of the Heart

Auscultation is that part of the physical examination involving the act of listening with a stethoscope to sounds made by the heart, lungs, and blood.

Aortic valve sound phenomena includes sounds, which are brief vibrations caused by momentary events and murmurs, which are the sound of turbulence as blood flows through some narrow orifice or tube (ie heart valves). The two sounds heard in everyone are the first sound (S1 or ‘Lub’, in lub-dub) caused by closing of the mitral and tricuspid valves, as the ventricles contract and pump blood into the aorta and pulmonary artery ( see figures 103, 104a, 104b, 104c ). The second sound (S2 or ‘Dub’) is caused when the ventricles finish ejecting, begin to relax and allow the aortic and pulmonary valves to close ( see figures 103, 104a, 104b, 104c ).

One common abnormal phenomena that can be heard with a stethoscope is a murmur, which is like a prolonged ‘whoosh’.

The murmur could be due to a narrowing of the aortic or pulmonary valve or to a leak through the mitral or tricuspid valves (both due to acquired or congenital causes, i.e. rheumatic fever or prior myocardial infarction, mitral prolapse), during systole or contraction of the ventricles.
But heart murmurs may also be heard when there is signicant narrowing of the mitral or tricuspid valve during diastole (during relaxation when the blood is flowing from the the left or right atrium into the respective ventricle) due to acquired ( i.e. rheumatic fever) or congenital causes.
Similarly, diastolic murmurs may be heard when the aortic or pulmonary valve leaflets do not adequately oppose each other (i.e. luetic disease, pulmonary hypertension).

The First Heart Sound

The first heart sound(S1) as recorded by a high-resolution phonocardiography consist of 4 sequential components:
(1) small low frequency vibrations, usually inaudible, that coincide with the beginning of left ventricular contraction and felt to be muscular in origin;

(2) a large high- frequency vibration, easily audible related to mitral valve closure (M1);

(3) followed closely by a second high frequency component related to tricuspid valve closure T1;

(4) small frequency vibrations that coincide with the acceleration of blood into the great vessel ( figure198a ). The two major components audible at the bedside are the louder M1 best heard at the apex followed by T1 heard best at the left lower sternal border. They are separated by only 20-30ms and at the apex are only appreciated as a single sound in the normal subject.

Echocardiographic Correlates and Splitting of the S1 one

Several studies have shown that the first high- frequency component of S1 coincides with the complete coadaptation of the anterior and posterior leaflets of the mitral valve. This sound is not due to the clapping together of the two delicate leaflets, but rather to the sudden deceleration of blood setting the entire cardiohemic system into vibration when the elastic limits of the closed tensed valves are met. It is unlikely that complete coaptation of the complex valve leaflets and final tensing are simultaneous; presumably it is a latter event is associated with vibrations perceived as M. For practical purposes, however, the resolution of M- mode echocardiography is inadequate to distinguish between these two events, and M1 and the "C" point of the mitral valve echocardiogram are considered to be coincident. Similar echocardiogram correlates are more difficult to demonstrate T1 in the normal subject because it is often impossible to clearly identify the onset of T1 as the two components of S1 are often synchronous or narrowly split ( figure198a ). However, when T1 is more widely separated from M1, identical echocardiographic correlates have been demonstrated in patients with wide splitting of S1 due to Ebstein's anomaly of the tricuspid valve. This exaggerated T1 or "sail sound" and its wide separation from M1 has been a helpful sign in the diagnosis of this entity. Wide splitting of S1 with normal sequencing ( M1, T1 ) is also present in right branch block of the proximal type as well as in left ventricular pacing, ectopic beats, and idio ventricular rhythms from the left ventricle due to of a delayed contraction of the right ventricle.In a similar manner pacing from the right ventricle and ectopic beats and idioventricular rhythms originating from the right ventricle will produce reverse splitting of S1 (T1, M1) due to delay in left ventricular contraction. Reverse splitting S1 may also be present in patients with hemodynamically significant obstruction of the mitral valve, as mitral valve closure is to delayed due to the increased left atrial pressure that must be overcome by the rising left ventricular pressure before closure can occur. Similar delay in M1 may also be found in mitral obstruction secondary to secondary to left atrial myxoma.

Hemodynamic Correlates of S1

In figure198b the sound and pressure correlates of M1 are shown. The first high-frequency component of M1 coincides with the downstroke of the left atrial "c" wave and is delayed from the left ventricular-left atrial pressure crossover by 30 ms. Similar delays following atrioventricular pressure crossover have been reported by other investigators in the past. These findings have cause considerable confusion regarding the origin of both M1 and T1, as it was assumed these sounds occurred at atrioventricular pressure crossover. However, the elegant studies the Laniado and al. recording both valve motion and phase flow across the mitral valve simultaneously resolved this issue. This study clearly established that forward flow continued for short period following left ventricular- left atrial true pressure crossover due to the inertia of mitral flow, with M1 occurring 20 to 40 ms later, coincidental with cessation of mitral flow and closure of the valve. An even greater delay between the occurrence of T1 and right ventricular-right atrial pressure crossover has been shown by Mills and associates, and the micromanometer study of O'Toole and al. have shown that T1 also coincides with the downstroke of the right atrial "c" wave. These hemodynamic data, together with echocardiographicm correlates of M1 and T1, confirm the primary role played by the atrioventricular valves in the genesis of S1.

Intensity of S1

The primary factors determining intensity of S1 are
(1) integrity of the valve closure,
(2) mobility of the valve,
(3) velocity of valve closure,
(4) status of ventricular contraction,
(5) transmission of characteristics of the thoracic cavity and thorax and
(6) physical characteristics of the vibrating structures.

Integrity of valve closure

In rare situations, usually in the setting of severe mitral regurgitation there is inadequate coaptation of the mitral leaflets to a degree that valve closure is not effective. As a result, abrupt halting of the retrograde blood column during the early ventricular contraction does not occur, and S1 may be markedly attenuated or absent. Such may be the case in severe mitral regurgitation due to the flail mitral leaflet as shown in figure 199a.

Mobility of the Valve

Severe calcific fixation of the mitral valve with complete immobilization will cause a markedly attenuated M1. This is most commonly seen in the setting of longstanding mitral stenosis as shown in figure 199b.

