Dobutamine Stress Echo: Difference between revisions
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==DSE to assess regional wall motion disorders== | |||
A stress echo is a test in which the position of the LV is looked at during rest and during exercise. The heart is charged by means of dobutamine intravenously. Dobutamine is a catecholamine with predominant β - receptor stimulator in which positive inotropic, chronotropic and dromotropic effects are caused in the heart. Dobutamine has a half-life of approximately 2 minutes. The inotropic and chronotropic effects induce myocardial ischemia by significantly narrowing the coronary artery. Echocardiography than regional wall motion detects disorders. DSE is also used to detect contractile reserve on myocardial damage after infarction. The reliability board for detecting coronary stenosis DSE is to compare myocardial perfusion scintigraphy and it is far superior to exercise ECG. | |||
A stress echo is a | |||
Advance is first made with the echo resting platelets : A | Advance is first made with the echo resting platelets: A PLAX, PSAX pm, AP4Ch and AP2Ch. | ||
At maximum heart rate are again | During the run of Dobutamine the heart is properly monitored using a 12 -channel ECG and blood pressure. With each increase in dose dobutamine (every 3 minutes see Table below) ECG and blood pressure is measured. The research is safe, but can cause symptoms such as: palpitations, chest pain, dizzy or light present in the head. The Dobutamine is stopped when reaching the [http://csecho.ca/cardiomath/?eqnHD=stress&eqnDisp=mphrage maximum heart rate] [(220 - age) x 0.85], severe complications or incidents, demonstrable new regional wall motion in more than one segment or an increase in end-systolic volume. In some cases the maximum heart rate has not been achieved, there may be need in the next Dobutamine, 0.25mg atropine co-administered with a maximum of 1 mg (at intervals of 1 minute). | ||
At maximum heart rate echo recordings are again made. Another PLAX, PSAX pm, AP4Ch and AP2Ch, are made exactly like the rest plates (otherwise do not compare the recordings with each other) that requires only routine of the sonographer. Then ensure that the heart rate is slow again.<cite>1</cite> | |||
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DSE with low- gradient aortic stenosis | ==DSE with low- gradient aortic stenosis== | ||
Low- gradient aortic stenosis is defined as a severe aortic valve stenosis (AVA < 1.0cm | |||
Low-gradient aortic stenosis is defined as a severe aortic valve stenosis (AVA <1.0cm<sup>2</sup>) with a transvalvular pressure gradient ≤30mmHg. A low- gradient aortic stenosis occurs in patients who have LV dysfunction with decreased ejection fraction. The assessment of the AGM in these patients may be overestimated because the calculated AVA is proportional to the displacement. A poorly functioning LV can exert enough pressure to the calcified aortic valve to open. At a fixed, or "true" stenosis in which the stroke volume increases, the gradient across the valve also increases relatively. In some patients, an increase in stroke volume results for only a limited increase in pressure gradient across the aortic valve. This phenomenon is called a "pseudo stenosis". DSE is a tool used to make a distinction between a true stenosis and a pseudo stenosis. | |||
Patients with pseudo- stenosis manifest an increase in the calculated AGM and a decrease in resistance of the valve as a response to an increase of the stroke volume. The reaction is different in patients with severe aortic stenosis | Patients with pseudo- stenosis manifest an increase in the calculated AGM and a decrease in resistance of the valve as a response to an increase of the stroke volume. The reaction is different in patients with severe aortic valve stenosis in whom dobutamine-induce increases transvalvular flow, giving an increase in the mean transvalvular gradient, but no change in AGM. | ||
A DSE study in a low- gradient aortic valve stenosis is given a low -dose dobutamine. That is, they | A DSE study in a low-gradient aortic valve stenosis is given a low-dose dobutamine. That is, they start to get 5μg/kg/min and gradually increase to a maximum 20μg/kg/min. | ||
