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NEHI/CMC Cardiology > Exercise Stress Testing > Flashcards

Exercise Stress Testing Flashcards

1
Q

What is the formula for max HR during stress testing?

A

220-age

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2
Q

What occurs during the initial stage of exercise?

A

increased ventricular HR, SV, and CO d/t vagal withdrawal and SNS stimulation Epi and Norepi release increases ventricular contractility at peak exertion Alveolar ventilation and venous return increase due to vasoconstriction

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3
Q

What happens physiologically during exercise progression?

A

Increased skeletal muscle blood flow Increased oxygen extraction Decreased peripheral resistance SBP, MAP, and PP usually increase DBP remains unchanged or may increase or decrease by approx 10 mmHg

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4
Q

What is defined as an inadequate SBP during exercise? What conditions cause this?

A

Inadequate rise in SBP is <20-30 mmHg or drop in SBP Results from aortic outflow obstruction, severe LV dysfunction, myocardial ischemia, BB’s

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5
Q

What occurs physiologically in the late phase of exercise?

A

Increased cardiac output due to primarily increased ventricular HR

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6
Q

What occurs physiologically during the post exercise phase?

A

Hemodynamics return to baseline within 6 minutes and often remain lower than pre-exercise for several hours, abrupt termination of exercise may cause precipitous drop in SBP d/t venous pooling and delayed immediate increase in SVR to match reduction in CO

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7
Q

What HR indicates a good result in a stress test?

A

80% max HR = good result, 90% max HR = excellent result

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8
Q

What is age-predicted max HR used to estimate?

A

The adequacy of stress to evoke inducible ischemia

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9
Q

What is a MET?

A

Metabolic equivalent, referring to the resting volume of oxygen consumption per minute for 70 kg, 40 y/o man

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10
Q

What does one MET equal?

A

VO2 3.5 mL/min/kg

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11
Q

What does a mean exercise capacity = 5 indicate?

A

high mortality risk

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12
Q

What is the double product?

A

Estimate of myocardial oxygen uptake during clinical exercise testing Calculated using HR x SBP Also known as a rate pressure product 10th percentile - 25000 90th percentile - 40000

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13
Q

What is Bruce protocol?

A

3- minute periods to allow achievement of steady state before workload is increased in an exercise stress test.

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14
Q

What is a modified Bruce protocol?

A

Two 3 minute warm up stages at 1.7 mph and 0% grade and 1.7 and 5% grade (used in older individuals or those who’s exercise capacity is limited by cardiac disease)

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15
Q

What is a stress test indicated for the evaluation of?

A

CP Prognosis and severity of CV disease Eval of therapy Screening for latent coronary disease Early detection of labile HTN Evaluation of CHF Evaluation of arrhythmia Pre-participation examination for sports Eval of congenital heart disease Stimulus to motivate change in lifestyle

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16
Q

What are the absolute CI of exercise stress testing?

A

AMI within 2 days, high-risk UA, uncontrolled arrhythmia, sx HF, acute PE or pulmonary infarct, acute myocarditis or pericarditis, acute aortic dissection, severe anemia, acute illness/infection, hyperthyroidism, symptomatic severe AS (moderate to severe defined as valve area between 0.5-1.5 cm2 and a mean gradient of 18-64mmHg)

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17
Q

What are the relative contraindications of exercise stress test?

A

LM coronary stenosis, moderate stenotic valvular heart disease, electrolyte abnormality, severe arterial hypertension (SBP >200, DBP >110), tachyarrhythmia or bradyarrhythmia, hypertrophic cardiomyopathy or other form of outflow obstruction, mental or physical impairment, high-degree AV block, CHD, severe ST-segment depression in at-rest “ischemia”

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18
Q

What is specific to HF patients undergoing cardiac stress testing?

A

ETT adds significant clinical info, impaired exercise capacity is a high prognostic indicator

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19
Q

What is specific to patients with hypertension in cardiac stress testing?

A

Exaggerated BP response is predictive of future HTN and potentially predictive of future mortality secondary to MI; associated with angiographic CAD

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20
Q

Why does a person with dilated cardiomyopathy need stress testing?

