Robert G. Carroll

CT determination of tibial tubercle lateralization in patients presenting with anterior knee pain

Anterior knee pain is commonly associated with patellofemoral malalignment. Both conventional radiographic measurements and CT measurements have been proposed to define and confirm the sometimes difficult clinical diagnosis of anterior knee pain secondary to patellofemoral malalignment. Using CT imaging with computerized technique to measure anatomic relationships, we evaluated patients (n=50) with anterior knee pain for excessive lateralization of the tibial tubercle. The symptomatic knee of each patient was compared with their asymptomatic knee as well as with the knees of patients with other causes of anterior knee pain (n=10) and with the knees of asymptomatic controls (n=10). The symptomatic knee of patients with suspected patellofemoral malalignment demonstrated significantly greater lateralization of the tibial tubercle (12.2±0.5 mm) than did the asymptomatic knee (9.0±0.7 mm). The symptomatic knees of patients with patellofemoral malalignment also demonstrated significantly greater lateralization of the tibial tubercle than did the knees of patients with other causes of anterior knee pain (5.9±0.9 mm). When a control population was added to the analysis, the patients with symptomatic patellofemoral malalignment demonstrated significantly greater lateralization of the tibial tubercle than did the controls (6.4±0.4 mm). Using a critical value of 9 mm lateralization, the CT diagnosis of patellofemoral malalignment had a specificity of 95% and a sensitivity of 85%. We conclude that CT determination of tibial tubercle position assists the diagnosis of patellofemoral malalignment.

Treatment of verapamil overdose with glucagon in dogs.

STUDY OBJECTIVE The purpose of this study was to evaluate the effectiveness of glucagon as a treatment for the hemodynamic effects of verapamil overdose in a canine model. DESIGN The study was performed in a nonblinded, controlled animal model. INTERVENTIONS Pentobarbital-anesthetized and instrumented dogs were maintained and observed for 60 minutes or until death. All animals were overdosed with 15 mg/kg i.v. verapamil over 30 minutes. Mean arterial pressure, heart rate, ECG, and cardiac output were monitored. The experimental group received a 2.5 mg glucagon i.v. bolus followed by a glucagon drip at 2.5 mg/hr. The control group received an equal volume of i.v. normal saline solution in the same fashion. Analysis was performed with the Dunnett and Tukey-Kramer methods, with alpha set at .05. RESULTS There were eight experimental and seven control animals, with mortality rates of 0% and 29%, respectively. The experimental group had increases in cardiac output and heart rate that were statistically significant at 45 and 60 minutes compared with those of the control group. In addition, there was a significant difference in heart rate at 30 minutes. No difference was noted between the groups for mean arterial pressure. CONCLUSION Glucagon appears to reverse both the bradycardia and the depressed cardiac output associated with verapamil overdose in a canine model.

Implications of adult education theories for medical school faculty development programmes

Adult education principles have impacted the approach used by many faculty development programmes. Underlying themes of immediacy of application, task centered opportunities to practice skills, and feedback on efforts are common to most popular approaches. Less common are instances where the need to know is initially communicated, or provision of opportunities to direct course content. Incorporation of sound adult educational principles into the design of faculty development programmes should enhance its reception by the faculty, and increase its value to the school.

Environmental temperature variations cause degradations in epinephrine concentration and biological activity

This study determined the biological consequence of temperature induced epinephrine degradation. Two different epinephrine preparations (1:1,000 and 1:10,000) were exposed to either cold (5 degrees C) or hot (70 degrees C) temperature. The exposure occurred for 8-hour periods each day in 4-, 8-, and 12-week intervals. Samples and identical controls were then chemically evaluated using high-pressure liquid chromatography (HPLC), and biological activity of samples showing chemical degradation was assessed in conscious rats. Epinephrine (1:10,000) underwent a significant degradation and a loss of concentration of the parent compound after 8 weeks of heat treatment. By 12 weeks, 64% of the epinephrine was degraded. A smaller (30%) but significant loss of cardiovascular potency was determined by blood pressure and heart rate responses in conscious rats. The degradation of epinephrine (1:1,000) was not statistically significant even after 12 weeks of heat exposure. No change was noted from control in either epinephrine concentration when exposed to cold temperatures. In conclusion, epinephrine (1:10,000) deteriorates in the presence of elevated temperature and should be protected from high temperatures when carried by EMS providers. The degradation products may possess biological activity.

