Hospital blood pressure measurement: staff and device assessment.

Evaluation of the ability of clinical staff to measure blood pressure as well as the functional state of hospital sphygmomanometers has consistently demonstrated marked deficiencies. In this study, the working order of all sphygmomanometers (manual and automated) in a teaching hospital was evaluated. Nursing staff were tested on their knowledge and use of such devices and were also asked to estimate the blood pressure from videotape. The accuracy of a commonly used automated device, Dinamap 8100, was also measured. Of 543 manual sphygmomanometers, 14% were in perfect working order although portable devices were more likely to be functional (47% of 36 units). In contrast, all 135 automated portable devices were in perfect working order although service requirements were seldom met. The mean time since last service was 18 months. There appeared to be an inverse correlation between the availability of automated and manual devices and the maintenance of wall-mounted bedside sphygmomanometers. Staff knowledge about manual devices was adequate as was their ability to accurately measure blood pressure using standardised videotape. Forty-two per cent of 31 nurses who completed the test were correct in 9 of 12 blood pressures. A comparison of this result with a comparable group of nurses tested in 1990 did not detect a significant change in competence. Direct evaluation of the commonly used Dinamap 8100 in 47 hospital patients demonstrated a poor correlation with a mercury sphygmomanometer with a D grade (fail) for systolic and a C grade for diastolic pressure. In summary, maintenance of manual sphygmomanometers was very poor, probably due to their lack of use by clinical staff. This was particularly true for units attached to bedside walls. Nursing staff demonstrated significant deficiencies in manual sphygmomanometer use although their skills were similar to those measured several years earlier. Because of the demonstrated inaccuracy of the Dinamap 8100 automated device, the strong trend towards the use of automated devices instead of manual sphygmomanometers within hospitals cannot be supported.

Hypertension treatment compliance: what do patients want to know about their medications?

While poor drug compliance is a significant impediment to the effective treatment of hypertension, knowledge of what patients wish to know about their medications in order to improve compliance is very limited. To develop a preliminary understanding of patients' medication requirements and expectations, a simple 30-item questionnaire was developed and administered to 66 patients who were either taking antihypertensive drugs, or about to commence antihypertensive drug treatment. Ninety percent of patients wanted to know about all possible side effects of medications as well as the most likely side effects. Ninety-six percent wanted to know if their drug treatment would keep them well. In addition, most patients wanted to avoid multiple medications, were concerned about the prospect of life-long treatment, and were worried about potential drug interactions. Effects of the drugs on their lifestyles as well as any lifestyle changes required to augment drug therapy were other issues of concern. The elderly were less interested in many of these issues. A strong desire for further knowledge about their disease was noted in most subjects (82%). If compliance with medication therapy is to be improved, a better understanding of patients' concerns and fears about medications is required, particularly in a relatively asymptomatic disease like hypertension.

Mechanism of lithium-induced polyuria in the rat.

