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R-wave Amplitude (r-wave + amplitude)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

R-wave Amplitude in Lead II of an Electrocardiograph Correlates with Central Hypovolemia in Human Beings

ACADEMIC EMERGENCY MEDICINE, Issue 10 2006
John G. McManus MD
Abstract Objectives Previous animal and human experiments have suggested that reduction in central blood volume either increases or decreases the amplitude of R waves in various electrocardiograph (ECG) leads depending on underlying pathophysiology. In this investigation, we used graded central hypovolemia in adult volunteer subjects to test the hypothesis that moderate reductions in central blood volume increases R-wave amplitude in lead II of an ECG. Methods A four-lead ECG tracing, heart rate (HR), estimated stroke volume (SV), systolic blood pressure, diastolic blood pressure, and mean arterial pressure were measured during baseline supine rest and during progressive reductions of central blood volume to an estimated volume loss of >1,000 mL with application of lower-body negative pressure (LBNP) in 13 healthy human volunteer subjects. Results Lower-body negative pressure resulted in a significant progressive reduction in central blood volume, as indicated by a maximal decrease of 65% in SV and maximal elevation of 56% in HR from baseline to ,60 mm Hg LBNP. R-wave amplitude increased (p < 0.0001) linearly with progressive LBNP. The amalgamated correlation (R2) between average stroke volume and average R-wave amplitude at each LBNP stage was ,0.989. Conclusions These results support our hypothesis that reduction of central blood volume in human beings is associated with increased R-wave amplitude in lead II of an ECG. [source]

Implant Experience with an Implantable Hemodynamic Monitor for the Management of Symptomatic Heart Failure

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2005
DAVID STEINHAUS
Introduction: Management of congestive heart failure is a serious public health problem. The use of implantable hemodynamic monitors (IHMs) may assist in this management by providing continuous ambulatory filling pressure status for optimal volume management. Methods and Results: The Chronicle® system includes an implanted monitor, a pressure sensor lead with passive fixation, an external pressure reference (EPR), and data retrieval and viewing components. The tip of the lead is placed near the right ventricular outflow tract to minimize risk of sensor tissue encapsulation. Implant technique and lead placement is similar to that of a permanent pacemaker. After the system had been successfully implanted in 148 patients, the type and frequency of implant-related adverse events were similar to a single-chamber pacemaker implant. R-wave amplitude was 15.2 ± 6.7 mV and the pressure waveform signal was acceptable in all but two patients in whom presence of artifacts required lead repositioning. Implant procedure time was not influenced by experience, remaining constant throughout the study. Conclusion: Based on this evaluation, permanent placement of an IHM in symptomatic heart failure patients is technically feasible. Further investigation is warranted to evaluate the use of the continuous hemodynamic data in management of heart failure patients. [source]

Electrocardiographic Alterations during Hyperinsulinemic Hypoglycemia in Healthy Subjects

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2008
Tomi Laitinen M.D.
Background: We evaluated the arrhythmogenic potential of hypoglycemia by studying electrocardiographic (ECG) changes in response to hyperinsulinemic hypoglycemia and associated sympathoadrenal counterregulatory responses in healthy subjects. Methods: The study population consisted of 18 subjects, aged 30,40 years. Five-minute ECG recordings and blood samplings were performed at baseline and during the euglycemic and hypoglycemic hyperinsulinemic clamp studies. PR, QT, and QTc intervals of electrocardiogram and ECG morphology were assessed from signal-averaged ECG. Results: Although cardiac beat interval remained unchanged, PR interval decreased (P < 0.01) and QTc interval (P < 0.001) increased in response to hyperinsulinemic hypoglycemia. Concomitant morphological alterations consisted of slight increases in R-wave amplitude and area (P < 0.01 for both), significant decreases in T-wave amplitude and area (P < 0.001 for both), and moderate ST depression (P < 0.001). Counterregulatory norepinephrine response correlated with amplification of the R wave (r =,0.620, P < 0.05) and epinephrine response correlated with flattening of the T wave (r =,0.508, P < 0.05). Conclusions: Hyperinsulinemic hypoglycemia with consequent sympathetic humoral activation is associated with several ECG alterations in atrioventricular conduction, ventricular depolarization, and ventricular repolarization. Such alterations in cardiac electrical function may be of importance in provoking severe arrhythmias and "dead-in-bed" syndrome in diabetic patients with unrecognized hypoglycemic episodes. [source]