Murmurs Flashcards
normal heart sounds
lub dub, lub dub
sounds of the valve closing projected on the chest wall
S1: tricuspid and mitral valve closing (AV valves)
S2: aortic and pulmonary valves closing (semilunar valves)
stages of the cardiad cycle
- late diastole: both chambers are relaxed and blood fills passively from A to V. The AV valves (M and T are open)
- Atrial systole
SA to AV node fires. Atria contraction. Forces the final amount of blood into the ventricles. - S1= AV valves M/T close (lub) to stop blood going from V (high pressure) back to A (lower pressure)
- Isovolumetric contraction
volume stays the same (same amount of blood)
but pressure increases in V.
*AV are closed
*Semilunar valves are closed (pulmonary artery and aorta still higher pressure) - Ventricular ejection
Ventricles contract and exceed the pressure of pulmonary arteries and aorta. the semilunar valves open and blood is ejected. - Isovolumetric relaxation
Ventricles relax (diasotle)
P/A is now higher than the ventricles so the semilunar valves snap shut (to prevent blood from moving from high PA to low V)
*S2 semilunar valves shut (dub) - Early diastole
Pressure in Atria now exceeds the Ventricles so the AV valves open. A is receiving blood, passive filling.
S1
S2
S3
S1: AV valves closing
S2: Semilunar valves closing
S3: blood filling from A to V in early diastole. if there is a lot of blood (HF) can bounce on the walls and cause a third heart sound. / rapid ventricular filling causes the coordinate tendinae to pull on their full length and twang (pregnancy, athletes, heart failure, LV failure
Diastole [S1] systole [S2}
definition of a murmur
turbulent blood flow
graded from 1-6
Systolic murmur
happens between S1 and S2 (S1 woooosh S2)
in systole, the M/T are closed and SL is open.
mitral / tricuspid valve cannot close (regurgitation)
aortic / pulmonary valve cannot open (stenosis)
Diastolic murmur
happens after S2 (S1, S2, wooosh, S1, S2)
M/T are open
SL are closed
mitral/tricuspid cannot open (stenosis)
aortic/pulmonary cannot close (regurgitation)
Mitral regurgitation
- systolic murmur
- ventricules are at a higher pressure than atria so M/T is shut (S1) to prevent blood flowing back to lower pressure in atria.
- if the M/T cannot close properly, the blood will continue to flow throughout systole into the atria
- heard best with bell of stethoscope over the apex, pt lying on the left lateral position
early opening snap suggests severe mitral stenosis (and a quiet S1)
= pansystolic / holosystolic murmur (i.e throughout systole)
dilated cardiomyopathy left ventricular dilation results in mitral regurgitation.
Tricuspid regurgitation
- systolic murmur
- pansystolic murmur
- can be heard 4-5th rib lower left border of the STERNUM
Aortic stenosis
*systolic murmur
the aorta/pulmonary valves cannot open (stenosis) so blood has to flow through a narrow opening from V to PA. at the beginning of systole there is a lot of blood trying to get through. this get’s quieter as blood passes and eventually the valves ‘snap’ open (ejection click)
= crescendo decrescendo murmur
- classically radiates to the carotids
- peripheral pulses are weak and delayed.
- aortic stenosis 2-3rd IC space right
- pulmonary stenosis 2-3rd IC left.
Carvello sign
tricuspid regurgitation is louder on inhalation. This is because the negative pressure (diaphragm goes down) means more blood goes back to RA so more blood is rushing into RA (tricuspid is R)
Aortic valve regurgitation
diastolic murmur
In diastole, the semilunar valves are shut because PA is higher pressure than V. blood leaks from aorta back to LV (loud, lots of blood then quietens)
= early diastolic decrescendo (high pitched blowing diastolic decrescendo murmur)
murmurs in summary
- systolic murmurs
- mitral regurgitation (pan systolic murmur)
- aortic stenosis (ejection click, crescendo decrescendo murmur) - diastolic murmur
- mitral stenosis (diastolic rumble)
- aortic regurgitation (early diastolic decrescendo)
S4 heart sound
in late diastole (atrial systole) the atrias contract and push the final amount of blood into the ventricles.
if the ventricles are very stiff, the atria has to push extra hard to push blood from A to V (e.g. in ventricular hypertrophy) this makes a fourth heart sounds
innocent murmurs (still’s murmurs)
heart walls are very thin- they vibrate when blood rushes (disappears with young age)
still’s murmur is heard over the left lower sternal border (common in young children)
mitral valve prolapse
the valves fall back into the atrium- papillary muscles and chordae tendinae are too weak to keep tethered.
