Auscultation of a heart: heart sounds, their splitting, reduplication

Auscultation of a heart: heart sounds, their splitting, reduplication. Adventitious heart sounds

Organic and functional heart murmurs.

Method of registration and coding of electrocardiogram (ECG). ECG-signs of hypertrophy of  heart chambers.

 

 

Аuscultation of a  heart

Auscultation involves listening for heart sounds with the stethoscope, similar to the procedure used in assessing breath sounds.

 

For most of this century, the stethoscope has served as a critical diagnostic tool in cardiovascular evaluation. With the advent of numerous new diagnostic modalities, however, especially ultrasonic imaging and Doppler techniques, cardiac auscultation is receiving less emphasis in teaching and practice. To compound this problem further, phonocardiography, ie, the graphic recording of heart sounds, which had served as a valuable means for teaching and documenting auscultation, has been largely discarded in this country. Although medical training directors and their students generally believe that cardiac auscultation is a skill that physicians should master, there appears to be a widespread belief that this skill is of secondary importance because the same information is readily obtainable through newer technological means. Possibly as a result of this attitude, there is no structured teaching of cardiac auscultation in three fourths of American internal medicine programs and two thirds of cardiology programs.¹This will inevitably lead to poor practice and teaching of this technique at all levels of training. Although not as well documented, the same process of attrition is probably affecting the other cognitive skills of history taking and bedside examination.

Conventional wisdom dictates that auscultatioot only provides important clinical information in itself but also is a cost-effective means to select additional tests. To support these assumptions, however, we must evaluate contemporary information concerning not only how auscultation can be used for additional test selection but also how it might, in comparison with other testing methods, provide a source of information of independent clinical value. For this reason, we shall examine a few specific examples in which auscultation can be used to achieve these ends. To maximize information gained through auscultation, however, we must attempt to identify sources of inaccuracy and suggest methods to correct these deficiencies, thereby allowing for more uniform and effective teaching and practice of this method.

Stetoscopes

A variety of stethoscopes are available for auscultation of heart sounds. Many stethoscopes have a separate bell and diaphragm. The bell is most effective at transmitting lower frequency sounds, while the diaphragm is most effective at transmitting higher frequency sounds.

Some stethoscopes combine these functions into a single surface such that the intensity of pressure of the stethoscope against the skin determines whether the stethoscope functions as a bell or a diaphragm. In addition, pressing the bell more firmly against the skin alters the frequencies that are loudest towards those of a diaphragm such that higher frequency sounds become louder and lower frequency sounds become softer.

 

Origin of heart sounds. The heart sounds are produced by the opening and closing of the valves and the vibration of blood against the walls of the heart and vessels. Normally two sounds – S₁ and S2 – are heard, which correspond  respectively to the familiar “lub dub” often used to describe the sounds. S₁ is caused by the closure of the tricuspid and mitral valves (sometimes called the atrioventricular valves). Right ventricular contraction follows tricuspid valve closure, and left ventricular contraction follows mitral valve closure. The contractions (systole) occur almost simultaneously, although the mitral valve (left side) closes slightly before the tricuspid valve (right side). Normally this split of the sounds is so close that it is not audible, except occasionally at the apex of the heart.

S₂ is the result of the closure of the pulmonic and aortic valves (sometimes called semilunar valves). Aortic valve closing (left side) occurs slightly before pulmonic valve closing (right side). The flow of blood into the aorta and pulmonary artery occurs following closure of their respective valves. The interval between S₂ and S₁ is diastole, or relaxation, of the heart. Normally the split of the two sounds in S₂ is distinguishable and widens during inspiration, since inspiration prolongs right ventricular filling and delays pulmonic valve closure. “Physiologic splitting” is a significant normal finding that should be elicited. “Fixed splitting”, in which the split in S₂ does not change during inspiration, is an important diagnostic sign of atrial septal defect.

The heart is usually auscultated by a stethoscope or a phonendoscope, but direct (immediate) auscultation is also used. The condition of the patient permitting, the heart sounds should be heard in various postures of the patient: erect, recumbent, after exersice (e.g. after repeated squatting). Sounds associated with the mitral valve’s pathology are well heard when the patient lies on his left side, since the heart apex is at its nearest position to the chest wall; aortic valve defects are best heard when the patient is in the upright posture or when he lies on his right side. The heart sounds are better heard if the patient is asked to inhale deeply and then exhale deeply and keep breath for short periods of time so that the respiratory sounds should not interfere with auscultation of the heart. The valve sounds should be heard in the order of decreasing frequency of their affection. The mitral valve should be heard first (at the heart apex); next follows the aortic valve (in the second intercostal space to the right of the sternum), the pulmonary valve (in the second intercostal space, to the left of the sternum), tricuspid valve (at the base of the xiphoid process), and finally the aortic valve again at the Botkin-Erb point. If any deviations from normal sounds have been revealed at these points, the entire heart area should be auscultated thoroughly.

 

http://www.youtube.com/watch?v=ax9B6g6gEOc

http://www.youtube.com/watch?v=falNFIx5PpI

 

The second 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  (the vascular component).

Both sounds can be heard over the entire precordium but their strength changes depending on the proximity of the valves involved in the formation of the first or second sound Therefore, in order to assess correctly the findings of auscultation, it is necessary to know the sites where the valves project on the chest wall (the auscultatory valve areas) and also areas where the sounds produced by a valve can be better heard.

The sites of projections of the valves on the anterior chest wall are very close to one another. The mitral valve projects to the left of the sternum, at the 3rd costosternal articulation, and the tricuspid valve, on the sternum midway between the 3rd left and 5th right costosternal articulations 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. Since all heart valves are projected on a small area of the chest, it is difficult to decide which of them is damaged if the valves are auscultated at sites of their actual projections.

Where to place your stethoscope

As with palpation of the heart, auscultation should proceed in a logical manner over 4 general areas on the anterior chest, beginning with the patient in the supine position.  The 4 percordial areas are examined with diaphragm, including:

1.                 Aortic region (between the 2nd and 3rd intercostal spaces at the right sternal border) (RUSB – right upper sternal border).

2.                 Pulmonic region (between the 2nd and 3rd intercostal spaces at the left sternal border) (LUSB – left upper sternal border).

3.                 Tricuspid region (between the 3rd, 4th, 5th, and 6th intercostal spaces at the left sternal border) (LLSB – left lower sternal border).

4.                 Mitral region (near the apex of the heard between the 5th and 6th intercostal spaces in the mid-clavicular line) (apex of the heart).

The auscultatory areas are as follows: (1) the area of the apex beat for the mitral valve because the vibrations are well transmitted by the muscle of the left ventricle and the cardiac apex is at the nearest distance to the anterior chest wall during systole; (2) the lower part of the sternum near its junction with the xiphoid process (the right-ventricular area); for the tricuspid valve; (3) the valve of the pulmonary trunk is best heard at its anatomical projection onto the chest, i.e. in the second intercostal space, to the left of the sternum; (4) the aortal valve is best heard in the second intercostal space, to the right of the sternum where the aorta is the nearest to the anterior chest wall. Moreover, the heart sounds which are associated with the contractions of the aortic valve or which develop during its affections can be heard to the left of the sternum at the 3rd and 4th costosternal articulation (the so-called fifth listening post at the Botkin-Erb point).

 

 

 

video: auscultation_of_a_heart

 

 

Auscultatory site	Chest location	Characteristics of heart sounds
Aortic area	Second right intercostal space close to sternum	S2  heard louder than S1 aortic closure heard loudest
Pulmonic area	Second left intercostal space close to sternum	Splitting of S2 heard best, normally widens on inspiration; pulmonic closure heard best
Erb’s point	Second and third left intercostal space close to sternum	Frequent site of innocent murmurs and those of aortic or pulmonic origin
Tricuspid area	Fifth right and left intercostal space close to sternum	S1 heard as louder sound preceding S2 (S1 synchronous with carotid pulse)
Mitral or apical area	Fifth intercostal space, left mid-clavicular line (third to fourth intercostal space and lateral to left midclavicular line in infants)	S1 heard loudest; splitting of S1  may be audible because mitral closure is louder than tricuspid closure S3 heard best at beginning of expiration with child in recumbent or left side-lying position, occurs immediately after S2, sounds like word “Ken-tuc-ky”     S1      S2    S3 S4 heard best during expiration with child in recumbent position (left side-lying position decreases sound), occurs immediately before S1 sounds like word “Ten-nes-see” S4        S1    S2

 

The first sound is produced by several factors. One of them is the valve component, i.e. vibrations of the cusps of the atnoventicular valves during the isometric contraction phase, when the valves are closed. The second component is muscular, and is due to the myocardial isometnc contraction. The intensity of myocardial and valvular vibrations depends on the rate of ventricular contractions: the higher the rate of their contractions and the faster the intraventricular pressure grows, the greater is the intensity of these vibrations. The first heart sound will thus be more resonant. The third component of the first heart sound 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 the blood during the ejection phase. The fourth component is atrial; it is generated by vibrations caused by atrial contractions. This fourth component gives rise to the first sound since the atrial systole precedes the ventricular systole. Vibrations caused therefore possible to find certain sites on the chest where sounds of eac valve can be better heard.

