Profiles of automated peritoneal dialysis prescriptions in the US 1997-2003.

Automated peritoneal dialysis (PD) is the dominant mode of delivery of PD in the US. Information about actual prescribing patterns has been limited. The present study examines cycler prescription use in large cohorts during the years 1997, 2000, and 2003. We observed trends consisting of increasing fill volumes, increasing time on cycler, lowering of the number of cycles, and a shift in the reason for utilization of tidal therapy. Monitoring of practice patterns is beneficial in identifying opportunities for practice enhancement. The findings of the present survey demonstrate trends that approach standard recommendations of the benefits of increasing fill volume whereas paying close attention to dwell time as a balance between cycle number and therapy duration. Furthermore, this survey shows that the cycler represents a flexible method to personalize PD therapy.

Electrocardiographic changes during acute treatment of hypertensive emergencies with sodium nitroprusside or fenoldopam.

BACKGROUND: Electrocardiograms are routinely obtained before and during the acute treatment of hypertensive emergencies, usually to rule out "ischemic changes." Despite a few anecdotal reports of electrocardiographic changes, little is known about the incidence and significance of such changes, or their relationship to the treatment used. METHODS: We prospectively analyzed 12-lead electrocardiograms from 21 patients admitted for hypertensive emergencies (average blood pressure, 222 +/- 4/140 +/- 3 mm Hg). Patients were randomly assigned to treatment with sodium nitroprusside (n = 11) or the dopamine receptor agonist fenoldopam mesylate (n = 10). Electrocardiograms were obtained at baseline and within 30 minutes of reaching goal blood pressure (diastolic blood pressure, 100 to 110 mm Hg). RESULTS: There was no significant effect of either drug treatment on PR interval, QRS duration, QT interval, or R-wave amplitude, and no major ST-segment changes were noted. During treatment with either drug, the average T-wave amplitude decreased in all leads except aVR. New T-wave inversions in lead V4 occurred in two and four patients after fenoldopam and nitroprusside treatment, respectively. There were no clinically apparent episodes of myocardial ischemia in any patient. CONCLUSIONS: Even in the absence of obvious myocardial ischemia, a decrease in T-wave amplitude, including T-wave inversion, occurs commonly during acute blood pressure reduction in hypertensive emergencies, an observation that may be explained by the accompanying acute changes in cardiac chamber volumes.

Torsade de pointes complicating acute myocardial infarction: the importance of autonomic dysfunction as assessed by heart rate variability.

Torsade de pointes is a polymorphic ventricular tachycardia associated with QT-interval prolongation rarely reported to occur in the setting of an acute myocardial infarction. Autonomic dysfunction has been implicated as a major stimulus for the development of this dysrhythmia. We describe the case of an 80-year-old woman who presented with an acute myocardial infarction and progressive QT-interval lengthening. An 89-beat run of torsade de pointes occurred during the time of the peak creatine phosphokinase (CPK) without electrolyte abnormalities or antiarrhythmic therapy. Assessment of autonomic tone using power spectral analysis of two consecutive 24-h Holter recordings was performed indicating that a transient decrease in heart rate variability and increase in sympathetic tone preceded the tachyarrhythmia. This case shows the potential usefulness of heart rate variability analysis as a marker for autonomic dysfunction and arrhythmogenesis, particularly during myocardial ischemia.

Informed consent in emergency research. Prehospital thrombolytic therapy for acute myocardial infarction.

Can the conscious patient in the midst of a medical emergency provide adequate informed consent for a clinical research protocol? Adequate consent is crucial to the ethical conduct of clinical trials, including those performed in emergency settings. We examine the problem of emergency informed consent. As an illustrative case, we discuss a pilot trial of prehospital thrombolytic therapy for myocardial infarction. Federal regulations for clinical research do not provide clear guidelines on emergency research in the conscious patient. Clinical investigators currently approach emergency consent in four ways: (1) avoid such research, (2) omit the consent process, (3) obtain deferred consent, or (4) obtain customary consent. We suggest a fifth alternative, two-step consent, which permits the conduct of emergency research while protecting the rights of the emergency research subjects. Such a process may serve as an alternative solution for future studies faced with the problem of informed consent in emergencies.

KIE: The problem of informed consent to research in emergency care is examined, using as an example a pilot trial of prehospital administration of thrombolytic therapy for acute myocardial infarction. Current federal regulations governing emergency care research are reviewed, along with four ways in which investigators currently approach emergency consent. The authors' use of a two-step process to resolve the problem of emergency consent is described. This approach allows the conduct of emergency research while protecting the rights of research subjects, and may offer a solution to the the ethical conduct of other studies faced with the problem of consent to emergency care.

Evaluation of patients for the need of thrombolytic therapy in the prehospital setting.

