There are unique problems associated with auscultating these subtle noises in the chest of a mechanically ventilated patient. How can you hear anything in there, one might ask, what with the wind howling through the ventilator tubing, and the rhythmic doof-doof of the balloon pump? I suppose one can make one's life rather easier by turning the ventilator rate to 1 per minute, turning the PEEP down to zero, and pausing the pump for a few seconds.
Anyway. The college places an unfair amount of emphasis on physical examination. The following past paper questions have involved heart sounds, murmurs, and cardiovascular examination findings in a broader sense:
From this table, one may observe certain trends:
Without further ado, one should at least know a little about the following physical signs.
This is the sound made by the mitral and tricuspid valves closing.
It indicates the beginning of systole. It is a loud, low-pitched LUB sort of sound.
This is the result of mitral valve leaflets remaining open at the end of diastole, rather than drifting back into a closed position as diastolic flow slows down. Such a wide-open mitral valve will slam shut loudly with the onset of systole, making the first heart sound louder than usual.
Conditions which produce slow or incomplete diastolic filling will cause a loud S1.
Well, its the reverse of the loud S1, and the opposite conditions cause it to develop.
Anything that slows the diastole allows the mitral valve to be almost completely closed by the time systole begins. For example:
This is the sound made by the aortic and pulmonary valves closing.
It indicates the end of systole. It is a quiet, high-pitched DUB sort of sound.
It is composed of A2 and P2, the aortic ad the pulmonary components, which correspond with the closure of the aortic and pulmonary valves.
It is normal for this sound to be split. The high pressure in the systemic circulation slams the aortic valve shut rather abruptly, almost angrily. In contrast, low pressure of the pulmonary circulation tends to close the pulmonary valve gently, and therefore the pulmonary component of the second heart sound (P2) is usually delayed by about 20-30 milliseconds.
It is also normal for increased right ventricular filling to cause a widening of the split. The more blood in the RV, the longer it takes to eject, and therefore the greater the delay until pulmonary valve closure.
In the spontaneously breathing patient, the delay is greatest during inspiration. Naturally, in the patient ventilated with positive pressure the delay is greatest during expiration (positive pressure being a barrier to diastolic filling)
Anything that delays the end of right ventricular systole can cause this sort of picture.
In this situation, P2 occurs before A2, and splitting widens during expiration (or inspiration in the mechanically ventilated patient). This only happens if the conduction to the left ventricle is delayed, or if the left ventricle is massively volume overload (and the right ventricle is not).
The S3 is a low-pitched mid-diastolic sound. It is generated by tightening of papillary muscles in the venricles and is associated with very rapid diastolic filling. The physiological S3 typically occurs in children and young fit people.
A pathological S3 is typically associated with a decreased ventricular compliance and increased atrial pressure, which could occur in either the right side or the left.
In fact, all the additional heart sounds are vaguely related to decreased ventricular compliance.
The S4 is a sound generated by the atria, and therefore absent in atrial fibrillation. It results from the reflection of an atrial pressure wave off the walls of a stiff non-compliant ventricle. Again, it can be due to right ventricular or left ventricular pathology.
Talley and O'Connor list a series of conditions associated with decreased left ventricular compliance, which sounds very similar to the list of conditions which cause the left ventricular S3. I will regurgitate the list here, and add some extra material.
This is a high-pitched sound occurring after S1, which one would expect to hear somewhere around the aortic or pulmonary auscultation window. Essentially, it is caused by congential stenotic disease of these valves. A congentially stenosed aortic valve is not calcified, it remains elastic and mobile - it is simply too small for its purpose. Consequently, when the hypertrophied left ventricle pushes against it, the valve "domes" into the aorta, and this produces the click.
Again, this is a high-pitched sound, but it occurs at some stage in the cardiac cycle which is not associated with systeole. It could happen after S1 or after S2, doest matter where. Itsn origin is the useless flailing of a prolapse valve leaflet, or (even more rarely) the lonely wiggle of randomly misplaced tricuspid valve leaflets in Ebsteins anomaly. The leaflets, as it occasionally comes into contact with other structures, produces all sorts of random noises, and these are all characterised as a "non-systolic ejection click".
This is a weird high-pitched sound occuring after S2. It happens when the stenotic mitral valve suddenly opens after a period of isovolumetric relaxation. Typically, it is followed by the diastolic murmur of mitral stenosis.
Though perhaps then coolest of all heart sounds, the pendunculated atrial myxoma plop is rare even among the population of genuine myxoma sufferers - apparently only 10% of them have this finding. Its the sound made by the tumour when it blocks the mitral valve in diastole. The first description of this as a plop comes from a 1960s paper which presents a case history of a 42-year old housewife, who had a 7cm atrial tumour.
Constrictive pericarditis can apparently result in a situation where the filling ventricle abruptly stops filling (when it meets the resistance of the fibrotic pericardium). This abrupt cessation of filling is called the "diastolic plateau" and patients with constrictive pericarditis who dont have a diastolic knock dont seem to have this plateau.