The first sound is produced during systole, after a long pause. It is best heard at the heart apex since the systolic tension of the left ventricle is more pronounced than that of the right ventricle. The first sound is longer and louder than the second heart sound. The second sound is generated during diastole, after a short pause, and is best heard at the heart base because it is produced by the closure of the semilunar cusps of the aortic and pulmonary trunk valves. As distinct from the first sound, the second sound is shorter and higher. The tone of the heart sounds may by the atrial systole are normally blended with vibrations caused by the ventricular systole, and are heard as one sound.

Perception of sounds generated in the heart depends on the distance from the valve to its projection on the chest wall and on sound conduction by the course of the blood flow It is change in pathology, and in order to differentiate between the first and second sounds it should be remembered that the first sound coincides in time with the apex beat (if the latter can be palpated) or with the pulse of the aorta and the carotid artery.

Intensity of the heart sounds may depend on conditions of the sound wave transmission, i.e. on the extracardiac causes. If subcutaneous fat or muscles of the chest are overdeveloped, or there are lung emphysema, liquid in the left pleural cavity, and some other affections that separate the heart from the anterior chest wall, the intensity of the heart sounds decreases. If conditions for sound transmission are improved (thin chest wall, the lung edges are sclerosed, the heart is pressed against the anterior chest wall by a growing tumour in the posterior mediastinum, etc.), the intensity of the heart sounds increases. The sounds can also be increased by the resonance in large empty cavities filled with air (a large cavern in the lung, large gastric air-bubble). The intensity of the heart sounds also depends on the composition of the blood flowing through the heart: if the blood viscosity decreases (in anaemia) the intensity increases.

The intensity of the heart sounds can decrease in decreased myocardial contractility in patients with myocarditis, myocardial dystrophy, cardiosclerosis, collapse, and 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. It occurs in physical and emotional strain, during exercise, and in patients with exophthalmic goitre. Changes in only one heart sound is very important diagnostically.

First heart sound diminishes in the mitral and aortic valve insufficiency. The cusps of the affected mitral valve fail to close completely the left atrioventricular orifice during systole. Part of the blood is thus regurgitated to the left atrium. The pressure of the blood against the ventricular walls and the cusps of the mitral valve is below normal, and the valvular and muscular components of the first heart sound markedly diminish. The period of closed valves is absent also during systole in the aortic valve insufficiency. It means that the valvular and muscle components of the first heart sound will also diminish significantly.

The second sound can be inaudible over the aorta if the aortic valve is much destroyer The second sound diminishes over the aorta in cases with marked hypotension; the second sound diminishes over the pulmonary trunk in cases with aortic valve incompetence (in very rare cases) and in decreased pressure in the lesser circulation.

         Two other heart sounds – S₃ and S₄ – may be produced. S₃ is the result of vibrations produced during ventricular filling. It is normally heard only in some children and young adults, but it is considered abnormal in older individuals. S₄ is caused by the recoil of vibrations between the atria and ventricles following atrial contraction, at the end of diastole. It is rarely heard as a normal heart sound; usually it is considered indicative of further cardiac evaluation.

 

 The third sound is caused by vibrations generated during quick passive filling of the ventricles with the blood from the atria during diastole of the heart; it arises in 0.15—1.12 s from the beginning of the second sound.

 

The fourth sound is heard at the end of ventricular diastole and is produced by atrial contractions during quick filling of the ventricles with blood.

 

The third and fourth sounds are low-pitch and soft and are therefore hardly heard iormal subjects. But they are clearly seen on a phonocardiogram. These sounds are better heard in immediate (direct) auscultation. The presence of the third and fourth sounds in the middle-aged usually indicates severe affection of the heart muscle.

 

The intensity of the murmur is next, graded according to the Levine scale:

·         I – Lowest intensity, difficult to hear even by expert listeners

·         II- Low intensity, but usually audible by all listeners

·         III – Medium intensity, easy to hear even by inexperienced listeners, but without a palpable thrill

·         IV – Medium intensity with a palpable thrill

·         V – Loud intensity with a palpable thrill. Audible even with the stethoscope placed on the chest with the edge of the diaphragm

·         VI – Loudest intensity with a palpable thrill. Audible even with the stethoscope raised above the chest.

 

A gallop rrhythm is auscultated in the case of increased intesity of III or IV sounds. The third heart sound results from vibration originating within the left ventricular walls, as this chamber active rapid expensil motion is a abruptly halted in early diastole. This sound is auscultated at direct above an apex of a heart, the best position when the ill lies. On PG adventitious III sound will be distant from beginning of the II sound on 0,12-0,15 sec. The occurence of pathological cardiac sound is conditioned by contraction of hypertrophic left atrium at loss of muscular component of ventriclularcontraction what cause by presence in ventriles of inflammatory-degenerative processes. On PCG it arises after 0,08-0,14 sec. from top of wave P on electrocardiogram, almost coincides with the end of the last one. In childrens and adolescents the IV sound is considered physiological. Presence of this sound in adult and elderly peoples is considered as a pathology, and in these cases it is called pathological IV sound.

Gallop rrhythm occurs at heavy lesions of cardiac muscle (inflammatory, degenerative, toxic), it is called as ” cry of a heart for help”.The gallop rrhythm is conditionally divides into protodiastolic (intensified III sound arises up though 0,12-0,2 sec. after second sound), mesodiastolic(at tachicardia descend coalescence of III and IV sounds and it is accepted at auscultation as a single sound) and presystolic (is conditioned by pathological IV cardiac sound). A gallop rhythm is better auscultated directly by ear (together with a note is accepted mild impetus transmitted from heart on thoracal cage in diastole phase) in the apical region at left lateral recumbent position of the patient, in III- IV intercostal spaes to the left.

 

 

Triple rrhythm (Rhithmus coeturnici) is a cardiac rhythm which is auscultated only in mitral stenosis and arises if there is presence of such an  adventitious sound as mitral click (or sound of opening of mitral valve) together with slapping first and second sounds. Slapping I sound (intensified I sound) is conditioned by fast reduction of left ventricle which is insufficiently filled with blood in diastole phase and oscillations of sclerotic usps of mitral valve, which one in diastole were in more relaxing condition because of small filling by blood the  left ventricle. On PCG the mitral click arises over 0,05-0,13 sec. after II sound and it creates the visibility of dualization of this sound, however as against true dualization is better auscultated on an apex of heart instead of for the basis. It causes by sudden effort of sclerotic valve cusps at transit of blood from the left atrium into the left ventricle. The interval teh  II sound and mitral click becomes more short, if stenosis is expressed more strongly. Rhithmus coeturnici is auscultated above heart  apex  and is conducted upwards and toward the axillary fossa.

 

Listen to Mitral Stenosis

 

In the case of pendulum rhythm the large (diastolic) heart pause is so shortened, that becomes an equal to small   (systolic) pause. The sound phenomenon, which   one arises thus,   reminds of even pendulum swinging.    Such   rhythm disturbance meets usually at heavy lesions of heart muscle . If pendulum rhythm is accompaning by sharp heart acceleration, this phenomenon is called as embriocardia.

An extra-pericardial-sound can occur in pericardial adhesion. It occures during diastole, 0.08-0.14s after the second sound, and is generated by the vibrating pericardium during the rapid dilatation of the ventricles at the beginning of diastole. The extra sound in adhesions in the pericardium can also arise during systole, between the first and the second heart sounds. This short and loud sound is also known as the systolic click. A place of best auscultation is teh bottom   of breastbone.

 

 

Another important category of heart sounds is murmurs, which are produced by vibrations within the heart chambers or in the major arteries from the back and forth flow of blood.

There are a number of other abnormal sounds, such as ejection clicks, snaps, gallops, and hums. It is beyond the scope of this discussion to elaborate on the gamut of adventitious heart sounds. The best approach is for the nurse to become familiar with normal heart sounds and to refer any questionable heart sound to a physician for further medical evaluation.

Differentiating normal heart sounds. In referring to Fig. 9.2, it is apparent that normally S₁ is louder at the apex of the heart in the mitral and tricuspid area and that S₂ is louder near the base of the heart in the pulmonic and aortic area. The doctor listens to each sound by inching down the chest in the sequence outlined in Table 9.1. If there is difficulty in deciding which sound is S₁ or S₂, especially when the rate is rapid, the carotid pulse should be simultaneously palpated with the index and middle finger while the heart sounds are auscultated. S₁ is synchronous with the carotid pulse. In addition to the areas listed in Table 9.1, the following areas should be auscultated for sounds, such as murmurs, which may radiate to these regions: the sternoclavicular area above the clavicles and manubrium, along the sternum and in interscapular region.

