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These places are where the blood is expected to go through when they pass the valve in question.
Systolic murmurs
• Aortic stenosis: narrowing of the aortic valve causing turbulent flow when blood is ejected.
Causing a systolic ejection murmur
○ Physiology of murmur:
▪ S1: this is normal, as the aortic valve has yet to open when the mitral valve shuts
▪ Shortly after the mitral valve shuts, the LV starts to contract --> this build up of
pressure will lead to an ejection click
▪ Blood will rush out of the stenosed aortic valve, it starts small and gets louder, and
then small again causing a crescendo-decrescendo murmur
○ This murmur is heard best at the aortic region
○ Can resonate into the carotid arteries, and can be heart as carotid bruits
• Pulmonic stenosis: narrowing of the pulmonary valve causing turbulent flow when blood is
ejected. Causing a systolic ejection murmur
○ Physiology
▪ As the mitral valve tries to close (and when S1 should occur), the hole in it will
allow blood to flow from LV into LA - so the murmur will start from S1
▪ Even as the LV continues to contract and aortic valve opens, LV still has higher
pressure than LA, so blood will continue to flow into LA. Note the intensity of the
murmur does not change.
▪ The backflow will occur all the way until the aortic valve closes (S2), after which
the mitral valve will open again and start a new cycle.
○ Best heard in the mitral area
○ Can radiate into the left axilla (the general direction in which the blood back flows)
• Tricuspid regurgitation: when the tricuspid valves cannot close properly, causing blood to flow
back into the RA during RV contraction. Causing a pan-systolic murmur
○ This murmur is quite similar to that of mitral regurgitation. But there are some
differences:
▪ Best heart in the tricuspid area
▪ Will not radiate into the left axilla.
• Mitral valve prolapse: when the mitral valve billows into LA as the LV contracts. Causing a mid
systolic non-ejection click.
○ Physiology
▪ The valve closes normally, and S1 is not altered.
▪ As the LV begins to contract, the mitral valve accelerates upwards into the LA, but
will be stopped by the chordae tendinae - this tensing of the chordae tendinae will
cause a click
▪ Some times, this condition occur with some mitral regurgitation as well, which will
be heard as a flat late systolic murmur after the click.
○ Heard best at the mitral area
Diastolic murmurs
• Aortic regurgitation: when blood backflows from the aorta into the LV due to incomplete
○ Physiology:
▪ Just when the aortic valve is supposed to close (S2), and before the mitral valve
opens to fill the LV, pressure in the aorta will exceed that of LV, causing a
turbulent backflow.
▪ After mitral valve opens to fill LV, pressure in LV starts to increase --> backflow will
diminish --> a decrescendo murmur in early diastole only.
○ Since the blood backflows, it is best heard along the left sternal border, not the aortic
area
• Pulmonic regurgitation: when blood backflows from the pulmonary artery into the RV due to
incomplete closing. Causing early decrescendo diastolic murmur
○ This murmur is very similar to aortic regurgitation, but will be heard in the upper left
sternum
• Mitral stenosis: narrowing of the mitral valve, causing flow from LA to LV to become turbulent.
Causing opening snap followed by mid diastole rumble
○ Physiology
▪ After aortic valve closes, the mitral valve opens. But due to stenosis, the leaflets
snap open and cause an opening snap
▪ Note that most of LV filling occurs at the beginning of diastole (due to greater
pressure difference at the start), therefore the turbulent murmur will be loudest in
early diastole, and will decrescendo as the flow decreases.
▪ In late diastole, the LA will contract to push leftover blood into LV --> flow
increases and the murmur will be louder --> pre-systolic accentuation
○ Best heard in the mitral area
• Tricuspid stenosis: narrowing of the tricuspid valve, causing flow from RA to RV to become
turbulent. Causing opening snap followed by mid diastole rumble
○ Quite similar to mitral stenosis murmur, except that it is better heard in the tricuspid
area
Effects of breathing
• Upon inspiration, the lungs expand and the intrathoracic pressure decreases:
○ More venous return to the right heart (think of blood being sucked in by vacuum - there
is decrease in central venous pressure, so the return gradient is increased) --> blood has
to flow faster --> louder right heart murmurs
▪ Note that this increased volume will make the pulmonary valve close a bit later
than it normally would
○ Breathing in will stimulate sympathetic activation, and this will cause vasoconstriction
and increase BP. The neural effect is probably larger than hydraulic effect.
○ Less blood return into left heart - as the expanded lungs compress on the blood
vessels --> softer left heart murmurs
▪ Note that the decreased volume will make the aortic valve close earlier than it
normally would
○ We would get a splitting of S2 as the aortic and pulmonary sounds become less
synchronised
• Upon expiration, the opposite to the above happens - we get louder left heart murmur and
softer right heart murmur.