Centrally mediated reduction in cardiac output elicits the enhanced hypotensive effect of clonidine in conscious aortic barodenervated rats

In a previous study, we showed that centrally mediated hypotensive responses are enhanced in aortic barodenervated (ABD) rats as compared with sham-operated (SO) rats. In the present study, we tested the hypothesis that the high basal total peripheral resistance (TPR) of ABD rats accounts for enhanced hypotensive responses to clonidine in this rat model. Aortic barodenervation resulted in acute increases in blood pressure (BP) and heart rate (HR) in anesthetized rats, associated with significant increases in plasma norepinephrine (NE) levels and TPR; cardiac index (CI) and stroke volume (SV) were not affected. After recovery from anesthesia, conscious ABD rats had significantly increased BP at 3 h after barodenervation; BP returned to SO levels by 48 h even though plasma NE levels and TPR remained significantly increased. On the other hand, CI and SV showed significant reductions, beginning at 3 h, and remained low throughout the postdenervation period (48 h); the reduction in CI offset the increase in TRP and may therefore account for the restoration of BP of ABD rats to normal levels. Beginning at similar baseline BP values, cumulative intracisternal (i.c.) doses of clonidine (0.02-2.5 micrograms) elicited greater decreases in BP and plasma NE levels in conscious ABD as compared with SO rats. These responses were centrally mediated because systemic administration of 0.12 micrograms clonidine, a dose that elicited near maximal hypotensive response after i.c. administration, affected neither BP nor plasma NE levels. Contrary to the hypothesis, the hypotensive effect of clonidine in ABD rats resulted exclusively from a reduction in CO (owing to reductions in both HR and SV) because TPR was not affected. These findings suggest that (a) in ABD rats, a reduction in CO offsets a sustained sympathetically mediated elevation in TPR and restores BP to normal levels; and (b) an enhanced hypotensive response to clonidine in ABD as compared with SO rats cannot be accounted for by a higher basal TRP but rather by elicitation of greater reductions in CO through a centrally mediated sympathoinhibitory action.

Ethanol-clonidine hemodynamic interaction in normotensive rats is modified by anesthesia

Our previous findings have shown that ethanol attenuates the decreases in plasma norepinephrine (NE) levels, and blood pressure elicited by centrally acting antihypertensive drugs in spontaneously hypertensive rats (SHRs). The present study investigated whether this interaction can be influenced by baseline blood pressure (BP) and sought direct evidence to support the involvement of the SNS by recording the sympathetic neural activity (SNA) of the splanchnic nerve. The conscious aortic barodenvervated (ABD) rat model was utilized because it exhibits greater hypotensive responses to clonidine compared with sham-operated (SO) rats. Although ABD and SO rats (332 + 33 vs. 227 + 18 pg/ml). Clonidine (30 micrograms/kg, i.v.) elicited significantly greater decreases in mean arterial pressure (MAP; -20.0 + 2.1 vs. -10.4 + 0.8 mm Hg) and plasma NE (-194 + 26 vs. -50 + 11 pg/ml) in conscious ABD vs. SO rats. Ethanol (1 g/kg, i.v.) reversed clonidine-evoked decreases in BP and plasma NE levels, but the interaction was more prominent in ABD rats. To support the hypothesis that the interaction occurs within the CNS, the effect of ethanol was studied on clonidine-evoked decreases in preganglionic SNA and BP in anesthetized rats. In contrast to its effects in conscious rats, ethanol augmented both the hypotensive and sympathoinhibitory responses to clonidine in anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of student performance in multiple-choice and long essay questions in the MBBS stage I physiology examination at the University of the West Indies (Mona Campus)

This retrospective study compared the performance of preclinical medical students in the multiple-choice question (MCQ) and long essay question components of a comprehensive physiology final examination. During the 3 yr analyzed, 307 students had an average score of 47% (SD 9.9) in the long essay questions and 64% (SD 9.9) in the MCQs. Regression analysis showed a significant correlation (r = 0.62, P < 0.01) between MCQs and long essay questions. When student performance was grouped by final course grade, a statistically significant correlation between MCQ and long essay scores existed only for the 210 students who received a passing grade (r = 0.20, P < 0.01). The MCQ and long essay question scores were not correlated for the 57 students who failed (r = 0.25, P = 0.06) or for the 40 students who achieved honors and distinctions (r = -0.27, P = 0.11). MCQ scores were significantly higher (P < 0.01) than essay scores for each of the groups when analyzed by two-way ANOVA. The results of this study suggest that for most students, the strong correlation between scores on MCQs and essay questions indicates that student performance was independent of testing format. For students at either end on the performance spectrum, the lack of correlation suggests that the performance in one of the testing formats had a strong influence on the final course grade. In addition, those students who failed the course were likely to be weak in both testing modalities, whereas students in all grade groups were more likely to perform better in the MCQs than in the long essay questions.

