Intraventricular blocks

Hypersensitivity to amide local anesthetics Stokes-Adams syndrome Wolff-Parkinson-White syndrome severe degrees of sinoatrial, atrioventricular (AV), or intraventricular block in the absence of an artificial pacemaker. 

The cardiac toxicity of quinidine includes A-V and intraventricular block, ventricular tachyarrhythmias, and depression of myocardial contractility. Ventricular arrhythmia induced by quinidine leading to a loss of consciousness has been referred to as quinidine syncope. This devastating side effect is more common in women than in men and may occur at therapeutic or subtherapeutic plasma concentrations. 

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. 

Disturbances of cardiac rhythm (e.g., tachycardia, atrial fibrillation, ventricular flutter, and A-V or intraventricular block) are the most frequent causes of death. Thus, management of cardiac function is critical. If the patient survives the early phase, recovery without sequelae is probable, and vigorous resuscitative measures are important. A major clinical problem is determining when a patient is no longer in danger. Many patients with mild overdose have been hospitalized... 

A new infarcted area suddenly masks totally or partially previous Q waves (Madias and Win, 2000) (Figure 5.39). The ECG may seem even normal or nearly normal due to cancellation of vectors. It should be ruled out that the disappearance or decrease of the Q wave is not secondary to the development of a new intraventricular block. Also ischaemia induced by exercise may mask transiently, due to ischaemia in the opposite sites, the Q wave of necrosis (Madias et al, 1997). 

A. The presence of nodal or ventricular rhythms in the setting of third-degree atrioventricular or intraventricular block. These are usually reflex escape rhythms that may provide lifesaving cardiac output, and abolishing them may result in asystole. 

The hypothesis of the role of HA in wakefulness stems from the observation that administration of the classical antihistamines (i.e. H3 receptor antagonists) induced sedation. These first-generation antihistamines, used to treat inflammatory reactions, could cross the blood-brain barrier and block the central Hi receptor (White Rumbold, 1988). The first study examining the effect of antihistamines on sleep-wakefulness in cats reported an increase in NREM sleep and a decrease in REM sleep (Jewett, 1968). Similar results were also obtained in dogs (Wauquier et ah, 1981) and humans (Risberg et ah, 1975 Bassano Caille, 1979 Nicholson et ah, 1985 Adam Oswald, 1986). Intraventricular application of HA in the anesthetized rat caused a dose-dependent decrease in the duration of narcosis, whereas intraventricular application of HA in conscious... 

Administration of HA and its effect on sleep-wakefulness Local application of HA (5, 30 and 60 pg) in the TMN region of cats increased the latency to sleep, increased arousal, and reduced NREM sleep in a site-specific, dose-dependent manner. The highest dose produced the maximal effect, which lasted for 6 h. The HA-induced arousal was completely blocked when the cats were pretreated intraperitoneally with the Hi receptor antagonist mepyramine (Lin et at, 1986, 1988). In rats, intraventricular administration of HA blocked the increase in delta and theta activity (0-6 Hz) in the EEG induced by repeated low-frequency stimulation of the midbrain reticular formation. This effect was blocked if specific thalamic nuclei were lesioned (Tasaka et at, 1993) or by simultaneous administration of an Hi receptor antagonist, but not by an H2 receptor antagonist (Tasaka et at, 1989). Application of HA... 

Using tactile startle, bufotenin, a hallucinogen that does not cross the blood-brain barrier readily, also produced biphasic dose-response effects when given intraventricularly (76). After systemic administration, however, low doses of indole hallucinogens have not been reported to increase tactile startle (73). Thus LSD (20-80 Mg/kg), DMT (0.25-1.0 mg/kg), and psilocin (2.5-5.0 mg/kg) did not increase tactile startle. A slightly higher dose of LSD (100 Mg/kg) did increase startle toward the end of the test session, perhaps because of blocking habituation (see below). 

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. 

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. 

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. 

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. 

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. 

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... 

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. 

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). 

The late activation of some areas of the LV due to delay in activation of this area explains the late QRS complex forces opposed to the infarction Q wave. This was related for many years as peri-infarction block . Currently, the combination of an infarction with some intraventricular zonal blocks is based on the concept of the hemiblocks, defined by Rosenbaum, Elizari and Lazzari (1968). Because hemiblocks are diagnosed mainly by the changes in the vector s direction in the FP, the electrocardiographic changes secondary to the association with MI will be evidenced also specially in the FP leads. 

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