If there is an increase in stroke volume, an increase in AVA | If there is an increase in stroke volume, an increase in AVA ≥0.3cm<sup>2</sup> and a small change in gradient produced after administering Dobutamine, there is an overestimation of the severity of aortic stenosis (=pseudo stenosis). | ||
A DSE may also demonstrate a severe aortic stenosis with low transvalvular pressure gradient or contractile reserve. Contractile reserve has a predictive value for mortality in surgery of aortic valve replacement. Recent studies have shown that perioperative mortality 5-8 % versus 32 % without contractile reserve in contractile reserve.<cite>2</cite> | A DSE may also demonstrate a severe aortic stenosis with low transvalvular pressure gradient or contractile reserve. Contractile reserve has a predictive value for mortality in surgery of aortic valve replacement. Recent studies have shown that perioperative mortality is 5-8% versus 32% without contractile reserve in contractile reserve.<cite>2</cite> | ||
==Indication DSE== | ==Indication DSE== | ||
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|Congestive heart failure | |Congestive heart failure | ||
|- | |- | ||
|Serious | |Serious tachyarrhythmia | ||
|- | |- | ||
|Serious | |Serious valve stenosis | ||
|- | |- | ||
|Hypertrophic obstructive cardiomyopathy | |Hypertrophic obstructive cardiomyopathy | ||
Latest revision as of 01:48, 7 February 2014
DSE to assess regional wall motion disorders
A stress echo is a test in which the position of the LV is looked at during rest and during exercise. The heart is charged by means of dobutamine intravenously. Dobutamine is a catecholamine with predominant β - receptor stimulator in which positive inotropic, chronotropic and dromotropic effects are caused in the heart. Dobutamine has a half-life of approximately 2 minutes. The inotropic and chronotropic effects induce myocardial ischemia by significantly narrowing the coronary artery. Echocardiography than regional wall motion detects disorders. DSE is also used to detect contractile reserve on myocardial damage after infarction. The reliability board for detecting coronary stenosis DSE is to compare myocardial perfusion scintigraphy and it is far superior to exercise ECG.
Advance is first made with the echo resting platelets: A PLAX, PSAX pm, AP4Ch and AP2Ch.
During the run of Dobutamine the heart is properly monitored using a 12 -channel ECG and blood pressure. With each increase in dose dobutamine (every 3 minutes see Table below) ECG and blood pressure is measured. The research is safe, but can cause symptoms such as: palpitations, chest pain, dizzy or light present in the head. The Dobutamine is stopped when reaching the maximum heart rate [(220 - age) x 0.85], severe complications or incidents, demonstrable new regional wall motion in more than one segment or an increase in end-systolic volume. In some cases the maximum heart rate has not been achieved, there may be need in the next Dobutamine, 0.25mg atropine co-administered with a maximum of 1 mg (at intervals of 1 minute).
At maximum heart rate echo recordings are again made. Another PLAX, PSAX pm, AP4Ch and AP2Ch, are made exactly like the rest plates (otherwise do not compare the recordings with each other) that requires only routine of the sonographer. Then ensure that the heart rate is slow again.[1]
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| DSE assessment on RWBS | DSE protocol |
|---|
| Relationship dobutamine concentration by weight and pump mode. Dobutamine 250mg in 50ml, pump speed in ml / h. (Copyright © OLVG) | |||||
|---|---|---|---|---|---|
| Time in minutes | |||||
| 0 | 0 | 3 | 6 | 9 | |
| Dobutamine in µg/kg/min | |||||
| 5 | 10 | 20 | 30 | 40 | |
| Weight in kg | Pump Stand | ||||
| 44 | 2.6 | 5.3 | 10.5 | 15.7 | 20.9 |
| 46 | 2.8 | 5.6 | 11.2 | 16.8 | 22.4 |
| 48 | 2.9 | 5.8 | 11.6 | 17.4 | 23.2 |
| 50 | 3.0 | 6.0 | 12.0 | 18.0 | 24.0 |
| 52 | 3.1 | 6.2 | 12.4 | 18.6 | 24.8 |
| 54 | 3.2 | 6.5 | 13.0 | 19.4 | 25.6 |
| 56 | 3.4 | 6.8 | 13.6 | 20.4 | 27.2 |
| 58 | 3.5 | 7.0 | 14.0 | 21.0 | 28.0 |
