Blood pressure dipping and salivary cortisol as markers of fatigue and sleep deprivation in staff anesthesiologists.

Anesthesiologists often work extended duty shifts that result in acute and chronic sleep loss and circadian disruption. Stress caused by sleep deprivation, together with excessive workload could contribute to acute increases in blood pressure (BP) and sympathetic nervous system activity. Non-dipping pattern of BP is considered an additional risk factor for cardiovascular events and target organ damage. We hypothesized that there would be significant changes of cardiovascular parameters when comparing work on call during the 24-hour in-hospital shift (24-HD) versus ordinary working day (8-HD) combined with changes of dipping pattern and altered diurnal cortisol secretion, measured by salivary cortisol (SC). Following local Medical Ethics Committee approval, 12 out of 36 staff anesthesiologists (8 male, 4 female), 33-61 years old, participated in this study. Ambulatory BP monitor was used for noninvasive 24-hour ambulatory BP and heart rate (HR) monitoring. Each participant was monitored continuously during the 8-HD, as well as during the 24-HD. Saliva for analysis of cortisol levels was collected six times a day (at 8 am, 11 am, 2 pm, 5pm, 8pm, and 11 pm) both during 8-HD and on 24-HD. There was a significant decrease in number of diastolic dippers on call vs. diastolic dippers on ordinary working day (4/12 vs. 10/12, p=0.036), and non significant decrease of systolic dippers (3/12 vs. 7/12, p =0.214). There were no significant differences in SC values between 8-HD and 24-HD at all observed time points. However, the SC values measured during the night were markedly elevated on both days compared with reference values and the shapes of SC curves were altered. The lack of diastolic BP dipping could be more sensitive indicator of stress among staff anesthesiologists than systolic BP dipping. The shape of SC diurnal curve in terms of elevated night values could be another indicator of their chronic fatigue.

The impact of hormone replacement therapy on metabolic syndrome components in perimenopausal women.

Hormone replacement therapy (HRT) is in use for more than a half of century, but the question of indications and ideal candidates for HRT remains unclear. Postmenopausal women are a population with the increasing risks for cardiovascular diseases which are the main cause of death in this group. Decline in oestrogen concentrations is linked to a number of changes in peri and postmenopause: increased total cholesterol, triglycerides, and low density lipoprotein, increased insulin resistance and impaired fibrinolysis. These changes are the main components of metabolic syndrome, the epidemic of the modern age. HRT is currently recommended as the gold standard for the management of vasomotor symptoms, but the benefit of HRT on components of metabolic syndrome and risk for cardiovascular events is still uncertain. In the initial reports from the Women's Health Initiative trial (WHI), overall health risks exceeded benefits in the cohort taking combined estrogen-progestin trial. Observational study in postmenopausal women, some meta-analyses and subsequent analyses of WHI had suggested that the timing of exposure to postmenopausal estrogen therapy may be an important factor in determining subsequent cardiovascular risk. It seems that the early therapy onset is a key factor in accomplishing positive results, but there are almost no surveys regarding the effects on the metabolic syndrome components in perimenopausal women. We hypothesized that the early, low dosage HRT in healthy perimenopausal women would have beneficial effects on the compounds of metabolic syndrome and could decrease the risk of cardiovascular events. Beneficial effect of HRT on cardiovascular diseases is due to the maintained integrity and functional status of the endothelium in younger women. We are aware of the fact that further studies are necessary to test the effects of different doses and routes of administration of HRT on cardiovascular outcomes.

[ISKRA guidelines on antimicrobial treatment and prophylaxis of urinary tract infections--Croatian national guidelines]. / ISKRA smjernice antimikrobnog lijecenja i profilakse infekcija mokracnog sustava--hrvatske nacionalne smjernice.

