The heart in modern practice; diagnosis and treatment

Front matter

Class T?C, (n 9. 1 Book H 5 Copyright N?__

COPYRIGHT DEPOSrr.

Pulmonary artery

Preface

It is well known that since the introduction of graphic methods of examination, extensive advances have been made in the knowledge of the heart in health and disease. Unfortunately, an acquaintance with this progress in cardi¬ ology can be gained only by a rather wide reading of the literature, as, at present, I am aware of no single book in English which is suitable to recommend to the student or physician who asks for the name of a single volume in w r hich he may read up on the subject. The interest in the study of the abnormal rhythms of the heart has been so great that many of the recent authors have limited them¬ selves to a presentation, often admirable it is true, of this aspect alone. There seems, then, in my opinion, to be a real need for a book which will incorporate the best of the new knowledge with that less recently acquired but which may be said to have stood the test of time. Such a book should preferably be brief enough as to be attractive to the bulk of the profession, whose opportunity to read upon a single aspect of medicine is limited. This little book is offered as an attempt, perhaps with indifferent success, to fill the above-mentioned need.

The attention of the reader is invited to the method in which the subject is presented. I refer to the division of the main part of the book into three sections, in which heart disease is described from an etiological, a functional, and a structural viewpoint, respectively. The importance of etiology does not receive sufficient emphasis when it is mentioned only in teaching or in an article contributed to

PREFACE a medical journal, but if we believe in it, and we do, the text-book should be written in a method that will stamp this on the reader’s mind. For instance, is it surprising that the average physician is hazy as to the effects of syphilis on the circulatory organs when it is realized that to find out what is known he must turn to the chapter on valvular affections for an account of aortic regurgitation, to another for syphilitic myocarditis, to another for heart-block and other arrhythmias occurring in syphilis, and to still others for aneurism and angina pectoris? Logically, this material should be brought together in some such man¬ ner as I have attempted in the chapter on “Cardiovascular Syphilis ” The day of the consideration of heart affections from the viewpoint of the structural change or anatomical lesion has passed; of greater importance is that of the functional condition and perhaps even more essential, to an intelligent conception, is the recognition of the etiolog¬ ical type. I have endeavored to present the subject as nearly in conformance with the above belief as is practi¬ cable. My excuse for insisting on this point is that it has been made a major feature of this book, which differs thereby from any other book with which I am acquainted.

It may appear that a proper balance has not been main¬ tained between the different subjects. Thus, the chapter on “ Artenosclerotic Heart Disease” is of equal length with that on “Septic Heart Disease ” though the former is of infinitely greater frequency and importance. However, certain subjects lend themselves to a brief presentation, while with others clearness demands greater space. I have sought for brevity with clearness.

Much as it is desirable, it was not found possible to avoid controversial subjects; cardiology is in process of

PREFACE change and physicians are not in agreement on all points. Whenever a point might be new to some readers, authority has been quoted. It is hoped that the references might stimulate collateral reading.

The electrocardiograms were made by the author in the laboratory of the Boston City Hospital.

It is a pleasure to acknowledge thanks to Austin W. Cheever, who kindly suggested most of the details of the antisyphilitic treatment recommended for cardiovascular syphilis.

W. D. R.

Section I Preliminary Considerations

CHAPTER PAGE

I. Anatomical, Physiological, and Embryological Considerations.. 15

II. Methods of Examination. 31

III. Methods of Examination (cont.)—Polygraphic Examination_ 49

IV. Methods of Examination (concl.)—Electrocardiographic Ex¬

amination . 64

V. The Normal Heart. 84

VI. The Classification of Heart Disease. 91

Section II Types Of Heart Disease (etiologic)