A

Determine exercise capacity, assess pulmonary response to LV dysfunction, determine grace of VE, evaluated effectiveness of treatment; often in this situation SV and CO cannot continue to meet exercise demands

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21
Q

Why would you stress test a person with HOCM?

A

It is not ideal to stress test someone with HOCM, can cause sudden death secondary to arrhythmia; may have CP, abnormal resting ECG, and exercise induced ST depressions are frequent; however ETT may be specially helpful to demonstrate the level at which significant events occur

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22
Q

What instructions does a patient receive in preparation for a stress test?

A

No eating or smoking 3 hours prior Water is fine Dress to exercise No unusual physical efforts for at least 12 hours prior to testing

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23
Q

What medication should you consider removing prior to stress testing?

A

Beta blocker - will attenuate exercise responses and limit test interpretation *potential for rebound tachycardia in pts with recent ACS

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24
Q

What should you be aware of when reviewing a patient’s daily medications prior to a stress test?

A

Potential for electrolyte abnormalities, hemodynamic effects

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25
Q

Why should the patient only grip the bar of the treadmill lightly?

A

It reduces workload and supports body weight when gripped tightly

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26
Q

Why is perceived exertion important?

A

It is generally a sound indication of relative fatigue which helps clinicians judge the degree of fatigue using the Borg scale

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27
Q

Why do patients not do a cool down period?

A

Cool down periods can eliminate the appearance of ST segment depression

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28
Q

What is an indication of a positive stress test?

A

J-point and ST80 depression of 1mV/1mm or more and/or ST segment slope within +/- 1mV/s in 3 consecutive beats

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29
Q

What is defined as an inadequate rise in SBP?

A

<20-30 mmHg or a drop Typically caused by aortic outflow obstruction, severe LV dysfunction, MI, or beta blockers

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30
Q

What is exercise induced hypotension indicative of?

A

In conjunction with other indicators of ischemia it is a poor prognostic indicator with 50% PPV of LM or triple vessel disease Also indicative of serious arrhythmias in patients with CAD, valvular HD, cardiomyopathy Can also occur in dehydration, patients on antihypertensives, or prolonged strenuous exercise

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31
Q

What are some reasons for tachycardia during submaximal exercise or recovery?

A

Deconditioning, prolonged bed rest, anemia, metabolic disorders, or any other cause of decreased vascular volume or peripheral resistance

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32
Q

What are the reasons for a low heart rate during submaximal exercise?

A

Exercise training, enhanced SV, drugs (beta blockers)

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33
Q

Define chronotropic incompetence

A

Failure to achieve 85% of age-predicted max HR or a low chronotropic index (HR adjusted to MET level), associated with increased mortality risk in pts with known CVD

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34
Q

What are the absolute indications for terminating an exercise stress test?

A

Drop in SBP >10mmHg when accompanied by other evidence of ischemia Moderate to severe angina Increasing nervous system symptoms (ataxia, dizziness, near syncope) Signs of poor perfusion (cyanosis, pallor) Technical difficulties in monitoring ECG or SBP Pt wants to stop Sustained VT ST elevation >/= 1 mm in leads without diagnostic q waves other than V1 or aVR

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35
Q

What are the relative indications for terminating an exercise stress test?

A

Drop in SBP >/= 10 mmHg from baseline with absence of other evidence of ischemia ST or QRS changes such as excessive ST depression (>2mm of horizontal or downsloping ST segment depression or marked axis shift Arrhythmias other than sustained VT Fatigue, SOB, wheezing, leg cramps, or claudication Development of BBB or IVCD that cannot be distinguished from VT Increasing CP Hypertensive response (SBP >250 mmHg and/or DBP >115 mmHg) Decreased skin temp, light perspiration, peripheral cyanosis (may indicate poor tissue perfusion due to inadequate CO with secondary vasoconstriction)

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36
Q

What parameters can be used to diagnose an ECG from exercise stress testing in a patient with baseline ST segment depression?

A

2mm additional ST segment depression or downsloping depression of 1mm or more in recovery (dx of CAD)

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37
Q

Why is Digoxin a confounder in stress ECG interpretation?

A

Produces ST segment response to exercise in 25-40% of healthy patients Directly related to age Requires two weeks off med to alleviate repolarization pattern

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38
Q

Why is LVH a stress ECG confounder?