Velocity of Valve Closure

The velocity of valve closure is the most important factor affecting the intensity of S1 and is determined by the timing of mitral valve closure in relation to the left ventricular pressure rise in early systole. The relative timing of left atrial and left ventricular systole may vary this relationship as shown in figure 199c in anesthesized dog preparation using the technique of sequential atrioventricular pacing. As the PR interval progressively decreased from 130 to 30 ms, there is a progressive increase in the intensity of M1 and progressive delay in M1 relative to the onset of left ventricular contraction. However, when left atrial and left ventricular systole occur almost simultaneously at a PR of 10ms S1 again becomes soft. At short PR intervals (30 to 70 ms) the mitral valve leaflets are maximally separated by atrial contraction at the onset of left ventricular systole. With ventricular contraction, the mitral valve closes at a high velocity with a large excursion. This results in a loud,late M1 occurring on the steeper part of the left ventricular pressure curve when the retrograde blood column is suddenly decelerated at the moment the elastic limits of the mitral valve are met. At longer PR intervals there is less separation of the mitral valve leaflets, which have already begun to close with the atrial relaxation. When left ventricular systole begins, there is less excursion of the mitral valve until tensing occurs, and S1 occurs earlier relative to the onset of left ventricular contraction at a lower left ventricular pressure. Thus, less force is applied to the mitral valve, its closing velocity is decreased, and less energy is generated when the column of retrograde blood is halted, resulting in a softer M1. Although simultaneous motion of the mitral valve is not shown in figure 199c, subsequent investigations using cineradiography and echocardiographic techniques to visualize the mitral valve during variations of the PR interval have further confirmed the relationship between the rate of mitral valve closure and the intensity of M1. The clinical finding of marked variation in the intensity of S1 in a patient with a slow heart rate will often alert the clinician at the bedside to the diagnosis of complete heart block with atrioventricular (AV ) dissociation. Other conditions in which there are beat to beat variations in the intensity of S1 include Mobitz type 1 heart block and ventricular tachycardia with AV dissociation. Variations in the intensity of S1 also occur with atrial fibrillation with both normal and stenotic atrioventricular valves. The loud S1 occurs in short RR intervals, while the softer S1occurs at longer RR intervals when the valve leaflets a partially closed. Mills and Craig have shown an excellent correlation between the closing rate of the anterior mitral leaflet and the amplitude of M1 in patients with atrial fibrillation without mitral obstruction. The position of the mitral valve at onset of ventricular systole may be altered not only by the relative timing of atrial and ventricular systole but also by altering the rate of left ventricle filling during atrial systole. Leonard and associates have shown that the timing and intensity of both S1 and S4 in hypertensive patients can be influenced by variations in venous return ( figure 199d ). It is suggested that the mitral leaflets have a greater separation when venous return is decreased to the noncompliant hypertensive left ventricle because there is more effective atrial volume transport to a relatively unfilled ventricle. As shown in the right panel of figure 199d, this results in a softer S4 that migrates toward an increased S1. When venous return is increased ( center panel) the atrial contribution of ventricular filling is now operating on the steep portion of the left ventricular pressure volume curve. The S4 becomes longer and earlier, and S1 is decreased in amplitude due to partially atriogenic closure of the mitral valve.

S1 in Pathological Conditions

Careful attention to the intensity of S1 is an extremely important aspect of cardiac auscultation often giving clues to the proper diagnosis and the degree of abnormality of the involved structures. The following conditions are examples where alterations in the intensive in the intensity of S1 play the key role in the correct diagnosis.

S1 in Mitral Stenosis

A loud, late M1 is the hallmark of hemodynamically significant mitral stenosis. When M M1 is loud, it is associated with a loud opening snap, and the intensity of both M1 and the opening snap correlated with valve motility ( figure 199e, left panel). When calcific fixation of the stenotic mitral valve occurs, M1 is soft and the opening snap is absent ( figure 199b ).The relationship between sound and pressure and echocardiographic mitral valve motion is shown in ( figure 199f ). Significance scarring of the mitral valve is the evident as a result of the rheumatic process. The increased left atrial pressure delays the time of pressure crossover between the left atrium and in the left ventricle. As a result in M1 occurs later and a much higher than normal left ventricular pressure at a time when there is a more rapid rate of development of left ventricular pressure. The presystolic gradient between the left atrium and the left ventricle prevents preclosure of the mitral valve leaflets. As a result, the closure of the leaflet begins from a domed position within the left ventricular cavity and takes place over a much greater distance than normal following the onset of left ventricular contraction. Both of these factors increase the velocity of mitral valve closure and the momentum of blood directed put the mitral valve leaflets, resulting in a loud M1 when the elastic limits of the stenotic mitral valve are met. for A similar mechanism is responsible for the booming S1 with aftervibrations and left atrial myxoma ( figure 199e, center panel).

S1 in Mitral Valve Prolapse

It has been reported that a loud M1 is heard over the apex in patients with nonrheumatic mitral regurgitation; this is indicative of holosystolic mitral valve prolapse ( figure 199e, right panel ). Patients with the more common middle to late systolic prolapse have a normal S1 while a soft or absent S1 may indicate a flail mitral valve ( figure199a ). The increased amplitude of leaflet excursion with prolapse beyond the line of closure explains the loud M1 associated with holosystolic prolapse. An alternative explanation may be a summation of a normal M1 an early noninjection click of valvular prolapse.

S1 and Left Bundle Branch Block

Left Bundle branch block (LBBB) M1 is decreased in intensity and is frequently delayed at times resulting in reversal of sequence of S1 ( figure199g ). The reason for the delay and the decreased intensity of M1 in this condition is multifactorial, with different mechanisms operative in different patients depending on the degree of completeness of the LBBB the site of the block (proximal versus peripheral), and especially the status of of left ventricular function. The primary factors involved are
(1) delay in one set of left ventricular contraction,
(2) a degree of left ventriclar dysfunction,
(3) presence of concomitant first-degree heart block, and
(4) presence of a non compliant left ventricle facilitating atriogenic preclosure of the mitral valve. It is likely that more than one factors operative in most patients with LBBB, with one or two factors predominating.

S1 in Acute Aortic Regurgitation

One of the important auscultatory findings in acute aortic regurgitation is eight is attenuation or absence of M1 as shown in figure199h . Severe regurgitation into a left ventricle that has not had time to adapt to the acute volume overload causes a marked increase in left ventricular- diastolic pressure resulting in resulting in premature closure of the normal mitral valve in middiastole. With the onset of left ventricular systole, minimal valve excursion occurs causing a marked reduction in the intensity of M1.