 

HEART MURMURS

Physiology of Murmurs

     Before trying to decipher what may be the underlying cause of a murmur, it is important to first understand what the normal heart sounds are, and what normal variations of these sounds may occur. It is assumed that you already understand the anatomy of the heart, and have read a basic physical examination textbook which describes the standard methods for auscultation.

     The most obvious of the heart sounds are the first and second sounds, or S1 and S2, which demarcate systole from diastole. The heart sound playing in the background on the introduction page of this site is a normal sinus rhythm, with a sharp S1 and S2 and no other significant sounds. S1 is the sound which marks the approximate beginning of systole, and is created when the increase in intraventricular pressure during contraction exceeds the pressure within the atria, causing a sudden closing of the tricuspid and mitral, or AV valves. The ventricles continue to contract throughout systole, forcing blood through the aortic and pulmonary, or semilunar valves. At the end of systole, the ventricles begin to relax, the pressures within the heart become less than that in the aorta and pulmonary artery, and a brief back flow of blood causes the semilunar valves to snap shut, producing S2.

     Although S1 and S2 are considered to be discrete sounds, you will notice that each is created by the near-instantaneous closing of two separate valves. For the most part, it is enough to consider that these sounds are single and instantaneous. However, it is worth remembering the actual order of the closures, because certain conditions can split these sounds into the separate valve components. During S1, the closing of the mitral valve slightly precedes the closing of the tricuspid valve, while in S2, the aortic valve closes just before the pulmonary valve. Rather than memorize this order, if you remember that the pressure during systole in the left ventricle is much greater than in the right, you can predict that the mitral valve closes before the tricuspid in S1. Similarly, because the pressure at the start of diastole in the aorta is much higher than in the pulmonary artery, the aortic valve closes first in S2. Knowing the order of valve closure makes understanding the different reasons for splitting of heart sounds easier.

     When listening to a patient’s heart, the cadence of the beat will usually distinguish S1 from S2. Because diastole takes about twice as long as systole, there is a longer pause between S2 and S1 than there is between S1 and S2. However, rapid heart rates can shorten diastole to the point where it is difficult to discern which is S1 and which is S2. For this reason, it is important to always palpate the PMI or the carotid or radial pulse when auscultating. The heart sound you hear when you first feel the pulse is S1, and when the pulse disappears is S2.

     When a valve is stenotic or damaged, the abnormal turbulent flow of blood produces a murmur which can be heard during the normally quiet times of systole or diastole. This murmur may not be audible over all areas of the chest, and it is important to first note where it is heard best and where it radiates to. Next, you should try to discern if the murmur occurs in systole or diastole by timing it against S1 and S2. Then, listen carefully to tell if the murmur completely fills that phase of the cycle (i.e., holosystolic), or if it has discrete start and end points. Regurgitant murmurs, like mitral valve insufficiency, tend to fill the entire phase, while ejection murmurs, like aortic stenosis, usually have notable start and end points within that phase. The quality and shape of the murmur is theoted. Common descriptive terms include rumbling, blowing, machinery, scratchy, harsh, or musical. The intensity of the murmur is next, graded according to the Levine scale:

• I – Lowest intensity, difficult to hear even by expert listeners
• II- Low intensity, but usually audible by all listeners
• III – Medium intensity, easy to hear even by inexperienced listeners, but without a palpable thrill
• IV – Medium intensity with a palpable thrill
• V – Loud intensity with a palpable thrill. Audible even with the stethoscope placed on the chest with the edge of the diaphragm
• VI – Loudest intensity with a palpable thrill. Audible even with the stethoscope raised above the chest.

     Finally, it is important to decide if this murmur is clinically significant or not. Just as a murmur can be caused by normal flow through a stenotic valve, it may also be created by high flow through a normal valve. Pregnancy is a common high-volume state where these physiologic flow murmurs are often heard. Anemia and thyrotoxicosis can cause high-flow situations where the murmur is not pathologic itself, but indicates an underlying disease process. Children also frequently have innocent murmurs which are not due to underlying structural abnormalities. How can a physician determine if a murmur is significant?

     The most important thing to consider is the clinical scenario. In a population of unreferred young adults, the prevalence of systolic murmurs ranges from 5% to 52%, with 86% to 100% of these patients having normal echocardiograms. Important questions to ask would include the presence of symptoms such as effort syncope, chest pain, palpitations, shortness of breath, or paroxysmal nocturnal dyspnea. In terms of the examination, there is no one way to rule in or out a murmur as being physiologic, but in general, physiologic murmurs tend to be located between the apex and left lower sternal border, have minimal radiation, occur during early to mid-systole, have a crescendo-decrescendo shape, and a vibratory quality. They will usually change intensity with positional maneuvers, becoming quieter on standing and louder with squatting. A Valsalva maneuver will decrease the intensity of the murmur because the increase in intrathoracic pressure will decrease venous return, which will decrease flow through the heart and lessen the turbulence. Additionally, they will not be correlated with additional audiologic findings, such as an S3 or S4.

     Examples of some common variations of normal heart sounds without an underlying structural pathology can be found via the links in the menu to the left.

 

At auscultation of a heart in series of cases, except for sounds, the sound phenomena termed as cardiac murmurs are auscultated. The murmurs can arise inside the heart (intracardial) and outside of it (extracardial). Intracardial murmurs more often are observed. They can arise at anatomical changes in structure of heart valves (organic murmurs) or infringement of function of non-affected valves (functional murmurs). Functional murmurs can be observed at augmentation of a blood flow rate or rising of blood viscosity.

Heart murmurs are produced as a result of turbulent flow of blood, turbulence sufficient to produce audible noise. They are usually heard as a whooshing sound. The term murmur only refers to a sound believed to originate within blood flow through or near the heart; rapid blood velocity is necessary to produce a murmur. It should be noted that most heart problems do not produce any murmur and most valve problems also do not produce an audible murmur.

The following paragraphs overview the murmurs most commonly heard in adults who do not have major congenital heart abnormalities.

         Regurgitation through the mitral valve is by far the most commonly heard murmur, producing a pansystolic/holosystolic murmur which is sometimes fairly loud to a practiced ear, even though the volume of regurgitant blood flow may be quite small. Yet, though obvious using echocardiography visualization, probably about 20% of cases of mitral regurgitation do not produce an audible murmur. Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is more common in older adults or in those individuals having a two, not a three leaflet aortic valve.Regurgitation through the aortic valve, if marked, is sometimes audible to a practiced ear with a high quality, especially electronically amplified, stethoscope. Generally, this is a very rarely heard murmur, even though aortic valve regurgitation is not so rare. Aortic regurgitation, though obvious using echocardiography visualization, usually does not produce an audible murmur.

Stenosis of the mitral valve, if severe, also rarely produces an audible, low frequency soft rumbling murmur, best recognized by a practiced ear using a high quality, especially electronically amplified, stethoscope.

         Other audible murmurs are associated with abnormal openings between the left ventricle and right heart or from the aortic or pulmonary arteries back into a lower pressure heart chamber.

 

 

At constant width of a lumen of a circulatory channel a murmur can arise in expense of augmentation of blood flow rate, as it is observed in thyrotoxicosis, fever, nervous exitation. Decreasing of blood viscosity (for example, in anemia) promotes augmentation of blood flow rate and also can serve as the cause of occureing of a murmur. The most often cause of ocureing of intracardial murmur are heart defects.

Conerning to the  time of appearance relating to phases of cardiac cycle (systole or diastole) systolic and diastolic murmurs are distinguished.

Systolic murmur arises when during a systole the blood meets any obstrution moving from one heart chamber to another or from heart towards large vessels. Systolic murmur is auscultated in stenosis of aoric rout   or pulmonary trunk, as in these heart defts during expulsion of blood from ventricles forward in systole  blood streammeetsobstruction (so this murmur is called systolic ejection murmur). Systolic murmur is auscultated also in mitral and trycuspide incompetene. Its ocureance can be explained in following order: during ventricular systole the blood stream will go not only to the aorta and pulmonary trunk, but also backwards towardsartium through not completely losed atrioventricular aperture, i.e. through a narrow aperture (systolic murmur of regurgitation).

Diastolic murmur occures whearrowing of the left or right atrioventricular apertures exists, as at these cases during diastole blood flow meets obstruction during motion from atriums to ventricles. Diastolic murmur is typical for incompetene of aortic or pulmonary trunk  valves — becouse of  blood buckflow from vessels to ventricles through the incompletelly closed  apertures of the changed valves.

