Presenting signs in the CVS.

The most pathetic presentations by candidates when they give their findings is in the findings in the heart. There is little attempt to synthesize the signs found into a viable diagnosis. The candidate will present signs which cannot exist together. Please try to understand the significance of each sign and present accordingly. The candidate is debating with himself/herself what to call the sign rather than if it is really present and what it means. Most candidates have memorised that the apex beat is “tapping” in mitral stenosis. They have no idea why. The tapping apex means that as there is less blood flowing into the left ventricle because the mitral valve is tight, the ventricle requires very little effort to contract hence is felt almost like a faint tap against the chest, indicating that there is only mitral stenosis present and there is no lateral displacement of the left ventricle. If the patient also has a mitral regurgitation and you have decided to use the term “mitral valve disease” which means both stenosis and regurg are present then the apex cannot be tapping. The left ventricle is full of blood which has gushed back into it from a leaky mitral valve, the chamber is dilated and is bumping against the chest way out towards the left axilla. So if you locate the apex beat in the anterior axillary line don’t describe the apex as tapping. The examiner immediately realises that you don’t know what you are talking about. Similarly if when you observe the praecordium and see lots of movement or pulsation don’t even think of a tapping apex.

Similarly there is some confusion about a “heaving” and a “thrusting” apex beat. In the seventies it was important for a clinician to determine if the apex beat indicated a hypertrophic ventricle i.e. heaving i.e. lifting up the palpating fingers but usually displaced only a little. Thrusting indicated a dilated chamber which was thrusting against palpating fingers and was outwardly displaced. Now it is a matter of semantics as an echocardiogram can easily settle the issue. However if you choose to use these terms explain what you mean.

Why are you examining the apex beat anyway? It tells you if there is cardiomegaly if it is displaced to the left unless the mediastinum has shifted as well. It tells you if there is a dilated chamber or a hypertrophic ventricle. A double apex beat may mean that both the right and left ventricles are forming the apex beat so there is right ventricular hypertrophy and rotation of the heart to the left.

Talk about the heart sounds before you talk about murmurs or pericardial rub or any added sound like a valve click. Heart sounds are classified as high frequency or low frequency sounds. What are the high frequency? High-frequency sounds arise from closing or opening valves, so both mitral and tricuspid valve closing sounds or the first heart sounds(M1 and T1), non-ejection sounds, opening snaps, aortic and pulmonary valve closure sounds or the second heart sound (A2 and P2), and early valvular ejection sounds. Prosthetic valve sounds are also high frequency.

Low-frequency sounds include the third heart sound (S3, which may be physiologic or pathologic), associated with early ventricular filling, and the fourth heart sound (S4), associated with the atrial contribution to ventricular filling in late diastole.

The first heart sound coincides with the carotid pulse. M1 (mitral first heart sound) which occurs first is slightly earlier but this difference cannot be determined by listening with a stethoscope. M1 is the louder component and is heard all over the precordium but the T1 component is heard over the tricuspid area only. How do we determine whether the S1 is loud or soft? S1 normally is louder than the second heart sound (S2) over the apex and along the lower left sternal border; intensity is reduced if S1 is softer than S2 over these areas. S1 intensity is likely to be accentuated if S1 is much louder than S2 over the left or right second interspace. 

When do we expect a change in the intensity of the first heart sound? The following factors influence the intensity of S1 so keep them in mind:

  • A wide open valve will close loudly and a partially open valve will close softly.
  • Length of the cardiac cycle: in tachycardia the valve is wide open; in bradycardia the valve is partially closed as it has had time to float up.
  • Mobility and structural integrity of the atrioventricular (AV) valves (eg, fibrosis, commissural fusion of the leaflets, tethering of the posterior mitral leaflet, etc).
  • A short PR interval.
  • Force of ventricular systolic contraction.

So what are the common causes of a loud first heart sound? Mitral or tricuspid stenosis, left atrial myxoma, high output states like patent ductus arteriosus, ventricular septal defect, pre-excitation syndrome and tachycardia.

When is the first heart sound going to be soft? When mitral regurgitation (MR) results from fibrosis and destruction of the valve leaflets (as in patients with rheumatic valve disease), which prevent an effective M1. In contrast, MR due to perforation of the valve leaflets from bacterial endocarditis may not be associated with a reduced intensity of S1. In severe aortic regurgitation the S1 will be soft because of premature closure. In some patients with bundle branch block the first sound is soft as well as in dilated cardiomyopathy. In hemodynamically significant aortic stenosis the first sound may be soft without calcification of the mitral valve.