Systolic Ejection Sounds

Ejection sounds are early systolic ejection events that can originate from either the left or the right side of the heart. These sounds have been classified as valvulara arising from deformed aortic or apulmonary valves or vascular or root events via caused by the forceful ejection of blood into the great vessels. Careful attention to the presence or absence of valvular ejection is of great benefit in defining the level of right or left ventricular outflowup track obstruction while root ejection sounds give insight into into abnormalitieshave of the great vessels with or without systemic or pulmonary hypertension.

Aortic Valvular Ejection Sounds

Aortic valvular ejection sounds are found in nonstenotic congenital bicuspid valves and in the entire spectrum of mild to severe stenosis of the aortic valve. This sound introduces the typical ejection murmur of the aortic stenosis, is widely transmitted, and is often best heard at the apex. As shown in the left panel of figure 199i, the aortic valvular ejection sound is delayed 20 to 40 msec after the onset of pressure rise in the central aorta and is coincident with the sharp anacrotic notch on the upstroke of the aortic pressure curve. Simultaneous sound, pressure and cineoangiographic studies have shown that this sound is coincident with the maximal excursion of the domed valve when its elastic limits are met. The abrupt deceleration of the oncoming column of blood sets the entire cardiohemic system into vibration, the lower frequency components being recorded as the anacrotic notch and the high-frequency components representing the valvular ejection sound. Inherent in this mechanism of sound production is the ability of the deformed valve to move. With severe calcific fixation of the valve, no excursion or piston like ascent of the deformed valve is possible. Therefore, no sudden tensing of the valve leaflets or abrupt decelebration of the column of blood occurs. As shown in the right panel figure 199i, neither an anacrotic notch on the up stroke of the aortic pressure nor a a valvular ejection sound is recorded in this situation.

Sound and motion correlates identical to those demonstrated by cineoangiography have been found with phonoechocardiography, clearly showing the onset of ejection sound to be coincident with the maximum opening of the valve ( figure199j ). The intensity of the ejection sound correlates directly with mobility of the valve, but there is no correlation between intensity and the severity of obstruction. In mobile nonstenotic bicuspid valves, the ejection sound is not only loud but also widely separated from S1 due to the prolonged excursion of the mobile valve the ( figure199k, left panel). The presence of an aortic valvular ejection sound is a valuable physical finding at the bedside; it not only defines the left ventriculare outflow obstruction at the valvular level but also gives insight into the mobility of the valve ( figure199k ).

Pulmonary Valvular Ejection Sounds

Pulmonary valve ejection sounds have identical sound and pressure correlates aortic as valvular ejection sounds. Echocardiographic correlations have also shown that the onset of the pulmonary injection sound occurs at the maximal excursion of the stenotic pulmonary valve. In contrast to the aortic valvular ejection sounds and to most right sided auscultatory events the pulmonary sound or ejection click decreases in intensity or disappears with inspiration and mild to moderate stenosis. The hemodynamic mechanism responsible for this phenomenon is shown in figure199l. In very mild valvular stenosis respiratory variation may be absent. In very severe valvular obstruction a vigorous con traction can completely preopen the pulmonary valve in diastole, causing a crisp of prejection sound. In this situation it has been shown that right ventricular pressure at the time of the atrial kick actually exceeds pulmonary artery end-diastolic pressure. As the severity of the pulmonic stenosis increases, both the excursion of the deformed valve and the right ventricular isovolumic contraction time decrease. The net effect of these to events is migration of the pulmonary ejection sound toward S1.

Aortic Vascular Ejection Sounds

Ejections sounds originating from the aortic root are common in systemic hypertension in the setting of a tortuous scleroitic aortic root, a tight noncompliant arterial tree and forceful left ventricular ejection. they are coincident with the stroke of the high fidelity central aortic pressure and have been interpreted as an exaggeration of the ejection component of a normal S1. Echocardiographic correlates, however, have shown that the sound occurs at the moment of complete opening of the aortic valve war and always on the pressure upstroke of a high fidelity aortic pressure curve.These observations have to the conclusion that this sound probably originates from the valve leaflets.

In contrast to the ejection sound of the stenotic aortic valve, these root sounds tend to be poorly transmitted from the aortic area and arenot heard well at the apex. It may be get difficult at times (if not impossible) to a differentiate this sound from the tricuspid component of a widely spread S1, which is best heard at the fourth left parasternal area and often increases with inspiration. The bedside decision as to whether this is T1 versus an ejection sound will often be dictated by the clinical situation. In either condition it should be emphasized in that the benign S1injection sound or the M1-T1 complexes frequently misinterpreted as a pathological S4-S1 sequence. Factors that favor the presence of an S4-S1 complex are an associated palpable presystolic apical impulse, optimal audibility of the S4 with stethoscope applied lightly at the apex, and a change the intensity of the S4 with maneuers that vary venous return ( figure199d ).

Pulmonary Vascular Ejection Sounds

Vascular or root ejection sounds may also arise from the pulmonary artery,and the common denominator is dilation of pulmonary artey .This dilation can be idiopathic or secondary to severe pulmonary hypertension. Although Laetham and others have stated that this sound is louder during expiration, there is no consensus on this point. Unlike splitting of S1, which is heard best at the mitral or tricuspid area, this sound is louder in the second and left intercostal spaces.

Echocardiographic correlates of the pulmonary root also show it to be coincide with complete opening of the pulmonary valve,occurring during the upstroke of the high-fidelity pulmonary artey pressure recording. This has led to the conclusion that these vascular ejection sounds may originate from semilunar valve cusps that undergone changes in structure in response to increasd pressure. Other investigators have found that the pulmonary root-ejection sounds in the setting of pulmonary hypertension coincide with the upstroke of thehigh-fidelity pulmonary artery tracing, while in bothidiopathic dilation of the pulmonary artery and atrial septal defect, this sound occurs during the upstroke of the pulmonary pressure tracing. It has been suggested that this sound is related to sudden checking of the rapidly accelerated blood column by the "tight" or "loose" pulmonary artery when its elastic limits are met. At present time it is not possible to state with certainty whether the coincidence of the sound with maximal opening of the pulmonary valve as found by some investigators is the cause and effect relation or chance relationship.

