No abstract available.
Dobutamine* ; Echocardiography, Stress* ; Myocardium*

No abstract available.
Adenosine* ; Dipyridamole* ; Dobutamine* ; Exercise Test*

No abstract available.
Dobutamine ; Echocardiography, Stress ; Liver Transplantation ; Liver

No abstract available.
Coronary Stenosis* ; Coronary Vessels* ; Dobutamine* ; Echocardiography, Stress* ; Female ; Humans

No abstract available.
Coronary Artery Disease* ; Coronary Vessels* ; Diagnosis* ; Dobutamine* ; Echocardiography, Stress*

> BACKGROUND: The accuracy of flow-related changes in aortic valve area (AVA) determined by the Gorlin formula or the continuity equation remains disputable. However, anatomic AVA can be determined by using by direct planimetry of transesophageal echocardiography (TEE). The purpose of this study was to assess the impact of changes in flow on AVA determined by TEE using direct planimetry. METHOD: Determination of AVA by TEE using direct planimetey was performed intraoperatively under three different hemodynamic conditions - pre-dobutamine (baseline) period, post-dobutamine period, post-CABG period - in 17 CABG patients and cardiac output (CO) with left ventricular ejection fraction (EF) were also determined by TEE simutaneously. The changes in aortic flow were induced by dobutamine infusion. RESULTS: AVA at pre-dobumaine period, post-dobutamine period, and post-CABG period were 2.99+/-0.80 cm2, 3.01+/-0.79 cm2, and 3.01+/-0.80 cm2, respectively. Before dobutamin infusion, CO and EF were 2.01+/-0.64 L/min and 47+/-10%. After dobutamine infusion, CO and EF were 3.03+/-1.05 L/min, 54+/-9% respectively and significantly increased by 54%, 18% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. After CABG, CO and EF were 3.86+/-1.86 L/min and 58+/-11% and also significantly increased by 98%, 26% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. However, despite of these significant hemodynamic changes, there were no significant changes in AVA and no significant correlations between these hemodynamic and AVA changes, neither at post-dobutamine period nor post-CABG period. CONCLUSION: The acute changes in CO and EF do not result in significant alterations in the anatomic AVA determined by TEE using direct planimetry. Thus, TEE using direct planimetry could be accurate and useful in the determination of AVA in hemodynamically unstable patient.
Aortic Valve* ; Cardiac Output* ; Dobutamine ; Echocardiography, Transesophageal* ; Hemodynamics ; Humans ; Stroke Volume*

> BACKGROUND: The accuracy of flow-related changes in aortic valve area (AVA) determined by the Gorlin formula or the continuity equation remains disputable. However, anatomic AVA can be determined by using by direct planimetry of transesophageal echocardiography (TEE). The purpose of this study was to assess the impact of changes in flow on AVA determined by TEE using direct planimetry. METHOD: Determination of AVA by TEE using direct planimetey was performed intraoperatively under three different hemodynamic conditions - pre-dobutamine (baseline) period, post-dobutamine period, post-CABG period - in 17 CABG patients and cardiac output (CO) with left ventricular ejection fraction (EF) were also determined by TEE simutaneously. The changes in aortic flow were induced by dobutamine infusion. RESULTS: AVA at pre-dobumaine period, post-dobutamine period, and post-CABG period were 2.99+/-0.80 cm2, 3.01+/-0.79 cm2, and 3.01+/-0.80 cm2, respectively. Before dobutamin infusion, CO and EF were 2.01+/-0.64 L/min and 47+/-10%. After dobutamine infusion, CO and EF were 3.03+/-1.05 L/min, 54+/-9% respectively and significantly increased by 54%, 18% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. After CABG, CO and EF were 3.86+/-1.86 L/min and 58+/-11% and also significantly increased by 98%, 26% than those measured before dobutamine infusion (p<0.01, p<0.01), respectively. However, despite of these significant hemodynamic changes, there were no significant changes in AVA and no significant correlations between these hemodynamic and AVA changes, neither at post-dobutamine period nor post-CABG period. CONCLUSION: The acute changes in CO and EF do not result in significant alterations in the anatomic AVA determined by TEE using direct planimetry. Thus, TEE using direct planimetry could be accurate and useful in the determination of AVA in hemodynamically unstable patient.
Aortic Valve* ; Cardiac Output* ; Dobutamine ; Echocardiography, Transesophageal* ; Hemodynamics ; Humans ; Stroke Volume*

