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J W Fasules

Publications and source records attributed to J W Fasules.

14 recordsLinked to original sources
PubMed1999

Blade and balloon atrial septostomy for left heart decompression in patients with severe ventricular dysfunction on extracorporeal membrane oxygenation.

Extracorporeal membrane oxygenation (ECMO) is used as circulatory support or bridge to transplantation in patients with severe left ventricular (LV) dysfunction. Left heart decompression is needed to reduce pulmonary edema, prevent pulmonary hemorrhage, and reduce ventricular distention that may aid in recovery of function. We reviewed our experience from November 1993 to December 1997 with 10 patients having severe LV dysfunction (7 myocarditis, 3 dilated cardiomyopathy) who required circulatory support with ECMO and who underwent left heart decompression with blade and balloon atrial septostomy (BBAS). Patients ranged in age from 1 to 24 years (median, 3 years). Indications for BBAS included left atrial/left ventricular distension (10), pulmonary edema/hemorrhage (9), or severe mitral regurgitation (2). BBAS was performed electively in eight patients and urgently in two patients. BBAS was performed while on ECMO in seven patients and pre-ECMO in three. A femoral venous approach was used in all patients. ECMO patients were fully heparinized. Transseptal puncture was required in nine patients while one patient had a patent foramen ovale. Blade septostomy was performed in all patients. Enlargement of the defect was then performed by stationary balloon dilation in nine and Rashkind balloon atrial septostomy in one. Balloon diameters ranged from 10 to 20 mm. Sequential balloon inflations were performed in some patients. Adequacy of the atrial septal defect (ASD) was confirmed by pressure measurement and echocardiography. Adequate left heart decompression was achieved in all patients. Pulmonary edema improved in nine of nine patients. Left atrial mean pressure fell from a mean of 30.5 mm Hg, (range, 12-50 mm Hg) to 16 mm Hg (range, 9-24 mm Hg). Left atrial to right atrial pressure gradient fell from a mean of 20 mm Hg pre-BBAS to 3 mm Hg post-BBAS. ASDs ranged in size from 2.5 to 8 mm (mean, 5.9 mm). Complications included needle perforation of the left atrium without hemodynamic compromise (one), ventricular fibrillation requiring defibrillation (one), and hypotension following BBAS which responded to volume infusion (two). Duration of ECMO ranged from 41 hr to 704 hr (mean, 294 hr). Seven patients survived and four patients had recovery of normal LV function. Of those who recovered, two had no ASD at follow-up while two ASDs are patent 14 days and 3 months post-BBAS. Three patients underwent successful cardiac transplantation. Three patients died, all of whom had multisystem organ failure with or without sepsis. A patent ASD was noted at transplant (three) or autopsy (two). No patient required a second BBAS. BBAS alleviates severe left atrial hypertension and pulmonary edema. In addition, BBAS avoids the potential bleeding complications of surgical left heart decompression. Stationary balloon dilation of the atrial septum is an effective alternative to Rashkind balloon septostomy in older patients. BBAS achieves left heart decompression that may permit recovery of LV function or allow extended ECMO support as a bridge to transplant.

Adolescent↗
PubMed1998

Pharmacokinetics and pharmacodynamics of ranitidine in neonates treated with extracorporeal membrane oxygenation.