Nonejection Sounds

The midsystolic click due to prolapse of the mitral or tricuspid valve is the most frequent cause of systolic nonejection sounds and is often associated with the systolic regurgitant Such sounds were first described in 1887 and termed "systolic gallop". Although origionally thought to be extracardiac in origin, confirmation of the valvular origin has been shown by angiographic, intra cardiac phonocardiographic and echocardiographic studies. The cause of the sound is due to tensing of the AV valves during systole. As with other high-frequency cardiac sounds, it is produced by vibrations of the entire cardiohemic system when the elastic limits of the prolapsed valve are suddenly reached.

The presence of a nonejection click on physical examination is sufficient to make the diagnosis of mitral valve prolapse. The sound has a sharp high-frequency clicking quality and, although often confined to the bit apex, can be transmitted widely on the precordium. It may be an isolated finding occurring most often in the middle to late systole or there may be multiple clicks, presumably as a result of different areas of the large redundant scalloped mitral leaflets prolapsing at different times ( figure199m ). Numerous echocardiographic studies have shown the presence of the characteristic and characteristic mid- to late systolic prolapse as well as holosystolic prolapse in patients with clicks. All of these patterns may be seen in the presence of an isolated systolic clicks, click and late systolic murmur, or the late systolic murmur alone. The click usually occurs at the time of maximal prolapse; the lack of exact correlation of maximal valvular prolapse and the auscultatory findings is the result of M-mode the echocardiographic technique, which allows visualization of only a small portion of the vave.

A feature of mitral valve prolapse is the variability of the auscultatory findings from examination to examination and even from to beat ( figure199n ). The timing of the click, or click and the late systolic murmur, vary considerably with changes in posture ( figure199o ). In the upright posture, the heart become smaller due to the decrease venous return,and the click moves earlier in systole. Angiographic studies have confirmed an earlier and greater degree of prolapse in the upright posture, compared to the supine position. Squatting, which causes an immediate increase in venous return and afterload increases left ventricular volume resulting in later prolapse and movement of the click toward S2. At the bedside these simple maneuvers are helpful in differentiating the nonejection click from early ejection sounds, a split S2 or an S3 .

Other physiologic and pharmacologic maneuvers that vary the loading conditions of the heart also causes changes in the timing of the auscultatory event. Phonocardiographic correlates during the inhalation of amyl nitrite have confirmed the cause- and effect relationship between the echocardiographically demonstrated prolapse and the timing of the click It has been demonstrated that echocardiographically determined left ventricular diameter was relatively constant at the time of the click during supine, upright and amyl nitrite conditions, indicating that a critical size was necessary for prolapse to occur. Increase contractility or velocity of shortening will also affect click timing as a critical size will be reached earlier in systole, The documentation of this consistent relationship of left ventricular size and the timing of the click is in keeping with what is thought to be the cause of mitral valve prolapse, that is, valvuloventricular disproportion or a valve too big for the ventricle. In general, maneuvers that decrease left ventricular volume volume such as sitting, standing, or strain of the Valsava maneuver as well as amyl nitrite administration causes the click to move closer to S. Manuevers that increase left ventricular volume (squatting, vasopressor infusion, and the supine position) moved the click toward S1. If the diastolic left ventricular volume is large enough that the critical prolapse size does not occur in systole, the click will be absent. Conversely, if the diastolic volume is too small the click will fuse with S1.

Although the most common cause of nonejection click is prolapse of the AVC valves, systolic sounds have been reported in patients with left-sided pneumothorax, adhesive pericarditis, atrial myxoma, left ventricular aneurysm, aneurysm of the membraneous ventricular septum associated with the ventricular septal defect and incompetent heterograft valves. The presence of these conditions can usually be recognized by the clinical setting and by the absence of its typical changes in the timing of the click associated with physiologic and pharmacologic and maneuvers.

The Second Heart Sound

Leatham has emphasized the importance of the S2 in the cardiac examination by labeling it the key to auscultation of the heart. To appreciate the significance of the normal and the abnormal S2, knowledge of its relationship to the hemodynamic events of the cardiac cycle is essential. In figure 200a, the two components of S2 are recorded simultaneously with the cardiac cycle by high fidelity catheter- tipped micromanometers. The A2 and the P2 are coincident with the incisura of the aorta and pulmonary artery pressure trace, respectively, and terminate the right and left ventricular ejection periods. Right ventricular ejection begins prior to left ventricular ejection, has a longer duration, and terminates after left ventricular ejection, resulting in P2 normally occurring after the A2. Right and left systole are nearly equal in duration, and the pulmonary artery incisura is delayed relative to the aortic incisura, primarily due to a larger interval separating the pulmonary artery incisura from the right ventricular pressure, compared with the same left- sided event. This interval has been called the "hangout interval", a purely descriptive term. Its duration is felt to be a reflection of the impedance of the vascular bed into which the blood is being received. Normally, it is less than 15ms in the systemic circulation and only slightly prolongs the left ventricular ejection time. In the low resistance, high- capacitance pulmonary bed, however, this interval is normally much greater than on the left, varying between 43 and 86ms, and therefore contributes significantly to the duration of right ventricular ejection. Awareness of this interval is essential for proper understanding of normal physiological splitting and for abnormal splitting seen in conditions where significant alterations in pulmonary vascular impedance have ccurred.

Echocardiographic Correlations and Mechanism of Sound Production

In figure 200b, the relationship between the aortic and pulmonary valve echocardiogram and A2 and P2 is shown. The first high-frequency component of both A2 and P2 is coincident with the completion of closure of the aortic and pulmonary valve leaflets. Identical correlation has been found by other investigators. As with sounds arising from the AV valves, A2 and P2 are not due to the clapping together of the valve leaflets but are produced by the sudden the deceleration of retrograde flow of the blood column in the aorta and pulmonary artery when the elastic limits of the tensed leaflets are met. This abrupt deceleration of flow sets the cardiohemicsystem in vibration; the low frequency of vibrations are recorded as in the incisura of the great vessels, while the higher frequency components result in A2 and P2. In further support of this theory are additional observations showing that the amplitude of A2 and P2 is directly proportional to the rate of change of the diastolic pressure gradient that develops across the valves, that is, the driving forces accelerating the blood mass retrograde into the base of the great vessels. This pressure gradient is the result of the level of diastolic pressure in the great vessel and the rate of pressure decline in the ventricle and is consistent with the well known clinical observation of increased intensity of A2 and P2 in systemic and pulmonary hypertension.

