Sinoatrial conduction time

Chronotropic effect negative. Ethanol (50%) extract of the fresh leaf, administered by gastric intubation to rats at a dose of 40 mL/kg, produced weak activity. Results were significant at p < 0.05 level ". Glycerin/ ethanol extract of the fresh leaf, administered intragastrically to dogs at a dose of 20 mg/kg, produced an increase in length of sinusal cycle (16%), sinoatrial conduction time (27%), and sinus node recovery time (31%) . 

Fentanyl enhances vagal tone and can cause bradycardia. In 27 children undergoing catheter ablation under propofol anesthesia, which has minimal effect on the sinus node, electrophysiological stimulation was performed before and after a bolus dose of fentanyl 2 micrograms/kg and a subsequent infusion of 0.075 micrograms/kg/minute [64 ]. There was an increase in calculated sinus node recovery time but no change in sinoatrial conduction time after fentanyl, suggesting that fentanyl -I- propofol impairs sinus node recovery and therefore... 

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells display pacemaker activity (phase 4 depolarization). The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. Thus, the PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated (ie, the intraventricular conduction time). The QT interval reflects the duration of the ventricular action potential.

Verapamil blocks both activated and inactivated L-type calcium channels. Thus, its effect is more marked in tissues that fire frequently, those that are less completely polarized at rest, and those in which activation depends exclusively on the calcium current, such as the sinoatrial and atrioventricular nodes. Atrioventricular nodal conduction time and effective refractory period are invariably prolonged by therapeutic concentrations. Verapamil usually slows the sinoatrial node by its direct action, but its hypotensive action may occasionally result in a small reflex increase of sinoatrial nodal rate. 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Transmembrane action potential of a sinoatrial node cell. In contrast to other cardiac cells, there is no phase 2 or plateau. The threshold potential (TP) is -40 mV. The maximum diastolic potential (MDP) is achieved as a result of a gradual decline in the potassium conductance (gK+). Spontaneous phase 4 or diastolic depolarization permits the cell to achieve the TR thereby initiating an action potential (g = transmembrane ion conductance). Stimulation of pacemaker cells within the sinoatrial node decreases the time required to achieve the TR whereas vagal stimulation and the release of acetylcholine decrease the slope of diastolic depolarization. Thus, the positive and negative chronotropic actions of sympathetic and parasympathetic nerve stimulation can be attributed to the effects of the respective neurotransmitters on ion conductance in pacemaker cells of the sinuatrial node. gNa+ = Na+ conductance. 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

By increasing the rates of ventricular contraction and relaxation, Epi preferentially shortens systole and usually does not reduce the duration of diastole. Epi speeds the heart by accelerating the slow depolarization of sinoatrial (SA) nodal cells that takes place during phase 4 of the action potential (see Chapter 34). The amplitude of the AP and the maximal rate of depolarization (phased) also are increased. A shift in the location of the pacemaker within the SA node often occurs, owing to activation of latent pacemaker cells. In Purkinje fibers, Epi accelerates diastolic depolarization and may activate latent pacemakers. If large doses of Epi are given, premature ventricular contractions occur and may herald more serious ventricular arrhythmias. Conduction through the Purkinje system depends on the level of membrane potential at the time of excitation. Epi often increases the membrane potential and improves conduction in Purkinje fibers that have been excessively depolarized. 

Concurrent use is unquestionably valuable and uneventful in many patients, but severe adverse effects can develop. This is well established. A not dissimilar adverse interaction can occur with verapamil , (p.841). On the basis of 6 reports, the incidence of symptomatic bradyarrhythmia was estimated to be about 10 to 15%. It can occur with different beta blockers, even with very low doses, and at any time from within a few hours of starting treatment to 2 years of concurrent use. The main risk factors seem to be ventricular dysfunction, or sinoatrial or AV nodal conduction abnormalities. Note that these are usually contraindications to the use of diltiazem. Patients with normal ventricular function and no evidence of conduction abnormalities are usually not at risk. Concurrent use should be well monitored for evidence of adverse effects. Changes in the pharmacokinetics of the beta blockers may also occur, but these changes are probably not clinically important. 

The T-channel and L-channel are widely distributed in the conductive system of the heart, especially the sinoatrial (SA) node. The first phase of cell depolarisation in the SA node will be started via the activation of the T-channel (allowing fast influx of extracellular calcitun ions), while the later phase of depolarisation will be controlled by the L-channel (slow influx). CCBs have no significant activity on the T-channel. Instead they shorten the L-channel opening time, which increases the penetration time required for Ca ions to completely depolarise the cell and hence this reduces the heart rate (negative chronotropic effect). 

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