While many studies have demonstrated a nephrogenic diabetes insipidus syndrome (NDI) with prolonged lithium (Li) treatment, experiments in the isolated rat papillary collecting duct have suggested that the defect may be due to a circulating factor that inhibits the action of arginine vasopressin (AVP). Since Li-treatment can produce a form of hyperparathyroidism and parathyroid hormone (PTH) can act as a partial agonist to AVP, in vivo and in vitro studies were performed on rats made polyuric by daily intraperitoneal (i.p.) Li (4 mmol/kg) treatment. Li-treatment for three weeks produced an increase in PTH (194 +/- 20 compared with 118 +/- 18 pg/ml in control rats; P < 0.01) as well as an increase in the plasma calcium concentration (2.38 +/- 0.05 compared with 2.25 +/- 0.04 mmol/liter; P < 0.05). Clearance studies were performed on water loaded Li-treated and control rats, and the defect in urine concentration was only observed with a low physiological concentration of AVP (10 mU/kg body wt over 5 min). Maximal urine osmolality was 328 +/- 31 compared with 613 +/- 81 mOsm/kg (P < 0.05) in controls. There was no detectable difference with a prolonged maximal physiological AVP concentration (10 mU bolus and 50 mU/kg body wt per hr) and papillary solute concentrations were unchanged. When Li-treated rats had been parathyroidectomized (PTX), a significant difference in urine concentration with the low AVP concentration could not be demonstrated when compared to non-PTX control rats. In the isolated papillary collecting duct preparation a medium was used that contained fresh plasma from Li-treated or control rats, both intact and PTX. Experiments using plasma from Li-treated intact rats produced only a 25.4 +/- 5.1% increase in diffusional water permeability with the addition of AVP (200 microU/ml) compared to 52.6 +/- 9.0% in control rats (P < 0.01). However, when plasma from Li-treated PTX rats was used, the AVP induced increase in water permeability (54.7 +/- 11.2%) was not significantly different from that observed in PTX control rats. These studies show that the NDI-like defect in Li-treatment is small and easily overcome by higher concentrations of AVP and suggests that the concentration defect is at least in part due to increased circulating levels of PTH acting as a partial agonist to AVP and thereby inhibiting its hydroosmotic action.

Acute effect of ethanol on renal electrolyte transport in the rat.

1. Despite human and animal studies, the direct effect of ethanol on renal water and electrolyte transport is poorly understood. The acute effect of increasing plasma concentrations of ethanol was evaluated in a water diuretic anaesthetized rat model which inhibits endogenous arginine vasopressin (AVP) release. 2. Ethanol at a plasma concentration of 1.69 +/- 0.28 mmol/L produced an immediate increase in urine flow (174 +/- 11 microL/min pre-ethanol and 189 +/- 13 and then 206 +/- 12 microL/min during the ethanol infusion; P < 0.01) as well as an increase in fractional sodium excretion (0.17 +/- 0.04 to 0.28 +/- 0.05 and 0.27 +/- 0.05%; P < 0.01). There was also a brief phosphaturia. These increases in electrolyte excretion had returned to control values by 20 min despite a further increase in the plasma ethanol concentration. 3. The urinary excretion of potassium, calcium and magnesium was not altered nor was glomerular filtration rate or renal plasma flow. 4. Ethanol at a mean concentration of 1.60 mmol/L did not alter the action of a maximal concentration of AVP (75 ng/kg) on water or electrolyte transport. However, the antidiuretic effect of a submaximal concentration of AVP (7.5 ng/kg) was augmented by ethanol at concentrations of 1.63 and 0.98 mmol/L. 5. These studies suggest that the ethanol induced diuresis commonly ascribed to inhibition of AVP secretion may also be due to other intrarenal effects of ethanol, possibly acting within the proximal tubule. These results also confirm recent in vitro findings that while ethanol does not inhibit the action of a maximal concentration of AVP, it does modulate the effects of lower AVP concentrations.

Hospital sphygmomanometer use: an audit.

Periodic evaluation over the past 20 years of the ability of clinical staff to accurately measure blood pressure, as well as the functional state of sphygmomanometers, has frequently demonstrated significant deficiencies. The data presented here are the results of a recent audit in the Newcastle area. Medical (48) and nursing (217) staff in five general hospitals (3 public, 2 private), were questioned on sphygmomanometer use, observed taking a blood pressure reading and asked to record blood pressures from a videotape. In addition, all hospital sphygmomanometers were checked to see if they were in working order. Of 463 sphygmomanometers evaluated, 58% were in perfect working order. There was a marked variation in the state of equipment between institutions (40 to 94%). Staff knowledge and technical ability in sphygmomanometer use was similar in doctors and nurses, with 69% of doctors and 71% of nurses knowing that phase V Korotkoff sounds best approximated adult diastolic blood pressure. Knowledge of appropriate cuff size and ability to use a sphygmomanometer was also similar between the two groups. However, doctors performed better in measuring systolic and diastolic blood pressures from a videotape (9.3 +/- 1.7 correct compared with 7.8 +/- 1.9 for nurses; P < 0.01). It was concluded that, with the exception of one hospital, the state of repair of sphygmomanometers was poor. Staff knowledge of sphygmomanometer usage and their ability to record blood pressure was satisfactory. However, not all practising health professionals are competent in using a sphygmomanometer.