Normal Physiologic Splitting

Normally during expiration, A2 (aortic valve component of second sound) and P2 (pulmonary valve component of second heart sound) are separated by an interval of less than 30ms and are heard by the doctor as a "single" sound. During inspiration, both components become distinctly audible as the splitting interval widens, primarily due to a delayed P2 ( figure 200c ). The delayed P2 and the early A2 are due to a complex interplay between dynamic changes in pulmonary vascular impedance and changes in systemic and pulmonary venous return.The net effect of these changes is the prolongation of the right ventricular ejection and a concomitant decrease in left ventricular ejection that results in widening of the splitting interval during inspiration. The splitting of S2 is usually best heard at the second or the left intercostal space.

Abnormal Splitting

All conditions in which abnormal splitting of S2 exist can be identified at the bedside by the presence of audible expiratory splitting (more than 30ms ), that is, the ability to hear two distinct signs during expiration ( fig. 200c ). This finding must be present when the patient is ausculted in both the supine and upright positions, as some normal patients have audible expiratory splitting in the recumbent position that becomes single when the upright position is assumed. There are three causes of audible expiratory splitting:
1. wide physiological splitting primarily due to delayed P2,
2. reverse splitting primarily due to delayed A2 and
3. narrow physiological splitting as seen in pulmonary hypertension , where A2 and P2 are heard as two distinct sounds during expiration at narrow splitting interval. In tables 1 and 2, the common causes of physiological splitting and reversed of S2 splitting are classified according to the abnormality of the cardiac cycle responsible for the altered timing of A2 and P2.
In each table the cardiac cycle has been divided into three phases:
1. the electromechanical couple interval, the time from the onset of the Q wave to the rise of ventricular pressure;
2. ventricular mechanical systole, the sum of the isovolumic contraction time plus the ejection time minus the hangout interval (abnormalities of this interval exclude those conditions in which prolongation of a hangout interval is primarily responsible for the increased ejection time); and
3. hangout or impedance interval, the time between the incisura out of the arterial trace and the ventricular pressure at the same level as incisura ( includes all conditions in which prolongation of this interval is primarily responsible for the increased ejection time).

Wide Physiologic Splitting of S2

An example of wide physiologic splitting of S2 due to delayed electrical activation of the right ventricle secondary to right bundle branch block is shown in figure 200d. In figures 200e and 200f, prolongation of right ventricular mechanical systole is secondary to severe pulmonary hypertension and pulmonary stenosis is responsible for the delayed P2. In figure 200g the classic fixed splitting of S2 found in atrial septal defect is demonstrated. A composite in figure 200h documents the role played by decreased impedance of the pulmonary vascular bed in the audible expiratory splitting found in atrial septal defect, idiopathic dilation of the pulmonary artery, and mild pulmonary stenosis with aneurismal dilation of the pulmonary artery. In each case there is a marked increase in the hangout interval as measured by high fidelity pressure tracings. In figure 199a, wide physiological splitting secondary to a decreased left ventricular ejection time is shown in a patient with acute mitral regurgitation. For a more detailed analysis of each of the conditions producing wide physiological splitting of S2 see table 1 references.

Reversed Splitting of S2

Almost all cases of reverse splitting of S2 are due to a delay in A2. As a result, the sequence of closure sounds is reversed, with P2 preceding A2. At the bedside this abnormality is recognized by paradoxical motion of A2 and P2 with respiration. During inspiration P2 moves toward A2 and the splitting interval narrows, whereas during expiration the two components separate, and audible expiratory splitting is present ( figure 200c ). The presence of paradoxical splitting S2 almost always indicates significant underlying cardiovascular disease.

Both right ventricular ectopic and paced beats produce a delay in the onset of left ventricular contraction resulting in reverse splitting of S2. The mechanism responsible is a delayed activation of the left ventricle, prolonging the Q to the left ventricular pressure rise interval. The most common cause of reverse splitting is complete LBBB, which can be due to delayed activation of the left ventricle, as seen in isolated proximal block ( figure 200i ) or prolonged mechanical systole ( primarily isovolumic contraction time), as seen in proximal or peripheral block invariably associated with significant left ventricular dysfunction ( figure 199a ). Delay often exist in the onset of left ventricular pressure rise when isovolumic contraction time is markedly prolonged, since in most cases of LBBB varying degrees of both mechanisms are present with one predominating. In the left panel of figure 200j reversed splitting of S2 is demonstrated in a patient with hypertrophic cardiomyopathy and is due to the large systolic pressure gradient and prolonged left ventricular relaxation. Although both of these mechanisms may contribute to to the reversed splitting observed in patients with valvular aortic stenosis an additional mechanism is shown in the right panel of figure 200j, where an exaggerated hangout in a intervalof 30ms is present and is primarily responsible for the delayed A2.

In hypertensive cardiovascular disease splitting is usually physiologic with the intensity increased. However, rare instances of reversed splitting do occur. the elevation of blood pressure produced by intravenous administration of methoxamine has been shown to produce reversed splitting in a normal subject due to prolongation of both left ventricular ejection time and the isovolumic contraction time in face of an increased afterload. Reverse splitting of S2 has also been reported in ischemic heart disease and during episodes of angina pectoris. The latter is extremely uncommon and has rarely been documented by phonocardiography. It is most likely due to a prolonged isovolumic contraction time of the ischemic left ventricle, although during angina it may also be due to an increase in systemic arterial pressure or transient left BBB. Decreased impedance and the systemic vascular bed can contribute to delayed A2 seen in poststenotic dilation of the aorta, as shown in the right panel of figure 200j. It also plays a role in the reverse splitting occasionally seen in both chronic regurgitation aortic and patent ductus arteriosus. Reverse splitting of S2 has been reported in some cases of type B Wolff- Parkinson-White syndrome where early activation of the right ventricle through an accessory pathway has caused P2 to occur prematurely.