These guidelines refer to diagnosis, antimicrobial treatment and prophylaxis of urinary tract infections in adults and children older than 12 years of age and cover lower urinary tract in females, uncomplicated pyelonephritis, complicated UTI with or without pyelonephritis, asymptomatic bacteriuria and recurrent UTI. These guidelines do not cover sexually transmitted diseases. The guidelines are primarily intended for use by general practitioners and specialists working in primary health care and hospitals. The members of the Working Group for the development of guidelines on antimicrobial treatment and prophylaxis of urinary tract infections were appointed by the Croatian Ministry of Health and Social Welfare. The project was financially supported by the Dutch government and professional assistance was provided by international consultants. The evidence for this guidelines is based on a systematic review of the literature, local antibiotic resistance data, the existing clinical protocols on the treatment and prophylaxis of UTIs, as well as suggestions and comments made by colleagues physicians during more than 50 continuous medical education courses held in the last three years on antimicrobial treatment and prophylaxis of UTIs. Draft version of the guidelines was available for comments on the web site http://iskra.bfm.hr and during the two-month piloting period the guidelines were widely presented to general practitioners, specialists working in primary care and hospitals--urologists, gynecologists, infectious disease specialists, nephrologists. The final version of the guidelines was approved by the Intersectoral Coordination Mechanism for the Control of Antimicrobial Resistance (ISKRA) Board.

Comparison between continuous ambulatory arterial blood pressure monitoring and standard blood pressure measurements among patients of younger and older age group.

The purpose of the study was to evaluate whether there is a difference between blood pressure measured in a physician's office and the average 24 hr continuous blood pressure monitored by hypertensive patients at home. If there is a difference between these two situations then is it possibly the result of a blood pressure response by the patient to the physician which is known as "white coat effect" or "white coat hypertension". We studied 80 hypertensive outpatients which were divided into two groups of 40 patients each--a younger patient group, with a mean age of 22.8 +/- 1.8 years, and an older patient group with a mean age of 50.3 +/- 5.7 years. They were selected because they had been diagnosed as essentially hypertension grade 1, according to 2007 ESH/ESC Guidelines, or the USA Joint National Committee Guidelines (JNC 7) (i.e., arterial blood pressure > 140/90 mm Hg and < 160/100 mmHg) and 35 were not having any antihypertensive treatment. All participants in the study went through a two-week "wash-out" period without medication. At the beginning of the study blood pressure was measured using the Riva-Rocci-Korotkoff method (mercury sphygmomanometer) after 5 minutes of rest and with the patient in the sitting position. The average of the two last measurements by sphygmomanometer was used in the analysis. The subsequent measurement was made by continuous ambulatory blood pressure monitoring (SpaceLabs 90207 device). Continuous ambulatory blood pressure monitoring revealed that 17 patients of the younger age group (42.5%) who were diagnosed hypertonic, according to mercury sphygmomanometeric measurement, were in fact normotonic. In the older age group only 7 (17.5%) of participants were normotonic during 24 hr blood pressure monitoring. The proportion of miss-diagnosed normotonic younger patients was directly related to elevated clinic blood pressure, which could be referred to as office hypertension or isolated clinic hypertension (white coat hypertension). This was statistically significant (chi2 = 5.95; p = 0.015). Hypertension diagnosed in younger patients based only on occasional doctor's office mesurements, using a mercury sphygmomanometer, could be miss-interpreted and treated as the start of arterial hypertension. This could sometimes have unwanted results due to the side effects of precipitate antihypertensive medication as well as the unnecessary cost of testing, cost of treatment, prevalence of white-coat hypertension at baseline, and the varying incidence of new hypertension after the initial screening. The results indicate a potential savings of 3-14% in the cost of care for hypertension, and a 10-23% reduction in treatment days when ambulatory blood pressure monitoring is incorporated into the diagnostic process. Therefore CABPM should be used as a legitimate method in the diagnosing of "white coat hypertension", particularly in young patients. The identification of white coat hypertensive"' patients should be followed by a search for metabolic risk or organ damage using the latest guidelines, and medication should start after an organ damage or cardiovascular risk assesement.

In-hospital cardiac arrest and resuscitation outcomes: rationale for sudden cardiac death approach.