 

The relation of murmur to systole or diastole determine to the same attributes, on which differentiate I and II sounds. The systolic murmur arises together with I sound during a systolic pause; it coincides with an apical beat and pulse on carotic arteries. The diastolic murmur arises after II sound during longdiastoli pause. Three kinds of diastolic murmur are distinguished:

1) protodiastolic, arising strightly at the beginning of diastole, at once after II tone,

2) mesodiastolic, auscultated a somewhat later after the II sound,

3) presystolic, appearing at the end of  diastole.

Concerning to timbre murmurs are devided on mild, blowing, or, on the contrary, rasping, scratching, sawing; musical murmurs are sometimes auscultated. Concerning to duration short and long murmurs are distinguished, onerning to loudness they are quiet or loud. The intensity of murmur can gradually decrease (decreasing or descendo murmur) or rise (increasing or desendo murmur). More often descendo murmurs are auscultated. The increasing character has presystolic murmur auscultated more often in narrowing of the left atrioventricular aperture strightly at the end of ventriclular diastole.

Murmurs are classified as: Tone and murmurs

1. Innocent, occurring in individuals with no anatomic or physiologic abnormality.

2. Functional, occurring in individuals with no anatomic cardiac defect but with a physiologic abnormality such as anemia.

3. Organic, occurring in individuals with a cardiac defect with or without a physiologic abnormality.The description and classification of murmurs are skills that require considerable practice and training. In general the doctor should be able to recognize murmurs as distinct swishing sounds that occur in addition to the normal heart sounds. The following information should be found:

1.  Location of the area of the heart where the murmur is heard best.

2.  Time of the occurrence of the murmur within the S1 S2 cycle.

3.  Evaluation of its intensity in relationship to the child’s position.  

 4.  Estimation of its loudness

Although the doctor consults with a physician whenever a murmur is identified, the following guidelines can be used in distinguishing between innocent and organic murmurs. Innocent murmurs generally are:

1.  Systolic, that is, they occur with or after S1.

2.  Of short duration and have no transmission to other areas of the heart.

3.  Grade III or less in intensity and do not increase over time.

4.  Usually loudest in the pulmonic area (second or third intercostal space along the left sternal border).

5.  Variable in relationship to position, respiration, and activity (for example, audible in the supine position but absent in the sitting position; may be louder with exercise, fever, anxiety, or anemia).

6.  Not associated with any physical signs of cardiac disease.  

7.  Usually of a low-pitched, musical, or groaning quality.

Gradations of Murmurs	(Defined based on use of an acoustic, not a high-fidelity amplified electronic stethoscope)
Grade	Description
Grade 1	Very faint, heard only after listener has “tuned in”; may not be heard in all positions. Only heard if the patient “bears down” or performs the Valsalva maneuver.
Grade 2	Quiet, but heard immediately after placing the stethoscope on the chest.
Grade 3	Moderately loud.
Grade 4	Loud, with palpable thrill (i.e., a tremor or vibration felt on palpation)
Grade 5	Very loud, with thrill. May be heard when stethoscope is partly off the chest.
Grade 6	Very loud, with thrill. May be heard with stethoscope entirely off the chest.

As noted, several different cardiac conditions can cause heart murmurs. However, the murmurs produced often change in complex ways with the severity of the cardiac disease. An astute physician can sometimes diagnose cardiac conditions with some accuracy based largely on the murmur, related physical examination and experience with the relative frequency of different heart conditions. However, with the advent of better quality and wider availability of echocardiography and other techniques, heart status can be recognized and quantified much more accurately than formerly possible with only a stethoscope, examination and experience.

Effects of inhalation/expiration

Inhalation pressure causes an increase in the venous blood return to the right side of the heart by increasing intrathoracic negative pressure making it more negative (pulling blood into the right side of the heart via a vacuum-like effect). Therefore,right-sided murmurs generally increase in intensity with inspiration. The increased (more negative)intrathoracic pressure has an opposite effect on the left side of the heart which is trying to move blood out to systemic circulation making it harder for blood to leave the left side of the heart. This causes left-sided murmurs to generally decrease in intensity during inspiration.

With expiration, the opposite haemodynamic changes occur. This means that left-sided murmurs generally increase in intensity with expiration. Having the patient lie supine and raising their legs up to a 45 degree angle facilitates an increase in venous return to the right side of the heart producing effects similar to inhalation-increased blood flow.

Interventions that change murmurs

There are a number of interventions that can be performed that alter the intensity and characteristics of abnormal heart sounds. These interventions can differentiate the different heart sounds to more effectively obtain a diagnosis of the cardiac anomaly that causes the heart sound.

 Murmurs are auscultated better at points of auscultation of those valves, in which they were formed. Only in some cases murmurs are better heard in a distance from a place of originating beouse of their good conduction. The murmurs are well spent on a direction of a blood flow; they are better auscultated in that range, where heart to a chest and where it is not covered mild.

The systolic murmur in mitral valve incompetene is best auscultated at heart apex; it can be conduted to axillary region or with blood bukflow from a left ventricle in the left atrium — to the  second and third intercostal space to the left of a breast bone.

The diastolic murmur iarrowing of the left atrioventricular aperture is usually auscultated on a circumscribed field in apex area.

The systolic murmur in stenosis of aortic rout is audible in the second intercostal space to the right of a breast bone. As a rule, he is well onduted with blood flow towards caroti arteries. As for this defeect rasping and loud (sawing, scratching) murmur is characteristic it can be determined by auscultation above all heart region and can be onduted to interscapular space.

The diastolic murmur aortic valve inompetence is often better auscultated not above the aorti valve, but at Botkin-Erb’s point, where it is onduted with blood bukflow from the  aorta to the  left ventricle.

The systolic murmur in thrycuspide valve inompetence is most well heard at the basis of  xiphoid process of the breast bone, as here right ventricle is closest adjoin to the chest. From here it can be conducted upwards and rightwards, towards the right atrium.

Rarely such defect is observedas  narrowing of right atrioventricular aperture.in thisase diastolic murmur is auscultated on a circumscribed field at the basis of  xiphoid process of a breast bone.

The systolic murmurs in the case of  of atrioventricular valves incompetence or iarrowing of rout of large vessels, are better auscultated in recumbent position of the patient.

The diastolic murmurs arising iarrowing of atrioventricular foramens or in aortic and  pulmonary trunk incompetence, are more easly auscultated in  vertical position of the patient.

 If some murmurs are simultaneously auscultated above different valves, it is necessary to decide, how much valves are affected as well as what is character of this lesion. The presence of systolic and diastolic murmurs above one of valves testifies to its combined lesion, i.e. about existence of both incompetence of the valve, and stenosis of its aperture. When above one of valves systolic murmur is auscultated, and above the another — diastolic, it testify about combined lesion of two valves.

More difficult is  to decide, is one valve or two  affected, if in different points the murmur in the same phase of cardiac cycle is auscultated. In this case it is necessary to pay attention to character of murmur. If in area of one valve the blowing murmur is mild, and above another — rasping, scratching, it means about different murmurs above two affected valves. Moving a stethoscope on a conditional line bridging valves, above which the murmur is auscultated, mark also change of its loudness. It helps to differentiate murmurs and character of their condution. For example, the systolic murmur at the mitral valve incompetence is onduted to axillary area; it can be auscultated above an aorta as well, but this murmur will not be onduted to carotic arteries as opposite to systolic murmur related to  stenosis of aortirout.

At auscultation of a heart it is necessary to be able to differentiate murmurs of a functional and organic origin, intracardiac and extracardiac murmurs. To differentiate functional and organic murmurs the following properties of functional murmurs are informative: 1) in the most cases functional murmurs are systolic; 2) the murmurs are changeable, can arise and decrease in intensity or even disappear at various positions of a body, after an exercise, stress, in different phases of respiration; 3) most often they are auscultated above a pulmonary trunk, less often — above heart apex, 4) the murmurs are short, seldom occupy all systole; mild and blowing in character; 5) the murmurs are usually auscultated on a circumscribed field and are not conducted far from the place of occurence; 6) The functional murmurs are not accompanied by other attributes of valvular lesions (enlargement of heart chambers, change of sounds etc.).

The extracardiac (extracardial) murmurs though comes up synchronously with activity of heart, but arise outside of it. 