VII. Rheumatic Heart Disease. 97

VIII. Septic Heart Disease. 119

IX. Cardiovascular Syphilis. 126

X. Arteriosclerotic Heart Disease. 142

XI. Hypertensive Heart Disease. 149

XII. The Heart in Hyperthyroidism. 160

XIII. The Heart in Diphtheria. 165

XIV. Congenital Heart Disease. 170

XV. Effort Syndrome : Irritable Heart. 175

Appendix

LIST OF ILLUSTRATIONS

no. PAGE

1. Anterior view of heart. frontispiece

2. Heart with part of interior exposed by the removal of a slice from the

anterior surface. 18

3. Curves of pressure in the left ventricle and right auricle. 24

4. Comparison between percussion and teleradiography in the determination of

the left cardiac border. 37

5. Arteriograms of pulsus altemans, and of pseudo-alternation. 52

6. Normal polygram. 52

7. Sinus arrhythmia. 52

8. 9. Auricular premature beats. Ventricular premature beat. 58

10. Paroxysmal tachycardia of auricular origin. 58

11. Auricular fibrillation. 59

12. Partial heart-block. 62

13. Complete heart-block. 62

14. The Einthoven triangle. 69

15. Normal electrocardiogram. 70

16. Ventricular preponderance. 71

17. Sinus arrhythmia. 74

18. Auricular premature beats. 75

19. Ventricular premature beats. 76

20. Paroxysmal tachycardia. 77

21. Auricular flutter. 78

22. Auricular fibrillation. 79

23. Partial heart-block. 80

24. Complete auriculo-ventricular heart-block, and intraventricular block.... 81

25. Combined arrhythmias. 83

26. Spirochetes in the myocardium. 126

27. Syphilitic myocarditis. 127

PLATES

PLATE PAGE

1. Rheumatic heart disease; healed mitral endocarditis with calcification

and rupture. Note the thickening and shortening of the chordae tendineae. 98-99

(Courtesy of Timothy Leary)

2. Rheumatic heart disease; acute infectious lesion of branch of the coronary

artery with surrounding myocarditis. 98-99

3. Large vegetations on the mitral valve, in septic heart disease due to the

pneumococcus. 120-121

4. Aneurism of the wall of the left ventricle with thrombus inside, associated

with coronary sclerosis and hypertensive heart disease. 244-245

5. Thrombi in the auricle. Note the corrugated surface of the large

thrombus. 270-271

Section I Preliminary Considerations

THE HEART IN MODERN PRACTICE

Chapter I Anatomical, Physiological, And Embryo- Logical Considerations

The following salient points of cardiac anatomy, phys¬ iology, and embryology have been selected as of most value in the clinical understanding of the heart.

ANATOMY

The heart is a somewnat conical-shaped mass of muscle, occupying the pericardial cavity in the middle mediasti¬ num. It is placed obliquely in the thorax; the base is directed backwards and corresponds to the fifth to eighth thoracic vertebras inclusive, while the apex points down¬ ward, forward, and to the left, at a level between the fifth and sixth costal cartilages and a little inside the left midclavicular line.

The heart cavity is divided into two lateral halves, and a transverse constriction further divides these latter into two cavities, the posterior on the two sides being called the auricles and the anterior the ventricles. The division of the heart into the four cavities is indicated by grooves upon its surface. In the groove indicating the auriculo-ventricular septum lie the main trunks of the nutrient vessels of the heart.

The right auricle is composed of a posterior and larger portion, the sinus venosus., and a smaller cavity placed in front and above, the right auricular appendix. Into the sinus venosus empty the superior and inferior vena? cava?, and its mesial wall is formed by the interauricular septum.

The Left Auricle is smaller than the right. It, too, consists of a principal cavity and an auricular appendix. The left auricular appendix is directed forward and to the right so that it overlaps the root of the pulmonary artery. The pulmonary veins, usually four but sometimes three in number, open into the upper part of the posterior wall of the left auricle.

The Ventricles are larger and the muscular layer forming their walls is much thicker than is that of the auri¬ cles. The right ventricle extends from the right auricle to near the apex and forms the larger part of the anterior surface of the heart. At its base, the right ventricle is prolonged into a conical pouch, the conus arteriosus or infundibulum, from which the pulmonary artery has its origin.

The left ventricle is longer than the right, beyond which it projects to form the apex of the heart. It appears on the anterior cardiac surface as a narrow strip along the left border, but forms a considerable portion of the posteroinferior surface. The thickness of the muscular wall of the left ventricle averages about three times that of the right ventricle.

Valves. —There are four valves in the heart, two be¬ tween the auricles and ventricles and two between the ven¬ tricles and the aortic and pulmonary arteries. These valves are formed by a reduplication of the endocardium and strengthened inside by a fibrous layer. At the attachment of each valve is an annular ring of dense fibrous tissue. The

ANATOMICAL CONSIDERATIONS cusps of the auriculo-ventricular valves are connected at their free margin by the chordae tendineae to the papillary muscles. These fibrous bands, or chordae tendineae, by limiting the play of the cusps, serve to prevent invagination of the latter into the auricles at the time of ventricular contraction. In the right heart, the valve has three sec¬ tions or cusps and hence its name, tricuspid. That of the left side has but two cusps and it is termed the bicuspid or mitral valve.

