The role of the generalist physician initiative in the merger of Hahnemann University and Medical College of Pennsylvania.

Unique in the history of academic medicine in the 20th century was the 1993 merger of two medical schools, Hahnemann University and The Medical College of Pennsylvania, to create Allegheny University of the Health Sciences, the largest private medical school in the United States. During the early, most critical phase of the merger process, the two faculties were brought together to plan and submit an application for The Robert Wood Johnson Foundation's Generalist Physician Initiative (GPI). This action had a profound and lasting impact on the merger of the two schools and the educational enterprise that subsequently evolved. The GPI grant was awarded to the merged school in the midst of this complex merger rife with major changes, all with their attendant fears and frustrations. During and just after the merger, at a time when faculty and staff were somewhat uncertain about the direction of the university, the GPI provided a focus with a clear set of goals and objectives. Despite the unprecedented changes occurring in the organization and personal and professional concerns, faculties from the two institutions were able to join in pursuing the generalist initiative and its associated curriculum reform. This single, pervasive effort was a significant factor in forming a unified faculty of a united school of medicine. This sense of unity was put to the test when, in July 1998 the university, along with its affiliated hospital system, filed for bankruptcy. The goals of this extraordinary action were to sell the hospitals to another organization, thereby removing from the university the burden of supporting hospital-based clinical programs and allowing the university to emerge as a freestanding academic institution focusing on its core mission of education and the principles embodied in the GPI.

Redesigning the surgery clerkship at MCP Hahnemann School of Medicine to address the educational needs of generalists.

This article describes how the surgery clerkship at MCP Hahnemann School of Medicine was redesigned to provide all students a well-rounded general professional education and to address the specific educational needs of generalists. During the 12-week clerkship, students spend eight weeks on two different general surgery rotations, which include significant experiences in outpatient settings. The evaluation and management of common general surgical problems, as well as the holistic approach to patient care, are emphasized. A nurse educator, recruited through funding obtained from The Robert Wood Johnson Foundation's Generalist Physician Initiative, provides formal instruction in holistic care and teaches bedside procedures. Two weeks are devoted to focused surgical subspecialty experiences addressing common conditions and are conducted primarily in outpatient settings. The remaining two weeks include an integrated musculoskeletal disease rotation, including orthopaedic surgery, rheumatology, physiatry, and radiology. Didactic teaching includes criteria for referral of patients from generalists to specialists. The new clerkship model has been well received by the students. Review of student logs for the first six months indicates the breadth of surgical experience has been maintained and appropriate balance achieved between simple and complex surgical cases. Further evaluation of the model will continue through longitudinal follow-up.

A statewide system to track medical students' careers: the Pennsylvania model.

In 1994 the Commonwealth of Pennsylvania announced a statewide Generalist Physician Initiative (GPI) modeled after The Robert Wood Johnson Foundation's GPI. Three-year grants totaling more than $9 million were awarded to seven of Pennsylvania's medical schools, including two that had already received GPI grants from the foundation. Stimulated by these initiatives, the state's six allopathic and two osteopathic medical schools decided to work together to develop a collaborative longitudinal tracking system to follow the careers of all their students from matriculation into their professional careers. This statewide data system, which includes information for more than 18,000 students and graduates beginning with the entering class of 1982, can be used to evaluate the impact of the Pennsylvania GPI, and it also yielded a local longitudinal tracking system for each medical school. This paper outlines the concept of the system, its technical implementation, and the corresponding implications for other medical schools considering the development of similar outcomes assessment systems.

Preserving the best of the art of teaching.

Teachers often develop unique methods to help students learn, but these techniques may be lost when they retire from the profession. In the 15 years that they have conducted the Effective Teaching Workshop: Improving Your Skills, the authors of this paper have observed presentations of many innovative teaching methods. The article describes five methods recently presented at the annual workshop: the use of a flipchart with slides; the use of Polarmotion overhead transparencies; an asthma simulation; a breast-mass simulation; and teamwork and game-playing. The authors present these techniques in the hope of reaching a broader audience, and to stimulate other teachers to submit descriptions of innovative teaching methods for possible publication in the Ideas for Medical Education column.

Evaluation of parallel pelvic/breast and male genital/rectal teaching programs.

