AUSCULTATION OF THE HEART.
Auscultation. Auscultation is the final step in the physical examination of the heart and must be performed in a quiet room with the patient and the physician in comfortable and relaxed circumstances. Air conditioners and fans should be turned off, and doors and windows closed to reduce background noise to a minimum. The examination usually begins with the patient in the recumbent position and always includes examination in the sitting position as well. Depending on the findings in these primary positions, the patient may also be examined in the left lateral decubitus position or after exercise. There are four prime areas for auscultation on the chest wall: apex, left lower sternal border, left second interspace, and right second interspace. It is often helpful, however, to move the stethoscope by small steps from one of these areas to the next to note changes in the amplitude and character of various auscultatory phenomena. The stethoscope should be applied over the carotid arteries in the neck, especially in the presence of a systolic murmur at the base of the heart, as murmurs generated in the great vessels may be heard over the upper chest and those of aortic valve disease may be heard in the neck. It is advisable to listen for murmurs over the back of the chest while the patient is sitting up.
The sounds produced by a working heart are called heart sounds. Two sounds can be well heard in a healthy subject, first sound (Is), which is produced during systole and the second sound (2s), which occurs during diastole. The 1st is produced by valve component, i.e. vibrations of the cusps of the atrioventricular valves during the isometric contraction phase, the 2nd component is muscular, and is due to the myocardial isometric contraction. The 3d component is the vascular one. This is due to vibrations of the nearest portions of the aorta and the pulmonary trunk caused by their distention with blood during the ejection phase. The 4th component is atrial, it’s generated by vibrations caused by atrial contractions.
The 2nd sound is generated by vibrations arising at the early diastole when the semilunar cusps of the aortic valve and the pulmonary trunk are shut (the valve component) and by vibration of the walls at the point of origination of these vessels (vascular component).
In order to assess correctly the findings of auscultation, it’s necessary to know the sites where the valves project on the chest wall and also areas where the sounds produced by a valve can be better heard. The mitral valve projects to the left of the sternum at the 3rd costosternal articulation, and the tricuspidal valve on the sternum midway between the 3rd left and 5th right costosternal articulation.The valve of the pulmonary trunk is projected in the 2nd intercostal space to the left of the sternum, the aortic valve is projected in the middle of the sternum at the level of the 3rd costosternal articulation.
The auscultatory areas are as follows: 1) area of the apex beat for the mitral valve; 2) the lower part of the sternum near its junction with the xyphoid process for the tricuspidal valve; 3) the 2nd intercostal space to the left of the sternum for the pulmonary trunk valve; 4) the 2nd intercostal space to the right of the sternum for the aortal valve. Moreover, the aortal valve can be heard to the left of the sternum at the 3rd and 4th costosternal articulation (Botkin-Erb point). The valve sounds should be heard in the order of decreasing frequency of the affection. The mitral valve should be heard first, next the aortic valve and pulmonary trunk valve, tricuspid valve, and finally the aortic valve at the Botkin-Erb point.
At each area, attention should first be directed to the normal sounds and rhythm, then to the abnormal sounds, and lastly to the murmurs. The normal first and second sounds can usually be easily identified by their differing character, but in disease this may be difficult, and auscultation should be carried out with a finger on the carotid pulse. The first heart sound (S1) can be identified by its occurrence coincident with the upstroke of the carotid pulse. The first sound is best heard at the apex, and the second sound (S2) will be found to be loudest in the second interspaces both to the right and to the left of the sternum. The second heart sound consists of two parts: A2, due to closure of the aortic valve; and P2, due to the closure of the pulmonary valve. Both components can be heard on both sides of the sternum in the second interspace, but A1 is the loudest component of S2 on the right side, and P2 is the major component of S2 heard on the left. The two components of the second sound are identified by their temporal relationships and not by the point of maximum audibility and, therefore, it is misleading to use the terms aortic area and pulmonic area. With inspiration, the pulmonary closure sound is delayed, the second sound splits, and P2 can be identified as the second component. Observation of the effects of respiration on the second sound is an important part of auscultation and will be discussed in more detail later.
The significance of a third heart sound depends upon the clinical setting in which it is heard. The S3 is frequently heard in children and adolescents, in whom it is termed a “physiologic” third heart sound and has no significance. The sound is apparently generated by the termination of rapid inflow of blood into the ventricle in early diastole. The third heart sound is heard with decreasing frequency with advancing age and is a rare finding in adults who have normal hearts.
A third heart sound in a patient with heart disease has special significance. In this setting, the S3 is termed a “pathologic” S3 or a “ventricular gallop” and is indicative of an abnormally large diastolic inflow, as in mitral regurgitation, or of ventricular failure.
The timing, character, and intensity are the same as in the case of the physiologic S3, but in this case, the generation of sound is probably related to reduced compliance of the ventricle. When the rate is rapid, as it often is in disease, the first, second, and third heart sounds are heard as a triple rhythm suggesting the sounds made by the hoofs of a galloping horse—hence the term “gallop rhythm.” An S3 gallop is usually much louder after exercise. Raising the legs increases venous return to the right heart and may bring out a gallop, which is difficult to hear at rest.
The fourth heart sound (S4) is also heard occasionally iormal subjects, but this is found less commonly than the S3. It may occur as a doubling of the first heart sound or as a sound in late diastole which suggests a presystolic murmur. The fourth sound is usually an indication of increased resistance to ventricular filling (decreased compliance) due to intrinsic myocardial disease or to an increased load as in the case of hypertension or outflow obstruction. It is generated in the ventricle in response to the thrust of forceful atrial systole. The significance again depends upon the setting. If the S4 is heard in a patient with other manifestations of heart disease, it is known as a “pathologic” S4 or an “atrial gallop.”
After these sounds have been identified, attention is turned to a search for abnormal sounds such as clicks and friction rubs. This is best done by listening in all four areas while concentrating on systole and then on diastole. Systole and diastole are normally silent and abnormal sounds and murmurs are best identified by asking the question: Is the period between S1 and S2 completely silent? and then asking the same question about the period between S2 and S1.
Effect of Respiration. More can be learned about the physiology of any organ system by observing its response to changing conditions or stress than by prolonged observation at rest. This general physiologic principle underlies the importance of careful observation of the effects of respiration on the heart. Normal quiet respiration results in phasic alterations in venous return, cardiac output, venous pressure, and arterial blood pressure. The response is often altered by disease.
All the hemodynamic changes depend upon the negative intrathoracic pressure which initiates inspiration. When the pressure within the chest becomes negative witli respect to that in the atmosphere and in the extrathoracic airways, air flows into the chest through the respiratory tree. The veins are similar to the trachea and bronchi in that they are conduits running into the thoracic cavity from outside. The decrease in intrathoracic pressure which initiates air flow into the trachea also initiates blood flow into the thorax from the extrathoracic portions of the superior and inferior venae cavae. Venous pressure in the neck veins falls witli inspiration. The return to the right atrium and right ventricle is, therefore, increased by the act of inspiration, and the output of the right ventricle into the lung is increased. The venous return to the left heart is decreased by inspiration, but this is less important than the phasic increase in right heart output which after a few heart beats results in a phasic change in left ventricular output. This variation in left ventricular stroke output is manifested by a phasic variation in arterial blood pressure of 5 to 8 mm Hg with the low point occurring coincident with inspiration. When this inspiratory decrease in blood pressure reaches 15 mm Hg a “pulsus paradoxus” is said to exist.
An important effect of respiration on physical signs is the change in the splitting of the second heart sound. Under normal circumstances, aortic valve closure precedes pulmonary valve closure, and, therefore, delay in right-ventricular emptying results in the separation or splitting of the two components (P2 and A2) of the second sound (S2). This normal increase in the interval between the two components of S2 is referred to as a physiologic splitting. If the splitting is due to left-ventricular disease or aortic stenosis, left-ventricular ejection is delayed, so that aortic valve closure follows rather than precedes pulmonary closure. In this situation, inspiratory delay in pulmonary valve closure results in a narrowing of the split between the two components of the second sound, whereas the two components move apart with expiration; hence, the designation paradoxical splitting.
The effect of respiration on physical signs is also important in establishing the diagnosis of atrial septal defect. When the two atria are in free communication, the inspiratory increment in venous return is divided between the right and left ventricles; the closure of both aortic and pulmonary valves is delayed; and, hence, the interval between the two events remains relatively constant. The majority of patients with ostium secundum atrial septal defect exhibit this sign—fixed splitting of the second heart sound.
Murmurs originating on the right side of the heart are made louder by inspiration, a fact which is useful in differentiating tricuspid from mitral regurgitation. Although theoretically one might expect a decrease in the intensity of the murmur of mitral regurgitation with inspiration, it actually changes very little, whereas the murmur of tricuspid regurgitation increases. This inspiratory increase is best observed in cases of minimal tricuspid regurgitation. In severe lesions, the murmur may be heard throughout both phases of the respiratory cycle.
The cardiovascular examination is not concluded with auscultation of the heart. Percussion of the thorax may reveal evidence of pleural effusion, and fine, moist rales in the lungs may be the earliest sign of pulmonary congestion. Hepatic enlargement and tenderness are signs of right heart failure. A careful search for edema about the ankles and over the sacrum should also be carried out.
Changes in the heart sounds.
The heart sounds may increase or decrease their intensity, the tone, the length, they may be split or reduplicated, or adventitious sound may appear.
Intensity of the heart sounds may depend on conditions of the sound wave transmission, i.e. on the extracardiac causes (subcutaneous fat or muscles of the chest are overdeveloped, the lungs emphysema, liquid in the left pleural cavity, etc)- the intensity of the heart sounds decreases. Thin chest wall, the lung edges are sclerosed, tumor in the posterior mediastinum, etc.-the intensity of the heart sounds increases.
The intensity of the heart sounds can decrease in decreased myocardial contractility in patients with myocardial dystrophy, myocarditis cardiosclerosis, collapse, accumulation of fluid in the pericardial cavity. Both heart sounds can be increased due to the effect of the sympathetic nervous system on the heart.
Changes in only one heart sound are very important diagnostically. The intensity of the 1st heart sound diminishes in the mitral and aortic valve insufficiency. In tricuspid and pulmonary valve failure, the diminution of the 1st sound will be better heard at the base of the xyphoid process. The 1st sound can be diminished at the apex in stenotic aortal orifice. In diffuse affections of the myocardium (due to dystrophy, cardiosclerosis, myocarditis) the 1st heart sound only may be diminished because its muscular component also diminished in this cases.
The 1st sound increases at the heart apex if the left ventricle is not adequately filled with blood during diastole (mitral stenosis). The 1st sound increases in tricuspidal valve stenosis at the base of the xyphoid process.
The 2nd sound over the aorta is diminished in aortic valve affections because either the cusps of the valve are destroyed or their vibrating power decreases due to developing cicatrices, the 2nd sound can be inaudible over the aorta if the aortic valve is much destroyed.
The 2nd sound may increase either over the aorta or over the
pulmonary trunk. If the sound is more intense over the aorta, it is say to be accentuated over the aorta, and if it’s stronger over the pulmonary trunk- accentuation of the 2nd sound over pulmonary artery is meant.
Reduplication of the heart sounds may be revealed by auscultation. Two short sounds, which quickly follow one another, are heard instead of one. It occurs in asynchronous work of the left and right chambers of the heart. Asynchronous closure of the atrioventricular valves splits the 1st sound, while asynchronous closure of the semilunar valves causes reduplication of the 2nd sound. If the two short sounds follow one another at a short interval, they are not perceived as two separate sounds, the sound is saided to be split.
Physiological reduplication or splitting of the 1st sound is due to asynchronous closure of the atrioventricular valves, e.g. during very deep expiration. Pathological reduplication of the 1st sound can occur in impaired intraventricular conduction (through the His bundle) as a result of delayed systole of one of the ventricles.
The 2nd sound is reduplicated more frequently than the 1st sound. Reduplication occurs due to asynchronous closure of the valve of the aorta and pulmonary trunk (essential hypertension, mitral stenosis, emphysema of the lungs, etc.).