BACKGROUND: Dobutamine, isoproterenol, and milrinone are inotropic agents with vasodilatory properties, and are frequently used perioperatively. We undertook to examine the effects of these three drugs on the pulmonary vasculature, excluding cardiovascular effects, by determining their effects on pulmonary artery pressure and hypoxic pulmonary vasoconstriction in an isolated rat lung model. METHODS: Thirty Sprague-Dawley rats were divided into a dobutamine group (n = 10), an isoproterenol group (n = 10) and a milrinone group (n = 10). Dobutamine 50microgram, 500microgram, and 5,000microgram, isoproterenol 0.4microgram, 4microgram, and 40microgram, and milrinone 2.5microgram, 25microgram, and 250microgram were added to perfusate sequentially during normoxic ventilation (21% O2-5% CO2-balanced N2). Baseline pulmonary artery pressure changes and subsequent hypoxic pressor responses during hypoxic ventilation (5% O2-5% CO2-balanced N2) were observed. RESULTS: Dobutamine, isoproterenol, and milrinone all decreased baseline pulmonary artery pressures and hypoxic pressor responses in a dose-dependent manner (P < 0.05). The last dose listed for each of the three drugs reversed hypoxic pulmonary vasoconstriction nearly completely. The calculated dose required to reduce the hypoxic pressor response to 50% of the initial response before drug administration (ED50) was 155microgram (95% CI: 80-263microgram) for dobutamine, 0.23microgram (95% CI: 0.011-0.75 microgram) for isoproterenol and 6.31microgram (95% CI: 3.1-10.8microgram) for milrinone. The relative potency of the drugs on HPV, based on ED50 was dobutamine 10: isoproterenol 0.015: and milrinone 0.41. CONCLUSIONS: Dobutamine, isoproterenol, and milrinone all reduced pulmonary vascular resistance and hypoxic pulmonary vasoconstriction in a dose dependent manner. (Korean J Anesthesiol 2004; 46: 454~461)
Animals ; Dobutamine* ; Isoproterenol* ; Lung* ; Milrinone* ; Pulmonary Artery ; Rats* ; Rats, Sprague-Dawley ; Vascular Resistance ; Vasoconstriction* ; Ventilation

BACKGROUND AND OBJECTIVES: Doppler myocardial imaging (DMI) has been suggested as a method of quantifying inducible ischemia during dobutamine stress echocardiography (DSE). Post-systolic motion (PSM) detected by DMI is related to peri-infarct ischemia during DSE. We hypothesized that PSM during DSE would predict recovery of dysfunctional myocardium after successful percutaneous coronary intervention (PCI). SUBJECTS AND METHODS: Thirty patients with dysfunctional myocardium in the left anterior descending coronary artery (LAD) territory were divided into two groups according to improvement of wall motion score index (WMSI) in the LAD territory at 6 months after successful PCI of the LAD. DMI was evaluated in the LAD territory during DSE. Fifteen patients showed improved WMSI (1.42+/-0.39) while the other 15 had unchanged WMSI (1.75+/-0.46) 1 month after PCI. Myocardial velocity was measured in the mid-septal, apico-septal, and basal anterior segments of the LAD artery territory. PSM was defined as a positive wave appearing after the curve of systolic ejection had reached the zero line. RESULTS: Although there was no difference between resting PSMs in both groups, PSM during DSE was significantly higher in the improved WMSI group than in the WMSI group where it was unchanged. CONCLUSION: PSM during DSE predicts recovery of dysfunctional myocardium after successful PCI.
Arteries ; Coronary Vessels ; Dobutamine ; Echocardiography, Stress ; Humans ; Ischemia ; Myocardial Stunning ; Myocardium ; Percutaneous Coronary Intervention

Hemostasis and a clear field are obtained by the local infiltration of a local anesthetic mixed with epinephrine. However, epinephrine may in itself, due to its cardiovascular effect, cause arryhthmia, heart failure, pulmonary edema, and even cardiac arrest. We describe a 10-year-old patient who developed ventricular premature contraction and acute pulmonary edema due to epinephrine infiltration during tonsillectomy. The patient recovered without any sequelae after intensive treatment involving fluid restriction, diuretics, dobutamine infusion, and oxygen by mask at 5 L/min.
Child ; Diuretics ; Dobutamine ; Epinephrine* ; Heart Arrest ; Heart Failure ; Hemostasis ; Humans ; Masks ; Oxygen ; Pulmonary Edema* ; Tonsillectomy*