Narrow Physiological Splitting

Narrow physiological splitting of S2 is a common finding in pulmonary hypertension, as shown in figure 200c. In contrast to the normal situation where only a single sound is heard expiration both A2 and P2 are easily heard, even though the splitting interval is less than 30ms because of the increased intensity and high frequency composition of P2. Narrow splitting, although common in severe pulmonary hypertension is not always the case as shown in figure 200f where wide splitting with an increase amplitude of P2 is present. It has been suggested that a wide split in pulmonary hypertension may indicate a more severely compromised ventricle than a normal split. Similar observations by others suggest that wide, persistent splitting becomes a useful sign of abnormal right ventricular performance in patients with primary pulmonary hypertension. In order to reconcile these differences responses in S2 when pulmonary hypertension develops, it is essential to appreciate that normally the duration of right and left ventricular systole is nearly equal and that a potential interval (the normally wide right sided hang out interval) can be encroached upon as a process of pulmonary hypertension progressively decreases the capacitance and increases the resistance of the pulmonary vascular bed ( figure 200c). In figure 200i, the sound and pressure correlates two patients with severe pulmonary are shown, one having narrow splitting of S2 and the other having wide splitting of S2. common to both the patients is marked narrowing of the normally wide right- sided hang out interval. In the center panel, the duration of right and left ventricular mechanical systole is nearly equal at the time of the pulmonary artery incisura, and splitting interval is narrow. In contrast, the right panel shows that there has been a marked prolongation of right ventricular mechanical systole in the face of chronic pressure overload, and the net effect is a delayed P2 resulting in wide splitting of S2. Thus, c spectrum of the width of splitting may be seen in pulmonary hypertension, depending on the degree of selective prolongation of right ventricular systole, always in this setting of a narrow hangout interval. Furthermore, it is clear that varying degrees of splitting may be seen in the same patient during different stages of the disease process, producing pulmonary hypertension. Similar hemodynamic correlates have been found and patients having hyperkinetic pulmonary hypertension secondary to large atrial septal defects.

Fixed splitting of S2 has occasionally been documented in severe right ventricular failure secondary to pulmonary hypertension. this has usually been attributed to the inability of the compromised right ventricle and to accept the augmented venous return associated with inspiration. The altered pulmonary vascular impedance associated with severe pulmonary hypertension may also play an important role in the diminished inspiratory split observed in such cases.

Single S2

All conditions listed in table 2 that delay A2 may produce a single S2 when the splitting interval becomes less than 30ms . Also, conditions in which one component S2 is either absentto or inaudible will produce a single S2 (for example, severe tetralogy of Fallot, severe semilunar valve stenosis, pulmonary atresia, and most cases of tricuspid atresia). In Eisenmenger's ventricular septal defect, the duration of right and left ventricular systole is necessarily equal and a loud, single S2 is appreciated because A2 and P2 occur simultaneosly. The most common cause of an apparent single S2 is the inability to hear the fainter of the two components of the sound (usually P2) because of emphysema, obesity, or respiratory noise. Another common cause of single S2 is seen in individuals over age 50. Although this has been attributed to a delayed A2, a decreased inspiratory delay in P2 has also been reported. This latter finding has been shown to be due to a decreased right - sided hangout interval, most likely related to aging changes in the pulmonary vascular bed.

Opening Snaps

Opening of the normal atrioventricular valve is almost always a silent event. However, it with thickening and deformity of the leaflets, usually rheumatic in origin, a sound is generated in early diastole in a manner analogous to the ejection sounds arising from the deformed semilunar valves. It has been proposed that the mechanism of production was a sudden stopping of the opening movement of the valve. Hemodynamic and angiograhic studies have shown sudden checking of the early diastolic descent of the funnel-shaped stenotic valve when its elastic limits were met. Phonoechocardiography has given an even more precise correlation of the opening snap with the maximal opening motion of the anterior mitral leaflet (figure 199e, left- panel).
The opening snap is a crisp, sharp sound that can be heard in the midprecordial location, usually best in the area from the left sternal border to just inside the apex. It may often be heard well at the base of the heart and is frequently not well heard at the maximal intensity of the diastolic murmur. The diastolic rumble generally follows the opening snap by a short interval. There is no variation in the intensity or timing of the mitral opening snap with respiration. as with ejection sounds of valvular origin, the intensity of the mitral opening snap correlates well with mobility of the valve. A loud opening snap is found in mobile stenotic valves with good excursion ( figure199e ), while the opening snap is absent with severe calcific fixation of the valve ( figure 199b, figure 200l ). The intensity of M 1 parallels the intensity of the opening snap; mobile valves having a loud opening snap have an accentuated M 1, and immobile valves having a decreased or absent opening snap have marked attenuation of M1. Although the presence of valvular calcification decreases valvular mobility and audibility of the opening snap, the sound is actually found in 50 to 60 percent of patients with calcific valve. The mere presence of valvular calcium does not preclude some mobility of the valve leaflets and therefore an opening snap ( figure200l ).
The opening snap follows A2 by an interval of 0.03 to 0.15 seconds. In patients with mild mitral stenosis, the interval is usually long, whereas with more severe stenosis the A2 -opening snap (A2-OS) interval is shorter. The A2-OS interval in atrial fibrillation can vary with cycle length as shown in figure 200m. With a short preceding RR interval, the left-atrium has not had time to empty, the left atrial pressure remains high, and the A2-OS is short. With a longer preceding RR interval that left atrial pressure falls and the A2 -OS widens. Increasing severity of mitral stenosis is usually accompanied by an increase in left atrial pressure and therefore a shortening of the A2-OS interval.The hemodynamics responsible for the timing of the opening snap are shown in figure 199f. The opening snap occurs at the maximal mitral valve opening shortly after left ventricular-left atrial pressure crossovers. Increasing severity of mitral stenosis is usually accompanied by an increasing left atrial pressure and therefore a shortening of the A2-OS interval.
Because this interval is multifactorially determined there is an imperfect correlation between the A2-OS interval and the mitral valve area.

Tricuspid valve stenosis can also produce an opening snap. This sound is frequently not detected because the findings of coexisting mitral stenosis, which is almost invariably present, overshadows those with the tricuspid stenosis. The maximal intensity of the tricuspid opening snap tends to be from closer to the left sternal border and, unlike the mitral snap the intensity of the tricuspid snap increases with inspiration. When present, it generally follows the mitral opening snap.

