Benzocaine-induced methemoglobinemia during an outpatient procedure.

Outpatient transesophageal echocardiography was performed in a 69-year-old man with a history of aortic valve repair. During the procedure the patient became markedly cyanotic and hypotensive. Oxygen saturation measured by pulse oximetry decreased from 97% to the mid-80s. The man's condition continued to deteriorate. On transfer to a critical care unit, blood analysis by co-oximetry showed methemoglobin saturation of 67.8%. The patient's condition improved significantly after intravenous administration of methylene blue 1 mg/kg. With increasing numbers of outpatient procedures performed under topical anesthesia, measures should be in place to deal with a potential life-threatening adverse event such as methemoglobinemia.

Cost-minimization analysis of intravenous adenosine and dipyridamole in thallous chloride TI 201 SPECT myocardial perfusion imaging.

OBJECTIVE: To conduct a cost-minimization analysis of intravenous adenosine and intravenous dipyridamole in thallous chloride TI 201 single-photon emission computed tomography (SPECT) myocardial perfusion imaging. DESIGN: A retrospective, open-label, cost-minimization analysis. SETTING: University hospital, outpatient nuclear medicine department. PATIENTS: Eighty-three patients undergoing dipyridamole TI 201 SPECT and 166 patients undergoing adenosine TI 201 SPECT. MAIN OUTCOME MEASURES: A cost-minimization analysis was conducted using a direct cost accounting approach estimating institutional costs. For the purpose of this study, sensitivity and specificity between adenosine SPECT and dipyridamole SPECT were assumed to be identical. Key costs evaluated included acquisition, administration, monitoring, treatment of adverse effects, follow-up care, and repeat tests. RESULTS: Adenosine increased heart rate and lowered blood pressure to a significantly greater extent than dipyridamole. The frequency of adverse reactions was not significantly different (p = 0.103) between adenosine (1.64 +/- 1.32 per patient) and dipyridamole (1.36 +/- 1.23 per patient). The frequency of prolonged and late-onset adverse effects was significantly greater for dipyridamole than for adenosine (p < 0.001). The frequency of adverse events requiring medical intervention was statistically greater for dipyridamole (24%) compared with adenosine (5%) (p < 0.00001). Total cost was significantly less for adenosine ($378.50 +/- $128.20 per patient) compared with dipyridamole ($485.60 +/- $230.40). Although adenosine had a significantly greater acquisition cost than dipyridamole (p < 0.0001), administration, monitoring, and adverse reaction costs were significantly less for adenosine than for dipyridamole. CONCLUSIONS: The cost of using dipyridamole is significantly greater than the cost of using adenosine despite adenosine's high acquisition cost. Adenosine is less expensive to use because of lower administration costs, monitoring costs, and adverse effect costs. Adenosine should be the agent of choice for pharmacologic vasodilation in the setting of myocardial perfusion imaging.

Outcomes and costs of positron emission tomography: comparison of intravenous adenosine and intravenous dipyridamole.

The objective of this study was to compare the cost of intravenous adenosine and intravenous dipyridamole in positron emission tomography (PET) in patients with coronary artery disease. A retrospective, open-label, case-control, cost-effectiveness analysis was performed in the out-patient nuclear medicine department of a university hospital. Thirty-six patients underwent dipyridamole PET, and 72 matched patients underwent adenosine PET. A cost-effectiveness analysis was conducted using a direct cost accounting approach to estimate institutional costs. Key costs evaluated included acquisition cost, administration cost, monitoring cost, cost of management of side effects, and cost of follow-up care. The total cost of adenosine PET and dipyridamole PET was divided by their respective predictive accuracies to provide a total cost adjusted for efficacy. Adenosine increased heart rate and lowered systolic blood pressure to a significantly greater extent than dipyridamole. The number of patients experiencing adverse drug reactions was significantly greater for adenosine (82%) than for dipyridamole (67%), but the frequency of prolonged (> 5 minutes) and late-onset side effects was significantly greater for dipyridamole than for adenosine. The frequency of side effects requiring medical intervention was also significantly greater for dipyridamole (53%) than for adenosine (6%). Although adenosine had a significantly greater acquisition cost than dipyridamole, costs of monitoring, management of side effects, and follow-up care were significantly less for adenosine than for dipyridamole. As a result, the total cost of using dipyridamole is significantly greater ($928.00 per patient) than the total cost of using adenosine ($672.00 per patient). Based on these results, adenosine may be the drug of choice for pharmacologic vasodilation for PET.

