Heart Sounds And Murmurs

Front 1

Back 1

a wave - transient venous distention due to RA contracting in late diastole

c wave - not seen - TV closes and buldges into RA as RV contracts

x descent = pressure decline following RA contraction

v wave = passive filling of RA from systemic veins during ventricular systole

y descent = loss of pressure as TV opens and rapidly fills RV

Front 2

constrictive pericarditis would affect what part of the JVP tracing?

Back 2

prominent y - represents descent of pressure in RA as TV opens and fills the RV

Front 3

tricuspid regurg would affect what part of the JVP tracing?

Back 3

prominent v = represents the passive filling of RA by the systemic veins while the TV is closed during ventricular systole -- think increased volume in RA

Front 4

Affect of RVH on JVP tracing?

Back 4

prominent a wave = contraction of RA in late ventricular diastole = transient venous distention

Front 5

Affectof tricuspid stenosis on JVP tracing

Back 5

prominent a wave = contraction of RA in late ventricular diastole = transient venous distention

Front 6

aortic valve shuts before the pulmonic valve because...

Back 6

difference in LVP and aortic pressure is greater than that between RVP and pulmonic pressure (remember, lungs are a low resistance system)

Front 7

location of aortic area - ascultation

Back 7

2-3rd rt intercostal space

Front 8

location of pulmonic area - ascultation

Back 8

2-3rd left IC space

Front 9

location of tricuspid area - asculation

Back 9

left lower sternal border

Front 10

location mitral area - ascultation

Back 10

apex

Front 11

factors that accentuate S1

Back 11

1. distance separating th eleaflets of the open valves at the onset of ventricular contraction

ex: shorter PR interval (ventircular filling following atrial contraction) = longer shutting distance for valves at onset of ventricular contraction = accentuated S1

ex: tachycardia (exercise, anemia, high CO output states) = accentuated S1

ex: lenthened PR interval = first degree AV nodal block = delayed onset of ventricular contraction= leaflets have smaller shutting distance = diminished S1

2. leaflet mobility

ex: increased mobility = widened shutting distance = louder S1

ex: mitral regurg = leaflets don't close all the way = diminished S1

ex: severe mitral stenosis = leaflets don't really move = diminished S1

3. rate in rise of Ventricular pressure

ex: LVH = leaflets drift together more rapidly = shorter distance to shut = diminished S1

Front 12

physiological splitting of S2 occurs during ____

Back 12

inspiration →chest expands → intrathoracic pressure becomes more negative → transient increase in capacitance of intrathoracic pulmonary veins so pulmonary arteries take longer to gain enough back pressure to closs the PV = P2 delay

Front 13

Causes of an accentuated S2

Back 13

pulmonary or systemic HTN causing diastolic pressure in the pulm vein/aorta to increase

Front 14

Aortic or pulmonary stenosis cause S2 to be (accentuated/diminshed)

Back 14

diminished - less movement due to stenosis so valve closure is less audible

Front 15

Widened Splitting of S2 (def and causes)

Back 15

interval between A2 and P2 are increased and audible upon expiration as well (think more delay in P2)

causes = pulmonary valve stenosis & RBBB

Front 16

Fixed Splitting of S2 (def and causes )

Back 16

widened interval that persists through respiration

cause = atrial septal defect (chronic right sided volume overload → increased capacitance of the right heart → delay in PV closure)

Front 17

Paradoxical splitting of S2 = revesed split (def and causes)

Back 17

heard in expiration and NOT inspiration (since P2 is delayed w/inspiratoin - so sounds are superimposed) = delay in Aortic Valve closure

causes = LBBB (delay in LV contraction) & Aortic stenosis (delay in LV ejection)

Front 18

Ejection clicks are heard shortly after _______ and conicide with the opening of the __________. Best heard at with the DP of the steth placed over the _______ areas. Causes are?

Back 18

S1 (early systole)

aortic or pulmonic valves

aortic or pulmonary areas (2-3rd IC space)

Causes = aortic or pulmonic valve stenosis (leaflets reach max opening just proir to ejection and slam shut - like a rubber band); dilation of the pulmonary artery or aorta (sudent tensing of root with onset of blood flow into vessel)

Front 19

Mid or Late systolic ejection clicks area result of _________

Back 19

Mitral or tricuspid valve prolapse

loudest over mitral or tricupsid areas

Front 20

extra sounds heard in diastole (list them)

Back 20

opening snap
S3
S4
pericardial knock

Front 21

Opening Snap (def and causes)

Back 21

sound heard when MV or TV opens (silent in the normal heart) due to M-stenosis or T-stenosis

heard between mitral and tricuspid areas just after A2 (when LVP just falls below LAP)

mitral stenosis more common than tricuspid stenosis

inspiratoin = physiological split + OS = 3 sounds

expiration = just OS = 2 sounds

milld stenosis = A2-OS = wide
severe = narrow

Front 22

S3 (def and causes)

Back 22

occurs in early diastole following opening of AV valves during ventricular rapid filling phase = tensing of chordae tendieae during rapid filling and expansion of the ventricle

low pitch sound
left sided = best heard at apex in left decubuitous position
right side = best heard at left lower sternal border

normal finding in children and young audlts → signifies a supple ventricule capble of normal rapid expansion in early diastole

indicative of volume overload in middle/older adults or increased transvavlular flow

causes = CHF and advanced mitral or tricuspid regurg

Ventricular gallop

Front 23

S4 (def and causes)

