Cardiac Anatomy

Posted on June 30, 2013 - 4:38pm


Note: Large images and tables on this page may necessitate printing in landscape mode.
(From: Skandalakis' Surgical Anatomy > Chapter 7. Pericardium, Heart, and Great Vessels in the Thorax >)


The anatomic and surgical history of the heart is shown in Table 7-1.

Table 7-1. Anatomic and Surgical History of the Pericardium, Heart, and Great Vessels in the Thorax

Unknown (Imhotep of Egypt?) 3000 BC Heart described as center of a system of blood vessels; pulse and heart were directly correlated
Hippocrates (460-377 BC)   Described the valves and chambers of the heart. Described the pericardium as "a smooth tunic which envelops the heart and contains a small amount of fluid resembling urine."
  Demonstrated that fluid could flow in only one direction through the aortic valve.
Herophilus (335-280 BC)   Described the pulmonary artery
Galen (130-ca.200)   Observed that the heart can beat independent of central nervous system control
Mondino de Luzzi (1270-1326)   Accurately described the anatomy of the heart; challenged Galen's view of the existence of pores in the interventricular septum
Leonardo Da Vinci (1452-1519)   Performed dissections and carefully illustrated heart anatomy; observed that air does not pass through the heart
Malpighi 1661 Discovered capillaries. Discovered the linkage between arteries and veins.
Scarpa (1747-1832)   Accurately illustrated the nerves of the heart
Romero 1819 Successfully opened pericardium
Schuch 1840 Performed pericardiocentesis without incision
Fick 1870 Reported a calculation of the cardiac output
Matas 1888 Reported effective occlusion of arterial aneurysm
DelVecchio 1895 Suture of wound in dog heart
Rehn 1896 Successful suture of stab wound in human right ventricle
Einthoven 1903 Performed first electrocardiograph yielding good tracings
Korotkoff 1905 Described his method of blood pressure measurement, now standard practice
Carrel and Guthrie 1905 Performed the first successful biterminal transplantation of a vein in a dog
Rehn, Sauerbruch 1913 Each independently introduced pericardiectomy
Berberich & Hirsch 1923 Published reproductions of living human angiograms
Cutler, Levine, and Beck 1924 Operated on stenosed mitral valves
Abbott & Dawson 1924 Published a paper on classification of cardiac malformations
Abbott 1936 Published Atlas of Congenital Cardiac Disease 
Forssman 1929 Performed a right-sided heart catheterization on himself
Dos Santos 1929 Reported the development of translumbar aortography
Claude Beck 1930s Provided important clinical and experimental descriptions that greatly enhanced the understanding of constrictive pericarditis: "Beck's triad" (small, quiet heart with elevated venous pressure)
Hyman 1932 Reported the development of the artificial cardiac pacemaker
Gross 1939 First successful closure of ductus arteriosus
Cournand 1941 Reported on cardiac catheterization and its clinical significance
Blalock and Taussig 1944 Performed the subclavian-pulmonary shunt in tetralogy of Fallot to increase pulmonary blood flow
Crafoord and Cross 1945 Aortic resection for coarctation
Harken 1946 Report of removal of foreign bodies from the heart
Sellors 1947 Performed first pulmonic valvotomy
Harken et al. 1948 Report of mitral valvuloplasty for mitral stenosis
Murray 1948 Closure of atrial septal defect
Bailey 1948 Performed a successful mitral valvulotomy
Gross 1949 Demonstrated that preserved arterial homographs could be used in the major arteries
Bigelow 1949 Demonstrated the use of deep hypothermia and cardiac arrest in cardiac surgery on a dog
Hufnagel 1951 Demonstrated that aortic insufficiency could be partially controlled with a caged plastic ball device in the descending aorta
Zoll 1952 Developed a cardiac pacemaker for clinical use
Gibbon 1953 Successfully closed an atrial septal defect; used cardiopulmonary bypass (heart-lung machine)
Voorhees 1953 Successfully used a synthetic arterial graft in a human
DeBakey & Cooley 1953 Resected abdominal aortic aneurysms and bridged with homografts
Lillehei 1955 Corrected cardiac congenital anomalies with cross-circulation
Lewis and Varco 1956 Corrected total anomalous pulmonary venous return
Mustard 1957
Akutsu & Kolff 1958 Implanted an artificial heart in a dog
Senning 1959 Correction of transposition of great arteries
Lower and Shumway 1960 First successful canine orthotopic cardiac transplants
Sones and Shirey 1962 Published landmark paper on selective coronary arteriography
Kolesov 1964 Performed first coronary artery bypass with internal mammary artery
Rashkind 1966 Introduced balloon atrial septostomy for correction of transposition of great arteries
Barnard 1967 Performed the first heart transplant in human
Stinson, Dong, Schroeder, Shumway 1969 Report of 13 heart transplants in humans
Favaloro 1969 Performed coronary artery bypass using saphenous vein
Cooley 1969 First to implant an artificial heart in human
DeVries 1982 First attempt at the permanent implantation of an artificial heart in a human
Bolman et al. 1985 Reported results of immunosuppressive cocktail of cyclosporine, prednisone, and azathioprine 
Ochsner and Eiswirth Jr. 1988 Reported 91% one-year survival after heart transplantation in humans (the Louisiana experience)
Battista et al. 1997 Performed the first partial left ventriculectomy

History table compiled by David A. McClusky III and John E. Skandalakis.

History Table References:

  1. Acierno LJ. The history of cardiology. New York: Parthenon, 1994.
  2. Barnard MS. Heart transplantation: an experimental review and preliminary research. S Afr Med J 1967;41:1260.
  3. Battista RJ, Verde J, Nery P, Bocchino L, Takeshita N, Bhayana JN, Bergsland J, Graham S, Houck JP, Salerno TA. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-38.
  4. Bolman RM, Elick B, Olivari MT, Ring WS, Arentsen CE. Improved immunosuppression for heart transplantation. J Heart Transplant 1985;4:315
  5. Beck CS, Moore RL. Significance of pericardium in relation to surgery of the heart. Arch Surg 11:689-821, 1925
  6. Beck CS, Grisvold RA. Pericardiectomy in the treatment of the Pick syndrome: experimental and clinical observations. Arch Surg 21:1064-1113, 1930
  7. Carrel A, Guthrie CC. The transplantation of veins and organs. Am Med 1905;10:1101.
  8. DeBakey ME, Cooley DA. Surgical treatment of aneurysm of abdominal aorta by resection and restoration of continuity with homograft. Surg Gynecol Obstet 1953;97:157.
  9. Ebert PA, Najafi H. The pericardium. In Sabiston DC Jr, Spencer FC (eds). Surgery of the Chest, 5th Ed. Philadelphia: WB Saunders, 1990, p. 1230.
  10. Gray SW, Skandalakis JE, Rowe JS, Symbas PN. Status of cardiac surgery: surgical embryology of the heart. In: Bourne GH (ed). Hearts and Heart-like Organs. New York: Academic Press, 1980.
  11. Harken DE, Ellis LB, Ware PF, Norman LR. The surgical treatment of mitral stenosis. I. Valvuloplasty. N Engl J Med 1948;239:804
  12. Lower RR, Shumway NE. Studies on orthotopic transplantation of the canine heart. Surg Forum 1960;11:18.
  13. Ochsner JL, Eiswirth CC Jr. Heart transplantation: the Louisiana experience. J La State Med Soc 1988;140:34.
  14. Sones FM Jr, Shirey EK. Cine coronary arteriography. Mod Concepts Cardiovasc Dis 1962;31:735-38.
  15. Stinson EB, Dong E, Schroeder JS, Shumway NE. Cardiac transplantation in man. Ann Surg 1969;170:588.
  16. Weisse AB. Medical Odysseys. New Brunswick NJ: Rutgers University Press, 1991.


Normal Development of Heart, Pericardium, and Great Vessels
During the first 20 days, the human embryo survives by diffusion. At that time, the genesis of the heart takes place by proliferation of mesenchymal cells. These cells, which are located in the splanchnic mesoderm, are known as the angiogenic clusters. The cells form a network of small blood vessels. The anterior central part of this network is the cardiogenic area, which is responsible for the formation of the heart and the dorsal aortas.
At the end of the third week, the primitive heart is formed by two endocardial heart tubes. These tubes unite to form a single heart tube. At the time of the union, cardiac jelly appears, surrounding the tubes. The myoepicardial mantle, which is of mesenchymal origin, surrounds the cardiac jelly.
The progressive genesis of specific heart parts takes place at this time:

   The endocardium, which is the endothelial lining of the heart, is formed by the endocardial tube.

 The muscular wall of the heart (myocardium) is formed by the myocardial mantle.

 The visceral pericardium, or epicardium, is also formed by the myoepicardial mantle.

Therefore, the cardiac wall is formed from inside to outside by the endocardium, myocardium, and epicardium.
Around the end of the third week, several embryologic entities appear. From above downward, they are the:

   Truncus arteriosus

 Bulbus cordis



 Sinus venosus


The student should not be confused by the use of the term "bulboventricular tube," which includes the aortic sac (from which the aortic arches will develop) and the primitive ventricle (which develops by expansion of the tube).
Next, a dextral looping takes place. The heart is nearly S-shaped. The atrium is positioned dorsal to the outflow tract (bulbus cordis), which represents the upper limb of the S. The ventricle is represented by the middle limb of the S, and the atrium by its lower limb.
It is not within the scope of this chapter to present the mechanisms of septation and the formation of the seven septa (atrial septum primum, atrial septum secundum, ventricular septum, aorticopulmonary septum, septum of the atrioventricular canal, canal septum, and truncal septum) which are responsible for the partitioning of the heart. Septation starts approximately at the middle of the fourth week and ends at the end of the fifth week.
The "parts of the developing heart should not be simplistically identified with the components of the full-term heart."2 To start with, the heart has one atrium and one ventricle. These septate around the end of the fifth week. The separation of the atrioventricular canal into right and left atrioventricular canals is accomplished by fusion of the endocardial cushions which develop at the dorsal and ventral walls of the heart.
The septum primum and septum secundum are responsible for the partitioning of the primitive atrium. The original right atrium, together with the sinus venosus and its right horn, is responsible for the final formation of the right atrium. The original left atrium, with participation of the terminal portions of the pulmonary veins, is responsible for the final formation of the left atrium.
At the end of the fourth week, the cardiac ventricles begin to form. The left ventricle arises from the ventricular portion of the primitive heart. During development, the bulboventricular fold disappears entirely. It is important to be aware of this in order to avoid thinking that it gives rise to the interventricular septum. As the muscular interventricular septum develops, it actually separates the heart tube ventricle (presumptive left ventricle) from the bulbus cordis (presumptive right ventricle). Because the primitive atrium and ultimately the definitive right and left atria shift to the right, the interventricular septum forms such as to fuse with the endocardial cushions, and the right atrium opens into the right ventricle, etc. Should this shift not occur, the double inlet malformation results. An exaggerated shift to the right results in a double outlet malformation.
The interventricular foramen is bounded by the ventricular muscular ridge, the endocardial cushions, and a neural crest derivative, the aorticopulmonary septum. The closure of this foramen at the end of the seventh week is effected by the development of the membranous portion of the interventricular septum by contributions from the three aforementioned structures. Thus the aorticopulmonary septum is involved in the formation of the left and right ventricular outlets as well as that of the pulmonary trunk and aorta.
The fusion of bulbar and truncal ridges around the fifth week is responsible for the partitioning of the bulbus cordis and truncus arteriosus, and therefore, for the reciprocally upward-spiraling formation of the ascending aorta and pulmonary trunk. The left pulmonary artery and the distal segment of the aortic arch communicate by means of the ductus arteriosus, a channel of variable length and diameter. The ductus arteriosus is derived embryologically from the sixth left aortic arch. At the time of birth, the ductus constricts, quickly becomes atretic, and thereafter remains as the ligamentum arteriosum.
The right common cardinal vein and the proximal part of the right anterior cardinal (right precardinal) vein are responsible for the development of both superior and inferior vena cavae. Most likely, the following three embryonic networks form parts of the inferior vena cava (IVC).

   The hepatic portion derives from the omphalomesenteric vein (right vitelline vein)

 The renal portion comes from the right subcardinal vein

 The sacrocardinal (subcardinal) or postrenal part comes from the right sacrocardinal vein

We quote Skandalakis and Gray3 on the development of the inferior and superior vena cavae:
The channels that will form the SVC are all present by the seventh week, and the definitive channel is already larger than the alternative pathways. By the end of the eighth week, almost all of the changes have been completed although the left supracardinal vein below the renal collar has not disappeared. It is probably the last of the old channels to vanish since it persists the most frequently as an anomalous left IVC.
The conducting system of the heart consists of the sinoatrial (SA) and atrioventricular (AV) nodes and the atrioventricular bundle. As reported by O'Rahilly and Müller,4 the conducting system appears at approximately 5 weeks. It is well developed at about the eighth week.
Congenital Anomalies
Pathogenetic classification of congenital cardiovascular malformations is summarized in Table 7-2. Syndromes featuring congenital heart disease are presented in Table 7-3.

Table 7-2. Pathogenetic Classification of Congenital Cardiovascular Malformations

I. Ectomesenchymal tissue migration abnormalities 
  Conotruncal septation defects
    Increased mitral aortic separation (a clinically silent, forme fruste)
    Subarterial, type I ventricular septal defect
    Double outlet right ventricle
    Tetralogy of Fallot
    Pulmonary atresia with ventricular septal defect
    Aorticopulmonary window
    Truncus arteriosus communis
  Abnormal conotrucal cushion position
    Transposition of the great arteries (dextro-)
  Branchial arch defects
    Interrupted aortic arch type B
    Double aortic arch
    Right aortic arch with mirror-image branching
II. Abnormal intracardiac blood flow 
  Perimembranous ventricular septal defect
  Left heart defects
    Bicuspid aortic valve
    Aortic valve stenosis
    Coarctation of the aorta
    Interrupted aortic arch type A
    Hypoplastic left heart, aortic atresia: mitral atresia
  Right heart defects
    Bicuspid pulmonary valve
    Secundum atrial septal defect
    Pulmonary valve stenosis
    Pulmonary valve atresia with intact ventricular septum
III. Cell death abnormalities 
  Muscular ventricular septal defect
  Ebstein's malformation of the tricuspid valve
IV. Extracellular matrix abnormalities 
  Endocardial cushion defects
    Ostium primum atrial septal defect
    Type III, inflow ventricular septal defect
    Atrioventricular canal
  Dysplastic pulmonary or aortic valve

Source: Clark EB. Growth, morphogenesis and function: the dynamics of cardiovascular development. In: Miller JM, Neal WA, Lock JA (eds). Fetal, Neonatal and Infant Heart Disease. New York: Appleton-Century-Crofts, 1989, p. 1-14; with permission.