mid systolic click- leaflet folds into atrium then stopped suddenly by chordae tendinae
mid systolic click followed by a late systolic murmur ?
mitral regurgitation and squatting / valsalva
If squat down- click comes later and murmur shorter. Squatting increase venous return so more LV in blood so more volume so there is more room for the leaflets and so they get forced back into the atrium a bit later
If stand/Valsalva- click comes sooner and murmur logger. Standing- less venous return- ventricle is smaller so the leaflet is forced out earlier in the contraction (why it’s longer)
Austin flint murmur
aortic regurgitation is so severe a jet blood forces the mitral valve shut which causes a rumbling mid diastolic murmur in mitral valve area with out opening snap sound
VSD
pan systolic murmur
*
RBBB
white split of second heart sound
ASD
ejection systolic murmur associated with split second heart sound over the pulmonary area (usually congenital)
Tricuspid regurgitation and heart failure
back flow of blood from RV to RA. This causes the right side of the heart to dilate and weaken. Back pressure on the IVC and poor ejection fraction
oedema, ascites, dyspnoea (HF)
murmur from chronic rheumatic fever
mitral stenosis (60%) aortic stenosis (30%)
opening snap after S2, followed by a rumbling mid-diastolic murmur.
Jones’ criteria
chronic rheumatic heart disease from previous untreated pharyngitis caused by a group A beta-haemolytic streptococcal infection.
+ evidence of previous sterptococcal infection
+ two or more of the following major Jones’ criteria
- migratory polyarthritis of large joints
- carditis
- subcutaenous nodules
- chorea
- erythma marinatum of the skin
or a diagnosis can be made with 1 from major and 2 from minor:
fever, arthralgia, elevated acute phase reactants
Patent ductus arteriousus
a continuous machine like murmur loudest at S2
pericarditis
fever, upper resp infection, pleuritic chest pain, ST elevation, PR depression on ECG
aggravated by movements / deep inspiration, non-radiating. improves when leaning forward
pericardial friction rub (scratchy, rubbing quality)
high pitched triphasic systolic and diastolic murmur
aortic stenosis and agina
angina can be a presenting feature of aortic stenosis.
angina- exertional chest pain and slow rising pulse
intra-cardiac tumour
atrial myxoma
fragments of the tumour break off and embolus into the cerebral arteries causing a TIA
murmur: atrial plop in early diastole
Infective endocarditis clinical features and murmur heard
constitutional upset- fever, night sweats, malaise, exertion dyspnoea, splinter haemorrhages and visible capillary pulsations in the nail bed (Quincke’s sign)
aortic regurgitation 2’ to infective endocarditis
coarctation of the aorta
hypertension in the upper extremities, hypotension in the lower extremities
long term hx of hypertension
painful, burning sensation in both legs
aortic lumen narrows distal to the arch vessels
CXR notching of the ribs.
bicuspid aortic valve without calcification
one of the most common congenital heart malformations in adults
early systolic ejection click
some degree of AR or AS
blowing early diastolic murmur and or systolic ejection murmur
susceptible to calcification and fibrosis
management for an MI
High Flow O2 (15L/min) Aspirin & Clopidogrel GTN Spray Morphine Beta Blocker
infective endocarditis symptoms
Splinter Haemorrhages/ Osler Nodes/ Janeway lesions
hypertrophic cardiomyopathy
hypertrophic obstructive cardiomyopathy / assymetric septal hypertrophy / idiopathic hypertrophic subaortic stenosis
inherited autosomal dominant
common cause of sudden death in young atheltes
endocarditis
streptococcus aureus is the most common cause of endocarditis (prosthetic valve replacement, IV drug use)
streptococcus viridians is more common after dental extraction.
endocarditis is an infection on a calcified aortic valve
multiple pulmonary emboli
evidence of right ventricular hypertrophy and pulmonary hypertension (loud P2)
collapse and reduced exercise capacity.
underlying cancer DVT
diagnose with CT and pulmonary angiogram
aortic stenosis
congenital bicuspid valve
rheumatic fever
slow rising pulse
narrow pulse pressure
non-displaced heaving apex bet
ejection systolic murmur that radiates to the carotids
symptoms of LV dysfunction and outflow tract obstruction
investigate:
CXR, ECG, echo, cardiac catheter studies
Mx: aortic valve replacement
if inoperable- diuretic therapy