A

If repolarization abnormalities are present it decreases specificity

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39
Q

What about LBBB makes it an stress ECG confounder?

A

Causes exercise induced ST-segment depression and is unrelated to ischemia, even up to 1 cm (therefore no level of ST depression that is diagnostic) *must do nuclear imaging without exercise* Rate dependent blocks typically precede chronic blocks that occur at rest LBBB occurring at a HR <125 bpm in pts with typical angina is frequently associated with CAD LBBB occurring at a HR >125 bpm occurrs more frequently in pts with normal coronary arteries Presence of intraventricular blocks at rest that disappear during exercise are rare

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40
Q

Why are RBBB confounders of stress ECG interpretation?

A

Exercise induced ST depression usually occurs with RBBB in anterior chest leads (V1-3) and is not associated with ischemia In L chest leads (V5-6) or inferior leads (II, aVF), test characteristics are similar to those of a normal resting ECG

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41
Q

What are the the potential changes seen in exaggerated atrial repolarization during a stress ECG?

A

Downsloping ST-segment depression in the absence of ischemia High peak exercise HR Absence of exercise-induced chest pain Markedly downsloping PR segments in inferior leads

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42
Q

Why is beta blocker therapy a confounder in stress ECG interpretation?

A

Inadequate HR response, sudden discontinuation may cause rebound effect leading to accelerated angina and HTN

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43
Q

Why are nitrates a confounder in stress ECG interpretation?

A

Can attenuate angina and ST depression associated with myocardial ischemia

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44
Q

Why is flecainide a stress ECG confounder?

A

Associated with exercise-induced VT

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45
Q

What changes does a torso placement of ECG leads cause?

A

Shifts axis to the R Increased voltage in inferior leads Disappearance of Q waves

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46
Q

True or false: electrode placement affects ST segment slope and amplitude?

A

True

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47
Q

Which leads have the highest diagnostic value?

A

Lateral precordial leads (V4-6) are capable of detecting 90% of all ST depression observed in multiple leads and are by themselves reliable markers for CAD Lead II has a high false-positive rate Inferior leads are of little value in identifying CAD during stress tests

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48
Q

What are the ideal diagnostic properties in abnormal ST segment changes in a stress ECG?

A

ST level measured relative to P-Q junction 3 consecutive beats in the same lead with stable baseline Measure at 60-80 ms after the J point (60 ms optimal with upsloping ST segment) HR >130

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49
Q

What is the most common ECG manifestation of ischemia?

A

ECG depression Downsloping > horizontal at predicting CAD; both more predictive than upsloping, but if slowly upsloping with a slope <1mV there is increased probability of CAD Positive: ST depression horizontal or downsloping >/= 1 mV for 60-80 ms

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50
Q

What is significant ST segment elevation?

A

>1mV elevation from baseline 60ms after the J point for three consecutive beats

51
Q

What is significant about ST-elevation without Q waves?

A

Only occurs in 1/1000 patients Indicator of proximal disease or vasospasm Higher risk for ventricular arrhythmias

52
Q

What is significant about ST elevation vs ST depression?

A

ST elevation localizes ischemia

53
Q

Where will ST elevation be seen in LAD blockage?

A

V2-4

54
Q

When ST depression is seen in the lateral leads which coronaries are blocked?

A

L Cx and diagonals

55
Q

Which coronary artery is blocked if ST elevation is seen in leads II, III, and aVF?

A

RCA

56
Q

If a person’s baseline ECG has Q waves suggestive of an old MI, why is ST segment elevation controversial?

A

Post MI ST elevation during exercise secondary to wall motion abnormalities - will have ST elevation in Q wave leads If accompanying ST depression is present it may indicate a second area of ischemia or reciprocal changes and may be indicative of multivessel CAD *imaging required*

57
Q

What is significant about ST elevation in patients with active variant angina (>2 spontaneous episodes/week)?

A

30% have exercise induced ST elevation induced by coronary vasospasm Ventricular arrhythmias are more frequent

58
Q

What are the causes of ST elevation?