True reduplication of the heart sounds should be differentiated from seeming doubling, which is connected with the appearance of adventitious sounds. The mitral valve opening sound is an example, this sound together with a loud 1st sound (snapping) and the 2nd sound to form a specific triple rhythm. An extrapericardial sound can occur in pericardial adhesion, it originates during diastole, 0,08-0,14 s after the 2nd sound, can also arise during systole, between the 1st and 2nd heart sounds (systolic click).
Changes in heart sounds can be due to intensified physiological the 3rd or 4th sounds. Intensification of one of these sounds gives a three-sound rhythm, known as the gallop rhythm. Protodiastolic, mesodiastolic and presystolic gallop rhythm are distinguished by the time of appearance of the extra sound in diastole.
If the heart sounds heard at the heart apex are similar in intensity, a peculiar auscultative picture resembles the tick-tack or fetal rhythm, known also as embryocardial or pendulum rhythm (severe cardiac failure, paroxysmal tachycardia, high fever, etc.).
CARDIAC MURMURS
The diagnosis of cardiovascular disease depends on the synthesis of all the available clinical information, but some objective finding must be taken as the primary point about which the differential diagnosis is developed. Heart murmurs, which are subject to precise description with regard to timing and location of maximal audibility, frequently form such a starting point. The murmur may serve as a basis for differential diagnosis in a patient ill with congestive failure, or it may be an incidental finding on routine examination.
Classification and Characteristics of Murmurs
ORIGIN AND SIGNIFICANCE. Not all heart murmurs are indicative of organic heart disease, a fact emphasized by their classification into three groups on the basis of the mechanism of production: 1) organic murmurs due to anatomic abnormalities within the heart or central circulation, the identification of which constitutes evidence for organic heart disease; 2) physiologic murmurs related to altered function within anatomically normal hearts, as with the systolic murmurs of anemia, thyrotoxicosis, and fever; 3) innocent murmurs that cannot be related either to altered anatomy or function. The mechanisms of production of the third type are unknown, but it is known that such murmurs are not associated with organic heart disease.
The importance of distinguishing between these three types of murmurs is obvious. It is sometimes necessary to employ cardiac catheterization and angiocardiography to solve the problem.
Innocent murmurs are usually systolic. Diastolic murmurs are rarely heard in the absence of organic heart disease. The innocent systolic murmurs are usually confined either to the first or to the middle part of systole, are not loud, are rarely accompanied by a thrill, and show variability with respiration or position or both. Final judgment about the significance of a particular murmur depends on the evaluation of that finding in relation to variation within the normal population and this judgment must be based on the examiner’s experience.
TIMING AND LOCATION. Standardization of classification and description is necessary if heart murmurs are to be of maximum value in differential diagnosis, if communication between one physician and another is to be effective, and if meaningful comparison is to be made between findings recorded at different times by the same physician.Further description with regard to intensity, character, and radiation also is possible and valuable.
Each of these time periods can be subdivided into thirds and murmurs classified according to their onset as early, mid, or late. Early diastole is sometimes referred to as protodiastole and late diastole as presystole. If a murmur lasts throughout systole, it is called pansystolic or holosystolic. The murmurs listed are divided vertically into three groups depending on point of maximum audibility. Those heard at apex and lower left sternal border have been grouped together under APEX because most of them can be heard in both places.
CHARACTER. The character of the murmur is sometimes described as crescendo or decrescendo to indicate progressive increase or decrease in intensity. The early-diastolic murmur of aortic regurgitation is classically decrescendo and the late-diastolic murmur of mitral stenosis is crescendo. The murmur of mitral stenosis is also described as presystolic or as an atrial systolic murmur, to indicate that it is related to atrial systole. The systolic murmur of aortic or pulmonary stenosis is best described as crescendo-decrescendo. The term “ejection systolic murmur” is applied to these and all other murmurs related to the ejection of blood into the great vessels. Since this term indicates that the examiner has information concerning the physiologic origin of the murmur, which he cannot get from auscultation alone, purely descriptive terms are preferable. The terms “diamond-shaped” and “Christmas tree” are applied to the early-systolic crescendo-decrescendo murmur and refer to its phonocardiographic appearance. The quality of a murmur is described as “harsh,” “blowing,” or “musical.” Although lacking in quantitative precision, these terms serve a useful purpose. Furthermore, the term “musical” used to describe a decre-scendo diastolic murmur indicates the possibility of an unusual cause of aortic regurgitation, such as rupture of an aortic leaflet.
The radiation of a murmur is of limited help, since it is, at least in part, a function of intensity. A loud murmur may be heard all
INTENSITY. Systolic murmurs are usually graded from 1 to 6 on the basis of intensity. The extremes of this grading system are easily defined, and the intermediate grades are determined with respect to these extremes. Grade 1 is the faintest audible murmur,not always heard initially, and identified only after careful auscultation under ideal conditions. Grade 6 is the loudest possible murmur, heard with the stethoscope removed from the surface of the chest. Grade 5 murmurs cannot be heard with the stethoscope removed from the chest but are audible when only one edge of the stethoscope is in contact with the chest wall. Grades 2, 3, and 4 lie between these extremes. The grade of a murmur is usually recorded as, for example, 2/6 and spoken of as 2 out of 6 to indicate that a six-part system of grading has been employed. Excellent agreement is obtained between the grading of experienced observers.
During auscultation of the heart, it’s necessary to differentiate between functional and organic, and between endocardial and exocardial murmurs. The following properties of functional murmers help differentiate them from organic murmurs: 1) functional murmurs in most cases are systolic, 2) functional murmurs are not permanent and may arise and disappear when patient changes his posture, after exercise and during various respiratory phases, 3) they are mostly heard over the pulmonary trunk and less frequently over the apex, 4) functional murmurs are transient and are rarely heard during the entire systole, they are soft and blowing, 5) functional murmurs are heard over a limited area and not transmit to long distances from their source, 6) functional murmurs are not accompained by other signs of valve affections (e.g. enlargement of heart chambers or changes in the heart sounds.)
Exocardial murmurs although synchronous with the heart work, they arise outside the heart. These are pericardial and pleurocardial friction sounds. The following signs can be used to differentiate pericardial friction sounds from intracardial sounds: 1) there is no complete synchronism of PFS with systole and diastole, friction sounds are often continious, their intensity increasing during systole or diastole, 2) PFS can be heard for short periods during various phases of the heart work, 3) PFS are not permanent and can reappear at intervals, 4) PFS are heard at sites other than the best auscultative points, they are best heard in the area of absolute cardiac dullness, at the heart base, at the left edge of the sternum in the 3rd and 4th intercostal space, their localization is inconstant and migrates even during the course of one day, 5) PFS are very poorly transmitted from the site of their generation, 6) PFS are heard nearer the examiner‘s ear than endocardial murmurs, 7) PFS are intensified if the stethoscope is pressed tighter to the chest and when the patient leans forward.
Pleuropericardial friction murmurs (PPFM) arise in inflammation of the pleura adjacent to the heart and are the result of friction of the pleura layers (synchronous with the heart work). As distinct from PFS PPFS is always heard at the left side of relative cardiac dullness. It usually combines with pleural friction sound and changes its intensity during respiration: increases during deep inspiration and decreases during expiration.
STUDY OF ARTERIAL PULSE
Pulse is the rhythmical vibration of the arterial walls caused by contractions of the heart, blood discharge into the arterial system, and changes in pressure in this system during systole and diastole. Pulse wave is transmitted due to the ability of arterial walls to distend and collapse. The velocity of the pulse wave varies from 4 to 13 m/s, i.e. exceeds significantly the linear velocity of the blood flow, which does not exceed 0.5 m/s even in large arteries.
Palpation of the pulse is the main method of examination of pulse. As a rule, pulse is studied first on the radial artery, since it is superficial and runs immediately under the skin and can thus be readily felt between the styloid process of the radial bone and the tendon of the internal radial muscle. The patient’s hand is grasped by the examiner so that the thumb of the right hand is placed on the dorsal side of the arm (near the radiocarpal joint) while the other fingers remain on the frontal side of the arm. As soon as the artery is found, it is pressed against the underlying bone. The pulse wave is felt by the examining fingers as a dilation of the artery. The pulse may be different on different arms, and therefore it should first be palpated simultaneously on both radial arteries. The condition of the vascular wall should be assessed simultaneously. To that end, the artery is pressed by the index and middle fingers of the left hand slightly above the point where the pulse is examined by the right hand. When the vessel stops pulsating under the fingers of the right hand, the arterial wall is felt. A normal artery is a thin elastic tube. In some diseases, for example, in atherosclerosis, the arteries change, their walls become firm, and the course more tortuous. If calcification is considerable, the artery walls are rough, tortuous tubes, sometimes with bead-like thickenings.
Various properties of pulse can be better understood if sphygmograms (pulse curves) are first studied. The diagnostic importance of the pulse will be described later.
Sphygmography. Pulsation of the vascular wall is recorded as a curve (sphygmogram) by an apparatus called sphygmograph. Special pick-ups convert mechanical oscillations of the vascular wall into electric pulses, which are amplified and recorded by an electrocardiograph.
Direct and volumetric sphygmography are distinguished. Direct sphygmography is used to record oscillations of the wall of any superficial artery, for which purpose a funnel is placed on the examined vessel. Volumetric sphygmography records total vibrations of the vascular wall that are converted into vibrations of a portion of the body (usually an extremity). Volumetric sphygmogram is taken by placing a special cuff on the extremity. Curves obtained by direct and volumetric sphygmography do not differ substantially. The distance of the artery from the heart is important for the shape of the pulse curve. Central and peripheral sphygmograms are distinguished accordingly. Central sphygmograms are taken from the carotid and subclavian arteries. Sphygmograms of the radial and femoral arteries, and also volumetric sphygmograms of the extremities are peripheral.
Fig. 36. Normal sphygmogram of the carotid (c) recorded simultaneously with ECG (a) and PCG (b).
Normal sphygmogram. Both the central and peripheral sphygmograms (Fig. 36) of a healthy individual have a sharp upstroke (the anacrotic wave), a peak of the curve, and a gradually declining downstroke (the catacrotic wave). The catacrotic limb of a peripheral sphygmogram has smaller waves one of which is more pronounced and is known as a dicrotic wave, which is due to repulsion of the blood from the closed aortic valve during early diastole. A central sphygmogram differs from a peripheral one by a pre-anacrotic vibration, a steeper anacrotic wave, a pronounced catacrotic incisura (corresponding to closure of the aortic valve), and a small dicrotic wave. In interpreting a sphygmogram, special attention should be paid to the shape of the pulse waves, the rate of ascent of the anacrotic wave and of descent of the catacrotic wave, the amplitude of the pulse wave, the height of the dicrotic wave, etc.
Properties of arterial pulse. The study of the arterial pulse gives information on the work of the heart and the condition of the circulatory system. The pulse should be taken in the following order. First the examiner must determine if the pulse can be equally felt on both arms. To that end both radial arteries should be palpated simultaneously and the magnitude of pulse waves on both hands compared (normally it is the same). The pulse wave on one arm may happen to be lower. It occurs in unilateral structural abnormalities in peripheral course of the artery, its constriction, compression by a tumour, or a scar, etc. Pulse may also be different when similar changes occur in the brachial or subclavian artery, or due to compression of large arterial trunks by the aortic aneurysm, mediastinal tumour, retrosternal goitre, or markedly enlarged left atrium. The smaller pulse wave may lag in time. If the pulse on the two arms is different, its further study should be carried out on that arm where the pulse wave is more pronounced. The following properties of pulse are examined: rhythm, rate, tension, filling, size, and form.
Rhythm. In healthy subjects, cardiac contractions and pulse waves follow one another at regular intervals: the pulse is said to be rhythmic or regular. When the cardiac rhythm is upset, pulse waves follow at irregular intervals: the pulse becomes arrhythmic, or irregular. Some pulse waves may be missing or they may appear prematurely, which is characteristic of extrasystole and also complete arrhythmia (fibrillation), in which pulse waves follow one another at irregular intervals.
