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Heart bundle branches

The Cardiac Cycle. The heart (Eig. lb) performs its function as a pump as a result of a rhythmical spread of a wave of excitation (depolarization) that excites the atrial and ventricular muscle masses to contract sequentially. Maximum pump efficiency occurs when the atrial or ventricular muscle masses contract synchronously (see Eig. 1). The wave of excitation begins with the generation of electrical impulses within the SA node and spreads through the atria. The SA node is referred to as the pacemaker of the heart and exhibits automaticity, ie, it depolarizes and repolarizes spontaneously. The wave then excites sequentially the AV node the bundle of His, ie, the penetrating portion of the AV node the bundle branches, ie, the branching portions of the AV node the terminal Purkinje fibers and finally the ventricular myocardium. After the wave of excitation depolarizes these various stmetures of the heart, repolarization occurs so that each of the stmetures is ready for the next wave of excitation. Until repolarization occurs the stmetures are said to be refractory to excitation. During repolarization of the atria and ventricles, the muscles relax, allowing the chambers of the heart to fill with blood that is to be expelled with the next wave of excitation and resultant contraction. This process repeats itself 60—100 times or beats per minute... [Pg.111]

Figure 39-2. The conducting system of the heart. Impulses originating in the node are transmitted through the atria to the AV node down the bundle of His and the bundle branches through the Flirkinje fi bers to the ventrides. Figure 39-2. The conducting system of the heart. Impulses originating in the node are transmitted through the atria to the AV node down the bundle of His and the bundle branches through the Flirkinje fi bers to the ventrides.
ECC first-degree heart block, right bundle-branch block, and arrhythmias... [Pg.1149]

Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles. Figure 13.3 Route of excitation and conduction in the heart. The heart beat is initiated in the sinoatrial (SA) node, or the pacemaker, in the right atrium of the heart. The electrical impulse is transmitted to the left atrium through the interatrial conduction pathway and to the atrioventricular (AV) node through the intemodal pathway. From the AV node, the electrical impulse enters the ventricles and is conducted through the AV bundle, the left and right bundle branches, and, finally, the Purkinje fibers, which terminate on the true cardiac muscle cells of the ventricles.
From the AV node, the electrical impulse spreads through the AV bundle or the bundle of His. This portion of the conduction system penetrates the fibrous tissue separating the atria from the ventricles and enters the interventricular septum where it divides into the left and right bundle branches. The bundle branches travel down the septum toward the apex of the heart and then reverse direction, traveling back toward the atria along the outer ventricle walls. This route of conduction of the impulse facilitates ejection of blood from the ventricles. If the impulse were to be conducted directly from the atria to the ventricles, the ventricular contraction would begin at the top of the chambers and proceed downward toward the apex. This would trap the blood at the bottom of the chambers. Instead, the wave of ventricular electrical stimulation and, therefore, contraction moves from the apex of the heart toward the top of the chambers where the semilunar valves are located and ejection takes place. [Pg.172]

The sequence of cardiovascular signs as serum magnesium increases from 3 mEq/L to 15 mEq/L is hypotension, cutaneous vasodilation, QT-interval prolongation, bradycardia, primary heart block, nodal rhythms, bundle branch block, QRS- and then PR-interval prolongation, complete heart block, and asystole. [Pg.909]

Despite concerns regarding safety and side effects, TCAs are appropriate for some patients. When starting a TCA, a baseline EKG is required. If the EKG reveals a second-degree or higher heart block, a bundle branch block, or a corrected QT interval exceeding 440 milliseconds, then a TCA should not be started. The initial doses should be low, especially in older patients or those with anxiety who are particularly sensitive to side effects. Over the first 7-14 days, the dose should be increased gradually to the lower end of the expected therapeutic range. After an additional 2-3 weeks, the dose may be increased further if necessary. [Pg.53]

Cardiovascular - Ang na pectoris aggravated, arrhythmia, arrhythmia atrial, atrial fibrillation, bradycardia, bundle branch block, cardiac failure, extrasystole, heart murmur, heart sound abnormal, hypertension, hypotension. Ml, palpitation, Q-wave abnormality, tachycardia, ventricular tachycardia (5% or less). [Pg.417]

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. [Pg.424]

Preexisting second- or third-degree AV block, right bundle branch block when associated with a left hemiblock (bifascicular block), unless a pacemaker is present to sustain the cardiac rhythm if complete heart block occurs recent myocardial infarction (Ml) presence of cardiogenic shock hypersensitivity to the drug. [Pg.459]

