The Sinoatrial Node
The sinoatrial node (SAN) is the pacemaker of the human heart ( Fig. 28.1 ). In visceroatrial situs solitus, the normal pattern of anatomic organization of the viscera and atria, the SAN normally is located to the right of the superior vena cava (SVC; see Fig. 28.1 , left upper diagram ). The SAN is located in the sulcus terminalis (the terminal sulcus), a shallow sulcus or depression that marks the termination of the right horn of the sinus venosus—the smooth venous tissue that includes the terminations of the SVC and the inferior vena cava (IVC). The sulcus terminalis also marks the beginning of the free wall of the right atrium (RA) with its characteristic musculi pectinati (pectinate muscles). Pecten is a Latin noun meaning “comb.” The pectinate muscles of the right atrial appendage (RAA) are remarkably parallel, like the teeth of a comb. The SAN is also known as the sinus node because it is located in the right horn of the sinus venosus (venous sinus). However, the pacemaker is immediately adjacent to the RA; hence sinoatrial node.
The sulcus terminalis externally, where the SAN is located, and the crista terminalis (terminal crest) internally both mark the junction of the right horn of the sinus venosus with the RA. The SAN is an invisible subepicardial structure. That is why you have to know where the SAN is, because you cannot see the SAN with the naked eye. This is also why the SAN was not discovered until 1907 by Sir Arthur Keith (1866–1955), while he was working with Martin Flack (1882–1931). Keith was an anatomist and anthropologist, a Scot from Aberdeen, who made many important contributions. For example, he was the first to understand that typical D-transposition of the great arteries (TGA) is caused by infundibular inversion.
In visceroatrial situs inversus, the location of the SAN is a mirror-image of its location in visceroatrial situs solitus (see Fig. 28.1 , upper right diagram ), that is, to the left of the entering SVC, in the left horn of the sinus venosus.
In the heterotaxy syndrome with visceroatrial situs ambiguus and asplenia (see Fig. 28.1 , left lower diagram ), there often are bilateral SVCs and bilateral SANs.
In the heterotaxy syndrome with visceroatrial situs ambiguus and polysplenia (see Fig. 28.1 , right lower diagram ), the SAN can be absent or difficult to locate.
Heterotaxy is derived from two Greek words. Heteros means “other or different.” Taxis means “arrangement.” The heterotaxy syndromes with asplenia, polysplenia, or a right-sided spleen mean that the situs—the pattern of anatomic organization of the viscera and atria—is different from situs solitus (normal) and from situs inversus (the mirror-image of normal).
Ambiguus is a Latin word meaning “uncertain or going about”; from ambigere, “to wander about.” In anatomy, ambiguus has the connotations of uncertain, unknown, undiagnosed. This is what we mean when we use these terms. Others have a different interpretation. In the heterotaxy syndrome with asplenia, they talk about bilaterally right atria (right atrial isomerism) or about bilaterally RAAs (RAA isomerism). In the heterotaxy syndrome with polysplenia, they talk about bilaterally left atria (left atrial isomerism) or about bilaterally left atrial appendages (LAA isomerism).
We think that the concept of atrial level mirror-imagery (isomerism) is anatomically incorrect. Why? Because bilaterally right atria (RAs) and bilaterally left atria (LAs) have never been documented anatomically, accurately speaking.
Bilaterally RA would have to have bilateral IVCs, bilateral SVCs, bilateral coronary sinus ostia, bilateral superior limbic bands of septum secundum, and a SAN bilaterally. No such case has ever been documented. Bilaterally LA would have to have a septum primum bilaterally, four pulmonary veins bilaterally, and no SAN bilaterally. Again, no such case has ever been documented in a single individual. (Siamese twins are excluded.)
Our friends and colleagues concede these points. But then they may retreat to atrial appendage isomerism. We agree that in the asplenia syndrome both atrial appendages often are broad, triangular, and bilaterally “rightish” in appearance. Similarly, in the polysplenia syndrome, we agree that the atrial appendages both often appear small and narrow, that is, bilaterally “leftish.” We think that the appearances of the atrial appendages—bilaterally “rightish” in asplenia and bilaterally “leftish” in polysplenia—are for hemodynamic reasons.
In asplenia the IVC typically is intact and the atrial septum is often poorly formed because of the presence of common atrioventricular (AV) canal. Consequently, the full systemic venous return often can flow into both atrial appendages, distending both, making both atrial appendages appear like RAAs.
In polysplenia, the IVC often is interrupted—absent between the renal veins and the hepatic veins. The blood flow of the hepatic and suprahepatic IVC is much less than normal, that is, no subhepatic systemic venous return. The systemic venous blood returns to the heart via the azygos vein and by the SVC.
