Injuries from interpersonal violence presenting to a rural health center in Western Kenya: characteristics and correlates.

OBJECTIVE: To define the scope of injury due to interpersonal violence in a medium-sized town in Western Kenya. DESIGN: Prospective, cross-sectional data collection and analysis. SETTING/SUBJECTS: Data were prospectively collected on all injured patients (n = 562) presenting to a health center in Western Kenya, 2002-2004. Age, gender, type, and severity of injury, relationship to assailant, disposition, and clinician's suspicion of alcohol use were recorded. MAIN OUTCOME MEASURES: Number of injuries due to interpersonal violence; correlation of gender, alcohol use, relationship to assailant, and type of injury. RESULTS: Interpersonal violence caused 43% of all injuries. Men and women were equally likely to suffer violent injuries (42% vs 45%); however, women were more likely to suffer injury from domestic violence (4.7% vs 7.0%) and sexual assault (0% vs 3.5%). Men and women were equally likely to know their assailant. Women were more likely to be injured by a spouse/partner (19% vs 1.3%), whereas men were more likely to be injured by an acquaintance (29% vs 16%). Alcohol use was more often suspected for victims of violent, as opposed to unintentional, injury (45% vs 16%). Men with violent injuries were more likely than women to be suspected of having used alcohol (51% vs 35%). CONCLUSIONS: Interpersonal violence is a leading cause of injury in Western Kenya. Although men and women are equally likely to be assaulted, women are more likely to be injured by a spouse, and men by an acquaintance. Alcohol use is common among those who suffer violent injuries in this population.

Peripheral and autonomic nervous system involvement in chronic GM2-gangliosidosis.

GM2-gangliosidosis (McKusick 268800 and 272800) is a rare hereditary, progressive disorder of ganglioside metabolism caused by deficiency of lysosomal beta-hexosaminidase (EC 3.2.1.52) activity. It is characterized by severe central nervous system involvement. Involvement of the peripheral and autonomic nervous system has been suspected but rarely documented in published case reports in the chronic form of the disease. Four patients, aged 24-29 years, with chronic GM2-gangliosidosis were examined prospectively for evidence of peripheral and autonomic nervous system dysfunction. All had nerve conduction studies, sympathetic skin responses and cardiac monitoring during the head tilt-table test. Three patients had objective evidence of autonomic dysfunction with abnormal sympathetic nervous skin responses and axonal sensorimotor polyneuropathy. None of the patients had evidence of significant cardiovascular autonomic dysfunction on the head tilt-table test. The peripheral and autonomic nervous system may be involved in patients with chronic GM2-gangliosidosis. In some cases, this may be clinically significant. On the other hand, cardiovascular autonomic instability is apparently not a significant problem in young adult patients with the disease.

Are diagnostic testing and admission rates higher in non-English-speaking versus English-speaking patients in the emergency department?

STUDY OBJECTIVE: To determine whether non-English-speaking patients who present to an emergency department have more diagnostic tests ordered, higher admission rate, and longer length of stay in the ED than English-speaking patients for 2 common complaints, chest pain and abdominal pain. METHODS: This prospective, comparative, observational study was conducted at a public hospital ED. The study group was composed of 324 patients (172 non-English-speaking and 152 English-speaking) presenting with nontraumatic abdominal pain (148) or chest pain (176). The main outcome measures were admission rates, length of stay in the ED, and diagnostic test and procedure ordering. RESULTS: The mean age for the total sample was 45.8+/-15.5 years (range 14 to 87 years); 45.4% (147/324) of the patients were male. For the non-English-speaking patients, the language distribution was Spanish (31.0%), other (9.0%), Cantonese (5.9%), Hindi (2.5%), Mien (1.5%), Arabic (1.9%), Russian (0.9%), Mandarin (0.6%), and Korean (0.3%). The admission rate was 37.8% for English-speaking patients versus 42.8% for non-English-speaking patients in the total sample (mean difference in proportions 5%, 95% confidence interval [CI] -6% to 16%; 34.2% for English-speaking versus 9.1% for non-English-speaking patients presenting with abdominal pain, mean difference in proportions 5%, 95% CI -11% to 21%) and 40.9% for English-speaking versus 45.8% for non-English-speaking patients presenting with chest pain (mean difference in proportions 5%, 95% CI -10% to 20%). Power was 80% to detect a 15% difference in admission rates at an alpha value of.05. There was no statistically significant difference in ordering of diagnostic tests between the non-English-speaking and English-speaking patients with chest pain. Non-English-speaking patients with abdominal pain had 5 tests ordered more often than English-speaking patients. The mean difference in proportions (with 95% CIs) for these tests were CBC count 18.4% (5.1% to 31.7%), serum electrolytes 17.9% (3.8% to 31. 9%), urinalysis 20.0% (4.5% to 35.6%), ECG 23.4% (8.6% to 38.2%), and abdominal computed tomographic scan 10.9% (1.0% to 20.8%). There was no statistically significant difference between English-speaking and non-English-speaking patients for ED length of stay in the total sample (mean difference 29.8, 95% CI -37.5 to 97.1 minutes; for the abdominal pain subgroup, mean difference 19.5, 95% CI -74.6 to 113.5 minutes; and for the chest pain subgroup, mean difference 37.9, 95% CI -58.0 to 133.8 minutes). CONCLUSION: Significantly more tests are ordered for non-English-speaking patients with abdominal pain in the ED, including 3 times as many abdominal computed tomographic scans. There is no increase in test ordering with non-English-speaking patients with complaints of chest pain in the ED. When comparing English-speaking and non-English-speaking patients, there were no statistically significant differences in admission rates or length of stay in the ED.