The Aortic and Pulmonary Valves each consist of three semilunar segments or cusps, the inner margins of which are free. Near the centre of the free margins of each cusp is a small nodule of fibrous tissue, termed the corpus Aurantii. These latter are to be distinguished from the thickenings produced by endocarditis. At the base of the aorta and of the pulmonary artery are small dilatations opposite each of the semilunar valve segments. These are known as the sinuses of Valsalva.

The Myocardium consists of bands and layers of muscle tissue intricately interlaced. The fibres of the bundle of His are the only fibres that are common to both auricle and ventricle. MacCallum’s studies of the myo¬ cardium have disclosed that by dissection the heart may be unrolled so that the four chambers can be separated and weighed separately, a matter of importance in careful studies of ventricular hypertrophy.

The Sino-auricular Node is a small mass of special¬ ized tissue located at the junction of the superior vena cava with the right auricle and immediately below the endo¬ cardium. This node is the seat of origin of the normal heart beat.

The Auriculo-ventricular Bundle of His (Fig. 2) is the only direct muscle connection between the auricles and ventricles. It arises from near the opening of the

Fig. 2.—Heart with part of interior exposed by the removal of a slice from the anterior surface. The auriculo-ventricular conduction bundle is represented schematically.

S. C.—Superior Cava.

P. A.—Pulmonary Artery.

R. A.—Right Auricle.

I. C.—Inferior Cava.

1. Auriculo-ventricular Node.

2. Bundle of His.

3. Right Branch. 9. Pulmonic Valve.

4. Left Branch. 10. Mitral Valve.

5. Right Auricular Appendage. 11. Papillary Muscle.

6. Tricuspid Valve. 12. Right Ventricle.

7. Interventricular Septum. 13. Left Ventricle.

8. Aortic Valve. 14. Cut Surface of Ventricular Vail.

( Gray'a: Anatomy, somewhat modified.)

coronary sinus, where it is connected with the annular and septal fibres of the right auricle. These fibres converge, form anode (node of Tawara), and continue as a compact

ANATOMICAL CONSIDERATIONS bundle which passes forward to the upper limit of the muscle portion of the ventricular septum, where it divides into right and left branches. These latter course down on either side of the ventricular septum to the right and left ventricles, respectively. Each limb is enclosed in a layer of connective tissue which isolates it from the mus¬ culature of the interventricular septum, but in the lower part of the ventricles each branch separates into numerous strands which enter the papillary muscles and spread over the entire inner surface of the ventricular muscle and form histological connections with the true cardiac muscle fibres. The right limb is the smaller of the two and usually enters the anterior papillary muscle by passing along the modera¬ tor band when that is present. The bundle of His consists of narrow, somewhat fusiform fibres, but the two branches and their terminal strands are composed of Purkinje fibres.

A bursa or lubricating mechanism is in relation with the main bundle, according to Curran , 1 and a special artery arising from the right coronaiy enters and follows the bundle. These facts suggest the possibility of the occur¬ rence of a bursitis from acute articular rheumatism or other infections, as causing certain cardiac symptoms.

The Purkinje Fibres are very much larger than the cardiac cells, and differ from them in several ways. In longitudinal section they are quadrilateral in shape. The central portion of each fibre contains one or more nuclei and is made up of granular protoplasm, with no indication of striations, while the peripheral portion is clear and has distinct cross striations. The fibres are intimately con¬ nected with each other, possess no definite sarcolemma, and do not branch.

1 The Anatomical Record, 1909, vol. iii, No. 12: 618.

The Arteries supplying the heart are the right and left coronaries. The right coronary artery rises from the anterior aortic sinus of Valsalva, passes forward to the auriculo-ventricular groove and after coursing to the right, divides into a transverse branch, which continues in the auriculo-ventricular groove to anastomose with the trans¬ verse branch of the left coronary artery, and a descending portion which supplies the right and posterior surface of the heart and finally anastomoses with the descending branches of the left coronary at the apex.

The left coronary has its origin in the left posterior sinus of Valsalva of the aorta. It, too, divides into a trans¬ verse and a descending branch. The former passes to the left in the auriculo-ventricular groove to anastomose with its fellow from the right coronary, and the descending branch, after supplying the left and part of the anterior cardiac surface, descends to the anastomosis at the apex.