Table 7-3. Syndromes Featuring Congenital Heart Disease

Name of Syndrome Clinical Features Cardiac Lesion Etiological Factors: Chromosomal Abnormalities
Asymmetric crying facies Asymmetric facies on crying (usually right sided) ? due to agenesis of anguli oris muscle. There may also be other congenital defects Septal defect or other abnormality  
Bonnevie-Ullrich More usually applied to Turner's syndrome with special features in the newborn. Prominence of redundant skin over back of neck; migratory edema and lymphangiectasia of hands and feet. Deepset nails See Turner's syndrome See Turner
Cri-du-chat Physical and mental retardation. Cat-like cry. Microcephaly. Hypertelorism. Epicanthic folds. Downward slant of palpebral fissures. Cleft palate Variable Partial deletion of short arm of chromosome 5
De Lange Physical and mental retardation. Small hands and feet. Bushy eyebrows. Thin lips with midline break in upper and notch in lower Variable. Ventricular septal defect Sporadic. ?Mutant gene
DiGeorge 3rd and 4th Aplasia of thymus gland impairs cellular immunity causing susceptibility to infections. Parathyroid hypoplasia causes hypocalcemia with tetany and convulsions. Physical and mental retardation. Choanal atresia Septal defects. Truncus arteriosus. Anomalies of great vessels; double aortic arch; interrupted arch Sporadic. Males/females: 2/1. Failure of 3rd and 4th branchial arch development
Down Mongoloid facies. Mental retardation. Hypotonia. Short metacarpals and phalanges Atrioventricular canal. Septal defect. Patent ductus. Tetralogy of Fallot 21 Trisomy (94%). 21 Trisomy/normal mosaicism (2.4%). Translocation (3.3%)
Ebstein Excessive breathlessness, cyanosis, syncope but many are symptom-free. Death sudden or from congestive heart failure Displacement of tricuspid valve into right ventricle. Large right atrium. Arrhythmia. Associated congenital heart lesions in one-third Sporadic
Ehlers-Danlos Hypermobility of joints, hyperelasticity of skin Atrial septal defect, atrioventricular septal defect, tetralogy of Fallot Autosomal dominant
Ellis-van Creveld chondroectodermal Growth retardation. Short extremities. Genuvalgus. Polydactyly, small thorax, hypoplasia of teeth and nails. Early cardiac or respiratory death in some Atrial septal defect (50%) Autosomal recessive
Holt-Oram Hypoplasia of thumb, radius, clavicles with narrow shoulders. Phocomelia may occur. Scoliosis Variable. Atrial, ventricular septal defect. Arrhythmia (frequent) Autosomal dominant
Hurler Characteristic facies with hypertelorism, protruding tongue. Physical and mental retardation later in first year. Kyphosis. Corneal opacities. Hepatosplenomegaly Infiltration of coronary arteries (narrowing) and valves (mitral incompetence) causes heart failure Autosomal recessive
Infantile hypercalcaemia (see Williams syndrome) Mental and physical retardation. Characteristic facies: epicanthic folds, hypertelorism, snub nose, carp mouth. Vomiting. Diarrhea, hypercalcemia inconstant (role uncertain) Supravalvar aortic stenosis. Pulmonary artery branch stenoses. Coarctation of aorta. Systemic hypertension Sporadic. Dietetic ?excess maternal vitamin D intake
Ivemark A syndrome associated with isomerism Anomalies of venous drainage. Endocardial cushion defects. Conotruncal abnormalities Sporadic
Kartagener Situs inversus. Absent frontal sinus in some. Bronchiectasis. Upper and lower airway infections frequent: pansinusitis, otitis, pneumonia Anomalies of venous return, endocardial cushions, septation, and great vessels. Dextrocardia Autosomal recessive
Laurence-Moon-Biedl-Bardet Mental retardation, obesity, hypogenitalism, retinitis pigmentosa Tetralogy of Fallot ?
Leopard, multiple lentigines Multiple dark spots on skin present at birth. Physical and mental retardation (mild). Hypogonadism Pulmonary stenosis. Prolonged P-R interval and QRS complex. Aortic stenosis Autosomal dominant
18 Long arm deletion Mental and physical retardation. Narrow or atretic auditory canal. Cleft palate. Long hands; tapering fingers. Undescended testicles Variable Long arm deletion of chromosome 18
Marfan Connective tissue defect resulting in tall stature, thin limbs, hypotonia, scoliosis, narrow palate, lens subluxation and lung malformation Dilation or aneurysm of aorta or pulmonary artery. Aortic valve and mitral valve incompetence (50%) Autosomal dominant
Noonan, Male Turner's Physical and some mental retardation. Characteristic facies with epicanthic folds; ptosis of eyelids; low-set ears. Webbed neck. Cubitus valgus. Pectus excavatum. Small penis. Undescended testicles. Occurs in male and female Pulmonary stenosis. Septal defect. Left ventricular obstruction or non-obstructive myopathy Sporadic. No chromosomal abnormality
Osteogenesis Fragile bones, blue sclera Weakness of the media of arteries, aneurisms, valvular incompetence Autosomal dominant
Pseudo-Hurler, Polydystrophy, Mucolipidosis III Physical and mental retardation. Similar to Hurler syndrome but milder Aortic stenosis and incompetence Autosomal recessive
Radial aplasia thrombocytopenia Absent or hypoplastic radius and sometimes other limb defects. Thrombocytopenia. Eosinophiliapenia Variable; 25% Autosomal recessive
Rubella Mental and physical retardation. Deafness, cataract, anemia, thrombocytopenia. Hepatosplenomegaly. Obstructive jaundice. Osteolytic trabeculation in metaphyses with subperiosteal rarefaction. Interstitial pneumonia Patent ductus. Pulmonary artery branch stenoses. Septal defect. Carditis. Lesions may cause heart failure Rubella virus transmitted from mother. May persist in excretions of infant for months
13 Trisomy Gross mental retardation. Microcephaly. Cleft lip and palate. Widespread skeletal abnormality. Single umbilical artery. Early death Ventricular and atrial septal defects. Patent ductus. Other gross defects 80% Trisomy for large part of D group (13 to 15) chromosome
18 Trisomy Mental and physical retardation. Small mouth and palpebral fissures. Short sternum. Limb abnormalities. Hirsutism. Single umbilical artery. Early death Ventricular and atrial septal defects. Patent ductus and other lesions Extra 18 chromosome
Turner Female with short stature. Ovarian dysgenesis. Lymphedema of hands and feet. Prominent ears. Web neck. Broad chest. Widely spaced nipples. Cutibus valgus. Horseshoe kidney. Buccal smear shows no female sex chromatin (Barr bodies) Cardiac defect in over 20% and of these 70% have coarctation of the aorta Sporadic. Chromosome pattern 45,XO (or mosaics XX/XO, XY/XO or part of X missing)
Gonadal dysgenesis
VATER VATER describes the main anomalies: Vertebral anomalies; vascular anomalies including ventricular septal defect and single umbilical artery; anal atresia; tracheoesophageal fistula and atresia; radial dysplasia; polydactyly; syndactyly; renal anomaly; single umbilical artery. Physical and mental retardation (but not in all Ventricular septal defect and other lesions Sporadic
Williams (see Infantile hypercalcemia syndrome) Physical and mental retardation. Coarse hair. Hypoplastic nails. Hypercalcemia occasionally found Supravalvar aortic stenosis. Peripheral pulmonary artery stenosis. Pulmonary valve stenosis. Ventricular septal defect Sporadic
Wolff-Parkinson-White Paroxysmal tachycardia which may cause heart failure, ECG: short P-R interval and slurred upstroke of QRS may be found between attacks Usually heart otherwise normal Accessory atrioventricular node and conducting bundle of Kent. Sporadic

Source: Arnold R. Heart disease in the neonate. In: Lister J, Irving IM (eds). Neonatal Surgery, 3rd ed. London: Butterworth 1990; with permission.

Clark (personal communication, 1992) correctly stated that it is impossible to classify all cardiac defects because of etiologic heterogeneity and phenotypic variability. It is not within the scope of this book to present all the congenital anomalies of the pericardium, heart, and great vessels. We will present a few here, and refer the interested student to Embryology for Surgeons.3

Pericardial Anomalies

Anomalies of the pericardium are shown in Table 7-4.

Table 7-4. Anomalies of the Pericardium

Anomaly Prenatal Age at Onset First Appearance (or Other Diagnostic Clues) Sex Chiefly Affected Relative Frequency Remarks
Congenital defects of the pericardium 5th-6th weeks At any age, if at all Male Rare Usually asymptomatic; more frequent on left
Pericardial cysts and diverticula 4th week Adolescence or later Male Rare Rarely symptomatic

Source: Skandalakis JE, Gray SW. Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.


Pericardial defects are usually asymptomatic. However, sudden death secondary to herniation and strangulation of the heart has been reported. Pericardiectomy is the treatment of choice in symptomatic patients, especially when cardiac herniation is present.

Isolated congenital absence of the pericardium was studied by Gatzoulis et al.5 Periodic stabbing chest pain was a presenting feature, and pericardioplasty benefitted the symptomatic patients. Chest x-rays and magnetic resonance imaging are necessary for diagnosis.

We quote Bennett6 on congenital foramen of the left pericardium:

Congenital foramen of the left parietal pericardium is uncommon. The condition has the potential to cause angina pectoris, myocardial infarction, or even death. [In 43 confirmed cases from the English language literature] the diagnosis, made at a mean age of 20 years (range 2 to 48) was five times more common in men. In 5 fatal cases, the heart had become incarcerated. In the remainder of cases, one-third were asymptomatic and two-thirds suffered a chest complaint that prompted diagnosis. Chest discomfort, dyspnea, and syncope were the most common symptoms. The most common finding at surgery... was a foramen at the base of the heart through which the atrial appendage had herniated. In eight instances, the rim of the defect lay upon and compressed the coronary circulation. Measures to remedy the disorder have included a variety of operations, some to enlarge the defect, others to close it, amputation of the atrial appendage, and, in two cases, myocardial revascularization. Surgery is appropriate in the majority of symptomatic patients and in all who are at risk for ventricular herniation.


Pericardial cysts, which are quite rare, vary in size from 1 cm to 15 cm. They are almost always asymptomatic. Occasionally, they communicate with the pericardial cavity; the term diverticulum is then more appropriate. Surgery is necessary for diagnostic confirmation.

Cardiac and Great Vessel Anomalies

The incidence of cardiac and great vessel anomalies is 3 to 5 per 1000 live births. It is beyond the scope of this book to discuss the wide variety of developmental defects that give rise to the broad spectrum of circulatory pathophysiology. The etiology of most of these defects is enigmatic. Surgery is the only appropriate treatment.

Several classifications are used for anomalies of the heart and great vessels. It is extremely important that pediatricians, as well as cardiac surgeons, understand the anatomy of the abnormal along with the pathophysiology of these malformations. We will list the three most common groups of abnormalities and their associated defects.


 Left to right shunts (acyanotic group)



– Uncomplicated septal ventricular or atrial defects


– Patent ductus arteriosus


 Right to left shunts (cyanotic group)



– Tetralogy of Fallot


– Truncus arteriosus


– Transposition of the great arteries


– Total anomalous pulmonary venous connection


– Tricuspid arteria


 Ventricular outflow obstruction



– Coarctation of the aorta


– Aortic stenosis


– Pulmonary valve stenosis


A fourth group of anomalies might include ectopia cordis, dextrocardia, and other rare malformations.

Congenital anomalies of the aorta are found in Table 7-5.

Table 7-5. Anomalies of the Aorta

Anomaly Prenatal Age at Onset First Appearance Sex Chiefly Affected Relative Frequency Remarks
Kinked aorta 7th week? None Equal Rare Asymptomatic
Aortic hypoplasia ? Young adulthood Male Rare  
Double aortic arch 7th week Infancy Equal Uncommon  
Right aortic arch 7th week Adulthood Male Uncommon  
Retroesophageal subclavian artery 7th week Any age Female Common Usually asymptomatic
Persistent third arch 7th week Childhood ? Very rare  
Cardioaortic fistula and aneurysm 6th week Adulthood Male Rare Some cases acquired
Coarctation of aorta 8th week or later Childhood Male Common  
Interruption of aortic arch Infancy Male Rare  
Coarctation of the abdominal aorta ? Adolescence or adulthood Equal Rare  
Patent ductus arteriosus At birth Childhood Female Common  
Persistent truncus arteriosus 4th to 7th weeks Childhood Male Rare  

Source: Skandalakis JE, Gray SW. Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.

Anomalies of the Superior Vena Cava

The anomalies of the superior vena cava (SVC) are left persistent superior vena cava and left persistent superior vena cava with failure of development of the coronary sinus. Awareness of an abnormal left superior vena cava is essential in order to avoid ligation during open heart surgery.

Left persistent superior vena cava is a common defect that originates in the fifth week and affects the sexes equally. Symptoms are related to associated cardiac defects only. A persistent left superior vena cava is not anomalous in complete situs inversus.