Acute effect of parathyroid hormone on urine concentration in the rat.

1. It has been demonstrated that parathyroid hormone can increase adenylate cyclase activity in the rat papilla, produce a small antidiuretic effect and in vitro can interfere with the action of arginine vasopressin on water transport. Clearance studies were performed in the anaesthetized water diuretic thyroparathyroidectomized rat to evaluate further the effect of parathyroid hormone on urine concentration in the presence and absence of arginine vasopressin. 2. A maximal phosphaturic concentration of rat parathyroid hormone (2 micrograms/kg) reduced urine flow from 125 +/- 7 to 81 +/- 9 microliters/min within 10 min (P < 0.01). Addition of a maximal antidiuretic concentration of arginine vasopressin (100 ng/kg) produced a delayed and diminished antidiuretic response when compared with a group of rats not pretreated with parathyroid hormone (47 +/- 5 compared with 27 +/- 5 microliters/min; P < 0.01). However, a supramaximal arginine vasopressin concentration (1000 ng/kg) produced a maximal antidiuretic effect in the presence of parathyroid hormone. 3. To evaluate further the inhibitory effect of parathyroid hormone on arginine vasopressin-induced antidiuresis, parathyroid hormone (2 micrograms/kg) was administered to one group of rats and a minimally effective arginine vasopressin concentration (7.5 ng/kg) to another group, which produced a similar antidiuretic effect. However, the subsequent effect of a maximal antidiuretic arginine vasopressin concentration (100 ng/kg) was again significantly blunted in the group pretreated with parathyroid hormone. 4. Parathyroid hormone produced only a small increase in mean plasma calcium concentration, and glomerular filtration rate was not altered by either hormone.(ABSTRACT TRUNCATED AT 250 WORDS)

The renal medulla in acute renal allograft rejection: comparison with renal cortex.

A retrospective cohort study was undertaken to evaluate the diagnostic value of the renal medulla in acute renal allograft rejection (ARAR). One hundred and ninety-five biopsies from 98 patients were randomly selected out of 565 transplant biopsies. Biopsies were graded blindly from Grade 0 (no rejection) to Grade 3 (severe rejection) using standard criteria; ARAR was confirmed by a fall in all cases of mean serum creatinine concentration from 0.331 +/- 0.182 to 0.184 +/- 0.079 mmol/l, with anti-rejection therapy. In the 43 biopsies which contained both cortex and medulla, the ARAR grades and the intensities of mononuclear cell, plasma cell, polymorphonuclear cell and eosinophil infiltrates, and of interstitial oedema and haemorrhage, were similar in cortex and medulla (Spearman's Rank Correlation r = 0.55-0.81, P < 0.001). The sensitivity, specificity and overall accuracy of medullary changes in predicting ARAR changes in the cortex were 77%, 100% and 38%, respectively. Acute vascular rejection changes could not be compared between renal cortex and renal medulla because of the anatomical differences between cortex and medulla. Further evaluation of ARAR in the all 195 biopsies, of which 188 had cortical tissue and 50 had medullary tissue, showed no significant differences in histological features (P > 0.05), except for more cortical biopsies with plasma cells (29%) than medullary biopsies with plasma cells (10%; P < 0.02). It is concluded that: (1) ARAR histological changes are similar in cortex and medulla; (2) the predictive value of ARAR medullary changes for cortical rejection changes has low sensitivity (77%) and high specificity (100%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effect of physiological concentrations of vasopressin on rat renal function.