AIM: To assess the frequency of cardiac arrest and outcomes and predictors of survival after cardiopulmonary resuscitation in hospitalized patients. METHODS: We prospectively analyzed the data on all patients who experienced cardiac arrest while hospitalized at the Split University Hospital between January and December 2003. Data were collected on patients' demographic characteristics, etiology and presentation of cardiac arrest, time, site, methods, and outcomes of cardiopulmonary resuscitation. RESULTS: Out of 120 cases of cardiac arrest among 32,861 hospitalized patients, 76.7% were witnessed. Ninety-six (80.0%) patients with cardiac arrest underwent resuscitation, and 22.5% of them were discharged alive. The survival rate was 20.0% at the Department of Internal Medicine, 29.2% in the Coronary Care Unit, and only 7.1% in other departments (P=0.058, chi2 test). Out of 92 patients with witnessed cardiac arrest, 28.3% survived to discharge, whereas only one of 28 patient with unwitnessed cardiac arrest survived to discharge (P=0.004, Fisher's exact test). More patients with cardiac arrest due to ventricular fibrillation or pulseless ventricular tachycardia survived than patients with asystole and pulseless electrical activity (47.6% vs 10.7%, respectively, P<0.001, Fisher's exact test). None of the patients with unclassified cardiac arrest survived until discharge. Cardiac arrest survivors were significantly younger (60.8+/-12.9 vs 71.1+/-11.7 years, P<0.001, Student t-test). Sex had no influence on survival. There were no significant circadian or hospital shift differences in the frequency rate of cardiac arrest, but the rate of successful resuscitation was lower during the night shift. CONCLUSION: The rate of successful resuscitation was higher in the coronary care unit, during the day and in younger witnessed cardiac arrest patients with ventricular fibrillation or pulseless ventricular tachycardia.

Effects of atenolol and propranolol on platelet aggregation in moderate essential hypertension: randomized crossover trial.

AIM: To compare the effects of a selective beta-blocker atenolol and a nonselective beta-blocker propranolol on platelet aggregation. METHODS: Twenty successive outpatients with moderate essential hypertension (6 women and 14 men, mean age-/+standard deviation 42.6-/+8.5 years) were randomized to either propranolol (40 mg three times a day) or atenolol (100 mg once a day) for the first two weeks, followed by a one-day washout period, and then a two-week administration of the alternative drug. Along with standard examinations and tests, circulating platelet aggregates were measured. RESULTS: There were no significant differences in creatinine, blood glucose, potassium, total cholesterol, hemoglobin, red blood cells (RBC), or platelets in three periods: baseline, atenolol, and propranolol period. Significant and comparable reductions in systolic and diastolic arterial pressure, body weight, heart rate, and HDL-cholesterol were recorded in both patient groups. The LDL-cholesterol concentration increased significantly in propranolol compared with both baseline and atenolol period. Serum triglycerides increased significantly with both medications. The number of circulating platelet aggregates decreased significantly with propranolol (0.99-/+0.19) in comparison with both atenolol (1.41-/+0.70; P=0.004, Wilcoxon matched pairs test) and baseline (1.59-/+0.94; P=0.002, Wilcoxon matched pairs test). CONCLUSION: Propranolol inhibits platelet aggregation more than atenolol and may have a favorable effect on the management of hypertension especially in patients with increased cardiovascular risk.

Effects of four antihypertensive monotherapies on cardiac mass and function in hypertensive patients with left ventricular hypertrophy: randomized prospective study.

