Bundle Branch

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... 

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.

ST-segment elevation of at least 1 mm in height in two or more contiguous leads, or new or presumed new left bundle-branch block... 

ECC first-degree heart block, right bundle-branch block, and arrhythmias... 

AFB Acid-fast bacillus aortofemoral bypass aspirated BBB Bundle-branch block, blood-brain barrier... 

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. 

The final portion of the specialized conduction system consists of the Purkinje fibers that extend from the bundle branches. These fibers, which... 

A fibrinolytic agent is indicated in patients with STE ACS presenting within 12 hours ofthe onset of chest discomfort who have at least 1 mm of STE in two or more contiguous ECG leads or a new left bundle-branch... 

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. 

Buna process, 22 111 Bundle branches, 5 80 Bundle of His, 5 80 Bundles scrap, 21 409 Bundpacker, 7 691 B nnagel formula, 23 473 Bunsen burners, 7 455—451, 458 Bunsenite, color, 7 331 Bunsen-Roscoe law, 19 108 Bunyaviruses, 3 138 Buoyancy... 

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. 

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). 

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. 

Use quinidine with extreme caution in incomplete AV block, because complete block and asystole may result. The drug may cause unpredictable dysrhythmias in digitalized patients. Use cautiously in patients with partial bundle branch block, severe CHF, and hypotensive states due to the depressant effects of quinidine on myocardial contractility and arterial pressure. 

Conduction abnormalities Use caution in patients with sick sinus syndrome, Wolff-Parkinson-White syndrome or bundle branch block. 

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. 

If second-or third-degree AV block, or right bundle branch block associated with a left hemiblock occurs, discontinue therapy unless a ventricular pacemaker is in place to ensure an adequate ventricular rate. 

Cardiovascular - Benign intracranial hypertension (pseudotumor cerebri) has been reported rarely. Bulging fontanels, as a sign of benign intracranial hypertension in infants, have been reported rarely. Changes in electrocardiogram (eg, nonspecific ST/T wave changes, bundle branch block) have been reported in association with pulmonary reactions. 

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. 

Godman MJ, Lassers BW, Julian DG. Complete bundle-branch block complicating acute myocardial infarction. N. Engl. J. Med. 1970 282 237. ... 

Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up. Circulation 1978 58 679-88. 

Stenestrand U, Tabriz F, Lindback J, England A, Rosenqvist M, Wallentin L. Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block. Circulation 2004 110 1896-902. 

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. 

Sade LE, Kanzaki H, Severyn D, Dohi K, Gorcsan J, III. Quantification of radial mechanical dyssynchrony in patients with left bundle branch block and idiopathic dilated cardiomyopathy without conduction delay by tissue displacement imaging. Am. J. Cardiol. 2004 94 514-8. 

Nelson GS, Berger RD, Fetics BJ, et al. Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block, [erratum appears in Circulation 2001 Jan 23 103 (3) 476]. Circulation 2000 102 3053-9. 

In contrast, intravenous fibrinolytic therapy is harmful without acute ST-segment elevation, a true posterior MI or a presumed new left bundle-branch block. 

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