1. The antidiuretic, pressor and electrolyte transport effects of arginine vasopressin (AVP) were simultaneously evaluated in the anaesthetized water diuretic rat. Increasing concentrations of AVP (7.5, 75 and 750 ng/kg bolus and per h), were used to produce plasma levels which approximate the physiological range (408 +/- 2.4, 35.7 +/- 12.5, 85.2 +/- 16.1 pg/mL respectively). 2. Administration of a minimally effective antidiuretic dose (7.5 ng) increased mean urine osmolality (from 101 +/- 7 to 312 +/- 89 mosmol/kg) without altering mean arterial pressure (MAP), renal plasma flow (RPF) or glomerular filtration rate (GFR). A maximal antidiuretic dose of AVP (75 ng) increased mean urine osmolality to 2002 +/- 109 mosmol/kg and was associated with significant mean increases in MAP (9 mmHg), RPF and GFR (25%) by 30-60 min. A further ten-fold increase in AVP (750 ng) produced a greater increase in MAP (116 +/- 6 to 134 +/- 7 mmHg; P < 0.01) as well as increasing RPF and GFR by 35.5 and 38.9% respectively. 3. Increasing concentrations of AVP also progressively increased the fractional excretion of sodium, potassium and phosphate. However, fractional calcium and magnesium excretion was significantly decreased with maximal and supramaximal concentrations. 4. These studies support evidence that AVP is a pressor hormone in physiological concentrations in baroreceptor intact animals. Its role in renal electrolyte transport is unclear. Measured increases in RPF and GFR with the maximal and supramaximal AVP concentrations appear to be correlated with the increase in MAP.

Effect of ethanol on water and chloride transport in the rat papillary collecting duct.

While it is believed that the effect of ethanol on human renal water homeostasis is indirect, amphibian membrane experiments have demonstrated direct effects albeit at high concentrations. To evaluate the direct effect of ethanol, diffusional water and chloride permeability was simultaneously measured in isolated rat papillary collecting ducts with increasing concentrations of ethanol (0, 0.12, 0.24, 0.48, 0.96 and 1.92 g%) both in the presence and absence of arginine vasopressin (AVP). Low concentration of ethanol (0.12 g%) increased basal water permeability by 9%. With increasing concentrations it then fell to control levels (0.48 g%) only to increase again with concentrations of 0.96 and 1.92 g% to a maximum increase of 26%. Similar changes in chloride permeability occurred. Water permeability in the presence of submaximal concentrations of AVP (20 microU/ml) was also significantly increased with lower concentrations of ethanol (0.12, 0.24 and 0.48 g%) but fell to control levels with higher concentrations. With the highest ethanol concentration (1.92 g%), submaximal AVP did not significantly increase water permeability. However water permeability was unaltered by increasing concentrations of ethanol in the presence of supramaximal AVP (2,000 microU/ml). These results demonstrate a direct effect of ethanol upon distal nephron water and chloride transport.

Acute pancreatitis and rhabdomyolysis: a new association.

Fourteen cases of acute severe pancreatitis complicated by non-traumatic rhabdomyolysis are described and compared to case controls. Pancreatitis of various aetiologies was confirmed by surgical diagnosis, laparotomy, abdominal paracentesis, CAT scan and post mortem. Pancreatitis was severe with a high Ranson prognostic score (7.4 +/- 0.5 vs controls 1.9 +/- 0.4, p less than 0.001), longer ICU admission and a mortality of 79%. Rhabdomyolysis occurred two to 19 days after the onset of pancreatitis (with a median CPK peak at 6.5 days) and was accompanied by multiple organ failure in 93% of cases. Severe rhabdomyolysis and myoglobinuric renal failure occurred in three patients out of 12 with acute renal failure. Hypocalcaemia was common (93%), severe (with a mean minimum value of 1.79 +/- 0.07 vs 2.34 +/- 0.04mmol/L, p less than 0.01) and prolonged (remaining abnormal for 5.2 +/- 0.8 vs 0.07 +/- 0.07 days, p less than 0.001). Intravenous calcium supplements were required in 50% of patients. Plasma phosphate, potassium, urate and anion gap were elevated (all p less than 0.05) and accompanying clinical features included fever, ascites, leucocytosis, hypoalbuminaemia and abnormal liver function tests. Rhabdomyolysis is associated with acute several pancreatitis, appearing as a late phenomenon in the context of severe prolonged hypocalcaemia, multiple organ failure and a poor outcome.