Back 23

occurs in late diastole and corresponds with atrial contraction → due to LA contracting against stiffented LV

caused by decreased ventricular compliance due to LVH or myocardial ischemia

atrial gallop

low pitch
best heard at apex in left lateral decubitous position

Front 24

pericardial knock (def and causes)

Back 24

due to abrupt cessation of ventricular filling in diastole

hallmark of constrictive pericarditis

Front 25

Mechanisms causing murmur

Back 25

1. flow across a partial obstruction

2. increased flow through normal structures

3. ejection into a dilated chamber

4. regurgitant flow across an incompetent valve

5. abnormal shunting of blood form one chamber to a lower pressure chamber

Front 26

Systolic Ejection murmur (def and causes)

Back 26

begins after S1 (isovolumetric contraction = both MV, TV and AV, PV valves are closed here) and terminates before (AV stenosis) or during S2 (pulmonary valve stenosis)

cresc (sig of ventricular constraction)/desc (sig of ventricular relaxation)

may be preceded by ejection click (mild aortic stenosis)

increased severity of stenosis = longer to eject blood across valve = later the murmur peaks in systole

Causes = aortic or pulmonic stenosis

Front 27

Aortic stenosis causes what type of murmurs and how can you tell the difference in degree of stenosis

Back 27

Systolic Ejection Murmur
radiates toward the neck
wide distribution, including apex

mild:
- ejection click
- early peaking cres/desc
- normal A2

moderate:
- peak of murmur in systole more delayed
- intensity of A2 lessens due to increasing leaflet rigidity
- prolonged ejection time so A2 merges with or occurs after P2
- may not have ejection click

severe:
- pakes late in systole
- A2 usually absent due to rigidity of leaflets
- no A-P splitting at all (no A2)

Front 28

unlike systolic ejection murmers seen with aortic stenosis, pulmonary stenosis ____________

Back 28

may extend beyond A2 if severe due to prolonged RV ejection time

only sometimes radiates toward neck or left shoulder
heart at 2-3rd left IC space

Front 29

Pansystolic/holosystolic murmurs (def and cuases)

Back 29

caused by regurgitatoin o fthe blood across an incompentant MV or TV or ventricular septal defect

uniform intensity throughout systole
turbulence heard as soon as ventricular pressure exceeds atrial pressure = righ after S1 so no gap (as with systolic ejection murmurs)

causes = mitral regurg, tricuspid valve regurg, ventricular septal defect

high pitched
blowing quality
increased intensity with inspirtation due to increase venous return to heart and increase regug flow (not true for VSD)

Front 30

Mitral Regurgitation Murmur

Back 30

Pansystolic/holosystolic murmur

blowing quality
high pitched
radiates toward left axilla
best heard at apex
intensity does not change with inspiration

Front 31

Tricuspid Valve Regurgitation murmur

Back 31

pansystolic/holosystolic murmur

bester heard along lower left sternal border

high pithced, blowing quality

intenstiy increases with inspiration due to increase venous return to the heart and increase right SV

Front 32

Ventricular Septal Defect Murmur

Back 32

pansystolic/holosystolic murmur

heard best and 4-6th IC space
may have assoc palpable thrill
intensity does not change with inspiration and murmur does not radiate to the axilla
smaller VSD = louder murmurs

Front 33

Late Systolic Murmur

Back 33

think mitral valve prolapse

usually preceeded with midsystolic click

begins in mid to late systole and ocntinues to the end of systole

Front 34

Early Diastolic Murmur

Back 34

regurgitant flow through the AV or PV

desc murmur - LVP<Aortic Pressure so maximum intensity at onset - intensity diminishes with lessened pressure gradient

AV = more common in adults

causes = AV regurg, PV regurg

Front 35

Aortic Regurg murmur

Back 35

Early diastolic murmur
desc
begins at A2
terminates before next S2
high pitched
best heard at left sternal border with pt sitting, leaning forward and exhaling

Front 36

PV regurg murmur

Back 36

early diastolic murmur
desc
due to presence of Pulm arterial htn
best heard at pulonic area
intensity may increase upon respiration
high pitched

Front 37

Mid to late diastolic murmurs

Back 37

due to turbulent flow across a steonitc MV or TV or less commonly from abnormally increased flow across a normal MV or TV

preceeded by an opening snap
begins after S2

intensity loudest at onset when pressure gradietn b/w atrium and ventricle is greatest→desc or disappears as gradient diminishes→intensity increases toward the end of diastole in pt with normal sinus rhythm when atrial contraction augments flow across the valve

degree to which murmur faces depends on stenotic severity → dissappears in mid to late systole if stensosis is mild and prolonged if severe

causes = MV stenosis, TV stenosis, hyperdynamic states (fever, anemia, hyperthyroidism, exercise), may acompnay advanced mitral regurg, tricuspid regurg, or atrial septal defect murmurs due to increased BV that must return across valve to the LV in diastole

Front 38

Continuous murmur

Back 38

begins in early systole → cresce to ints max at S2 → decresc until next S1

due to presitent pressure greadient b/w two structures during systole and diastole

cause = PDA

Front 39

To and fro combined murmur

Back 39

diamond shaped ejection murmur in systole and desc murmur in diastole

sound does not extend through S2

cuases = pt with both aortic stenosis and regur; pt with both pulmonic stenosi and regurg