A

Infarction (if persists >3 months, suggests ventricular aneurysm) Vasospastic angina Pericarditis Early repolarization Acute myocarditis Hyperkalemia Acute cor pulmonale IHSS Cerebrovascular hemorrhage Cardiac tumor, cardiac sarcoidosis Hypothermia

59
Q

What are the causes of ST depression?

A

Ischemia: ST depression is transient, downsloping or horizontal NonSTEMI Reciprocal changes Severe HTN Severe AS Cardiomyopathy Anemia Hypokalemia Severe hypoxia Digitalis: scooped appearance, <1 mm, seen in multiple leads Sudden excessive exercise Glucose load LVH Hyperventilation MVP Intraventricular conduction delay Preexcitation syndrome (WPW) Severe volume over load (aortic or mitral regurg) SVTs Use of TCAs

60
Q

What is the significance of early repolarization?

A

In an asymptomatic patient it is benign: elevation of the J point/”fishhook” deformity, ST elevation upward and concave in precordial leads and leads with the tallest R waves, reciprocal ST depression in aVR, tall/peaked/slightly asymmetrical T waves with notch and slur on R wave, vertical axis, shorter/depressed PR interval, abrupt transition, counterclockwise rotation, presence of U waves, sinus bradycardia Increased in males <50 May normalize with exercise

61
Q

What may occur at the sinus node in patients with severe ischemic heart disease?

A

Sinus arrest immediately after exercise (rare)

62
Q

What happens to the PR segment during exercise?

A

Shortens by as much as 0.10-0.11 s and slopes downward in inferior leads - potential for false positive ST depression in inferior leads

63
Q

Which medications and conditions predispose a patient to a first degree AV block post exercise?

A

Digoxin, propranolol, verapamil, myocarditis

64
Q

What happens to the QRS complex during exercise?

A

Q wave becomes slightly more negative at max exercise Increase in R wave amplitude during submaximal exercise with decline at max exercise Sharp decrease in R wave observed in lateral leads at max exercise and into first minute of recovery S wave more negative in lateral and vertical leads J point depressed in lateral leads to max depression at max exercise, gradually returns to preexercise values in recovery - j pt depression more common in elderly patients Resting J point elevation (early repolarization may develop an isoelectric J junction with exercise = normal finding

65
Q

what are the causes of poor R wave progression?

A

LVH, RVH Pulmonary disease (COPD, chronic asthma): RAD, RAA, persistent precordial S waves LBBB, LAH, IVCD Cardiomyopathy Chest wall deformity Normal variant Lead misplacement

66
Q

What happens to the T wave during exercise?

A

Gradual decrease in T wave amplitude in all leads during early exercise At max exercise, T wave begins to increase At 1 minute recovery, amplitude is equivalent to resting values in lateral leads Morphology is influenced by body position, respiration, hyperventilation, drug therapy, ischemia/necrosis Low risk pt = normalization of inverted T waves with exercise (non dx)

67
Q

What happens to the U wave during exercise?

A

Difficult to identify with a HR >130 U wave inversion is associated with LVH, CAD, AR, MR: abnormal LV distensibility Exercise-induced U wave inversion is a marker for ischemia and suggests LAD CAD

68
Q

What is the effect of exercise on pre-excitation syndromes?

A

Provoke, abolish, or no effect on anomalous AV conduction in patients with WPW When exercise does not interfere with preexisting anomalous AV conduction, significant ST depression can be observed during exercise ST depression may not be due to ischemia but may be a false-positive occurrence Low prevalence of tachyarrhythmias during or after exercise in WPW patients

69
Q

What do the Q waves look like in a normal ECG?

A

Small and narrow septal q waves: lateral leads (I, aVL, V4-6) Moderate to large Q waves and/or T wave inversion: III, aVF, aVL, aVR, V1

70
Q

What do normal T waves look like on a resting ECG?

A

Isolated T wave inversion in leads III, aVF, or aVL most likely not ischemia when QRS is also negative in these leads T wave abnormality alone is not diagnostic of any particular condition, except for hyperkalemia

71
Q

What type of T waves are characteristic of LVH, LBBB, chronic pericarditis, or electrolyte abnormality?

A

T wave inversion

72
Q

What do T waves look like in hyperkalemia?