 

The pericardial friction is develops in change of visceral and parietal pericardiac layers, when the fibrin (is postponed at a pericarditis), or cancerous nodules are deposied on them. The mechanism of recation of  pericardial friction is similar to the mechanism of crepitation of a pleural friction, only instead of respiratory movements the cause of its appearance is the movements of a heart during  systole and diastole. Pericardial friction can have a various sound characteristics; sometimes it is similar to  pleural friction, reminds a crunch of snow; the very quiet murmurs similar to a rustle of a paper or reminding a scratch is occasionally auscultated. The pericardial friction differs from intracardiac murmurs by the following attributes: 1) not always precisely coincides with  systole and diastole, quite often is auscultated during all cardiac cycle, only strengthening during  systole or diastole; 2) during short time can be auscultated in different phases of a cardiac cycle, during  systole, diastole; 3) it is changeable, disappear and appear again; 4) does not coincide on localization with points of the best auscultation of valves; is most well auscultated in area of absolute heart dullness, at its establishment, at the left edge of a breast bone in third — the fourth intercostal spaces; the localization it is changeable and can vary within a day; 5) is weakly onducted from the place of ocurence; 6) is felt by closer to an ear of an examiner, than intracardial murmurs; 7) strengthens at pressing of a stethoscope to a hest wall and at inclination of a trunk forward, as thus of a leaf of a pericardium adjoin more intimately.

The pleuropericardial friction murmur arises in inflammation of  pleura, immediately accumbent to heart, owing to friction of pleural layers, synchronic with activity of a heart. As opposite to pericardial friction it is auscultated on the left edge of relative cardiac dullness; is usually combined with  pleural friction and changes the intensity in different phases of respiration strengthens at a penetrating inspiration, when the edge mild adjoins to more closely to the heart, and weakens at expiration, at fall of edge mild sharply.

 

Term	Description
Tachycardia	Increased rate
Bradycardia	Decreased rate
Pulsus altemans	Strong beat followed by weak beat
Pulsus bigeminus	.Coupled rhythm in which beat is felt in pairs because of premature

     This is a typical example of the late-peaking murmur of aortic stenosis. Notice that the murmur is in later systole, with a harsh quality and a crescendo-decrescendo shape. Because this is late-peaking, it would suggest a more severe stage of aortic stenosis than an early peaking murmur. Additionally, there is a nearly-absent S2, again indicating that the valve is poorly mobile and severely diseased.

     You are listening to a typical example of a murmur caused by mitral valve regurgitation. Mitral valve regurgitation is usually either a congenital condition or a consequence of rheumatic heart disease, marked left ventricular dilatation, acute infective endocarditis, or papillary muscle dysfunction secondary to acute or prior myocardial infarction.

     This murmur is usually best heard at the apex, with radiation into the axilla. Because the mitral valve is unable to contain the blood within the ventricle for the entire systolic period, it is a holosystolic murmur. The quality of the murmur is usually described as blowing, and, as subtly demonstrated in the sample you are hearing, it is often associated with an S3 because of the left atrial volume overload. Although S1 is due to a combination of mitral and tricuspid valve closure, the mitral valve is the louder aspect. Because the valve closure in mitral regurgitation is incomplete, S1 may be noticeably quieter. Finally, in severe regurgitation, the pressure in the left ventricle quickly equalizes with venous pressure in the left atrium during the start of diastole. The result is that the aortic valve may close prematurely and may, although not present in this sample, occasionally result in a widely split S2.

     A maneuver which may increase the intensity of mitral regurgitation is transient arterial occlusion. When blood pressure cuffs are used to completely occlude the brachial artery for a short period, the resultant increase in arterial resistance causes the left ventricle to increasingly favor the regurgitant mitral valve as an outlet for flow. This flow increase will enhance the intensity of the murmur.

     Before trying to decipher what may be the underlying cause of a murmur, it is important to first understand what the normal heart sounds are, and what normal variations of these sounds may occur. It is assumed that you already understand the anatomy of the heart, and have read a basic physical examination textbook which describes the standard methods for auscultation.

     Click on the links to the left to hear the available diastolic murmurs.

     You are listening to a typical murmur caused by aortic valve regurgitation. Aortic regurgitation is mostly seen in males, with a 3:1 ratio as compared to females. In 2/3 of cases, the regurgitation is secondary to rheumatic heart disease, and may have a component of aortic stenosis. Aortic regurgitation may also be primarily congenital or associated with syphilis infection, Marfan syndrome, or valvular deterioration due to infective endocarditis. 

 

       

     The murmur of aortic regurgitation is complex. The left ventricle is typically dilated secondary to extreme volume overload, as it must handle both the forward flow delivered from the left atria as well as the regurgitant flow from the aorta. This large volume of blood is ejected rapidly during systole, and an early mid-systolic flow murmur is frequently audible over the right upper sternal border with radiation into the neck.

     The most notable aspect of the murmur is the diastolic sound produced as the blood flows retrograde back into the left ventricle. This murmur is usually characterized as blowing, decrescendo, and heard best in the third left intercostal space. In severe regurgitation, it may be holodiastolic. It radiates widely along the left sternal border.

     Finally, a third murmur, known as an Austin Flint murmur, may be detected. This is a soft, rumbling, low-pitched, late diastolic murmur which is heard best at the apex. It is thought to be due to a functional mitral valve stenosis, as the backflow of blood from the aorta presses on the anterior leaflet of the mitral valve, slightly occluding the flow from the atria. The atrial kick just before systole accentuates this flow, producing the Austin Flint murmur.

     Any maneuver which increases systemic vascular resistance will increase the murmur of aortic regurgitation, as it will tend to favor backflow into the ventricle. This includes handgrip and isometric excercise.

     You are listening to a typical example of the murmur produced by mitral valve stenosis. As opposed to aortic regurgitation, mitral stenosis has a female preponderance, with the female:male ratio being about 2:1. Almost all cases of mitral stenosis are rheumatic in origin, although congenital causes can occur.

             

     The murmur of mitral stenosis is best heard at the apex with little radiation. It is nearly holodiastolic with pre-systolic accentuation due to the atrial kick. It is usually described as low-pitched, decrescendo, and rumbling, and can be heard best with the patient in the left lateral decubitus position. The murmur appears about 0.08 seconds after S2, and is heralded by an “opening snap”. This is a brief, loud sound which is caused as the stenotic valve suddenly halts its normal opening at the start of diastole

Why do we still need cardiac auscultation?

Auscultation represents the acquisition of mechanical vibrations from the surface of the body that encompass the frequency range of sound. Vibrations below this range (<20 cycles per second) are defined as “infrasonic,” and although not audible, they are usually readily palpable or visible and constitute a source of information supplementing that obtained from the sounds alone. Examples of infrasonic vibrations are provided by precordial motion (thrusts or heaves) and arterial and venous pulses. Although the general subject of cardiac auscultation has been reviewed recently,7 the diagnostic value of this technique and how it relates to other testing modalities are presented specifically in a few important examples below.

The audible fourth heart sound (and its simultaneous accentuated presystolic apical thrust) usually provides evidence of a forceful left atrial contraction combined with reduced left ventricular compliance—findings indicating diastolic dysfunction of the left ventricle. Studies of the accentuated and palpable presystolic apical thrust (“A” wave of the apexcardiogram), which usually accompanies the fourth sound, have provided direct evidence for increased ventricular stiffness (reduced compliance) in such cases. In general, Doppler and echocardiographic techniques (E/A velocity ratio, E-wave deceleration time, isovolumic relaxation time, and atrial filling fraction) and nuclear ventriculography (peak filling rate, time to peak filling rate, and one-third filling rate) have had some success in the detection and confirmation of diastolic dysfunction of the ventricles, but factors such as ventricular preload and the gradient of pressure between left atrium and left ventricle may influence diastolic filling patterns independent of ventricular stiffness. Thus, the fourth sound may provide one of the few direct clues of diastolic dysfunction, a finding of clearly useful and independent value.

The third heart sound, when encountered in the older individual without primary valvular disease or states marked by high cardiac output, usually signifies reduced systolic function of one or both ventricles together with increased filling pressure within the affected chamber. When encountered in this setting, this sound virtually ensures that the left ventricular ejection fraction is below 50%; moreover, it is regularly present when the ejection fraction drops below 30%. The presence of this sound has even been found to signal the likely efficacy of inotropic agents such as digitalis glycosides in treatment of the underlying disorder. Even when found in the setting of primary valvular disease (except for mitral regurgitation), the third sound usually signals the presence of systolic dysfunction together with elevation of left ventricular filling pressure. Imaging techniques that demonstrate ventricular enlargement and reduced systolic wall motion provide similar information, but the third sound additionally signifies the presence of an abnormally high filling pressure, and thus decompensation, of the involved ventricle.

A diastolic sound resembling the third sound but earlier in timing characterizes the pericardial “knock” sound of pericardial constriction; when such a sound is combined with careful evaluation of the precordial motion and jugular venous pulse, this diagnosis is strongly supported. Although imaging techniques may demonstrate pericardial thickening or calcification, they do not provide prima facie evidence for hemodynamic interference of ventricular filling. A variety of echocardiographic signs have been described in pericardial constriction, but to date no single sign is best or pathognomonic in making this diagnosis. Even hemodynamic information obtained through cardiac catheterization may not provide clear differentiation between pericardial constriction and myocardial restrictive disease ; however, if one combines this information with precordial motion and timing of the early diastolic sound, clear diagnosis may become possible.