So the systemic venous return flows into the atrial level predominantly in a superior-to-inferior direction, passing behind (dorsal to) the atrial appendages, and failing to dilate the atrial appendages, which therefore are bilaterally undistended and bilaterally “leftish” in appearance.
But what about the SAN data? Remember that the SAN is often just called the sinus node, not the sinoatrial node. The SAN tells you where the sinus venosus and SAN are located. It does not necessarily tell you that all of the other features of the RA are there also. So, a bilateral SAN does not mean that the RA is bilateral. Instead, it only means that the sinus venosus and the SAN are bilateral. Similarly, bilateral absence of the SAN means bilateral absence of the SAN, not that a LA is bilateral.
It also should be mentioned that “partial” isomerism is a conceptual error, such as isomerism of the right or LAAs only. Consider D-glucose and L-glucose. These are real isomers.
Isomerism applies to complex structures such as the atria (see Fig. 28.1 , left upper and right upper diagrams ), and like D-glucose and L-glucose molecules, in which all asymmetrical groups are mirror-images. There are four asymmetrical groups. If only one or two asymmetrical groups were mirror-images, but the other asymmetrical groups were not mirror-images, these two molecules would not be mirror-images (isomers). Isomerism is an all-or-nothing phenomenon. “Partial” isomerism—of the appendages only, but not the whole atria—is a mistake. Mirror-imagery (isomerism) applies to the whole structures, like the whole D- and L-glucose molecules, not to just some, but not all, of the asymmetrical parts of these molecules, or of other structures such as cardiac atria.
The Internodal and Interatrial Conduction Pathways
There are three internodal conduction pathways ( Fig. 28.2 ) between the SAN and the AVN: the anterior, middle, and posterior internodal pathways. There is one interatrial conduction pathway between the RA and the LA: the Bachmann bundle.
The Atrioventricular Node and the Atrioventricular Bundle
Now that we have briefly considered the variable locations of the SAN in visceroatrial situs solitus, in visceroatrial situs inversus, and in visceroatria situs ambiguus (see Fig. 28.1 ), it is now time to consider the variations in the location of the AVN and the AVB.
Where is the AVN? Mentally, draw a line between the right atrial ostium of the coronary sinus and a point slightly below the anteroseptal commissure of the tricuspid valve adjacent to the atrial septum. I say draw this line mentally, not with a sucker in the operating room, because a sucker can get stuck on this line, and pulling it off this line can damage the invisible AVN and/or the invisible AVB. For convenient brevity, we call this line the coronary sinus–membranous septum line. Others use the triangle of Koch to localize the invisible AVN and AV (or His) bundle. The triangle of Koch is formed by (1) the origin of the septal leaflet of the tricuspid valve, (2) the Thebesian valve of the coronary sinus, and (3) the Eustachian valve of the IVC and its anterior extension, the tendon of Todaro. The AVN is close to the apex of the triangle of Koch.
Because the Thebesian valve of the coronary sinus and the Eustachian valve of the IVC are variable in their morphology and can be absent, and because the tendon of Todaro is difficult to visualize grossly (but is well seen histologically), we prefer to use the coronary sinus–membranous septum line to localize the AVN and the AVB.
Historical Note
Wilhelm His, Jr. (1863–1934) described the AVB in 1893; it is now widely known as the His bundle, or the AVB of His. Born in Basel, Switzerland, he moved to Leipzig, Germany as a child. He became a German citizen and a physician. In 1907, he became the director of the first medical clinic at the Charité Hospital in Berlin. He served in the army in World War I, during which he saw and described trench fever. He had a long-standing interest in gout and diet.
Walter Karl Koch (1880–1962) was a German physician from Berlin. He was a cardiologist, surgeon, and pathologist who described the triangle of Koch in which the AVN is sometimes referred to as Koch’s node.
Adam Christian Thebesius (1686–1732) was a German anatomist who worked at Leiden, the Netherlands. He described the small veins of the heart, the Thebesian veins. He also described the coronary sinus and its valve, the Thebesian valve, in 1708.
Bartolomeo Eustachio (1524–1574) was a professor in Rome at the Collegia della Sapienza. In 1552, he completed a superb set of anatomical plates, Tabulae Anatomicae, drawn by himself. These plates remained unprinted in the Papal Library for 162 years. Finally, Pope Clement XI presented the engraved plates to his physician Lancisi. On the advice of Morgagni, Lancisi published these plates with his own notes in 1714. They were the first anatomic plates on copper. These plates were more accurate in delineation than those of Vesalius. These plates revealed that Eustachius (Latin spelling of his name) had discovered the Eustachian valve of the IVC, the Eustachian tube, the thoracic duct, the adrenal glands in 1563 and the abducens (sixth) cranial nerve. Eustachio (Italian spelling of his name) also described the origins of the optic nerves, the cochlea, the pulmonary veins, and the muscles of the throat and neck. He also gave the first correct picture of the uterus, and he wrote the best description of his time of the structure of the teeth, giving the nerve and blood supply in 1563. Eustachio is regarded as a genius of discovery.
