Anatomy stuff Flashcards
2 intra atrial bundles
Bachmann’s bundle- SN to L auricle. more resistant to hyperkalemia. straddles intraatrial groove
Inferior inter-atrial fascicle- connect RA-LA along path of coronary sinus. ends at ligament of Marshall (remnant of LCrVC and extends between upper and lower PV)
4 parts of AV junction
1 preferential pathways (nodal approaches) along R atrial wall and IAS and atrionodal bundles
2 proximal AV bundle (inferior nodal extension
3 Compact AVN
4 non-penetrating and penetrating portions of distal AV bundle
membranous IVS is distal boundary of AV junction
Atrionodal bundles (nodal approaches) 3
1 superior atrionodal bundle- continuation of anterior internodal tract. runs supero-anterior portion of medial wall of RA near interventricular septal ridge
2 medial atrionodal bundle- continuation of medial internodal tract. runs along supero-medial portion of coronary sinus ostium under the epicardial layer of the RA medial wall-opposite medial portion of the tendon of Todaro
3 lateral atrionodal bundle- continuation of posterior internodal tract. runs along inferolateral portion of coronary sinus ostium under epicardial layer of the infero posterior portion of the RA medial wall
froms the proximal AV bundle (inferior nodal extension)
Triangle of Koch
At base of RA
Boundaries- TV septal leaflet, tendon of todaro, coronary sinus orifice
AVN (bundle of his) at apex
Tendon of Todaro
continuation of eustachian valve of the CaudalVC and valve of coronary sinus
Thebesian valve
valve of CS
Valve of Vieussens
The valve of Vieussens is one of two valves of the coronary sinus, which can be found at the junction to the great cardiac vein in the majority of individuals and might be of clinical importance for specific cardiac catheterization procedures.
CTD embryo
The heart is the first embryonic organ to develop function.1 It develops from being a tubular peristaltic pump to a four-chambered muscular organ with synchronous contractions. During primary septation of the heart, the distal part of the bended tube forms the sinus venosus. The right arm of the sinus venosus is integrated into the right atrium, forming, at a later stage, the sinus of the cava veins, whilst the left arm eventually forms the CS.2 The CS receives the venous myocardial blood from the main coronary vein, originated in the cardiac apex and following the diaphragmatic surface of the heart from the left side, over the left atrial atrioventricular groove, towards the right atrium
The embryogenesis of CTD is explained as the persistence of the right valve of the sinus venosus generating a division within the right atrium.3, 4, 5, 6 This intra-atrial membrane may be perforate or imperforate3, 7 and creates two distinct chambers. When the CTD is perforate, it creates a physiological-pressured CrRA receiving the cranial venous drainage, connected to a high-pressured CdRA receiving the CdVC venous return. This differential resistance against the caudal venous return is responsible for caudal right-sided CHF signs (i.e. ascites), named Budd-Chiari-like syndrome by some authors8, 9 and makes CTD one of the differentials to be considered in young dogs presenting with ascites
Gerbode defect
all in vet med- thoracic trauma or infection. Type A- LVOT to RA. Type B LVOT to RV then through TV defect to RA
Communications between the left ventricular outflow tract and right atrium (which may also communicate with the right ventricle), or Gerbode type defects, were first classified in humans by Gerbode et al. as variations of congenital membranous ventricular septal defects (VSDs) usually associated with deformities or perforations in the septal leaflet of the tricuspid valve. Some of these defects are believed to occur secondary to spontaneous aneurysmal transformation and closure of VSDs by tricuspid valve tissue. The normal attachment of the septal leaflet of the tricuspid valve occurs in the membranous ventricular septum and divides it into two portions, a supravalvular (atrioventricular) portion, separating the left ventricle and right atrium, and infravalvular (interventricular) portion separating the ventricles. Depending on the morphology of the deformity, shunting of blood flow occurs from the left ventricular outflow tract into the right atrium, right ventricle, or both, and occurs throughout both phases of the cardiac cycle. Infravalvular defects account for approximately two thirds of cases of LVOT–RA shunts seen in humans and are usually congenital. They allow shunting of blood from the left ventricle into the right ventricle and ultimately into the right atrium, by way of the abnormal tricuspid valve. Supravalvular defects occur in only one third of cases in humans and are more likely to be acquired. These defects allow for direct communication between the left ventricle and right atrium and greater left to right shunting of blood flow than simple VSDs because of the larger pressure gradient present between these two chambers during systole as compared with the LVOT–RV systolic pressure gradient. The end result is often biventricular volume overload and 4 chamber cardiac enlargement. The majority of shunting of blood flow in LVOT–RA shunts occurs during systole, though because left ventricular pressure is consistently higher than right atrial pressure during the cardiac cycle, some diastolic shunting of blood flow does occur
Incomplete fusion of the distal aortopulmonary septum results in:
an aortopulmonary window. Additional defects allowing communication between the ascending aorta and the pulmonary circulation include truncus arteriosus, anomalous origin of one of the pulmonary arteries from the aorta, or an aberrant vessel connecting the great vessels.
