On ridges, crests, and rings of fire: just location, or does the catheter point to the origins of focal tachycardia?
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OBJECTIVE: In the majority of patients with chronic atrial fibrillation the arrhythmia will persist after correction of the underlying structural abnormality. The maze procedure is an effective surgical method to eliminate atrial fibrillation and to restore atrial contractility. METHODS: In this study we used radiofrequency energy to create lines of conduction block in both atria during cardiac surgery as a modification of the maze III procedure. One hundred twenty-two patients with atrial fibrillation for at least 1 year and structural heart disease underwent open heart operation and a radiofrequency modified maze procedure. RESULTS: In 108 (89%) of 122 patients mitral valve surgery was performed, and in this group 86 patients (80%) underwent 121 concomitant procedures. Fourteen patients (11%) underwent cardiac surgery not involving the mitral valve. The additional crossclamp time required for the left atrial part of the radiofrequency modified maze procedure was 14 +/- 3 minutes. The in-hospital mortality rate was 4.1%. The overall 39-month survival was 90%, and freedom of atrial flutter or atrial fibrillation was 78.5% +/- 5.1%. Eighty-nine survivors with sinus, atrial rhythm, or atrioventricular sequential pacemaker had Doppler echocardiography, and right atrial transport function was documented in 83% and left atrial transport function in 77% of patients. CONCLUSION: We concluded that the radiofrequency modified maze procedure as an adjunctive procedure is safe, time-sparing, and effective in eliminating atrial fibrillation and restoring atrial transport function.
UNLABELLED: Laparoscopic surgery is associated with systemic and splanchnic hemodynamic alterations. Recent data suggest that small-dose dobutamine may attenuate the reduction in splanchnic blood flow associated with increments in intraabdominal pressure. We conducted this study to analyze the effects of dopamine and dobutamine on the hepatic circulation in this setting. Twenty-one pigs were anesthetized and mechanically ventilated. A flow-directed pulmonary artery and carotid artery catheters were inserted. Perivascular flow probes were placed around the main hepatic artery and the portal vein. CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mm Hg. After 60 min, animals received dopamine (5 microg x kg(-1) x min(-1); n = 8), dobutamine (5 microg x kg(-1) x min(-1); n = 8), or saline (n = 5) for 30 min. Pneumoperitoneum induced significant increases in heart rate, mean arterial pressure, and systemic vascular resistance, with decreases in cardiac output and hepatic artery and portal vein blood flows. Dobutamine infusion, in contrast to dopamine, corrected, at least in part, cardiac output, systemic vascular resistance, and hepatic artery blood flow alterations, but neither drug restored total hepatic blood flow. IMPLICATIONS: Hepatic blood flow decreases during laparoscopic surgery. A small-dose infusion of neither dobutamine nor dopamine corrects the total hepatic blood flow impairment, but the former is able to restore the hepatic arterial blood supply in an animal model mimicking this condition.
OBJECTIVE: To review the clinical use of central venous pressure measurements. DATA SOURCES: The Medline database, biographies of selected articles, and the author's personal database. DATA SYNTHESIS: Four basic principles must be considered. Pressure measurements with fluid-filled systems are made relative to an arbitrary reference point. The pressure that is important for preload of the heart is the transmural pressure, whereas the pressure relative to atmosphere still affects other vascular beds outside the thorax. The central venous pressure is dependent upon the interaction of cardiac function and return function. There is a plateau to the cardiac function curve, and once it is reached, further volume loading will not increase cardiac output. CONCLUSIONS: If careful attention is paid to proper measurement techniques, central venous pressure can be very useful clinically. However, the physiologic or pathophysiological significance of the central venous pressure should be considered only with a corresponding measurement of cardiac output or at least a surrogate measure of cardiac output.
OBJECTIVE: Outcome after trauma with severe hemorrhagic shock is still dismal. Since the majority of blood is present in the venous vessels, it might be beneficial to perform venous recruiting via the airway during severe hemorrhagic shock. Therefore, the purpose of our study was to evaluate the effects of negative expiratory pressure ventilation on mean arterial blood pressure, cardiac output, and short-term survival during severe hemorrhagic shock. DESIGN: Prospective study in 21 laboratory animals. SETTING: University hospital research laboratory. SUBJECTS: : Tyrolean domestic pigs. INTERVENTIONS: After induction of controlled hemorrhagic shock (blood loss approximately 45 mL/kg), 21 pigs were randomly ventilated with either zero end-expiratory pressure (0 PEEP; n = 7), 5 cm H2O positive end-expiratory pressure (5 PEEP; n = 7), or negative expiratory pressure ventilation (up to -30 cm H2O at the endotracheal tube during expiration; n = 7). MEASUREMENTS AND MAIN RESULTS: Mean (+/-sd) arterial blood pressure was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (38 +/- 5 vs. 27 +/- 3 mm Hg; p = .001) and the 5 PEEP animals (38 +/- 5 vs. 20 +/- 6 mm Hg; p < .001) after 5 mins of the experiment. Cardiac output was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (3.1 +/- .4 vs. 1.9 +/- .9 L/min; p = .001) and 5 PEEP animals (3.1 +/- .4 vs. 1.2 +/- .8 L/min; p < .001) after 5 mins of the experiment. All seven negative expiratory pressure ventilation animals, but only three of seven 0 PEEP animals (p = .022), survived the 120-min study period, whereas all seven of seven 5 PEEP animals were dead within 35 mins (p < .001). Limitations include that blood loss was controlled and that the small sample size limits the evaluation of survival outcome. CONCLUSIONS: When compared with pigs ventilated with either 0 PEEP or 5 PEEP, negative expiratory pressure ventilation during severe hemorrhagic shock improved mean arterial blood pressure and cardiac output.
