Heart murmurs Flashcards
1
Q
Define murmur
A
Sound made by turbulent blood flow - usually through a valve but not always
2
Q
LO: Explain the anatomy/ physiology of the heart and the mechanisms that can cause murmurs:
What are the components of a heart valve?
A
- A - posterior leaflet of bicuspid (mitral) valve
- B- chordinae tendinae
- C- anterior papillary muscle
- D - left ventricle inflow portion
Ring around valve = annulus
3
Q
LO: Explain the anatomy/ physiology of the heart and the mechanisms that can cause murmurs:
What could cause a heart murmur?
A
- Valve leaflet problems:
- infective endocarditis
- rheumatic fever
- calcified valve
- bicuspid aortic valve
- mitral valve prolapse
- Valve annulus or aortic root problems:
- connective tissue disease e.g. Marfan’s, syphilis
- Chordae/papillary muscle problems:
- inferior myocardial infarct resulting in rupture and acute Mitral regurgitation
4
Q
Examination of a murmur
A
- Peripherally –> infective endocarditis signs (splinter haemorrhages, janeway lesions, osler’s nodes), heart failure signs (peripherl oedema, pulmonary oedema, hypertrophied heart - heaves)
- Ausculation: listen at all 4 regions
- whilst listening palpate the carotid pulse
- use bell and diaphragm to listen for mitral valve –> bell for low pitched murmurs
- listen for radiation to the axilla (MR) and carotid (AS)
- accentuating manouevres –> louder on inspiration (RIGHT murmur), on expiration (LEFT).
- palpation:
- thrills = palpable murmur, fingetips in 2nd i/c spaces
- Heave = hypertrophied heart, contraction felt extra strong
- apex beat displacement = heart muscle has moved within the chest i.e DILATION.
5
Q
What is Levine’s heart sound scale?
A
- 1 - lowest intensity, difficult to hear even by experts
- 2- low intensity usually audible to all listeners
- 3- medium intensity easy to hear even by inexperienced listeners, but without palpable thrill
- 4- medium intensity with palpable thrill
- 5- loud intensity with a palpable thrill. Audible with even edge of diaphragm
- 6- loudest intensity with palpable thrill. Audible even with stethoscope raised above the chest.
6
Q
How should you describe a murmur?
Zero to finals mnemonic SCRIPT
A
- Zero to finals pnemonic - SCRIPT
- Site - where is the murmur loudest (could add on expiration/ inspiration too)
- Character - soft, blowing, crescendo (getting louder) or decrecendo (getting quieter) or crescendo-decrescendo (describes change in intensity throughout the cardiac cycle)
- Radiation - to the axilla as in mitral regurgitation or to the carotids as in aortic stenosis
- Intensity - grading - 1 barely audible to 6 heard without steth
- Pitch - high pitch indicates high velocity, low pitch indicates low velocity. higher pitched if higher pressure gradient e.g. aortic stenosis higher pitch as greater pressure diff between LV and aorta, vs mitral stenosis low pitch lower pressure between LA and LV.
-
Timing - systolic, diastolic, pan systolic (entirety of systole, cannot distinguish s1 and s1). Systole occurs between S1 and S2 heart sounds. Diastole occurs between S2 and S1.
- in timing could include duration –> early, midsystolic (e.g. systolic ejection murmur, will be able to hear both S1 and S2 clearly), late or holo/Pan - e.g. lasting entirety of systole = pansystolic murmur (hard to distinguish S1 and S2 from each other).
7
Q
What is aortic stenosis?
Key features in a history?
A
Aortic stenosis = obstruction of blood flow across the aortic valve due to aortic calcification and narrowing. Progressive disease, presents after a long subclinical period (20 years).
- Key symptoms = decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure
- HF sx –> paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, SOB, syncope on exertion
8
Q
What is the pathophysiology of aortic stenosis?
A
- Active process of inflammation after endocardial injury
- Valvular endocardium is damaged is damaged as a result of abnormal blood flow across the valve
- initiates inflammatory process - leads to deposition of calcium on the valve
- calcificaition is slow and subclinical until disease is advanced
- progressive calcium deposition limits aortic leaflet mobility, produces stenosis
9
Q
What is the normal aortic valve anatomy?
A
- Normal aortic valve anatomy:
- aortic (and pulmonary) valves are semilunar - each with 3 cusps that meet in the midline
- the sinuses are behind each cusp = pocket like spaces that fill with blood and close the valve during ventricular diastole
- the coronary arteries also fill during diastole, - left CA arises of the left posterior aortic sinus and the anterior aortic sinus gives rise to the right coronary artery
10
Q
What are the causes /aetiology of aortic stenosis?
A
- Normal tricuspid valves in 80% of cases –> calcification leads to aortic sclerosis (thickening but no flow limitation)
- Congential Unicuspid and bicuspid valves (20%) –> experience abnormal shear and mechanical stress from birth –> stenosis earlier than tricuspid valves
- Rheumatic disease –> autoimmune inflammatory reaction triggered by streptococcus infection
- CKD - abnormal calcium homeostasis
11
Q
Complications of aortic stenosis?