The pathway of left persistent superior vena cava is as follows:


 It develops from the union of the left subclavian and left internal jugular veins


 It receives the superior intercostal vein and the accessory hemiazygos vein


 It travels downward in front of the aortic arch and in front of the left pulmonary artery and left pulmonary vein


 After entering the pericardium, it is related to the posterior wall of the left atrium and the posterior atrioventricular groove


 It forms the coronary sinus after receiving the great cardiac vein


The anatomic pathway of left superior vena cava with failure of coronary sinus development is similar to that of persistent left superior vena cava. A left superior vena cava with failure of coronary sinus development empties into the upper part of the left atrium between the left superior pulmonary vein and the atrial appendage. It bypasses the coronary sinus, which is not developed and not formed (unroofed coronary sinus).



 Anomalous pulmonary veins may enter the superior vena cava. These veins must be recognized and avoided during surgery.


 An absent left brachiocephalic vein may indicate a left superior vena cava. This may be detected by palpation of an enlarged coronary sinus or by entrance of the left superior vena cava into the coronary sinus slightly above the left atrial appendage.


 Curtil et al.7 reported 27 cases of left retroaortic brachiocephalic vein as follows.


A retrospective study was made of 5218 congenital [pediatric] cardiopathies. . .. A left retro-aortic brachiocephalic vein was demonstrated in 27 patients, i.e. an incidence of 0.5%. The chief cardiopathy in these patients was a tetralogy of Fallot in 25 cases (93%). Among these 25 cases of Fallot's tetralogy the aortic arch was rightsided in 19 cases (70%). . .. The embryological origin of the left retro-aortic brachiocephalic vein. . . derives from the inferior (but not superior) transverse plexuses, connecting the two anterior cardinal veins.


 Referring to left persistent superior vena cava, Hammon and Bender8 wrote, "Complications are usually related to the magnitude of operation for associated anomalies and not to the operative therapy for this uncommon situation."


 The two operations for persistent superior vena cava are



– Simple ligation


– 'Roofing' of the coronary sinus using pericardium or part of the left atrium. This directs the blood into the right atrium.


 Standardized terminology for congenital heart, pericardial, and great vessel disease is still evolving. Mavroudis and Jacobs9 have provided an introduction to the work of the International Congenital Heart Surgery Nomenclature and Database Project, and we urge the interested student to study the April 2000 issue of Annals of Thoracic Surgery.



Knowledge of detailed cardiac anatomy is a prerequisite for successful surgery. Nowhere is this more important than in the setting of congenital cardiac malformations.—R.H. Anderson, B.R. Wilcox10

In this chapter, the anatomy of the pericardium, heart, and great vessels is reviewed in some detail. Advances in surgical instrumentation, techniques, and medication have facilitated the development of cardiac surgical procedures for repair of congenital cardiac defects, correction of cardiac vascular insufficiency, replacement of diseased cardiac valves, implantation of electronic devices for regulation of pacemaking activity, and replacement of the heart itself. The reader seeking the particulars of surgical procedures relating to the correction of congenital malformations or of pathologic processes should consult appropriate texts that treat thoracic or cardiac surgery in detail.


Topographic Relations

The pericardial sac and the heart within reside in the mediastinum, an area between the pleural sacs. It is bounded anteriorly by the sternum and posteriorly by the thoracic vertebrae.

The mediastinum is divided arbitrarily into superior and inferior portions by a transverse plane passing through the sternal angle of Louis and the T4 intervertebral disk (Fig. 7-1). The inferior mediastinum is further subdivided into anterior, middle and posterior sections. The middle mediastinum is defined by the pericardium and its contents: the heart (Fig. 7-2) and the roots of the eight great vessels (aorta, pulmonary trunk, superior and inferior vena cavae, and four pulmonary veins).

In front of the pericardium are the structures of the anterior mediastinum. These include the first four sternebrae, the lower part of the thymus, and connective tissues. Behind the pericardium are the principal contents of the posterior mediastinum: the aorta, the esophagus, the azygos system, and the fifth through the eighth thoracic vertebrae. Above is the superior mediastinum; below, the diaphragm forms a lower limit for the middle mediastinum.


The pericardial sac, or parietal pericardium, is formed by two layers: an outer fibrous layer and an inner serous layer, responsible for secretion of the fluid film within the pericardial sac (Fig. 7-3). The simple squamous epithelium (mesothelium) that forms the serous lining of the pericardial cavity is a portion of the primitive embryonic celom. Therefore, it is similar to the lining of the pleural and peritoneal cavities. At the points of exit of the vessels from the pericardial sac, the fibrous layer becomes continuous with the adventitia of the vessels and the pretracheal fascia. There the serous lining is also reflected over the surface of the heart, as the visceral pericardium or epicardium. Deep to this layer is a variably thick lamina of connective tissue, which can be thought of as representing the fibrous layer of the pericardial sac.


The parietal and visceral layers of pericardium form a closed sac, the pericardial cavity. Two topographic areas within the sac are of special importance. One of these is a part of the pericardial cavity called the oblique sinus. It is found behind the heart, and is bounded superiorly and on either side by the left atrium, pulmonary veins, and inferior vena cava. The esophagus is related posteriorly to this space.

The second space of note within the pericardial sac is the transverse sinus. This is a potential space behind the pulmonary artery and ascending aorta. It is bounded from behind by the front of the atria and the superior vena cava. The surgeon can place a digit or two, or a ligature, into this space without dissection, and quickly clamp the great arteries.

The transverse sinus is separated from the oblique sinus by the venous mesocardial reflection. The venous mesocardial reflection runs from the pericardial sac to the dorsum of the left atrium between the uppermost right and left pulmonary veins. From a clinical standpoint, the pericardium should be considered a single entity, a closed fibroserous sac (see Fig. 7-3).

In the cadaver, the pericardial cavity contains between 40 and 60 ml of fluid. Much more can be accommodated if the increase in quantity is gradual.


The pericardial sac is roughly conical in shape. It is fused at its base to the diaphragm, and fused at its apex to the adventitia of the great vessels and pretracheal fascia. Two other minor points of fixation are the superior and inferior sternopericardial ligaments.

The relations of the pericardium are as follows:


 Anterior: The fibrous pericardium is related to the sternum and the costal cartilages, but is separated from them, for the most part, by the anterior medial reflections of the left and right pleurae (the costomediastinal reflections). The pericardium is thus covered by the pleurae, except over a small bare area on the left at the level of the fourth to sixth cartilages. This is known as the "bare area of Edwards," or the "cardiac dull space." The latter term is attributable to the lack of resonance to percussion at this point.


 Posterior: The right and left bronchi, lymph nodes, esophagus and its nerve plexus, descending thoracic aorta, and vertebral reflection of pleura are all related to the posterior portion of the pericardium (Figs. 7-4, 7-5)


 Lateral: Mediastinal pleurae, phrenic nerves, and pericardiacophrenic vessels


 Inferior: Diaphragm, peritoneum, and inferior vena cava


 Superior: Roots of the great vessels, the left brachiocephalic vein, the left recurrent laryngeal nerve, and the left superior intercostal vein


William Osler envisioned an "abdominal area of romance where the head of the pancreas lies folded in the arms of the duodenum." We like to think that within the chest cavity also there is a love affair, with the lungs embracing the pericardial sac and the heart.

Vascular Supply


About 80 percent of the blood to the pericardium comes from the right and left internal thoracic arteries by way of their pericardiacophrenic branches (Fig. 7-6). In addition, the lower pericardium is supplied by branches of the superior phrenic arteries. The posterior portion receives branches from the bronchial and esophageal arteries and mediastinal twigs from the descending thoracic aorta. All of these vessels anastomose freely.


The veins follow the arteries. They empty into the azygos and hemiazygos veins, the internal thoracic veins, and the superior phrenic veins.


The pericardium is drained by three groups of lymph nodes:


 Anterior mediastinal nodes


 Diaphragmatic nodes


 Inferior tracheobronchial nodes


Warren11 reported on pericardial malignancies:

Malignancies rarely arise from the pericardium. Mesothelioma, the most common of these, is usually unresectable and almost always incurable. Malignancies may secondarily involve the pericardium by direct extension...More frequently, malignancies may involve the pericardium by a process of retrograde lymphangitic spread or hematogenous dissemination. These patients present with a symptomatic pericardial effusion and occasionally pericardial tamponade. Subxiphoid pericardiostomy and drainage is a safe procedure that provides effective and durable symptomatic relief in these terminally ill patients.


Nerve fibers from the vagus nerves, the phrenic nerves, and the cardiac branches of the recurrent laryngeal nerves supply the parietal pericardium. Sympathetic fibers arise from the cervical and upper thoracic parts of the sympathetic chains, and from the stellate ganglia. The fibers reach the pericardium by way of the aortic and cardiac plexuses.

Surgical Applications


Aspiration of the fluid contents of the pericardial sac may be necessary for the diagnosis or treatment of pericardial effusion caused by trauma, secondary manifestations of heart disease, infection, or neoplasms. Cardiac tamponade may also be produced from central venous catheters. Unexplained hypotension, tightness of the chest, and shortness of breath are the signs and symptoms of cardiac tamponade. Collier et al.12 advised emergency echocardiogram for diagnosis, but for prevention advised that the tip of the catheter should be outside of the cardiac silhouette on chest X-rays. It is obvious that the greater the accumulated amount of fluid, the easier the aspiration, but the more desperate the patient's condition.

Remember Beck's Triad of cardiac tamponade:


 Small, quiet heart


 Falling atrial pressure


 Rising venous pressure


We quote from Schrump and Nguyen13 on malignant pericardial effusion:

Malignant pericardial effusion is frequently an indication of advanced, incurable malignancy. Hence, the goals of intervention include relief of symptoms and prevention of recurrence...Surgical interventions (subxiphoid pericardiostomy) or medical interventions (ultrasound-guided percutaneous tube pericardiostomy and sclerotherapy) have acceptable risks and provide excellent results. We favor surgical drainage as the primary approach for patients with malignant pericardial effusion because of its simplicity and extremely high success rate without the need for intrapericardial instillation of sclerosing agents and tube manipulations that may be associated with patient discomfort. Recurrent malignant pericardial effusion can be managed either by repeat pericardiostomy or insertion of a shunt. Patients responding to treatment with complete control of the effusion should have a meaningful survival with life expectancy (average, 9 months) contingent on the histology of the underlying malignancy.

Parasternal Approach

The needle is inserted into the fifth or sixth intercostal space 2 cm lateral to the apical impulse, or just medial to the left border of the cardiac dullness. The needle is then directed to the right shoulder. The parasternal position of the internal thoracic artery and vein must be remembered to avoid hemothorax from their laceration.

Abdominal (Paraxiphoid) Approach

The needle is inserted 1 cm below and 1 cm to the left of the xiphoid, between it and the left costal arch, pointing in the direction of the left shoulder. This is the preferable route, because the needle will transgress neither the pleural nor the peritoneal cavities; most importantly, it is less likely to cause injury to a coronary artery.

Olsen et al.14 recommended pericardial-peritoneal window for patients with malignant and non-infectious benign pericardial effusions, including those with tamponade.


Indications include constrictive pericarditis, and malignant or benign constrictive effusion.


For the drainage of the pericardial space and/or partial pericardiectomy, two approaches may be used, the subxiphoid and the anterolateral.

For the subxiphoid approach, a midline incision is made from approximately the xiphoid process to approximately halfway above the umbilicus. The xiphoid process is then resected. With downward traction of the diaphragm, the anterior pericardium is exposed and resected.

For the anterolateral approach, an anterolateral thoracotomy at the left fifth intercostal space is made, and part or all of the left anterolateral pericardium is removed.

For total pericardiectomy, median sternotomy is the best approach, although the "clamshell" bilateral submammary incision may be used in special cases. The pericardium is removed from the aorta and pulmonary artery above to the diaphragm below, and from the left to the right pulmonary veins.

Inflammatory Response to Pericardial Trauma

In some patients, opening of the pericardium may be accompanied by fever, pericardial and pleural effusion, and/or pain. These manifestations have been termed 'postpericardiotomy syndrome.' Injury to the pericardium and the presence of blood in the pericardial cavity appears to be the cause. Salicylates and corticosteroids provide relief from the symptoms. The condition is usually self-limiting.


External Topographic Features


The projection of the living heart on the chest wall (Fig. 7-7) is highly variable. It depends upon the position of the body and other factors such as age and obesity. There are four anatomic landmarks, identified in Figure 7-7 by Roman numerals I-IV:

I, Superior vena cava Second right intercostal space or third right costal cartilage, 1.2 cm lateral to the right sternal margin
II, Inferior vena cava Sixth right costal cartilage, 1 cm lateral to the right sternal line
III, Apex Fifth left intercostal space, 6 cm lateral to the left sternal line or 9 cm lateral to the midline
IV, Tip of left auricle Second left costal cartilage, 1.2 cm lateral to the left sternal margin

If you connect the four Roman numerals as indicated below, the figure so outlined (Fig. 7-7) provides a rough approximation of the projection of the heart. This projection can never be taken for granted, because the heart is not rigidly fixed in the thorax:


 I and II with a convex line (SVC to IVC)


 II and III with a straight line (IVC to apex)


 III and IV with a convex line (apex to tip of left auricle)


 IV and I with a straight line (tip of left auricle to SVC)


The projection of the four cardiac valves (Fig. 7-8) is approximately as follows:


 P, Pulmonary valve: Third left sternochondral junction


 A, Aortic valve: Left sternal line at third left intercostal space, just below and medial to the pulmonary valve projection


 M, Mitral valve: Fourth left sternochondral junction


 T, Tricuspid valve: Right sternal line at fourth left intercostal space


The location of the points of best auscultation of these valves is different from their actual projections. Valve sounds are best heard at the following sites (Fig. 7-8):


 P, Pulmonary valve: Second left intercostal space, adjacent to the sternum


 A, Aortic valve: Second right intercostal space, adjacent to the sternum


 M, Mitral valve: Fourth or fifth left intercostal space, near the midclavicular line (apex beat)


 T, Tricuspid valve: Fourth or fifth left sternochondral junction, near the end of the sternum (right lower sternal line)


According to Waller and Schlant,15 the weight and size of the heart vary, depending on such factors as age, sex, body length, epicardial fat, and general nutrition. Edwards16 stated that the adult human heart averages 325 ± 75 g in men and 275 ± 75 g in women.

