Changes In Cardiac Conduction Research Articles

Electrocardiographic determination of perioperative myocardial ischemia and stunning.

Many modalities are available for monitoring for ischemia. Electrocardiography (ECG) is the most suitable modality for monitoring for perioperative ischemia. The detection and monitoring of myocardial stunning is more difficult. T wave inversion or peaking may be caused by ischemia. However, numerous nonischemic causes may lead to perioperative T wave changes. Inverted T waves may also indicate myocardial stunning. ST deviation is the most commonly used feature of ischemia. ST depression may be indicative of subendocardial ischemia while ST elevation may be associated with transmural ischemia or injury. Perioperatively, ST deviation may be caused by many nonischemic causes. Fixed ST deviation may be caused by left ventricular hypertrophy (LVH), cardiac conduction changes, old MI, coronary artery disease, and other causes such as drugs, including digitalis. New ST deviation may be caused by changes in body position. During cardiopulmonary bypass, ST deviation may be caused by hypothermia and defibrillation. ST deviation may be caused by new cardiac conduction changes and pericarditis. Ischemia may cause changes in other features of the ECG including the R wave, Q wave, U wave, QRS axis, and the angle between QRS axis and T wave axis. However, the specificity of these features for ischemia is even lower than that of the ST segment.

Frequency dependent effects of tocainide, quinidine, and flecainide on conduction as reflected in the rise time of the monophasic action potential in the isolated guinea pig heart

The aim was to evaluate a possible correlation between intraventricular conduction and the rise time of the ventricular monophasic action potential upstroke. This evaluation was performed by estimating the onset rate kinetics for changes in the monophasic action potential rise time and cardiac conduction upon abrupt shortening of the interstimulus interval in the in vitro perfused guinea pig heart. 21 Duncin Hartley guinea pigs, 520-800 g, were used for the studies. The animals were anaesthetised and the hearts rapidly excised and perfused horizontally in the Langendorff manner. It was shown that the rise time onset rate (expressed as the inverted number of action potentials needed to reach 63% of the new steady state level) was very fast (greater than 0.5) for tocainide, very slow for flecainide [0.09(SEM 0.009]) and intermediate for quinidine [0.29(0.070)]. These values are similar to onset rates previously reported from studies of Vmax in intracellular recordings. Moreover, similar onset rates were obtained for simultaneously measured frequency dependent changes in cardiac conduction. These findings suggest that, at least for drugs restricting sodium entry into the cell, effects on Vmax could be predicted from monophasic action potential rise time data from the isolated guinea pig heart. The possibility of using the monophasic action potential rise time as a measure of local cardiac conduction provides an opportunity for in vivo studies of the temporal beat by beat relationship between conduction and repolarisation, factors that are important for the initiation and maintenance of many arrhythmias.

Isradipine in the treatment of hypertension: a clinical profile

Isradipine (DynaCirc, PK 200-110) is a new calcium channel blocker of the dihydropyridine class. In controlled, double-blind, clinical trials isradipine is an effective first-line monotherapeutic agent in the treatment of hypertension, regardless of patient age or race. Isradipine is safe and well tolerated, with few adverse effects reported, and does not cause significant changes in cardiac conduction or the force of cardiac contraction. In addition, it does not adversely affect the lipid profile, carbohydrate tolerance, or renal function. Long-term experience with isradipine indicates that the antihypertensive efficacy is maintained without problems of tachycardia or tachyphylaxis.

Influence of sodium on desmethylimipramine (DMI)-induced changes in cardiac conduction

Influence of sodium on desmethylimipramine (DMI)-induced changes in cardiac conduction

Cardiorespiratory effects of brevetoxin (PbTx-2) in conscious, tethered rats

The cardiorespiratory effects of various doses of brevetoxin (0–100 μg PbTx-2/kg) were studied in conscious, tethered rats, After surgical preparation and a 24 hr recovery, toxin or vehicle was infused into the tethered, awake rats for 1 hr. They were then monitored for 6 hr or until death. Toxin-infused rats had decreased core and peripheral temperatures and decreased respiratory rates; these values were all low in the 100 μg/kg group at the time of death. Blood gas values remained within normal limits, except terminally. Electrocardiographic (ECG) disturbances, noted in all groups given ≥25 μg/kg, included heart block, premature ventricular contractions and idioventricular rhythms. It was concluded that brevetoxin causes changes in cardiac conduction and multiple changes in nervous system function.

Action potential correlates of pressure-induced changes in cardiac conduction.

Microelectrode studies were undertaken to determine the cellular bases for hydrostatic pressure effects on impulse propagation and refractoriness in cardiac muscle. Canine Purkinje fibers, at 37 degrees C, were exposed to increases in hydrostatic pressure to 150 ATA. At 150 ATA membrane excitability was depressed and the maximum upstroke velocity (Vmax) of the action potential was reduced by 10%. Furthermore, the curve relating Vmax to takeoff potential (membrane responsiveness relation) shifted downward and to the right with the half inactivation voltage shifting in the hyperpolarizing direction by about 4 mV. Decreases in excitability and responsiveness occurred concomitantly with pressure-induced decreases in impulse conduction. Action potential duration (APD) increased significantly at 150 ATA. APD measured at -20 mV, -60 mV, and at maximum repolarization averaged 20.7, 15.5, and 13.5% longer than their respective 1-ATA values. The combined effects of increased APD and depressed responsiveness account for increased tissue refractoriness. The implications of the findings with regard to the arrhythmogenic nature of high hydrostatic pressure are discussed.

Cadmium Feeding: Apparent Depression of Atrioventricular‐His‐Purkinje Conduction System

Male rats were exposed to 0, 10 and 130 p.p.m. cadmium administered in 0.5% saline drinking water for 71 days. Biweekly records of ECGs, Hct, body weight and blood levels of cadmium were made. Rats exposed to 130 p.p.m. cadmium showed slower growth rates and declining Hct indicative of acute cadmium poisoning. At the end of the experimental period, carotid artery blood pressures and whole heart cadmium levels were determined. Although no significant blood pressure changes were observed in the experimental groups, the cadmium content of the hearts of the higher dose group was significantly higher than in the hearts of the lower dose group. The PR interval of the ECG was lengthened progressively and to the same extent in both experimental groups with continued cadmium feeding. These experiments offer evidence that the accumulation of even moderate amounts of cadmium will be manifested in marked changes in cardiac conduction without overt signs of cadmium poisoning.

Effects of chronic lead treatment on some cardiovascular responses to norepinephrine in the rat

Rats were treated with lead via the mother's milk from birth to weaning. After a lead-free period of approximately 4 months, responses to norepinephrine were tested. Neither the pressor effect nor the enhancement of myocardial cAMP accumulation caused by norepinephrine was altered by prior lead treatment. However, norepinephrine caused significantly more cardiac arrhythmias in lead-treated animals than in controls. Even doses of norepinephrine which caused no significant ECG abnormalities in control animals were arrhythmogenic in lead-treated rats. It is concluded that lead treatment causes changes in cardiac conduction which are not readily reversed by termination of lead exposure.

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.