Synthetic human parathyroid hormone-related protein and rat renal electrolyte transport.

The effect of parathyroid hormone (PTH)-like peptide PTH-related protein (PTHrP)(1-34) from a human cancer cell line on renal electrolyte transport was compared with human PTH(1-34) in a thyroparathyroidectomized anesthetized rat model. Comparing submaximal, maximal and supramaximal phosphaturic concentrations of hPTH with the same PTHrP concentrations, no significant difference could be demonstrated in the urinary excretion of calcium, magnesium, inorganic phosphate or cAMP. Even the small (30.3%) and brief (45 min) reduction in fractional water excretion with the maximal (1 nM/kg/h) hPTH concentration was approximated by PTHrP. It is concluded that the structural homology between hPTH and PTHrP allows a similar action on renal electrolyte transport, including the partial agonist effect of higher concentrations of PTH on vasopressin-induced water transport.

Increased dietary sodium chloride in patients treated with antihypertensive drugs.

Eleven patients on a normal diet with mild to moderate essential hypertension satisfactorily treated with diverse hypotensive agents entered a randomized double-blind cross-over study to evaluate the effect of additional sodium chloride (100 mmol slow sodium) compared with placebo on blood pressure control over a 6 week period. Despite excellent tablet compliance, sodium chloride failed to significantly alter mean supine or erect blood pressure. These findings as well as a review of the relevant literature suggest that excess dietary sodium does not jeopardize blood pressure control in such patients.

Acute dialysis hypercalcemia and dialysis phosphate loss.

During maintenance hemodialysis in patients with chronic renal failure, acute elevations of the plasma calcium are common, although of doubtful significance. Because the mechanisms for this hypercalcemia are unclear, calcium, magnesium, and inorganic phosphate mass transfer data was collected during routine hemodialysis. While the increase in the plasma calcium did not significantly correlate with the gain of calcium from the dialysate nor with the dialysate calcium concentration, there was a significant positive correlation between the degree of hypercalcemia and the loss of body phosphate (r = 0.66, P less than 0.05, n = 15). Hemodialysis without ultrafiltration and concomitant hemoconcentration depressed the dialysis hypercalcemia by 46% (P less than 0.001). However, continuous infusion of 33.5 mmol of phosphate during a 5-hour dialysis period, which reduced the plasma phosphate fall (1.53 +/- 0.16 to 0.87 +/- 0.08 mmol/L, P less than 0.01, in the control group; compared with 1.59 +/- 0.19 to 1.35 +/- 0.11 mmol/L, not significant [NS], in the phosphate infusion group) abolished the hypercalcemia (2.38 +/- 0.07 to 2.54 +/- 0.04 mmol/L, P less than 0.01, in the control group and 2.39 +/- 0.06 to 2.41 +/- 0.04 mmol/L, NS, in the phosphate infusion group). It is suggested that during routine hemodialysis, the loss of inorganic phosphate from the body is excessive, and that phosphate as well as calcium is released from the intracellular pool in response to the rapid fall in the plasma phosphate concentration. Such rapid, repetitive, and excessive losses of phosphate, particularly from bone, may be an important cause of renal osteodystrophy.

Effect of posture on clearance of atrial natriuretic peptide from plasma.