A
- Long standing pressure overload leads to left ventricular hypertrophy
- results in relative ischaemia of left ventricular myocardium, consequent angina, arrhythmias and left ventricular failure.
- cardiac output can hardly increase during exercise –> exercise induced symptoms
- blood pressure falls, coronary ischaemia worsens, myocardium fails and arrhythmias develop –> can lead to heart failure
- Backup of blood in the LV leads to increased LV diastolic pressure –> lead to pulmonary hypertension and pulmonary oedema
12
Q
Key features in the history for aortic stenosis?
A
- Exertion breathlessness
- angina
- syncope
13
Q
What are the key examination features of aortic stenosis?
A
-
Examination: Palpation
- Heaving apex beat (LV hypertrophy)
-
Examination: Pulse:
- carotid arterial pulse –> delayed and plateaued peak, decreased amplitude, gradual downslope
- in elderly with rigid carotid vessels this sign may not be present
- pulsus alternans (alternating strong and weak pulse) may be due to left ventricular systolic dysfunction
- slow rising pulse –> due to the stenosis pulse rises slow
- narrow pulse pressure –> systolic hypertension to allow blood across aortic valve
-
Examination: BP:
- systolic hypertension (to compensate and push blood across aortic valve)
-
Murmur itself:
- ejection systolic murmur in aortic region
- loudest in expiration (Left sided murmurs loudest on expiration)
- radiation to the carotids
14
Q
What investigations would be appropriate in suspected aortic stenosis?
A
- Bedside:
- ECG –> detect LVH, depressed ST segment and T wave inversion in leads orientated to LV, leads 1, aVL, V5 and V6
- may find arrhythmias
- Bloods:
- U&E’s
- cardiac biomarkers
- CBC
- consider ABG if hypoxaemic
- Imaging:
- CXR –> may have post stenotic dilatation of ascending aorta, valve may show as calcified
- increased cardiothoracic ratio if HF occured
- Multimodal imaging: for preoperative planning and postoperative detection of complications
- Doppler echocardiography –> diagnose and determine severity of aortic stenosis
- see thickened, calcified and immobile aortic cusps, LVH
- cardiac catheterisation if unsure –> measure the LVEDP and LVSP to calculate EF
- exclude CA with coronary angiography
- Doppler echocardiography –> diagnose and determine severity of aortic stenosis
15
Q
Management of aortic stenosis?
A
- Surgical: All symptomatic patients should have aortic valve replacement, asymptomatic patients for regular review
- Balloon valvuloplasty –> dilate valve with balloon only in childhood or adolescence for tempporary relief
- valve replacement –> if EF< 50%, low/intermediate risk
- adjunct: anticoagulants, abx prophylaxis vs risk of endocarditis
- if stables, transthoracic USS every 3-5 years if mild stenosis
- 1-2 years if moderate
16
Q
Prognosis of aortic stenosis?
A
- Replacements are at risk of dissection
- 2-3 year survival from onset of sx without surgery
- 8-34% symptomatic patients die suddenly
17
Q
Define pulmonary stenosis
A
- obstruction of blood flow from the right ventricle to the distal pulmonary vasculature due to pathological narrowing
- 90% of cases due to valve stenosis but can occur below the level of the valve (subvalvular), in the pulmonary arteries or supravalvular
18
Q
What are the causes of pulmonary stenosis?
A
- majority are congenital –> malformation of the bulbus cordis, fetal endocarditis, Noonan syndrome, congenital rubella syndrome, tetraology of fallot
- acquired is rare –> endocarditis, carcinoid syndrome, myocardial tumours or external compression
19
Q
What is the pathophysiology of pulmonary stenosis?
A
- if not severe and congenital hyperplasia of cardiac tissue compensates
- In adults, hypertrophy occurs
- obstruction to RV empyting results in RV hypertrophy, leads to RA hypertrophy
20
Q
What are the key features in the history for pulmonary stenosis?
A
- severe pulmonary obstruction - incompatible with life
- lesser degrees of obstruction –> fatigue, syncope, symptoms of R sided HF:
- dysponea/SOB
- orthopnea
- paroxysmal nocturnal dysponea
- ankle/leg/ abdo swelling
- couging and wheezing
- dizziness
- fatigue
- difficulty exercising/ ADL’s
21
Q
Key features in examination - pulmonary stenosis
A
- Signs of R sided HF: lung crackles (pulmonary oedema), peripheral oedema, ascites, raised JVP, hepatomegaly, cyanosis (if severe)
- Murmur itself:
- harsh mid systolic ejection murmur -may have an ejection click
- best heard on inspiration (R sided murmur)
- left of sternum in 2nd IC space
- often feel a thrill
- pulmonary closure sound delayed and soft
22
Q
Investigations for pulmonary stenosis?