Pulse rate in normal conditions corresponds to the rate of cardiac contractions and is 60—80 per minute. If the heart rhythm is accelerated (tachycardia), the number of pulse waves increases and the pulse rate increases accordingly (pulsus frequens); slowed cardiac rhythm (bradycardia) is characterized by a respective slowing of the pulse (pulsus rarus). The pulse rate is counted for one minute. If the pulse is arrhythmic, the heart beats should also be counted and compared with the pulse rate. During frequent and irregular contractions of the heart, some systoles of the left ventricle can be so weak that the blood is not ejected into the aorta or the amount of the discharged blood is very small and the pulse wave does not reach the peripheral arteries. The difference between the heart rate and the pulse is called the pulse deficit while the pulse itself is called pulsus deficient. The greater the deficiency, the worse is the effect it produces on the circulation of blood.
Pulse pressure is determined by the force that should be applied to the pulsating artery to compress it completely. This property of pulse depends on the magnitude of the systolic arterial pressure. If arterial pressure is normal, the artery can be compressed by a moderate pressure. A normal pulse is therefore of moderate tension. The higher the pressure, the more difficult it is to compress the artery; such a pulse is called pulsus durus (hard or high-tension pulse). If the arterial pressure is small, the artery is easy to compress and the pulse is soft (pulsus mollis).
Volume of pulse. Pulse volume shows the artery filling with blood, which in turn depends on the amount of blood that is ejected during systole into the arterial system and which produces variations in the artery volume. Pulse volume depends on the stroke volume, on the total amount of circulating blood, and its distribution in the body. If the stroke volume is normal and the artery is sufficiently filled with blood, the pulse is said to be full,(pulsus plenus). In abnormal circulation and blood loss, the pulse volume decreases (pulsus vacuus).
Pulse size. The pulse size implies its filling and tension. It depends on the expansion of the artery during systole and on its collapse during diastole. These in turn depend on the pulse volume, fluctuation of the arterial pressure during both systole and diastole, and distensibility of the arterial wall. Pulse wave increases with increasing stroke volume, great fluctuations in the arterial pressure, and also with decreasing tone of the arterial wall. This pulse is called large-volume pulse or pulsus magnus. A large-volume pulse is characterized by a high amplitude of pulse fluctuations on a sphygmogram, and it is therefore also called high pulse (pulsus altus). Large-volume or high pulse is characteristic of aortic valve incompetence in thyrotoxicosis, when the pulse wave increases due to the high difference between systolic and diastolic arterial pressure. Such a pulse may develop in fever in connection with decreased tone of the arterial wall.
Pulse wave decreases with decreasing stroke volume and amplitude of pressure fluctuations during systole and diastole and with increasing tone of the arterial wall. The pulse wave and the pulse become small (pulsus parvus). Pulse is small when the amount of blood discharged into the arterial system is small, and the rate of its discharge is low. This is observed in stenosis of the aortic orifice or of the left venous orifice, and also in tachycardia and acute cardiac failure. The pulse wave may be quite insignificant (barely perceptible) in shock, acute cardiac failure and massive loss of blood. This pulse is called thready (pulsus filiformis).
In normal conditions, pulse is rhythmic and the pulse wave uniform. Such a pulse is called uniform (pulsus aequalis). In cardiac rhythm disorders, when the heart contracts at irregular intervals, the pulse wave becomes non-uniform, and this pulse is called unequal (pulsus inaequalis). In rare cases (in rhythmic pulse), high and low pulse waves alternate. This is alternating pulse (pulsus alternans). It is believed that this pulse is due to alternation of heart contractions that vary in force. It usually occurs in severe myocardial affection.
Pulse character (Fig. 37a). This depends on the rate of change in the arterial pressure during systole and diastole. If much blood is discharged into the aorta during systole and the pressure in the aorta increases rapidly, while during a diastole this pressure quickly falls, the arterial wall will expand and collapse quickly as well. This pulse is called quick pulse (pulsus celer or pulsus saliens). On a sphygmogram this pulse gives a steeper anacrotic rise and sharp catacrotic fall (Fig. 37b). Quick pulse is characteristic of aortic incompetence, since in this condition the stroke volume and systolic pressure increase, while during diastole the pressure falls rapidly due to blood regurgitation into the left ventricle. Pulse in such cases is not only quick but also high (pulsus celer et altus). Quick pulse is less characteristic of thyrotoxicosis or nervous strain.
Slow pulse (pulsus tardus) is, on the contrary, connected with slow rise and fall of pressure in the arterial system and its small fluctuation during the cardiac cycle (Fig. 37c). This condition is characteristic of aortic stenosis: blood ejection from the left ventricle is difficult and the pressure in the aorta therefore increases slowly. The puke wave decreases and the pulse is therefore not only slow but also small (pulsus tardus et parvus).
Fig. 37. Sphygmograms. a—normal pulse; b—quick and high pulse; c—small and low pulse.
Other changes in the arterial pulse. Sometimes, when the pulse wave decreases, another wave can be detected which is connected with increasing dicrotic wave; this wave normally is not detectable and can only be seen on a sphygmogram. If the tone of the peripheral arteries decreases (e.g. in fever or infectious diseases), the dicrotic wave can be detected by palpation as well. This pulse is called dicrotic (pulsus dicroticus). Paradoxical pulse (pulsus paradoxus) is also distinguished. It is characterized by smaller pulse waves during inspiration. It develops in cases with adherent pericardium due to compression of large veins and decreased blood filling of the heart during inspiration.
After the examination of pulse on the radial artery has been finished, it is studied on other vessels, e.g. on the temporal, carotid, femoral, popliteal arteries, dorsalis pedis and other arteries. Examination of pulse on other arteries is especially important in suspected affections of these arteries (obliterating endocarditis, atherosclerosis, thrombosis of the vessels).
The femoral artery is readily palpable in the groin, better with the straightened and slightly outwardly turned thigh. The pulse of the popliteal artery is well palpated in the popliteal fossa with the patient in the prone position. The posterior tibial artery is palpated in the region of the condyle of the internal malleolus. The dorsalis pedis artery is felt on the dorsal surface of the foot in the proximal part of the first intermetatarsal space. The pulse taken on the latter two arteries is very important for diagnosis of obliterating endarteritis.
The pulse of the carotid arteries should be examined carefully, one after the other, beginning with a slight pressure on the arterial wall, because of the danger of the carotid reflex: the heart may slow down markedly (or even stop) and the arterial pressure drop significantly. The clinical signs of this reflex are vertigo, faint, and convulsions.
Some diseases of the cardiovascular system are characterized by different pulse in the upper and lower extremities. When the aortic isthmus is constricted (coarctation), the pulse waves in the lower extremities decrease significantly, whereas they remaiormal, or even increase, in the carotid arteries and the arteries of the upper extremities. In Takayasu’s disease (pulseless disease), in the presence of obliterating arteritis of large vessels originating from the aortic arch, the pulse decreases or disappears at all in the carotid, axillary, brachial, and radiant arteries.
Velocity of the pulse wave. An additional method of examination of the arterial system is determining velocity at which the pulse wave is propagated; this is used to assess the elasticity of the vascular walls. The firmer the wall, the higher the velocity at which the pulse wave is propagated.
In order to determine velocity of pulse wave propagation (V), it is necessary to know the length of the vessel (L), and the pulse wave lag time (t) on the periphery at instantaneous sphygmography at two points of the vascular system. The pulse wave velocity can then be calculated from the formula:
In order to determine the velocity of pulse wave, two sphygmograms are usually taken synchronously from the carotid and femoral arteries (see “Sphygmography”). One pickup is placed at the bifurcation of the carotid artery (at the level of the upper thyroid cartilage) and the other, on the femoral artery, in the region of the inguinal ligament. A measuring tape is then used to measure the distance from the jugular fossa to the first pickup (l1) and to the second one (l2). The true length of the vessel (L) can be found by subtracting two lengths from the jugular fossa to the pickup on the carotid artery (2l1) from the sum of the lengths l1 and l2 because the direction in which the pulse wave propagates in the carotid artery is opposite to that in the aorta. It follows that L = (l1 + l2) — 2 x l1 = l2 — l1 Once the length of the vessel is known, the lag time is now determined for the pulse wave at the periphery, i.e. the period lasting from the anacrotic ascent on the sphygmogram of the femoral artery to the anactrotic ascent on the carotid sphygmogram (in hundredth fractions of a second). The higher the velocity of pulse wave, the less the time lag.
Once the length and lag time of the pulse wave have been determined, one can find the velocity of the pulse wave mainly in the descending aorta. Iormal cases it varies from 4.5 to 8 m/s. This velocity increases with age. It also increases in atherosclerosis and essential hypertension. The pulse wave velocity decreases in hypotension, anaemia, heart diseases, and thrombosis of the abdominal artery.
STUDY OF CAPILLARIES
Capillaries are examined by inspection and capillaroscopy.
Capillaroscopy is the method of studying capillaries of intact surface epithelial coats (e.g. skin or mucosa). Slight-magnification microscopes with common diffuse day-light illumination, or special capillaroscopes may be used for the purpose. Capillarography is a photographic modification of capillaroscopy. It gives graphic patterns.
Capillaroscopy is mostly used to study capillaries at the edge of the nail bed of the ring finger. In order to clarify the skin, it is coated with a drop of peach-kern or cedar oil. Iormal conditions, the capillaries can be seen as elongated pale red loops against the yellowish pink background. The arterial bend of the capillary is normally narrower and shorter than the venous one; the transition part of the loop is usually rounded. Figure-eight-shaped loops sometimes occur. The number of capillaries is 16—20 in the field of vision. The blood flow is almost indiscernible in them; it is continuous and faster in the arterial bend than in the venous one. The capillaroscopic picture changes during vascular spasms, congestions, and in diabetes mellitus.
STUDY OF VENOUS PULSE
Venous pulse is studied by inspection and phlebography.
Phlebography is the recording of the venous pulse. Vibrations of the venous walls connected with the change in filling of the large veins located close to the heart are recorded in the form of a curve (phlebogram). The principle underlying phlebography is similar to that used in sphygmography. Phlebograms of the jugular veins, where the pulsation is more pronounced, are usually taken. A phlebogram of the cardiac cycle in healthy subjects includes a number of waves (Fig. 38). These are positive (a, c, v) and negative (x, y) pulse waves. Their origination is explained as follows.
1. The positive wave a appears during contraction of the right atrium. At this moment, emptying of the venae cavae from the inflowing peripheral venous blood is delayed; the veins become overfilled and swollen.
2. Wave c follows wave a after an insignificant descent of the curve. It is associated with ventricular systole and arises due to transmission of pulsation of the carotid artery that runs in the vicinity of the jugular vein.
Fig. 38. Phlebograms. /—normal; 2—positive venous pulse.
3. Next follows the negative wave x, which is caused by a systolic collapse and is explained by filling of the right atrium with venous blood during ventricular systole; the veins are emptied and collapse. Fast emptying of the veins is facilitated by the falling intrathoracic pressure due to heart contraction and discharge of the systolic blood to the peripheral vessels.
4. Positive wave v comes at the end of the ventricular systole with the closed tricuspid valve. It is connected with accumulation of blood in the atria which holds back the delivery of new portions of blood from the venae cavae.
5. Wave v is followed by a new collapse of the vein (the diastolic collapse y) which begins with opening of the tricuspid valve and delivery of blood into the right ventricle. This promotes the inflow of blood from the venae cavae into the right atrium and collapse of the vein.
In the analysis of a phlebogram, it is useful to pay attention to the shape and width of separate waves and their relation to the sphygmographic findings. A phlebogram shows the activity of the right heart chambers and pressure fluctuation in the right atrium. A normal phlebogram has a sharp wave a; this form of the venous pulse curve is called atrial. If sphygmogram and phlebogram are taken simultaneously, the maximum ascent of the normal sphygmographic curve corresponds to the negative deviation (x) of the phlebogram, because atrial diastole and blood flow into the atria from the veins begin during ventricular systole and blood ejection into the arterial system. Hence another name of a normal venous pulse, negative venous pulse.