Maximum benefit from thrombolytic therapy in acute myocardial infarction is obtained with early therapy. The earliest possible time to treat is during the initial evaluation of the patient in the home or ambulance, which requires accurate diagnosis of acute myocardial infarction in the prehospital setting. In our study, paramedics evaluated patients who had chest pain with a 12-lead ECG transmitted by cellular telephone and a checklist for inclusion and exclusion criteria for thrombolytic therapy. This information was transmitted to a hospital-based telemetry physician who diagnosed or excluded acute myocardial infarction and made a mock decision to withhold or administer a thrombolytic agent. Forty-eight patients with chest pain were evaluated. Six were diagnosed as having overt acute myocardial infarction by the hospital-based telemetry physician. All six patients had the diagnosis substantiated by both ECG and enzyme studies on hospital admission. Based on the data supplied by paramedics, two of these six patients were considered eligible for thrombolytic therapy by the physician. Hospital evaluation confirmed the prehospital decision to treat with a thrombolytic agent. In addition, all other patients were appropriately diagnosed as ineligible. Prehospital ECG diagnosis resulted in two patients going directly to the catheterization lab, thereby bypassing the emergency department. Overt acute myocardial infarction can be accurately identified by a prehospital-acquired 12-lead ECG transmitted to a hospital-based physician. Our study demonstrates that in conjunction with specially trained paramedics, the hospital physician can decide whether to administer thrombolytic therapy to such patients in the prehospital setting.

Cellular telephone transmission of 12-lead electrocardiograms from ambulance to hospital.

Currently, only single-lead, serial telemetry rhythm strips can be transmitted from ambulances. Triage of patients with chest pain and administration of thrombolytic therapy in ambulances is limited by the lack of specific electrocardiographic (ECG) diagnosis. A new technique is described using cellular telephone transmission of simultaneous 12-lead ECGs from ambulance to hospital to overcome this limitation. A portable 12-lead ECG installed in an ambulance was connected via modern link to a cellular telephone and digitized ECG information was transmitted to an ECG device in the hospital emergency room. Paramedics in the field placed adhesive patch electrodes and attached ECG wires. Field ECGs from 23 patients were compared with corresponding transmitted ECGs. There were no differences in heart rate, PR interval, QRS duration, QT interval or R- and T-wave axes. Baseline and transmitted ECGs had identical morphologic characteristics. Differences in R-wave amplitude in 5 transmitted tracings compared with hospital-recorded ECGs resulted in computer diagnosis of left ventricular hypertrophy by voltage, possibly due to differences in patient position. Twelve-lead ECGs can be easily transmitted from a moving ambulance using cellular telephones. This allows diagnosis before hospital arrival, improves prehospital triage of patients and may facilitate prehospital therapy with lidocaine or streptokinase. In addition, the cellular telephone link can convey both verbal and digitized information and thus improve on current telemetry systems.

Optimal ECG monitoring during percutaneous transluminal coronary angioplasty of the left anterior descending artery.

During percutaneous transluminal coronary angioplasty (PTCA) frontal ECG leads are routinely monitored. The detection of ST segment deviation during the procedure is important for decisions regarding guiding catheter seating and the timing of balloon inflation and deflation. ST segment deviation appears on intracoronary electrograms in the absence of changes on the surface ECG in many patients, while the reverse is true in some individuals. When a precordial lead is employed, V5 or V6 is most commonly selected. The surface ECG leads most sensitive for monitoring ischemia during left anterior descending angioplasty are not known. In nine lead surface ECGs recorded during balloon inflation, a small degree of ST segment elevation occurred in leads I, aVL, and V5. Lead V2 demonstrated an increase in ST displacement from 0.0 +/- 0.03 mV to 0.29 +/- 0.25 mV during coronary occlusion (p less than 0.01). We conclude that if V5 or V6 is used as a single precordial lead, surface ECG alterations are easily overlooked. During left anterior descending occlusion the most sensitive surface lead is V2. Optimal ECG monitoring during PTCA in some cases should involve surface lead V2 or the intracoronary lead.

R wave of the surface and intracoronary electrogram during acute coronary artery occlusion.

Increases in electrocardiographic R-wave amplitude in humans have been described with positive and negative dynamic exercise test findings, episodes of variant angina and myocardial ischemia and infarction. The role of factors other than acute reversible ischemia in the genesis of these R-wave size alterations is unclear. To evaluate the contribution of acute ischemia to changes in R-wave size in the absence of other confounding variables, electrocardiograms were recorded before and during coronary angioplasty balloon inflation. The frontal leads and V1, V2, V5 and V6 were recorded during the last 10 seconds of coronary occlusion in 20 patients and intracoronary epicardial electrograms were recorded continuously during balloon inflation in 10 patients. Inflations were 8 +/- 2 atm for 52 +/- 36 seconds. Chest pain occurred in 26 of 30 patients with balloon inflation and ST elevation occurred in 22. No significant increases in R amplitude were noted in any lead or in the sum of the R waves in all leads, including intracoronary electrograms. In contrast, R amplitude tended to decrease. The initial decrease in both surface and epicardial R amplitude was similar to the first of the biphasic changes observed in animal models. An increase in R-wave amplitude is not by itself always a marker for myocardial ischemia, but depends on severity and duration of the process.

Change in ventricular cavity size: differential effects on QRS and T wave amplitude.