Pelvic/breast (PB) and male genital/rectal (GR) programs were evaluated to learn if male and female students differed in their reactions to the programs and if observations of the programs confirmed students' reactions. In-depth interviews were conducted with male and female teaching associates to uncover the need for program improvements beyond those suggested by observation and student reactions. Participating in the PB program were 74 men and 85 women; 79 men and 90 women took part in the GR program. Sex differences were found in the GR program: Female students admitted to greater anxiety about examining male genitalia prior to the program (p = .009) and expressed more dissatisfaction with the timing (too late in the curriculum p = .006). Male students were less likely than females to improve their ability to communicate as a result of the GR program (p = .009). Observations and interviews indicated that the programs were successful in teaching technical skills but that they needed further work in integrating technical and communication training, especially during GR examination training.

Modulation of arachidonic acid metabolites and vulnerability to ventricular fibrillation during myocardial ischemia in the cat.

To determine the relative importance of arachidonic acid pathway products on vulnerability to ventricular fibrillation (VF), we examined the effects of synthesis inhibitors and a receptor blocker acting in the cyclooxygenase (C) and lipoxygenase (L) pathways on VF thresholds in a feline model of coronary occlusion. Thresholds for the induction of VF wer measured before and after a 5-minute coronary occlusion in drug-treated animals and control subjects. Animals were treated with BW755c, a dual L and C inhibitor, CGS-8515, and L inhibitor, FPL-55712, a leukotriene receptor blocker, or sulfinpyrazone, a C inhibitor. BW755c, CGS-8515, and FPL-55712 all prevented an otherwise significant fall in VF threshold during coronary occlusion (p less than 0.01) independent of an effect on effective refractory period, heart rate, or blood pressure. In contrast, sulfinpyrazone, the only compound devoid of an effect on the L pathway, did not protect against an occlusion-related fall in VF threshold. BW755c and CGS-8515 inhibited the synthesis of L and C metabolites coincident with their protection against VF (p less than 0.01). We conclude that agents that antagonize the effects of L products protect against enhanced ventricular vulnerability during acute ischemia, whereas C inhibition alone may not afford this protection.

A study skills workshop as an integral part of orientation to medical school: the establishment of self-directed learning.

The MCP Program, a prematriculation academic support service workshop for all incoming students, combines techniques of learning style identification, study skills, time management and stress control. This has resulted in higher class performance, the formation of collegial relationships and an early emergence of professional behaviors and leadership.

Effect of thromboxane synthetase inhibition on vulnerability to ventricular arrhythmia following coronary occlusion.

Release of thromboxane (TXA2) during acute myocardial infarction may be an important contributing factor in the genesis of ventricular fibrillation (VF). We assessed the effect of selective TXA2 inhibition on vulnerability to VF after total occlusion of the anterior descending coronary artery in chloralose-anesthetized cats. Animals were pretreated with vehicle or with CGS-13080, a TXA2 synthetase inhibitor, 3.0 or 9.0 mg/kg intravenously. There was an apparent dose-dependent protective effect following CGS-13080 administration, in which the decrease in VF threshold following coronary occlusion was attenuated. Also, the incidence of spontaneous ventricular arrhythmia in the first 30 minutes after occlusion was reduced by two thirds in the 9.0 mg/kg CGS-13080 group compared to the vehicle-treated animals. This protective effect does not appear to be due to a change in hemodynamics, effective refractory periods, or extent of ischemia. TXA2 released during coronary occlusion appears to be arrhythmogenic, and inhibiting its synthesis may be protective.

Arrhythmia inducibility and ventricular vulnerability in a chronic feline infarction model.

Ventricular tachyarrhythmias are the cause of sudden cardiac death in ischemic heart disease. Reliable animal models are necessary to study techniques for identifying individuals at risk and to develop effective modes of therapy. The purpose of the present study was to evaluate the inducibility of ventricular tachyarrhythmias and vulnerability to ventricular fibrillation and to correlate these findings with changes in ventricular refractoriness in a chronic feline model. Twelve conditioned cats were randomly divided into two groups: group A, sham-operated controls (n = 5); or group B, permanent occlusion of the left anterior descending coronary artery (n = 7). Two weeks later, the following measurements were made: (1) assessment of refractory periods at several ventricular sites; (2) inducibility to ventricular tachyarrhythmias; and (3) determination of ventricular fibrillation threshold. After electrophysiologic testing, the animals were killed and the hearts were studied histologically. Ventricular fibrillation thresholds were significantly lower in group B compared with group A (13 +/- 3 vs 46 +/- 9 mA; p less than 0.01). One of the sham-operated controls had induction of nonsustained ventricular tachycardia, while six of the group B animals had reproducible, inducible ventricular tachyarrhythmias (p less than 0.01). There was a significant dispersion in effective refractory periods between normal and infarcted sites in group B (46 +/- 6 msec) not seen in group A (12 +/- 2 msec, p less than 0.01). The group A cats demonstrated minimal damage to the myocardium or cardiac architecture. Group B cats demonstrated extensive, transmural, homogeneous infarcts of approximately 30% of the anterior wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of bretylium and clofilium on dispersion of refractoriness and vulnerability to ventricular fibrillation in the ischemic feline heart.