Francesco Todaro (1839–1918) was an Italian physician who described the Todaro tendon.
The Atrioventricular Node and Atrioventricular Bundle Continued
In 1958, Maurice Lev, who was one of my teachers and an outstanding investigator of the conduction system in congenital heart disease, published a paper concerning the conduction system in common AV canal ( Fig. 28.3 ). In a right lateral view of the opened RA, common AV valve, and right ventricle (RV), many of the most important anatomic details are shown, including the ostium of the coronary sinus, the posteroinferior AVN, the penetrating portion of the AVB, and the branching portion of the AVB.
In 1973, Jack Titus published a study of the normal human cardiac conduction system ( Fig. 28.4 ). This is a left posterolateral view. Titus found that in the average adult, the AVN measures 7.5 mm in length. Then the AVB begins. The first 1.5 to 2.0 mm are unbranched. This unbranched portion of the AVB penetrates from the atrial level to the ventricular level. Branching occurs at the ventricular level. The left posterior bundle branch travels to the posteromedial papillary muscle group of the left ventricle (LV). The left anterior bundle branch runs to the anterolateral papillary muscle group of the LV. Some fascicles of the left bundle branch (LBB) travel down the left ventricular septal surface between the anterior and posterior LBBs. The right bundle branch (RBB) is 1 mm wide (diameter) and about 50 mm in length.
The normal branching AVB runs immediately beneath the membranous septum, and beneath the right coronary and noncoronary leaflets of the normal aortic valve. The membranous septum and the branching AVB vary between 6.5 and 20 mm in length.
Surgical Relevance
Now you can see how misplaced surgical sutures (or devices) can produce various kinds of iatrogenic heart block:
- 1.
If the misplaced suture is superficial, the result can be RBB block (RBBB).
- 2.
If the misplaced suture is deeper, the result can be RBBB and left anterior hemiblock.
- 3.
If the misplaced surgical suture is even deeper, the result can be complete heart block. These are some of the reasons why a good understanding of the conduction system is so important in the interventional transcatheter management and in the surgical management of congenital heart disease.
The Communicating Atrioventricular Node
Many studies have confirmed that the communicating AVN usually is located posteroinferiorly, quite close to the right atrial ostium of the coronary sinus (see Fig. 28.3 ). By communicating AVN we mean an AVN that is confluent with the AVB and its branches. As we shall soon see, there is such a thing as a noncommunicating AVN, that is, an AVN that communicates with nothing.
The Course of the Atrioventricular Bundle
Many studies have confirmed that the branching portion of the AVB usually runs beneath (or inferior to) (1) the membranous portion of the ventricular septum normally, as in Fig. 28.4 ; or (2) inferior to the usual type of ventricular septal defect (VSD) between the infundibular septum above and the ventricular septum below (an infundibuloventricular type of VSD, as in tetralogy of Fallot); or (3) inferior to an AV septal defect, as in the complete form of common AV canal (see Fig. 28.3 ).
Why are the LBBs so much bigger than the RBB? The LBB enters the LV first and massively. The RBB enters the RV second, as a single, slim bundle (see Fig. 28.4 ). Why is there such a difference between the LBB and the RBB of the conduction system? It is hard to answer questions like this. But it is worth remembering that the RV is only about 36% as old phylogenetically as is the LV—180 million years (RV) as opposed to at least 500 million years (LV). And, of course, the LV is the systemic pump, whereas the RV is the lung pump. Fish and amphibia do not have an RV, whereas higher reptiles (such as alligators and crocodiles), birds, and mammals normally all do. Thus, in the evolution of our phylum Chordata (the Chordates), the RV and the RBB are Johnnies-come-lately compared with the LV and the LBB (see Fig. 28.3 ). The two fascicles, or radiations, of the LBB—the superior (or anterior) and the inferior (or posterior)—are clearly shown (see Fig. 28.3 ).
The Atrioventricular Conduction System in Transposition of the Great Arteries {S,L,L}
One of the most important form of congenital heart disease with AV situs discordance is congenital physiologically corrected TGA {S,L,L}. To the best of my knowledge, the location of the AV conduction system in TGA {S,L,L} was first figured out correctly and presented comprehensibly in 1973 and 1974 by Robert Anderson et al , ( Figs. 28.5 through 28.9 ), a great achievement.
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