Anterior or Sternocostal Surface

The right atrium and auricle, the atrioventricular groove, and the right ventricle and pulmonary outflow tract, or conus arteriosus, form the anterior surface of the heart. The anterior right ventricle is typically in nearly direct contact with the sternum. Occasionally, a small portion of the left ventricle participates in the formation of the anterior surface (Figs. 7-9, 7-10).



 With median sternotomy, the atrial appendages in a normal heart are located clasping the arterial pedicle (Fig. 7-11) in most cases.


 If the atrial appendages are on the same side of the pedicle, they produce an anomaly known as juxtaposition of the appendages. This anomaly can also be associated with congenital heart disease.


Posterior Surface

The posterior surface of the heart consists of the left ventricle, the atrioventricular and posterior interventricular sulci, the left atrium and its four (or five) pulmonary veins, and a portion of the right atrium (Figs. 7-12, 7-13).

Diaphragmatic or Inferior Surface

The inferior (or diaphragmatic) surface of the heart is formed by the right one-third of the right ventricle, the posterior interventricular sulcus, the left two-thirds of the left ventricle, and a small portion of the right atrium at the entrance of the inferior vena cava. In contrast to the rounded, convex form of the anterior and left sides of the heart, this surface is noticeably flattened from its contact with the diaphragm.

Relations of the Borders of the Heart


 Superior: The roots of the great vessels extend obliquely from the third right costal cartilage to the left second costal cartilage, and form the superior border. A line drawn across the sternum at the level of the second intercostal space is said to approximate the "clinical base" of the heart, indicating the general level of the cardiac attachment of the great vessels.


 Right: The right border is formed by the terminal part of the superior vena cava, right atrium, and suprahepatic inferior vena cava. It extends from the third right costal cartilage, 1.3 cm from the right sternal border, to the sixth right costal cartilage.


 Left (oblique or pulmonary): The left border is formed by the convexity of the pulmonary trunk, the tip of the left auricle, and the left ventricle. It extends from the second left costal cartilage, 1.3 cm from the left sternal border, to the apex of the heart. This is usually located just inferior to the left nipple and slightly medial to the midclavicular line in the fifth intercostal space, about 9 cm from the midline.


 Inferior: The inferior border is formed by both ventricles. It extends from the sixth right costal cartilage, 1 cm from the right sternal line, to the apex of the heart.


 Apex: The apex of the heart is formed by the junction of the left and inferior borders in the fifth left intercostal space, 6.5 cm from the left sternal border. It is usually composed of the tip of the left ventricle.



As soon as the pericardium is opened, one can see two irregular lines of fat deposits on the external surface of the heart. These lines indicate the groove or sulcus that separates the atria from the ventricles, and the groove that separates the left and right ventricles.


The atrioventricular sulcus almost encircles the heart. It is interrupted only by the conus or infundibulum of the right ventricle (pulmonary trunk) anteriorly. Beginning to the right of the infundibulum, the sulcus descends to the right side of the diaphragmatic border, passing to the left of the entrance of the inferior vena cava. It continues deeply under the coronary venous sinus and left atrium, and ascends again to the left side of the infundibulum.

Anteriorly, the atrioventricular sulcus separates the right atrium from the right ventricle, and contains the right coronary artery and the small cardiac vein. Posteriorly, it separates the left atrium from the left ventricle, and contains the coronary sinus, the great cardiac vein, and the circumflex branch of the left coronary artery.


The interventricular sulcus indicates the position of the underlying interventricular septum between the right and left ventricles. On the anterior surface, it leaves the coronary sulcus just to the left of the infundibulum (the pulmonary trunk), and curves gracefully in a reverse sigmoid form to the diaphragmatic surface, to the right of the apex. It continues on the posterior surface, ascending to join the coronary sulcus at the "crux." The crux is the small posterior region where all four major chambers are most closely approximated.

The anterior portion of the interventricular sulcus contains the anterior interventricular (left anterior descending) branch of the left coronary artery and the great cardiac vein of Galen. In the majority of people, the posterior portion contains the posterior interventricular (posterior descending) branch of the right coronary artery (which can sometimes arise from the left circumflex) and the middle cardiac vein.


The interatrial sulcus separates the atria. Anteriorly, it is covered by the pulmonary trunk and aorta; posteriorly, it is very faint. The interatrial sulcus is not a useful landmark.

Fibrous Cardiac Skeleton

The skeleton of the heart is usually described as a framework of fibrous "rings," the valve anuli, encircling the mitral, tricuspid, aortic, and pulmonary orifices, interconnected by dense aggregates of connective tissue. These fibrous elements provide both sites of origin and insertion for the muscular bands which form the walls of the chambers, the interventricular septum, and the papillary musculature (Figs. 7-14, 7-15, 7-16).

The four rings are mutually supported and held together by the right and left fibrous trigones, and by the conus tendon. From the right side of the aortic ring, the membranous portion of the interventricular septum extends downward to meet the muscular portion of the septum. The right fibrous trigone, often also referred to as the central fibrous body, joins the aortic, mitral, and tricuspid valve anuli or rings.

The left fibrous trigone, considerably less distinct than the right trigone, joins the mitral anulus to that of the aorta. The aortic and pulmonary valve rings are joined together by a stout band of fibrous tissue, the tendon of the conus.

The myocardium of the atria and the myocardium of the ventricles are separated, and also electrically insulated from each other, by the mitral and tricuspid rings and by the right fibrous trigone. Normally, the sole functional interconnection of the myocardia is through the atrioventricular bundle (of His), which perforates the right fibrous trigone to reach the top of the muscular septum. Thereafter, it divides into the broad left bundle branch and the narrow right bundle branch.

For a more detailed description of the fibrous skeleton, the reader should consult Zimmerman17 and Zimmerman and Bailey.18

Lal et al19 questioned the presence of the tendon (or ligament) of the infundibulum. We present their summary of their findings.

The fibrous skeleton of the heart has featured prominently in anatomical and surgical descriptions, although all its purported components are difficult to demonstrate. In descriptions of the skeleton, there have been repeated references to the presence of a tendon (or ligament) between the aortic and pulmonary roots. Such a tendon is rarely, if ever, discussed in the context of surgical procedures being carried out on the ventricular outflow tracts. Our study was undertaken, therefore, to investigate the existence and nature of such a tendon or ligament. Serial transverse sections were made through roots of the aorta and pulmonary trunk in an intact fetal heart. In addition, ten normal adult hearts were dissected to display the components of the fibrous skeleton of the heart. No discrete fibrous or elastic structure could be detected in the tissue plane between the aortic sinuses and the subpulmonary muscular infundibulum, although a fascial strand was observed in one heart. Apart from this specimen, the space between the free-standing muscular subpulmonary infundibulum and the sinuses of aorta bearing the coronary arteries was occupied only by loose fibroareolar tissue. The initial presence of the ligament was described following studies of animal and macerated human hearts. Subsequently, it would seem its existence has been passed on through generations of morphologists and surgeons without its presence being reconfirmed. We have been unable to demonstrate any structure approximating to the initial illustrations.

So-called "accessory bundles" (of Kent) are atypical muscle fibers which, by bypassing the atrioventricular node and the normally intervening fibrous skeleton, interconnect atrial and ventricular muscle. Such cardiac muscle fibers can form an alternative conduction pathway which, not being subject to the normal delay of the stimulating impulse provided by the atrioventricular node, leads to early ventricular excitation, or to Wolff-Parkinson-White syndrome.

The membranous part of the interventricular septum is composed of a pars interventriculare lying beneath the septal leaflet of the tricuspid valve, and a pars atrioventriculare just superior to the attachment of the septal leaflet, forming part of the floor of the left atrium. Defects of the membranous septum usually result in ventricular communication through the pars interventriculare, but can sometimes result in left ventricle/right atrium communication through the pars atrioventriculare.

Chambers of the Heart


General Relations

The right atrium lies between the openings of the superior and inferior venae cavae. Blood enters the right atrium from the venae cavae, and leaves it to enter the right ventricle. Together, the right atrium and the right ventricle form the physiologic "right heart."

The relations of the right atrium:


 Superior: Superior vena cava


 Anterior: Pericardium, right lung, right mediastinal pleura


 Posterior: Right pulmonary veins, left atrium


 Lateral: Pericardium, right phrenic nerve and pericardiacophrenic vessels, right lung, right mediastinal pleura


 Medial: Ascending aorta, left atrium; the right auricle is related to the right and anterior wall of the ascending aorta


 Inferior: Inferior vena cava


External Features

The chief external features of the right atrium include the following, from above downward:


 Superior vena cava


 Right auricle over the root of the aorta


 Coronary sulcus separating the right atrium from the right ventricle


 Sulcus terminalis


 Inferior vena cava


The sulcus terminalis is a shallow groove and is not always obvious. It starts at the right side of the superior vena cava and ends at the right side of the inferior vena cava. The sulcus corresponds to an internal ridge between the right atrium and the right auricle, the crista terminalis. The groove and the ridge separate the smooth posterior portion of the atrium, the sinus venarum, from the anterior trabeculated auricle, which is the right half of the primitive atrium. The sinus venarum is derived from the embryonic right horn of the sinus venosus.

Internal Features

The principal feature of the interior of the right atrium is the crista terminalis, corresponding to the externally-seen sulcus terminalis (see above). This ridge separates the posterior, smooth area of the atrium (sinus venarum) from the anterior rough area (trabeculated region), the atrium proper, and its auricle. The trabeculations extend outward to the margin of the auricle (Fig. 7-17). They are also called the musculi pectinati, for their fancied resemblance to the teeth of a comb.

The fossa ovalis on the interatrial septal wall is a depression marking the site of the prenatal atrial communication, the foramen ovale. The margin of the fossa, the limbus fossa ovalis, is formed by the edge of the septum secundum. The floor is formed by the septum primum of the fetal heart. The limbus is absent inferiorly, and is continuous with the left leaf of the inferior vena cava. In about 15 percent of the population, the floor of the fossa ovalis is not entirely sealed shut. Usually, this has no physiologic significance, for the higher pressure within the left atrium keeps the floor of the fossa pressed shut against the limbus.

Taylor and Taylor20 support the hypothesis that the right atrial appendage, the pectinate muscles, and the terminal crest evolved to supply blood to the conducting myocardium of the sinus part of the right atrium. Like the right ventricle, the right atrium is structured as a single and completely finished unit. The interpectinate spaces and the thebesian sinusoids offer suggestions to the topography of the conducting pathway and the sinus node.


The openings of the right atrium include the following anatomic entities


 Orifices of the superior vena cava and inferior vena cava


 Coronary sinus


 Several minute orifices of small veins


 Several small, irregular openings in each of the four chambers of the heart


 Atrioventricular orifice


The orifice of the superior vena cava is at the uppermost portion of the sinus venarum. The orifice of the inferior vena cava is at the posteroinferior portion of the sinus venarum. It is guarded by the proper (eustachian) valve of the inferior vena cava.

The coronary sinus is on the medial wall of the atrium, between the orifice of the inferior vena cava and the attachment of the septal cusp of the tricuspid valve. It is guarded by the thebesian valve. This opening is said to be large enough to admit the tip of the surgeon's little finger. It may occasionally be covered by a multi-perforated net of tissue, the network of Chiari.

We quote from Ortale et al.21 on their cadaveric studies of the coronary sinus and its tributaries:

Knowledge of the tributaries and the relationships of the coronary sinus are important in cardiac surgery, especially when dissecting the coronary arteries, as well as in the area of the arteriovenous trigone...An anastomosis of approximately 1.0 mm in calibre was observed between the anterior and posterior interventricular veins in 19% of specimens. Myocardial bridges were detected above the anterior interventricular vein or its tributaries in 8% of specimens. The great cardiac vein formed the base of the arteriovenous trigone of Brocq and Mouchet with the bifurcating branches of the left coronary artery in 89% of specimens and formed an angle accompanying these arterial branches in 11%. In the trigone the anterior interventricular and great cardiac veins were superficial to the arteries in 73% of specimens. The left marginal vein was present in 97% of specimens, emptying into the great cardiac vein in 81% of cases and into the coronary sinus in the remaining 19%. The small cardiac vein was present in 54% of specimens. In the coronary sulcus the great cardiac vein was adjacent to the circumflex branch of the left coronary artery in 76% of specimens and to the right coronary artery in 5%; in 19% there was no relationship with either artery. The coronary sinus maintained a relationship with the right coronary artery in 46% of specimens and with the left coronary artery in 32%; in 22% it had no relationship with these vessels.

There are several minute orifices of small veins. These are the anterior cardiac veins. They arise on the anterior surface of the right ventricle, and cross the right coronary artery to reach the margin of the auricle.

Variably small, irregular openings on the medial wall of the right atrium mark the sites of entry of the venae cordis minimae (thebesian veins), which drain venous blood from the musculature of the chamber. Such openings are present in all four chambers of the heart. Since their number is inversely proportional to the pressure within the chamber, they are most numerous in the right atrium and least numerous in the left ventricle.

The atrioventricular orifice, which occupies the entire left anterior wall of the atrium, is surrounded by a fibrous ring. It is guarded by the tricuspid valve leaflets. In the adult heart, the orifice admits three fingers.



 The sinus node is located beneath the epicardial surface of the terminal sulcus, at the base of the superior vena cava. The terminal sulcus is located between the triangular appendage and the sinus venarum.


 There are four eponymous entities associated with the internal surface of the right atrium.



– Waterston's groove: The superior limbus is a fold of the interatrial sulcus, which is named Waterston's groove. It is located between the fossa ovalis and the opening of the superior vena cava. There is no inferior limbus.