Role of adenosine receptors in the paradoxic bradycardia response of rats to inferior vena cava occlusion during an infusion of isoproterenol.

BACKGROUND: In susceptible humans, vasodepressor reactions are induced by restriction of venous return (upright tilting) and administration of isoproterenol. Because paradoxic bradycardia is a major manifestation of vasodepressor reactions, and allowing for extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined whether adenosine receptors mediate the paradoxic bradycardia reaction. METHODS AND RESULTS: Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. We studied whether dipyridamole, an adenosine transport inhibitor, and aminophylline (nonselective) or DPCPX (selective) A1 antagonists augmented or inhibited paradoxic bradycardia, respectively, during inferior vena cava occlusion. The maximum changes in R-R during 60 seconds of inferior vena cava occlusion were that (1) in control, the rate accelerated (DeltaR-R, -9.7+/-0.8 ms, P<0.001); (2) during isoproterenol (0.8 microg . min-1), paradoxic bradycardia occurred (DeltaR-R, +92.0+/-32.0 ms, P<0.001); (3) during isoproterenol but after dipyridamole, paradoxic bradycardia occurred at a much lower dose of isoproterenol (0.2 microg . min-1), and the magnitude was increased at all doses (at 0.8 microg . min-1 isoproterenol, DeltaR-R, +195.6+/-27.6 ms, P<0.001 versus isoproterenol alone, DeltaR-R, +92.0+/-32 ms); (4) during isoproterenol and dipyridamole, atropine did not block paradoxic bradycardia, but cervical vagotomy inhibited paradoxic bradycardia (DeltaR-R, +5.6+/-1.8 ms, P<0.001 compared with isoproterenol and dipyridamole alone); and (5) during isoproterenol alone, aminophylline or DPCPX blocked paradoxic bradycardia (DeltaR-R, -5.4+/-1.0 ms, and DeltaR-R, -2.6+/-0.5 ms, respectively, each P<0.001 compared with isoproterenol alone). CONCLUSIONS: The adenosine A1 receptor mediates the paradoxic bradycardia reflex during inferior vena cava occlusion in the face of isoproterenol via vagal afferents.

Induction of paradoxic bradycardia in rats by inferior vena cava occlusion during the administration of isoproterenol: the essential role of augmented sympathetic tone.

