Toxic methemoglobinemia after topical anesthesia for transesophageal echocardiography.

Topical benzocaine spray is an anesthetic agent that is commonly used during transesophageal echocardiography (TEE). This agent is believed to be relatively safe because of very low systemic absorption. We report a case of toxic methemoglobinemia induced by benzocaine use for pharyngeal anesthesia during TEE. Physicians who perform TEE and use benzocaine or other topical anesthetics need to be familiar with this potential complication and have the necessary treatment readily available.

Myocardial imaging with a new transpulmonary lipid-fluorocarbon echo contrast agent: experimental studies in pigs.

The development of echo contrast agents that can provide reliable opacification of the myocardium after intravenous injection is an important advancement for the clinical application of contrast echocardiography. In this study, the hemodynamic effects and echocardiographic characteristics of a new lipid-fluorocarbon echo contrast agent, Aerosomes MRX 115 (ImaRx Pharmaceutical Corp., Tucson, Ariz.) were studied in six anesthetized ventilated pigs. Intravenous injection of this new agent in doses ranging from 0.0005 to 0.01 ml/kg produced significant measurable and visible myocardial opacification without any effect on heart rate, systemic pressure, partial pressure of oxygen, or left ventricular systolic function. The two largest doses (0.005 and 0.01 ml/kg), however, resulted in mild reversible increases in mean pulmonary artery pressure of 12 and 16 mm Hg, respectively. In four animals, epicardial images were obtained before and during coronary artery occlusion. Intravenous contrast injection during coronary occlusion permitted delineation of the hypoperfused myocardial segment. This capability may further expand the utility of contrast echocardiography.

Metabolic adaptation to a gradual reduction in myocardial blood flow.

BACKGROUND: Studies during 20% to 50% reductions in regional coronary blood flow have revealed a number of metabolic and functional adaptations that suggest the heart downregulates energy requirements and contractility in response to ischemia. In contrast to prior studies of sudden changes in coronary blood flow, we tested whether the heart could reduce ATP consumption commensurate with a gradual decrease in coronary blood flow or whether transient metabolic abnormalities are a necessary trigger in this process. METHODS AND RESULTS: From 0 to 35 minutes, mean left anterior descending coronary artery blood flow was reduced by approximately 1% per minute in 10 acutely anesthetized and instrumented swine. Coronary blood flow then was held constant between 35 and 60 minutes at the resulting 35% net blood flow reduction. Although systemic hemodynamics remained stable, a significant decrease in regional left ventricular systolic wall thickening developed (from control value of 45 +/- 11% to 18 +/- 11% at 60 minutes, P < .001) without a sustained decrease in the phosphorylation potential (as assessed by a < 2% decrease in either the transmural or subendocardial phosphocreatine-to-ATP ratio) and with minimal myocardial lactate production (4 +/- 44 mumol.min-1 x 100 g-1). CONCLUSIONS: Metabolic markers of ischemia such as ratio of phosphocreatine to ATP, ATP content, lactate content, and lactate production were blunted during this protocol of gradually worsening ischemia. Thus, contractile abnormalities of mild ischemia can develop with minimal metabolic evidence of ischemia. The downregulation of myocardial energy requirements can almost keep pace with the gradual decline in coronary blood flow.

Metabolic aspects of hibernating myocardium.

Myocardial hibernation describes the clinical entity of a dysfunctional region of myocardium with reduced flow that shows improvement in function after flow is restored. It is postulated that despite the reduced flow, metabolic activity is sufficient to prevent tissue necrosis. Experimental work in animals supports this. A moderate reduction in flow to a region of the left ventricle in pigs initially results in the typical metabolic picture of ischemia: ATP and PCr fall and anaerobic metabolism is present. However, over the next hour, a hypometabolic response occurs that eliminates almost all metabolic findings of ischemia despite ongoing flow reductions. This appears to be an actively and tightly regulated response. The reduction in systolic function is an important part of the hypometabolic state, but cannot fully account for the downregulation of energy use.

Spontaneous echo contrast and hemorheologic abnormalities in cerebrovascular disease.