– Tendon of Todaro: Todaro's tendon is a fibrous cord under the endocardium, 1 mm in diameter (see Fig. 7-15). It extends from the right fibrous trigone of the heart (elliptical mass between the aortic, mitral, and tricuspid openings) to the valve of the inferior vena cava. To be more anatomically correct, its pathway is from the right atrial wall to the medial end of the valve of the inferior vena cava.


Kozlowski et al.22 studied the morphology of the tendon of Todaro in histologic sections of human hearts from fetal stage to older adults, and reported the following:

The tendon of Todaro, found in the right atrium of the heart, has considerable clinical importance in the fields of both cardiac surgery and invasive cardiology...In fetal hearts...a very well-developed, white structure was observed, convexed into the lumen of the atrium...In the group of hearts of young adults, it was also possible to follow the course of the tendon of Todaro macroscopically. However, the older the heart was, the less the convex was visible, and in older adults it was completely invisible. In the hearts of older adults the tendon of Todaro formed very small ribbons of connective tissue. In the adult heart, the examined tendon was located the deepest and did not connect to the endocardium...[T]he tendon of Todaro is a stable structure, occurring in all examined hearts even when it is not macroscopically visible.

Ho and Anderson23 declared the tendon of Todaro or its surrogate (a projected line between the eustachian valve and the central fibrous body) to be a landmark to locate the atrial components of the AV conduction axis, and a reliable border for the triangle of Koch.


– Triangle of Koch: The triangle of Koch is the home of the atrioventricular node. Its inferior border is Todaro's tendon; the superior border is the septal leaflet of the tricuspid valve. The base is the post-eustachian sinus.


– Sinus of Keith: The sinus of Keith is a pouch above the orifice of the coronary sinus. It is related to the tricuspid valve and to the extension of the terminal crest.


 The right atrial surface of the fossa ovalis is located between the triangle of Koch and the opening of the superior vena cava.


 An aneurysm of the aortic sinus of Valsalva may rupture into the right atrium because of the proximity.



General Relations

The right ventricle lies behind the sternum and to the left of the right atrium. It receives blood from the right atrium, and expels it through the pulmonary artery. The myocardium of the right ventricle is thicker than that of the atria, and thinner than that of the left ventricle.

The relations of the right ventricle are:


 Superior: Right auricle and pulmonary trunk


 Anterior: Pericardium, left pleura, anterior margin of the left lung, sternum, and costal wall of the thorax


 Posterior: Interventricular septum


 Inferior: Pericardium, central tendon of diaphragm


External Features

The right ventricle forms most of the sternocostal surface of the heart. The atrioventricular groove on the right margin marks the boundary between the two chambers, and contains the right coronary artery. Its dextral margin, the acute margin, forms a relatively sharp angle between the sternocostal surface and the diaphragmatic surface.

Internal Features

The crista supraventricularis divides the ventricle into the inflow tract (an inferior, roughened, and trabeculated region) and the infundibulum (a superior, smooth, outflow tract) (Fig. 7-18).

The trabeculae carneae of the rough inflow tract are muscular ridges or bundles of the myocardium. One bundle forms a muscular bridge from the interventricular septum and anterior wall of the right ventricle to the base of the anterior papillary muscle. It has been named the septomarginal trabeculum or, more commonly, the moderator band. In about half of individuals, the moderator band is very clearly identifiable; in others, it is variably less so. The term 'moderator band' comes from the fact that the right bundle branch of the conducting system passes in a subendocardial position along the surface of the band, often visible as a narrow, light streak of tissue.

Slender strands of pale tissue, the cardiac pseudotendons, can be seen passing to the walls of the chamber near the base of the anterior papillary muscle. The pseudotendons can be seen particularly well near the apex of the chamber. They typically contain slender strands of specialized cardiac muscle for conducting the contractile impulse to the working myocardium.

Arising from the trabeculae carneae are pyramidal or cylindrical muscular projections, the papillary muscles. Although named anterior, posterior, and septal because of their relative positions in the chamber, the form and number of papillary muscles is quite variable, especially the septal papillary muscles. Often, the anterior papillary muscle provides anchorage for slender, tendinous chordae tendineae that pass to the anterior and posterior leaflets of the tricuspid valve. The more posteriorly situated papillary muscle is attached to the posterior and septal cusps.

One little papillary muscle, the papillary muscle of the conus, is of more significance than its diminutive size might indicate. The papillary muscle of the conus is located at the medial end of the crista supraventricularis, the junction of the smooth and rough portions of the chamber. It is at the location of this muscle that the right bundle branch commonly attains a subendocardial position in the right ventricle, where it can often be discerned. The papillary muscle of the conus is, in some instances, represented only by a few chordae tendineae that arise at the margin of the crista supraventricularis and pass to the septal cusp of the tricuspid valve.

Right Atrioventricular Opening

The right atrioventricular opening is oval, 4 cm in its longest axis, and admits the tips of three fingers. The opening is guarded by three leaflets (anterior, posterior, and septal [medial]) of the tricuspid valve. The leaflets arise peripherally from the fibrous atrioventricular (tricuspid) anulus of the cardiac skeleton. Their free margins are attached by several complex tiers of chordae tendineae to the papillary muscles (Fig. 7-19).

Pulmonary Orifice

The pulmonary trunk leaves the uppermost part of the smooth-walled outflow tract (the infundibulum) through the fibrous pulmonary ring. It is guarded by three semilunar cusps (anterior, right, and left). Each cusp consists of a crescentic lunule which has a thickened nodule midway along its arc. Adjacent cusps are interconnected by the commissures of the valve.


General Relations

The left atrium forms two-thirds of the base of the heart. It receives the blood carried by the pulmonary veins, and discharges its blood to the left ventricle. It is related to other structures as follows:


 Superior: Left bronchus and right pulmonary artery


 Anterior: Proximal ascending aorta and proximal pulmonary trunk


 Posterior: Anterior wall of the oblique sinus of the pericardial cavity, esophagus, right pulmonary veins


 Right: Right atrium and interatrial septum


 Left: Pericardium and left pulmonary veins


 Inferior: Left ventricle


External Features

The most striking features of the left atrium are the four pulmonary veins, two on each side. The veins are enveloped, together with the superior and inferior venae cavae, in a serous pericardial sleeve.

In some hearts, a small vein (the oblique vein of the left atrium) can be seen on the left extremity of the chamber, near the entrance of the left inferior pulmonary vein. This normally small vessel drains into the coronary venous sinus. It represents the termination of the embryonic left common cardinal vein. In a small percentage of individuals, it is much enlarged as a left-sided superior vena cava. In these circumstances, the coronary venous sinus can be very large in diameter.

Internal Features

Like the right auricle, the left auricular appendage is trabeculated; the left is much smaller, however. But the left auricle does not possess a crista terminalis as does the right auricle. The pectinate muscles of the right auricle arise from the crista terminalis. The remainder of the interior of the left atrium is quite smooth and relatively featureless, although a few small openings of venae cordis minimae (thebesian veins) may be seen.

The two right pulmonary veins open, one above the other, on the right wall of the atrium. In some cases, three right pulmonary veins may end separately there, with the vein from each of the three lobes of the right lung retaining its independence. The two left pulmonary veins, similarly arranged, open in the posterior wall. In other words, the orifices of the four pulmonary veins are located near the corners of the left atrium. The bicuspid (mitral) valve and its opening occupy the entire anterior wall of the atrium.


General Features

The left ventricle forms the apex and the left surface of the heart, and participates in forming the sternocostal and diaphragmatic surfaces. Its myocardium is three times as thick as that of the right ventricle, and produces about three times the pressure. It receives blood from the left atrium, and expels it through the ascending aorta.

The relations of the left ventricle to other structures:


 Superior: Left atrium


 Anterior: Pericardium, left sternocostal wall of the thorax, lingula of the left lung


 Lateral: Pericardium, left mediastinal pleura, left lung, left phrenic nerve, and pericardiacophrenic vessels


 Medial: Interventricular septum


 Inferior: Diaphragm


External Features

The left ventricle is longer than the right, and forms the apex of the heart. The separation of the two ventricles is marked anteriorly by the anterior descending branch (left anterior descending artery [LAD]) of the left coronary artery and the great vein of Galen. Posteriorly, the separation is indicated by the posterior descending artery (usually a branch of the right coronary) and the middle cardiac vein. The rounded left (oblique) border is associated with the left marginal branch of the left circumflex artery. Superiorly, the ventricle is bounded by the great cardiac vein and the circumflex artery lying in the atrioventricular sulcus. Just above the sulcus are the left auricle, coronary venous sinus, and the left inferior pulmonary vein.

Internal Features

The cavity of the left ventricle is separated by the anterior leaflet of the mitral valve into an inflow tract and an outflow tract on the right. The smooth portion of the outflow tract, just beneath the aortic valve, is the aortic vestibule.

Here, the trabeculae carneae are more numerous and more interlaced than those of the right ventricle. They are best developed at the apex and on the posterior wall. They are absent in the region of the aortic vestibule.

Two papillary muscles are present: the anterior from the sternocostal wall, and the posterior from the diaphragmatic wall. Each is attached by tiers of chordae tendineae to both leaflets of the mitral valve. The upper portion of the interventricular septum is relatively smooth, with a lighter coloration. This is due to the downward cascade of the left bundle branch of the cardiac conduction system, just beneath the endocardium, and to a thin lamina of connective tissue.

Pseudotendons are a prominent feature of the chamber. There are numerous strands near the apical region. Occasionally, there are rather thick strands leaving the septal surface and bridging the chamber to reach the free wall or papillary musculature. These tendonlike structures typically contain a core of cardiac muscle, specialized for conduction.

The left atrioventricular orifice is oval and is slightly smaller than the right opening. It admits the tips of two fingers.

Two leaflets guard the opening forming the mitral valve (Fig. 7-20). The anterior (septal) leaflet is large, and semicircular or triangular in shape. The smaller posterior leaflet is known as the Merklin leaflet. The leaflets insert on the left atrioventricular fibrous anulus. Their free margins are attached by chordae tendineae to the papillary muscles. The scalloped margin of the posterior leaflet gives the impression of indistinct minor leaflets, often at opposite sides of the valve. Each of the valve leaflets possesses thickened nodules (nodules of Albinus) on its free margin, near the central points of apposition of the leaflets. Similar nodules are present on the tricuspid valve leaflets.

The aortic orifice lies in the superior wall of the ventricle, to the right of the atrioventricular opening and posterior to the orifice of the pulmonary trunk. Three semilunar cusps (right, left, and posterior) form the aortic valve (Fig. 7-21). Behind each of the cusps is an expanded region at the aortic base called the aortic sinus (of Valsalva).

The right coronary artery arises from the right aortic sinus; the left coronary artery takes origin at the left coronary sinus. The posterior sinus is often designated as the noncoronary sinus. It is located just cranial to the membranous part of the interventricular septum and to the site of entry of the left bundle branch of the conduction system into the left ventricle. In about 40 percent of people, the right conus branch of the right coronary artery leaves the right coronary sinus separately, with the result that there are two orifices behind the right aortic valve cusp.

Each of the cusps of the aortic semilunar valve has a free, crescentic border called a lunule. The lunule has a small, thickened nodule at its midpoint, the nodule of Arantius. The pulmonary semilunar valve possesses similarly named nodules, which strengthen the central point of apposition of the cusps in diastole. Adjacent lunules are interconnected by an intervening commissure that provides the fibrous framework supporting the cusp margin.


The following anatomic entities can be seen from an atrial aspect: the aortic valve, mitral valve, tricuspid valve, and right and left coronary arteries (Fig. 7-22).

Vascular Supply


There is a lack of uniformity in the terminology used to describe the positions of the coronary arterial ostia in relation to the aortic valve. Nomina Anatomica24 presents the terms right, left, and posterior. We agree with Turner and Navaratnam25 that this nomenclature is more appropriate for the embryologic disposition of the fetal heart. To describe the corresponding adult positions, they suggest the terms anterior, left posterior, and right posterior.

Muriago and colleagues26 reported the location of the coronary arterial orifices of the normal heart as follows (Figs. 7-23, 7-24, 7-25):

The left coronary artery arose within the left posterior aortic sinus (of Valsalva) in 16 (69%) [necropsy] specimens, above the sinutubular junction in five (22%), and at the level of the junction in two (9%). The distance of the left orifice from the zone of apposition between the left posterior and anterior aortic leaflets was between 13% and 61% of the width of the aortic sinus at the sinutubular junction. The right coronary artery arose within the aortic sinus in 18 (78%) specimens, above the junction in three (13%), and at the level of the junction in two (9%). The distance of the orifice from the zone of apposition between the leaflets hinged from the anterior and right posterior aortic sinuses was between 5% and 62% of the width of the aortic sinus at the sinutubular junction. An accessory coronary orifice was found in the anterior aortic sinus in 17 (74%) specimens, whereas a third orifice in this sinus was found in five hearts. The coronary arterial orifices are usually located within the aortic sinuses below the sinutubular junction, but are rarely centrally located. Accessory coronary arterial orifices are found in the majority of the anterior aortic sinuses.

Left Coronary Artery

The left coronary artery arises from a single ostium in the left coronary sinus behind the left cusp of the aortic valve. It divides rather quickly to form the anterior descending (anterior interventricular) artery and the left coronary circumflex artery (Figs. 7-26, 7-27).

Reich et al.27 reported a case of a 14-month-old girl in whom the left main coronary artery and the right coronary artery arose from separate ostia in the right sinus of Valsalva.

A left single coronary artery with a single orifice in the left aortic sinus was reported by Koizumi et al.28 The artery bifurcated into the anterior ventricular and circumflex arteries.

Left Anterior Descending Artery (LAD). The left anterior descending artery travels in the interventricular sulcus toward the acute margin near the apex. There it anastomoses with the posterior descending coronary artery, usually a branch of the right coronary artery. A variable number of deeply perforating septal branches pass from the LAD into the anterior part of the interventricular septum (Fig. 7-27). The first of these is usually the largest, and arises adjacent to the pulmonary valve. This branch regularly supplies the region of bifurcation of the common atrioventricular bundle, and is, therefore, of critical importance.

The LAD usually gives off several "diagonal" branches, so named for their oblique course toward the left side and the apex, passing parallel with the underlying superficial layer of cardiac muscle.

Left Circumflex Artery. The left circumflex coronary artery passes in the left coronary sulcus to reach the posterior surface of the left ventricle. En route, it gives off one or more diagonal branches to the anterior and anterolateral left ventricle, a left marginal branch (arteria margo obtusa) that is frequently large, and branches to the posterior surface of the left ventricle and left atrium.

The left coronary circumflex artery may give origin to the posterior interventricular (posterior descending) artery and the artery to the atrioventricular node; this occurs most frequently in males. This pattern of coronary distribution is referred to as left coronary dominance.

The term "coronary dominance" relates to the blood supply of the interventricular septum. In almost all cases, the LAD branch of the left coronary artery supplies the anterior two-thirds of the interventricular septum.

If the right coronary artery provides the posterior descending branch supplying the posterior one-third of the septum, an opportunity exists for the development of rich anastomotic interconnections within the septum between the left and right coronary arteries. These interconnections can provide potentially critical collateral supply in the event of coronary arterial disease. This form of coronary distribution is referred to as right coronary dominance.

When the left circumflex artery provides the posterior descending supply to the septum (left coronary dominance), an important potential communication between right and left coronary arteries within the interventricular septum is absent. In the event of gradual occlusion of the anterior descending or the main left coronary artery, branches of the posterior descending artery can provide collateral supply to the septum. Of course, the supply of the interventricular septum can, therefore, be in jeopardy in the event that both the anterior descending and posterior descending arteries are derived from a diseased left coronary artery.

Right Coronary Artery

After its origin from the right coronary sinus of Valsalva, the right coronary artery usually supplies all of the right atrium (together with the sinoatrial node) and the right ventricle. Right coronary arterial dominance results when the right coronary artery supplies the posterior descending artery. In this circumstance, it also provides supply to part of the left atrium posteriorly, part of the posterior surface of the left ventricle, the posterior papillary muscle of the left ventricle, and the atrioventricular node.

The first significant branch of the right coronary artery, the artery to the conus, usually passes in counterclockwise fashion around the conus or infundibulum. There, it frequently anastomoses with a branch of the LAD, forming the so-called arterial circle of Vieussens (Fig. 7-26).

The conus artery often rises from a separate ostium behind the right coronary cusp. This phenomenon, seen more often in older individuals, is probably attributable to growth and expansion of the region of the aortic sinus, wherein the origin of the conus artery becomes gradually incorporated into the base of the aortic valve. Coronary circulation originating from a single coronary ostium is rare. Neil et al.29 described the anatomic course of the right coronary artery arising from a solitary coronary ostium in the right coronary sinus.

Knowledge of the exact anatomy of anomalous coronary arteries of aortic origin is essential for surgical procedures. Felmeden et al.30 stated that the most common of these anomalies is an aberrant origin of the main left or right coronary artery from the wrong sinus of Valsalva.

Topaz et al.31 reported the occurrence of a variant posterior interventricular (posterior descending) coronary artery and its relation to the right coronary artery:

Acute thrombotic occlusion of an infarct-related artery is frequently found in patients presenting with myocardial infarction. In a patient with acute inferior wall myocardial infarction complicated by continuous chest pain and hemodynamic instability, emergency diagnostic coronary arteriography demonstrated a patent, infarct-related, 'pseudo' right coronary artery while, in fact, this vessel was a rare anatomic variant of the posterior interventricular branch with very early origin from the right coronary artery and the true right coronary artery was completely occluded by a thrombotic obstruction. Accurate anatomic-angiographic interpretation of the angiogram was crucial for successful performance of emergency recanalization and revascularization of the true right coronary artery with laser and balloon angioplasty. Once antegrade flow was restored another rare coronary variant was discovered, i.e., a sinoatrial node artery arising from the middle portion of the newly patent right coronary artery.

Nerantzis et al.32 reported that in somewhat fewer than 10 percent of cases, the right coronary artery perfused not only the right ventricle, but also supplied about half of the left ventricle by extending branches.

Nerantzis and Koutsaftis33 reported a case in which the left coronary artery arose in a common trunk with the right coronary artery from the right aortic sinus and proceeded via the ventricular septum to the left heart.

Sinoatrial Artery

The next branch of the right coronary artery regularly arises from the deeper aspect of the right coronary artery. It ascends the anterior wall of the right atrium, which it supplies; thereafter, it enters the sinoatrial node. In about 40 percent of individuals, this artery is derived from an anterior left atrial branch of the left coronary artery.

The right coronary artery passes in the right atrioventricular sulcus. It gives off several branches to the anterior surface of the right ventricle and a right marginal branch (arteria margo acutus) before reaching the diaphragmatic surface of the right ventricle, which it regularly supplies. As noted earlier, in most individuals, the right coronary artery crosses the crux. Near the crux, it gives origin to the posterior descending artery. At this same location, it provides origin to the atrioventricular nodal artery and a terminal branch to the diaphragmatic surface of the left ventricle.

Sow et al.34 used dissection of 45 specimens to study the artery of the sinoatrial node. They found a solitary artery in 88.89% and double arteries in 11.11%. In 64.45%, the artery arose from the right coronary artery; in 24.44%, the artery arose from the left coronary artery; in 11.11%, it arose from both. The pathway of the artery arising from the right coronary artery was variable, while the pathway from the left coronary artery was relatively uniform. Sow and colleagues suggested that some arrhythmias during cardiac surgery could be secondary to disturbance of the arterial supply of the sinoatrial node.

Coronary Distribution and Anastomoses

From the arteries visible beneath the epicardium, perforating branches enter the myocardium. Small branches from the perforators arborize immediately to supply the outer two-thirds of the myocardium (class A vessels). The perforating arteries continue, without further branching, to end in a large subendocardial plexus (class B vessels). The papillary muscles are thus supplied by class B vessels. Homocoronary and intercoronary anastomoses between branches of the right and left coronary arteries can be of great significance in cardiac function and coronary vascular disease.

Intercoronary anastomoses (Fig. 7-26) are commonly present at the following sites:


 About the base of the pulmonary conus, between the left anterior descending branch of the left coronary, and the conus branch of the right coronary artery


 In the interventricular sulci, between the anterior descending and posterior descending arteries


 On the diaphragmatic surface of the left ventricle, between terminal twigs of the right coronary artery and the left coronary circumflex artery


 Within the interventricular septum, between perforating septal branches of the anterior and posterior descending arteries



For the most part, the coronary veins pass with the coronary arteries, usually lying superficial to them (Fig. 7-28).

The great cardiac vein (of Galen) arises near the apex in the interventricular sulcus. It ascends to the atrioventricular sulcus, where it turns to the left in company with the left coronary circumflex artery. At the obtuse margin, the great cardiac vein joins the oblique vein of the left atrium (this is where the coronary venous sinus has its embryologic beginning). The coronary venous sinus empties into the right atrium, to the left of the opening of the inferior vena cava.

The oblique vein (of Marshall) of the left atrium drains the posterior wall of the left atrium. It is the vestigial remnant of the left common cardinal vein. Its junction with the great cardiac vein marks the beginning of the coronary venous sinus. If the embryonic left common cardinal vein is retained, bilateral superior venae cavae will be present, with great enlargement of the coronary sinus occurring with the formation of the left superior vena cava.

The posterior vein or marginal vein of the left ventricle ascends the diaphragmatic surface of the left ventricle, draining it. It ends in the coronary sinus.

The middle coronary vein passes upward in the posterior interventricular sulcus, superficial to the artery. It receives tributaries from both ventricles and the interventricular septum. It ends in the coronary sinus, near its termination.

The small cardiac vein arises on the acute margin of the right ventricle. It passes in the right coronary sulcus to join the extreme right end of the coronary venous sinus.

The anterior cardiac veins, three or four variably sized veins, arise from the sternocostal surface of the right ventricle. They cross superficial to the right coronary artery and pierce the margin of the right auricle to drain directly into it. Some anterior cardiac veins join the small cardiac vein.


The lymphatic flow passes from the lymphatic capillaries to the epicardial vessels which follow the coronary arteries. At the right and left collecting trunks, the lymphatic flow diverges. From the right collecting trunk, it passes to the mediastinal nodes. From the left collecting trunk, it passes to the caval node of the tracheobronchial group, which is located between the aorta and the superior vena cava.



The intrinsic innervation of the heart is provided by the cardiac conduction system. The parts of the system are named the sinoatrial node, the atrioventricular node, the three internodal pathways, the atrioventricular bundle (bundle of His), the left bundle and its branches, the right bundle, and the ventricular system of Purkinje fibers (Figs. 7-29, 7-30).

Some researchers believe there are specialized cells that conduct the electrical forces in the atria while others believe there are only preferential pathways. We are grateful to our esteemed colleague J. Willis Hurst for permission to quote from his Ventricular Electrocardiography35 on the different theories of cardiac conduction.

Anton Becker, one of the modern authorities on the conduction system of the heart,36-39 does not believe that there is any specialized conduction tissue within the atria. However, he maintains that there are preferential electrical pathways within the atria, pointing out that the right atrium is a "bag of holes."39 There are five such holes, created by the openings of the superior and inferior vena cava, the opening of the coronary sinus, the fossa ovalis, and the opening of tricuspid valve.39 There are also five "holes" in the left atrium. They are the openings of four pulmonary veins and the opening of the mitral valve. By comparison, each ventricle has only two "holes." Becker also points out that some of the tissue surrounding some of the holes in the atria is fibrous tissue and not muscle.39The remaining atrial tissue, made up of atrial cells crowded together, forms the preferential electrical pathways. These preferential electrical pathways are called internodal tracts. They are labeled as the anterior, middle, and posterior tracts. The anterior tract was first described by physiologist Jean Bachmann40,41 of the Emory University School of Medicine. It travels anteriorly from the sinus node to reach the atrioventricular node, and simultaneously travels into the left atrium.41 The middle tract travels from the sinus node and passes posteriorly around the superior vena cava and down the atrial septum to reach the atrioventricular node. The posterior tract travels posteriorly through the crista terminalis and down the posterior portion of the atrial septum to the atrioventricular node.41 James41has depicted the internodal tracts.


The nerve supply of the heart originates from cardiac branches of the vagus nerves (parasympathetic), and from fibers of the sympathetic trunk (Fig. 7-31). For all practical purposes, this is the extrinsic innervation. With organ transplantation (liver, heart, etc.), it has been found that the transplanted anatomic entity can function well without any extrinsic innervation.


The sympathetic system includes cervical cardiac branches, cervicothoracic branches from the stellate ganglion, and thoracic visceral nerve branches from the first four thoracic levels of the sympathetic chains. These fibers are cardio-accelerators, vasodilators, and sensory (for pain).

Figures 7-32 and 7-33 offer a highly diagrammatic presentation of the sympathetic and parasympathetic systems of nerve supply to the heart.

Parasympathetic (Vagus Nerves)

The parasympathetic system includes one cervical branch, one or two cervicothoracic branches at the thoracic inlet (via the main vagus or right recurrent laryngeal nerve), and two to four thoracic branches from the main vagus nerve and its left recurrent branch. The parasympathetic fibers of the vagus nerve are principally cardio-inhibitory, the cholinergic fibers effecting a reduction of the rate of depolarization of cardiac pacemaker muscle fibers. Most of the nerve fibers carried by the vagus are sensory, with those from the heart carrying information from baroreceptors, stretch receptors, chemoreceptors, and so on.

According to O'Rahilly,42 the topographic anatomy and pathways of these cardiac nerves are extremely variable. We agree. The thoracic surgeon should be familiar with variations of the cervical, cervicothoracic, and upper thoracic cardiac nerves. These nerves end, variably, at the connective tissue of the heart and within the adventitia of the vessels.

In a study of human hearts, Armour et al.43 noted the presence of far more ganglion cells on the atria and ventricles than had been reported previously, with an estimate of more than 14,000 neurons. This finding provides some evidence of an intrinsic cardiac neuronal synaptic network of great complexity. The presence of unipolar and bipolar neurons (usually assumed to be sensory neurons), in addition to multipolar cells (parasympathetic?), is intriguing. It underscores our lack of understanding of the possible highly complex cardiac visceral neuronal network. The atrial component of this network, in particular, may have implications applicable to the methodology employed in cardiac transplantation.



 The vagus nerves transmit their general sensory fibers from viscera upward, to superior and inferior sensory ganglia at the base of the skull, and then into the brain. Pain fibers carried by erstwhile sympathetic cardiac nerves are transmitted from the sympathetic chains by communicating rami, to upper thoracic spinal nerves, and thence to the spinal cord. Of course, the above statements are oversimplifications, for we know that there are communications between vagal and sympathetic cardiac nerves.


 The anatomic distribution of cardiac pain



– Anterior chest (retrosternal)


– Neck


– Lower jaw


– Left shoulder


– Left arm, medial aspect


– Left hand


– Right arm (occasionally)


 Preganglionic sympathetic fibers synapse with cervical and thoracic ganglia. Postganglionic sympathetic fibers travel together within cardiac branches of the sympathetic trunk. Are there synapses with certain cardiac ganglion cells? We do not know.


 Preganglionic vagal fibers are distributed to the cardiac ganglia via the vagus. Postganglionic vagal fibers provide rich innervation to the sinoatrial and atrioventricular nodes, resulting primarily in a negative chronotropic effect; that is, they act to reduce the rate of contraction.


 To what degree are postganglionic parasympathetic fibers distributed to ventricular muscle? If this distribution does occur, what are the effects? We are not sure.


 The cardiac plexus is formed by the meeting of the sympathetic and parasympathetic fibers at the base of the heart (Fig. 7-34). It is formed anterior to the bifurcation of the trachea, superior to the bifurcation of the pulmonary trunk (very close to its adventitial wall), and at the posteromedial aspect of the arch. A study by Mizeres44 emphasized that the cardiac plexus is a single anatomic entity. It is not composed of superficial (below the aortic arch and anterior to the right pulmonary artery) and deep (posterior to the aortic arch and anterior to the tracheal bifurcation) entities, as has often been described (Fig. 7-35).


 The right vagus nerve acts especially upon the sinoatrial node. The left vagus nerve acts chiefly upon the atrioventricular node. This is reflective of embryonic association of the right vagus with the right horn of the sinus venosus and the left vagus with the left horn, each of which contained specialized pacemaking cells.



Sinoatrial Node

The primary pacemaker of the heart, the sinoatrial or sinus node (Fig. 7-36) is an elongated, ellipsoidal mass of tissue. It lies at the junction of the superior vena cava and the right auricle at the cranial end of the sulcus terminalis. The node varies from about 0.5 to 1.5 cm in length, and 1 to 5 mm in thickness.

It might, indeed, be said that the connective tissue of the sinoatrial node forms an apparent, enormous adventitia of the sinus nodal artery. Specialized pacemaking cells are located within the connective tissue of the sinoatrial node.

The artery of the sinus node is an early rising branch of the right coronary artery in most people, with the artery reaching the node after ascending the anterior wall of the right atrium. In other people, the artery arises from the proximal part of the left coronary or the left circumflex artery. In these circumstances, the artery first passes up the anterior wall of the left atrium. Then it passes in counterclockwise fashion around the base of the superior vena cava to enter the node.

Arising from the sinus node are anterior, middle, and posterior internodal pathways (see earlier discussion). These allow rapid transmission of the stimulating electrical impulse to the atrioventricular node. The contractile impulse spreads in radial fashion through the atrial myocardium. Numerous parasympathetic ganglion cells can be found in the vicinity of the sinoatrial node in the connective tissue beneath the epicardium.

The principal internodal pathway in humans passes along the crista terminalis and under the inferior vena caval orifice to reach the atrioventricular node. The other two paths course, in curving fashion, anterior to the superior vena cava (the anterior pathway), or posterior to the superior vena cava (the middle path), then down through the interatrial septum to reach the atrioventricular node. The anterior path gives off a branch which passes over a thin band of muscle (Bachmann's bundle) to reach the left atrium, for the activation of its musculature.

Atrioventricular Node

The atrioventricular node is a small nodule of tissue lying beneath overlying myocardium of the medial wall of the right atrium. The AV node is located on the right fibrous trigone, in a triangular region bounded by the ostium of the coronary sinus, the septal cusp of the tricuspid valve, and the membranous part of the interventricular septum.

Parasympathetic ganglion cells can be detected in the loose connective tissue adjacent to the node. The fibers of the atrioventricular node are specialized in structure (narrow and serpiginous in form, with a paucity of intercalated disks) for a temporary delay of the stimulating impulse, although they can also function as a secondary cardiac pacemaker. In that function, the fibers depolarize at a slower rate (about 40/min versus 70/min).

The arterial supply of the AV node is usually derived from the right coronary artery as it crosses the crux posteriorly. This is the region where the four major chambers are most closely approximated. The artery that crosses the crux, be it the terminal part of the right coronary or the left coronary circumflex, exhibits a horseshoe-shaped curve into the region of the crux. From this site, the atrioventricular nodal artery arises. Collateral arterial supply for the node is received from an anterior atrial branch of the left coronary artery, by way of a small vessel which passes through the lower part of the interatrial septum, the so-called "arteria anastomotica auricularis magna" (of Kugel).

James45 gave a succinct description of the anatomic entity that bears his name, the U-turn of James:

At the crux, the crossing coronary artery makes a deep "U"-turn beneath the posterior interventricular vein, and emerges into the epicardium again on the other side (Figs. 7-37, 7-38, 7-39); this observation is true whether the crossing artery comes from the right or the left side. The plane of this turn is usually perpendicular (though it may skew) to the interatrial and interventricular septa, and the turn itself passes through their junction. The atrioventricular node artery arises from this "U"-turn, and its point of origin is usually near the deepest penetration of the turn.

That this "U"-turn has escaped the attention of most anatomists is not surprising, because of its surface appearance. Casual inspection suggests both the left circumflex and the right coronary arteries commonly meet at the crux and form parallel descending arteries (Fig. 7-40). Actually, this is so unusual that it may be considered a rare exception. As a rule, either the left or right coronary artery alone (most often the latter) makes its "U"-turn and supplies all the visualized posterior descending arteries near the interventricular sulcus. . . The deceptive appearance of the surface anatomy of these arteries at the crux has undoubtedly led to some mistaken classifications of coronary artery distribution.

The triangle of Koch is another structure associated with the pathway of the artery of the atrioventricular zone. Ferguson and Cox46 describe it as "bounded by the annulus of the tricuspid valve inferiorly, the tendon of Todaro superiorly, and a line drawn between the coronary sinus and the tricuspid annulus posteriorly" (Fig. 7-41).

Sow et al.47 studied the artery of the atrioventricular node by dissection of 38 anatomic specimens, with the following findings:


 In most cases, the artery is solitary


 In rare cases, the artery is double


 In most cases, the artery originates at the level of the U-turn of James, on the right side. On the left side, the artery originates from the terminal part of the circumflex artery


 Respect for the triangle of Koch, the base of the interatrial septum, and the region of the intersection of the cardiac sulci will avoid injury to the artery of the atrioventricular node


Atrioventricular Bundle

The atrioventricular bundle arises from the deep part of the atrioventricular node. It penetrates the right fibrous trigone to reach the upper part of the muscular interventricular septum, deep to the membranous part of the septum. Here, it immediately gives origin to a broad left bundle branch. Ensheathed in insulating collagenous tissue (the "sheath of Curran"), it then proceeds along the top of the muscular septum before appearing in a subendocardial position in the right ventricle. Here, it emerges as the right bundle branch, adjacent to the papillary muscle of the conus in the vicinity of the crista supraventricularis.

Bundle Branches

The right branch is compact and narrow as it passes along the moderator band (trabecula septomarginale) to the anterior papillary muscle of the right ventricle. Beyond this point, smaller fascicles pass in all directions to the right ventricular myocardium; some fibers pass back up upon the interventricular septum, others enter the myocardium of the ventricular wall.

The left bundle branch, as noted before, makes its appearance in the left ventricle just beneath the non-coronary cusp of the aorta. It shortly divides into an anterior fascicle (the left anterior superior branch) and a posterior fascicle (the left posterior inferior branch) (Fig. 7-29); these pass subendocardially down the interventricular septum, ensheathed in a lamina of collagenous tissue. Near the apex, numerous strands of fibers (some of which are independent and long enough to be called pseudotendons) carry the specialized cells (of Purkinje) to all parts of the ventricle. As they enter the ventricular substance, the cell types become almost indistinguishable from normal working myocardium.

Small fascicles from the common bundle or the proximal portion of the main branches serve the nearby muscular fibers of the interventricular septum. These are called the paraspecific fibers of Mahaim. They are observed more frequently in infant than in adult hearts. During repairs of congenital malformations such as interventricular septal defects, the atrioventricular bundle is vulnerable to injury in the region of the membranous interventricular septum.

Great Vessels in the Thorax

Great Arteries


The pulmonary trunk begins at the pulmonary orifice of the right ventricle. Externally, it arises smoothly from the infundibulum. The first 4 cm of the trunk lie within the pericardium, which envelops the pulmonary trunk and the aorta in a common sleeve of serous pericardium.

At its origin, the pulmonary trunk is anterior. The proximal end of the trunk lies between the anteromedial tips of the two auricles. The pulmonary trunk passes backward and to the left, lying in the concavity of the aortic arch. Here, it bifurcates: the left pulmonary artery passes anterior to the descending aorta; the right pulmonary artery passes posterior to the ascending aorta and the superior vena cava. A persisting portion of the ductus arteriosus (which is sometimes not occluded) connects the superior border of the trunk with the inferior part of the aortic arch.

A large embolus, most likely arising from the lower extremity venous network, can obstruct the pulmonary trunk or its branches. This event frequently results in the patient's demise. Embolectomy for pulmonary embolism employs either of two procedures. The closed procedure may be accomplished by cannulation of the femoral vein or of the right internal jugular vein under fluoroscopy, and by possible removal of the thrombus by suction. The open procedure is by median sternotomy, incision of the pulmonary artery, and removal of thrombi from the right and left pulmonary arteries and their branches, with the help of a Fogarty catheter.


The aorta leaves the heart almost vertically, behind the pulmonary trunk and the medial tip of the right auricle. It gives off the right coronary artery from the right aortic sinus and the left coronary artery from the left aortic sinus.

The ascending aorta lies wholly within the pericardium, the upper limit of which is at the level of the plane of the sternal angle and the T4/T5 intervertebral disk. This plane marks the end of the ascending aorta, the beginning and the end of the aortic arch, and the beginning of the descending aorta. It also coincides with the:


 Division of the superior and inferior mediastina


 Junction of the left and right brachiocephalic veins to form the superior vena cava


 Closest approximation of the right and left mediastinal pleurae


 Bifurcation of the trachea


Coady et al.48 stated that their study supports the role of genetic factors influencing familial aggregation of thoracic aortic aneurysms (TAA). TAA in association with multiplex pedigrees represent a new risk factor for aneurysm growth. Pedigree analysis suggests genetic heterogeneity. The primary mode of inheritance seems to be autosomal dominant, but X-linked dominant and recessive modes are also evident.

Great Veins


The superior vena cava is formed by the junction of the right and left brachiocephalic (innominate) veins. The superior vena cava receives the azygos venous arch, and enters the pericardium to the right of the ascending aorta. No valve guards its entrance into the right atrium.

The entire length of the vessel is 7 cm, and half of it lies within the pericardium. The relations of the extrapericardial portion are:


 Anterior: Sternocostal junction, right pleura


 Posterior: Right vagus nerve, right pulmonary artery, mouth of the azygos arch, pleura


 Right: Right phrenic nerve, azygos arch, pleura


 Left: Ascending aorta



The right vagus nerve descends to the left of the arch of the azygos vein.

Within the pericardial cavity, the relations of the superior vena cava are:


 Anterior: Free in the pericardial cavity


 Posterior: Left atrium, right pulmonary artery, posterior and lateral pericardium


The pericardium is fixed firmly to the wall of the superior vena cava. Intrapericardial mobilization is possible after careful division of these pericardial attachments.

According to Iannettoni and Orringer,49 superior vena cava syndrome (obstruction of the SVC) is secondary to mediastinal malignancy in 75 percent of cases, and due to benign processes in 25 percent of cases. Clinical presentation of the syndrome includes "facial and upper extremity edema, distention of the veins of the head, neck, arms, and upper thorax, and a dusky rubor of these areas suggesting cyanosis."

Schindler and Vogelzang50 indicate that for the patient with superior vena cava syndrome (SVCS) secondary to malignant process, radiation and anticoagulation provide inadequate relief of symptoms and that the best palliation may be obtained with techniques such as thrombolysis, angioplasty, and stents. The above authors find that SVCS secondary to the benign process is more problematic, and point out that the long-term results of stenting are not yet known. They suggest that the risks and benefits of stenting versus surgical bypass should be assessed for these patients.

According to Downs et al.,51 perforation frequently occurs at the junction of the SVC and right atrium during central venous catheterization.


The inferior vena cava pierces the diaphragm at the level of the eighth thoracic vertebra, and enters the right atrium at the level of the xiphisternal joint. Its entrance is guarded by a fold of tissue, the eustachian valve. This part of the intrapericardial inferior vena cava is about 1 cm long. An extrapericardial portion is nearly or wholly nonexistent. If it is present, it is related to the right pleura and the right phrenic nerve. Practically speaking, the "thoracic" and the intrapericardial portions are identical.

For more information about the inferior vena cava, we strongly recommend that the reader consult Surgery of the Chest by Sabiston and Spencer52 and Embryology for Surgeons by Skandalakis and Gray.3


The pulmonary veins are fixed to the pericardium. Within the pericardium, they are barely visible over only a part of their circumference; the dorsal mesocardium effectively conceals their more superior and lateral aspects. Together with their mesocardial attachments, the inferior vena cava and the posterior aspect of the left atrium, the pulmonary veins form superior and lateral limits for the oblique pericardial sinus.

Of the four veins, the left inferior is the most visible; the right inferior is the least so. In 25 percent of individuals, the left pulmonary veins join within the pericardium to form a common left pulmonary vein. In only 3 percent is a common right pulmonary vein formed in this manner.

During surgery, it is prudent to identify the location of all pulmonary veins for septal defects, since partial anomalous drainage may be present.53


The wall of the heart is composed of three layers: the epicardium, the myocardium, and the endocardium. The wall contains the fibrous skeleton for the attachment and support of the valves, nerves (internal conducting system), arteries, veins, and lymphatics.

The epicardium consists of connective tissue supporting the lining of mesothelial cells. In the myocardium, there are special muscle fibers containing large mitochondria and sarcoplasmic reticulum. There is no regeneration or replacement of the cardiac cells. They do not divide; they are succeeded by fibrous connective tissue. The endocardium is composed of smooth endothelial cells. The fibrous skeleton is composed of dense connective tissue.

Histology of the pericardium and great vessels will not be addressed here.


It is a daunting task to present the physiology of the heart, pericardium, and great vessels in any anatomy book. The subject is far too complex for the scope of this chapter.

A striking example of these wonders can be found in Severs'54 description of the cardiac muscle cell:

The cardiac myocyte is the most physically energetic cell in the body, contracting constantly, without tiring, 3 billion times or more in an average human lifespan. By coordinating its beating activity with that of its 3 billion neighbors in the main pump of the human heart, over 7000 liters of blood are pumped per day, without conscious effort, along 100,000 miles of blood vessels.

