What health plans should know about clinical practice guidelines--round-table discussion.

Quality is the watchword for health plans that wish to survive to see the new century, and accreditation by the National Committee for Quality Assurance is becoming quality's indispensable stamp. Practice guidelines are an imperative for that accreditation. Here's what seven managed care leaders had to say about guidelines in a recent round-table discussion.

Can residents be trained to counsel patients about quitting smoking? Results from a randomized trial.

STUDY OBJECTIVE: To evaluate the effectiveness of two teaching interventions to increase residents' performance of smoking cessation counseling. DESIGN: Randomized controlled factorial trial. SETTING: Eleven residency programs, in internal medicine (six), family medicine (three), and pediatrics (two). Programs were located in three university medical centers and four university-affiliated community hospitals. PARTICIPANTS: 261 residents who saw ambulatory care patients at least one half-day per week, and 937 returning patients aged 17 to 75 years who reported having smoked five or more cigarettes in the preceding seven days. Of the 937, 843 were eligible for follow-up, and 659 (78%) were interviewed by phone at six months. INTERVENTIONS: Two interventions (tutorial and prompt) and four groups. The tutorial was a two-hour educational program in minimal-contact smoking cessation counseling for residents. The prompt was a chart-based reminder to assist physician counseling. One group of residents received the tutorial; one, the prompt; and one, both. A fourth group received no intervention. MEASUREMENT AND RESULTS: Six months after the intervention, physician self-reports showed that residents in the tutorial + prompt and tutorial-only groups had used more counseling techniques (1.5-1.9) than had prompt-only or control residents (0.9). Residents in all three intervention groups advised more patients to quit smoking (76-79%) than did control group residents (69%). The tutorial had more effect on counseling practices than did the prompt. Physician confidence, perceived preparedness, and perceived success followed similar patterns. Exit interviews with 937 patients corroborated physician self-reports of counseling practices. Six months later, self-reported and biochemically verified patient quitting rates for residents in the three intervention groups (self-reported: 5.3-8.2%; biochemically verified: 3.4-5.7%) were higher than those for residents in the control group (self-reported: 5.2%; biochemically verified: 1.7%), though the differences were not statistically significant. CONCLUSION: A simple and feasible educational intervention can increase residents' smoking cessation counseling.

Smoking cessation counseling by resident physicians in internal medicine, family practice, and pediatrics.

Residents in primary care specialties care for many patients who smoke cigarettes, but little is known about their smoking cessation counseling (SCC). We surveyed 309 residents (72 family practice, 171 internal medicine, and 66 pediatrics residents) in 13 programs to determine their practices, knowledge, attitudes, and training in SCC. More than 90% thought physicians are responsible for SCC, the majority routinely took smoking histories, and 80% attempted to motivate patients to quit smoking. However, 25% or fewer reported discussing obstacles to quitting, setting a quit date, prescribing nicotine gum, scheduling follow-up visits, or providing self-help materials. Family practice residents used more SCC techniques (1.8) than did internal medicine (0.8) and pediatrics (0.1) residents. Only 54% of residents reported recent SCC training and 13% reported formal SCC training. Recent training correlated with the number of counseling techniques used. Residents in primary care specialties report positive attitudes but inadequate practice and training in SCC.

Clinical pharmacology of carvedilol in normal volunteers.

The mechanism of the vasodilatory action of carvedilol (BM 14190), a new antihypertensive agent, was investigated in normal volunteers. Intra-arterial blood pressure and ECG were monitored continuously. Carvedilol (1 mg/min for 15 minutes) produced a rapid reduction in blood pressure and a transient increase in heart rate. At the end of infusion, systolic and diastolic blood pressure were reduced by 23% (-32.3 mm Hg) and 18% (-13.6 mm Hg), respectively, whereas heart rate was not different from baseline. At the doses used, the hypotensive effect of carvedilol was greater than that of labetalol (36 and 72 mg in 15 minutes). Carvedilol and labetalol antagonized isoproterenol-induced hypotension and tachycardia, at serum levels greater than or equal to 8 and 20 mg/ml, respectively. Both drugs antagonized phenylephrine pressor effects. A similar degree of inhibition (25% of control) of pressor effects was observed for carvedilol and labetalol when their respective serum concentrations were 23 ng/ml and 80 ng/ml. Neither carvedilol nor labetalol had any effect on AII pressor responses. Carvedilol serum levels as high as 150 ng/ml failed to inhibit AII-induced pressor responses. Our results suggest that at the doses used in this study, carvedilol has both alpha 1-and nonselective beta-receptor blocking properties. Moreover, carvedilol is approximately three to five times more potent than labetalol in blocking alpha 1-and beta-receptors and in reducing blood pressure.

Mechanism of the vasodilatory effect of carvedilol in normal volunteers: a comparison with labetalol.

In a single blind parallel design, saline (n = 9), labetalol i.v. (40 mg n = 4, 80 mg n = 3), and carvedilol i.v. (15 mg n = 8) were given to volunteers with blood pressure (BP) recorded intraarterially. The effect of these treatments on the response to challenge doses of angiotensin II (to give a rise in mean BP of 20-25 mm Hg), isoproterenol (to give an increase in heart rate of 30-35 beats/min), and phenylephrine (to give a rise in mean BP of 20-25 mm Hg) were studied. The dose of i.v. carvedilol employed gave a greater fall in BP than the dose of labetalol used. Carvedilol appeared to be about four times more potent than labetalol in inhibiting the tachycardia to isoprenaline. Likewise, from inhibition of the pressor response to phenylephrine, it is concluded that carvedilol is four times more effective at the alpha receptor than labetalol. Neither drug was found to antagonize the pressor effects of angiotensin. Calculation of the half-life of carvedilol gave values of 2.2 to 9 h. The volume of distribution was found to be 1.54 l/kg and the total body clearance was 0.521 l/h/kg.