The size of separate waves on phlebograms changes in pathology. The waves may increase, decrease, or disappear. For example, with difficult blood outflow from the right atrium (in stenotic right atrioventricular orifice, or increased pressure in the right ventricle), the contractile force of the atrium and the a wave increase. The a wave broadens and becomes lower, or it can even disappear altogether in progressive weakness of the right atrium, and blood congestion in it. Since the blood pressure does not fall significanlty during diastole either, emptying of the veins becomes difficult. The negative x wave therefore levels and disappears. As a result, the activity of the right ventricle can only be seen on the phlebogram: the vein swells during ventricular systole (positive v wave) and collapses during diastole (negative y wave). This form of the venous pulse is called ventricular.
If ventricular venous pulse is recorded synchronously with sphygmogram, one can see that the maximum ascent of the curve on the sphygmogram corresponds not to the systolic collapse of the vein but to the positive deviation, the v wave. This explains another name of the pulse, positive venous pulse (see Fig. 38).
Positive ventricular venous pulse is observed in tricuspid incompetence, pronounced venous congestion in the greater circulation, in fibrillation and complete transverse heart block.
AUSCULTATION OF VESSELS
Auscultation of arteries. Arteries of medium calibre, such as the carotid, subclavian, or femoral artery, are usually auscultated. The artery is first palpated, then heard by a phonendoscope without applying pressure, since stenotic murmurs may otherwise appear. Sounds and murmurs can be heard over arteries. These can be generated either in the arteries themselves or be transmitted from the heart and aortic valves. The transmitted sounds and murmurs can only be heard on the arteries that are located close to the heart, such as the carotid and the subclavian arteries.
Two sounds can be heard on the carotid and subclavian arteries in healthy persons. The first sound is due to the tension of the arterial wall distended by the running pulse wave, and the second sound is transmitted onto these arteries from the aortic semilunar valve. One systolic sound can sometimes be heard on the femoral artery. Like the first sound of the carotid and subclavian arteries, the second sound is generated by the vibration of the tensed arterial wall when the pulse wave passes it. In aortic incompetence, the first sound over the arteries becomes louder because of the higher pulse wave, and it can be heard at greater distances from the heart, e.g. on the brachial and radial arteries. Two sounds can sometimes be heard on the femoral artery in aortic incompetence. This doubled tone (Traube’s doubled tone) is generated by intense vibration of the vascular wall during both systole and diastole.
Sounds heard over the arteries are mostly systolic. Systolic sound produced by the stenosed aortal orifice is usually well transmitted onto the carotid and subclavian arteries. Systolic sound associated with decreased viscosity of blood and increased flow rate (e.g. in anaemia, fever, exophthalmic goitre) can also be heard on these vessels. Systolic sound sometimes appears in stenosis or aneurysmal dilation of large vessels. The Vinogradov-Duroziez doubled tone can be heard in aortic incompetence over the femoral artery when it is compressed by a stethoscope bell. The first of these tones is stenotic murmur, which is due to the blood flow through a narrowed (by the pressure of the stethoscope) vessel, while the second sound is explained by the accelerated backflow to the heart during diastole.
Auscultation of veins. Neither sounds nor murmurs are normally heard over veins. Auscultation of the jugular veins, over which the so-called nun’s murmur may be heard, is diagnostically important. This is a permanent blowing or humming sound, which is produced by accelerated flow of blood with decreased viscosity in anaemic patients. It is better heard on the rijght jugular vein and becomes more intense when the patient turns the head in the opposite side.
MEASURING ARTERIAL PRESSURE
The pressure of the blood in the arterial system varies rhythmically, attaining its maximum during systole and lowering during diastole. This is explained as follows: when blood is ejected during systole it meets resistance of the arterial walls and of the blood contained in the arterial system; the pressure in the arteries thus increases to cause distention of the arterial walls. During diastole the arterial pressure falls and remains at a certain level due to the elastic contraction of the arterial walls and resistance of the arterioles, owing to which the blood flow into the arterioles, capillaries, and veins continues. It follows therefore that arterial pressure is proportional to the amount of blood ejected by the heart into the aorta (i.e. the stroke volume) and the peripheral resistance.
Arterial pressure is expressed in millimetres of mercury column. The normal systolic {maximal) pressure varies from 100 to 140 mm Hg and diastolic {minimal) from 60 to 90 mm Hg. The difference between systolic and diastolic pressure is called the pulse pressure (normally it is 40—50 mm Hg). Arterial pressure can be measured by a direct or indirect method. In the direct method, the needle or a cannula is introduced directly into the artery and connected to a pressure gauge. This method is mostly used in heart surgery.
Three techniques exist to take blood pressure indirectly. These are auscultatory, palpatory, and oscillographic. The auscultatory method is commonly used in medical practice. The method was proposed by N. Kbrotkoff in 1905 and is used to measure systolic and diastolic blood pressure. A sphygmomanometer is used to read pressure. It consists of a mercury or a spring manometer which is connected to a cuff and rubber bulb used to inflate the cuff through a connecting tube. A valve on the bulb is used to admit air into the cuff and the manometer, and to hold pressure at the needed level. A more accurate instrument is a Riva-Rocci mercury manometer. This is a mercury container communicated with a thin vertical glass tube attached to a scale graduated in millimetres from 0 to 300.
The pressure in the brachial artery is usually measured. To that end, the arm of the patient is freed from tight clothes and a cuff is attached snugly and evenly onto the arm (a finger-breadth between the cuff and the skin). The inlet socket of the cuff should be directed downward, 2—3 cm above the antecubital fossa. The arm should be placed comfortably on a level surface, the palm up; the muscles of the arm should be relaxed. The phonen-doscope bell is placed over the brachial artery in the antecubital space, the valve on the bulb is closed, the air is pumped into the cuff and the manometer. The pressure of the air in the cuff that compresses the artery corresponds to the mercury level as read off the instrument scale. Air is pumped into the cuff until pressure inside it is 30 mm above the level at which the brachial or radial artery stops pulsating. The valve is then opened slowly to release air from the cuff. Using the phonendoscope, the brachial artery is auscultated and the readings of the manometer followed. When the pressure in the cuff drops slightly below systolic, tones synchronous with the heart beats are heard. The manometer readings at the moment when the tones are first heard are taken as the systolic pressure. This value is usually recorded to an accuracy of 5 mm Hg (e.g. 135, 130, 125 mm Hg, etc.).
N. S. Korotkoff described four phases of sounds that are heard during measurement of arterial pressure. The first phase is the appearance of the tone over the artery. The tones arise at the moment when the pressure in the artery during systole becomes slightly above the pressure in the cuff and the first portions of blood pass into the vessel below the point of constriction to cause pulsation of the relaxed wall of the emptied vessel. Although the tones appear at a pressure slightly below the systolic one, this difference is insignificant and is disregarded. As air pressure in the cuff continues decreasing, greater amount of blood passes the compressed portion of the vessel and the pulsation of the arterial wall below the point of constriction intensifies. The tones become louder, and murmurs caused by the blood turbula-tion below the constricted point join the tones (second phase). A further reduction of the air pressure inside the cuff decreases pressure on the artery and the sounds disappear. The tone loudness increases during this time because the pressure in the cuff still remains above diastolic. The artery below the point of compression remains relaxed, and since greater amounts of blood pass into the vessel during each systole, pulsation of the vessel is intensified and the tones become louder. The moment when loud tones become audible is designated as the third phase. When pressure inside the cuff equals diastolic one, and the blood flow is no longer obstructed, the pulsation of the vessel suddenly decreases. This moment is characterized by a marked weakening and disappearance of the tones (fourth phase).’
The palpatory method is only used to take systolic pressure. As the air is released from the cuff slowly, the radial artery is palpated. When the pressure in the cuff drops slightly below the systolic one, the first weak pulse tones appear.
The oscillographic method is used to record systolic, mean, and diastolic pressure in the form of an oscillogram, and also to assess the tones of the arteries, elasticity of their wall and patency. When blood passes the compressed portion of the artery during systole, the pressure in the cuff increases, and pressure fluctuations are recorded as a curve on a paper chart by an oscillo graph. A simple oscillograph consists of a cuff, a manometer, and recording device. Pulsation of large arteries (e.g. brachial or femoral artery) is studied by oscillography. To that end, the artery in question is compressed by air which is pumped into the cuff. When the artery is compressed completely, the oscillograph only records insignificant vibrations due to the pulse thrust against the blind end of the compressed artery. The release valve is then opened and the pressure in the cuff begins decreasing. As soon as it equals the systolic pressure (to be more exact, as soon as the pressure becomes slightly lower than the systolic one), pulsations appear in the vessel wall, they are recorded as waves of small amplitude. As the pressure continues falling in the cuff, the amplitude of the waves increases. 1 The maximum oscillations correspond to the so-called mean or dynamic blood pressure. The concept of the mean arterial pressure was formulated by I. Sechenov in 1861. According to Sechenov, this is constant pressure that might (without pulsation) ensure movement of the blood in the system at the same rate. Normal mean pressure is from 80 to 100 mm Hg. Mean pressure can only be determined from an oscillogram. It can approximately be calculated by the following formula: Pmean = Pdiastolic + 1/3 Ppulse. As the pressure in the cuff further drops, the amplitude of oscillations decreases. The moment when the oscillations disappear (the last wave on the oscillogram) corresponds to the level of diastolic pressure.
Oscillograms taken at symmetrical points of the upper and lower extremities of healthy persons have a similar pattern. If patency of vessels decreases, oscillations of the affected artery decrease markedly or disappear altogether. Any indirect method of measuring systolic pressure may give somewhat exaggerated results because artificial compression of the vessel imposes additional resistance to the blood flow not only by the vascular wall itself but also the tissues surrounding the vessel. Systolic pressure may also be influenced by the hydraulic impact arising at the blind end of the artery compressed by the cuff as it meets the thrust of the pulse wave. Arterial pressure of healthy subjects varies physiologically within a certain limit depending on physical exertion or emotional strain, the posture, time of meals, and other factors. [Die lowest pressure is normally observed at rest, before breakfast, in the morning, i.e. in conditions under which basal metabolism occurs. This pressure is therefore called basal. When pressure is taken for the first time, it may appear slightly higher than actual which is explained by the patient’s response to the procedure. It is therefore recommended that pressure be taken several times at a run without taking off the cuff but only deflating it completely. The last and the least value should be considered the closest to the true pressure. A transient increase in the arterial pressure may occur during heavy exercise (especially in persons who are unaccustomed to it), in excitation after taking alcohol, strong tea or coffee, in heavy smoking or during attacks of intense pain.
Many diseases are attended by changes in arterial pressure. Elevation of systolic pressure over 140 mm and of diastolic over 90 mm Hg is called arterial hypertension. A drop in the systolic pressure below 100 mm and of diastolic below 60 mm Hg is known as arterial hypotension. Longstanding elevation of arterial pressure occurs in essential hypertension, many renal diseases (glomerulonephritis, vascular nephrosclerosis), in certain endocrinological diseases, and heart diseases, etc. Systolic pressure alone is sometimes elevated, whereas diastolic pressure remains normal or decreased. This causes a marked increase in the pulse pressure. This condition occurs in aortic incompetence, thyrotoxicosis, less markedly in anaemia of any aetiology and atherosclerotic affections of the vessels.
Arterial pressure may be decreased due to constitutional properties in asthenic persons, especially in the upright position (orthostatic hypotension). As a pathological symptom, hypotension occurs in many acute and chronic infectious diseases, Addison’s disease, etc. A sudden drop in the arterial pressure occurs in profuse blood loss, shock, collapse, or myocardial infarction. Systolic pressure alone sometimes decreases while diastolic pressure does not change or even increases. This causes a decrease in the pulse pressure. The phenomenon is observed in myocarditis or exudative and adhesive pericarditis when cardiac output decreases to cause the corresponding fall in the systolic pressure. Pulse pressure decreases also in the presence of stenotic aortal orifice.
