A study was conducted to determine the patterns of opioid use in patients under the care of specialist palliative care (SPC) teams in Trent Region, both in the community and in inpatient settings. The design was a survey of point prevalence by case note and drug chart review. The case notes and prescription records of 1007 patients were reviewed, and data collected on age, sex, diagnosis, date of referral, care settings, opioid form and dose on referral, and most recent opioid form and dose. Nine hundred and seventy patients had cancer; their ages ranged from 18 to 98 years (mean 66.5; median 69). Care was delivered by community specialist nurse for 39%, hospice daycare (DC) for 31%, hospice based homecare for 11%, hospice inpatient unit (IPU) for 15%, hospice outpatient (OP) for 5%, and other for 0.5%. There was no record of medication in 2% of the notes. No opioids had been prescribed for 43% of patients (range 24% IPU to 49% DC), 10% of patients were using weak opioids only (range 0.9% IPU to 16% OP), and 45% of patients were using strong opioids (range 39% DC to 75% IPU), the majority being on morphine (87% of total strong opioids). Daily oral morphine equivalence (OME) dosages ranged form 0.4 mg to 3600 mg (mean 166; median 60; mode 60). Dose changes under SPC ranged from -780 mg to +3900 mg OME, 42% patients having had no change in their dosage and 15% having reduced their opioid dose whilst under SPC. This survey challenges the popular impression that patients receiving SPC require large doses of morphine. The highest prevalence of potent opioid prescribing was in hospice IPUs, largely owing to the use of parenteral diamorphine. Conversely, IPUs had the lowest prevalence of weak opioids. Staff caring for patients with cancer must consider the need for downward as well as upward titration of opioid dosages.

Diastolic time intervals (DTIs) were calculated from simultaneous recordings of a phonocardiogram, apexcardiogram, and echocardiogram in 84 patients with hypertrophic cardiomyopathy and 35 patients with hypertrophy secondary to chronic pressure and volume loading and were compared with those in 31 normal subjects. The isovolumetric relaxation period (IRP) was measured as the interval from the aortic closure sound (A2, phonocardiography) to the opening of the mitral valve (MO, echocardiography) and the interval from A2 to the 0 point of the apexcardiogram was used as an index of total relaxation. Their difference, the MO-0 interval, was also calculated. In 12 patients with volume loading secondary to mitral regurgitation there was no significant difference in any of the DTIs compared with those in normal subjects. There was a wide range of IRPs (from 10 to 90 msec), and hemodynamic correlation in a representative patient with a short A2-MO interval revealed that this was due to premature MO secondary to a high V wave in the wedge pressure. In 12 patients with volume loading secondary to chronic aortic regurgitation there was an increase in the IRP (83 + 26 vs 62 + I I msec; p < .001) and a decrease in the MO-0 interval (48 + 27 vs 67 + 15 msec; p < .01), with no significant difference in their sum (the A2-0 interval). Hemodynamic data in one patient demonstrated that prolonged IRP was secondary to the large pressure drop from the A2 to the MO. In 11 patients with chronic pressure overload secondary to valvular aortic stenosis and in the 84 patients with hypertrophic cardiomyopathy there was no significant difference in the IRP as compared with that in normal subjects; in patients with these conditions the MO-0 interval was significantly increased, as was the A2-0 interval in the patients with hypertrophic cardiomyopathy. In four of the patients with aortic stenosis and in 15 patients with hypertrophic cardiomyopathy, the IRP was more than 2 SDs below the mean value in normal subjects. Hemodynamic correlation at cardiac catheterization in patients with both conditions demonstrated that a delayed A2 was primarily responsible for the abbreviated A2-MO interval and that this was secondary to a large left ventriculoaortic pressure gradient and/or the "hangout" phenomenon. In this situation A2 is an inappropriate marker of the onset of rapid left ventricular pressure decline and the A2-MO interval is not a valid reflection of diastolic relaxation. We conclude that the duration of DTIs is multifactorially determined and that none of these noninvasively measured intervals is a consistently valid gauge of left ventricular relaxation. In left ventricular hypertrophy, in which alterations in preload, afterload, and the timing of A2 are common, as are primary changes in the rate of left ventricular pressure decline, the duration of these intervals will represent the net effect of all of their determinants. Circulation 68, No. 1, 76-87, 1983

No abstract

Previous reports have demonstrated that patients with hypertrophic cardiomyopathy have a prolonged isovolumic relaxation period as a result of a delay in mitral valve opening, reflecting a reduced rate of fall of left ventricular pressure. This period as measured from the aortic closure sound (A2 on phonocardiogram) to the opening of the mitral valve (on echocardiogram) was determined in 84 patients with hypertrophic cardiomyopathy and compared with findings in 31 normal volunteers. The duration of the isovolumic relaxation period in the 84 patients had a wide range from 0 to 160 ms (mean 71 +/- 32) that was not significantly different from that in normal subjects (63 +/- 11 ms). However, it was possible to identify a group of 15 patients with an extremely short isovolumic relaxation period, 2 standard deviations below the normal range. This shortening was due to a marked delay in aortic closure sound (A2) due to late left ventricular-aortic pressure crossover, as well as early opening of the mitral valve secondary to elevated left atrial pressure, which was confirmed by hemodynamic correlations and digitized echocardiographic data. In this subset of patients, A2 is a poor marker of the onset of rapid left ventricular pressure decline and, thus, the interval from A2 to mitral valve opening is not a valid reflection of left ventricular relaxation. It is concluded that in hypertrophic cardiomyopathy, both the timing and sequence of relaxation are abnormal, as is the rate of relaxation. Furthermore, the isovolumic relaxation period is multifactorially determined and depends not only on the rate of left ventricular pressure decline, but also on the magnitude of the pressure drop from A2 to mitral valve opening. All of these determinants must be kept in mind when the isovolumic relaxation period is used as a measure of left ventricular relaxation.