Ejection Click of Aortic Stenosis (AS)5 6

• Diagnostic of valvular AS and is absent in supravalvular or subvalvular AS.

• It corresponds to the notch in the upstroke of the aortic pressure tracing or the carotid pulse tracing (Fig. 6).

  This notch apparently results from maximal opening and abrupt deceleration of the flexibly stenotic aortic valve.

• Intensity of the sound decreases with calcification. Seen only with pliable valves and is absent in severe calcific AS.

• Calcification of the aortic valve is a rule beyond the age of 40 years. Hence, presence of aortic ejection click in adults suggests either mild AS or presence of congenital bicuspid aortic valve.

• Presence of an aortic EC in the child is diagnostic of congenital bicuspid aortic valve.

• Absence of other signs of AS in the presence of aortic EC strongly suggests the presence of bicuspid aortic valve.

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Fig. 6 Physiological basis of ejection click in aortic stenosis.

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Fig. 6 Physiological basis of ejection click in aortic stenosis.

Ejection Click (EC) of Pulmonary Stenosis (PS) 7 8

• Diagnostic of valvular PS.

• It is the only right-sided acoustic event that softens (diminishes) with inspiration.

• Mechanism of inspiratory decrease in the pulmonary EC.

  • In PS, the right ventricle (RV) is stiff and hypertrophied.

  • During inspiration, when more blood enters the RV, it fails to distend normally. As a result, the RV pressure increases, and exceeds that of the pulmonary artery pressure, which falls slightly. The pulmonary valve is partially open (domed or tensed position) prior to onset of ventricular contraction (Fig. 7a). When the RV contracts, excursion of the partially opened pulmonary valve is reduced and therefore the EC is softer and occurs earlier.

  • During expiration, venous return to the right heart is decreased. At the same time, the pulmonary artery pressure also rises slightly. As the pulmonary artery end-diastolic pressure exceeds the RV pressure, the pulmonary valve leaflets are in a closed or slack position (Fig. 7b). With ventricular systole, the valve opens quickly and then abruptly halts, producing the ejection sound.

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Fig. 7 (a and b) Respiratory variation of pulmonary ejection click.

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Fig. 7 (a and b) Respiratory variation of pulmonary ejection click.

The S1–pulmonary EC interval is directly related to RV isovolumic contraction time. With increasing severity of PS, the isovolumic systolic interval shortens resulting in early onset of EC.

• Mild-to-moderate PS–EC becomes soft and occurs earlier.

• Severe PS–the RV may become so stiff that a vigorous atrial contraction opens the pulmonary valve completely, producing a click in late diastole.

• Very severe PS–the EC fuses with S1 and may not be identified

Vascular clicks 9: They occur in the presence of normal aortic and pulmonary valves. They result from rapid distension of the dilated proximal aorta or pulmonary artery at the onset of ejection.

Mechanism: Vascular clicks result from increased pressure, increased flow, and dilatation of the great vessels (Fig. 8).

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Fig. 8 Mechanism of vascular clicks.

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Fig. 8 Mechanism of vascular clicks.

Causes:

A. Aortic vascular click.

1. Systemic hypertension.

2. Aneurysm of the ascending aorta.

3. Aortic regurgitation.

4. Tetralogy of Fallot–anterior dilated aorta.

5. Anemia and thyrotoxicosis–hyperkinetic circulatory states.

B. Pulmonary vascular click.

1. Pulmonary hypertension.

2. Idiopathic dilatation of the pulmonary artery.

3. Left-to-right shunts.10

4. Hyperkinetic circulatory states.

Clinical characteristics of vascular and valvular clicks11 are shown in Table 2.

Aortic vascular and valvular clicks can be identified, based on associated clinical features (Table 3).

Pulmonary clicks can be differentiated, based on respiratory variation and associated clinical features (Table 4).

Significance

Aortic vascular click is associated with aortic root dilation in the form of aortic sclerosis with tortuous aortic root, systemic hypertension, ascending aortic aneurysm and aortic regurgitation due to aortic root pathology.

Pulmonary vascular click is associated with pulmonary hypertension and pulmonary arterial dilatation.

Differential diagnosis: ECs may be confused with a split S1 or a S4 followed by an early S111 (Tables 5 6).