A
- Bedside -
- ECG - RA and RV hypertrophy, can be normal
- pulse oximetry - cyanosis
- ABG - cyanosis and resp f
- Bloods - U&E’s, FBC - Hb and HCT for cyanosis, long term hypoxaemia leads to increased RBC production, inflammatory markers (CRP), blood cultures
- imaging - CXR - can be normal can show prominent pulmonary artery owing to post stenotic dilatation, R A/V enlargement or cardiomegaly, decreased pulmonary vascularity
- Doppler echocardiogram - confirms diagnosis, visualise pulmonary vavle and stenosis, classifies severity by measuring transvalvular gradient
23
Q
Management of pulmonary stenosis?
A
- Mild disease - observation, cardiology follow up into adulthood
- moderate disease -
- surgical - percutaneous balloon pulmonary valvuloplasty or surgical valvuloplasty (cutting of contricted valve)
- adjunct - endocarditis prophylaxis with ABX
- severe/critical disease
- first line percutaneous ballon pulmonary valvuloplasty, second line surgical valvuloplasty plus ABX endocarditis prophylaxis PLUS o2
24
Q
What is a flow murmur/ innocent murmur?
A
- Rapid flow of blood during ejection causes turbulence especially at pulmonary or aortic outlet –> not a valvular or cardiac issue
- occurs in hyperdynamic states such as:
- anaemia
- thyrotoxicosis
- fever
- pregnancy
25
Q
Describe a flow murmur
A
- murmur is early systolic, short duration, pulmonary area and increased with inspiration or aortic aread and increase with expiration
26
Q
Define atrial septal defect
what types are there?
A
- congenital failure of formation of the atrial septum ergo allowing left- right shunting of blood in the atria
- NOTE: Patent foramen ovale is NOT ASD
-
Included:
- ostium secundum
- ostium primum
- sinus venosus defect
- coronary sinus defect
27
Q
Refresh: cardiac embryology - how does heart form, what areas does the heart tube dilate into/ what do they then form?
A
- Heart forms from cardiogenic cell clusters, that cluster together to form two heart tubes, these fuse with lateral folding of the embryo forming a single heart tube
- Heart tube dilates into several different regions - Truncus arteriosus (will form aorta and pulmonary artery), bulbus cordis (will form outflow tracts of ventricles), ventricles, atria, and sinus venosus (inflow tract of R atria, with Inferior and superior vena cava).
- The heart then becomes split into r and l sides, with first atrial septal formation, formation of endocardial cushion in interventricular area, and finally growing out of muscular septum/endocardial cushion and spiral septum in truncus arteriosus to form ventricular septum.
28
Q
How do the atria become split into R and L sides?
A
- Septum primum grows off the roof of the common atria towards the endocardial cushion in the AV canal
- Septum primum grows down to meet it, the foramen inbetween the endocardial cushion and septum primum - foramen primum
- septum primum contacts endocardial cushion closing foramen primum
- holes form higher in septum primum to form foramen secundum
- to the right of septum primum, a 2nd septum develops called septum secundum
- grows over foramen secundum and towards endocardial cushion but doesnt fully contact it, hole that remains = foramen ovale
- septum secundum = rigid and tough, septum primum = floppy and acts like a valve
- in the embryo, R sided pressure is greater than L due to fluid filled lungs, allowing blood to bypass the lungs and creating R-L shunt
- allows oxygenated blood from placent to enter systemic circulation
29
Q
What is an ostium secundum?
A
- foramen secundum or ostium secundum = hole in septum primum
- not the same as foramen ovale, which is an opening in the septum secundum
- blood is able to flow through the foramen ovale and through the foramen secundum, from RA to LA
- 70% ASD
30
Q
What is ostium primum?
A
Hole remaining in atrial development due to failure of the septum primum to contact the endocardial cushion
accounts 20% ASD
31
Q
what is a sinus venosus defect?
A
- atrial septal defect - only 10% of all ASD’s
- can occur near superior vena cava, inferior vena cava or be associated with anomalous pulmonary venous connection
32
Q
what is a coronary sinus defect?
A
interatrial communication that lies outside confines of interatrial septum and allows L to R shunt through ostium of coronary sinus
39
Q
Define mitral regurgitation?
What is the anatomy of the mitral valve?
A
- Mitral regurgitation = backflow of blood from the left ventricle to the left atrium due to mitral valve insuffiency
- mitral valve consists of anterior and posterior leaflets, a mitral annulus, anterolateral and posteromedial papillary muscles and chordae tendineae.
- any faults in any of these parts (mechanical/infectious/ traumatic/ degenerative/congenital/metabolic) can lead to mitral regurgitation.
56
Q
What is aortic regurgitation?
A
- Diastolic leakage of blood through the aortic valve into the left ventricle
- Causes:
- Disease of the valve or the aortic root
- rheumatic heart disease commonest in developing world
- congenital bicuspid valve and aortic root dilation in developed world
- root dilation –> marfan’s or ehlers danlos, secondary to syphilis, reactive arthritis/ankylosing spondylitis, aortic dissection
- valvular –> congenital, infective endocarditis, rheumatic fever and rheumatoid arthritis.