A

Tall, peaked T waves seen throughout ECG, small P waves, PR interval short

73
Q

What are tall peaked T waves seen only in specific sets of leads indicative of?

A

Impending infarction, secondary to potassium leak

74
Q

T wave inversion can occur during MI and persist for months, true or false?

A

True

75
Q

What might flat T waves be indicative of?

A

Ischemia, cardiac scarring, evolving infarction, hypokalemia, or nonspecific

76
Q

Describe an ECG consistent with pericarditis.

A

Widespread ST elevation that is concave and upward, unrelated to coronary artery distribution PR depression in all leads except aVR and V1 where PR segment elevation will be seen Stage I: diffuse ST elevation, may last up to two weeks, absence of reciprocal changes, no T wave inversion, ST depression in aVR, V1 Stage II: return of ST segments to baseline, flattening of T wave; may last days to several weeks Stage III: inversion of T waves in opposite direction of ST segment at end of second or third week Stage IV: gradual resolution of T wave changes, may last up to 3 months No Q waves Normal R wave progression Possible low voltage Arrhythmias uncommon

77
Q

Describe an ECG in which evidence of LVH is present.

A

Deepest S wave in V1 or V2 + tallest R wave in V5 or V6 >/= 35 mm and/or R wave in aVL >/= 12 mm LV strain: asymptomatic ST depression and T wave inversion in at least one lead: I, aVL, V4-6 LAA: m-shaped (notched) and widened P wave (>/= 0.12 sec) in I, II, aVL; deep negative component to P in V1 Additional Voltage Criteria: R >/= 20 in any inferior lead deep S >/= 20-25 in V1 or V2 R >/= 25 in V5 R >/= 20 V6

78
Q

Describe the appearance of an ECG showing RVH.

A

RAD or indeterminant axis RAA: peaked, pointed P waves in inferior leads incomplete RBBB Low voltage, especially if emphysema present Persistent precordial S waves Strain Tall R in V1

79
Q

What are four reasons exercise may induce arrhythmia?

A

Diuretic therapy Digitalis therapy Recent ingestion of alcohol or caffeine may exacerbate arrhythmias Myocardial ischemia

80
Q

What is the physiology behind arrhythmia generation during exercise?

A

Enhanced sympathetic tone, increased MVO2, or both Immediate post exercise phase is more dangerous due to circulating catecholamine levels and generalized vasodilation

81
Q

Why do some arrhythmias disappear with exercise?

A

Ectopy overridden by sinus tach secondary to vagal withdrawal and increased sympathetic stimulation

82
Q

What are the most common arrhythmias during exercise in order of appearance?

A

Ventricular, supraventricular, fusion Prevalence is directly related to age and cardiac abnormalities Concerning in pts with FHx of SCD or personal history of cardiomyopathy, valvular HD, or severe myocardial ischemia

83
Q

What kind of arrhythmia is fairly common during the early stage of exercise and immediate recovery?

A

Sinus arrhythmia with periods of sinus bradycardia and wandering atrial pacemaker

84
Q

Are PAC’s diagnostic of heart disease?

A

No, they can occur in normal hearts as well as diseased hearts

85
Q

In what percentage of patients does exercise induced AF and flutter occur?

A

<1% May be healthy or rheumatic HD, hyperthyroidism, WPW, or cardiomyopathy

86
Q

What is the incidence of paroxysmal junctional tachycardia?

A

Rare

87
Q

What are exercise induced supraventricular arrhythmias typically due to?

A

Old age, pulmonary disease, recent alcohol ingestion, excessive caffeine intake, occasionally CAD

88
Q

What might one find on physical exam immediately post exercise in someone with LV dysfunction?

A

Gallop, precordial bulge new MR murmur suggests papillary muscle dysfunction and may be related to transitory myocardial ischemia Preferable to have patient lie supine for exam, but allow those who develop orthopnea to sit up Severe angina or ominous arrhythmias after exercise may be lessened by allowing pt to sit up, bc ischemia may be decreased due to lower LV wall tension

89
Q

What responses are typical of myocardial ischemia during exercise stress testing?Q

A

angina, ST depression, ST elevation in leads without Q waves

90
Q

What responses are likely secondary to ischemia or LV dysfunction in exercise stress testing?