Conditions with OS

1. Diseased atrioventricular valves.

   1. MS

   2. Tricuspid stenosis (TS)

2. Normal atrioventricular valves, but excess blood flow from mitral valve into LV

   1. VSD

   2. Patent ductus arteriosus (PDA)

   3. Mitral regurgitation (MR)

3. Rare conditions wherein a mitral OS is heard in the presence of a normal mitral valve are16:

   1. Tricuspid atresia with a large atrial septal defect (ASD).

   2. Idiopathic second- and third-degree heart block.

   3. Thyrotoxicosis.

   4. Tetralogy of Fallot occurring after a Blalock–Taussig procedure.

Characteristic Features of OS

• Sharp, high-pitched, crisp sound heard with the diaphragm of the stethoscope.

• Best heard in the supramammary area between the apex and the LLSB, but it has a wider area of radiation. It is loudest in the fourth left interspace, occasionally in the third, and slightly above and to the right of the area in which the diastolic murmur is best heard (i.e., the supramammary area). It is next best heard at the apex, left sternal border, and at the base of the heart in the aortic position, with the least common location being the pulmonary area.

• Usually heard 40 to 120 milliseconds after the second heart sound, it precedes the mid-diastolic murmur by a short interval. The S2–OS interval is influenced by the heart rate (HR) and tends to shorten with tachycardia. During atrial fibrillation (AF) and sinus arrhythmias, the interval duration depends on the length of the preceding cardiac cycle.

Best audible in recumbent position. Exercise can augment its audibility by increasing the HR as OS is louder at higher rates.

Clinical Significance

Mitral stenosis (MS) 17 18 19:

• Mitral OS followed by a mid-diastolic murmur is characteristic of MS and not a flow rumble across a nonstenotic valve.

• Presence of a crisp OS suggests that the mitral valve leaflets are mobile and pliable.

• It softens or disappears as the leaflets become ore calcific and immobile.

• The S2–OS interval helps in assessment of the left atrial pressure and severity of MS.

  • In severe MS, because of higher left atrial pressure, the transmitral gradient develops immediately after mitral valve opening (MO), resulting in an OS almost just after S2.

  • In mild mitral stenosis, the OS occurs later in diastole due to delayed transmitral gradient.

  • In addition, in severe MS, the OS is followed by a longer murmur, as it takes more time for blood to pass through the stenotic mitral valve and for the pressure gradient to dissipate once the mitral valve opens.

  • Intervals < 70 milliseconds suggest severe MS, and > 100 milliseconds are compatible with mild obstruction.

  • An A2–OS interval of ≥ 80 milliseconds indicates the left atrial mean pressure is normal (9 to 12 mm Hg).

  • An A2–OS interval of < 60 milliseconds indicates a markedly elevated left atrial mean pressure (25 to 36 mm Hg).

  • When the A2–OS interval was 60 to 80 milliseconds, there was an overlap of mean pressure value (12 to 25 mm Hg).20

  • Reduction of < 20% of the interval on exercise suggests an increase of < 35% left atrial mean pressure.

  • Whereas a decrease of the A2–OS interval > 30% is associated with > 40% increase of the left atrial mean pressure.

OS is a useful diagnostic sign in MS, especially when other signs have been missed on casual examination. Its presence prompts for a more thorough search for the latent mid-diastolic murmur. Absence of OS in a confirmed case of MS indicates either

1. mild MS; b. calcified immobile valve c. associated significant MR.

Tricuspid Stenosis (TS): OS in TS was first described by Rivero Carvallo (1952–53)21 as a sound from the diseased tricuspid valve and defined as “chasquido de apertura de la trictspide.” The sound is similar in almost all respects to the OS of the mitral valve except for its area of audibility. It is shorter in duration, occurs earlier and relatively lower pitch than the mitral OS, and best heard over the xiphisternum and right lower end of the sternum22

Differential diagnosis: OS could be confused for split second heart sound or third heart sound (Table 9 Fig. 14).

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Fig. 14 Occurrence of time intervals of opening snap and its mimics.

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Fig. 14 Occurrence of time intervals of opening snap and its mimics.

The time intervals of opening snap and its mimics play an important role in identifying its character and is depicted in Fig. 14.

The sequence of events would be split S2, OS, and then S3 in view of occurrence and intervals (Fig. 15).

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Fig. 15 Sequence of events in relation with opening snap.

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Fig. 15 Sequence of events in relation with opening snap.