The presence of an ejection sound (ejection click) or opening snap usually signifies improper opening of semilunar valves or atrioventricular valves, respectively. For example, an ejection sound in an ostensibly normal individual generally signifies abrupt cessation of the motion of an abnormal semilunar valve before it reaches full opening. This finding usually indicates the need for an echocardiogram, which can identify and characterize an abnormal semilunar valve, such as a malformed or bicuspid aortic valve. On the other hand, opening sounds usually indicate proper functioning of mechanical prosthetic valves, and their loss may warn us of impending or actual malfunction of these devices. Thus, serial auscultatory evaluation may provide important collateral information in the assessment of prosthetic valves and lead to proper selection of imaging techniques, such as transesophageal echocardiography.

A mid or late systolic click is most likely diagnostic of mitral (or tricuspid) valve prolapse, even though echocardiograms may fail to confirm this finding.

 Echocardiograms commonly fail to demonstrate prolapse when an isolated systolic click is found in the absence of a systolic murmur of mitral regurgitation, a fact probably attributable to the inability of this technique to detect minor prolapse of limited portions of the leaflets. On the other hand, “prolapse” is often diagnosed from the echocardiogram in the absence of any auscultatory abnormalities. This is generally considered a benign clinical finding and, for the most part, probably reflects the inaccuracies of echocardiographic criteria for diagnosis. Thus, to avoid overdiagnosing this disorder, with its attendant psychological and insurance problems, careful auscultation of the patient in different positions and at different times must be considered in arriving at a final diagnosis and also is superior to echocardiography for clinical management and follow-up. Therefore, in the total absence of auscultatory abnormalities, there is usually little justification for performing an echocardiogram to search for mitral prolapse and no need for prophylaxis against infective endocarditis.

Proper identification and classification of audible systolic murmurs usually enables us to identify their mechanism and likely source. Very often, Doppler techniques demonstrate minor regurgitation across atrioventricular valves that does not produce audible murmurs, a finding that is usually clinically insignificant, for such patients generally suffer from no hemodynamic consequences and there is no evidence that antibiotics are necessary to prevent bacterial endocarditis. Conversely, Doppler study may not reveal the origin of audible murmurs, as exemplified by many crescendo-decrescendo murmurs produced by ejection of blood into the great vessels. Thus, to understand the origin and significance of a given systolic murmur, one must first categorize its type on the basis of its auscultatory characteristics and then consider this in the light of the Doppler results. By use of certain appropriate maneuvers, one can usually distinguish between ejection murmurs originating in the aortic outflow tract in contrast with pansystolic murmurs produced by mitral or tricuspid regurgitation. If such a murmur is characterized by skilled examiners as an innocent-type ejection murmur, further testing is generally unnecessary. On the other hand, a long, late-peaking, crescendo-decrescendo murmur may signal the presence of severe aortic or pulmonic stenosis and require confirmation by echo-Doppler techniques.

 

Phonocardiographic registration of auscultation data

A Phonocardiogram or PCG is a plot of high fidelity recording of the sounds and murmurs made by the heart with the help of the machine called phonocardiograph, or “Recording of the sounds made by the heart during a cardiac cycle.” The sounds are thought to result from vibrations created by closure of the heart valves. There are at least two: the first when the atrioventricular valves close at the beginning of systole and the second when theaortic valve closes at the end of systole. It allows the detection of subaudible sounds and murmurs, and makes a permanent record of these events. In contrast, the ordinary stethoscope cannot detect such sounds or murmurs, and provides no record of their occurrence. The ability to quantitate the sounds made by the heart provides informatioot readily available from more sophisticated tests, and provides vital information about the effects of certain cardiac drugs upon the heart. It is also an effective method for tracking the progress of the patient’s disease. 

Software provides tools to display heart signal and to estimate its basic statistics  that are presented in the format of Intensity Score (%); Frequency Score (mean Frequency and Mean Half-Bandwidth) and Time Duration Score (%).

 

Normal heart sounds

Aortic stenosis

 

Aortic stenosis

 

Method of registration and coding of electrocardiogram (ECG). ECG-signs of hypertrophy of  heart chambers.

Electrocardiography (ECG or EKG from Greek: kardia, meaning heart) is a transthoracic (across the thorax or chest) interpretation of the electrical activity of the heart over a period of time, as detected by electrodes attached to the surface of the skin and recorded by a device external to the body. The recording produced by thisnoninvasive procedure is termed an electrocardiogram (also ECG or EKG).

An ECG is used to measure the rate and regularity of heartbeats, as well as the size and position of the chambers, the presence of any damage to the heart, and the effects of drugs or devices used to regulate the heart, such as a pacemaker.

Most ECGs are performed for diagnostic or research purposes on human hearts, but may also be performed on animals, usually for diagnosis of heart abnormalities or research.

The conduction system of the heart consists of four structures:

1. The sinoatrial (SA) node, located within the rig atrial wall near the opening of the superior vena cava

2. The atrioventricular (AV) node, also located within the right atrium but near the lower end of the septum

3. The atrioventricular bundle (bundle of His), which extends from the atrioventricular node along each side of the interventricular septum

4. Purkinje fibers, which extend from the atrioventricular bundle into the walls of the ventricles. The electric impulses from this conduction system can be recorded on an electrocardiogram.

The sinoatrial node initiates the heart’s conduction system. It also possesses -an intrinsic rhythm that maintains a constant heart rate. For these reasons it is called the body’s pacemaker. The sinoatrial impulse spreads throughout the atria to cause depolarization. As the atria contract, impulses spread to the atrioventricular node to stimulate the ventricles. The atrioventricular node is the only normal pathway by which the impulses from the atria can be transmitted to the ventricles. The impulses then spread to the atrioventricular bundle and Purkinje fibers to cause simultaneous depolarization of the ventricles.

                                                                                                               

Heart conductive system

 

A cardiac cycle is composed of sequential contraction (systole) and relaxation (diastole) of both the atria and ventricles. First, the atria contract, ejecting blood into the relaxed ventricles. Then, as the atria relax, the ventricles contract to eject blood into the pulmonary artery and aorta. During the period of atrial diastole blood enters the atria from the systemic and pulmonary veins, thus completing one cardiac cycle.

         Electrocardiography is the method of graphic registration of operating heart biopotentials from the body surface. Potential difference appears at this moment between stimulated part of myocardium and the area at the state of rest. This potential difference is fixed by electrocardiograph in the form of EGG waves.

Electrocardiography (ECG or EKG) records the electrical impulses generated from the heart muscle and provides a graphic illustration of the summation of these impulses and their sequence and magnitude.

This method occupies one of the first places in the store of instrumental methods of patient examination. Due to it we are able to determine pathology of heart automatism, stimulation and conductivity.

Heart systole is preceded by its stimulation. During this time physical-chemical properties of cellular membrane are changed. ionic composition of intercellular and intercellular liguid undergoes  changes  accompanied  by  electric  current generation.

Modern electrocardiographs are of the same structure as voltage measuring instruments. They have the following parts: perceiving device,  amplifiers, galvanometer, registrating device, apparatus supply unit. The main principle of operation is based on the perception of potential difference oscillations prodused during myocardium stimulation by electrodes located on the body of examined patient. This low voltage is amplified 600-700 times by electron tubes.

Electrodes are put on lower one third of both forearms and left shin. Red wire with one relief ring is connected to the electrode on the right arm, yellow wire with two relief rings is connected to the electrode on the left arm, green wire with three relief rings is connected to the electrode on the left leg.

Augmented unipolar leads  from extremities are aVR, aVL, aVF; a being the first letter of the English word “augmenteg” which means amplified; V being the first letter of the English word “Voltage”; R,L,F are the first letters of the English words “Right”, “Left”, “Foot”; aVR is an active electrode on the right arm, indifferent from connected left arm and left leg; aVL is an active electrode on the left arm, indifferent from connected right arm and left leg; aVF is an active electrode on the left leg, indifferent from connected right and left arms.

Chest leads are used for more accurate diagnostics of myocardium diseases, they are:

1)    electrode is located on the left edge of breast – bone in IV intercostal  space;

2)    electrode is located on the right edge of breast – bone in IV intercostal  space;

3)    electrode is situated on the left peristernum line between IV and V intercostal  space;

4)    electrode is put on the left medium clavicle line in V intercostal  space;

5)    electrode is located on the left front axial line in V intercostal  space;

6)    electrode is placed on the left axial line in V intercostal  space.