Bretylium has been shown to have a pronounced antifibrillatory effect. The purpose of this study was to examine the effects of bretylium on changes in vulnerability to ventricular fibrillation (VF) and refractoriness which occur during acute myocardial infarction. Right ventricular VF thresholds and effective refractory periods (ERP) at six left ventricular sites were measured before and serially after left anterior descending coronary occlusion in chloralose-anesthetized cats. In eight untreated animals, there was a decrease in VF thresholds of 73% (p less than 0.01) immediately after occlusion and dispersion of refractoriness (DR) (maximum difference in ERP between normal and ischemic left ventricular sites) increased from 18 +/- 4 to 50 +/- 6 msec (p less than 0.01). Five of eight animals manifested spontaneous VF within the first minutes of occlusion but none had nonsustained VF. Pretreatment with bretylium (10 to 20 mg/kg intravenously) increased resting ERP from 181 +/- 9 to 201 +/- 9 msec (p less than 0.05) and VF threshold from 32 +/- 5 to 85 +/- 7 mA (p less than 0.001). Bretylium also prevented spontaneous VF in all eight animals and abolished occlusion-related changes in VF and DR. Fourteen animals were similarly studied using clofilium, a bretylium congener which is devoid of sympatholytic effect (no effect on blood pressure response to bilateral carotid artery occlusion). Clofilium increased resting ERP and VF thresholds at both low (0.5 mg/kg intravenously) and high doses (5 mg/kg intravenously). High-but not low-dose clofilium blunted the fall in VF threshold after coronary occlusion. In addition, DR correlated with VF threshold changes at both doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of site of stimulation on measurement of ventricular vulnerability in the normal and ischemic feline heart.

Site of stimulation is an important variable in the inducibility of ventricular tachycardia in both non-human animal infarction models and in humans; that is, proximity of the stimulating electrode to the site of reentry facilitates the induction of sustained arrhythmia. Whether site of stimulation is decisive in measurement of vulnerability to ventricular fibrillation (VF) during acute coronary occlusion has not been fully evaluated. We measured VF thresholds in 9 chloralose-anesthetized cats at 2 right ventricular and 3 left ventricular sites (2 endocardial, 3 intramural) before and after abrupt occlusion of the anterior descending coronary artery. VF thresholds were measured using a single stimulus of increasing intensity delivered during ventricular drive. Although VF thresholds were lower at endocardial sites, there were no significant differences in VF threshold among any of the sites tested at control. After occlusion, VF thresholds fell to a similar extent at all 5 sites tested. The percent reduction in VF threshold at any site was not influenced by the sequence of testing. VF may be precipitated from multiple sites and, unlike ventricular tachycardia, does not represent an isolated focus of arrhythmogenicity.

Effect of sulfinpyrazone on ventricular arrhythmia, prostaglandin synthesis, and catecholamine release following coronary artery occlusion in the cat.

We examined if inhibition of endogenous prostaglandin (PG) synthesis reduced the severity of ventricular arrhythmia and the incidence of ventricular fibrillation (VF) following occlusion of the left anterior descending coronary artery (LAD) in anesthetized cats. We also determined whether the PGs were interacting in a facilitory manner with the sympathetic nervous system to produce arrhythmia and VF after LAD occlusion. Sulfinpyrazone, an inhibitor of cyclo-oxygenase enzyme, or vehicle was administered intravenously to cats 1 h before LAD occlusion. Sulfinpyrazone completely (p less than 0.001) inhibited the release of 6-keto-PGF1 alpha into the great cardiac vein following LAD occlusion. Sulfinpyrazone (100 mg/kg) significantly (p less than 0.001) reduced the amount of ventricular arrhythmia and the incidence of VF (p less than 0.05) in the 1st h after LAD occlusion. In addition to 6-keto-PGF1 alpha sulfinpyrazone also (p less than 0.001) inhibited the increase in plasma norepinephrine from the heart due to sympathetic nervous system stimulation following LAD occlusion. Since sulfinpyrazone was ineffective in increasing the dose of digoxin required to produce arrhythmia and death, sulfinpyrazone apparently did not depress cardiac excitability. Finally, the extent of infarction resulting from LAD occlusion was not different in sulfinpyrazone-treated animals compared with control. These data indicate that sulfinpyrazone, by inhibiting endogenous PG synthesis in the heart following LAD occlusion, may prevent a facilitory interaction between PGs and the sympathetic nervous system that contributes, in part, to the development of ventricular arrhythmia and VF normally associated with this event.