The OS and second component of split-second sound can be differentiated clinically, based on the best audible site and interval. Deep breathing technique is of great value, especially since both the sounds are heard. Differentiation of opening snap from S3 rarely poses a dilemma in clinical reality.

Fig. 16 summaries the confusion among the additional sounds around first and second heart sound in practice.

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Fig. 16 Additional sounds causing confusion around S1 and S2.

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Fig. 16 Additional sounds causing confusion around S1 and S2.

Differential Diagnosis

S3 gallop is the most common differential diagnosis. A pericardial knock occurs closer to the S2 than S3 gallop, which occurs 100 to 200 milliseconds after S2. Pericardial knock is of higher pitch and louder than S3.

Tumour Plop1 2 3 4

Early diastolic low-pitched sound heard just after S2 (Fig. 18). It is heard 80 to 150 milliseconds after the second heart sound. It may or may not be followed by a diastolic murmur. It is heard in left atrial myxoma.

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Fig. 18 Tumour plop.

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Fig. 18 Tumour plop.

Other Diastolic Sounds

1. Vegetation plop25: an early diastolic sound occasionally heard in endocarditis. This sound is produced when a large vegetation over the mitral valve moves into the LV during early diastole.

2. High-frequency early diastolic sounds are occasionally heard in the following:

1. MVP–sound is related to rapid movement of the prolapsed MV into LV before opening of the mitral valve.

2. Hypertrophic cardiomyopathy–sound is related to contact of the anterior mitral leaflet (AML) with the interventricular septum (IVS) in early diastole, especially in patients with small LV cavity.

3. Severe MR due to ruptured chordae.

Characteristic Features26 27 28 29 30

• Scratchy/leathery/grating sound–like the two pieces of sandpaper rubbing together. Loud enough to mask other cardiac murmurs.

• May present as a soft blowing murmur and confuse with other cardiac murmurs.

• Best heard with the diaphragm of the stethoscope.

• Best heard with firm pressure of the diaphragm during held inspiration and in leaning forward position or leaning over position (Fig. 19)

• May be localized or widespread and best heard at the lower sternal border.

• Although synchronizes with the heartbeat, it does not strictly correlate with the systole or diastole.

• It has three components–atrial systole, ventricular systole, and rapid filling phase of the ventricle (Fig. 20)

  • However, it may present as one component or two.

  • The order of the most audible component is ventricular systole > atrial systole > rapid filling phase.

  • The three-component sound in heard in less than 50% cases.

  • Usually a to-and-fro rub is heard representing the ventricular systole and atrial systole.

  • Single component is rare and heard in myocarditis, following transmural MI, resolving stage of pericarditis, and in the presence of atrial fibrillation.

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Fig. 19 Best position to auscultate for pericardial friction rub.

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Fig. 19 Best position to auscultate for pericardial friction rub.

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Fig. 20 Components of friction rub.

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Fig. 20 Components of friction rub.

Inconsistency is a striking feature of pericardial rub. It is usually transitory or evanescent, persisting for few hours or days. Its intensity, character, duration, and site of audibility also varies over a period.

Differential Diagnosis

1. Pleural rub (Table 10).

2. Systolic or to-and-fro murmur (Table 11).

3. Means–Lerman scratch in thyrotoxicosis–a to-and-fro high-pitched sound heard over the left second space

4. Hamman’s sign/mediastinal crunch–acute mediastinal emphysema, usually postopen heart surgery.

5. Sail sound in Ebsteins’s anomaly.

6. Pacemaker heart sound–twitching of the intercostal muscles or the diaphragm during artificial pacing.

7. Pleuropericardial rub: A pleuropericardial rub, resulting from friction between the inflamed pleura and parietal pericardium, can often be confused for a pericardial rub. This happens in dry pleurisy when the anterior margin of the lung is affected. The adjacent heart is involved, and the friction rub now confronts cardiac rhythm rather than the respiratory movements. This movement occurs with beating of the heart and disappears with deep respiration or cessation of breathing.

8. Movement of transvenous pacing lead or balloon floatation catheter across the tricuspid valve produces an early systolic superficial scratching sound that may be confused for a single component friction rub. These sounds usually disappear with alteration of the patient’s position

9. Inadvertent entry of air into the RV cavity and its movement with RV systole and diastole produces a slushing or crunching sound (mill wheel murmur) which mimics pericardial rub.