BACKGROUND AND PURPOSE: Spontaneous echo contrast (SEC) is thought to represent a risk factor for cardioembolic stroke. In vitro studies suggest that SEC results from interaction between red cells and fibrinogen. To better understand the relation between SEC and stroke and to investigate the in vivo genesis of SEC, we examined the relation between SEC, the constituents of the blood, and plasma and serum viscosity in patients with acute stroke or chronic cerebrovascular disease. METHODS: Fifty patients with acute stroke or chronic cerebrovascular disease referred for transesophageal echocardiogram (TEE) were studied by transthoracic echocardiography and TEE. Complete blood count, fibrinogen, albumin, gamma-globulin, and plasma and serum viscosity determinations were made. Left atrial SEC was graded as absent, mild, or marked by means of TEE. RESULTS: SEC was absent in 31 patients, mild in 10 patients, and marked in 9 patients. Higher grade of SEC was associated with a significantly greater percentage of patients with atrial fibrillation and larger left atrial dimension. Atrial fibrillation was present in 23% of the patients in the SEC absent group, 50% of the patients in the mild SEC group, and 78% of the patients in the marked SEC group (P < .01). Left atrial diameter averaged 3.8 +/- 0.6 cm in the SEC absent group, 4.3 +/- 1.1 in the mild SEC group, and 4.9 +/- 0.7 in the marked SEC group (P < .001). Hematocrit, white blood cell count, and platelet count did not differ among the three groups. Fibrinogen, gamma-globulin, plasma viscosity, and serum viscosity values were all significantly higher in the presence of SEC (P < .05). Fibrinogen values were 361 +/- 97 mg/dL in the SEC absent group and 427 +/- 135 mg/dL in the marked SEC group. gamma-Globulin levels were 0.75 +/- 0.23 g/dL in the SEC absent group and 1.06 +/- 0.48 g/dL in the marked SEC group. Both plasma viscosity (1.97 cp) and serum viscosity (1.64 cp) were higher in the marked SEC group than in the SEC absent group (1.77 and 1.50 cp, respectively). CONCLUSIONS: In patients with acute stroke or chronic cerebrovascular disease, the severity of SEC was not related to albumin, hematocrit, white cell count, or platelet count but rather to elevated fibrinogen levels and concomitant increases in both plasma and serum viscosity. Moreover, increasing grade of SEC was associated with significantly increased left atrial diameter and a higher percentage of patients in atrial fibrillation.

Effect of lung denervation on development of pulmonary edema.

The objective of this study was to determine the relationship of an intact nervous system to the lung in the development of pulmonary edema. After unilateral denervation of a lung by autotransplantation, eight dogs were subjected to a period of increased intracranial pressure with air. A significant increase in pulmonary artery pressure and a 20% right-to-left shunt developed in all animals. The innervated lung of the animals subjected to increased intracranial pressure developed higher wet/dry lung weight ratios and 51Cr platelet counts compared to denervated lungs and to the five control innervated lungs. Thus intrapulmonary platelet sequestration and pulmonary edema occurred only in the intact innervated lung. These findings support the thesis that pulmonary edema following elevation of the intracranial pressure with air is the result of neurally induced alterations in pulmonary hemodynamics and platelet sequestration that could possibly lead to an increase in pulmonary vascular permeability.

Goretex and autogenous vein in the canine model.

Thirty Goretex grafts of 6 mm internal diameter, 30 mu fibril length, 30 mg/cc density and 0.5 mm wall thickness were placed as end-to-side bypass grafts in canine femoral arteries. Handling characteristics, patency and healing properties were compared with autogenous jugular veins which were anastomosed into the opposing femoral arteries. Autogenous veins were easier to anastomose and they showed a patency rate of 87% over a 16 week observation period. The Goretex grafts had a 50% patency rate during the same period. Goretex grafts failed because of technical errors (9), graft kinks (5), infection (3) and neointimal fibrous hyperplasia (2). This canine model has previously been used to evaluate all currently available biologic and synthetic vascular grafts. Goretex grafts demonstrated the highest rate of technical failures, but the lowest incidence of neointimal fibrous hyperplasia when compared to other grafts previously tested in this model.

Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization.

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.

Extrahepatic portal hypertension: a retrospective analysis.

A retrospective analysis of 19 patients with esophagogastric or intestinal varices secondary to extrahepatic portal hypertension was conducted. Nine patients had onset of bleeding during childhood. In six of eight pediatric patients in whom a shunt was performed no major bleeding occurred during the follow-up period. In seven adults with pure extrahepatic portal hypertension the four shunting procedures effected permanent control of bleeding. In two of three adults in whom portal vein thrombosis was associated with liver disease, shunting was successful. An emergency procedure was infrequently required. Multiple recurrences of bleeding episodes prior to decompression was the rule. Postshunt encephalopathy was never seen. In those patients in whom a shunt thrombosed or could not be performed, recurrent bleeding occurred uncommonly, and was readily managed to bedrest and transfusion.