Pressure changes in the brachial and certain other arteries (of the lower extremities in particular) are diagnostically important. Aortic coarctation (congenital stenosis of the aorta) is characterized by considerably lower pressure in the femoral arteries compared with the brachial arteries. In order to measure pressure in the femoral artery, the cuff is placed on the thigh of the patient who is in the prone position. The pulse is auscultated in the popliteal fossa. Pressure on both arms and both legs is sometimes measured.
MEASURING VENOUS PRESSURE
Venous pressure is measured in millimetres of water column. In healthy subjects it varies from 60 to 100 mm H20. Direct and indirect phlebotonometry are used to measure venous pressure. The direct method is more accurate. The phlebotonometer is a manometer comprising a glass tube (inner diameter of 1.5 mm) fixed in a stand with a scale graduated from 0 to 350. The lower end of the glass tube is connected by rubber tubing to a needle. Before measuring venous pressure, the tubes are sterilized and filled with isotonic sodium chloride solution. The level in the glass tube is adjusted to zero and the rubber tube is then stoppered by a clamp. Venous pressure is measured with the patient at complete rest in lying position. The instrument is adjusted so that the zero reading of the scale be at the level of the right atrium (at the lower edge of the pectoralis major muscle). Venous pressure in the ulnar vein is usually measured. The vein is punctured by the needle and connected to the apparatus through the rubber tube. The clothes should not compress the arm; the tourniquet on the vein should not be kept for a long time because venous congestion may influence the result of measurement. The needle is then connected to the apparatus, the pressure in the vein levelled (for 1—2 minutes), and the clamp is removed from the rubber tubing to admit the blood into the system: the column of isotonic sodium chloride solution in the glass tube reads venous pressure.
Venous pressure can be determined tentatively by raising the arm until the vein is emptied and the limb becomes pallid. The height (in millimetres) to which the arm is raised from the level of the right atrium corresponds tentatively to the venous pressure. It is pretty constant in healthy subjects at rest. Physical exertion and nervous strain can elevate the pressure. The respiratory phases have a substantial effect on venous pressure. During inspiration the intrathoracic pressure decreases to intensify the venous outflow to the heart and thus to reduce the venous pressure. During deep inspiration the pressure increases. Measuring venous pressure is important for diagnosing diseases and assessing functional condition of the cardiovascular system, especially so if this examination is carried out repeatedly.
ELECTROCARDIOGRAPHY.
Electrocardiography is a method of graphic recording of electric current generated in the working heart, 12-lead electrocardiography recording wide use: 3 standard leads, six chest and 3 unipolar limb leads. Special leads are also used in some cases.
Bipolar limb leads. Moist cloths are placed on the lower third of both arms and less (red on the right arm, yellow – left arm, green – left leg, black – on the right leg. 3 bipolar limbs leads are distinguished: I – (L arm-R arm), II (R arm – L leg). III (L arm – L leg). Chest leads: the electrode is placed at 6 positions: 1) R sternal border, 4th ICS, 2) L sternal border, the 4th ICS, 3) parasternal line, between the 4th and 5th ICS, 4) L midclavicular line, the 5th ICS, 5) L anterior axillary line, the 5th ICS, 6) L midaxillary line, the 5th ICS. Unipolar limb leads AVR, AVL, AVF. AVR -the active electrode is located on the R arm, electrodes of the L arm and L leg are connected together to form the central terminal of apparatus. AVL – active electrode on the left arm, R arm and L leg electrodes together for form the central electrode, AVF – active electrode on the L leg, R arm and L arm electrodes together.
Normal electrocardiogram has the following elements: 1) positive waves P, R, T, negative waves Q and S, the positive wave U is accidental, 2) P-Q, S-T, T-P and R-R intervals, 3) QRS and ORST complexes. Each of these elements characterizes the time and sequence of excitation of various parts of the myocardium.
Cardiac cycle begins with excitation of the atria (P wave, ascending portion – R atrium, descending – L atrium). The wave is small, its amplitude 1-2 mm, the length is 0,08-0,1 s. P-Q interval extends from the beginning of the P wave to the beginning of the Q (or R) wave and includes the time of pulse propagation in the atria and its physiological delay in the AV node (normal length is 0,12-0,18 s). Excitation of the ventricles corresponds to the QRS complex. Its waves vary in size and are different in various leads. The length QRS from the beginning of the Q wave to the end of the S wave is 0,06-0,1 s. This is the time of intraventricular conduction. Q wave corresponds to excitation of the interventricular septum. Its amplitude doesn’t normally exceed 1/4 amplitude of the R wave. The R wave corresponds to almost complete excitation of both ventricles. The negative S wave is recorded in full excitation of the ventricles. At the moment of complete depolarization of the myocardium, the potential difference is absent and the electrocardiogram is therefore a straight line (the S-T interval). S-T interval may be displaced from the isoelectric line to not more than I mm. The T wave corresponds to the repolarization of the ventricular myocardium. The QRST complex corresponds to electrical systole of the ventricles, T-P interval – electrical diastole. The R-R interval corresponds to the time of one cardiac cycle.
The electrocardiogram is interpreted as follows:
1. Regularity of the cardiac rhythm is first determined. The P wave should be before QRS complex, R-R intervals should be equal.
2. The heart rate is calculated, for this duration of one cardiac cycle
should be determined (R-R interval) in seconds, after 60 sec: (divide)
R-R interval in seconds ,we obtained heart rate.
3. Voltage of the electrocardiogram is determined. To that end, the amplitude of R waves is measured in standard leads. Normal amplitude is 5-15 mm. If the sum of amplitudes of R waves in all three main leads is less than 15 mm, the electrocardiogram voltage is considered decreased.
4. Electrical axis of the heart is determined by the shape of QRS complexes in standard leads, described by Einthoven triangle. The position of the electrical axis changes with changes of the position of the heart in the chest. If the diaphragm is low, the E.A. is more vertical, if the diaphragm is high, the EA is more horizontal.
5. The length and size of electrocardiogram elements (P wave,P-Q interval, QRS complex) are then determined, moreover, the direction of the P and T waves is determined. It is difficult to overestimate the clinical importance of electrocardiography, it is used to reveal disorders of heart activity, diagnose coronary circulatory disorders. Electrocardiogram can reveal enlargement of heart chambers. If the atrium is enlarged the P wave changes. Since an enlarged atrium is slower excited, the length of the P wave becomes longer than 0,1 sec. The amplitude of the P wave changes if hypertrophy of atrium present. Enlargement of the left atrium changes P wave in I and II lids, enlargement of the right-in the II and III leads. Ventricular hypertrophy causes the following changes in electrocardiogram: 1) the position of the EA is changed – in left ventricular hypertrophy it deviates to the left, and R ventricular -to the right, 2) amplitude of the QRS and its length increase, 3) recovery of the myocardium is upset, ST segment id displaced and the T wave changes, 4) in L ventricular hypertrophy the amplitude of S wave in the R chest leads increases, the amplitude of the R wave in the left chest leads increases too.
In the R ventricular hypertrophy the changes of the S and R waves are the reverse, i.e. a high R appears in the R chest leads, and a deeper S wave in the L chest leads.
Electrocardiography is used for functional examination of cardiovascular system. Combination of electrocardiography with functional tests helps reveal latent coronary insufficiency and differentiate between functional and organic disorders. Exercise testing is commonly used. At once electrocardiogram taken at rest. The patient is then asked to perform exercise (ascend and descend stairs, 2 step test, etc.) and electrocardiogram are taken then -immediately after the exercise, in 3 and 6 min. A bicycle ergometer is now also used, оr treadmills.
Exercise electrocardiography is a standard procedure for investigation of patients in whom a diagnosis of angina pectoris is being considered as well as in the follow-up of patients who have had a myocardial in-farction or thrombolytic therapy. The apparatus required is not expensive, and the test is available in many doctors’ offices. The aim of an exercise test is to induce the symptoms of which the patient is complaining in the laboratory, in the presence of a physician, and with an ECG running continuously.
Safety Precautions
There is a small but significant (1:10,000) risk in exercising patients with angina until they develop pain or have to stop because of fatigue or severe shortness of breath. The risk mainly stems from the possibility that the patient may have developed a myocardial infarction since last seen, but ventricular arrhythmias, myocardial infarction, collapse, and sudden death may occur during the test. Care must be taken prior to testing to make sure that the patient’s symptoms have not changed, and a 12-lead ECG is taken at rest in the supine and upright positions and compared with the most recent previous ECG. An exercise test should never be done without a doctor present and resuscitation equipment available. The physician in charge must strike a balance between failing to stress the patient enough to bring out symptoms and encouraging excessive and dangerous over-exertion. It is, however, safer for patients with angina to bring on their pain in a laboratory than in the course of their daily activities.
Technique
The exercise stress consists of walking on a motor-driven treadmill or pedaling a cycle ergometer. Several patterns of graded exercise are in common use. The commonest is the Bruce protocol, in which the test is divided into four stages, each lasting 3 minutes. In stage I, the patient walks at 1.7 mph at a 10% grade; in stage II, the speed is increased to 2.5 mph at a 12% grade; in stage III, the speed is 3.4 mph and the grade 14%; and in stage IV, the speed is 4.2 mph and the grade 16%. Comparable protocols are used for cycle ergometer exercise. Other protocols are available for more gradual increase in workload.
Blood pressure is often measured by sphygmoma-nometry during the test, but the values obtained tend to be unreliable because of the motion of the patient and the noise of the treadmill.
The patient is instructed to stop exercise when anginal discomfort would ordinarily cause him or her to stop, or when shortness of breath or fatigue requires cessation of exercise. This is called a “symptom-limited” stress test. The physician stops the test if arrhythmia develops or the patient shows obvious signs of distress. Marked (> 3 mm) ST depression or a falling blood pressure is also an indication to stop.
The heart rate is monitored and the ECG continuously observed during the test. A significant increase in heart rate is sought. Since the maximal heart rate that can be achieved during exercise by normal subjects decreases with age, the expected heart rate for a given patient is obtained from tables, and about 85% of this value used as a target. A rough guide to the maximal heart rate is 220 beats/min minus the patient’s age in years. In practice, most patients with angina of effort develop chest pain at heart rates below 130/min. The ECG is recorded during the first 3 minutes of recovery, since ST-T wave changes sometimes do not develop until after exercise. Exercise electrocardiography is often combined with thallium-201 imaging. The radionuclide is injected at the height of exercise and the images obtained after recovery. If the patient is unable to exercise, thallium imaging can be combined with a drug that increases coronary blood flow, such as dipyridamole, adeno-sine, or increases myocardial oxygen demand, such as dobutamine.
It is possible to obtain stable tracings even during severe exercise on a cycle ergometer or treadmill. Although various lead systems have been used, a single unipolar lead or a bipolar lead from the right subclavicular region to the apex beat, with an indifferent electrode on the head or left shoulder, will detect ischemic changes in the ECG during exercise almost as effectively as more complicated lead systems. In practice, three leads are monitored continuously, usually I, II, and Vg, and every 3 minutes all 12 leads are recorded.
Results
The changes of myocardial ischemia occur during exercise and are virtually always visible in the left ventricular leads (Ґ5 is probably the best). They consist of flat or downsloping ST-T wave depression with T wave inversion. Junctional depression and up-sloping ST segments are not significant, although ST depression of 2 mm and a duration of 0.08 s are considered definite positive findings indicating ischemia. ST depression of 1—2 mm is deemed equivocal.
There is some relationship between the ease with which electrocardiographic changes can be provoked, their magnitude, the length of time they last, and the severity and prognosis of the coronary lesions. Patients with significant left main coronary artery lesions often show marked ST depression with minimal exercise.
Interpretation
The significance of electrocardiographic changes during exercise is greatest in patients with a normal resting tracing who develop “their pain” during the test. Digitalis therapy and the presence in the body of beta-adrenergic blocking agents make interpretation difficult. Digitalis produces ST-T wave changes that may mimic ischemia, and propranolol reduces the heart rate and makes pain less likely to be the limiting factor during exercise. Exercise testing may establish a diagnosis of ischemic heart disease, but the significance of the results is not easy to determine.