The pharmacokinetics and pharmacodynamics of ranitidine were studied in 13 term neonates with stable renal and hepatic function who were treated with extracorporeal membrane oxygenation (ECMO). Ranitidine was initially administered as a single 2 mg/kg dose over 10 minutes and intragastric pH was monitored to determine response. Within 90 minutes after administration of ranitidine, intragastric pH for all of the patients whose initial reading was < or = 4 had increased to > 5. Intragastric pH remained > 4 for a minimum of 15 hours. Mean +/- 1 standard deviation elimination half-life was 6.61 +/- 2.75 hours, and 41.5 +/- 22.2% of the single dose was eliminated in urine within 24 hours. Total plasma clearance of ranitidine correlated well with estimated glomerular filtration rate. Twenty-four hours after the initial dose, a continuous infusion of ranitidine (2 mg/kg/24 hr) was started and continued for 72 hours or until ECMO was discontinued. Eleven patients completed 48 hours of continuous infusion and seven completed all 72 hours. Plasma clearance and elimination half-life were determined from steady-state plasma ranitidine concentrations 24, 48, and 72 hours after the start of the infusion. There were no significant differences in clearance between these intervals. These data suggest that for term neonates with stable renal and hepatic function, ranitidine does not need to be administered more frequently than every 12 hours. A continuous infusion of 2 mg/kg/24 hours maintained intragastric pH above 4 in more than 90% of our patients, and in our opinion is the preferred method for delivering ranitidine to term neonates undergoing ECMO who require H2 antagonists. Response to therapy should be monitored by repeated measurement of gastric pH and the dose should be adjusted accordingly.

Extracorporeal Membrane Oxygenation↗
PubMed1997

Prolonged extracorporeal life support for bridging to transplant: technical and mechanical considerations.

Through July 1995, the Extracorporeal Life Support Organization (ELSO) registry listed 87 patients who received extracorporeal life support (ECLS) as a bridge to cardiac transplantation with a survival rate of 41%. At Arkansas Children's Hospital, 17 patients (aged between two days and 24 years) with diagnoses of dilated cardiomyopathy (seven), postcardiotomy (seven) and acute viral myocarditis (three) were bridged with ECLS. Mechanical complications only occurred in two patients, neither of which necessitated withdrawal of ECLS. Decompression of the left heart was performed in 11 patients, six via a surgically placed vent and five with a blade/balloon artial septostomy. Documented infection occurred in 11/17 patients, but only one patient died from infection. Fifteen of 17 patients (88%) recovered or were transplanted, of which 13 (76%) were discharged home. With left-heart decompression and appropriate treatment of infection, ECLS may be used as a bridge to cardiac transplantation or until the return of cardiac function.

Adolescent↗
PubMed1994

Pulmonary hypertension and arterial changes in calves with a systemic-to-left pulmonary artery connection.

The pathogenic mechanisms by which increased pressure and flow lead to pulmonary vascular disease are poorly understood, especially in newborns. To study the pathophysiological correlations and timing of the development of structural changes in response to high flow in nonhypoxic neonates, a model of high pulmonary flow was developed in newborn calves by anastomosis of the isolated left pulmonary artery (LPA) to the aorta. LPA pressure and flow increased acutely. LPA pressure reached near-systemic levels by 10 wk, whereas LPA flow was maximally increased at 1 mo before decreasing in several calves. Right pulmonary arterial pressure remained normal, and ventricular hypertrophy did not develop. Morphometric evaluation of the left lung demonstrated decreased arteriolar diameter, increased medial thickness, muscularization of arterioles at the bronchoalveolar junction, luminal obliteration of small arteries, and dilation lesions. The LPA pressure and vascular changes were greater and developed over a shorter time period than did prior models of nonhypoxic flow-induced pulmonary vascular changes. Lesser degrees of decreased arteriolar diameter and muscularization of small vessels were seen in the right lung, indicating a difference in the vascular response to moderately increased flow vs. increased pressure and flow. Thus, calves with an isolated LPA-to-aortic anastomosis simulate the hemodynamic and pulmonary vascular changes seen in newborns with congenital heart defects. Such calves may serve as models to assess effects of mechanical stresses on a newborn's vasculature.

Anastomosis, Surgical↗
PubMed1994

Extracorporeal life support of neonates with congenital cardiac defects: techniques used during cardiac catheterization and surgery.