The intensity of the first sound may vary in atrial fibrillation, a-v dissociation, premature beats and auscultatory alternans when one beat is heard loudly and one is heard softly. This is usually associated with pulsus alternans and electrical alternans.

Wide splitting of S1 is a feature of Ebstein anomaly which is associated with right bundle branch block. The extra early systolic sound around S1 is also referred to as the “sail sound.

The Second Heart Sound consists of two components: aortic and pulmonary valve closure sounds, traditionally designated as A2 and P2, with the valve cusps vibrating for 4 ms. The onset of A2 occurs with the dicrotic notch of the aortic root pressure pulse S2 occurs after the peak of the carotid pulse and coincides with its downslope.The two components of S2 are best heard with the diaphragm of the stethoscope and over the left second interspace, close to the sternal border.

A2 is widely transmitted to the right second interspace, along the left and right sternal border, and to the cardiac apex. P2 is normally best heard and recorded over the upper left sternal border and is poorly transmitted. S2 is best heard when patients are semi-recumbent (30 to 40 degrees upright) with quiet inspiration.

Increased intensity of A2 often occurs in:

  • Systemic hypertension.
  • Coarctation of the aorta.
  • Ascending aortic aneurysm; a “tambour” quality of A2 is commonly heard.
  • When the aortic root is relatively anterior and closer to the anterior chest wall, as in tetralogy of Fallot and transposition of the great arteries.

Increased intensity of P2 often occurs in:

  • Pulmonary arterial hypertension of any etiology (most common, even with pulmonary regurgitation).
  • Idiopathic pulmonary artery dilation.
  • Atrial septal defect (ASD); P2 is increased considerably and frequently greater than A2 over the left second interspace.

Decreased intensity of A2 occurs in:

  • Conditions that affect the mobility and integrity of the aortic valve
  • Severe aortic regurgitation (AR) or stenosis
  • Hypotension

Decreased intensity of P2 occurs in:

  • Conditions that affect the mobility and integrity of the pulmonary valve.
  • Pulmonary stenosis and regurgitation.
  • Significant RV outflow obstruction associated with a soft and delayed P2. The low pulmonary artery pressures also play a role in attenuating P2.

Splitting of S2 — Under normal physiologic conditions, the A2 and P2 components of S2 vary with inspiration. A2 and P2 are usually fused during the expiratory phase of continuous respiration, but during the inspiratory phase, separation of A2 and P2 occurs; the degree of splitting varies from 0.02 to 0.06 seconds.

Wide splitting of S2 occurs in the following conditions:

  • Right bundle branch block (RBBB),
  • artificial pacing from the LV,
  • Wolff-Parkinson-White (WPW) syndrome with LV preexcitation.
  • Premature beats and an idioventricular rhythm of LV origin (QRS complex of RBBB morphology) are also associated with wide splitting.

Hemodynamic causes:

  • Pulmonary valve, infundibular, supravalvular, or pulmonary branch stenosis, and pulmonary arterial hypertension.

Wide and fixed splitting of S2 – Fixed splitting of S2 has been defined as ≤20 ms of variation in the A2-P2 interval between the inspiratory and expiratory phases of respiration. One common cause of wide and fixed splitting of S2 is a large interatrial communication (ASD, common atrium) and left-to-right or bidirectional shunt; abnormally wide splitting of S2 occurs, and respiratory variations of the A2-P2 intervals are minimal or absent.

The S2 may be single because the A2 component is absent if there is severe calcification of the aortic valve or if the aortic valve is practically destroyed in aortic regurgitation. The P2 component may be absent with congenital absence of the pulmonary valve, pulmonary atresia, or truncus arteriosus. Remember that the P2 is difficult to hear due to emphysema, obesity, or pericardial effusion.

S3 and S4 are low frequency heart sounds heard during ventricular filling. S3 and S4 are best heard with the bell of the stethoscope. First identify the S1 and S2, then auscultate along the left sternal border both in inspiration and expiration for these sounds in the lateral decubitus position.

S3 occurs as the rapid filling phase of diastole is completed It appears to be related to a sudden limitation of the movement during ventricular filling along its long axis. It is closer to the second heart sound.