Although many factors have been reported to change the R wave amplitude of the electrocardiogram (ECG), few observations have been made of the associated changes in T wave amplitude. We hypothesized that changes in R and T wave amplitude should parallel each other. To test this hypothesis, R and T wave amplitudes were measured in 15 normal subjects during increased and decreased left ventricular dimensions induced by infusion of methoxamine and by Valsalva maneuver, respectively, as well as during changes in the proximity of the left ventricle to the chest wall (i.e., shift in patient position from supine to left lateral position). Simultaneous nine-lead ECGs and two-dimensional-guided M mode echocardiograms of the left ventricle were recorded at rest and under each experimental condition. R wave amplitude increased as the left ventricular lateral wall moved closer to the V5 and V6 electrodes. Alterations in R wave amplitude seen with changes in left ventricular chamber size were primarily caused by radial movement of the left ventricle in relation to the chest wall. Proximity of the left ventricle to the chest wall was therefore a major determinant of R wave amplitude. In contrast, T wave amplitude varied directly with alterations in left ventricular chamber size but was unaffected by changes in proximity to the recording electrode on the chest wall. Left ventricular chamber size, and possibly the associated alteration in endocardial-to-epicardial surface area ratio, appeared to be the major determinants of T wave amplitude.

Relation of electrocardiographic R-wave amplitude to changes in left ventricular chamber size and position in normal subjects.

Although exercise-induced changes in electrocardiographic R-wave amplitude have been ascribed to changes in left ventricular (LV) size, QRS axis, heart rate and ischemia, the physiologic mechanism remains unclear. To clarify the relation between R-wave amplitude and changes in LV size and position, simultaneous 9-lead electrocardiograms and targeted M-mode echocardiograms were recorded from 15 normal subjects. Recordings were made at rest, during Valsalva maneuver and during methoxamine infusion. LV diastolic dimension increased with methoxamine and decreased with Valsalva maneuver (p less than 0.001). R-wave amplitude in leads V5 and V6 varied directly with LV dimensions (p less than 0.001). The correlation coefficient between the change in R-wave amplitude in V5 or V6 and the change in LV dimension was 0.81 (p less than 0.01). No significant changes in R-wave amplitude were seen in electrocardiographic leads I, II, III, aVR, aVL, aVF or V1. Distance from the chest wall to the LV posterior wall correlated with change in R-wave amplitude (r = 0.79, p less than 0.001). Change from supine to left lateral position moved the left ventricle closer to the lateral chest wall in association with a 41 +/- 8% increase in R-wave amplitude in V5 and V6 (p less than 0.001). In conclusion, there is a direct and a dynamic relation between R-wave amplitude and LV chamber size. Chamber size and distance from the left ventricle to leads V5 or V6 interact as major determinants of R-wave amplitude.

Supernormality: recent developments.

The major advance in our understanding of supernormality is the following hypothesis. Focal accumulations of extruded potassium ion in unstirred-clefts (invaginated extensions of the extracellular space in Purkinje fibers) cause threshold to fall by virtue of the early effects of hyperkalemia: lowering of threshold and acceleration of conduction. These effects rapidly dissipate in diastole as ionic equilibration takes place; threshold rises and assumes its late diastolic value. It is not known if this mechanism is applicable to the supernormality of specialized atrial fibers. Comparing the strength interval curves of supernormality and triggered automaticity the fall in threshold during the upstroke of the late after-depolarisation occurs later than the supernormal phase and is followed by a threshold rise (during the downstroke of the after-potential). Supernormality does not correspondingly show this biphasic change in the strength interval curve.

Electrophysiological changes in the canine atrium and ventricle during progressive hyperkalaemia: electrocardiographical correlates and the in vivo validation of in vitro predictions.

The electrophysiological response to hyperkalaemia was reinvestigated in the whole dog for several reasons including: the paucity of comparative electrophysiological and electrocardiographical studies in which atrial and ventricular tissues were simultaneously investigated; the contrast between the clarity of findings in previous in vitro studies as compared with the rather conflicting results in earlier in vivo investigations; and the difficulty in validating the extrapolation from in vitro results and theory to the in vivo situation because of deficiences in the literature. Biphasic alterations in atrial and ventricular conduction times as well as excitability in response to progressively increasing hyperkalaemia were documented. The alterations in conduction times were reflected quite accurately by relevant electrocardiographical changes. Experiments in the whole animal were designed to test predictions based on membrane theory: the results offering strong support for the validity of extrapolating from the in vitro to the in vivo situation. The results of this study should help clarify and render interpretable many of the seemingly conflicting results in the literature.

The junctional premature beat: an instructional exercise in modes of concealment.

?The relative brevity of the main His bundle refractory period compared with that of the A-V node above, and the trifascicular system below, makes it likely that premature beats originating in the His bundle will encounter physiologic delay, or block in both antegrade and retrograde modes. Two clinical cases of junctional premature beats are presented, which demonstrate many facets of concealment (antegrade, retrograde and bidirectional). Hitherto unreported is a ventricular echo which was induced by a junctional premature beat, the antegrade concealment of which was due to functional trifascicular block.