A. “False-Positive” Results: Results are generally interpreted as “false-positive” if changes occur in the ECG in patients whose coronary arteries are found to be normal at angiography. False-positive exercise results may be due to misinterpretation of the coronary angiograms. Atherosclerotic changes may be missed because of overlapping vessels or inadequate or technically unsatisfactory views. Typical angina with a normal coronary angiogram does, however, undoubtedly occur, especially in young women. There is increasing evidence that “ischemic” ST depression can result from a failure of coronary arte-rioles to properly vasodilate with exercise, a loss of coronary vascular reserve. ST-T wave changes can also result from autonomic nervous system influence. The results of exercise tests are less reliable in patients with abnormal resting ECGs and in those in whom pain does not develop. The magnitude of the ST depression is also related to the significance of the test, both regarding severity of coronary arterial obstruction and prognosis.
B. “False-Negative” Results: “False-negative” results are assumed if coronary disease is seen on angiography in patients in whom no changes occurred in the ECG during exercise. False-negative results are common, especially in patients who do not develop pain or a high enough heart rate or in asymptomatic persons. If the coronary arteriograms are taken as the “gold standard” for diagnosis, this result is not surprising. There is no necessary or inevitable relationship between the presence of obstructive lesions in the coronary circulation and the presence of ischemic pain or changes on an ECG, but significant lesions are usually present when angina and electrocar-diographic changes are found on exercise. Coronary artery disease is undoubtedly present in a pre-symptomatic (latent) form in many “normal” persons past middle age. “False-negative” results are most common when only one coronary vessel is significantly obstructed, especially in the presence of isolated circumflex vessel disease.
C. Interpretation in Other Uses: Exercise tests are also used to assess the fitness of normal persons in particular occupations, eg, airline pilots. The interpretation of changes in the ECG induced by exercise in such cases is less reliable than in patients with chest pain.
In recent years, exercise tests have been commonly used as a means of assessing patients with recent myocardial infarction. If the patient develops chest pain or changes in the ECG during the test, the prognosis is worse, and if ST segment depression is 2 mm or greater or if it occurs at low double-product (heart rate x systolic blood pressure), coronary arteriogra-phy is indicated. The time after an infarction at which it is safe to do an exercise test is an open question. In many institutions, heart rate-limited stress tests (limited to a heart rate of 120/min) are done before the patient leaves the hospital to identify patients with severe ischemia. It is probably just as well in patients without heart failure or angina on minimal activity to wait until 3 weeks after the infarction and then do a symptom-limited stress test to risk-stratify the patient.
4. STRESS ECHOCARDIOGRAPHY
A recent advance in stress testing has been the detection of changes in wall motion by two-dimensional echocardiography brought about by exercise or infusion ofdobutamine. Imaging is done immediately after exercise on the treadmill or bicycle, with the patient supine or with the left side down. Imaging is done during infusion of increasing amounts of do-butamine: 5, 10, 20, and 30 Jig/kg/min. Iormal patients, there is an increase in contractility of all ventricular walls, resulting in hyperkinesis brought about by sympathetic and catecholamine stimulation. In patients with significant obstructive coronary artery disease, exercise or dobutamine precipitates myocardial ischemia in those segments supplied by the obstructed coronary arteries, resulting in failure to increase wall motion or the development of hypokinesis or akinesis of those segments.
The specificity and sensitivity of both exercise and dobutamine stress echocardiography are equivalent to or better than those of exercise electrocardiography (Marcovitz, 1992). The specificity of stress echocardiography decreases when there is resting abnormal wall motion by echocardiography.
5. MYOCARDIAL ST SEGMENT MAPPING
This procedure, still in the research phase, is another form of investigation designed to follow the progress and assess the size of myocardial infarc-tions. It is moderately expensive and involves multiple ECGs recorded from different sites of the precor-dium. In patients with anterior infarcts, the extent of the area over which ST elevation can be detected bears a relationship to the size of the infarcted area. By summing the total extent of ST elevation in 30 or so electrocardiographic leads placed in standard positions oh the surface of the left chest, it is possible to obtain a numerical assessment that bears a relationship to infarct size. Unfortunately, changes in position of the heart and thickness of the chest wall vary greatly from patient to patient, and this detracts from the general usefulness of the technique.
Pharmacological tests are used to differentiate between functional and organic disorders in coronary circulation. Amyl nitrite and nitroglycerin are used for this purpose. The original electrocardiogram is compared with electrocardiogram taken after medicine intake. Disappearance of signs of myocardial ishaemia after taking drugs indicates the functional character of coronary disorders. Inderal and potassium choride are used for differentiation between neuroendocrine and metabolic disorders and coronary insufficiency in cases with changed terminal parts of ventricular complex(ST interval and T wave).
Heart Defects
The valves of the heart or its septa are involved in heart diseases. The defects may be either congenital or acquired. Congenital heart defects develop during the intrauterine period as a result of abnormal formation and growth of the heart and vessels. Botallo’s duct patency (open passage between the aorta and the pulmonary artery), a defect of the interventricular septum, narrow pulmonary artery, open oval orifice (which is normally open in the foetus only), and some other defects are congenital. Acquired defects result from various diseases such as rheumatism, atherosclerosis, syphilis, sepsis, etc.
The mitral valve is commonly affected; less frequently involved is the aortic and the tricuspid valve, and the pulmonary trunk valve is affected still less often. Stenosis and incompetence of the valves are distinguished. Stenosis is characterized by contraction of the lumen through which the blood is passed. Incompetence of the valve is its incomplete closure which causes regurgitation, i.e. backflow of the blood. Stenosis and incompetence often occur simultaneously. Their clinical picture is characterized by the summation of the symptoms peculiar to each defect.
Mitral Incompetence
The bicuspid (mitral) valve is affected in rheumatic endocarditis by cicatricial changes in its tissues. The valve leaflets (and their tendons) shorten to account for the incomplete closure of the valve during systole. As a result, a slit remains in the valve through which the blood is regurgitated from the ventricle into the left atrium. This condition is called mitral incompetence (regurgitation). This defect rarely occurs alone and it usually combines with stenosis of the left atrioventricular orifice. A combined mitral defect then develops. Symptoms of both mitral regurgitation and a stenosed atrioventricular orifice are seen in such patients.
Organic and functional bicuspid incompetence are distinguished. Organic mitral incompetence is due to the affection of the valve by endocarditis, while functional mitral incompetence is the widening of the atrioventricular orifice which cannot be efficiently closed by a normal mitral valve. This defect usually occurs in an enlarged heart.
In mitral incompetence the left atrioventricular orifice is closed incompletely and during systole, as the blood is injected into the aorta, part of it is regurgitated into the left atrium. As a result, the atrium now contains both the blood ejected from the ventricle and the blood returned from the pulmonary vessels. The left atrium is distended by the excess blood and becomes hypertrophied.
During diastole in addition to the normal amount of blood (60-70 ml), the loft ventricle also receives the blood from the left atrium that was ejected from the ventricle during systole. This causes dilatation and hypertrophy of the left ventricle. The heart performs extra work to compensate for the disordered circulation of blood in mitral incompetence. This condition is called cardiac compensation.
The distended and hypertrophied muscle of the left ventricle weakens with time and the blood outflow from the left atrium becomes difficult. The blood pressure in the left atrium, thus, increases to cause congestion in the lesser circulation. The increased pressure intensifies the action of the right ventricle which also becomes hypertrophied later. Blood congestion in the veins of the greater circulation now develops. The heart becomes unable to compensate for the upset blood circulation. This is called cardiac decompensation or circulatory insufficiency.
Symptoms. In the absence of cardiac decompensation, the patient has no complaints. The early decompensation stage is manifested by exertional dyspnoea. As the disease progresses further, the patient complains of palpitation, edema in the evening, and especially after physical strain. When decompensation is pronounced, dyspnoea develops at rest, the patient complains of right hypochondriac pain and edema of the legs. Examination reveals cyanotic erythema on the face (the patient looks younger). The apex beat of the distended and hypertrophied heart is displaced to the left and down; the beat is intensified and its pulsation extends over a larger area.
Percussion of the heart reveals the broadening of its borders to the left due to dilatation of the left ventricle and upwards as a result of dilatation of the left atrium. These changes are obvious by x-ray. In severe cases the heart is also enlarged to the right due to dilatation and hypertrophy of the right ventricle. Auscultation reveals weakening of the first sound at the apex due to the absence of the closure of the valves. A systolic murmur can be heard at the apex, which changes but little during respiration. The systolic murmur is due to the backward blood flow from the left ventricle to the left atrium during systole, which causes turbulence in the blood flow and vibration of the sclerosed mitral valve cusps. The second sound is accentuated over the pulmonary artery in the second left intercostal space because of the increased blood pressure in the lesser circulation.
Prognosis. The course of this heart disease is rather calm. The valvular incompetence remains compensated during a prolonged period of time and the progress of the circulatory insufficiency is slow. The patients often live to old age without being aware of their disease. Developing circulatory insufficiency impairs the prognosis.
Mitral Stenosis
Stenosis of the left atrioventricular orifice occurs as a result of rheumatism. The leaflets of the mitral valve adhere to one another narrowing the atrioventricular orifice to 0.5-1 sq cm as opposed to the normal 5-6 sq cm. The blood flow from the left atrium to the left ventricle is, thus, obstructed.
During diastole the blood flow from the left atrium to the left ventricle is difficult and the atrium is emptied incompletely. A new portion of blood from the pulmonary veins is added to the remaining blood and the atrium is distended and hypertrophied. This causes blood congestion in the lesser circulation, which in turn causes dilatation and hypertrophy of the right ventricle and congestion in the greater circulation. The left ventricle is affected but little since a decreased amount of blood is delivered into it through the stenosed orifice.
Symptoms. The patients complain of exertional dyspnoea, and palpitation; some patients complain of pain in the heart and spit up blood (due to an overload in the lesser circulation). The tip of the nose, the external ears, and the lips are cyanotic. The cardiac beat is not intensified, but pulsation in the epigastrium increases due to distension and hypertrophy of the right ventricle. ‘Cat’s purring’ (a diastolic thrill) can often be palpated at the heart apex. Percussion reveals upward displacement of the heart’s border due to enlargement of the left atrium and displacement to the right due to enlargement of the right ventricle. More specific changes become obvious by x-rays. The absolute cardiac dullness increases due to dilatation of the right ventricle.
Auscultation of the heart reveals a loud and snapping first sound at the apex. This is due to incomplete filling of the left ventricle with blood. The second sound markedly increases over the pulmonary artery because of the increased blood pressure in the lesser circulation. The opening sound of the mitral valve and diastolic murmur are often heard at the heart apex. The diastolic murmur can be heard during early diastole (protodiastolic murmur), during the middle of diastole (mesodiastolic murmur), or at the end of diastole (presystolic murmur).
Mitral stenosis is characterized by a low (small) pulse. Fibrillation is also characteristic. As fibrillation develops, the circulatory insufficiency rapidly increases. Fibrillation is characterized by a markedly decreasing murmur or even its complete absence.
Prognosis. The prognosis of mitral stenosis depends on the degree of affection and the presence of complications (first of all thromboembolism, fibrillation, and lung infarction). Embolism is caused by parietal thrombi that that are torn off from the distended left atrium. Distension of the atria promotes development of fibrillation. Lung infarction with subsequent blood spitting arises as a result of obstruction of the pulmonary vessels by the thrombi torn off from the right atrium, obstruction of the veins in the lower extremities, or thrombosis of the pulmonary vessels due to decelerated circulation. Heart failure develops comparatively early, but it can be adequately managed for protracted periods of time.
Aortic Incompetence
Incompetence of the aortic valve develops in rheumatism, syphilis, subacute septic endocarditis, and in transition of sclerosis from the aorta onto the valve. This heart disease often combines with other valvular diseases. Aortic incompetence alone is usually characteristic of syphilis. During diastole an affected aortic valve fails to close completely and part of the blood is regurgitated from the aorta into the left ventricle. The blood from the left atrium also enters the ventricle to distend it and cause hypertrophy.