Baldasseroni S, Opasich C, Gorini M, et al. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure a report from the Italian network on congestive heart failure. Am. Heart J. 2002 143 398-405. [Pg.62]

Xiao HB, Lee CH, Gibson DG. Effect of left bundle branch block on diastolic function in dilated cardiomyopathy. Br. Heart J. 1991 66 443-7. [Pg.64]

Flecainide is contraindicated in patients with preexisting second- or third-degree heart block or with bundle branch block unless a pacemaker is present to maintain ventricular rhythm. It should not be used in patients with cardiogenic shock. [Pg.180]

In the case of patients with preexisting heart disease and patients older than 40 years, an electrocardiogram should be obtained before the initiation of TCA treatment. TCAs should not be used in patients with bundle branch block unless all other options have failed. [Pg.42]

Early reports on imipramine noted that some patients developed first-degree heart block, as well as other bundle branch patterns, but it took almost 15 years to clarify that these conduction delays were the only adverse effects at therapeutic plasma concentrations. It is now well documented that increased PR, QRS, or QT intervals occur with all standard TCAs, at or slightly above their therapeutic plasma levels. [Pg.146]

Cx40 was found in sinus node cells, atrium, AV node, AV bundle and bundle branches and Purkinje fibers. Cx45 was expressed at low levels in Purkinje fibers and ventricles of the canine heart [Kanter et al., 1993a, b, ]. [Pg.29]

FIGURE 23-2 Schematic representation of the conduction system of the heart. Conduction normally follows the pathways indicated by the dashed lines. Impulses originate in the sinoatrial node and are transmitted to the atrioventricular node. Impulses are then conducted from the atrioventricular node to the ventricles by the bundle of His and bundle branches. [Pg.323]

Abbreviations DM, diabetes mellitus HR, heart rate HTN, hypertension LBBB, left bundle branch block SBP, systolic blood pressure STEMl, ST-segment elevation myocardial infarction. ... [Pg.466]

Other risk factors for complete heart block were left bundle branch block, first degree atrioventricular block, female gender, volume of alcohol, and number of septal perforators treated (27-29). [Pg.607]

Septal ablation related mortality at experienced centers is currently 1% to 2%, similar to that of surgical myectomy (Table 4). Conduction system abnormalities are relatively common complications of septal ablation, Permanent right bundle branch block occurs in about 50% of patients and transitory complete heart block in 60% and permanent pacemakers required for high grade atrioventricular block in about 5% to 20%, Concerns of late occurrence of complete heart block following septal ablation mandates in-patient monitoring for 4 to 5 days,... [Pg.611]

Care should be taken in patients with a recent myocardial infarction who show evidence of impaired conduction (first-degree heart block, bundle-branch block, or prolongation of the QTC interval), since tricyclic antidepressants can theoretically add to the already increased risk of ventricular fibrillation in such patients (31). Reviews in earlier editions of Meyler s Side Effects of Drugs discussed these effects and gave practical guidelines on the use of tricyclic antidepressants in patients with heart disease (32). [Pg.9]

In a 72-year-old woman cibenzoline was associated with left bundle branch block and heart failure (11). Excess cibenzoline accumulation was suspected, because of reduced renal function, but plasma cibenzoline concentrations were not reported. [Pg.740]

In a review of 60 original articles detailing 1835 courses of intravenous and/or oral flecainide in both placebo-controlled and comparative studies as well as a large number of uncontrolled studies, unwanted cardiac events occurred in 8% of patients (7). The cardiac events were hypotension (1.3%), heart failure (0.4%), sinus node dysfunction (1.6%), bundle branch block (1.0%), atrial dysrhythmias (1.6%), and ventricular dysrhythmias (1.3%). However, in 8505 patients, 5507 of whom were administered flecainide for more than 4 weeks and most of whom took dosages of 100-300 mg/day, cardiac adverse effects occurred in only about 2% and non-cardiac effects in... [Pg.1371]

Brugada R, Brugada J, Antzelevitch C, Kirsch GE, Potenza D, Towbin JA, Brugada P. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation 2000 101(5) 510-15. [Pg.1374]

Intracardiac conduction disturbances should not be considered as absolute contraindications to epidural anesthesia there were only nine cases of sinus bradycardia, easily reversed with atropine sulfate, in 66 patients (123). However, rare cases of complete heart block and complete left bundle branch block have occurred (SEDA-21, 132) (124). [Pg.2128]


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