These vessels occasionally arise by a common trunk or their number may be increased to three or more.

Veins. —The coronary sinus receives the majority of the veins draining the blood from the substance of the heart. It terminates in the right auricle between the opening for the inferior vena cava and the tricuspid valve. Its orifice is guarded by a semilunar valve (the coronary valve).

The anterior cardiac veins, comprising three or four small vessels, empty direct into the right auricle. The veins of Thebesius, consisting of a number of minute ves¬ sels arising in the substance of the heart, empty mostly into the auricles, but a few empty into the ventricles.

The Nerves of the heart are derived from the super¬ ficial and the deep cardiac plexuses, and from these plex-

ANATOMICAL CONSIDERATIONS uses obtain fibres from the vagus and sympathetic nerves. The superficial cardiac plexus lies under the arch of the aorta, while the deep cardiac plexus is under the tracheal bifurcation. The nerves from the plexus are freely dis¬ tributed on the surface and in the substance of the heart, many of the separate filaments being furnished with small ganglia.

The Pericardium is a serofibrous sac in which the heart and the commencement of the great vessels are con¬ tained. It consists of an outer fibrous layer and an inner layer of serous type. The fibrous layer blends with the central portion of the diaphragm and with the external coat of the great vessels. There are several prolongations of this outer layer (called ligaments of the pericardium) which attach it to the sternum, diaphragm, and vertebral column (by way of the cervical fascia). On the lateral surface of the pericardium is found the phrenic nerve as it passes downward to the diaphragm. The serous layer lines the fibrous pericardium and is invaginated by the heart so that it is described as consisting of a parietal and of a visceral layer.

The Internal Mammary Arteries, to be avoided in paracentesis of the pericardium, descend on the inner tho¬ racic wall about one half an inch from the sternal margins.

The Pulmonary Artery rises from the conus arteri¬ osus slightly anterior and to the left of the aorta. It passes obliquely to the left and under the arch of the aorta, where it divides into right and left branches. The artery averages but two inches in length. It is connected to the aortic arch by a short fibrous cord, the ligamentum arteriosum. This latter is the remnant of the fetal ductus arteriosus.

The Aorta rises from the base of the left ventricle, ascends a short distance, then arches backward and to the left to descend on the left side of the vertebral column. The ascending portion starts behind the left half of the sternum at the level of the lower border of the third costal cartilage and passes upward and forward to the right to the level of the upper border of the second right costal cartilage. The ascending portion is contained within the pericardium. When the aorta is distended it is about one quarter of an inch from the posterior surface of the sternum. This space is occupied by loose areolar tissue and the remains of the thymus gland.

The transverse arch of the aorta lies upon the trachea, esophagus, and thoracic duct, and the left recurrent laryn¬ geal nerve winds around it.

PHYSIOLOGY

The Events That Occur During a Single Car¬ diac Cycle.— A complete cardiac cycle is the time from any given feature of the heart beat until that feature is again produced. For example, if we begin with the clos¬ ure of the semilunar valves, the sequence of events is as follows:—At that moment the second heart sound is heard and the ventricle is quickly relaxing from its previous contraction. For a brief interval the auriculo-ventricular valves remain closed and for the moment the ventricles are shut off on both sides. The blood is flowing steadily into the auricles and dilating them. As soon as the ventricles relax completely the pressure of the blood in the auricles presses open the auriculo-ventricular valves, and from that moment until the beginning of auricular systole the blood from the large veins is filling both auricles and ventricles.

PHYSIOLOGICAL CONSIDERATIONS

The ventricular walls become more tense and the auriculo-ventricular valves are floated into position ready for closure. The auricular systole sends a sudden wave of blood into the ventricles, which closes the auriculo-ventricular valves . 2 The contraction of the auricles also momen¬ tarily blocks or retards the flow from the large veins, whence the auricular wave in the jugular veins. Ventric¬ ular systole follows immediately upon auricular systole. As the ventricles enter into contraction, the first sound is audible, and for a brief moment the ventricular cavities are again shut off on both sides. Soon the rising intra¬ ventricular pressure opens the semilunar valves and a stream of blood is forced into the aorta and pulmonary artery. During ventricular systole, the auricles continue to receive blood from the large veins; the venous flow is never completely blocked, but at most experiences a slight retardation during the very brief auricular systole. At the end of ventricular systole the intraventricular pressure falls below that in the aorta and pulmonary artery and the excess of arterial pressure closes the semilunar valves, thus completing the cardiac cycle.

