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Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Delayed conduction through the bundle branches can result in incomplete or complete bundle branch block (BBB), but does not cause a bradycardia.
Autopsy Cardiac Examination
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
The bundle branches connect with a very widespread subendocardial layer of Purkinje cells, which are the finest branches of the conduction system before the impulse for contraction passes into the ordinary myocardium. Purkinje cells have specialized tight junctions for rapid conduction and have scanty myofibrils appearing empty and vacuolated when compared with contractile myocytes. The conduction system down to the peripheral ventricular system is totally isolated from the ordinary myocardium. In the normal heart, the only electrical connection between atria and ventricles is via the bundle of His which is only 2 mm in diameter. In the embryo, conduction tissue develops around the whole circumference of the atrioventricular rings, but is steadily isolated as the connective tissue matrix of the valve rings develop, finally leaving the bundle of His as the only connection.
The QRS complex
Published in Andrew R Houghton, Making Sense of the ECG, 2019
A block of either of the bundle branches delays the electrical activation of its ventricle, which must instead be depolarized indirectly via the other bundle branch. This prolongs the process of ventricular depolarization, and so the QRS complex is wider than 3 small squares. In addition, the shape of the QRS complex is distorted because of the abnormal pathway of depolarization.
Tests for the identification of reflex syncope mechanism
Published in Expert Review of Medical Devices, 2023
Michele Brignole, Giulia Rivasi, Artur Fedorowski, Marcus Ståhlberg, Antonella Groppelli, Andrea Ungar
A predominant CI reflex syncope (bradycardic phenotype) is diagnosed in the case of documentation of a syncopal asystolic pause >3 s or of an asymptomatic asystolic pause >6 s. The finding of a rapid decrease in heart rate concomitant with syncopal event may suggest a mixed mechanism including both hypotension and bradycardia as causes of reflex syncope. No or minimal changes in HR rather suggest a predominant hypotensive mechanism. In both these cases, diagnosis should be confirmed with other tests allowing for confirmation of the hypotensive component of syncope. The caution should be taken when extrapolating such results onto an inferred non-bradycardic hypotensive mechanism of syncope as alternative explanations may include psychogenic pseudosyncope and other syncope mimics, as well as transient neurological causes. Conversely, sudden onset AV block (and ventricular pause/s), triggered by atrial or ventricular premature beats, in patients with bundle branch block or structural heart disease suggests an intrinsic conduction disturbance [57].
Use of Crotalidae equine immune F(ab’)2 antivenom for treatment of an Agkistrodon envenomation
Published in Clinical Toxicology, 2021
B. Z. Wilson, J. Larsen, G. Smelski, S. Dudley, F. M. Shirazi
During the patient’s hospitalization, his pain and swelling remained well controlled (Figure 2b). His fibrinogen remained stable but his platelets slowly declined to a nadir of 132,000/mm3 at 30 h post-envenomation at which point he was given an additional 4 vials of F(ab’)2AV (Figure 3). His troponin-I climbed to a peak of 0.65 mg/mL at 17 h post-envenomation. Serial electrocardiograms demonstrated an incomplete left bundle branch block with no ischemic or transient changes. Echocardiogram demonstrated impaired left ventricular function. He was evaluated by cardiology whom recommended medical management with beta-blocker and an angiotensin converting enzyme inhibitor. Due to concerns for coagulopathy, aspirin was initially deferred on admission but started prior to discharge. The patient’s creatinine peaked at 1.91 mg/dL, and declined to 1.73 mg/dL prior to discharge. The patient’s baseline creatinine was not available.
Block of branching portion of bundle of His from catheter shaft during ablation of left ventricular outflow tract ventricular premature complexes
Published in Baylor University Medical Center Proceedings, 2021
Ayman Haq, Ali Yousif, Hafiza Khan, Brian Deville, Mustafa Dohadwala
The AV node is located within the apex of the triangle of Koch2 and transitions into the bundle of His, which can be divided into the penetrating bundle of His and branching bundle of His. The penetrating bundle of His is completely encased by the central fibrous body, which is within the membranous septum along the apex of the triangle of Koch on the right side and inferior to the noncoronary cusp and right coronary cusp on the left side (Figure 3).3 The branching bundle of His is not protected by the central fibrous body and begins as the bundle of His gives rise to the left bundle branch and terminates at the origin of the right bundle branch. It is in proximity to the aortic ring, below the noncoronary cusp and right coronary cusp along the left ventricular crest.4 The left bundle branch runs inferiorly and anteriorly from the branching portion, while the right bundle branch emerges on the right side as direct continuation of the bundle of His (Figure 3).1