AIM: To compare the effects of four antihypertensive drugs, which have reportedly different effectiveness in reducing myocardial mass. METHODS: A randomized, double-blind, prospective study included 80 hypertensive patients with left ventricular (LV) hypertrophy confirmed both electrocardiographically and echocardiographically. We investigated the effects of indapamide, nicardipine, propranolol, and chlorthalidone on arterial blood pressure and LV mass and function. RESULTS: Sixty-four patients (34 men and 30 women) completed the 6-month study. No significant differences in antihypertensive effects of the four medications were found. The average decrease in systolic and diastolic blood pressure was 12.8% and 10.4%, respectively. All four antihypertensive medications caused pronounced reduction in LV mass, between 7.9% in the propranolol group and 10.1% in the nicardipine group, with no significant difference between the groups. In patients receiving diuretics, predominant decrease was observed in LV mass and LV mass index. In patients treated with propranolol, the thickness of both the LV wall and interventricular septum was reduced, whereas the reduction in LV mass, LV wall and interventricular septum thickness was found in patients treated with nicardipine. There was no significant correlation between the changes in LV mass and other variables (blood pressure, and systolic and diastolic function). Systolic function did not improve with the reversion of LV hypertrophy in any group of patients, but improvement was observed in some indices of diastolic function. The early and late LV filling velocity and their ratio did not improve significantly, either. Clinically relevant side effects were not observed. CONCLUSION: All four antihypertensive monotherapies achieved a comparable control of hypertension and reduction in LV hypertrophy.

Prospective controlled trial of two nifedipine extended release formulations in the treatment of essential hypertension.

The aim of this study was to assess the pharmacodynamic equivalence of two different slow-release formulations of nifedipine (CAS-21829-25-4). In a prospective, controlled, double-blind clinical trial, 42 patients with essential hypertension (sitting diastolic blood pressure (DBP) 95-114 mmHg) underwent an initial washout, drug free period of 2 weeks, after which they were randomized to receive either 30 mg of nifedipine in the test preparation "XL" (Nifecard) or 30 mg of nifedipine in a reference formulation, "LA", during six weeks. The response to treatment was assessed by measuring the blood pressure (BP) every two weeks (standard office mercury sphygmomanometry) and by 24-h ambulatory blood pressure monitoring (ABPM). Of the 42 included patients 36 (85.5%) completed the trial: 19 on "XL" and 17 on "LA". After 2 weeks of therapy the DBP decreased by about 11% (-13.4 mmHg) and 10% (-9.5%), respectively, after 4 weeks the mean decrease versus the end of the placebo period reached about 14% (-15.5 mmHg) and 11% (-13 mmHg), and at the end of the trial the DBPs were lower by about 13% (-14.5 mmHg) in both groups. In all these measurements the within group differences were significant (p < 0.001), while the between groups differences were not (p > 0.05). Quite comparable results were obtained with ABPM, e.g. in the "XL" group the systolic blood pressure at the end of the study was lower by 12.3% (-4.6 mm Hg) and in the "LA" group, by 10.6% (-9.0 mm Hg); p = 0.358. The adverse effects were similar in both groups and they required neither particular interventions nor withdrawal from the study. The drugs under study were comparably effective and well tolerated antihypertensives.

Comparison of ondansetron with metoclopramide in the symptomatic relief of uremia-induced nausea and vomiting.

BACKGROUND: Nausea and vomiting are well-known gastrointestinal complications in chronic renal failure and are frequent indications for the commencement of dialysis. Although the administration of antiemetic drugs (metoclopramide and, recently, ondansetron) is usually mentioned, there are scanty data on their effects. METHODS: A double-blind crossover study was done in 10 uremic patients. All the patients were uremic and suffered from nausea and vomiting. The drugs were randomly administered intravenously (either metoclopramide 10 mg or ondansetron 8 mg) 2 h after blood drawing for laboratory tests either on the 1st or on the 3rd study day at the same time. The outcomes were scored after 24 h of follow-up by (1) one of us (D.P.; 1-3 points: 1 = no effect; 2 = moderate effect - decreased frequency of vomiting, and 3 = good effect - no vomiting), and (2) by the patients (1-5 points). RESULTS: The results obtained showed that ondansetron was more effective in controlling nausea and vomiting than metoclopramide, either objectively (2.80 +/- 0.422 vs. 1.40 +/- 0.699, p < 0.005) or subjectively (4.10 +/- 0.738 vs. 2.10 +/- 0.994, p < 0.005). CONCLUSIONS: We conclude that at the dosage level studied ondansetron is about twice as effective as metoclopramide in the symptomatic relief of uremia-induced nausea and vomiting.