The effect of posture on plasma atrial natriuretic peptide (ANP) levels during a constant iv infusion of the 28-amino acid polypeptide was investigated in 8 normal men. alpha-Human ANP was infused at a constant rate of 0.5 micrograms/min (162 pmol/min) while the men were supine, then erect, and finally when supine again. Plasma ANP levels rose from 10.9 +/- 1.6 (+/- SEM) to 33.3 +/- 2.4 pmol/L after 60 min of constant infusion with the men in the supine position. On standing, plasma ANP increased further to 40.6 +/- 3.4 pmol/L, then fell to 32.2 +/- 2.7 pmol/L with resumption of supine posture. The calculated MCR of ANP fell from a mean of 7.7 to 5.7 L/min on standing, but rose again to 7.6 L/min upon lying down. We conclude that body posture has a significant effect on the rate of clearance of ANP from plasma.

Effects of captopril on circulating T lymphocyte subsets.

Six patients treated with captopril for severe essential hypertension were studied to determine whether the drug significantly altered circulating peripheral blood T (Thymus derived) lymphocytes and T lymphocyte subsets. OKT3+ (functionally mature T lymphocytes), OKT4+ (class II major histocompatibility complex [MHC] reactive T lymphocytes) and OKT8+ (class I MHC reactive T lymphocytes) T lymphocytes were monitored using monoclonal antibodies and flow cytometry before commencement of treatment and then at intervals during 14 months of captopril administration. Results showed a significant increase in the absolute numbers of OKT4+ cells at 2 h (p less than 0.05) and a decrease at 12 weeks (p less than 0.01) during captopril treatment. These findings indicate that captopril has an effect on cellular immunity in vivo.

Effect of trial therapy on subsequent therapy. A review of patients with hypertension who have completed a pharmacological intervention study.

After a clinical trial was completed in which two commonly used antihypertensive agents (prazosin and propranolol) were compared, 20 previously untreated men with moderate, asymptomatic, essential hypertension returned to the care of their general practitioners. Twelve months later 17 patients who were still attending the same doctor demonstrated improved blood pressure control with a decrease in their lying diastolic blood pressure from 96 +/- 2 mmHg to 91 +/- 2 mmHg (P less than 0.01). Only two of the 17 patients had not by then achieved satisfactory control. Eleven patients (65%) were still taking at least one of the trial medications; clinicians seemed to prefer prazosin (10 patients). Only one of seven patients was still taking propranolol although five patients had begun treatment with other beta-blocking agents. One patient had ceased drug treatment. This survey indicates that many general practitioners are able to maintain or even improve blood pressure control in patients whose blood pressure has been stabilized initially. However, the reasons for the medication preference were unclear and studies of the clinical behaviour that influences a general practitioner's choice of medication are required.

Effect of indomethacin on urine concentration and dilution in the rat.

The precise role of prostaglandins in modulating urine concentration and dilution is unclear. Evidence in vitro has recently cast doubt on the accepted theory that renal prostaglandins inhibit the hydro-osmotic effect of vasopressin. Urine clearance studies were performed on indomethacin treated (prostaglandin deficient) and control anaesthetized water diuretic rats both before and during the addition of vasopressin in maximal (10 m-units) and supramaximal (100 m-units) concentrations. Before the addition of vasopressin, indomethacin treatment inhibited the excretion of a water load by 48.7%. The mean papillary sodium concentration was also greater in this group of rats. Vasopressin (10 m-units) increased the urine osmolality in control and indomethacin treated rats; however, the mean urine osmolality was greater in the indomethacin group (1521 +/- 103 compared with 1120 +/- 98 mosmol/kg; P less than 0.01), as was the papillary sodium concentration. A ten-fold increase in vasopressin depressed the papillary sodium concentration to a level similar to that in the control group and produced a marked natriuresis. Consequently, the mean urine osmolalities and urine flows were similar in control and indomethacin treated rats. These experiments suggest that a major function of renal prostaglandins is to increase the ability of the kidney to excrete a water load. Renal prostaglandins do not interfere with the vasopressin induced increase in distal nephron water permeability.