Cardiac Conduction (cardiac + conduction)

Distribution by Scientific Domains

Terms modified by Cardiac Conduction

  • cardiac conduction defect
  • cardiac conduction system

  • Selected Abstracts


    Acute Effects of Low Doses of Red Wine on Cardiac Conduction and Repolarization in Young Healthy Subjects

    ALCOHOLISM, Issue 12 2009
    Matteo Cameli
    Background:, Moderate to high blood concentrations of ethanol have been shown to yield acute changes in cardiac electrophysiological properties, but the effect of low concentrations have never been assessed. The role of concomitant changes in clinical variables or cardiac dimensions is also still unknown. This study aimed at exploring the acute effects of low doses of ethanol, administered as Italian red wine, on conduction, depolarization, and repolarization electrocardiographic (ECG) intervals in a population of healthy subjects. Methods:, Forty healthy young volunteers drank a low quantity of red wine (5 ml/kg), and an equal volume of fruit juice in separate experiments. Heart rate, P-wave duration, PR interval, QRS duration, QT interval, corrected QT interval, QT dispersion, and corrected QT dispersion were assessed at baseline and after 60 minutes from challenge. Results:, Mean blood ethanol concentration after drinking was 0.48 ± 0.06 g/l. Compared to the control challenge, significant changes after red wine intake were observed in P-wave duration (from 101 ± 11 to 108 ± 14 milliseconds, p = 0.0006), PR interval (from 153 ± 15 to 167 ± 17 milliseconds, p < 0.0001), QT interval (from 346 ± 28 to 361 ± 24 milliseconds, p < 0.0001), and corrected QT interval (from 388 ± 24 to 402 ± 30 milliseconds, p = 0.0006). None of these changes showed correlations with modifications in clinical or echocardiographic variables. In multivariate analyses aimed at exploring predictors of ECG changes, none of the variables entered the final models. Conclusions:, Low doses of red wine acutely slow cardiac conduction and prolong repolarization in normal individuals. These changes are poorly predictable. The potential arrhythmogenic impact of these effects is worthy of exploration. [source]


    Hypertonic Saline Treatment of Severe Hyperkalemia in Nonnephrectomized Dogs

    ACADEMIC EMERGENCY MEDICINE, Issue 9 2000
    Justin L. Kaplan MD
    Abstract. Objectives: To determine whether a hypertonic saline bolus improves cardiac conduction or plasma potassium levels more than normal saline infusion within 15 minutes of treatment for severe hyperkalemia. Previously with this model, 8.4% sodium chloride (NaCl) and 8.4% sodium bicarbonate (NaHCO3) lowered plasma potassium equally effectively. Methods: This was a crossover study using ten conditioned dogs (14-20 kg) that received, in random order, each of three intravenous (IV) treatments in separate experiments at least one week apart: 1) 2 mmol/kg of 8.4% NaCl over 5 minutes (bolus); 2) 2 mmol/kg of 0.9% NaCl over one hour (infusion); or 3) no treatment (control). Using isoflurane anesthesia and ventilation (pCO2= 35-40 torr), 2 mmol/kg/hr of IV potassium chloride (KCl) was infused until conduction delays (both absent p-waves and ,20% decrease in ventricular rate in ,5 minutes) were sustained for 15 minutes. The KCl was then decreased to 1 mmol/kg/hr (maintenance) for 2 hours and 45 minutes. Treatment (0 minutes) began after 45 minutes of maintenance KCl. Results: From 0 to 15 minutes, mean heart rate increased 29.6 (95% CI = 12.2 to 46; p < 0.005) beats/min more with bolus than infusion and 23.4 (95% CI = 2.6 to 43.5; p < 0.03) beats/min more with bolus than control. No clinically or statistically significant difference was seen in heart rate changes from 0 to 30 minutes. Decreases in potassium from 0 to 15 minutes were similar with bolus, infusion, and control. Conclusions: In this model, 8.4% NaCl bolus reversed cardiac conduction abnormalities within the first 15 minutes after treatment, more rapidly than did the 0.9% NaCl infusion or control. This reversal occurred despite similar reductions in potassium levels. [source]


