, reaching 0.3 mV (3 mm) of horizontal ST segment depression at the end of exercise. severe ischemic response.
The J point at peak exertion is depressed 2.5 mm, the ST segment slope is 1.5 mV/sec, and the ST segment level at 80 msec after the J point is depressed 1.6 mm. “ slow upsloping ” ST segment at peak exercise indicates an ischemic pattern in patients with a high coronary disease prevalence pretest. 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.
abnormal at 9:30 minutes ES test and resolves in the immediate recovery phase. 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.
LEAD aVR 1mm or greater ST elevation – significant predictor of LMCA, Proximal LAD or multivessel CAD As an isolated marker, high sensitivity, moderate specificity & high – ve predictive value
CHANGES IN QRS Exercise induced BBB are rare < 0.5% or less If EI LBBB occurs @ HR > 125, CAD is unlikely IF EI LBBB occurs @ lower heart rates => death & major cardiac events EI RBBB no risk