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Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 +/- 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1-3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.
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Atrial fibrillation (AF) leads to remodeling of the left atrium (LA) and left atrial appendage (LAA), resulting in atrial myopathy. Reduced LA and LAA function in chronic AF leads to thrombus formation and spontaneous echo contrast (SEC). The effect of inotropic stimulation on LAA function in patients with chronic AF is unknown. LAA emptying velocity (LAAEV) and maximal LAA area at baseline and after dobutamine were measured by transesophageal echocardiography in 14 subjects in normal sinus rhythm (NSR) and 6 subjects in AF. SEC in the LA was assessed before and after dobutamine. LAAEV increased significantly in both groups. However, the LAAEV at peak dobutamine in patients with AF remained significantly lower than the baseline LAAEV in patients who were in NSR (P = 0.009). Maximal LAA area decreased significantly with dobutamine in both groups, but LAA area at peak dose of dobutamine in patients with AF remained greater than baseline area in those in NSR (P = 0.01). Despite the increase in LAAEV, SEC improved in only two of five patients. We conclude that during AF, the LAA responds to inotropic stimulation with only a modest improvement in function.
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PURPOSE: To study clinical and physiologic aspects of Z-stent therapy for superior vena cava (SVC) syndrome secondary to malignant disease. MATERIALS AND METHODS: Signs and symptoms of SVC syndrome were classified, graded, and scored in 11 cases. Six patients with caval pressure higher than 22 mm Hg peripheral to the stenosis underwent stent therapy. RESULTS: Immediately after Z-stent implantation into the stenotic lesion, the diameter of the constriction increased from 3.3 mm +/- 2.0 (mean +/- standard deviation) to 14.0 mm +/- 3.2, the mean caval pressure peripheral to the stenosis decreased from 26.6 mm Hg +/- 2.5 to 8.9 mm Hg +/- 0.7, and the symptom score decreased from 6.7 +/- 1.8 to 1.3 +/- 1.4. The caval pressure, lesion diameter, and symptom score correlated highly with each other. One complication--transient pulmonary edema attributable to volume overload caused by reperfusion--was observed. Mean survival exceeded 7.1 months. CONCLUSION: Stent placement could be a useful treatment for refractory SVC syndrome.
Mean circulatory filling pressure (MCFP) has been measured after vagally induced cardiac arrest in 11 nonpregnant and 10 near-term pregnant rabbits, anesthetized with pentobarbital sodium. MCFP was 6.1 +/- 0.4 (SD) mmHg in the nonpregnant and 7.2 +/- 0.4 mmHg in the pregnant animals. The difference of 1.1 mmHg was significant (P < 0.001). Sympathetic blockade with bretylium tosylate (10 mg/kg) reduced MCFP by 0.4 mmHg in both nonpregnant and pregnant rabbits. Vascular capacitance was examined in the two groups. Unstressed vascular volume and vascular compliance were derived from measurements of MCFP after increasing blood volume by 8 and 16% or reducing it by 8%. The unstressed vascular volumes, 33.9 +/- 3.9 (SD) ml/kg in the nonpregnant and 35.1 +/- 3.2 ml/kg in the pregnant group, were not significantly different, but compliance in the pregnant group (4.0 +/- 0.6 ml.kg-1.mmHg-1) was significantly greater than in the nonpregnant rabbits (3.4 +/- 0.6 ml.kg-1.mmHg-1) (P < 0.05). We conclude that there are changes in vascular capacitance in rabbit pregnancy, probably not related to alterations in vasomotor activity, but these are insufficient to fully compensate for the increase in blood volume, thus leading to the rise in MCFP.
