The college, for some anachronistic reason, still has profound fondness for the physical act of human examination. The candidates are expected to be  expert at auscultating cardiac murmurs and distinguishing between them. The following past paper questions have involved heart sounds, murmurs, and cardiovascular examination findings in a broader sense:

Cardiovascular Examination Findings in CICM SAQs
  • Question 24.2 from the first paper of 2019 - clinical features of right heart failure
  • Question 16 from the first paper of 2016 - AR severity, indications for AVR, causes of systolic murmur.
  • Question 2 from the second paper of 2015 – clinical and TTE assessment of right heart failure
  • Question 14.2 from the first paper of 2013 – Aortic regurgitation vs. mitral stenosis
  • Question 26.3 from the second paper of 2011 – 4 causes of a diastolic apical murmur
  • Question 5.3 from the second paper of 2010 -  double peak arterial pulse
  • Question 5.4 from the second paper of 2010 – clinical featurs of Tetralogy of Fallot
  • Question 3.2 from the first paper of 2010 - causes of a diastolic apical murmur
  • Question 12.1 from the second paper of 2009 – causes of an irregularly irregular pulse
  • Question 24.2 from the first paper of 2009 – features of pulmonary hypertension
  • Question 24.6 from the first paper of 2009- causes of a diastolic apical murmur
  • Question 7.1 from the second paper of 2008 – signs of ASD, VSD and PDA
  • Question 13.1 from the first paper of 2008 – features of severe aortic stenosis
  • Question 27 from the first paper of 2008 – causes of a pan-systolic murmur

In order to improve this situation, I wanted a one-page summary of all the possible clinical signs that one may be asked about the significance of.
And here it is.

Respiratory variation

Timing in cardiac cycle

Characteristic features

Murmur

Causes of this valve pathology

Louder on inspiration

Systolic

Large pulsatile liver;
Huge cannon C waves in the CVC trace.

Tricuspid regurgitation

  • Rheumatic heart disease
  • Infective endocarditis
  • RV papillary muscle infarction
  • Trauma (steering wheel injury)
  • Ebstein’s anomaly

Split of P2 varies with respiration;
Opening click
Not radiating to carotids
S4 may be present

Pulmonic stenosis

  • Congenital
  • Carcinoid syndrome

Fixed split P2

Atrial septal defect

  • Congenital
  • Myocardial infarction

Diastolic

Left sternal edge
Presystolic pulsation of the liver

Tricuspid stenosis

  • Rheumatic heart disease

Signs of pulmonary hypertension

Pulmonic regurgitation

  • Pulmonary hypertension
  • Infective endocarditis
  • Congenital absence of the pulmonary valve.

Louder on expiration

Systolic

Louder with Valsalva

 

S4 is present
Loudest at left sternal edge
No click
Quieter with isometric hand grip

HOCM

  • autosomal dominant (sarcomeric heavy chain or troponin gene mutation)
  • Friedreich's ataxia

No S4
Loudest at apex
Systolic click
Louder with isometric hand grip

Mitral prolapse

  • Papillary muscle failure due to ischaemia
  • Myxomatous degeneration
  • Marfans syndome

Quieter with Valsalva

 

Radiates to carotids
Ejection systolic
Plateau pulse

Quieter with isometric hand grip

Aortic stenosis

  • Degenerative calcification
  • Congenital bicuspid valve
  • Rheumatic heart disease

Loud S3
Soft or absent S1
Maximal at apex
Radiates to axilla
Pan-systolic

Louder with isometric hand grip

Mitral regurgitation

  • Mitral valve prolapse
  • Age-associated
  • Rheumatic heart disease
  • Infective endocarditis
  • Papillary muscle failure due to ischaemia
  • Dilated cardiomyopathy
  • Marfan's syndrome
  • Rheumatoid arthritis,
  • Ankylosing spondylitis;

