Intraventricular conduction block

Cardiac toxicity is generally the result of drug-induced depression of cardiac conduction (e.g., atrioventricular block, intraventricular conduction block) and systemic vasodilation. These effects may progress to severe hypotension and cardiac arrest. 

This information will be useful in understanding when and why bradyarrhythmias and/or intraventricular conduction abnormalities may occur during an evolving ACS (see Arrhythmias and intraventricular conduction blocks in ACS p. 250). 

Fig. 10.13 (A) Lead II ECG in a patient with syncope intraventricular conduction block but no documented AV block at rest. (B) On exercise 2 1 AV block occurs and 1 1 AV conduction returns during the recovery period. A subsequent electrophysi-ological study revealed infranodal AV block at an atrial pacing rate of 110/min and a permanent pacemaker was implanted. No further syncope occurred.

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. 

Adverse reactions occurring in at least 3% of patients include angina first-degree AV block CHF intraventricular conduction delay palpitations proarrhythmia ventricular tachycardia dizziness fatigue headache constipation dyspepsia nausea/vomiting unusual taste blurred vision dyspnea. About 20% of patients discontinued treatment due to adverse reactions. 

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. 

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. 

Contraindications Complete AV block, development of thrombocytopenic purpura during prior therapy with quinidine or quinine, intraventricular conduction defects (widening of QRS complex)... 

A 22-year-old woman took an overdose of propafenone (amount unknown) and developed tetany and then generalized convulsions requiring intravenous clonazepam (44). She had a low blood pressure and first-degree atrioventricular block associated with prolonged intraventricular conduction. She was intubated and given intravenous fluids, equimolar sodium lactate, dopamine, and adrenaline. Her cardiac conduction returned to normal. 

Atrioventricular block, intraventricular conduction defects, and ventricular dysrhythmias on electrocardiogram... 

A. Cardiac disturbances, including hypotension and bradycardia, are the most common manifestations of poisoning. Atrioventricular block, intraventricular conduction disturbances, cardiogenic shock, and asystole may occur with severe overdose, especially with membrane-depressant drugs such as propranolol. The ECG usually shows a normal QRS duration with increased PR intervals QRS widening occurs with massive intoxication. 

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... 

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). 

Intravenous phenytoin is effective for the treatment of cardiac arrhythmias, but fatal ventricular asystole secondary to i.v. phenytoin has been reported (60 ). Massive overdose from oral Garoin (phenytoin plus phenobarbitone) has produced right bundle branch block (19 ). It has been suggested that the stopping of diphenylhydantoin before anaesthesia for surgery may precipitate atrioventricular or intraventricular conduction defects during the anaesthesia (30 ). 

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

Uncontrolled CHF cardiogenic shock sinoatrial, AV and intraventricular disorders of impulse generation or conduction (eg, sick sinus node syndrome, AV block) in the absence of an artificial pacemaker bradycardia marked hypotension bronchospastic disorders manifest electrolyte imbalance hypersensitivity to the drug. 

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. 

Contraindications Bradycardia bronchospastic disorders cardiogenic shock electrolyte imbalance sinoatrial, AV, and intraventricular impulse generation or conduction disorders, such as sick sinus syndrome or AV block, without the presence of a pacemaker uncontrolled CHF... 

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