    Cells migrating from the neural crest contribute to the innervation of the venous pole of the heart

    JOURNAL OF ANATOMY, Issue 1 2008
    Victoria Hildreth
    Abstract Cells migrating from the neural crest are known to septate the outflow tract of the developing heart, and to contribute to the formation of the arterial valves, their supporting sinuses, the coronary arteries and cardiac neural ganglia. Neural crest cells have also been suggested to contribute to development of the venous pole of the heart, but the extent and fate of such cells remains unclear. In this study, in the mouse, it is shown that cells from the neural crest contribute to the parasympathetic and, to a lesser extent, the sympathetic innervation of the venous pole of the heart. Nerves within the venous pole of the heart are shown to be of mixed origin, with some being derived from the neural crest, while others have an alternative origin, presumably placodal. The neurons innervating the nodal tissue, which can exert chronotropic effects on cardiac conduction, are shown not to be derived from the neural crest. In particular, no evidence was found to support previous suggestions that cells from the neural crest make a direct contribution to the myocardial atrioventricular conduction axis, although a small subset of these cells do co-localize with the developing left bundle branch. We have therefore confirmed that cells from the neural crest migrate to the venous pole of the heart, and that their major role is in the development of the parasympathetic innervation. In addition, in some embryos, a population of cells derived from the neural crest persist in the leaflets of the atrioventricular valves, but their role in subsequent development remains unknown. [source]


    The pharmacological properties of anisodamine,

    JOURNAL OF APPLIED TOXICOLOGY, Issue 2 2007
    Jay M. Poupko
    Abstract Anisodamine is a naturally occurring atropine derivative that has been isolated, synthesized and characterized by scientists in the People's Republic of China. Like atropine and scopolamine, anisodamine is a non-specific cholinergic antagonist exhibiting the usual spectrum of pharmacological effects of this drug class. It appears to be less potent and less toxic than atropine and displays less CNS toxicity than scopolamine. Anisodamine has been shown to interact with and disrupt liposome structure which may reflect its effects on cellular membranes. Experimental evidence implicates anisodamine as an anti-oxidant that may protect against free radical-induced cellular damage. Its cardiovascular properties include depression of cardiac conduction and the ability to protect against arrhythmia induced by various agents. Anisodamine is a relatively weak ,1 adrenergic antagonist which may explain its vasodilating activity. Its anti-thrombotic activity may be a result of inhibition of thromboxane synthesis. The T1/2 of anisodamine in humans is about 2,3 h. Numerous therapeutic uses of anisodamine have been proposed including treatment of septic shock, various circulatory disorders, organophosphorus (OP) poisoning, migraine, gastric ulcers, gastrointestinal colic, acute glomerular nephritis, eclampsia, respiratory diseases, rheumatoid arthritis, obstructive jaundice, opiate addiction, snake bite and radiation damage protection. The primary therapeutic use of anisodamine has been for the treatment of septic shock. Several mechanisms have been proposed to explain its beneficial effect though most mechanisms are based upon the assumption that anisodamine ultimately acts by an improvement of blood flow in the microcirculation. Preliminary studies suggest another important therapeutic use of anisodamine is for the treatment of OP poisoning. Additional research is needed to delineate further the clinical usefulness of anisodamine relative to other anti-muscarinic drugs such as atropine and scopolamine. Copyright © 2006 John Wiley & Sons, Ltd. [source]


    Acute Effects of Low Doses of Red Wine on Cardiac Conduction and Repolarization in Young Healthy Subjects