An early diastolic sound can also be caused by the right or left atrial myxoma ( figure199e ). The tumor "plop" occurs at the maximal diastolic descent of the myxoma.
Although an opening snap is rarely found in patients with normal valves, it may be heard in situations where high flow exists across the AV valves.An early diastolic sound is frequently present in large atrial septal defects, coincident with maximal opening of the tricuspid valve. Opening snaps have also been observed in severe mitral regurgitation in reports prior to the routine use of echocardiography. It may well be that some of these patients had severe mitral regurgitation of rheumatic origin with typical diastolic doming of the deformed valve, as seen with mitral stenosis (figure 200l, right panel ). Other conditions in which functional opening snaps have been bound include large ventricular septal defects, thyrotoxicosis, and tricuspid atresia with a large atrial septal defect. The opening snap must be differentiated from other early diastolic sounds such as the S3, the pulmonary component of a widely split S2 and a pericardial knock. At the bedside differentiation of an opening snap from P2 is made by noting that the maximum intensity is near the apex rather than at the pulmonary area and that there is a lack of movement with respiration. During continuous respiration, it is often possible to appreciate three sounds on inspiration, occurring in rapid sequence in the pulmonary area, and only two components on expiration.

The Fourth Heart Sound

Precordial vibrations resulting from atrial contraction are normally neither palpable nor audible. Under pathologic conditions, forceful atrial contraction generates a low-frequency sound (S4) just prior to S1 (also termed the atrial diastolic gallop or the presystolic gallop).
Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction. The S4 follows the onset of the P wave of the ECG by approximately 70 ms. Audibility of the S4 depends not only on its intensity and frequency but also on its separation from S1 The degree of this separation is determined primarily by the PR interval, but it is also somewhat influenced by the PS4 and the QS1 interval. A loud S1 may also mask the audibility of a preceding softer S4.
The S4 is best heard at the apex impulse with the patient turned in the left lateral position. It varies considerably with respiration, usually being heard best during expiration. Both the intensity and timing of the S4 are closely related to the end-diastolic volume of the ventricle. Maneuvers that increase venous return increase the audibility by increasing the intensity of the sound and by causing it to occur earlier, thereby separating it further from S1 (Fig. 199d) Decreased venous return does the opposite. Audible fourth heart sounds are usually accompanied by a palpable presystolic apical impulse in the absence of obesity, emphysema, etc., but occasionally palpable presystolic impulses are not audible. The S4 generated by a forceful right atrial contraction is usually heard best at the lower left sternal border. Unlike the left-sided S4, it tends to be accentuated with inspiration (Fig. 200q). It is also accompanied by prominent "a" waves in the jugular venous pulse and is occasionally audible over the right jugular vein.
As with the S3, both the ventricular origin of this sound due to the abrupt deceleration of the atrial contribution to late diastolic filling and the impact theory have been proposed. It is likely that the former is responsible for the sounds recorded within the ventricular cavities or on their epicardial surfaces, while the latter mechanism is responsible for the S4 ausculted at the chest wall.
Regardless of the exact mechanism of production, the presence of an S4, particularly when associated with a palpable presystolic apical impulse, is an abnormal finding. Although considered to be a normal finding in older subjects by some investigators. Many other experienced cardiologists feel strongly that a definite S4 in a middle- or older person is not likely to br a normal event.the study by Reddy and associates has shed light on this controversity, showing that the absolute intensity of S4 does not decrease with age as does the absolute intensity of S1, resulting in a relative increase in the intensity of S4 compared to S1. This relative change in intensity may well explain the increased frequency of recordable and audible fourth heart sounds in older subjects. Conditions such as obesity, emphysema, or barrel-chest deformity may hinder the clinical detection of both an S4 and an apical presystolic impulse.
The common pathologic conditions in which S4 is heard are listed in Table 5 below. A forceful atrial contraction into a hypertrophied noncompliant ventricle almost always produces an early and easily audible and recordable S4. The severe left ventricular hypertrophy present in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy is responsible for the loud S4 recorded in Fig. 199d, Fig. 200r and Fig. 200s. In each case, the S4 is associated with a prominent apical presystolic impulse and is widely separated from S1. Although Goldblatt et al. have reported that an S4 in patients with aortic stenosis correlates with a peak systolic gradient of 70 mmHg or more and a left ventriculat end-diastolic pressure of 13 mmHg or greater, Caulfield and associates have modified this observation, stating that an S4 is good evidence of significant aortic stenosis only in patients under age 40.

Fourth Heart Sound (S4), Atrial diastolic Gallop,
and Presystolic Gallop and Pericardial Knock

Physiologic --recordable, rarely audible



Decreased ventricular compliance

Ventricular hypertrophy
Left or right ventricular outflow obstruction
Systemic or pulmonary hypertension
Hypertrophic cardiomyopathy

Ischemic heart disease
Angina pectoris
Acute myocardial infarction
Old myocardial infarction
Ventricular aneurysm

Idiopathic dilated cardiomyopathy
  Excessively rapid late diastolic filling secondary to vigorous atrial systole
Hyperkinetic states
Arteriovenous fistula
Acute atrioventricular valve incompetence
Heart block


An audible S4 with a palpable presystolic impulse is common in patients with ischemic heart disease during an acute episode of angina and in the early phases of transmural myocardial infarction. Its prevalence is also increased in patients with prior myocardial infarction. However, audible fourth heart sounds in patients with ischemic heart disease without prior infarction is quite uncommon. In patients with left ventricular aneurysm or idiopathic or ischemic cardiomyopathy, abnormal fourth heart sounds are commonly present and often associated with an S3, producing a quadruple rhythm. If tachycardia is present or if the PR interval is prolonged, S3 and S4 may fuse, giving rise to a loud summation gallop (Fig. 200n).

Quadruple rhythms are common in hyperkinetic states where the S3 is due to excessively rapid early diastolic filling and the S4 results from a forceful atrial contraction into a volume-loaded ventricle. With varying degrees of tachycardia, incomplete summation may occur, simulating a diastolic rumble, or complete fusion may occur, generating a loud summation gallop (Fig. 200n). In acute incompetence of the AV valve, vigorous atrial contraction into an acutely volume-loaded ventricle produces an S4 associated with a presystolic apical impulse (Fig. 199a).At times it may be difficult to appreciate because of the masking effect of the loud systolic murmur. This contrasts with most patients with chronic mitral regurgitation, who do not have an S4 but rather frequently have an S3.

Presystolic and isolated diastolic fourth heart sounds as well as summation gallops may be heard with varying degrees of heart block. First-degree heart block facilitates audibility of the S4 because it further separates S4 from Si. In 2:1 heart block, an isolated S4 may be heard in diastole and also a presystolic S4 may be audible because of the increase in diastolic volume. In complete heart block, S4 may be heard randomly throughout diastole, and when it occurs simultaneously with rapid early ventricular filling, a loud summation gallop may occur (Fig. 200t). Fourth heart sounds have also been reported in ventricular systole when atrial contraction occurred during systole in a patient with heart block. The occurrence of an S4 when the mitral valve is closed excludes its ventricular origin due to either a pressure or volume change and is in keeping with the impact theory of S4 sound production.

