Stephen Schmaltz

Upper Gastrointestinal (GI) pH in Young, Healthy Men and Women

The pH in the upper gastrointestinal tract of young, healthy men and women was measured in the fasting state and after administration of a standard solid and liquid meal. Calibrated Heidelberg capsules were used to record the pH continuously over the study period of approximately 6 hr. In the fasted state, the median gastric pH was 1.7 and the median duodenal pH was 6.1. When the meal was administered the gastric pH climbed briefly to a median peak value of 6.7, then declined gradually back to the fasted state value over a period of less than 2 hr. In contrast to the pH behavior in the stomach, feeding a meal caused a reduction in the median duodenal pH to 5.4. In addition, there was considerable fluctuation in the postprandial duodenal pH on an intrasubject basis. The pH in the duodenum did not return to fasted state values within the 4-hr postprandial observation period. There was no tendency for the duodenal pH to be related to the gastric pH in either the fed or fasted phases of the study. Furthermore, pH in the upper GI tract of young, healthy subjects appears to be independent of gender. The differences in upper GI pH between the fasted and the fed state are discussed in terms of dosage form performance and absorption for orally administered drugs.

Accountability Measures — Using Measurement to Promote Quality Improvement

Measuring the quality of health care and using those measurements to promote improvements in the delivery of care, to influence payment for services, and to increase transparency are now commonplace. These activities, which now involve virtually all U.S. hospitals, are migrating to ambulatory and other care settings and are increasingly evident in health care systems worldwide. Many constituencies are pressing for continued expansion of programs that rely on quality measurement and reporting. In this article, we review the origins of contemporary standardized quality measurement, with a focus on hospitals, where such programs have reached their most highly developed state. We discuss some lessons learned from recent experience and propose a conceptual framework to guide future developments in this fast-moving field. Although many of the points we make are relevant to all kinds of quality measurement, including outcome measures, we focus our comments on process measures, both because these account for most of the measures in current use and because outcome measures have additional scientific challenges surrounding the need for case-mix adjustment. We write not as representatives of the Joint Commission articulating a specific new position of that group, but rather as individuals who have worked in the fields of quality measurement and improvement in a variety of roles and settings over many years.

Upper gastrointestinal pH in seventy-nine healthy, elderly, North American men and women.

Gastric and duodenal pH levels were measured in 79 healthy, elderly men and women (mean ± SD = 71 ± 5 years) under both fasted and fed conditions using the Heidelberg capsule technique. The pH was recorded for 1 hr in the fasted state, a standard liquid and solid meal of 1000 cal was given over 30 min, then the pH was measured for 4 hr postprandially. Results are given as medians and interquartile ranges: fasted gastric pH, 1.3 (1.1–1.6); gastric pH during the meal, 4.9 (3.9–5.5); fasted duodenal pH, 6.5 (6.2–6.7); and duodenal pH during the meal, 6.5 (6.4–6.7). Although fasted gastric pH, fasted duodenal pH, and duodenal pH during the meal differ statistically from those observed in young subjects, the differences are not expected to be clinically significant in terms of drug absorption for the majority of elderly subjects. Following a meal, gastric pH decreased from a peak pH of 6.2 (5.8–6.7) to pH 2.0 within 4 hr in most subjects. This rate of return was considerably slower than in young, healthy subjects. Nine subjects (11%) had a median fasted gastric pH >5.0, and in five of these subjects the median pH remained >5.0 postprandially. In this group, drugs and dosage forms which require an acidic environment for dissolution or release may be poorly assimilated.

Evaluation of the predictive value of ICD-9-CM coded administrative data for venous thromboembolism in the United States