To investigate the effect of a fall of intrathoracic pressure on left ventricular (LV) hemodynamics and relaxation, simultaneous micromanometric recordings of LV and aortic pressures were performed at rest and during two graded Mueller maneuvers in 16 patients undergoing cardiac catheterization for aortic valve stenosis (n = 8) or chest pain (n = 8). The reductions (means +/- SE) of airway pressure during the lesser and greater maneuvers were 26 +/- 1 and 42 +/- 1 mmHg, respectively. Simultaneously, LV isovolumic-developed pressure increased by 9 +/- 3 and 21 +/- 4 mmHg, respectively (P < 0.03 for both). During the greater maneuver, the individual changes of the time constant of LV isovolumic relaxation (tau) correlated with the changes of LV isovolumic-developed pressure (r = 0.73; P = 0.002). In patients with a > 20-mmHg rise in isovolumic-developed pressure, tau increased by 10.3 +/- 4.6 ms. By multiple-regression analysis, the change of tau was related directly to the change of isovolumic-developed pressure (standardized coefficient beta = 0.80; P = 0.001) and inversely related to the resting systolic LV-aortic pressure gradient (beta = -0.37; P = 0.050). The other hemodynamic changes were independent of aortic valve stenosis. In conclusion, during the Mueller maneuver, the LV isovolumic contraction load increases and tau lengthens, particularly with higher elevations of LV systolic load.
A series of phenylethanolamines bearing a 2-[1-phenylpropyl] substituent on the nitrogen atom was evaluated in vitro for activity at beta(1)- and beta(2)-adrenoceptors. As previously observed, the presence of 3,4-dihydroxy substitution on phenylethanolamine is required for potent activation of both subtypes, whereas the 3,5-dihydroxy analog showed selectivity for the beta(2)-subtype. Replacement by a carboxyl group of the 4-hydroxyl group on the aralkyl nitrogen substituent produced only a small reduction in beta(1) potency (5-fold), whereas beta(2) potency was reduced by more than 100-fold. Hence this structural class includes agonists having either a beta(1), nonselective beta(1)/beta(2) or beta(2) selectivity profile.
BACKGROUND: The isthmus between the inferior vena cava and the tricuspid annulus has been shown to be involved in the reentry circuit of common atrial flutter. The effects of radio-frequency catheter ablation of this isthmus were examined in the canine model of atrial flutter due to reentry around the tricuspid annulus. METHODS AND RESULTS: A model of atrial flutter was prepared in 11 of 14 dogs by creating intercaval and connected transverse lesions (Y-shaped lesion). Bipolar electrodes were attached at 24 atrial sites, and computer-assisted mapping was performed. Stable atrial flutter with a cycle length of 133 +/- 11 ms was repeatedly induced by rapid atrial pacing in all dogs, and atrial mapping revealed reentry around the tricuspid annulus including the isthmus. In 6 dogs, the isthmus was ligated during atrial flutter (mechanical ablation). In the other 5 dogs, a 7F large-tip electrode catheter was placed at the isthmus under a fluoroscopic control. Radiofrequency energy (25 W for 30 s) was delivered to three sequential sites from the tricuspid annulus to the inferior vena cava to ablate the isthmus linearly. Atrial flutter was terminated in all dogs after mechanical and radio-frequency ablation of the isthmus and was not induced again. Atrial pacing from the posterior left atrium during sinus rhythm demonstrated intra-atrial conduction block at the isthmus after ablation. Pathological examination of the isthmus showed transmural myocardial damage. CONCLUSIONS: Linear radiofrequency ablation of the isthmus can induce intra-atrial conduction block and is effective as a curative therapy for atrial flutter when the reentry circuit involves the isthmus.
It is not known how the decrease in left ventricular contractility following endotoxin exposure is mediated, or whether this decrease is preventable by antibodies to tumor necrosis factor-alpha (TNF alpha). Four groups of six anesthetized and instrumented pigs were pretreated with ovine polyclonal antibody to human TNF alpha (anti-TNF alpha), nonspecific IgG, or saline, and then treated with either endotoxin or saline. We measured hemodynamics and left ventricular pressures (Millar catheter) and volumes (conductance catheter). Left ventricular contractility was assessed using the slope (Emax) of the end-systolic pressure-volume relationship. Four hours after the start of endotoxin infusion in the nonspecific IgG pretreated group, Emax had decreased by 44 +/- 6% (p < 0.05), mean arterial pressure had decreased from 115 +/- 7 mm Hg to 70 +/- 10 mm Hg (p < 0.05), and cardiac output was rapidly decreasing after an initial increase (p < 0.05). Anti-TNF alpha significantly reduced the decrease in Emax (11 +/- 9%, p < 0.05), and the systemic hypotension (108 +/- 15 mm Hg to 99 +/- 6 mm Hg, p < 0.05), at 4 h, and prevented the late decrease in cardiac output. This suggests that TNF alpha is an important early mediator in sepsis leading to decreased left ventricular contractility.