S4 occurs during the atrial filling phase after the P wave on the electrocardiogram (ECG) and coincides with atrial systole and a waves of the atrial pressure pulse, and with the apical impulse.

An abnormal S3 or S4 tends to be louder and of higher pitch (sharper) and is frequently referred to as a “gallop.” S3 is the ventricular gallop, and S4 is the atrial gallop. S3 and S4 can be fused during tachycardia to produce a loud diastolic filling sound, termed a “summation gallop. Gallops can be seen and palpated.

LV gallops

Clinical significance of S3 — Although an S3 can be heard in healthy young children and adults. it is usually abnormal in patients over the age of 40 years, suggesting an enlarged ventricular chamber. An S3 gallop is an important and common early finding of HF associated with dilated cardiomyopathy and may also be heard in patients with diastolic HF (although less frequently than with systolic HF), aortic valve disease, and coronary artery disease (CAD). In such patients, an S3 gallop is usually associated with left atrial pressures exceeding 20 mmHg, increased LV end-diastolic pressures (>15 mmHg), and elevated serum brain natriuretic peptide (BNP) concentrations. An S3 is nearly always present in severe chronic mitral regurgitation.

Clinical significance of S4 — An audible S4 is generally abnormal in young adults and children. Effective atrial contraction and ventricular filling are both required for production of atrial gallop sounds. Thus, this sound is usually absent in atrial fibrillation and in significant AV valve stenosis. S4 can be heard in many healthy older adults without any other cardiac abnormality, due to decreased ventricular compliance with age. An S4 is always abnormal when it is palpable, regardless of patient age.

Pericardial knock is heard in constrictive pericarditis. it is earlier than an S3 and is best heard in inspiration.

Ejection clicks can originate both from the aorta and the pulmonary artery and often sound like a split S1. An aortic ejection click is present in aortic valve stenosis, bicuspid aortic valve, aortic regurgitation, and with aneurysm of the ascending aorta. Pulmonary ejection sounds tend to be present in clinical conditions associated with a deformed pulmonary valve and pulmonary artery dilation, including pulmonary valve stenosis, idiopathic dilation of the pulmonary artery, and chronic pulmonary arterial hypertension of any etiology.

Midsystolic click — Prolapse of the mitral valve is the most common cause for a non-ejection midsystolic click; the timing coincides with maximal prolapse of the mitral valve into the left atrium.

Opening snap — The opening snap is a high-frequency, early diastolic sound associated with mitral or tricuspid valve opening. This opening of the AV valves, which is normally silent, becomes audible in the presence of pathologic conditions. It indicates that the valve is still mobile. Commonest cause is mitral stenosis.

Tumor plop — Early diastolic sounds (tumor “plop”) are occasionally heard in atrial myxoma. These sounds appear to occur when tumors move into the ventricle and come to a sudden halt.

 You can then discuss the murmurs you have found which I am not discussing here. You must then discuss the presence or absence of heart failure.

Volume assessment — There are three major manifestations of volume overload in patients with HF: pulmonary congestion, peripheral edema, and elevated jugular venous pressure. Pulmonary congestion is manifest by rales and if severe rhonchi are audible too. In the milder form lymphatic and venous capacitance may increase in the lungs so that crepitations may not be heard. Elevated jugular venous pressure is usually present if peripheral edema is due to HF, since it is the high intracapillary pressure that is responsible for fluid movement into the interstitium. With the patient sitting at 45º jugular venous pressure can be estimated from the height above the right atrium of venous pulsations in the internal jugular vein. The height of external jugular vein pulsations may also be helpful but care must be taken to avoid spurious interpretation. Look for peripheral edema, scrotal edema, sacral edema, ascites and pleural effusion.

Please make up your mind about what diagnosis you have found. Present with confidence. Make your presentation with confidence and make sure that you have your findings right. Remember the heart sounds!!!

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I am a Professor of Medicine and a Nephrologist. Having served in the Army Medical College, Pakistan Army for 27 years I eventually became the Dean and Principal of the Bahria University Medical and Dental College Karachi from where I retired in 2016. My passion is teaching and mentoring young doctors. I am associated with the College of Physicians and Surgeons Pakistan as a Fellow and an examiner. I find that many young doctors make mistakes because they do not understand how they should answer questions; basically they do not understand why a question is being asked. My aim is to help them process the information they acquire as part of their education to answer questions, pass examinations and to best take care of patients without supervision of a consultant. Read my blog, interact and ask questions so that I can help you more.

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