Diastolic

Quiet S1
No opening snap
Collapsing pulse

3rd, 4th left intercosdtal space

Aortic regurgitation

  • Rheumatic heart disease
  • bicuspid valve
  • seronegative arthropathy, eg. ankylosing spondylitis;
  • Marfan's syndrome
  • Aortitis (e.g. syphilis, rheumatoid arthritis,
  • dissecting aneurysm.
  • infective endocarditis

Loudest at apex

Austin Flint  murmur

Loud S1
Opening snap
Best heard with the bell  in the left lateral position
Loudest at the apex

Mitral stenosis

  • Rheumatic heart disease
  • Congenital parachute valve

Rules of thumb:

  • Right sided murmurs become louder on INspiration
  • Left sided murmurs become louder on EXpiration
  • The only murmurs louder with Valsalva are HOCM and mitral prolapse

The timing of murmurs within the cardiac cycle

This is my attempt to graphically represent the timing of murmurs.

a graphical representation of cardiac murmurs

Murmurs which are best heard with the bell of the stethoscope

Generally speaking, low pitched sounds are meant to be auscultated with the bell.

  • Mitral stenosis
  • third heart sound

Murmurs which are louder on inspiration (increased preload)

Right-sided murmurs are usually louder with inspiration; left sided murmurs are usually softer (this is one way of distinguishing between them)

  • Tricuspid regurgitation
  • Tricuspid stenosis
  • Pulmonic regurgitation
  • Pulmonic stenosis

Murmurs which are louder on expiration (decreased preload)

Left sided murmurs are usually louder with expiration. Right-sided ones are quieter.

  • Aortic regurgitation
  • Aortic stenosis
  • Mitral regurgitation
  • Mitral stenosis

Murmurs which are louder on leaning forward with deep expiration

This manoeuvre brings the left side of the heart closer to the chest.

  • Aortic regurgitation and stenosis are heard best in this position
  • Pericardial friction rub is also most audible in this way

Murmurs which are louder with the Valsalva manoeuvre (decreased preload)

One could write an entire monograph on the four phases of the Valsalva manoeuvre. Let us limit ourselves to discussing what happens in Phase 2 (during "straining") with decreased preload the prevalent condition.

  • The systolic murmur of hypertrophic cardiomyopathy (HOCM) becomes louder
  • Mitral prolapse murmurs get louder
  • All other murmurs become quieter because less blood is available in the heart

Murmurs which are quieter with squatting (increased preload)

Suddenly squatting from a standing position increased preload and afterload; the increased blood in the chambers increases the loudness of all murmurs, except...

  • The systolic murmur of hypertrophic cardiomyopathy (HOCM) becomes quieter
  • All other murmurs become louder because more blood is available in the heart

Murmurs which are louder with the isometric hand grip (increased afterload)

  • All murmurs become louder EXCEPT aortic stenosis and HOCM

Distinguishing pansystolic murmurs

Which pan-systolic murmur is it? It could be mitral regurgitation, tricuspid regurgitation, a VSD or an aortopulmonary shunt of some sort.
 
Inspiration and expiration

  • Mitral regurgitation and VSD will be louder on expiration;
    • however MR is best heard at the apex and in the left lateral position, whereas the VSD is loudest along the sternal border
  • Tricuspid regurgitation will be louder on inspiration.
  • The aortopulmonary shunt, though most audible in systole, is in fact a continuous murmur (it just so happens that the diastolic component is quiet).

Distinguishing midsystolic crescendo-decrescendo murmurs

Which ejection systolic murmur is it? It could be aortic stenosis, pulmonic stenosis, ASD or the LVOT obstruction of HOCM.

First: is it right-sided or left-sided?
Inspiration and expiration

  • Pulmonic stenosis and ASD will both be louder with inspiration
  • Aortic stenosis and the LVOT murmur of HOCM will be louder with expiration.

Louder with inspiration: must be either pulmonic stenosis or ASD, but which is it?
The atrial septal defect creates an ejection systolic murmur by causing greater flow across the pulmonic valve.  To differentiate between them, one needs to examine the S2 split in inspiration and expiration.