Study of the diagram, Fig. 3, showing the relation of the pressure in the auricle, ventricle, and aorta, should aid one to visualize the events in a cardiac cycle. The latter is commonly divided into two periods: that of contraction or systole, and that of relaxation or diastole. At an aver¬ age heart rate of 72 per minute, the cardiac cycle occupies about 0.8 of a second, and this may be divided approxi¬ mately as follows: auricular systole 0.1, ventricular systole 0.3, and the common pause of the heart as 0.4 of a second, respectively. Diastole, as commonly determined, is the

2 Henderson, Y., and Johnson, F. E.: Heart, 4:69, 1912-1913.

period of ventricular diastole, and auricle systole is de¬ scribed as late diastolic or presystolic. In hearts beating at a slow rhythm, the greater part of ventricular filling may be completed in early diastole, which is then followed by

Fig. S.—Curves of pressure in the left ventricle and right auricle; the radial and jugular pulse tracings are placed above and below to show their time-relations.

A. V. C. and A. V. O., closure and opening of the auriculo-ventricular valves, respectively; S. O. and S. C., opening and closure of semilunar valves, respectively; pr., presphygmic period; po., postsphygmic period. The time intervals of some of the periods are marked above and below in seconds.

(This diagram is from one published by Thomas Lewis, with slight modification.)

a period of comparative rest. This resting phase is termed diastasis.

Contrary to the general impression, the apex of the heart, from which the pericardium has not been removed, does not twist forward and to the right with contraction, but, according to Starling , 3 there is then a definite descent

Starlixg, E. H.: Human Physiology, third edition, 1920, p. 947.

PHYSIOLOGICAL CONSIDERATIONS of the base downward toward the apex. The heart tends to be fixed by its attachment to the vena? cava?. This fact is a factor in an enlargement of the right ventricle being manifest to the left rather than to the right.

The Heart Sounds. —The first heart sound is largely muscular in origin. It begins with the “setting” of the ventricles, and continues until the highest intraventricular pressure has been produced. The systole of the ventricles then continues in silence the discharge of blood into the aorta until its sudden termination, which is marked by the second sound. The second sound is associated with the closure of the aortic and pulmonary valves. The actual sound is due to the relaxed semilunar cusps suddenly being put into a state of tension; a comparable somid may be pro¬ duced by suddenly drawing taut a fold of a handkerchief held between one’s hands. A second sound is possible with¬ out a perfect closure of the valve. The closure of the mitral and tricuspid valves is relatively quiet and probably contributes but little to the volume of the first heart sound . 4 The loudness and intensity of the first sound has been found 5 to be directly proportional to the intracardiac ten¬ sion, and especially to the tension developed during the isometric period i.e ., before the opening of the semilunar valves.

Mechanism of the Heart Beat. —On inspection the exposed heart is seen to contract and relax in rhythmic succession. The contraction wave starts at rhythmic intervals at the sino-auricular node, then spreads centrifugally over the auricles, like the rings from a stone thrown into a millpond, meets a slight delay at the auriculo-ventricular bundle, and thence proceeds through the right and left branches to the Purkinje fibres, where it is distributed to the muscular fibres of the ventricular walls. Other parts of the specialized tissue, namely, the auriculo-ventricular (Tawara) node and the conduction bundle on the ventricular side of the node, have the power of stimulus production, but the rate of this is slower than that of the sino-auricular node, and therefore, save in abnormal conditions, the heart contracts in response to stimuli received from the higher centre, the sino-auricular node.

It now seems established that the myogenic theory of the production and transmission of the heart beat is correct. The nerves have been shown to control the heart beat but do not initiate it or conduct the contraction wave. The vagus inhibits and the sympathetic accelerates the beat, each counteracting the other. The heart with its nerve connections severed may continue to beat.

Immediately after the muscle fibres of the heart have contracted they exhibit a refractory stage in that they fail to respond to stimulation. Restoration of excitability at once commences and increases progressively during dias¬ tole. When the cardiac muscle is stimulated it either does not contract at all, or does so to the fullest possible extent at the time. The amount of contraction does not depend on the strength of the stimulus employed, but varies according to the time at which the stimulus is received. When a stimulus is received early in diastole the resulting contraction is weaker than that of the previous cardiac cycle. Within limits, the amount of contraction varies directly in proportion to the length of the previous diastole. This principle serves to explain the fact that the more

PHYSIOLOGICAL CONSIDERATIONS rapid the heart rate the greater is the possibility of cardiac failure.

Gaskell has described five fundamental functions of cardiac muscle, namely: stimulus production, excitability, conductivity, contractility, and tonicity. The terms are somewhat theoretical, to be sure, but very useful in the dis¬ cussion of the various features of the heart’s activity. In abnormal conditions of the heart it is rare that the disturb¬ ance is limited to but one of the five fundamental functions mentioned above.

The Physiology of Muscular Exercise. —The out¬ put of the heart varies from 3 to 5 litres per minute in individuals at rest, it is raised by moderate exercise to 8 or 9 litres, and during heavy muscular exercise it may reach 20 litres or even more. It is of importance to consider briefly the conditions associated with this increase in the cardiac output.

At the onset of exercise, a constriction of the splanchnic vessels takes place and this diverts much of the blood into the muscles, and increases the pressure in their vessels. The increase in the blood supplied to the active muscles enables the latter, by their contractions, to expel a greater volume of blood into the veins and thence back to the heart. The heart then drives the blood out again into the muscles. Thus, in a certain sense, it can be seen that the mechanism, by which during exercise a greater volume of blood circulates through the active muscles, is largely de¬ pendent upon the activity of the latter. If the exercise is continued, some dilatation of the vessels in the working muscles usually occurs, and this results in a further in¬ crease in the blood supplied to these same muscles and enables them to return more blood to the heart.

It has been said above that during exercise there is a greater volume of blood returned to the heart, which is then called upon to propel it forward if the increased cir¬ culation is to be maintained. In other words, the output of blood from the heart must be augmented. The physi¬ ologists state that this may be accomplished by an increase in the number of contractions per minute and by a greater output per beat. The former certainly occurs, but as regards the latter there is some disagreement.

During diastole the heart is filled passively by the blood flowing in from the veins, and if the pressure of the latter is increased (in exercise) the heart undergoes a greater distention or dilatation. Dilatation is, therefore, a per¬ fectly normal process, and the extent to which it can take place, under physiological conditions, is ultimately limited by the pericardium. * 6

It has been shown 7 that the ventricles never pass in a single systole from utmost fulness to extreme contraction. The same observers hold that under normal conditions [i.e., when the pressure of the venous return is not decreased) the amplitude of the beat is determined by the duration of diastole; in other words, the systolic discharge is less when the heart rate is accelerated. The output per beat may be increased, however, during exercise when the heart rate is not quickened, as apparently occurs in individuals habitu¬ ated to exercise.

An understanding of the physiology of exercise makes more intelligible many of the phenomena observed in the study of the heart both in health and in disease. The

0 Bainbridge, F. A.: The Physiology of Muscular Exercise, Longmans,

Green and Co., 1919, p. 54.

7 Henderson, Y., and Barringer, T. B., Jr.: Amer. Jour. Physiol., xxx:366 (March, 1913).

EMBRYOLOGICAL CONSIDERATIONS subject is, unfortunately, complex and further presenta¬ tion will not be attempted here.

EMBRYOLOGY

The Circulatory System in the early embryo is that of a single tube or artery whose wall at a certain point possesses the power of rhythmic contractions. The spe¬ cialized part of this primitive tube later undergoes a sort of S-shaped twist, and by a complex process of evolution develops into the heart. There are many modifications which may occur in the above-mentioned development, and some of these are recognized in the condition termed “con¬ genital heart.” The variability in the relation of the right and left vagus nerves to the sino-auricular node and the auriculo-ventricular bundle may, in part, be due to differ¬ ences in the evolution of the heart. There are several structures in the heart which possess particular significance as regards the fetal circulation.

The Foramen Ovale is in the interauricular septum and is freely open until about the middle of fetal life, when a fold of tissue grows up from the posterior wall of the left auricle and acts as a valve in permitting the passage of blood only in the direction of right to left auricle.

The Eustachian Valve is a fold of tissue projecting upward in front of the orifice of the inferior vena cava and tends to divert the blood from this vessel through the fora¬ men ovale into the left auricle.

The Ductus Arteriosus (ductus Botalli) is a short tube, about 10 mm. in length at birth and 2 mm. in diameter. In fetal life it forms the continuation of the pulmonary artery, and opens into the aorta just beyond the origin of the left subclavian artery. It conducts the greater part of the right ventricular blood stream into the aorta.