The effect of sulfinpyrazone on the response to sympathetic nervous system stimulation.

The purpose of this study was to determine if sulfinpyrazone has a direct action on sympathetic nerve endings to prevent release of the transmitter. Pre-synaptic and post-synaptic events as well as direct sympathetic nervous system stimulation were tested in 15 alpha-chloralose anesthetized cats before and 1 hour after sulfinpyrazone (100 mg . kg-1, i.v.). Heart rate response to cardiac accelerator nerve stimulation or to increasing doses of isoproterenol was not significantly depressed by sulfinpyrazone. In addition, no alteration in the reflex activation of the sympathetic nervous system in response to histamine was observed following sulfinpyrazone. Both norepinephrine and epinephrine levels were similar to those levels reported previously by Smith and Robinson for (7) untreated cats. We conclude sulfinpyrazone has no direct depressing effect on the sympathetic nerve endings and that this mechanism cannot explain the reported beneficial effect of sulfinpyrazone on coronary occlusion induced arrhythmias.

Role of the adrenergic nerve terminal in digitalis-induced cardiac toxicity: a study of the effects of pharmacological and surgical denervation.

This study determined whether the protective action of bretylium against ouabain-induced ventricular arrhythmia in the cat is related to an action of bretylium on the adrenergic nerve terminal. Bretylium pretreatment (20 mg/kg, i.v.) administered 2 h prior to ouabain (2 micrograms/kg/min, i.v. until death) increased the dose of ouabain to produce premature ventricular contraction, ventricular tachycardia, and death from 77.2 +/- 5.2 to 107.7 +/- 6.7 micrograms/kg; from 84.9 +/- 5.2 to 113.9 +/- 7.1 micrograms/kg; and from 108.8 +/- 4.0 to 146.7 +/- 5.7 micrograms/kg, respectively (p less than 0.05). Surgical denervation 2 weeks prior to the experiment or 6-hydroxydopamine (6OH dopamine), 20 mg/kg, i.v., administered 3 or 14 days prior to the ouabain infusion did not protect against the arrhythmogenic effects of ouabain. When bretylium was administered to cats pretreated with 6OH dopamine 3 days prior to the ouabain infusion or to surgically denervated cats, the protective action against ouabain-induced arrhythmia did not develop. Since 6OH dopamine and surgical denervation prevented the action of bretylium on ouabain-induced ventricular arrhythmia, it appears that bretylium is acting on the adrenergic nerve terminal. Thus, agents like bretylium that act on the adrenergic nerve terminal, leaving it structurally intact but not functional, are effective against ouabain-induced ventricular arrhythmia while procedures which cause the degeneration of the adrenergic nerve terminal, such as 6OH dopamine and surgical denervation, are not. These observations indicate that for the protective effect of sympathectomy against ouabain-induced arrhythmia to develop, the adrenergic nerve terminal must be present, although not functional as far as adrenergic neurotransmission is concerned. Changes in the heart rate or blood pressure did not appear to be a factor in the protective effect of bretylium.

The action of reserpine, 6-hydroxydopamine, and bretylium on digitalis-induced cardiotoxicity.