INTRODUCTION: Testing human susceptibility for vasodepressor reactions involves combining venous return restriction by passive upright tilting and administering isoproterenol. While sympathetic tone is usually increased by the stimuli that incite a vasodepressor reaction, it is not known if the increased sympathetic tone is an essential or passive component of the mechanism that triggers the reaction. Given that paradoxic bradycardia is a major manifestation of vasodepressor reactions and allowing for the possible extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined the role of sympathetic tone in the paradoxic bradycardia reaction. Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. To examine the role of increased sympathetic tone on this reaction, we studied whether carotid artery perfusion (80 to 100 mmHg) during inferior vena cava occlusion, a maneuver that blunts the rise in sympathetic tone, inhibits paradoxic bradycardia. METHODS AND RESULTS: The maximum changes in R-R were measured during 60 seconds of inferior vena cava occlusion as follows: (a) in control the heart rate accelerated (delta R-R - 10.2 +/- 2.3 msec, P < 0.001); (b) during an infusion of isoproterenol, paradoxic bradycardia occurred (delta R-R + 140.6 +/- 18.2 msec, P < 0.001), and this was inhibited by common carotid artery perfusion (delta R-R - 6.6 +/- 1.5 msec, P < 0.001); and (c) following carotid sinus denervation and during an infusion of isoproterenol, paradoxic bradycardia was induced without and with carotid artery perfusion (delta R-R + 122.6 +/- 12.0 msec, P < 0.001; delta R-R + 151.8 +/- 12.7 msec, P < 0.001, respectively). CONCLUSIONS: Since carotid artery perfusion during inferior vena cava occlusion inhibits paradoxic bradycardia only when the carotid sinus is innervated, we conclude that carotid artery perfusion blocks the reaction by increasing carotid sinus afferents, thereby limiting the increased sympathetic tone during inferior vena cava occlusion, and not as a result of cerebral perfusion. Thus, the paradoxic bradycardia resulting from inferior vena cava occlusion requires activation of sympathetic tone as a result of carotid sinus hypotension.

Verapamil blockade of the paradoxic bradycardia in rats induced by inferior vena cava occlusion during the administration of isoproterenol or calcium: the role of Ca2+.

It has been postulated that the vasodepressor reaction results from a vigorous ventricular contraction in the face of a reduced cardiac volume. Paradoxic bradycardia is a major manifestation of vasodepressor reactions. Allowing for the possible extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined calcium's role, an essential component of cardiac contraction, in the paradoxic bradycardia reaction. Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion, and we examined calcium's role by studying whether verapamil inhibits and CaCl2 causes paradoxic bradycardia, respectively. The maximum changes in R-R were measured during 60 s of inferior vena cava occlusion under the following conditions: (i) in control, the rate accelerated (R-R-21.8 +/- 2.4 ms (mean +/- SE), p < 0.001); (ii) during isoproterenol, paradoxic bradycardia occurred (R-R 98.0 +/- 8.1 ms, p < 0.001), and this was inhibited by verapamil (R-R 5.0 +/- 2.1 ms, p > 0.05) and restored by CaCl2 (R-R 109.3 +/- 6.5 ms, p < 0.001); (iii) during CaCl2 (without isoproterenol), paradoxic bradycardia also occurred (R-R 82.1 +/- 22.9 ms, p < 0.001), and this was also inhibited by verapamil (R-R -18.5 +/- 4.7 ms, p < 0.001). We conclude that verapamil inhibits the inferior vena cava occlusion induced paradoxic bradycardia caused by either isoproterenol or calcium, and these findings support the concept that increased cardiac contractile force triggers a vasodepressor reaction.

Paradoxic bradycardia (vasodepressor reaction) induced by inferior vena cava occlusion: the role of alpha- and beta-adrenergic receptors and their interaction.

Vasodepressor reactions, characterized by paradoxic bradycardia, were induced in rats when the inferior vena cava was occluded during an infusion of isoproterenol. The effects of alpha-adrenergic receptors and their interaction with beta-adrenergic receptors on the vasodepressor reaction were examined. Inferior vena cava occlusion was performed for 60 s, and the maximum changes in R-R were measured in 44 rats: (i) in control conditions, during phenylephrine (alpha 1-adrenergic agonist), and during a combined infusion of phenylephrine and isoproterenol the R-R shortened significantly (-16.8 +/- 1.4, -24.1 +/- 2.2, and -4.9 +/- 1.2 ms, respectively); (ii) isoproterenol and phentolamine and prazosin (nonselective and selective alpha-adrenergic antagonists) prolonged the R-R paradoxically (+89.2 +/- 9.5, +58.9 +/- 4.1, and +64.4 +/- 10.2 ms, respectively); (iii) atropine and right vagotomy did not affect the phentolamine-induced R-R prolongation (+66.0 +/- 2.4 and +73.8 +/- 13.7 ms, respectively), but it was blocked by left vagotomy (-9.6 +/- 1.1 ms); (iv) propranolol inhibited the prazosin-induced R-R prolongation (-14.3 +/- 2.8 ms,); (v) epinephrine (alpha- and beta-adrenergic agonist) shortened the R-R interval (-9.5 +/- 2.2 ms), but following prazosin, epinephrine induced R-R prolongation (+13.7 +/- 6.0 ms,); (vi) norepinephrine induced R-R prolongation (+21.0 +/- 6.7 ms). It was concluded that (i) paradoxic bradycardia (vasodepressor reaction) dependent on vagal afferents can be induced by reduced venous return in the presence of excess exogenous beta 1-adrenergic stimulation (isoproterenol) or when endogenous alpha-adrenergic tone is antagonized (phentolamine or prazosin); (ii) the reaction can be blocked by alpha 1-adrenergic stimulation; and (iii) epinephrine does not induce paradoxic bradycardia, whereas norepinephrine does, and this may be due to the stronger alpha-stimulating properties of epinephrine.

Vasodepressor reaction induced by inferior vena cava occlusion and isoproterenol in the rat. Role of beta 1- and beta 2-adrenergic receptors.

BACKGROUND: Testing for the susceptibility of vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. We developed an experimental rat model in which vasodepressor reactions are induced when the inferior vena cava is occluded during an infusion of isoproterenol. The reactions are characterized by the development of paradoxical bradycardia during the period of inferior vena cava occlusion. METHODS AND RESULTS: Inferior vena cava occlusion was performed for 60 seconds, and the maximal changes in RR interval were measured during seven states as follows: (1) when inferior vena cava occlusion was performed under control conditions in 40 rats, the rate accelerated in all 40 rats (delta RR, -15.6 +/- 1.9 milliseconds in 25 rats, P < .001; delta RR, -13.3 +/- 1.7 milliseconds in 10 rats, P < .001); (2) when inferior vena cava occlusion was performed in 25 rats during an infusion of isoproterenol, a vasodepressor reaction was observed in all rats as the heart rate slowed (delta RR, +92.7 +/- 8.3 milliseconds, P < .001); (3) when inferior vena cava occlusion was performed in 10 rats during an infusion of dobutamine, a selective beta 1-agonist, a vasodepressor reaction was observed in all rats as the heart rate slowed (delta RR, +63.3 +/- 10.6 milliseconds, P < .001); (4) when inferior vena cava occlusion was performed in 5 rats during an infusion of salbutamol, a selective beta 2-agonist, vasodepressor reaction was not observed as the heart rate accelerated in all rats (delta RR, -11.4 +/- 2.8 milliseconds, P < .002); (5) the vasodepressor reaction induced by either dobutamine or isoproterenol was inhibited by atenolol, a selective beta 1-adrenergic receptor antagonist; (6) the vasodepressor reaction induced by isoproterenol was inhibited by propranolol (lipophilic) and sotalol (nonlipophilic) beta-blockers and there was a dose-dependent attenuation by propranolol of the maximal RR interval slowing during inferior vena cava occlusion; and (7) butoxamine, a selective beta 2-adrenergic receptor antagonist, attenuated but did not block the vasodepressor reaction observed during an infusion of isoproterenol. CONCLUSIONS: Reduced cardiac volume combined with beta 1-adrenergic stimulation can stimulate a vasodepressor reaction in rats. beta 2-Adrenergic receptors play little or no role in the reaction. The vasodepressor reaction can be blocked by selective or nonselective beta 1-adrenergic antagonists independent of the drug's ability to penetrate the central nervous system. The application of these findings to humans remains to be elucidated.

Effect of prolonged oral terbutaline therapy on glucose tolerance in pregnancy.

OBJECTIVE: Our objective was to elucidate the pathophysiologic effects and potential reversibility of terbutaline-induced changes in carbohydrate metabolism. STUDY DESIGN: We prospectively evaluated serum glucose, insulin, glucagon, C-peptide, and pancreatic polypeptide levels in response to a 100 gm glucose challenge (oral 3-hour glucose tolerance test) in 17 obstetric patients without complications who were given terbutaline (5 mg orally every 4 hours) for 5 consecutive days between 24 and 32 weeks' gestation. Each patient served as her own control, with day 1 representing pretreatment, day 7 the treatment phase, and day 14 the posttreatment evaluation. Body mass index and posttreatment serum terbutaline levels were also measured. RESULTS: A significant initial treatment effect (day 1 versus 7) was observed for glucose (elevated), insulin (elevated), insulin/glucose ratio (elevated), and pancreatic polypeptide (elevated). A significant delayed treatment effect (day 1 versus 14) was also observed for insulin (elevated), insulin/glucose ratio (elevated), and pancreatic polypeptide (elevated). Body mass index directly correlated with postchallenge measures of insulin, insulin/glucose ratio, pancreatic polypeptide, and C-peptide. Posttreatment serum terbutaline levels directly correlated with pancreatic polypeptide, but not with other parameters. CONCLUSIONS: Our data support a dose-independent, terbutaline-induced glucose intolerance mediated by glucagon and caused by diminished insulin sensitivity.