10. Swallowing sounds produced by vibration of vocal cords during swallowing.

Clinical Significance31 32 33 34 35

1. Acute MI–a pericardial rub after acute MI suggests a transmural infarction and a contraindication to anticoagulation. It is responsible for persistent pain after MI and a reason for pyrexia after acute MI. Prompt relief is seen with steroids.

2. Rheumatic carditis–suggests pan carditis and response with steroids.

3. Postheart surgery–suggests pericardiotomy pericarditis.

4. Chronic renal failure- intensification of dialysis

5. Infective endocarditis–myocardial abscess/ring abscess.

6. Liver abscess–extension into the pericardium.

7. Malignancy–pericardial involvement.

8. Patients in shock heart failure–look for cardiac tamponade.

9. Fever with septic foci–pyogenic pericarditis.

10. Fever of unknown origin–tuberculosis.

Hamman’s crunch36 37–Multiple crunchy sounds heard when the heart beats against the air-filled tissues. These precordial crackles correlate with the heartbeat and not respiration.

They are seen in the following:

Pneumopericardium–postcardiac surgery, postresuscitation, or postpericardiocentesis

Pneumomediastinum–spontaneous mediastinum emphysema or Boerhaave syndrome.

Characteristics Features

• A metallic click before the carotid pulse (occurs in diastole after S2) is an auscultatory sign of mitral valve replacement, and a click just after the carotid pulse (occurs in systole, after S1) is heard in aortic valve replacement (Fig. 21).

• A mitral prosthetic sound is heard louder in the mitral area and an aortic prosthetic sound over the aortic area.

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Fig. 21 Mitral and aortic prosthetic sounds.

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Fig. 21 Mitral and aortic prosthetic sounds.

Classical click–Loud, high-frequency metallic closing sounds are typically heard with tilting disc and bileaflet valves. They can be heard even without a stethoscope. A soft opening sound may also be heard.

Ball and caged valves (Star–Edwards)–They have easily audible opening and closing sounds. These sounds are distinct, high-pitched prominent sounds (relatively low-pitched compared with disk and leaflet valves) which can be easily distinguished from normal heart sounds. Both the opening and closing sounds are of equal intensity. The sounds can be very loud, depending on the prosthetic model and composition of the ball. The sounds correspond to the maximal excursion of the ball and its subsequent seating.

Classical clicks are not heard with tissue valves; instead, low-pitched sounds different from the normal heart sounds are heard

Auscultatory features: Auscultatory features38 39 40 of different prosthetic valve in mitral and aortic position are mentioned in Table 12.

Table 12

Auscultatory features of different prosthetic valves

Type and design of valve	Mitral area	Aortic area
Abbreviations: AC, aortic closing; AO, aortic opening; MC, mitral closing; MO, mitral opening.
Ball valves (e.g., Starr–Edwards)	Opening sound (MO) heard in diastole MO louder than closing sound (MC) A2–MO interval 70–110 milliseconds	Opening sound (AO) heard in systole AO louder than closing sound (AC) S1–AO is 70 milliseconds
Tilting disc valves (e.g., Medtronic–Hall)	MO is soft and may not be audible. A2–MO 50–90 milliseconds	AO is soft and may not be audible S1–AO is 40 milliseconds AC is louder than AO
Bileaflet valves (e.g., St. Jude)	–	Loud AO and AC
Bioprosthetic valves	MC louder than MO MO audible in 50% A2–MO interval 100 milliseconds	AC louder than AO AO may be absent S1–AO interval 30–80 milliseconds

Note: TTK Chitra41 is a low-cost, high-quality single leaflet tilting disc. In contrast to other disk valves, valve closing sounds are soft and dull due to the use of ultrahigh-molecular weight polyethylene disc; hence, less disturbing in a lean person

Of the commonly used mechanical valves, the sounds associated with Duromedics Edwards (33.5 dB) and Björk–Shiley Monostrut valves (31 dB) are significantly louder than St Jude Medical (24 dB) and Carbomedics (25 dB) valves.42 43

Clinical Significance

Muffled or absent normal prosthetic sound is a clue to valve failure or thrombosis.

Diminished or Absent Closing Sound is a Sign of Malfunction

Ball variance is a term used to describe the physical changes in a ball valve, which results in changes in the intensity of the opening and closing sounds. It is related to specific model of the ball valve, which is rarely in use nowadays.