A

Chronotropic incompetence, decreased SBP, poor exercise capacity *better recognized by hx of HF or by PE (confirm by echo or imaging)

91
Q

Why would you stress test someone post MI?

A

Risk stratification and assessment of prognosis Predictors of adverse outcome: ST depression > 1mm (esp at low level of exercise or in presence of compensated HF), functional capacity < 5 METs, inadequate BP response (peak SBP < 110 mmHg or < 30 mmHg rise from resting level) Assessment of adequacy of therapy and need for other diagnostic or treatment options (pts taking BB post MI should continue taking at the time of exercise)

92
Q

How do you assess the prognosis of someone with chronic ischemic HD via exercise stress test?

A

Excellent exercise tolerance: good prognosis regardless of anatomical extent of CAD Low mortality risk if > 7 METs with normal exercise ECG and no chest discomfort High mortality risk if pt has both angina and significant ST depression at low level of exercise

93
Q

What is the prognosis of a patient with silent myocardial ischemia during stress testing?

A

Greater risk for SCD d/t lack of intact warning system Ischemia is silent in ~60% of pts with ischemic ST depression

94
Q

What are the guidelines for ETT post CABG?

A

> 5 years post = greater diagnostic and prognostic utility Ischemic response more likely indicates graft occlusion, stenosis, or CAD progression in native circulation

95
Q

What are are the statistics for restenosis post PTCA?

A

Occurs in ~20-40% of patients, usually within 6 months More common in patients with DM, proximal LAD disease, or suboptimal post-PTCA (suboptimal angiographic result, impaired coronary vascular reserve in successfully dilated vessel, incomplete revascularization) Predictive value of exercise ECG to detect restenosis early after PTCA is suboptimal Serial conversion of initially normal ETT to abnormal test 6 months post PTCA, particularly at lower level exercise workloads, is usually associated with restenosis

96
Q

Are exercise-induced arrhythmias an independent risk factor for mortality or coronary events?

A

No

97
Q

What are the reasons for performing stress testing in valvular HD?

A

Quantify disability Reproduce exercise-induced symptoms Evaluate responses to medical and surgical interventions Identify concurrent CAD (high prevalence of false-positive responses: ST depression not due to ischemia, baseline ECG abnormalities in LVH) Determine when surgery is indicated on basis or a reduction in final functional capacity or abnormal hemodynamic response

98
Q

What are the mechanisms for exercise induced syncope in AS?

A

Carotid hyperactivity LV failure Arrhythmia LV baroreceptor stimulation

99
Q

What should you do in the setting of AS with abnormal BP response during ETT?

A

2 minute cool down walk at a lower stage of exertion to avoid LV volume overload

100
Q

What symptoms should be focused on when performing ETT on a patient with AS?

A

Sx BP response Slowing HR Ventricular and atrial arrhythmias

101
Q

What is a typical ETT result in a patient with AR?

A

Normal exercise capacity until severe Decreases in diastolic duration and regurgitation volume favor forward output As myocardium fails, HR tends to slow, and EF and SV decrease

102
Q

What is a typical ETT result in a patient with MS?

A

Normal or excessive increase in HR during exercise SV cannot be increased Normal rise of CO is attenuated and may eventually fall during exercise, accompanied by exercise-induced hypotension

103
Q

What is the typical result of an ETT in a patient with MR?

A

Mild to moderate MR maintains normal CO during exercise BP, HR, and ECG responses normal If MR occurs suddenly during exercise as a result of ischemic papillary muscle dysfunction - a flat response in SBP can occur Severe MR: pts do not necessarily have decreased CO and limited exercise capacity - hypotensive result can develop and arrhythmias frequently occur

104
Q

What is the criteria for disability in terms of METs as put forth by social security?

A

5 METs without signs or symptoms

105
Q

What is the age related decline in max HR?

A

~1 bpm/yr d/t decreased beta adrenergic response (major contributor to reduction in aerobic capcity)

106
Q

What happens to SBP response with age?

A

Increased response to maximal aerobic exercise (more pronounced in women)

107
Q

What happens to LV function during strenuous exercise with age?

A

Blunted increase/less complete emptying

108
Q

What work-up is necessary in an ED patient to exclude ACS prior to exercise stress testing?

A

2 sets of cardiac enzymes at 4 hour intervals that are normal ECG at time of presentation and pre-exercise show no significant changes Rest ECG has no abnormalities that preclude accurate assessment of exercise ECG patient is asymptomatic or has minimal atypical CP from admission to time results are available from second set of enzymes

109
Q

What is the sensitivity and specificity of ETT?

A

61-73% sensitive (percentage of pts with disease who will have an abnormal test), 59-81% specific (percentage of pts without disease who will have a normal test)

110
Q

What type of patients have have a high false positive rate?

A

Premenopausal women

111
Q

Define chronotropic incompetency?

A

HR < 120 not d/t drugs

112
Q

What indicates a positive ETT?

A

Strong positive > 2.5 mm ST depression, >1 mm elevation in leads without Q waves Chronotropic incompetence High risk patients have ischemic changes in recovery >2mm lasting >6 minutes in multiple leads

113
Q

What are the markers of exercise capacity?

A

Maximal exercise duration Maximal MET level achieved Maximum workload achieved Maximum HR HR-BP product

114
Q

In what time frame should you attempt to perform stress testing on a patient if they have symptoms of UA?

A

Low-risk out patient: within 72 hours Low or intermediate risk inpatient: unless cath is indicated when free of sx or active HF for a minimum of 8-12 hours, after 2-3 days, maybe earlier

115
Q

When performing ETT post MI what should be the predetermined end points?

A

HR of 120 bpm or 70% predicted max HR or peak MET level of 5 at 4-7 days post (submaximal) Sx limited at 14-21 days post if no predischarge ETT performed Sx limited at approx 3-6 weeks if early ETT was submaximal Perform prior to discharge in pts who have undergone cardiac cath if coronary lesion of borderline severity Perform in pts with complete LBBB, preexcitation syndrome, LVH, digoxin therapy, > 1mm resting ST depression, V paced rhythm Periodic monitoring in pts who continue to participate in exercise training or cardiac rehab

116
Q

What are the indications for performing ETT in asx pts?

A

DM pts with plans to start a vigorous exercise regimen Pts with multiple risk factors: cholesterol >240, SBP >140, DBP >90, smoking, DM, FHX of MI or SCD in first degree relative younger than 60 Eval of men >45 and women >55: who plan to begin vigorous exercise, involved in occupations in which impairment might impact public safety, those at high risk of CAD d/t other disease

117
Q

What are you looking for during the echo portion of an ETT?

A

Wall motion abnormality (increases the sensitivity and specificity)

118
Q

What are the limitations of echo in ETT?

A

Technical quality of images (COPD and obesity) Timing of aquisition of images Learning curve Operator dependent Reproducibility

119
Q

What percentages of CAD probability determine the need for ischemic evaluation in women?

A

Low probability (<20%): no test d/t high probability of false positive Intermediate probability (20-80%): perfusion imaging or stress echo High risk (>80%): perfusion imaging or stress echo; consider direct angiography

120
Q

What is one reason women have higher incidence of false positives on ETT?

A

Greater catecholamine release leading to coronary vasoconstriction and test result augmentation

121
Q

What anatomical factor results in higher incidence of false positives in women in thallium and technesium 99 tests in women?

A

Breast shadow

122
Q

What are the indications for pharmacologic stress echo?

A

Unable to exercise Simultaneous eval of ischemia and myocardial viability Preoperative risk assessment in major surgery Inability to achieve target HR during exercise bc of beta-blocker or CCB

123
Q

What are the indications for myocardial perfusion imaging?

A

Suspected false +/- ETT Resting ST changes LBBB, RBBB, LVH, digitalis, WPW, pacemaker Elderly pts with decreased functional capacity and possible CAD Pts with chronic debilitation and possible CAD Women with +ETT and low or intermediate probability CAD Inability to exercise Pts taking bb or other negative chronotropic agents Prognosis of known CAD Detecting post PCI or CABG ischemia Assessing myocardial viability Risk evaluation in noncardiac surgery patients Assessment of functional significance of documented coronary stenosis

NEHI/CMC Cardiology (6 decks)

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