Shaver,J.A.,MD and Salerni,R.,MD,Hurst's The Heart,Auscultation of the Heart,PP.253-314.


Levine and Harvey described a musical, apical systolic high-pitched, musical, sonorous, and vibratory, are best heard at the apex in late systole, and are frequently intermittent. They may vary strikingly with respiration, from beat to beat, and from examination to examination. They are often preceded by clicks and originate in the mitral valve. They are associated with ballooning of the mitral valve or mitral regurgitation (or both), and their unusual quality is secondary to the high-frequency vibrations of the mitral apparatus. The systolic "whoop" or "honk," together with late systolic murmurs, with or without associated clicks, is part of a continuum representing abnormalities of the mitral valve apparatus of varying etiologies. Similar honking noises, with or without clicks, may arise from the tricuspid valve and also have been produced by transvenous pacemaker catheters situated across the valve. These murmurs are best auscultated at the fourth left intercostal space and have the typical inspiratorv augmentation of tncuspid murmurs.

215. Levine SA, Harvey SP. Clinical Auscultation of the Heart, 2d ed. Philadelphia: Saunders; 1959.Shaver,J.A.,MD and Salerni,R.,MD,Hurst's The Heart,10th Edition,Auscultation of the Heart,PP.267

Innocent Murmurs

Innocent murmurs are always systolic ejection in nature and occur without evidence of physiologic or structural abnormalities in the cardiovascular system when peak flow velocity in early systole exceeds the murmur threshold. These murmurs are almost always less than grade 3 in intensity and vary considerably from examination to examination and with body position and level of physical activity. They are not associated with a thrill or with radiation to the carotid arteries or axillae. They may arise from flow across either the normal LV or RV outflow tract and always end well before semilunar valve closure.

Innocent murmurs are found in approximately 30 to 50 percent of all children. In young children, especially children aged 3 to 8 years, the vibratory systolic (Still's) murmur is common. It has a very distinctive quality described as "groaning," "croaking," "buzzing," or "twanging." It is heard best along the left sternal border at the third or fourth interspace and disappears by puberty. Considerable controversy exists as to the origin of the vibratory systolic murmur. Regardless of the exact cause, most authorities agree that this murmur originates from flow in the LV outflow tract.

Innocent systolic ejection murmurs also have been attributed to flow in the normal RV outflow tract and have been termed innocent pulmonic systolic murmurs because the site of their maximal intensity is auscultated best in the pulmonic area at the second left interspace with radiation along the left sternal border. These are low to medium in pitch, with a blowing quality, and are common in children, adolescents, and young adults. Stein et al.,who used high fidelity catheter tipped micromanometers to record intracardiac sound and pressure in the aorta and pulmonary artery in adults with normal valves, invariably recorded the ejection murmur in the region of the aortic valve. They concluded that these murmurs, despite their precordial location, were aortic in origin.
In adults over age 50, innocent murmurs due to flow in the LV outflow tract are often heard and may be of a higher frequency, with a musical quality, and frequently loudest at the apex. They may be associated with a tortuous, dilated sclerotic aortic root, often in the setting of systolic hypertension. Mild sclerosis of the aortic valve also may be present.

The preceding descriptive breakdown of innocent murmurs is based primarily on age, precordial location, and distinctive acoustic qualities. Since all these murmurs are equally innocent, and because there is considerable overlap among them with respect to origin, transmission, and frequency composition, they are best characterized as systolic ejection murmurs without associated abnormailities of thee cardiovascular system. Since both innocent and pathologic ejection murmurs have the same mechanism of production it is the "the company the murmur keeps" that affords the differential diagnosis of the pathologic systoloic ejection murmur from the innocent murmur.

For a murmur to be considered innocent, the examination of the cardiovascular system must disclose no abnormalities. Blood pressure and contour of the carotid, femoral, and brachial arteries always should be evaluated carefully. For example, a seemingly innocent murmur in the setting of hypertension, particularly in a younger patient, always should suggest the diagnosis of coarctation of the aorta, which can be diagnosed readily by palpation of weak or nearly absent femoral pulses and confirmed by taking the blood pressure in the lower extremities. There should be no elevation of the jugular venous pulse, and the contour of the jugular pulse should be normal, without exaggeration of either the a or v wave. Evidence of cardiac enlargement on physical examination should be absent, and palpation of the apex in the left lateral position should show no evidence of a presystolic impulse, sustained systolic motion, or hyperdynamic circulation. On auscultation, normal physiologic splitting should be present. A physiologic S3 is often present in association with an innocent murmur in children and young adults but should not be heard after age 30. An S4 is rarely heard in normal children and adults (younger than 50 years) and always should be considered to be abnormal when associated with a presystolic impulse. Systolic ejection sounds of valvular origin as well as midsystolic nonejection sounds should be absent because their presence points to minor abnormalities ot the semilunar and AV valves, respectively (see Fig. 211).

The remainder of the physical examination should show no evidence of a cardiac cause of pulmonary or systemic congestion. In almost all patients with innocent murmurs, the ECG and the cardiac silhouette on chest x-ray shouId be normal.
The supraclavicular arterial murmur or bruit is a common finding in normal individuals, particularly children and adolescents. These murmurs are maximal in intensity above the clavicles and tend to be louder on the right, although they are often heard bilaterally. The bruit begins shortly after SI, is diamond-shaped. and is of brief duration, usually occupying less than half of systole. Although the exact mechanism is unknown, it is related to peak flow velocity near the origin of the normal subclavian, innominate, or carotid artery. When particularly prominent, this murmur may transmit to the basal region of the heart and simulate a systolic ejection murmur. However, unlike the cardiac ejection murmur, the supraclavicular murmur is always louder above the clavicles than below them. Complete compression of the subclavian artery may cause the murmur to disappear completely, whereas partial compression occasionally may intensify it. Hyperextension of the shoulders is a simple bedside maneuver that may decrease the intensity of the murmur and cause it to disappear completely. In the adult, the supraclavicular murmur must be distinguished from the murmur of true organic carotid obstruction, this latter being longer, often extending through S2 and are frequently associated with a history suggestive of transient ischemic attacks.