Adverse Effect of Helicopter Flight on the Ability to Palpate Carotid Pulses

STUDY OBJECTIVE To determine if the air medical helicopter environment compromises the ability to palpate carotid pulses. DESIGN Using a carotid pulse model, flight nurses were tested for their ability to palpate the simulated carotid pulse at normal (120/80 mm Hg) and low (80/60 mm Hg) blood pressures on the ground and during helicopter flight. SETTING Palpation tests were performed during flight in an MBB BO-105 twin-turbine engine, single-rotor air medical helicopter; control palpation tests were performed on the ground. TYPE OF PARTICIPANTS Ten flight nurses. MEASUREMENTS AND MAIN RESULTS Tracings of pulsatile pressure from the carotid pulse model verified its ability to simulate a wide range of arterial pressures. Analyses of variance for repeated measures, including polynomial contrasts, were performed to compare the number of correct detections of the presence or absence of pulse pressures in flight with the number of correct detections in the two control conditions for both carotid pulse pressures. The mean in-flight number of correct detections was lower than both the preflight and postflight control tests, which were themselves nearly equal, at each simulated carotid pulse pressure. The quadratic terms for both the 120/80 mm Hg trial (F1,14 = 9.28; P = .0087) and the 80/60 mm Hg trial (F1,18 = 5.69; P = .0283) were statistically significant. CONCLUSION Factors associated with transport of patients in an MBB BO-105 helicopter impair the ability of flight nurses to detect carotid pulses in a simulated physiologic model.

Reduced oxygen consumption precedes the drop in body core temperature caused by hemorrhage in rats.

ABSTRACT This study examines the early time course in core temperature change and oxygen consumption at 4 levels of hemorrhage. Chronically instrumented rats were acclimatized to a respirometry chamber for 30 min. The rats were briefly (10 min) removed from the chamber for a fixed volume hemorrhage of 0 mL/kg (sham), 8 mL/kg, 16 mL/kg, 24 mL/kg, or 32 mL/kg. Rats were then returned to the chamber, and oxygen consumption and body core temperature were monitored for the next 2 h. Oxygen consumption (control 1.26 mL O2/g/h) fell significantly 5 min after hemorrhage in all but the sham and 8 mL/kg hemorrhage groups, with the decrease proportional to the hemorrhage volume. The 32 mL/kg hemorrhage group showed the greatest decrease, to 0.47 mL O2/g/h. Body core temperature (control 37.5°C) fell more gradually, declining to 35.6°C 110 min after the 24 mL/kg hemorrhage, and to 33.2 °C at 6 h after the 32 mL/kg hemorrhage. In the 16 mL/kg hemorrhage group, oxygen consumption fell significantly by 5 min after hemorrhage, but a drop in body temperature was not seen until 25 min after hemorrhage. The data from this study indicate that the drop in core temperature does not cause the observed decrease in oxygen consumption. In fact, the timing and magnitude of the drop in oxygen consumption indicate that the reduced metabolic rate may mediate the hemorrhage‐induced drop in body core temperature in conscious rats.

Reduced metabolic rate accompanies the hemorrhage-induced hypothermia in conscious rats

The mechanism for the hemorrhage-induced drop in body temperature is unknown. This study determined the alterations in cutaneous heat exchange and metabolic heat production caused by a moderate hemorrhage in conscious rats. Chronically instrumented rats were subjected to a 16 ml/kg hemorrhage, followed by a 4-h recovery period, while monitoring body core temperature and cutaneous temperature. Cutaneous heat transfer was disrupted by housing the animals at an elevated (28 degrees C) ambient temperature. A separate group of experiments measured the change in oxygen consumption in the post-hemorrhage period. Moderate hemorrhage caused a drop in body core temperature which stabilized at 0.7+/-0.3 degrees C below control in the second hour following hemorrhage. Disruption of cutaneous heat exchange by reducing the thermal gradient did not diminish the hemorrhage-induced hypothermia. Hemorrhage caused a significant decline of oxygen consumption (-0. 21+/-0.05 ml O(2)/g per h). This 16% drop in resting oxygen consumption was prevented by immediately retransfusing the aspirated blood back into the rat. These data indicate that a decrease in metabolic heat production mediates the drop in body core temperature caused by moderate hemorrhage in conscious rats.