OBJECTIVE To determine the positive predictive value of International Classification of Disease, 9th Revision, Clinical Modification (ICD-9-CM) discharge codes for acute deep vein thrombosis or pulmonary embolism. MATERIALS AND METHODS Retrospective review of 3456 cases hospitalized between 2005 and 2007 that had a discharge code for venous thromboembolism, using 3 sample populations: a single academic hospital, 33 University HealthSystem Consortium hospitals, and 35 community hospitals in a national Joint Commission study. Analysis was stratified by position of the code in the principal versus a secondary position. RESULTS Among 1096 cases that had a thromboembolism code in the principal position the positive predictive value for any acute venous thrombosis was 95% (95%CI:93-97), whereas among 2360 cases that had a thromboembolism code in a secondary position the predictive value was lower, 75% (95%CI:71-80). The corresponding positive predictive values for lower extremity deep-vein thrombosis or pulmonary embolism were 91% (95%CI:86-95) and 50% (95%CI:41-58), respectively. More highly defined codes had higher predictive value. Among codes in a secondary position that were false positive, 22% (95%CI:16-27) had chronic/prior venous thrombosis, 15% (95%CI:10-19) had an upper extremity thrombosis, 6% (95%CI:4-8) had a superficial vein thrombosis, and 7% (95%CI:4-13) had no mention of any thrombosis. CONCLUSIONS ICD-9-CM codes for venous thromboembolism had high predictive value when present in the principal position, and lower predictive value when in a secondary position. New thromboembolism codes that were added in 2009 that specify chronic thrombosis, upper extremity thrombosis and superficial venous thrombosis should reduce the frequency of false-positive thromboembolism codes.

Hospital performance trends on national quality measures and the association with joint commission accreditation

BACKGROUND Evaluations of the impact of hospital accreditation have been previously hampered by the lack of nationally standardized data. One way to assess this impact is to compare accreditation status with other evidence-based measures of quality, such as the process measures now publicly reported by The Joint Commission and the Centers for Medicare and Medicaid Services (CMS). OBJECTIVES To examine the association between Joint Commission accreditation status and both absolute measures of, and trends in, hospital performance on publicly reported quality measures for common diseases. DESIGN, SETTING, AND PATIENTS Performance data for 2004 and 2008 from U.S. acute care and critical access hospitals were obtained using publicly available CMS Hospital Compare data augmented with Joint Commission performance data. MEASUREMENTS Changes in hospital performance between 2004 and 2008, and percent of hospitals with 2008 performance exceeding 90% for 16 measures of quality-of-care and 4 summary scores. RESULTS Hospitals accredited by The Joint Commission tended to have better baseline performance in 2004 than non-accredited hospitals. Accredited hospitals had larger gains over time, and were significantly more likely to have high performance in 2008 on 13 out of 16 standardized clinical performance measures and all summary scores. CONCLUSIONS While Joint Commission-accredited hospitals already outperformed non-accredited hospitals on publicly reported quality measures in the early days of public reporting, these differences became significantly more pronounced over 5 years of observation. Future research should examine whether accreditation actually promotes improved performance or is a marker for other hospital characteristics associated with such performance. Journal of Hospital Medicine 2011;6:458–465.

Electrophysiologic effects of epinephrine in humans

The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.

Differences in QRS configuration during unipolar pacing from adjacent sites: Implications for the spatial resolution of pace-mapping

To examine the spatial resolution of unipolar pace-mapping, 12 lead electrocardiograms (ECGs) recorded during pacing from each of the poles of a quadripolar catheter (5 mm interelectrode distance) were examined. Unipolar pacing was performed from each of the poles at late diastolic threshold, twice threshold and 10 mA at a cycle length of 500 ms. In 15 patients, pacing was performed at the right ventricular apex and in 14 at various left ventricular sites. Pacing from the distal catheter pole at threshold (index ECG) was used to simulate the site of origin of ventricular tachycardia, and all other ECGs were compared with the index ECG. Electrocardiograms were evaluated by two independent observers for 1) minor configuration differences (notch, new small component, change in the amplitude of individual components or change in QRS shape); 2) major differences in configuration (new large component, marked change in the amplitude of an existing component or two minor changes); and 3) peak to peak changes in amplitude. Minor differences in configuration were seen in a mean 2.4 +/- 1.9, 4.6 +/- 2.4 and 4.4 +/- 2.9 leads during pacing at 5, 10 and 15 mm from the distal electrode (index site). Major differences in configuration were seen in a mean of 0.3 +/- 0.5, 2.1 +/- 2.1 and 3.7 +/- 2.3 leads during pacing at 5, 10 and 15 mm from the index site. Differences in amplitude were seen in a mean of 3.1 +/- 2.2, 5.6 +/- 2.5 and 6.8 +/- 3.0 leads per ECG during pacing at 5, 10 and 15 mm from the index ECG pacing site, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of Nonsustained Ventricular Tachycardia Guided By Electrophysiological Testing