Symptoms. The patients complain of headache, dizziness, pain in the heart, palpitation, and pulsation in the neck. Dyspnoea develops in later stages. Signs of circulatory insufficiency are late, but once they have appeared, their progress is rapid. Cardiac asthma is an especially unfavourable sign. During examination the following symptoms are revealed: pallor, pulsating arteries (first of all, the carotid artery on the neck). The carotid pulsation can be so strong that the head shakes with each systole (Musset’s sign). When a finger nail is pressed slightly, the capillary pulse can be seen in the quick filling and emptying of the vessels of the nail bed. The pulse of the radial artery is usually high, the pulse wave is jumpy and high too. Systolic pressure is elevated, while diastolic is always low and sometimes falls to zero. The pulse pressure (the difference between the systolic and diastolic pressure) is very high. These symptoms are caused by ejection of a big volume of blood by the left ventricle into the aorta and the rapid backflow of part of his blood into the left ventricle. The apex beat is intensified and displaced tг the left, and down (to the 6-7th intercostal space).
Percussion reveals broadening of the cardiac dullness area to the left. Chest X-rays show the horizontal position of the heart, which looks like a sitting duck (aortic heart). Auscultation reveals weak and dulled first sound due to the absence of complete closure of the valves. A diastolic murmur can be heard at the listening point over the aorta; the sound is conducted to the Botkin-Erb point. This murmurs best heard when the patient stands upright. A systolic murmur appears at the apex. The murmur is functional: it arises due to a sharp dilatation of the left ventricle which accounts for distension of the left atrioventricular orifice.
The course of the disease depends largely on the disease that caused the aortic incompetence. In most patients the course is benign because the powerful muscle of the left ventricle compensates for the incompetence. Decompensation may be absent in these patients; some patients remain unaware of their disease. Once circulatory insufficiency develops, its progress is rapid; cardiac asthma is a common manifestation of the insufficiency. The prognosis is worse in patients with syphilitic affections of the aortic valve. The valvular disease in these patients is attended by the affection of the aorta and the coronary arteries of the heart.
Stenosis of Aortic Orifice
Stenosis of the aortic orifice is not infrequent, but even today it often remains unrecognized. The main cause of aortic stenosis is rheumatism; less frequently it develops secondary to subacute septic endocarditis. In some cases the disease is caused by calcification of the aortic valve. Cases in which the aortic orifice alone is afflicted are rare; more frequently stenosis of the orifice combines with aortic valve incompetence.
During systole the blood from the left ventricle of patients with aortic stenosis is ejected into the aorta through a contracted orifice and part of the blood remains in the ventricle. During diastole a normal portion of blood from the left atrium is added to this remaining blood in the left ventricle distending it; a more powerful contraction of the ventricle then follows. The left ventricle has to perform more work and, thus, becomes hypertrophied and dilatated.
Symptoms. Patients with aortic stenosis rarely present complaints. Some patients feel pain in the heart due to incomplete filling of the coronary vessels of the heart; syncopes (especially during heavy exercise) may occur. Dyspnoea and palpitation develop during the late stages of the disease. The examination of the patient reveals pallor which is due to insufficient blood supply to the peripheral vessels.
The pulse is slow; the pulse wave rises slowly and is not high; the blood is slowly ejected into the aorta through a contracted aortic orifice. Pulse pressure decreases. The apex beat is displaced to the left and intensified. A systolic thrill (cat’s purring) can be detected in the second intercostal space, to the right of the sternum. A coarse systolic noise can be heard over the same listening point. This sound is conducted by the blood stream to the carotid arteries. The murmur is caused by the blood passing into the aorta through a narrow orifice during systole.
Prognosis. The disease is characterized by a slow progress. The patient leads a normal life. Development of angina pectoris and circulatory insufficiency worsens the prognosis significantly. The circulatory insufficiency is manifested by cardiac asthma.
Tricuspid Incompetence
This disease can be either organic, when the tricuspid valve is attacked by endocarditis, or secondary, when the valve incompetence develops due to dilatation of the right ventricle and distension of the fibrous ring. As a result, the valve cannot completely close the tight atrioventricular orifice. Secondary incompetence occurs more frequently. It occurs in mitral incompetence, in myocarditis, and pulmonary heart. The organic form of the disease occurs in rare cases. It develops as a result of rheumatic endocarditis combined with mitral and aortic incompetence. Cases in which the tricuspid valve alone is affected are extremely rare. In tricuspid incompetence the blood is ejected during systole, from the right ventricle to the right atrium causing its considerable dilatation.
Symptoms. Patients with tricuspid incompetence complain of exertional dyspnoea and dyspnoea at rest, discomfort in the epigastrium, and oedema. Examination of the patient reveals cyanotic skin with an icteric hue. The neck veins are swollen and pulsating. The liver is enlarged and also pulsates during systole. Pulsation of the neck veins and the liver is explained by ejection, during systole, of the blood from the right ventricle into the right atrium from where the blood is ejected into the vena cava. Percussion reveals enlargement of the cardiac dullness to the right. Auscultation at the 4th right costosternal articulation reveals weakening of the first and second heart sounds, and also a systolic murmur. The pulse is usually fast and small. The arterial pressure does not change significantly.
Prognosis. Since tricuspid incompetence often combines with other heart defects, the prognosis depends largely on these other defects. Tricuspid incompetence diminishes congestion in the lungs decreasing dyspnoea and improving the general condition of the patient.
Prophylaxis and Treatment of Heart Defects
Unless a heart defect is attended by heart failure, the patient can continue with his routine occupation. Some patients are unaware of their disease. No special treatment is necessary for patients with compensated heart diseases. But they may not be regarded as healthy individuals either. Relapses of rheumatic endocarditis may develop in patients with a heart disease. The affected valves are more easily attacked by infection thaon-involved valves. Cardiac decompensation finally develops in most patients with heart diseases. It follows, therefore, that such patients are exposed to two dangerous factors: possible relapse of endocarditis and circulatory insufficiency.
The main prophylactic measures should be directed at preventing exacerbations of endocarditis or circulatory insufficiency.
This is attained by protecting the patient from various infections primarily from rheumatism, and also by eliminating infection, foci in the mouth, nasopharynx, paranasal sinuses, and the genitalia (in women). Various infectious diseases exacerbate rheumatism. Antibiotics of prolonged action should, therefore, be administered for infections during the course of the disease and also during the first days of convalescence.
The work regimen and leisure time should be organized correctly for patients with compensated heart diseases. They should avoid overstrain, but light physical work is necessary for training the heart muscle and the coronary vessels. It should be recommended that patients with compensated heart diseases have adequate night rest and rest during the day, exercise moderation in eating and drinking, abstain from alcohol and smoking.
Prophylaxis of heart diseases is prevention and correct treatment of rheumatism and endocarditis, and also sanation of infectious foci in the mouth, paranasal sinuses, etc.
No treatment is needed in cardiac compensation. Sanatoria and health resorts are effective. Patients with heart diseases feel better in the fresh air and in mild climates.
A stenosed left atrioventricular orifice or aortic stenosis can only be corrected surgically. If a patient has active rheumatism or circulatory insufficiency, he should be given conservative treatment before surgical intervention. Patients with severe circulatory insufficiency and significant changes in the myocardium are not operated on. Artificial valves are implanted surgically in patients with valvular incompetence.
Heart Diseases and Pregnancy
Pregnancy and labour are often complicated in patients with heart diseases. Late toxaemia of pregnancy and eclampsia are frequent in these patients. Premature withdrawal of the amniotic fluid and uterine inertia occur more frequently in women with heart diseases. Cardiac decompensation is a severe complication of pregnancy. Circulatory insufficiency occurs in about 50 per cent of all patients with heart diseases and they should, therefore, be hospitalized three times: during early pregnancy (to decide if the pregnancy may be preserved), during the middle of the pregnancy, (28-32nd week when the load on the heart is maximum), and near the end of pregnancy (3-4 weeks before labour) to prepare the woman for labour and to decide which way of parturition is best for the patient.
During early pregnancy (to 14 weeks) an artificial abortion is indicated in women with endocarditis, aortic incompetence, mitral stenosis, combined mitral disease, and also organic diseases of the heart which are attended by symptoms of circulatory insufficiency during early pregnancy. Abortion at later terms is indicated if all measures to eliminate circulatory insufficiency prove ineffective. The method by which the pregnancy is interrupted should be chosen separately in each particular case. Caesarean section is performed in extreme necessity: 1—in recurrent rheumatic carditis; 2—in cardiac asthma; 3—in pronounced mitral stenosis.
Salicylates, butadiene, amidopyrin, and antibiotics are prescribed for exacerbations of rheumatic carditis. In the presence of symptoms of late toxaemia, magnesium sulphate should be administered promptly.
Circulatory Insufficiency
The supply of nutrients to the bodily organs and tissues becomes insufficient in circulatory disorders. Circulatory insufficiency arises due to decreased contractile power of the myocardium and the muscular coat of the vessels. The share of the vascular and cardiac components may be different in various diseases. Either the cardiac or vascular failure may prevail in circulatory insufficiency. In some cases one of these components may be very significant while the other be so mild that heart failure or vascular insufficiency can be regarded separately. Some patients develop cardiovascular insufficiency (myocardial infarction, etc).
Vascular insufficiency may be acute or chronic. Acute vascular insufficiency is of greater clinical significance. Chronic vascular insufficiency is manifested by hypotension, i.e. decreased arterial pressure.
Acute vascular failure manifests by syncope, collapse, and shock. The vascular failure develops as a result of decreased blood filling of the vessels due to: 1—decreased volume of circulating blood (withdrawal of part of the circulating blood to the blood depots, usually in the abdominal organs or some other vessels); 2—loss of blood or fluid; 3—transition of the liquid component of the blood to the tissues. Acute vascular failure arises in many diseases and conditions such as: 1—infectious diseases (lobar pneumonia, louse-borne typhus); 2— profuse blood loss; 3—injuries; 4—anaphylactic shock; 5—food poisoning; 6—severe pain; 7—frights, etc.
Syncope is a form of acute circulatory failure, with a transient loss of consciousness due to a sudden decrease of blood supply to the brain. As a rule, blood rapidly flows to the abdominal vessels during syncope. Syncope occur in persons with a weak nervous system (frights), or when a patient sharply stands up (or sits) from a horizontal position.
The skin of a patient with syncope is pallid and covered with cold sweat; the pupils are contracted; the pulse is small and weak.
Collapse is another form of circulatory failure arising in upset regulation of the vascular tone. Collapse occurs in severe infections, profuse bleeding, vomiting, diarrhoea, and other conditions attended by a significant loss of fluid.
The patient is very weak but conscious. The skin is pallid and covered with cold sweat. The pulse is fast and weak, the arterial pressure, low, the respiration is rapid and shallow.
Shock is the most severe form of acute circulatory failure. It usually occurs in burns, grave injuries, myocardial infarction, and allergy (anaphylactic shock).
The symptoms of a shock depend mostly on the disease which causes the shock. The patient is conscious but complains of weakness. The temperature drops below normal values, the limbs are cold, the face is pinched, the pupils are dilated, skin is pallid and covered with cold sticky sweat. The patient is thirsty, the tongue is dry, the pulse is fast, small, and soft. The visible neck veins are collapsed.
Treatment and care. The patient in a syncope should be placed so that his legs are slightly elevated (above the head level) to facilitate the blood supply to the brain. The patient’s chest should be stripped of his clothes. Cold water should be sprayed over the patient’s face and ammonia spirit put to his nose. As a rule, these measures are sufficient to recover the patient to his senses. If, however, these measures fail to help, 1 ml of cordiamine or mesaton should be injected subcutaneously.