Neonatal patients with congenital cardiac defects require proper diagnosis often by cardiac catheterization before surgical repair. In our institution, patients whose echocardiograms reveal surgically correctable lesions, but who are severely decompensated, have been placed on Extracorporeal Life Support (ECLS) prior to catheterization or surgery. Subsequent management of ECLS and cardiopulmonary bypass (CPB) are dictated by the surgical procedure. Hypothermia can be utilized while on ECLS to facilitate low-flow CPB, or circulatory arrest. Total extracorporeal circulation may be performed with the ECLS circuit, or the patient may be transferred to a conventional CPB circuit during the procedure. If required, post surgical ECLS can be facilitated through prior cannulation. We have found pre-operative institution of ECLS, in the neonate with severe congenital cardiac defects, provides immediate control of hemodynamic and respiratory problems, lowers the risk of cardiac catheterization, and reduces the usage of blood products during surgery.

Cardiac Catheterization↗
PubMed1993

Mobile extracorporeal membrane oxygenation.

Transport of critically ill neonates in need of extracorporeal membrane oxygenation can be risky. Their extreme cardiorespiratory instability may delay or even preclude conventional transport to an extracorporeal membrane oxygenation center. We report the use of a UH-1 helicopter specially adapted for mobile extracorporeal membrane oxygenation support to transport a critically ill neonate.

Acidosis↗
PubMed1992

Extracorporeal membrane oxygenation for cardiac failure after congenital heart operation.

Despite continuing improvement in myocardial protection and surgical technique, the repair of complex congenital heart lesions can result in cardiopulmonary compromise refractory to conventional therapy. In a 29-month period, 24 patients (aged 14 hours to 6 years) were treated with extracorporeal membrane oxygenation (ECMO) 28 times for profound cardiopulmonary failure. Four patients required ECMO after each of two cardiopulmonary bypass procedures. Seventeen patients required ECMO to be initiated in the operating room: 12 (71%) were weaned successfully from ECMO, and 8 (47%) survived. Seven patients had ECMO initiated in the intensive care unit: 6 (86%) were weaned, and 5 (71%) survived. Serial echocardiograms demonstrated substantial recovery of cardiac function in 18 of 21 instances (86%) of ventricular failure from myocardial dysfunction. Overall, 18 of 24 patients (75%) were successfully weaned from ECMO including all 4 who underwent 2 ECMO treatments. We conclude that ECMO can successfully salvage children who have serious cardiopulmonary failure immediately after a congenital heart operation and that long-term survival is possible after two ECMO treatments.

Cardiac Output, Low↗
PubMed1992

Pharmacokinetics and pharmacodynamics of bumetanide in neonates treated with extracorporeal membrane oxygenation.

Eleven term neonates treated with extracorporeal membrane oxygenation received bumetanide to treat volume overload. All patients had stable renal function, no history of prior diuretic therapy, and no overt evidence of hepatobiliary disease or hypoalbuminemia. Pretreatment creatinine clearance was 35.2 +/- 4.5 ml/min per 1.73 m2 (range, 20.3 to 57.5). Bumetanide, 0.095 +/- 0.003 mg/kg, was administered for 2 minutes into the postmembrane side of the extracorporeal membrane oxygenation circuit. Serial plasma and urine samples were collected for measurement of bumetanide and electrolyte concentrations. Total plasma and renal clearances for bumetanide were 0.63 +/- 0.11 and 0.16 +/- 0.04 ml/min per kilogram, respectively. The steady-state volume of distribution (0.44 +/- 0.03 L/kg) and the elimination half-life (13.2 +/- 3.8 hours) were greater than similar values reported in previous studies of bumetanide disposition in premature and term neonates who were not treated with extracorporeal membrane oxygenation. At observed rates of bumetanide excretion, the diuretic, natriuretic, and kaliuretic responses were linear. Significant diuresis, natriuresis, and kaliuresis were observed, although the duration of these effects was less than expected given the prolonged renal elimination of bumetanide. Nonrenal elimination of bumetanide was variable (47.2% to 96.9%) but higher than expected; this may explain the relatively brief diuretic and kaliuretic response.