This study determined whether the protective effect of reserpine against ouabain-induced ventricular arrhythmias in the cat is due to an action of the drug on the adrenergic nerve terminal. Reserpine (5 mg/kg i.p.) administered 24 h prior to ouabain (2 micrograms/kg per min i.v., until death) increased the dose of ouabain to produce premature ventricular contractions, ventricular tachycardia, and death from 77.3 +/- 5.2 to 105.0 +/- 6.0; 84.9 +/- 5.2 to 132.7 +/- 9.1; and 108.8 +/- 4.0 to 165.7 +/- 10.4 micrograms/kg, respectively (P less than 0.05). When 6-hydroxydopamine (6OHDA; 20 mg/kg i.v.) was given 3 days prior to the experiment, the protective effect of reserpine was not evident. When bretylium (20 mg/kg i.v., 2 h prior to ouabain) was administered to animals previously treated with reserpine, the dose of ouabain which produced premature ventricular contractions, ventricular tachycardia, and death was increased to 109.0 +/- 7.2; 146.1 +/- 12.6; and 165.8 +/- 7.6 micrograms/kg, respectively (P less than 0.05). However, the magnitude of this protective action was similar to that produced by reserpine alone. Lathers et al. (Fed. Proc. 40, 672, 1981) reported that bretylium alone provides protection of a similar order of magnitude as reserpine. Thus, the effects of reserpine and bretylium were not additive; this indicates that the two agents may be acting on the same locus or they may be acting at different sites with the action of one drug masking or blocking the action of the other. Since 6OHDA prevented the action of reserpine on ouabain-induced ventricular arrhythmia and since 6OHDA only produces degeneration of adrenergic nerve terminals, it is probable that the protective effect of both reserpine and bretylium is due to an action at the adrenergic nerve terminal. The heart rate and blood pressure were not involved in the antiarrhythmic effects of reserpine.

Effect of prostaglandin synthesis inhibition and sympathectomy on ouabain-induced arrhythmia in cats.

The purpose of this study was to examine the importance of endogenous prostaglandins (PGs) and sympathectomy on the arrhythmogenic action of ouabain. Cats, anesthetized with dial-urethane, were infused intravenously with ouabain continuously. The dose of ouabain necessary to produce arrhythmia (AR), ventricular tachycardia (VT), and death was determined. Pretreatment with sulfinpyrazone at 100 mg kg-1 i.v. 1 h before glycoside infusion was used to inhibit PG synthesis. Removal of endogenous PGs with sulfinpyrazone reduced the cardiotoxic dose of ouabain. Sympathetic influences were removed by: (a) destroying sympathetic nerve terminals with 6-hydroxydopamine (6-OHDA); (b) depleting nerve terminal catecholamines with reserpine; or (c) preventing catecholamine release from the nerve terminal with bretylium. Reduction of sympathetic influences with reserpine or bretylium increased the cardiotoxic dose of ouabain; whereas removal of nerve terminals with 6-OHDA did not alter the toxic dose of ouabain from that found in control animals. When endogenous PG synthesis was inhibited with sulfinpyrazone the protective effects of reserpine and bretylium were eliminated. These results suggest that endogenous PGs protect against the arrhythmogenic action of ouabain, not only by interfering with catecholamine influences at the sympathetic nerve terminal, but also by a mechanism independent of sympathetic inhibition. Furthermore, the protective action of agents which diminishes the cardiotoxic action of ouabain by interfering with sympathetic influences is lost when endogenous PGs are removed. Finally, 6-OHDA, which destroys the sympathetic nerve terminals, removes both the arrhythmic influence of the catecholamine as well as the protective influence of the PG, resulting in no net change in the cardiotoxic dose of this glycoside.

Changes in vagal activity and response to muscarinic receptor agonists with age.

The response to vagal nerve and muscarinic receptor stimulation was evaluated in young (90 day), adult (365 day) and old (730 day) male F-344 rats anesthetized with urethane. Bilateral vagotomy produced a significant increase in heart rate in the young and adult animals (p < 0.05), while no change in heart rate occurred in the old animals. Stimulation of the right vagus nerve produced a frequency dependent decrease in response to right vagus nerve stimulation with age (p < 0.05; analysis of variance), i.e., old animals had a smaller decrease in heart rate over the same frequency range of nerve stimulation than either the young or adult animals. The effect of age on the response of the muscarinic receptor was examined using cumulative doses of methacholine administered by bolus injection. Methacholine produced a dose dependent decrease in heart rate and blood pressure. The heart rate response to methacholine was diminished in the older animals (p < 0.05; analysis of variance). Similar results were obtained after atropine although the doses of methacholine employed were much greater. In contrast, although methacholine decreased blood pressure in all animals at each age there was no change in the hypotensive response to methacholine with age. These data indicate that there is a diminution in vagal control of heart rate with age as well as the response of the vagus nerve to stimulation. Furthermore, the response of the muscarinic receptor in the heart declines with age while that in the peripheral vasculature does not.