The P wave represents the electric activity associated with the sinoatrial node and the spread of the impulse over the atria. It is a wave of depolarization.

ECG graph paper

The output of an ECG recorder is a graph (or sometimes several graphs, representing each of the leads) with time represented on the x-axis and voltage represented on the y-axis. A dedicated ECG machine would usually print onto graph paper which has a background pattern of 1mm squares (often in red or green), with bold divisions every 5 mm in both vertical and horizontal directions.

It is possible to change the output of most ECG devices but it is standard to represent each mV on the y axis as 1 cm and each second as 25 mm on the x-axis (that is a paper speed of 25 mm/s). Faster paper speeds can be used, for example, to resolve finer detail in the ECG. At a paper speed of 25 mm/s, one small block of ECG paper translates into 40 ms. Five small blocks make up one large block, which translates into 200 ms. Hence, there are five large blocks per second. A calibration signal may be included with a record. A standard signal of 1 mV must move the stylus vertically 1 cm, that is, two large squares on ECG paper.

 

Layout

By definition, a 12-lead ECG will show a short segment of the recording of each of the 12-leads. This is often arranged in a grid of four columns by three rows, the first columns being the limb leads (I,II and III), the second column the augmented limb leads (aVR, aVL and aVF) and the last two columns being the chest leads (V1-V6). It is usually possible to change this layout, so it is vital to check the labels to see which lead is represented. Each column will usually record the same moment in time for the three leads and then the recording will switch to the next column, which will record the heart beats after that point. It is possible for the heart rhythm to change between the columns of leads.

Each of these segments is short, perhaps one to three heart beats only, depending on the heart rate, and it can be difficult to analyse any heart rhythm that shows changes between heart beats. To help with the analysis, it is common to print one or two “rhythm strips”, as well. This will usually be lead II (which shows the electrical signal from the atrium, the P-wave, well) and shows the rhythm for the whole time the ECG was recorded (usually 5–6 sec). Some ECG machines will print a second lead II along the very bottom of the paper in addition to the output described above. This printing of lead II is continuous from start to finish of the process.

The term “rhythm strip” may also refer to the whole printout from a continuous monitoring system, which may show only one lead and is either initiated by a clinician or in response to an alarm or event.

Placement of electrodes

Ten electrodes are used for a 12-lead ECG. The electrodes usually consist of a conducting gel, embedded in the middle of a self-adhesive pad onto which cables clip. Sometimes the gel also forms the adhesive. They are labeled and placed on the patient’s body as follows

The classical 12-lead ECG can be extended in a number of ways in an attempt to improve its sensitivity in detecting myocardial infarction involving territories not normally “seen” well. This includes an rV4 lead, which uses the equivalent landmarks to the V4 but on the right side of the chest wall and extending the chest leads onto the back with a V7, V8 and V9.

The Lewis lead or S5 has the LA electrode placed in the second intercostal space to the right of the sternum with the RA at the fourth intercostal space. It is read as lead I and is supposed to demonstrate atrial activity much better to aid in identification of atrial flutter or broad-complex tachycardia.

A posterior ECG can aid in the diagnosis of a posterior myocardial infarction. This is performed by the addition of leads V7, V8 and V9 extending around the left chest wall toward the back.

Algorrhythm of ECG registration

 

Registration performs fare from electric motors and other electrical devices.

Tested person may have rest before registration in 10-15 minutes. This procedure needs 2-hour interval after eating or worm procedures.

For better contact between electrodes and skin use solution NaCl 5-10 % or special electrode past or electrode gel. Otherwise hindrances in ECG curve may occur. They will stand in the way of ECG analysis

 

 

ECG registration performs in quiet breathing in patients.

Registration begins from standard voltage 1 mV from the electrocardiograph for regulation of amplitude in ECG. Usually standard voltage amplitude is 10 mm. Then continue registration of bipolar limb leads, the next – unipolar limb leads and afterwards – unipolar chest leads.

 

ECG analysis

The main elements of ECG curve are:

– Waves P, Q, R, S and T. Sometimes U wave may occur;

– Segments – P-Q (from the end of P wave to beginning of Q wave), S-T (from the end of S wave until beginning of T wave);

– Intervals, which characterize certain time period of heart activity – P-Q (from the beginning of P wave to beginning of Q wave), Q-T (from beginning of Q wave to end of T wave);

– Complexes – atrial, which is presented by P wave, and ventricular -QRST.

a) P wave in healthy persons, is obligatory positive in I, II, AVF, V2-V6 leads. P wave may be negative in III, AVL and V1, either positive or biphasic. Normally in II lead its amplitude is 2.5 mm, duration – 0.1 s.

b) P-Q interval reflects duration of AV-conduction, which is spreading of potential by AV node, His bundle and its branches. This interval lasts 0.12-0.20 s and depends on heartbeat rate.

c) QRST complex reflects spreading of excitation by ventricles. It hole amplitude is higher 5 mm of the waves are signed by capital letters. Otherwise it used little letters. ORS duration in II lead is not more than 0.1 s.

d) Q wave normally in II lead is less then 1/4 of R amplitude duration is 0.03 s. Normally in AVR deep and wide Q waves may be recorded. In V1, V2 – Q wave is particularly absent.

e) R-view usually is recorded in all leads; exalt AVR, which may be absent. In unipolar chest leads R amplitude gradually increases from V1 to V4 and some decreases in V5 and V6. So normally in unipolar chest leads both increasing R-amplitude and S-amplitude occurs. S-wave has amplitude not more than 20 mm, but it varies from lead to lead.

j) S-T –segment corresponds to excitation of both ventricles. Normally in bipolar and unipolar leads it lies on baseline and don’t move more than 0.5 mm. In V1-V3 deviation upward to 2 mm may occur.

h) T-wave normally is positive in I, II AVF, V2-V6, TI>TIII, TV6>TV1. T-wave has sloping ascend part and sleep descending part. In III, AVL, V1 T-wave may either be positive, negative or bipolar. In II lead T-amplitude is 5-6 mm, duration – 0.16-0.24 s.

i) Q-T interval is electrical systole of ventricles. Its duration directly depends on heartbeat rate. Proper duration may calculated by Buzett formula:

Q-T=K√¯R-R¯, where

K=0.37 in male or 0,40 in female

f) U-wave may be recorded in unipolar chest leads, which reflects excitation fare of excitability after electrical systole of ventricles myocardium. U-wave usually is positive and small.

Axis

The heart’s electrical axis refers to the general direction of the heart’s depolarization wavefront (or mean electrical vector) in the frontal plane. With a healthy conducting system, the cardiac axis is related to where the major muscle bulk of the heart lies. Normally, this is the left ventricle, with some contribution from the right ventricle. It is usually oriented in a right shoulder to left leg direction, which corresponds to the left inferior quadrant of the  hexaxial reference system, although −30° to +90° is considered to be normal. If the left ventricle increases its activity or bulk, then there is said to be “left axis deviation” as the axis swings round to the left beyond −30°; alternatively, in conditions where the right ventricle is strained or hypertrophied, then the axis swings round beyond +90° and “right axis deviation” is said to exist. Disorders of the conduction system of the heart can disturb the electrical axis without necessarily reflecting changes in muscle bulk.

Clinical lead groups

Of the 12 leads in total, each records the electrical activity of the heart from a different perspective, which also correlates to different anatomical areas of the heart for the purpose of identifying acute coronary ischemia or injury. Two leads that look at neighbouring anatomical areas of the heart are said to be contiguous. The relevance of this is in determining whether an abnormality on the ECG is likely to represent true disease or a spurious finding.

 

Diagram showing the contiguous leads in the same color

 

Category	Color on chart	Leads	Activity
Inferior leads	Yellow	Leads II, III and aVF	Look at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)
Lateal leads	Green	I, aVL, V5 and V6	Look at the electrical activity from the vantage point of the lateral wall of left ventricle     The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads. •   Because the positive electrodes for leads V5 and V6 are on the patient’s chest, they are sometimes referred to as the low lateral leads.
Septl leads	Orange	V1 and V2	Look at electrical activity from the vantage point of the septal wall of the ventricles (interventricular septum)
Anterior leads	Blue	V3 and V4	Look at electrical activity from the vantage point of the anteriorsurface of the heart (sternocostal surface of heart)

In addition, any two precordial leads next to one another are considered to be contiguous. For example, though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another. A common saying to remember the contiguous leads is “I see all leads” (inferior, septal, anterior and lateral).

Lead aVR offers no specific view of the left ventricle. Rather, it views the inside of the endocardial wall to the surface of the right atrium, from its perspective on the right shoulder

13. ECG analysis begins with estimation of control voltage and paper speed. Another analysis at usual performs in this order.