Using transesophageal echocardiography to manage critically ill patients. What role in hemodynamic instability, MI, embolic disease, trauma?

When transthoracic echocardiographic images are suboptimal, transesophageal echocardiography offers a new window for visualization of the heart and thoracic aorta. It can be performed at bedside in 15 to 20 minutes. Complications (emesis, hypoxemia, hypotension) are rare and easily reversed or averted by administration of naloxone or flumazenil. Indications include evaluation of hemodynamic instability, ventricular function, mitral regurgitation, ventricular septal defects, aneurysm, endocarditis, intracardiac sources of embolus, valve pathology, aortic dissection, intra-aortic debris, and trauma. Results can be analyzed immediately and used to guide further evaluation, medical therapy, or surgery.

Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs.

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 +/- 8.4 to 178.5 +/- 11.3 mmHg (P less than 0.01) and left ventricle end-diastolic pressure from 3.5 +/- 0.7 to 8.9 +/- 1.0 mmHg (P less than 0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 +/- 1.9 to 4.80 +/- 1.2 ms/mmHg (P less than 0.01) for the pulse interval relationship and from -2.51 +/- 0.53 to -1.14 +/- 0.32 beats . min-1 . mmHg-1 (P less than 0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. beta 1-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic baroreceptor characteristics in dogs with chronic high output failure.

It has been shown that the arterial baroreflex is depressed in heart failure. The role of alterations in afferent discharge as a possible mechanism for this depression has not been investigated previously. Single unit aortic baroreceptor activity was recorded from six normal dogs and from nine dogs, each with a chronic aorto-caval fistula (AVF). At the time of the acute experiment, mean arterial blood pressure (MABP) was not significantly different in the two groups of dogs; however, pulse pressure was significantly higher in the AVF dogs (45.7 +/- 2.4 mm Hg vs, 24.4 +/- 2.0 mm Hg; p less than 0.001). Left ventricular end-diastolic pressure (LVEDP) was higher in the AVF dogs (31.3 +/- 2.0 vs 5.6 +/- 1.8 mm Hg; p less than 0.001). AVF dogs had elevated heart weight/body weight ratios. The relationship of systolic aortic pressure to systolic discharge was examined by changing aortic pressure with aortic and vena caval occluders. The peak gain (normalized to maximum discharge) averaged 2.19 +/- 0.27 in the normal dogs compared to 1.15 +/- 0.09 in the AVF group (p less than 0.01). Saturation pressures and maximum discharge rates were greater in the AVF dogs although the threshold pressures were not different in the two groups. This data suggests that there is an attenuated response of aortic baroreceptor discharge in dogs with chronic volume overload and this abnormality may partially be responsible for the abnormal baroreflex in heart failure.

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog.

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Attenuation of arterial baroreflex control of heart rate by left ventricular receptor stimulation in the conscious dog.

The purpose of this investigation was to determine whether left ventricular receptor stimulation attenuates the arterial baroreflex control of heart rate in the conscious dog and to determine the role of cardiac efferent sympathetic and parasympathetic pathways in any interaction observed. Mean arterial blood pressure-heart rate function curves, which characterized arterial baroreflex control of heart rate, were constructed before (control) and during an infusion of veratrine into the left circumflex coronary artery. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range (maximum minus minimum heart rate) were reduced during intracoronary infusion of veratrine. The mean arterial blood pressure-heart rate relationship also was shifted to a lower pressure during intracoronary infusion of veratrine. In order to study the role of cardiac efferents in this interaction, we constructed mean arterial blood-pressure-heart rate curves during cholinergic blockade, cholinergic blockade plus intracoronary infusion of veratrine, beta 1-adrenergic blockade, and beta 1-adrenergic blockade plus intracoronary infusion of veratrine. The addition of intracoronary infusion of veratrine during cholinergic blockade produced a shift of the mean arterial blood pressure-heart rate curve down the ordinate axis (heart rate) and to a lower pressure; however, peak sensitivity and heart rate range remained unchanged. The addition of intracoronary infusion of veratrine during beta 1-adrenergic blockade resulted in reductions in peak sensitivity and heart rate range. These data indicate that left ventricular receptor stimulation attenuates arterial baroreflex control of heart rate and that the reduction of sensitivity and heart rate range is mediated by parasympathetic motoneurons common to both reflex arcs. On the other hand, resetting to a lower operational set point may be mediated by cardiac sympathetic motoneurons common to both reflex arcs.