| 60 | 3.6 | 7.2 | 14.4 | 21.6 | 28.8 |
| 62 | 3.7 | 7.4 | 14.8 | 22.2 | 28.8 |
| 64 | 3.8 | 7.6 | 15.2 | 22.8 | 30.4 |
| 66 | 4.0 | 8.0 | 16.0 | 24.0 | 32.0 |
| 68 | 4.1 | 8.2 | 16.4 | 24.6 | 32.8 |
| 70 | 4.2 | 8.4 | 16.8 | 25.2 | 33.6 |
| 72 | 4.3 | 8.6 | 17.2 | 25.8 | 34.4 |
| 74 | 4.4 | 8.8 | 17.6 | 26.4 | 35.2 |
| 76 | 4.6 | 9.2 | 18.4 | 27.6 | 36.8 |
| 78 | 4.7 | 9.4 | 18.8 | 28.2 | 37.6 |
| 80 | 4.8 | 9.6 | 19.2 | 28.8 | 38.4 |
| 82 | 4.9 | 9.8 | 19.6 | 29.4 | 39.2 |
| 84 | 5.0 | 10.0 | 20.0 | 30.0 | 40.0 |
| 86 | 5.1 | 10.2 | 20.4 | 30.6 | 40.8 |
| 88 | 5.3 | 10.6 | 21.2 | 31.8 | 42.4 |
| 90 | 5.4 | 10.8 | 21.6 | 32.4 | 43.2 |
| 92 | 5.5 | 11.0 | 22.0 | 33.0 | 44.0 |
| 94 | 5.6 | 11.2 | 22.4 | 33.6 | 44.8 |
| 96 | 5.8 | 11.6 | 23.2 | 34.8 | 46.4 |
| 98 | 5.9 | 11.8 | 23.6 | 35.4 | 47.2 |
| 100 | 6.0 | 12.0 | 24.0 | 36.0 | 48.0 |
| 102 | 6.1 | 12.2 | 24.4 | 36.6 | 48.4 |
| 104 | 6.2 | 12.4 | 24.8 | 37.2 | 49.6 |
| 106 | 6.4 | 12.8 | 25.6 | 38.4 | 51.2 |
| 108 | 6.5 | 13.0 | 26.0 | 39.0 | 52.0 |
| 110 | 6.6 | 13.2 | 26.4 | 39.6 | 52.8 |
DSE with low- gradient aortic stenosis
Low-gradient aortic stenosis is defined as a severe aortic valve stenosis (AVA <1.0cm2) with a transvalvular pressure gradient ≤30mmHg. A low- gradient aortic stenosis occurs in patients who have LV dysfunction with decreased ejection fraction. The assessment of the AGM in these patients may be overestimated because the calculated AVA is proportional to the displacement. A poorly functioning LV can exert enough pressure to the calcified aortic valve to open. At a fixed, or "true" stenosis in which the stroke volume increases, the gradient across the valve also increases relatively. In some patients, an increase in stroke volume results for only a limited increase in pressure gradient across the aortic valve. This phenomenon is called a "pseudo stenosis". DSE is a tool used to make a distinction between a true stenosis and a pseudo stenosis.
Patients with pseudo- stenosis manifest an increase in the calculated AGM and a decrease in resistance of the valve as a response to an increase of the stroke volume. The reaction is different in patients with severe aortic valve stenosis in whom dobutamine-induce increases transvalvular flow, giving an increase in the mean transvalvular gradient, but no change in AGM.
A DSE study in a low-gradient aortic valve stenosis is given a low-dose dobutamine. That is, they start to get 5μg/kg/min and gradually increase to a maximum 20μg/kg/min.
If there is an increase in stroke volume, an increase in AVA ≥0.3cm2 and a small change in gradient produced after administering Dobutamine, there is an overestimation of the severity of aortic stenosis (=pseudo stenosis).
A DSE may also demonstrate a severe aortic stenosis with low transvalvular pressure gradient or contractile reserve. Contractile reserve has a predictive value for mortality in surgery of aortic valve replacement. Recent studies have shown that perioperative mortality is 5-8% versus 32% without contractile reserve in contractile reserve.[2]
Indication DSE
| Indications for DSE |
|---|
| Suspected coronary artery disease |
| Inability to perform bicycle test |
| Known for determining coronary ischemia before and after revascularization |
| Known coronary artery disease to determine areas of ischemia |
| Preoperatively, to assess risk, with large myocardial infarction. |
| Detection of viability |
Contra-indication DSE
| Contra-indications for DSE |
|---|
| Acute myocardial infarction (≤ 4-10 days) |
| Unstable angina |
| Known relevant main stem stenosis |
| Congestive heart failure |
| Serious tachyarrhythmia |
| Serious valve stenosis |
| Hypertrophic obstructive cardiomyopathy |
| Acute pericarditis, myocarditis, endocarditis |
| Aortic dissection |
References
- Krahwinkel W, Ketteler T, Gödke J, Wolfertz J, Ulbricht LJ, Krakau I, and Gülker H. Dobutamine stress echocardiography. Eur Heart J. 1997 Jun;18 Suppl D:D9-15. DOI:10.1093/eurheartj/18.suppl_d.9 |
- Lange RA and Hillis LD. Dobutamine stress echocardiography in patients with low-gradient aortic stenosis. Circulation. 2006 Apr 11;113(14):1718-20. DOI:10.1161/CIRCULATIONAHA.105.617159 |