1) Determining of impulse origin. Pay attention to proper order of waves in ECG. If P wave in II lead is positive and recorded before QRS complex is believed to determine pacemaker in SA node.

2) Heart rhythm evaluation by measuring of R-R duration. Normally adjacent R-R intervals duration may differ from each other not more 0.1 s. Usually II lead is examined.

3) Determining of heart rate. In proper rhythm 60 s is divided to R-R duration in seconds, which is calculated using paper speed.

4) Evaluation of ECG voltage. If in bipolar limb leads the lowest R wave is smaller than 5 mm and RI+RII+RIII less than 15 mm, the ECG voltage is decreased. Otherwise it is normal.

5) EMP direction determining.

– Visual method: needs measuring R amplitude in all bipolar limb leads. If true, that RII>RI>RIII, the EMP direction is near 30º-69º, that is normal;

– Graphic method use Baily co-ordinate. If in Einthoven’s triangle put through the center parallel to leads axes we’ll get Baily’s co-ordinate. Than in any two bipolar limbs leads it is necessary to determine summary amplitude of QRS waves. Upward waves have positive meaning and downward are negative. Summary amplitude put on corresponding axis with (+) or (-) sign. In this point lined perpendicular to lead axis. Next time determined cross point of two drown perpendiculars. When join this point to Baily’s co-ordinate center we’ll obtain the EMP direction outward the center.

6) ECG elements analysis. Pay attention to form, amplitude and duration of waves and intervals. Measure deviation from baseline if it occurs. Compare the results with normal rate.

The QRS complex (wave) is actually composed of three separate waves: the Q wave, the R wave, and the S wave. They are all caused by currents generated when the ventricles depolarize before their contraction. Because ventricular depolarization requires septal and right and left ventricular depolarization, the electrical wave depicting these events is more complex than the smooth P wave.

The P-R interval is measured from the beginning of the P wave to the beginning of the QRS complex. It is termed P-R instead of PQ because frequently the Q wave is absent. This interval represents the time that elapses from the begin Q-T intervalning of atrial depolarization to the beginning of ventricular depolarization.

The T wave represents repolarization of the ventricles. The Q-T interval begins with the QRS complex and ends with the completion of the T wave. It represents ventricular j depolarization and repolarization. This interval varies with j the heart rate. The faster the rate, the shorter the Q-T interval. Therefore in children this interval is normally shorter than in adults.

The S-T segment is normally an isoelectric (flat) line that I connects the end of the S wave to the beginning of the T wave. The T-P interval represents atrial and ventricular polarization in anticipation of the next cardiac cycle.

An electrocardiogram is taken by placing leads or electrodes on the skin to transmit elective impulses back to a recording machine. By means of telemetry the pattern of electrical impulses can be demonstrated on an oscilloscope. The position of the electrodes on the body and the manner in which they are attached to the electrocardiogram machine influence the type of recording. Usually the electrodes are attached to the body with a rubber strap or a type of adhesive (for continuous monitoring). An electrolyte lubricant or electrolyte-soaked gauze is placed between the skin and lead to increase conductivity.

The PQRST complex is plotted on graph paper. Each small block represents 0.04 second horizontally and I mv (millivolt) vertically. By counting the number of squares intersected by the complex, one can calculate the various intervals, such as the P-R or Q-T interval, and the amplitude (height) of each wave. Other information supplied by electrocardiogram includes heart rate, rhythm, abnormalities; of conduction, muscular damage (ischemia), hypertrophy, effects of electrolyte imbalance, influence of various drugs, and pericardial disease. However, the electrocardiogram gives no direct information concerning the mechanical performance of the heart as a pump triumph and satisfaction in having gone through the experience.

Electrocardiogram of a healthy person is distinguished by considerable variability that is why general regularities typical for all ECGs were conclude:

1)    wave P – stimulation of right (ascending part) and left (descending part of wave) atrium;

2)    interval P-Q – time of impulse passage from atriums to ventricules;

3)    wave Q – stimulation of right ventricle basis, interventricle membrane;

4)    wave R – stimulation transition to left ventricle basis;

5)    wave S – stimulation of both ventricles;

6)    waveT – ventricular repolarisation;

7)    interval T-P – heart diastole;

8)    interval Q-T – ventricle systole;

9)    interval R-R – complete cycle of heart operation.

9.    1) regularity of heart rhythm;

2)    heart rhythm frequency;

3)    ECG voltage;

4)    location of electric heart axis:

5)    amplitude and duration of waves and intervals;

6)    interval QRST.

Following the indicated sequence in ECG decoding we can state about the norm and pathology of heart automatism, stimulation and conductivity.

 

Hypertrophy of heart chambers

If the atrium is enlarged and its myocardium is hypertrophied, the P wave changes. Since an enlarged atrium is slower excited, the length of the P wave becomes longer than 0.1 s. The amplitude of the P wave increases because a higher potential is generated to excite the large mass of the myocardium. If dystrophic or sclerotic changes occur in the myocardium, the shape of the P wave changes: it becomes serrated and split (with two phases). Enlargement of the left atrium changes the P wave in standard leads I and II. Enlargement of the right atrium changes the P wave in standard leads II and III.

Hypertrophy of the left atrium

Hypertrophy of right left atrium

 

Ventricular hypertrophy causes the following changes in ECG: (1) the position of the electrical axis is changed: in left-ventricular hypertrophy it deviates to the left, and in right-ventricular hypertrophy to the right; (2) the amplitude of the ventricular complex and its length increase, i.e. the time of excitation of the ventricles increases; (3) the recovery of the myocardium is upset and this shows itself in the changed terminal part of the ventricular complex of the ECG, namely, the S-T segment is displaced and the T wave changes; (4) in left-ventricular hypertrophy, the amplitude of the S wave in the right chest leads increases: the amplitude of the R wave in the left chest leads increases too. In right-ventricular hypertrophy the changes in the S and R waves are the reverse, i.e. a high R wave appears in the right chest leads, and a deeper S wave in the left leads.

Hypertrophy and chamber enlargement

Because of the thin-walled nature of the atria, from an ECG point of view, one cannot talk about “atrial hypertrophy” but only about enlargement. Conversely, thickening of the ventricle may result in increased voltages seen on the surface ECG, and we can then discuss “ventricular hypertrophy”.

Left ventricular systolic overload/hypertrophy (LVH)

The absence of LVH on ECG means nothing, as the features are insensitive. If however they are present, LVH is very likely. Because the criteria were formulated on white males, they are very insensitive in e.g. black women.

Systolic overload results in increased QRS deflections, with the sum of the S in V1 and the R in V5 or V6 over 35mm indicating hypertrophy. (In the above picture, also note the predominantly negative deflection of the P wave in V1, suggesting left atrial enlargement). A host of other criteria have been proposed. Useful are:

1)    electric axis of the heart is deflected to the left;

2)    high wave R appears in the left chest leads and deep wave S  appears in the right chest leads;

3)    duration and amplitude of the ventricle complex increase;

4)    segment S-T displacement and wave Т change.

T wave axis changes can be predicted knowing Schamroth’s rule .

 

 

LV   hypertrophy

RV hypertrophy

A number of ECG abnormalities have been associated with right ventricular hypertrophy. These include:

•      right axis deviation;

•      A tall R wave (bigger than the S) in V1;

•      A `little something’ in V1 (an initial slur of the QRS, a small r, or a tiny q).

•      Increased VAT in V1

•      left-sided RS or rS complexes, partial or complete RBBB, or RS complexes in the mid-precordial leads.

Whenever you see a tall R in V1, consider the following differential:

•      posterior myocardial infarction

•      RV hypertrophy

•      Right bundle branch block

•      Wolff-Parkinson-White syndrome (with an appropriately placed accessory pathway)

•      Other rare causes such as dextrocardia, Duchenne muscular dystrophy, and so on

•      and, of course, incorrect lead placement

Main symptoms of the right ventricle hypertrophy:

1)    electric axis of the heart is deflected to the right;

2)    high wave R appears in the right chest leads and deep wave S appears in the left chest leads;

3)    duration and amplitude of the ventricle complex increase;

4)    segment S-T displacement and wave Т change.

 

RV hypertrophy. High R vaves in right ECG leads

Hypertrophy

Hypertrophy criteria are fairly straightforward; we will be looking for enlargement of any of the four chambers.

1. LVH: (Left ventricular   hypertrophy). Add the larger S wave of V1 or V2 (not both), measure in mm, to the larger R wave of V5 or V6. If the sum is > 35mm, it meets “voltage criteria” for LVH. Also consider if R wave is > 12mm in aVL. LVH is more likely with a “strain pattern” which is asymmetric T wave inversion in those leads showing LVH.

 

2. RVH: (Right ventricular hypertrophy). R wave > S wave in V1 and R wave decreases from V1 to V6.