    ALCOHOLISM, Issue 12 2009
    Matteo Cameli
    Background:, Moderate to high blood concentrations of ethanol have been shown to yield acute changes in cardiac electrophysiological properties, but the effect of low concentrations have never been assessed. The role of concomitant changes in clinical variables or cardiac dimensions is also still unknown. This study aimed at exploring the acute effects of low doses of ethanol, administered as Italian red wine, on conduction, depolarization, and repolarization electrocardiographic (ECG) intervals in a population of healthy subjects. Methods:, Forty healthy young volunteers drank a low quantity of red wine (5 ml/kg), and an equal volume of fruit juice in separate experiments. Heart rate, P-wave duration, PR interval, QRS duration, QT interval, corrected QT interval, QT dispersion, and corrected QT dispersion were assessed at baseline and after 60 minutes from challenge. Results:, Mean blood ethanol concentration after drinking was 0.48 ± 0.06 g/l. Compared to the control challenge, significant changes after red wine intake were observed in P-wave duration (from 101 ± 11 to 108 ± 14 milliseconds, p = 0.0006), PR interval (from 153 ± 15 to 167 ± 17 milliseconds, p < 0.0001), QT interval (from 346 ± 28 to 361 ± 24 milliseconds, p < 0.0001), and corrected QT interval (from 388 ± 24 to 402 ± 30 milliseconds, p = 0.0006). None of these changes showed correlations with modifications in clinical or echocardiographic variables. In multivariate analyses aimed at exploring predictors of ECG changes, none of the variables entered the final models. Conclusions:, Low doses of red wine acutely slow cardiac conduction and prolong repolarization in normal individuals. These changes are poorly predictable. The potential arrhythmogenic impact of these effects is worthy of exploration. [source]


    Effects of Sex and Age on Electrocardiographic and Cardiac Electrophysiological Properties in Adults

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001
    TARESH TANEJA
    TANEJA, T., et al.: Effects of Sex, and Age on Electrocardiographic and Cardiac Electrophysiological Properties in Adults. Although differences in patient sex in heart rate and QT interval have been well characterized, sexual differences in other cardiac electrophysiological properties have not been well defined. The study population consisted of 354 consecutive patients without structural heart disease or preexcitation who underwent clinically indicated electrophysiological testing in the drug-free state. Atrial, AV nodal, and ventricular effective refractory periods (AERP, AVNERP, VERP) were determined at a pacing cycle length of 500 ms using an 8-beat drive train and 3-second intertrain pause. There were 124 men and 230 women with a mean age of 45 ± 19 and 47 ± 18 years, respectively The sinus cycle length (SCL) was longer in men than in women (864 ± 186 and 824 ± 172 ms, respectively, P < 0.05). The QRS duration was significantly longer in men (90 ± 12 ms) than women (86 ± 13 ms) (P < 0.005). The HV interval was 48 ± 9 ms in men and 45 ± 8 ms in women (P < 0.05). The sinus node recovery time (SNRT) was significantly longer in men than in women (1215 ± 297 ms and 1135 ± 214 ms, respectively, P < 0.05). AERP and VERP were similar in both sexes. Aging did not influence sexual differences in cardiac electrophysiological properties, although, it independently prolonged the SCL, PR, and QT intervals, AH and HV intervals, SNRT, AVNERP, and the AV Wenckebach cycle length. The SCL, QRS duration, HV interval, and SNRT were significantly longer in men than in women. Aging prolonged cardiac conduction and increased the SCL but the effects were similar in both sexes. AERP and VERP were unaffected by aging or sex. [source]


    Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

    ANAESTHESIA, Issue 8 2010
    G. Cave
    Summary Intravenous lipid emulsion is established therapy for bupivacaine induced cardiotoxicity. The benefit of combined hypertonic saline and lipid treatment is unexplored. In this experiment, sedated rabbits were resuscitated from bupivacaine-induced asystole with intravenous lipid according to the Association of Anaesthetists of Great Britain and Ireland's guideline, or by identical lipid dosing with hypertonic saline: 6 mEq.kg,1 21% sodium chloride. Early electrocardiography QRS prolongation was less with lipid plus hypertonic saline (mean (SD) QRS 0.19 (0.07) s lipid only vs 0.09 (0.01) s lipid plus hypertonic saline; p = 0.003) at 9 min though not different from the lipid only group at 20 min. No difference was observed in rates of circulatory return (7/10 lipid only and 9/10 lipid plus hypertonic saline; p = 0.58) or survival (5/10 lipid only and 6/10 lipid plus hypertonic saline; p = 1.00). Some benefit to cardiac conduction may be afforded by hypertonic saline co-administered with lipid emulsion in bupivacaine-induced cardiotoxicity. [source]