The interested student will find a storehouse of information in the most recent edition of Hurst's The Heart.55 The quadruplex fundamental mechanics of cardiac muscle (preload, afterload, contractility, and heart rate), nervous control, and regulation of blood flow are explained in depth in this text.


The complex anatomy of the heart, its location, and its multiple potential problems (both congenital and acquired) do not permit detailed coverage of cardiac surgery in this book. Therefore, we will present only some selected applications.

The excellent works of Kubik and Healey,56 Edwards et al.,57 and Wilcox and Anderson58 provide information on this subject.

The era of minimally invasive surgery for the heart lies ahead. It must be emphasized that this work is currently in a most embryonic state. By all means, the student of cardiac surgery should be familiar with this promising horizon that perhaps will play a great role in treating coronary artery disease and other heart disease. Fishman et al.59 reported that minimally invasive direct coronary artery bypass (MIDCAB) avoids median sternotomy. This reduces cardiac surgical trauma.

Approaches to the Right Side of the Heart

Two incisions provide a pathway for this approach: median sternotomy and right anterolateral thoracotomy.

The anatomic entities involved are:




 Superior vena cava




 Left atrium


 Right pulmonary artery


 Azygos vein


 Right pulmonary veins


The length of the superior vena cava is approximately 7 cm. Its proximal half is outside the pericardium; its distal or caudal half lies within the pericardium, emptying into the right atrium. The azygos vein empties into the posterior wall of the superior vena cava, just above the pericardium.

The topography of communication between the azygos vein and the superior vena cava should be remembered if ligation of the SVC is absolutely necessary. Cerebral edema and death may follow a sudden ligation of the superior vena cava if the azygos vein is obstructed. However, ligation that takes place between the azygos and the right atrium does not jeopardize survival if the azygos system is intact and unobstructed.

The anatomic logic of ligation of the superior vena cava must be remembered. We want to emphasize that the above-mentioned ligation should be performed ONLY if it is absolutely necessary. The azygos and hemiazygos systems of veins are quite variable; remember that this is the venous drainage collateral network between the superior vena cava and the inferior vena cava.

The entrance of the superior vena cava into the pericardial cavity is located to the right of the aorta. Posteriorly, it is attached to the left atrium and right pulmonary artery. The four pulmonary veins enter the left atrium through its lateral wall.

Bouchard et al.60 advised that aortic valve replacement can be accomplished through a ministernotomy approach. Perioperative results are similar to those obtained through a conventional sternotomy.

Approaches to the Left Side of the Heart

The incision usually used for this approach is median sternotomy; rarely posterolateral thoracotomy is used. With either of these two incisions, the left side of the heart, the great arteries, and the pulmonary veins can be exposed. Ali et al.61 reported higher cost effectiveness and greater patient satisfaction with subtotal median sternotomy than standard sternotomy.

Protect the left phrenic nerve and the pericardiophrenic artery and vein; these are attached to the left side of the pericardium. An anterior approach in relation to the neurovascular bundle is mentioned by Wilcox and Anderson.58

The descending aorta is exposed using anterior retraction of the left lung and division of the mediastinal pleurae posterior to the left vagus nerve. The recurrent laryngeal nerve should be protected in its passage around the lower border of the ligamentum arteriosum; prepare carefully and avoid traction of the vagus nerve.

Surgical Applications of Coronary Circulation

Given the high incidence of coronary arterial atherosclerosis and its associated mortality, it is readily understandable that coronary arterial bypass is one of the most common surgical procedures. Surgery is performed to forestall likely myocardial infarction or to relieve ischemic symptoms, persistent angina, and/or congestive heart failure from severe occlusive disease of the coronary arteries.

The internal thoracic arteries and segments of the radial artery or saphenous veins are the commonly used conduits to bypass occluded, or nearly occluded, arterial segments. One end of the vein graft is anastomosed with the ascending aorta and the other to the coronary artery distal to its stenosis or occlusion. The graft must be appropriately oriented with regard to the valves within so that arterial flow is not impeded. The internal thoracic artery is released from its parasternal position, then transected (usually at the sixth intercostal space), and its end is anastomosed to a coronary artery distal to the occlusive process.

Jones et al.62 reported that surgical myocardial revascularization using the internal thoracic artery, the gastroepiploic artery, the radial artery, the inferior epigastric artery, and other arterial and venous conduits, has benefited hundreds of thousands of patients.

Percutaneous transluminal coronary angioplasty is a less invasive procedure for enhancing coronary arterial flow; compressing the arterial plaque expands the size of the functional arterial channel. The balloon-tipped catheter is introduced by way of the femoral or brachial artery. With the aid of direct fluoroscopy, the catheter is advanced to the aorta and the selected coronary ostium.



 The superior intercostal vein between the phrenic and vagus nerves can be ligated with impunity.


 The left thoracic duct heads toward the left subclavian vein. This duct can also be ligated with impunity. Pérez et al.63 presented a case of left pleural chylothorax as a complication of coronary artery bypass graft.


 In most cases, section of the upper five thoracic dorsal roots will stop cardiac pain.


 Similar results can be obtained from cutting the rami communicantes to the upper five spinal nerves. The variability of the number and courses of these rami must be kept in mind in performing sectioning of these nerves, however.


 Sternobronchial fistula complicating coronary surgery was reported by Mand'ak et al.64


Anatomy of Cardiac Transplantation

This not a presentation of technique. We simply present the anatomic entities involved with donor cardiectomy and recipient transplantation.

Spann and Van Meter65 reported that cardiac transplantation is an effective and life-saving option for patients with congestive heart failure who do not respond to medical treatment.

Anatomy of Cardiectomy (Donor)


1. Vertical midline incision of the sternum and abdominal wall


2. Division of the pericardium


3. Careful dissection of the superior vena cava


4. Careful dissection and separation of the aorta from the main pulmonary artery


5. Careful exposure of the right superior pulmonary vein


6. The superior vena cava is ligated


7. Incision of the superior vena cava and right superior pulmonary vein for decompression of the heart


8. Distal ascending aorta is cross-clamped


9. Excision of the heart by transection of the inferior vena cava, all pulmonary veins, distal ascending aorta, and right and left pulmonary arteries


Anatomy of Orthotopic Cardiac Transplantation (Recipient)


1. Cross-clamping of the aorta


2. Incision of the right atrium down to the coronary sinus


3. Division of the aorta and pulmonary artery close to the valves


4. Incision of the left atrium at the dome with extension of the incision to the atrial septum


5. Right atrial excision


6. The remnants of the atrium are divided, being extremely careful to preserve adequate tissue around the pulmonary veins


7. Removal of the heart


8. Anastomoses



a. Left atrium


b. Right atrium


c. Pulmonary artery


d. Aorta



Blunt cardiac trauma can be just a contusion or rupture to the cardial wall. According to Mayfield and Hurley,66 blunt chest injury is responsible for 5% of American highway deaths each year. In an autopsy review after blunt chest trauma, Parmley et al.67 reported a 64% incidence of cardiac rupture, with only a 7% survival of more than 30 minutes. Tassiopoulos et al.68 and Symbas et al.69 presented discussions of cardiac rupture due to blunt trauma.


A variety of complications can occur during or following cardiac procedures. Many of them are minimized or avoided when the surgeon is well informed about the anatomy of the heart and great vessels, has accurately diagnosed the cardiac lesion, and has planned for its correction.

Roe70 stated:

When cardiac surgery is contemplated, the functional pathology and the operative plan must be established from the diagnostic studies. Evaluation and decision based on operative findings have proved to be treacherous. Surgical exposure is restricted and visualization in the collapsed, empty heart can easily mislead the operator about the presence or severity of functional pathology. Ventricular septal defects can be multiple and obscure; anomalous or fistulous pathways may be difficult to identify. Pathological anatomy of a valve often correlates poorly with functional performance. . . External localization of critically obstructive lesions in coronary arteries is obscured by the diffuse character of the atherosclerotic process.

It is, therefore, axiomatic that safe and effective thoracic surgery cannot be performed without accurate, reliable, and unmistakable diagnostic studies. The surgeon subjects his patient to unjustifiable risk if he cannot be personally satisfied that the studies are of sufficient quality and validity to remove uncertainty about the appropriate procedure, or if he believes that reliable decisions can be made on the basis of operative findings. He must also be certain about the absence of associated pathology which could jeopardize the outcome or require simultaneous attention.

Pericardial Complications


The heart, coronary vessels, internal thoracic vessels, and lungs can be injured by careless paracentesis. Possible results include perforation of the stomach, perforation of the colon, pneumothorax, and pneumopericardium.

Bleeding can occur secondary to laceration of the coronary artery, right ventricle, and/or right atrium. Tamponade, hemopericardium, and (rarely) hemothorax are also possible complications.

Pericardiotomy and Pericardiectomy

Contamination of the pleural cavity can be avoided by using the subxiphoid approach.

Bleeding is a possible complication of pericardiectomy.

Complications of Approach

Median Sternotomy

Many of the complications from this incision are due to preexisting, predisposing factors. Median sternotomy in the presence of a greatly enlarged right ventricle or an aneurysm adhering to the posterior plate of the sternum may result in trauma of these structures and major hemorrhage, whether the surgery is being performed for the first time or, especially, when it is being re-done.

A study by Demetriades et al.71 concluded that subclavian and axillary vascular injuries are highly lethal. For surgical exposure they advised clavicular incision; for proximal injuries, a median sternotomy is added to provide access to both right and left subclavian vessels (Fig. 7-42, Fig. 7-43, Fig. 7-44).

Bleeding to a much less catastrophic degree may be caused by injury of other organs such as the thymus (particularly its veins), the internal thoracic or inferior thyroid artery, and the lungs.

Unilateral injury (or extremely rarely, bilateral injury) of the vagus or phrenic nerve may occur, resulting in paralysis of a vocal cord or the hemidiaphragm. Excessive spreading of the upper third of the sternotomy can result in brachial plexus injury, due to its stretching or compression against the first rib.

Awareness of the presence of predisposing factors and meticulous surgical technique prevent complications. Infection is a later complication, resulting in mediastinitis.

To interested readers, we highly recommend the book Median Sternotomy: Historical Perspective and Current Application by Dalton and Connally.72

Lateral Thoracotomy Through the 4th, 5th, or 6th Interspace

Immediate complications of lateral thoracotomy are very rare. Bleeding may occur from the intercostal vessels or the internal thoracic artery, or from the lung when it is adherent to the chest wall. Extremely rare but potentially devastating complications include cerebrospinal fluid leakage (with or without pneumocephalus), and paraplegia following packing of the costal spine junction of the incision with Gelfoam.

Postthoracotomy chest pain is a common late sequela of lateral thoracotomy. Pain is occasionally due to neuroma formation of the intercostal nerve. In the majority of cases, the cause of pain is unknown.

Cardiac Complications

Ischemic and structural injuries to the heart are common complications of cardiac procedures. Ischemic injury of the myocardium can be minimized or prevented by protecting the heart during cross-clamping of the aorta. This is accomplished by antegrade and retrograde perfusion of the coronary arteries with cardioplegic solution. Supplementary local hypothermia is achieved by placing ice saline slush on the heart.

Precise knowledge of the anatomy of the heart, and of congenital or acquired lesions, coupled with precise surgical technique, will result in minimizing or avoiding other anatomic complications of cardiac surgery. Here, it may be of value to emphasize again some important cardiac structures.


 The sinoatrial node is located under the anterolateral junction of the superior vena cava and the right atrial appendage. According to Bolling,73 its blood supply is the sinus node artery springing from the right (60%) or the circumflex artery, which may pass anterior or posterior to the superior vena cava.


 The atrioventricular node is located within the triangle of Koch (which consists of the anulus of the tricuspid valve, the coronary sinus ostium, and Todaro's tendon). It is found at the muscular atrioventricular septum on the right atrial side of the central fibrous tendon. In most cases, it is located just above the coronary sinus. The atrioventricular node may be injured during mitral procedures due to the close relation of its left part to the anulus of the mitral valve. The posterior descending artery primarily supplies the node.


 The pathway of the bundle of His starts from the atrioventricular node. According to Bolling,73 it travels on the left side of the ventricular septum in 80% of cases. After passing between the septal and anterior leaflets of the tricuspid valve, it finally bifurcates beneath the commissure of the right and noncoronary cusps of the aortic valve into left and right branches.


 Supraventricular accessory conduction pathways are not present in the area between the left and right fibrous trigones, because there is no atrial muscle in proximity to the ventricle. According to Titus,74 another area lacking supraventricular accessory pathways is the pyramidal space, which consists of the fibrous trigone, epicardium, and left ventricular posterior superior process. This space contains fat pads, coronary sinuses, the atrioventricular node artery and possible posterior septal pathways.73 The four anatomic areas where accessory conduction pathways can occur are shown in Figure 7-45.


Complications of Great Vessels

Pulmonary Trunk

The anatomic complications of surgery of the pulmonary trunk (artery) are those following embolectomy for pulmonary embolism, employing either a closed or open procedure. Bleeding is an anatomic complication in both procedures. In the open procedure, complications are those usually associated with thoracotomy complications. Mortality is very high.

Thoracic Aorta

We will present the complications of only the following two surgical procedures: correction of patent ductus arteriosus and correction of coarctation of the aorta.


Complications include:


 Bleeding secondary to a tear at the wall of the ductus, or by misplacement and slippage of a clamp, with bleeding from the aorta or pulmonary artery


 Bleeding from the incision of the chest wall, with hemothorax


 Injury of the left recurrent nerve


 Injury of the left phrenic nerve


For further information we recommend the excellent book Surgery of the Chest, by Sabiston and Spencer.52


Complications include:


 Bleeding secondary to slippage of a nonserrated clamp, or from a tear of an aneurysmal intercostal artery


 Injury of the thoracic duct with chylothorax


 Injury of the left recurrent nerve


 Paraplegia secondary to poor collaterals, and distal hypotension secondary to cross-clamping of the aorta


 Mesenteric vasculitis which may culminate in ischemia or gangrene of the affected bowel


 Severe delayed hypertension


 Read an Editorial Comment




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