In addition to the abovementioned, there are a whole symphony of weird sounds produced by artificial heart valves and pacemakers
These tend to be the result of a high pressure chamber draining into a low pressure chamber. For instance, the murmur of mitral regurgitation is a pan-systolic murmur. Non-standard plumbing of the greater vessels tends to also produce such sounds when one of the two vessels is inder higher pressure.
These tend to involve a ventricle ejecting blood through some sort of stenotic orifice, be it a conventional valve or some sort of catastrophically narrow outflow tract. They follow a classical crescendo-decrescendo pattern.
These are the outcome of some sort of regurgitant valve, leading backwards out of a ventricle. So by that lame definition, they are represented by only tricuspid and mitral regurgitation. Specifically, the mitral valve needs to be actually prolapsed in order to generate a late systolic murmur. Or, the papillary muscles need to be somehow damaged.
This tends to occur together with aortic stenosis.
Blood regurgitating back through the aortic valve forms a high-pitched early diastolic murmur, best heard at the 3rd and 4th intercostal spaces.
There may be an Austin Flint murmur in late diastole.
Question 16 from the first paper of 2016 asked for five clinical signs of severity, whereas Question 30.3 from the second paper of 2018 only asked for four (and gave more marks for them). UpToDate gives the following list of features associated with chronic AR:
Signs of widened pulse pressure:
Chacteristic auscultatory findings:
Indications for aortic valve replacement, as given in the 2014 AHA/ACC guidelines, are as follows:
Blood regurgitating back through the pulmonic valve forms an early diastolic murmur along the left sternal border. They also call it the Graham Steell murmur. Generally speaking, unlike TR, this murmur is not associated with a presystolic pulsation of the liver.
This tends to be associated with a loud S1 and an opening snap.
It is best heard in the left lateral position, with the bell of the sthethoscope. It is louder on expiration.
This is best heard at the left sternal edge. It is louder on inspiration.
The tumour makes various sounds, but usually one expects to hear a diastolic murmur as the blood finds its way around the mass in diastole.
Named after Dr C.F. Coombs from Bristol, it is a "short mid-diastolic rumble" associated with rheumatic mitral valve disease, and which disappears with resolving valvular disease.
This one is named after Austin Flint, whose monumental contribution one can still find scanned into the cavernous archives of Google. Its a murmur of the aortic regurgitation jet hitting the apex of the left ventricle in diastole. Flint said of the murmur,
"“Oftener rough than soft. The roughness is often peculiar. It is a blubbering sound, resembling that produced by throwing the lips or the tongue into vibration with the breath of respiration.”
This murmur can be distinguished from mitral stenosis by the absence of a loud S1 and the absence of an opening snap.
I shant repeat myself.
The persisitng connection between the pulmonary artery and the aorta is a noisy one. This is usually a constant "machinery" murmur, maximal at the first left intercostal space.
Similarly to the PDA, but of unnatural origin, this is a communication between the pulmonary circulation and the aorta.
This is oe mumrur you might not hear maximally at the praecordium! The fistula itself will be where the sound is maximal.
This a benign phenomenon.
This is freakishly rare. The sinuses of Valsalva are the anatomical dilatations of the ascending aorta, which either give rise to the coronary arteries, or (posteriorly) are "blind". If one ruptures, it is bad news. The sound it makes will probably be heard best aroiund the parasternal areas.
In 1960, Tabatznik Randall and Hersch proudly examined two hundred and fifty seven South African Bantu women and foudn this murmur in about 15% of them. It is though to originate from the turbulent flow around the sites of anastomosis between the internal mammary arteries and the intercostal arteries.
The following table may be found in the SAQ discussion notes , where it is used to answer Question 16 from the first paper of 2016. Specifically, that question asked for five different causes of a systolic murmur, and their "auscultatory characteristics".
|Atrial septal defect||
The following table may be found in the SAQ discussion notes , where it is used to answer Question 14.2 from the first paper of 2013.
|Feature||Aortic regurgitation||Mitral stenosis|
|Rhythm||usually sinus||usually AF|
|First heart sound||Normal S1||Loud S1|
|Second heart sound||Soft S2 (A2)||Normal S2 (M2)|
|Additional sounds||Third heart sound (S3)||Opening snap|
|Pulse quality||Collapsing pulse||Small pulse pressure|
|Where is it loudest||3rd intercostal space, parasternally||Apex|
|When is it loudest||Sitting forward, during expiration||In a left lateral position|
|Pitch, quality||Decrescendo||low-pitched, rumbing|
Signs of LV failure,
displaced apex beat
|Coexisting disease||Infective endocarditis, ankylosing spondylitis, other seronegative arthropathies, Marfans.||Pulmonary hypertension|
For whatever reason, the college frequently ask for four causes of a diastolic murmur loudest at the apex. This has come up three times:
Those causes are:
The college has also previously asked about the characteristic auscultation findings in tetralogy of Fallot (Question 5.4 from the second paper of 2010). Those findings are:
• An ejection systolic murmur: either pulmonic stenosis or RVOT obstruction
• Right ventricular heave
• A loud single second sound