S2 splitting with inspiration and expiration

  • Pulmonic stenosis and ASD will both cause a widely split P2.
  • In pulmonic stenosis, the P2 split is greater with inspiration.
  • In ASD with P2 split is fixed: i.e. inspiration and expiration will not alter the timing of the P2 split (because the pressure equalises between the atria via the ASD)

Louder with expiration: must be either AS or HOCM, but which is it?
Valsalva manoeuvre to distinguish between AS and HOCM

  • AS is quieter with Valsalva
  • HOCM LVOT obstruction is usually the only other murmur which is LOUDER with Valsalva

Radiation into the neck

  • Aortic stenosis is usually the only one that radiates to the carotids.

Distinguishing end-systolic murmurs

These are basically murmurs of the faulty mitral valve, regurgitating into the left atrium during systole. Typically, mitral prolapse is a murmure of late systole, which ends with the second heart sounds. But lets say you suck at timing murmurs. How do you tell a mitral prolapse murmur from an aortic stenosis or any other mid-systolic murmur?

Well.

  • Mitral prolapse starts with a mid-systolic click. Nothing else can click like that.
  • Mitral prolapse, like HOCM, is the only other murmur which gets louder with the Valsalva manoeuvre.

How can you differentiate mitral prolapse from HOCM?

  • The hand grip manoeuvre, which increases afterload, helps tell these two apart.
    • In HOCM, the murmur gets quieter with increased afterload
    • In mitral valve prolapse, the murmur gets louder.

Distinguishing diastolic murmurs

These could be damn near anything. Diastolic murmurs are hard enough to hear, let alone time according to whether they are late middle or early.

Really, there are 4 left-sided murmurs one should be familiar with, and two right-sided murmurs.

Louder on expiration

  • Aortic regurgitation
  • Mitral stenosis
  • Austin Flint murmur of aortic regurgitation
  • Carey Coombs murmur of acute rheumatic fever

Louder on inspiration

  • Pulmonary regurgitation
  • Tricuspid stenosis

Distingusihing between the left-sided diastolic murmurs:

  • Mitral stenosis is best heard with the bell, and is low pitched
  • With mitral stenois, there is usually an opening snap shortly after S2
  • With mitral stenosis, there is usually a loud S1
  • Aortic regurgitation is best heard with the diaphragm, and is high-pitched.
  • There is no opening snap and the S1 is soft with aortic regurgitation

Distinguishing between pulmonary regurgitation and tricuspid stenosis

  • Tricuspid stenosis is freakishly rare; typicaly its a diastolic murmur heard best at the left sternal edge. .
    • Unlike pulmonic regurgitation, tricuspid stenosis causes a presystolic pulsation of the liver, which is caused by the forceful contraction of the atrium against a stenotic valve.
  • Pulmonic regurgitation is also freakishly rare; they call it the Graham Steell murmur. It is typically the result of pulmonary artery dilatation in the context of pulmonary hypertension. If there is no sign of pulmonary hypertension, you may be listening to an aortic regurgitation instead.

Clinical and echosonographic features of right heart failure

Features if the RV which can be assessed on TTE:

  • RV size: LV size on apical 4-chamber view
  • RV diameter
  • RV wall thickness
  • Tricuspid annular plane systolic excursion (TAPSE) or S-PRIME on apical 4-chamber view
  • Right ventricular systolic pressure gradient to right atrium using tricuspid regurgitation (TR) jet. Ventricular septal motion (D-shaped septum) that can indicate pressure or volume overload
  • Tissue Doppler and E/E’ ratios

Clinical features:

  • Elevated Jugular venous pressure
  • Right ventricular heave
  • Right ventricular third heart sound
  • Pleural effusion

References

Clinical Examination of the Critically Ill Patient, 3rd edition by L.I.G. Worthley - which can be ordered from our college here.

Clinical Examination: whatever edition, by Talley and O'Connor. Can be acquired any damn where.

Flint, Austin. Compendium of Percussion & Auscultation, and of the Physical Diagnosis of Diseases Affecting the Lungs and Heart. W. Wood & Company, 1870.

Chapter 27 by Sylvia Crawley of Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition