24 Stress Echocardiography Flashcards

1
Q

What are the indications for stress echo?

A

Diagnosis of suspected CAD, risk assessment for known CAD, identification of viable myocardium before revascularisation, localisation of myocardial ischaemia (identification of culprit before revascularisation) and assessment of myocardial perfusion following revascularisation.

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2
Q

What are the contraindications for stress echo?

A

The 72 hours following ACS, known LM disease, HF with symptoms at rest, lethal arrhythmias, severe LVOT obstruction, severe systemic hypertension (SBP >220mmHg or DBP >120mmHg), recent PE, thrombophlebitis or DVT, hypokalaemia and/or active endocarditis, myocarditis or pericarditis. There are other contraindications for atropine and vasodilators.

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3
Q

What are the stress echo principles?

A

If the oxygen demand is greater than the oxygen supply, myocardial ischemia occurs. Stress echo identifies RWMAs and areas of abnormal LV function during rest and/or stress.

In patients with severe CAD, myocardial ischemia is not induced at rest because the arterioles downstream of the stenosis dilate to increase maintain blood and oxygen supply. However, myocardial ischemia is induced with stress because increased oxygen demand is greater than the ability of the arterioles to dilate and therefore the oxygen supply. Therefore, patients with severe CAD show normal myocardial perfusion and myocardial function at rest but show myocardial ischemia and RWMAs with stress.

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4
Q

Describe the stress echo protocol?

A

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5
Q

What are the 3 stressors used in stress echo?

A

Exercise, dobutamine and vasodilators.

Exercise and dobutamine induced myocardial stress by increasing myocardial oxygen demand. Vasodilators cause cause dilatation of normal coronary arteries, but not dilatation of abnormal coronary arteries.

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6
Q

What are the 4 responses to stress echo?

A

A normal response is indicated by normal contractility (normokinesis) at rest and normal or increased contractility (hyperkinesis) with stress.

An ischaemic response is indicated by normokinesis at rest but decreased (hypokinetic), absent (akinetic) or paradoxical (dyskinetic) contractility with stress. Normally, an ischemic response is due to CAD.

A necrotic response is indicated by abnormal contractility (hypokinesis or akinesis) at rest and with stress. Normally, this is due to a scarred myocardium due to myocardial infarction.

A viability response is indicated by abnormal contractility (hypokinesis or akinesis) at rest but an improved response with stress.

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7
Q

How is myocardial viability assessed with stress echo?

A

Administer dobutamine and assess myocardial function at low and high stress levels to assess myocardial viability.

A viability response is indicated by abnormal contractility (hypokinesis or akinesis) at rest but an improved response with stress.

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8
Q

How are myocardial stunning and myocardial hibernation differentiated?

A

Myocardial stunning and myocardial ischemia are reversible but stunning requires time whilst hibernation requires revascularisation.

If the myocardium is stunned, the improvement in myocardial contractility will be maintained throughout the stress. A stunned myocardium shows a temporary decrease in myocardial contractility which improves with time. This is due to acute ischemia followed by reperfusion (e.g. angina or heart attack).

If the myocardium is hibernating, the improvement in myocardial contractility is present at low levels of stress but absent at high levels of stress (biphasic response). A hibernating myocardium shows a permanent decrease in myocardial contractility will not improve spontaneously but will improve with revascularisation. Myocardial hibernation protects the heart by decreasing myocardial contractility, and therefore myocardial oxygen demand. This is due to chronic ischemia.

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9
Q

How is the WMSI and calculated?

A

Calculate the WMSI by adding the individual wall motion scores and dividing by the number of segments scored. If all the LV segments are normokinetic, the WMSI is 1, but, if there are abnormal LV segments, the WMSI is >1.

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10
Q

How is the ischemic threshold calculated?

A

The ischemic threshold is the HR at which the ischemia was first present.
Ischemic threshold = (HR at first sign of ischemia) / (220-age) x 100

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11
Q

Why and how is dobutamine stress echo used to assess low grade low flow AS?

A

It is difficult to assess AS severity in patients with LV dysfunction because the small AVA, calculated by the continuity equation, may be due to true AS or low CO, and the low AV velocities and gradients may underestimate AS severity. Therefore, it is difficult to differentiate low gradient low flow true AS (AVA <1cm2, mean PG <30mmHg and LVEF <40%) from functional AS. Therefore, dobutamine stress echo is used to differentiate true AS from functional AS.

An IV dobutamine infusion is administered at 5μg/kg/min with increases to 10 and 20 at 5 minute intervals if required. In patients with true AS, the AVA will be constant (<1.2cm2) but the mean PG will increase (>30mmHg) with stress. However, in patients with functional AS, the AVA will increase more relatively and the mean PG will increase less relatively with stress.

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12
Q

What are contractile reserve and flow reserve in the assessment of AS using dobutamine stress echo?

A

A LV contractile reserve and AV flow reserve are indicated by an increase in the SV by ≥20% with dobutamine stress. If there is no LV contractile reserve (increase in SV of <20%), it is true AS, and, if there is LV contractile reserve there is functional (pseudo) AS.

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13
Q

Why is stress echo used to assess MS?

A

In patients with MS with symptoms which are not proportional to the echo measurements, exercise stress echo is performed to identify patients who would benefit from treatment. Treatment is indicated in patients with exertional dyspnoea with a mean transmitral PG of >15mmHg and PASP of >60mmHg.

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14
Q

Why is stress echo used to assess pulmonary hypertension?

A

In patients with suspected pulmonary hypertension but normal PASP at rest, exercise stress echo is performed to show an increase in PASP during exercise to diagnose pulmonary hypertension, assess severity, and guide management.

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15
Q

What is the stress protocol?

A

Before the stress echo, stop beta blockers 48 hours before.

During the stress echo, perform an ECG and a BP at baseline, every minute and at recovery.

During the stress echo, optimise the images using harmonics or contrast to visualise the LV endocardial borders (contrast if >2 endocardial borders not visualised). The stress echo views include PLAX, PSAX, A4C and A2C. Assess the size and function.

After the stress echo, monitor the patient until they are asymptomatic with their ECG and BP back at baseline.

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16
Q

What are the exercise, dobutamine and vasodilator stress echo protocols?

A

Exercise stress echo is performed using a treadmill or a bicycle with an increase in work in 3 minute intervals until maximum HR.

An IV dobutamine infusion of 5μg/kg/min is administered with the infusion increasing every 3 minutes.

In dipyridamole stress echo, an IV dipyridamole infusion of 0.56mg/kg is administered over 4 minutes and then no infusion for 4 minutes. Acquire the images at baseline and at 4 minutes.

In adenosine stress echo, an IV adenosine infusion of 140μg/kg/min is administered over 6 minutes. Acquire the images at baseline and at 3 minutes.

Vasodilators cause a mild increase in HR and decrease in BP. Vasodilator stress echo is less sensitive and specific than exercise or dobutamine stress echo so is only used if the others are contraindicated.

17
Q

How is the LV assessed in the stress protocol?

A

Display the images side by side. Assess the LV wall motion based on the level of systolic endocardial excursion (normally >5mm) and systolic endocardial thickening (normally >50%) using the 16-segment model at baseline, low stress, high stress and recovery.