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Biomedical subjects

R P Holland

Publications and source records attributed to R P Holland.

12 recordsLinked to original sources
PubMed1981

Nonspatial determinants of electrograms in guinea pig ventricle.

Theory states that the extracellularly recorded potential (epsilon) is determined by spatial and nonspatial factors. Spatial factors include the boundary between areas with different transmembrane voltages (Vm) and the relationship of the boundary to the extracellular electrode. Nonspatial factors include the Vm across the boundary [transmembrane potential gradient (TPG)] and a conductivity term (C sigma). Few studies have investigated the nonspatial factors experimentally due to the difficulty in separating the nonspatial from the spatial determinants. Our model rendered the spatial factors constant, permitted the simultaneous recording of epsilon and Vm, and allowed the manipulation of Vm and C sigma across the boundary. Epsilon and the TPG were related predictably with changes in [K+]o, [Na+]o, temperature, conduction, stimulus rate or prematurity, and hypoxia. In the presence of a constant TPG, epsilon could be affected by a change in C sigma caused by hypoxia and a metabolic poison. The effects of the nonspatial determinants on epsilon could be modeled using electrical circuit analogues. Nonspatial determinants must be considered in studies using electrocardiographic measures as an index of ischemia.

Action Potentials↗
PubMed1979

Study of 'Vivalan' in geriatric patients suffering from depression.

Twenty elderly depressed patients were entered into a study of Vivalan (viloxazine; 150-200 mg daily). Significant falls in Hamilton and Zung ratings occurred by Day 7 of treatment and further significant improvements were noted over the following 2 weeks. These changes were also reflected in global assessments. Headache was reported in six patients and nausea in three. Vivalan had no significant effect upon blood pressure and absence of anticholinergic side-effects proved an advantage in the treatment of elderly patients with depressive illness.

Aged↗
PubMed1977

TQ-ST segment mapping: critical review and analysis of current concepts.

Controversy and confusion surround many aspects of TQ-ST segment mapping today. Technical standards pertaining to the recording and measurement of the TQ-ST deflection have not been uniformly established nor has the correlative value of the deflection as an indicator of myocardial injury been clearly ascertained. The TQ-ST deflection is believed to originate primarily although not exclusively as a result of extracellular potassium accumulation in the ischemic region and subsequent establishment of a transmembrane potential gradient during diastole and systole at the ischemic boundary. Nonspatial factors (including electrolytes, antiarrhythmic agents, heart rate) influence the TQ-ST deflection by altering this gradient. Spatial factors (including ischemic area and shape, electrode location) alter the relative position of the ischemic boundary to the electrode site and as such can be analyzed with the solid angle theorem. Further study of the complex behavior of the TQ-ST segment deflection, particularly in the presence of pharmacologic intervention, is necessary before mapping techniques can be used reliably in clinical studies designed to quantitate and modify ischemic damage.

Coronary Disease↗
PubMed1977

Spatial and nonspatial influences on the TG-ST segment deflection of ischemia. Theoretical and experimental analysis in the pig.

Spatial and nonspatial aspects of TQ-ST segment mapping were studied with the solid angle theorem and randomly coded data from 15,000 electrograms of 160 anterior descending artery occlusions each of 100-s duration performed in 18 pigs. Factors analyzed included electrode location, ischemic area and shape, wall thickness, and increases in plasma potassium (K(+)). Change from control in the TQ-ST recorded at 60 s (DeltaTQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, DeltaTQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) DeltaTQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) DeltaTQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123+/-18%, DeltaTQ-ST at IS sites decreased (-38.1+/-3.6%), and sum of DeltaTQ-ST at IS sites increased by only 67.3+/-10.3%. In RV NIS Pos DeltaTQ-ST became Neg. With increased K(+), DeltaTQ-ST decreased proportionately to log K(+) (r = 0.97+/-0.01) at IS and NIS sites on the epicardium and precordium. TQ-ST at 60 s was obliterated when K(+) = 8.7+/-0.2 mM. All findings were significant (P < 0.005) and agreed with the solid angle theorem. Thus, a transmembrane potential difference and current flow at the IS boundary alone are responsible for the TQ-ST. Nonspatial factors affect the magnitude of transmembrane potential difference, while spatial factors alter the position of the boundary to the electrode site.

Animals↗
PubMed1976

The QRS complex during myocardial ischemia. An experimental analysis in the porcine heart.

Although ST segment deflections have been widely utilized as a means of assessing the degree of underlying ischemic injury, the relationship of QRS complex alterations to the ischemic process is poorly understood. In this study we made a beat-to-beat analysis of the QRS complex in terms of ventricular activation time (CT) and R wave voltage (V) in the acutely ischemic porcine myocardium and analyzed the relationship of these responses to changes in the area of ischemic involvement, altered myocardial energy demands, and plasma [K+]0 levels. With the onset of ischemia the QRS complex underwent a specific and reproducible biphasic sequence with an initial decrease in CT and V indicating a transient increase in the conduction velocity of the ischemic tissue. Subsequently both CT and V returned briefly to control and then increased dramatically, now indicating a marked decrease in conduction velocity. The time when CT first began to increase (Tc) was shortened by enlarging the area of ischemia or after an inotropic intervention and was lengthened by decreasing the area of ischemia or with administration of propranolol. Moreover Tc was found to be inversely proportional to plasma [K+]0 in the range 3.4-8.8 mM, above which the initial decrease in CT and V was no longer present. We conclude that this biphasic sequence of QRS alterations in early myocardial ischemia is attributable to a progressive leakage of potassium out of the ischemic cells which in turn alters both the time-course and transmural pathway of the activation process through the ischemic tissue. These changes are related to both inotropic state and the area of ischemic involvement.

Animals↗
PubMed1976

Cases of overdosage with viloxazine hydrochloride (Vivalan).

Twelve cases of viloxazine overdosage are reported. All patients recovered without sequelae and no ECG abnormalities were observed. Gastric lavage was performed in most cases and was probably beneficial. As viloxazine is rapidly absorbed (Bayliss & Case 1975, Case & Reeves 1975) lavage should be carried out as soon as possible after the tablets are taken. Since the drug is almost exclusively excreted in the urine, it is suggested that forced diuresis be carried out to reduce blood levels as quickly as possible.

Adolescent↗
PubMed1975

Precordial and epicardial surface potentials during Myocardial ischemia in the pig. A theoretical and experimental analysis of the TQ and ST segments.

The solid angle theorem was used to analyze the relationships between TQ and ST segment deflections recorded from precordial and epicardial locations and the time course, size, shape, and transmural location of the ischemic process in the ventricular myocardium. Mathematical predictions were compared with experimental data from the intact heart. Precordial electrograms obtained in anesthetized close-chest pigs were compared with epicardial electrograms recorded directly from the heart's surface. Various areas of ischemia were produced by occluding large and small coronary artery branches, and the resultant changes in ischemic shape were delineated with Thioflavin S injections and postmortem ultraviolet photography. Formally derived equations and cumulative experimental data were in close agreement, suggesting that in the ischemic ventricle (1) TQ depression always accompanies ST elevation, (2) TQ and ST segment changes in magnitude and polarity are complex functions of ischemic size, shape, and transmural location; (3) precordial electrocardiogram (ECG) ST segment elevation is directly related to ischemic size; and (4) epicardial ECG ST segment elevation is inversely related to ischemic size. It is thus concluded that precordial and epicardial ECG TQ and ST segment deflections are complex functions of ischemic geometry and that their accurate interpretation with respect to ischemic size and shape and in the presence of pharmacological interventions is often difficult and may be misleading.

Action Potentials↗