The treatment and care of the patient in collapse or shock are the same. The cause that provokes the acute circulatory failure should first of all be eliminated (control of poisoning, arrest of bleeding). The patient should be placed in the horizontal position to improve the blood supply to the brain and to increase the venous blood flow to the heart. The patient should be warmed (blanket, hot water bottles to the feet). In the presence of the pain syndrome, pain should be removed by subcutaneous or intravenous injection of narcotics (morphine, pantopon, promedol). The treatment should be directed mainly at increasing the vascular tone and the amount of liquid in the body. Camphor, caffeine, or cordiamine should be administered subcutaneously. These preparations act on the vasomotor centers in the medulla oblongata and also increase the volume of the circulating blood, elevate the blood pressure, and improve the contractile function of the myocardium.
Mesaton (0.5-1 ml of 1 per cent solution) or norepinephrine (0.3-0.5 ml of a 0.1 per cent solution) are administered intravenously to treat collapse and shock. Later these preparations are administered dropwise through a needle or through a permanent tube. The solution is prepared by adding 1-2 ml of a 1 per cent mesaton or 1-3 ml of a 0.1 per cent norepinephrine solution to 500 ml of isotonic sodium chloride solution or the same amount of 5 per cent glucose solution. The solution is administered at a rate of 20-40 drops per minute, so that the systolic arterial pressure is between 100 and 110 mm Hg. In order to increase the hypertensive effect of norepinephrine, 1 ml of a 0.1 per cent atropine sulphate solution is added to the dropper.
Corticosteroids are administered in a deep collapse or shock. From 30 to 90 mg of prednisolone or 100-200 mg of hydrocortisone are added to the system with mesaton or norepinephrine. Ion-reactive collapse or shock it is reasonable to use hypertensin which is ten times more effective thaorepinephrine. Dextran, polyglucin, or other blood substitute (800-1000 ml) should be infused intravenously or even intra-arterially. Biological tests and tests for individual compatibility should be done before administering sera.
Heart failure. This is the decreased contractile function of the myocardium. Acute and chronic heart failure are distinguished. In heart failure the load on the heart exceeds its pumping capacity. The heart load is determined by the amount of blood delivered to the heart and the resistance which the blood meets as it is ejected from the heart. Heart failure can be caused by fatigue of the myocardium (in heart diseases, hypertension, etc.), disordered blood supply to the myocardium through the coronary vessels (in ischaemic heart disease), upset metabolism in the myocardium, and toxic effect of substances on the myocardium.
Heart failure is further divided into right and left ventricular failure. Right chambers of the heart undergo changes in right ventricular heart failure: the right atrium and ventricle are hypertrophied and dilatated. Right ventricular heart failure is characterized by venous congestion in the greater circulation (swelling of the neck veins, enlargement of the liver, oedematous legs and the sacrum, extension of oedema onto the abdominal, pleural, and pericardial cavities).
The venous pressure increases. Cyanosis and tachycardia are also characteristic of right ventricular heart failure.
Left ventricular heart failure is characterized by hypertrophy and dilatation of the left heart chambers. Blood is congested in the lesser circulation. Most patients develop dyspnoea and night attacks of asthma, cough, and rales in the lungs. The venous pressure does not increase but tachycardia, is observed.
Acute right ventricular heart failure occurs in embolism of the pulmonary artery, lobar pneumonia, paroxysmal tachycardia, paroxysmal fibrillation, atrial flutter, and the like conditions. Dyspnoea, cyanosis, acute hepatic enlargement attended by right hypochondriac pain, nausea, vomiting, and abdominal flatulence are characteristic. Oedema soon develops.
Acute left ventricular heart failure develops in diseases involving mostly left chambers of the heart (essential hypertension, atherosclerotic cardiosclerosis, myocardial infarction, acute nephritis, aortic incompetence). Acute left ventricular heart failure is manifested by cardiac asthma and lung oedema.
Cardiac asthma is characterized by attacks of asphyxia which occur mostly during the night time. The patient assumes a forced posture: he sits still in his bed. Attacks of asthma are attended by cough with expectoration of sputum (sometimes with streaks of blood). Auscultation reveals dry rales in the lungs (moist rales in their lower parts). If medication is ineffective and the condition of the patient-worsens, the picture of lung oedema develops. Cyanosis rapidly progresses, the respiration becomes gurgling, and the amount of moist rales in the lungs rapidly increases. The pulse becomes thready and the patient loses his consciousness. This condition requires urgent measures to be taken.
Treatment and care. The patient with an acute heart failure should be ensured a complete bed-rest. His head should be slightly raised. In the absence of collapse, blood-letting is indicated as an urgent measure (300-500 ml). Immediately following the phlebotomy, 0.25-0.5 mg of strophanthin (diluted in 20 ml of a 40 per cent glucose or isotonic sodium chloride solution) should be administered. Morphine or pantopon should be administered for severe dyspnoea. Inhalation of oxygen and counterattractive means (hot water bottles to the legs, hot water baths, mustard plasters to the legs, tourniquetes on the thighs to provoke venous engorgement) are indicated as well. In order to release load on the lesser circulation and to stimulate dehydration, strong diuretics (lasix, urea) and also ganglioblocking drugs (pentamine, dicoline, arphonad) should be administered intravenously. Antifoaming measures should be taken in progressive oedema of the lungs: oxygen is given to breathe through a nasal tube (96 per cent alcohol should be used instead of water to humidify the gas). Inhalation should continue for about 30 minutes.
Chronic heart failure develops gradually with slowly increasing pathological processes which cause the failure (heart defects, cardiosclerosis, essential hypertension, etc.).
The following symptoms are characteristic of chronic heart failure. The earliest and constant symptom is tachycardia. It is first exertional but later occurs at rest. Dyspnoea is an early symptom, of left ventricular heart failure. It may be exertional (provoked by physical effort), dyspnoea at rest, paroxysmal dyspnoea (coming in attacks), or in the form of Cheyne-Stokes’ respiration. Dyspnoea is caused by the oxygen deficit of the organs and tissues. Orthostatic dyspnoea (dyspnoea in the erect position) occurs due to blood congestion in the lesser circulation. Dyspnoea may develop when the patient lies: the blood flows from the legs to the thoracic viscera, the diaphragm rises to impair lung ventilation, and the patient sits up to lessen dyspnoea. The Cheyne-Stokes’ respiration is characterized by alternation of waxing and waning of the breathing depth with regularly recurring periods of apnoea. This condition usually occurs at night in patients with severe and late heart failure.
Increased venous pressure is an important symptom of chronic right ventricular heart failure. It arises due to blood congestion in the greater circulation. The pressure first rises in the atria and then in the veins. Engorgement of the veins is quite obvious, especially on the neck.
Oedema is accumulation of fluids in subcutaneous cellular tissue and in the bodily cavities. Heart failure is characterized by oedema of the legs and the lumbar regions, which intensifies by the end of the day. In later stages of heart failure, fluids are accumulated also in serous cavities such as the pleural cavity (hydrothorax), pericardium (hydropericardium), and the abdomen (ascites). Cracks and trophic ulcers develop on the skin overlying pronounced oedema (mainly on the legs).
Cyanosis is an early symptom of heart failure. The cyanotic colour is more obvious on the fingers and toes, the tip of the nose, the lips, i.e. at sites where the bloodflow rate is slowed down. Later cyanosis spreads over the other parts of the body. Cyanosis arises due to the slow bloodflow and underoxidation of haemoglobin.
Congestion in the lungs is caused by difficult blood outflow from the lungs to the left atrium. If congestion is chronic, the lungs become consolidated and lose their elasticity. Congestion in the lungs manifests clinically by dyspnoea, cough, and moist rales in the lower portions of the lungs.
Congestive hepatic enlargement is connected with the congestion of blood in the veins. The liver becomes firm and tender. A protracted congestion of blood in the liver stimulates the growth of fibrous tissue which accounts for secondary cirrhosis of the liver.
Chronic heart failure is characterized by myocardial dysfunction, decreased cardiac output (decreased minute volume), and decelerated blood flow. The amount of the circulating blood, on the contrary, increases.
During the progress of heart failure the number of its symptoms increases. The patient first complains of exertional dyspnoea, palpitation, and cyanosis. Later even an insignificant exercise provokes dyspnoea; the neck veins swell, the patient complains of right hypochondriac pain (due to hepatic congestion), and oedema. If heart failure further progresses orthopnoea and ascites develop, oedema intensifies, the urine output decreases, and the patient loses weight (cardiac cachexia).
Three stages of chronic heart failure are distinguished according to Strazhesko and Vasilenko by gravity of the affection. During the first stage heart failure is manifested by exertional dyspnoea and tachycardia. The second stage is also characterized by oedema, cyanosis, hepatic enlargement, and congestion in the lungs that can be quickly removed by the appropriate treatment. During the third stage dyspnoea occurs at rest, the cyanosis is pronounced, tachycardia and oedema are constant, the liver is cirrhosed, and liquid accumulates in the abdominal and pleural cavities. The internal organs are attacked by dystrophic changes.
The treatment of chronic heart failure depends on the stage of the disease. Dietary restrictions are necessary at all stages of the disease. The amount of liquid should be restricted to 500-800 ml daily; the salt intake should be restricted as well. The more severe the course of heart failure, the lesser the amount of liquid and salt should be taken. The food should be easily assimilated and cause no flatulence. Bed-rest should be recommended to the patient. Hypnotics and sedatives should be given for deranged sleep.
No special medication is required in the first stage. Cardiac glycosides (digoxin or isolanid, 0.00025 g 2-3 times daily) should only be administered for pronounced tachycardia. Patients with heart failure in the 2nd or 3rd stage should be hospitalized. Cardiac glycosides and diuretics are the main preparations to eliminate signs of cardiac decompensation. Digitoxin (0.0001 g, 3 times daily), digoxin, and isolanid should be given per os. If these preparations fail to produce the desired effect or if heart failure is significant, cardiac glycosides (strophanthin or corglycon) should be administered intravenously. They should be injected slowly, during 3-4 minutes. Care should always be taken against overdosage of cardiac glycosides. The first signs of poisoning are nausea and vomiting, decreased diuresis, and extrasystoles. In the presence of these signs the administration of these preparations should immediately be suspended and potassium salts (10 per cent potassium chloride solution, 20 ml 3-4 times daily) administered instead.
Diuretics are effective to control heart failure: hypothiazid (50-100 mg), lasix (80-120 mg), brinaldix (0.02-0.04 g), and etacrynic acid (0.1-0.2 g) are given in the morning.
Patients with the third stage of the disease should be prescribed bpd-rest and diet. Cardiac glycosides and diuretics should be administered. Oxygen (a mixture containing 60 per cent of oxygen) should be given to breathe in severe hypoxia. The gas mixture is given through a mask, nasal tubes, or in oxygen tents. Vitamin B1 and cocarboxylase are used to improve nutrition. Cardiotonics (cordiamine, camphor) are widely used.
Prophylaxis of circulatory insufficiency is primarily treatment of the disease to which cardiac decompensation is secondary. Dispensary care of patients and timely treatment of the disease preclude aggravation of circulatory insufficiency.
Patient care. The patient should observe strictly the regime and the diet. The prescribed preparations should also be taken according to the physician’s order. If dyspnoea develops or the daily diuresis decreases with the development of oedema, the patient should be placed in bed. Rest will be helpful in mild cases. In the presence of cardiac decompensation, cardiac glycosides and diuretics should be administered in addition to complete bed-rest.
The patient’s bed should be comfortable and soft. Adjustable beds suit the purpose best of all. Bed linens should be straightened regularly. The patient’s anal region should be washed after each defaecation. The skin also requires a thorough care. The skin dries and thins on the oedema-affected legs. Even minute scratches become leaking to release the fluid. The skin, thus, macerates and the danger of erysipelatous inflammation arises. Dry skin should be treated with vaseline or lanolin. If oedema is pronounced, the sites where the legs contact each other should be treated with talcum. The diuresis should be measured in heart failure: the increasing or decreasing amounts of daily urine indicate changes in the patient’s condition. The patient should be weighed at least once a week; decreasing body weight indicates elimination of oedema. Proper care of the patient is, to a certain measure, important for the success of general treatment.