Analysis of Variance↗
PubMed1992

Evaluation of the reconstructed carotid artery following extracorporeal membrane oxygenation.

Over a 12-month period, 28 neonatal patients in respiratory failure were supported with extracorporeal membrane oxygenation (ECMO), and 11 of these underwent successful repair of the right carotid artery post-ECMO. Nine of 11 were studied with duplex color-flow Doppler imaging between 14 and 109 days of age and again at 1 year of age. A velocity ratio (A/B) of the peak systolic velocity above the level of the anastomosis to the peak systolic velocity below the anastomosis was measured to assess the degree of stenosis, if any, at the repair site. Antegrade flow through the carotid was detected post-ECMO in 8 of 9 infants, and antegrade and retrograde flow was documented in 1 infant. A/B ratios ranged from 1.00 to 8.60 (A/B ratio of 1 is normal; 2.0 indicates at least a 50% obstruction to flow). Four of 9 patients had ratios greater than 2.0, and 8 of 9 exhibited some evidence of obstruction. Follow-up scans were performed on 8 of 9 infants between 12 and 18 months of age. All infants examined showed marked improvement in A/B ratio and patency of the vessel, documenting that initial narrowing of the vessel is reversible. No infant had evidence of embolic phenomena to the right side of the brain by magnetic resonance imaging. Repair of the common carotid artery post-ECMO is technically feasible without increasing the risk of brain injury.

Blood Flow Velocity↗
PubMed1987

Neither anticoagulant nor nonanticoagulant heparin affects monocrotaline lung injury.

The administration of monocrotaline to rats causes pulmonary vascular leak within 1 wk followed in 2-3 wk by perivascular proliferation and fatal pulmonary hypertension. Possibly blocking the proliferation might block the pulmonary hypertension, providing insight into its mechanism. Because heparin, given as an antiproliferative agent, reduced hypoxic pulmonary hypertension in mice, it might also block monocrotaline-induced pulmonary hypertension. Alternatively, anticoagulation could worsen the lung injury. We found that heparin (300 and 600 U/kg sc twice daily) inhibited clotting in rats given monocrotaline but did not change the vascular leak, the right ventricular pressure, the right ventricular hypertrophy, the increased medial thickness of the pulmonary arterioles, or the production of a slow-reacting substance of anaphylaxis-like material by the lungs. A nonanticoagulant heparin fragment (2 mg/kg sc twice daily), given to avoid anticoagulation also did not influence the monocrotaline injury. Thus neither anticoagulant nor nonanticoagulant heparin either attenuated or worsened the measured effects of monocrotaline.

Animals↗
PubMed1985

Increased lung vasoreactivity in children from Leadville, Colorado, after recovery from high-altitude pulmonary edema.

Cardiac catheterization was performed on seven children after recovery from high-altitude pulmonary edema. All were life-long residents at elevations above 10,000 feet. Three of the seven had developed pulmonary edema without antecedent travel to low altitude but had an upper respiratory infection. Response of pulmonary arterial pressure to 16% inspired oxygen in all seven was compared with that in six well children who resided at a similar altitude and had no history of high-altitude pulmonary edema. With hypoxia the susceptible patients had a greater mean pulmonary arterial pressure (56.3 +/- 23.8) than the nonsusceptible children (18.8 +/- 3.9, p less than .05). Comparison with historical hemodynamic responses in children at high altitudes showed a similar greater mean pulmonary arterial pressure in the susceptible children. Thus, in children from high altitudes, increased pulmonary vasoreactivity to hypoxia may play a role in the pathogenesis of high-altitude pulmonary edema. The development of pulmonary edema in high-altitude residents with upper respiratory infections and no antecedent low-altitude journey is consistent with the presence of other factors such as inflammation, which may play a role in the pathogenesis of the edema. The finding of right ventricular hypertrophy on an electrocardiogram in children from high altitudes may be predictive of their susceptibility to high-altitude pulmonary edema.

Altitude↗