Heart intraventricular conduction

Hypersensitivity or idiosyncrasy to quinidine or other cinchona derivatives manifested by thrombocytopenia, skin eruption or febrile reactions myasthenia gravis history of thrombocytopenic purpura associated with quinidine administration digitalis intoxication manifested by arrhythmias or AV conduction disorders complete heart block left bundle branch block or other severe intraventricular conduction defects exhibiting marked QRS widening or bizarre complexes complete AV block with an AV nodal or idioventricular pacemaker aberrant ectopic impulses and abnormal rhythms due to escape mechanisms history of drug-induced torsade de pointes history of long QT syndrome. 

Cardiovascular effects If a ventricular pacemaker is operative, patients with seconder third-degree heart block may be treated with mexiletine if continuously monitored. Exercise caution in such patients or in patients with preexisting sinus node dysfunction or intraventricular conduction abnormalities. 

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. 

Intraventricular conduction delay often leads to late activation of the left ventricular free wall with significant mechanical consequences. The mechanical consequences of abnormal electrical activation of the heart have long been recognized [58, 60, 86]. These include dyssynchrony between the atria. 

Shamim W, Francis DP, Yousufuddin M, et al. Intraventricular conduction delay a prognostic marker in chronic heart failure. Int. J. Cardiol. 1999 70 171-8. 

Cazeau S, Leclercq C, Lavergne T, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N. Engl. J. Med. 2001 344 873-80. 

Higgins SL, Hummel JD, Niazi IK, et al. Cardiac resynchronization therapy for the treatment of heart failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias, [see comment]. J. Am. Coll. Cardiol. 2003 42 1454-9. 

Mexiletine is contraindicated in the presence of cardiogenic shock or preexisting second- or third-degree heart block in the absence of a cardiac pacemaker. Caution must be exercised in administration of the drug to patients with sinus node dysfunction or disturbances of intraventricular conduction. 

Tricyclic antidepressants have effects on heart rate (HR), blood pressure (BP), and three distinct measures of the electrocardiogram (EKG). The EKG parameters affected are (1) the PR interval, which represents depolarization of the aorta (2) the QRS duration, which represents intraventricular conduction time and (3) the QTc, which represents the depolarization and subsequent repolarization of the ventricles, corrected for cardiac rate. 

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. 

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.

Acute overdose may be rapidly fatal without treatment and indeed has even been described as a means of suicide. (Chloroquine may now be bought from pharmacies in the UK without a prescription.) Puhnonciry oedema is followed by convulsions, cardiac arrh5dhmias and coma as little as 50 mg/kg can be fatal. These effects are principally due to the profound negative inotropic action of chloroquine. Diazepam was found fortuitously to protect the heart and adrenaline (epinephrine) reduces intraventricular conduction time this combination of drugs, given by separate i.v. infusions, improves survival. 

Quinidine has anticholinergic properties that can result in the blockade of impulses from the vagus nerve to the heart. This would prevent the slowing of the heart rate that is ordinarily produced by normal vagal stimulation. The resulting increased heart rate counters the direct depressant effect on the pacemaker. This can understandably complicate therapy from the clinical standpoint. The effectiveness of quinidine and procainamide treatment can be traced on ECG by the increase in the Q-T interval, which can be attributed to the increased duration of systole, as well as decreased intraventricular conduction velocity. 

Although no clinically important changes in scrum digoxin levels appear to occur during concurrent use, the occurrence of arrhythmias in a few patients indicates that good monitoring is advisable. It has been pointed out that the addihve effects of both drugs on intranodal and intraventricular conduction may be excessive in some patients with heart disease. More study is needed. 

In advanced heart failure, it is common to see abnormal electrical conduction. Heart failure patients can have first-degree heart block and/or intraventricular conduction delay. The intraventricular conduction delay is usually manifest as left bundle branch block. It has been estimated that one-third of patients with systolic heart failure have a QRS duration greater than 120 ms (3). 

These conduction disturbances typically worsen overall cardiac function. The AV delay seen with first degree heart block can lead to suboptimal contribution of atrial systole, less filling time for the LV, and worsened mitral regurgitation (4,5). The intraventricular conduction abnormality can lead to regional LV wall motion delay, which is termed LV dyssynchrony. In LBBB, the LV lateral wall typically depolarizes late and therefore, contracts late. This delayed contraction of the LV lateral wall occurs when the septum is already in its relaxation phase. On echo, it can be seen that the relaxed septum moves paradoxically away from the lateral wall late in systole. This is inefficient contraction since the septum and lateral walls are not moving in unison to... 

Disordered electrical and mechanical ventricular activation can compromise cardiac function. Pacing technology has been nsed to att pt to correct the inter- and intraventricular conduction in an effort to optimize cardiac performance. The earliest attempts were performed during surgery when epicardial leads were placed over the lateral left ventricle free wall. Later, the coronary sinus was utilized to activate the left ventricle. Cardiac-resynchronization therapy (CRT) for treatment of patients with congestive heart failure and ventricular dyssynchrony can have a remarkable beneficial effect. Use of this technology continues to evolve. 

Management of a Biventricular Device. It has been estimated that up to 38% of patients with moderate to severe congestive heart failure due to left ventricular systolic dysfunction have intraventricular conduction delays with wide QRS complexes and ventricular dyssynchrony (79). Cardiac resynchronization therapy using a biventricular pacemaker is now a Class I indication therapy for systolic heart failure in patients with a QRS complex > 120 ms and left ventricular ejection fraction < 35% (80). Although cardiac resynchronization therapy decreases heart failure hospitalizations (81,82), as the overall number of patients with biventricular pacemakers and ICDs increase, more critical care patients will present with implanted biventricular devices, and familiarity with the management of these devices will become increasingly important. 

Cardiac abnormalities (e.g., pathological heart block, valvular disease, intraventricular conduction defects other than isolated right bundle branch block, angina pectoris, arrhythmia, coronary artery disease). 

May be conducted or nonconducted (blocked) through AV node and heart depending on status of the AV node and intraventricular conduction system. 

Acute cardiovascular reactions to procainamide administration include hypotension, A-V block, intraventricular block, ventricular tachyarrhythmias, and complete heart block. The drug dosage must be reduced or even stopped if severe depression of conduction (severe prolongation of the QRS interval) or repolarization (severe prolongation of the QT interval) occurs. 

Propafenone is contraindicated in the presence of severe or uncontrolled congestive heart failure cardiogenic shock sinoatrial, A-V, and intraventricular disorders of conduction and sinus node dysfunction, such as sick sinus syndrome. Other contraindications include severe bradycardia, hypotension, obstructive pulmonary disease, and hepatic and renal failure. Because of its weak (3-blocking action, propafenone may cause possible dose-related bronchospasm. This problem is greatest in patients who are slow metaboUzers. 

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