Endobronchial irradiation with 192Ir in the treatment of malignant endobronchial obstruction.

From Jan 1, 1983 to April 30, 1989, 32 patients underwent 38 endobronchial treatments with 192Ir, bronchoscopically inserted for treatment of endobronchial obstructions secondary to bronchogenic carcinoma. Thirty-four of the 38 treatments were far enough apart to allow separate response analysis. Thirty of the 34 patients were symptomatically improved or stable; 22 of 24 patients who could be evaluated roentgenographically showed improved or stable chest roentgenograms, and ten of 12 patients evaluated bronchoscopically demonstrated improved patency of bronchial lumen.

Use of telemetry functions in the assessment of implanted antitachycardia device efficacy.

Twenty patients (aged 50 +/- 21 years and mean left ventricular ejection fraction 37 +/- 17%) with recurrent ventricular arrhythmias were treated with an investigational, implantable combined antitachycardia-pacing cardioverter defibrillator. The device's telemetry capabilities include both stored (1-second snapshots) and real-time display of endocardial and device-circuit signals. The device can store these before, during and after up to 50 tachycardia and antitachycardia pacing episodes. All stored events are indexed to a 24-hour internal clock. During 10.1 +/- 5.1 months of follow-up, the device was used in 11 of 20 patients. In the entire group, antitachycardia pacing was activated on 44 +/- 14 occasions per patient (total 874) and shock delivery occurred on 8 +/- 14 occasions per patient (total 156). Reconstruction by stored telemetry of all device-therapy episodes was possible. Twenty-six percent of all shocks delivered were not appropriate and were due to atrial arrhythmias in 2 patients and dysfunction of the sensing lead in 3. The absence of a relation between symptoms and appropriate shock delivery was documented in 1 patient. Antitachycardia pace acceleration occurred in 5.3% of cases; 7% of attempts at pacing were unsuccessful and needed shock therapy. It is concluded that the enhanced telemetry available in newer antitachycardia devices enables more accurate assessment of device use and enhances diagnosis of inappropriate therapy delivery.

Vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

UNLABELLED: Testing for the susceptibility for vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. To explore the basis of the vasodepressor test in humans, the present experiment examined whether a reduced cardiac volume coupled with adrenergic stimulation causes a vasodepressor reaction in rats. Vasodepressor reaction was defined as paradoxical heart rate slowing in conjunction with hypotension during inferior vena caval occlusion. Inferior vena caval occlusion was performed for 60 s and the maximum changes in R-R were measured during seven states as follows. (A) Under control conditions inferior vena caval occlusion alone accelerated the rate in 32 of 32 rats (delta R-R, -13.9 +/- 1.7 ms, p less than 0.001). (B) When inferior vena caval occlusion was performed during an infusion of isoproterenol (0.5-1.0 micrograms.min-1), a vasodepressor reaction was observed in all rats as the heart rate slowed (delta R-R, +138.1 +/- 14.8 ms, p less than 0.001). The vasodepressor reaction was further examined during isoproterenol and inferior vena caval occlusion under five additional states. (C) After atropine the vasodepressor reaction was unchanged (delta R-R, +132.7 +/- 24.8 ms, p less than 0.001). (D) After bilateral vagotomy the paradoxical slowing was eliminated. (E) After intrapericardial lidocaine the paradoxic slowing was eliminated. (F) After bilateral stellectomy nonsignificant slowing was still present, but this was markedly reduced when compared with B (p less than 0.001). (G) Following chronic chemical sympathetic denervation with 6-hydroxydopamine the paradoxic bradycardia was eliminated. CONCLUSIONS: (1) Reduced cardiac volume combined with adrenergic stimulation can stimulate a vasodepressor reaction; (2) the vasodepressor reaction requires signalling by the afferent but not efferent vagal fibers; (3) the bradycardia is mainly due to withdrawal of sympathetic efferent tone.

Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

Vasodepressor reactions were induced in 27 rats by a combination of inferior vena caval occlusion and an infusion of isoproterenol. A vasodepressor reaction was defined as paradoxical heart rate slowing during inferior vena caval occlusion. The R-R intervals were measured at 5-s intervals before, during, and after 60 s of inferior vena caval occlusion. The purpose of this study was to examine the role of the right and left vagus nerve and the right and left stellate ganglia in this reflex. Under control conditions inferior vena caval occlusion accelerated the rate (R-R, -15.9 +/- 0.9 ms). During an infusion of isoproterenol (0.5-1.0 micrograms.min-1), inferior vena caval occlusion produced paradoxical rate slowing, i.e., a vasodepressor reaction (R-R, +75.0 +/- 2.2 ms). The vasodepressor reaction was examined during inferior vena caval occlusion and isoproterenol under the following additional states: atropine methyl bromide or right vagotomy did not alter the reaction; left vagotomy eliminated the reaction; and right or left stellectomy greatly reduced the vasodepressor reaction. We conclude the following: (1) left vagal afferents mediate the vasodepressor reaction; (2) cardiac sympathetic fibers participate in the vasodepressor reaction by withdrawing efferent tone through the right stellate ganglion, and by generating the afferent signal, which triggers the vasodepressor reaction through the left stellate ganglion.

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat.

Ventricular tachycardia or ventricular fibrillation was electrically induced in 38 normal rats (group 1) and 24 sympathetically denervated rats (6-hydroxydopamine) (group 2). The time for spontaneous reversion to sinus rhythm was measured during (1) control, (2) isoproterenol, and (3) the combination of isoproterenol and phenylephrine. The time for spontaneous reversion was the same in both groups in the three states. The reversion time was prolonged threefold by isoproterenol, and restored to control values when phenylephrine was added to the infusion of isoproterenol. The tachycardia duration and the refractory period were inversely related: log10 (tachycardia duration) = 3.466-0.091 (refractory period). Ventricular tachycardia/fibrillation induction was examined as follows: (i) Ventricular tachycardia/fibrillation was induced in 100% of normal rats (group 1), but only 42% of the denervated rats (group 2, p less than 0.001); (ii) during isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of rats of both groups; and (iii) when phenylephrine was added to isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of group 1 rats versus 82% of group 2 rats, (p = NS). These observations suggest (1) the induction of ventricular tachycardia/fibrillation is highly dependent on intact sympathetic innervation, and (2) exogenous adrenergic agonists modulate the duration of ventricular fibrillation through their effects on ventricular refractory period, independent of sympathetic innervation.

A follow-along study of participants in a longitudinal transition program for youths with mild disabilities.

Descriptive data are presented on the employment patterns of youths with mild disabilities who participated in a transition program with an intensive postsecondary component. Data on employment rates, positive and negative job changes, participation in continuing education, and access to benefit packages are reported for 94 youths who participated in the program over a 4-year period. Program participants had favorable outcomes when compared with a national sample, but they stabilized at an entry level of work participation. Their rates of entry into postsecondary education were also greater than the national sample, but advances were nominal.

Effects of posture, Valsalva maneuver and respiration on atrial flutter rate: an effect mediated through cardiac volume.

The effects of passive upright tilting from 0 degrees to +60 degrees (n = 27), Valsalva maneuver (n = 16) and respiration (n = 10) on the rate of atrial flutter were studied in 27 patients. After tilting to +60 degrees, the atrial flutter cycle length shortened in all patients from 247.5 +/- 7 to 236.7 +/- 6.9 ms (range of shortening 1 to 21 ms, p less than 0.001). The Valsalva maneuver (strain of 40 mm Hg) shortened the flutter cycle length during the strain (phase 2) from 242.2 +/- 4.6 to 230.5 +/- 5 ms (range of shortening 2 to 19 ms, p less than 0.001). In 10 patients whose respiration was monitored, the flutter cycle length consistently prolonged during inspiration and shortened during expiration. Combined beta-adrenergic and muscarinic receptor blockade in six patients did not significantly alter the flutter cycle length at rest or the effects of the various maneuvers on the changes in flutter cycle length. This study revealed that the atrial flutter cycle length can be shortened by passive upright tilting, the strain phase of the Valsalva maneuver and expiration. Changes in flutter cycle length were independent of autonomic tone, implying that by decreasing cardiac volume, these maneuvers affect characteristics of the atrial flutter circuit, thereby producing dynamic changes in the rate of atrial flutter.