Two hundred eighty patients with spontaneous nonsusfained ventricular tachycardia were treated based on the results of electrophysiological testing. Seventy‐nine patients had no evidence of structural heart disease, 134 had coronary artery disease, 43 had idiopathic dilated cardiomyopathy, and 24 patients had miscellaneous types of heart disease. Sustained monomorphic ventricular tachycardia was induced during electrophysiological testing in the drug free state in 52 of 280 patients (19%). Ventricular tachycardia was induced more frequently in patients with coronary artery disease (32%) than in any of the other groups (P < 0.001). The patients with inducible sustained monomorphic ventricular tachycardia underwent a mean of 1.9 ± 1.3 drug trials. Twenty‐five patients had the induction of ventricular tachycardia suppressed by pharmacological therapy and were treated with the drug judged to be effective during electropharmacological testing. Twenty‐seven patients continued to have inducible sustained monomorphic ventricular tachycardia despite antiarrhythmic therapy and were discharged on the drug that made induced ventricular tachycardia best tolerated. Forty‐five of 280 patients (16.1%) died during a mean follow‐up period of 19.6 ± 14.4 months, There were 15 sudden cardiac deaths, 21 nonsudden cardiac deaths, 6 noncardiac deaths, and 3 deaths that could not be classified. Sudden cardiac death mortality was lowest in the patients without structural heart disease (0% at 2 years), intermediate in the patients with coronary artery disease and miscellaneous heart disease (4% al 2 years), and highest in the patients with idiopathic dilated cardiomyopathy (13% at 2 years; P < 0.01 for pairwise comparisons). No patient treated with a drug that had suppressed the induction of sustained ventricular tachycardia died suddenly during the follow‐up period whereas four of 27 patients who were discharged on “ineffective antiarrhythmic drugs” and 11 of 228 patients without inducible sustained ventricular tachycardia experienced sudden cardiac death during the follow‐up period. By multivariate analysis, ejection fraction and inducible ventricular tachycardia during the predischarge eiectrophysiological test were independent predictors of sudden cardiac death. In conclusion, in patients with spontaneous nonsustained ventricular tachycardia: (1) Arrhythmia inducibility varies depending on the underlying heart disease. Ventricular tachycardia is most often inducible in patients with coronary artery disease and least often in patients without structural heart disease; (2) With the exception of patients with idiopathic dilated cardiomyopathy, management of patients with nonsustained ventricular tachycardia guided by electrophysiological testing appears to result in a low incidence of sudden cardiac death although effects on total mortality are less impressive; and (3) Patients with idiopathic dilated cardiomyopathy and patients with other heart diseases who continue to have inducible ventricular tachycardia despite antiarrhythmic drug therapy are at substantial risk of sudden cardiac death.

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Magnitude and time course of beta-adrenergic antagonism during oral amiodarone therapy☆

To examine the presence and time course of beta-adrenergic antagonism produced by amiodarone, the heart rate, QT interval and arrhythmia frequency in response to graded doses of isoproterenol were evaluated in eight patients treated with oral amiodarone for sustained ventricular tachycardia. Measurements were made before and every 2 days after beginning oral amiodarone therapy (600 mg twice daily). Isoproterenol was given in doses of 12.5, 25 and 50 ng/kg body weight per min. The mean heart rate at rest decreased from 73.1 +/- 17.8 beats/min on day 0 to 57.8 +/- 15.0 beats/min after 12 days of amiodarone therapy. A significant linear decline in heart rate at rest was observed until day 6 (p less than 0.05 for all comparisons). On all days isoproterenol produced a progressive increase in heart rate that reached 115.5 +/- 20.2 beats/min on day 0 and 94.2 +/- 18.5 beats/min on day 12. Amiodarone blunted the heart rate increase produced by isoproterenol on days 2 to 12 (p less than 0.05 versus day 0). This effect was present by day 2 and did not change significantly thereafter. The mean corrected QT (QTc) interval increased from 430 +/- 30 ms on day 0 to 449 +/- 63 ms on day 12. A significant linear increase in QTc interval was observed until day 6 (p less than 0.05 for all comparisons). There was no systematic effect of isoproterenol on the QTc interval. Five of eight patients had a significant number of isoproterenol-induced premature ventricular complexes. Ventricular ectopic activity in response to isoproterenol was abolished after 4 days of amiodarone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)