Oh baby! A labor and delivery staffing system measures patient census and acuity.

The unique characteristics of labor and delivery units make it difficult to plan clinically and fiscally justified staffing patterns. This article presents an effective technique to measure patient census, track patient acuity, and determine required and actual nursing care hours.

Ultrastructural evidence of thyroid damage in amiodarone-induced thyrotoxicosis.

Amiodarone-induced thyrotoxicosis occurs in 2-12.1% of patients on chronic amiodarone treatment. In most cases its pathogenesis is related to iodine overload in the presence of preexisting thyroid abnormalities, such as multinodular or diffuse goiter or autonomous nodule. A minority of patients show apparently normal glands or pictures of non-autoimmune thyroiditis. However, there is recent evidence of a direct toxic effect of amiodarone, with consequent release of iodothyronines into the circulation. We report a patient with amiodarone-induced thyrotoxicosis with toxic thyroid effects demonstrated by electron microscopy in a fine-needle aspiration biopsy. There were three main pathologic findings: multilamellar lysosomal inclusions, intramitchondrial glycogen inclusions--both ultrastructural findings indicating thyroid cell damage--and a microscopic morphological pattern of thyroid cell hyperfunction. No inflammatory changes were found. Plasma thyroglobulin levels were high. The patient proved to be a non responder to simultaneous administration of methimazole (starting dose 30 mg/day) and potassium perchlorate (1000 mg/day for 40 days), while still taking amiodarone, thus providing evidence against a possible pathogenetic role of iodine overload. Dexamethasone (starting dose 3 mg/day) was added to methimazole. After three months euthyroidism had been restored and plasma thyroglobulin level substantially decreased. Subsequent subclinical hypothyroidism developed, which persisted after stopping antithyroid treatment and required substitution treatment with levothyroxine. In view of the primary role of lysosome function in the proteolysis of thyroglobulin molecules and of the energy-requiring carrier-mediated transport of monoiodotyrosine across the lysosomal membrane for iodine salvage and reutilization, we suggest that the pathological lysosomal and mitochondrial changes observed could be an ultrastructural marker for subsequent hypothyroidism in amiodarone-induced thyrotoxicosis. Our observations suggest the usefulness of ultrastructural thyroid evaluation and serial plasma thyroglobulin determinations to thoroughly evaluate the underlying pathogenetic mechanisms in amiodarone-associated thyrotoxicosis with apparently normal thyroid glands. Moreover, more knowledge of its pathogenesis could improve both prognostic stratification and treatment guides.

Intravenous amiodarone vs propafenone for atrial fibrillation and flutter after cardiac operation.

The safety and efficacy of amiodarone and propafenone in converting atrial fibrillation or flutter after cardiac surgery were compared in a randomized double-blind trial. Eighty-four patients with sustained atrial tachyarrhythmias of more than 30 min' duration, stable hemodynamic status and neither preoperative atrial arrhythmias nor treatment with other antiarrhythmis drugs, were randomized to receive amiodarone (46 patients: 5 mg/kg over 15 min and then 15 mg/kg over the subsequent 24 h for non-converting) or propafenone (38 patients: 2 mg/kg over 15 in and then 10 mg/kg over the subsequent 24 h for non-converting). Nine of the 46 patients (19.5%) receiving amiodarone converted to sinus rhythm within 1 h following bolus injection compared with 17 of 38 patients (44.7%) treated with propafenone (P < 0.05). Within the 24 h study, 38 of 46 patients (82.6%) given amiodarone and 26 of 38 patients (68.4%) given propafenone were converted to sinus rhythm (P = NS). A significantly progressive reduction in ventricular response, already evident at 10th min from the start of treatment, was achieved in both groups of patients. Side effects occurred in six patients given propafenone (15.7%) and in five given amiodarone (10.8%) (P = NS). The two drugs were equally effective in converting postoperative atrial fibrillation and/or flutter after 24 h although propafenone was superior within the first hour.

Beta-blocking effect of propafenone based on spectral analysis of heart rate variability.

RR variability was analyzed in 15 patients with ventricular arrhythmias to evaluate whether the antiarrhythmic action of propafenone is associated with alteration of neural control mechanisms. Before drug administration, spectral analysis of RR variability was characterized by 2 major components at low and high frequency, which are considered to reflect sympathetic and parasympathetic modulation of the heart period. After propafenone (600 to 900 mg/day), there was a marked reduction in RR variance (826 +/- 184 to 412 +/- 77 ms2; p < 0.05), although the mean RR interval was unchanged. The drug significantly reduced the low-frequency component (52 +/- 6 to 28 +/- 4 nu) and augmented the high-frequency component (39 +/- 6 to 55 +/- 5 nu). As a result, the low-/high-frequency ratio (an index of sympathovagal balance) decreased from 2.0 +/- 0.4 to 0.6 +/- 0.1. A positive correlation between serum levels and drug-induced changes in the low-frequency component was also observed. Furthermore, the increase in the low-frequency component induced by tilt (53 +/- 5 to 79 +/- 3 nu) was markedly attenuated after drug administration (27 +/- 5 to 54 +/- 7 nu). Thus, propafenone administration is associated with changes in spectral components that are consistent with a beta-blocking effect of the drug.

Effects of mexiletine, propafenone and flecainide on signal-averaged electrocardiogram.

The effects of mexiletine, propafenone and flecainide on the parameters of signal-averaged electrocardiogram in 40 subjects with symptomatic and repetitive ventricular arrhythmias were studied. Mexiletine (n = 16) suppressed ventricular arrhythmias in 10 patients and did not produce any significant changes in filtered QRS duration (fQRS), root mean square voltage of the final 40 ms of filtered QRS (RMS40) or low amplitude terminal component duration (LAS40). Acute (n = 8, 450 mg) and chronic (n = 16, 600-1200 mg.day-1) administration of propafenone determined a significant increase in fQRS (from 123 +/- 2.2 to 139 +/- 3 ms) and a reduction in RMS40 (from 54 +/- 8.8 to 34 +/- 6.7 microV); as a consequence the incidence of ventricular late potentials rose from 43 to 62%. The observed effects were independent of anti-arrhythmic efficacy, which was 86% for this drug. Acute (n = 8, 200 mg) and chronic (n = 13, 200-300 mg.day-1) administration of flecainide was associated with a marked prolongation in fQRS (from 123 +/- 2.8 to 138 +/- 4.1 ms) and a reduction in RMS40 (from 69 +/- 11.5 to 47 +/- 11 microV); thus determining an increase in the incidence of ventricular late potentials from 29 to 48%. Changes in signal-averaged electrocardiogram were not related to drug efficacy, which was 81%. These data indicate that 1c anti-arrhythmic drugs consistently modified the parameters of signal-averaged electrocardiogram; the observed changes might reflect an inhomogeneous slowing of intramyocardial impulse propagation.

Identification of propafenone metaboliser phenotype from plasma and urine excretion data.

The aim of the study was to validate a test based on analyses of urine to identify the propafenone metaboliser phenotype during routine chronic therapy. Twenty seven patients chronically treated with propafenone were studied. A debrisoquine test was performed in 10. Propafenone and its metabolites in plasma and urine were measured by HPLC. Propafenone, 5-hydroxypropafenone and N-depropylpropafenone concentrations in plasma were 1.09, 0.182 and 0.101 ng.ml-1, respectively. Total recovery of the administered dose in urine was 30.7%. Two patients were identified as PM, based on the result of the debrisoquine test (log D/4OHD of 1.26 and 1.36). This finding was confirmed by the propafenone metabolic ratio in urine, but the plasma data did not permit clearcut separation of the phenotypes. Propafenone/5-hydroxypropafenone in plasma was not a good predictor of metabolizer phenotype. Although the number of patients who completed all three tests was limited, it is concluded that analysis of propafenone/5-hydroxypropafenone in urine collected between two consecutive doses at steady-state is more practical than the debrisoquine test and more specific than determining the propafenone/5-hydroxypropafenone ratio in plasma, for identification of the propafenone metaboliser phenotypes.

Signal averaging of pre- and post-extrasystolic beats in patients with ventricular arrhythmias.

To evaluate the effects of premature ventricular beats on the impulse conduction of adjacent sinus cycles, we compared the high amplification signal-averaged electrocardiogram parameters of the pre- and post-extrasystolic beats with those of the remaining sinus cycle. According to the duration of filtered QRS (fQRS), to the voltage of root mean square of the terminal 40 ms (RMS 40) and to the duration of low amplitude terminal components of the sinus cycles, ventricular late potentials were detected in nine out of 29 subjects. Patients with an abnormal signal-averaged electrocardiogram exhibited a longer fQRS (146 +/- 6 versus 116 +/- 2 ms), a reduced RMS40 voltage (18 +/- 2 versus 80 +/- 10 microV) and a prolonged duration of less than 40 microV components (42 +/- 4 versus 17 +/- 2 ms). Analysis of the pre-extrasystolic beats did not reveal any significant variation in the above parameters, showing a mean difference of 0.44 +/- 2.4 ms; 0.02 +/- 1.14 microV; 1 +/- 1.9 ms and of -1.45 +/- 1.02 ms; 3.5 +/- 8.6 microV; -0.7 +/- 0.84 ms respectively, for patients with and without ventricular late potentials. In addition, no significant variation was observed when the post-extrasystolic beats were considered. These results indicate that the sinus cycles adjacent to premature ventricular discharges do not present variations of signal-averaged electrocardiogram parameters that may suggest an influence of the ectopic beats on their intramyocardial impulse propagation.

Myopathy during amiodarone treatment: a case report.

The case of a 69-year-old woman who developed muscle weakness on chronic amiodarone treatment is reported. Muscle biopsy showed vacuolar alterations and a marked accumulation of amiodarone and of its metabolite desethylamiodarone was found in the muscle sample despite normal blood levels. Amiodarone-induced morphological alterations of the muscle may be related to the actual tissue concentration rather than to the blood level.

[Propafenone in ventricular hyperkinetic arrhythmias. Dynamic ECG evaluation of the acute oral test and short-term treatment]. / II propafenone nelle aritmie ipercinetiche ventricolari. Valutazione mediante ECG dinamico del test orale acuto e della terapia a breve termine.

The antiarrhythmic efficacy of Propafenone (PF) was evaluated in 24 patients with ventricular hyperkinetic arrhythmias by means of 24-hour Holter monitoring. The drug was administered as an acute bolus (450 mg) and, subsequently, in continuous therapy for 7 days at an average dose of 600 mg/day followed by a 5 days wash-out. The results of our study can be summarized as follows: High antiarrhythmic efficacy of the drug and good tolerability: 19 out of 24 patients showed, in continuous therapy, suppression of ventricular tachycardias (VT), reduction greater than or equal to 90% of couples, reduction greater than or equal to 70% of ventricular premature beats (VPBs). High predictivity value of the oral acute test with PF, (91.6%). Occurrence of first degree atrioventricular block in 4 patients (16.5%) and left bundle branch block in 3 patients (12.5%) with chronic treatment.