Murmurs

Question 1

Aortic Stenosis

Answer 1

Narrowing of aortic valve orifice
Usually due to fibrosis and calcification from “wear and tear”
Presents in late adulthood-bicuspid aortic valve increases risk with syncope, angina and dyspnea

Can be consequence of chronic rheumatic valve disease, coexisting mitral stenosis and fusion of the aortic vavle commissurse distinguish RF from normal wear and tear

Quality: Crescenco-decrescedno systolic ejection murmur
Loudest at base; radiates to carotids
Pulses are weak with delayed peak 
low pulse pressure
Carotid upstrokes: tardus et brevis 
S4 gallop

Clinical: angina, syncope

Pathophys:
increased LV pressure during systole
LV hypertrophy (pressure overload)
LA hypertrophy

Complications:
Concentric left ventricular hypertrophy
Angina and syncope with exercise (imbalance between O2 supply and demand)
Microagniopathic hemolytic anemia-RBCs are damaged
CHF

Avoid hypotensive meds

Question 2

Aortic Regurgitation

Answer 2

Backflow of blood from the aorta into the left ventricle during diastole

Due to: aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis) most common cause is isolated root dilation, syphilis

Features:
Early, blowing diastolic (after S2) decrescendo murmur
Wide pulse pressure leading to bounding pulses, nail bed pulses, femoral pulses and head bobbing
Displaced PMI-volume overload

Pathophys:
Acute: increased LV pressure, LA pressure, pulmonary edema
Chronic: volume overload of LV, high systolic pressure
Wide pulse pressure
Low diastolic pressure decreases O2 delivery to myocardium

Complications:
LV dilation and eccentric hypertrophy

Physical Exam:
Increased during handgrip (increased systemic pressure-afterload more gets regurgitated), vasodilators decrease intensity of murmur
ERBs pipnt

Question 3

Mitral Valve Prolapse

Answer 3

Ballooning of mitral valve into left atrium during systole

Due to: myxoid degeneration (Movat pentachrome stain) of the valve (fibrosa layer) and expansion of spongiosa making it floppy
May be seen in Marfan or Ehlers-Danlos, RF, or chordae rupture
Elongated, attenuated or occasionally ruptured chordae tendineae
Fibrous thickening of valve leaflets at points of contact

Features:
Late systolic crescendo murmur with midsystolic click (due to sudden tensing of chordae tendinae)

Physical Exam:
Occurs earlier in maneuvers that decrease venous return (standing or Valsava)
Decrease in sound while squatting (increased systemic resistance decrease left ventricular emptying)

Complications:
infectious endocarditis, arrhythmia, and severe mitral regurgitation

Question 4

Mitral Regurgitation

Answer 4

Reflux of blood from the left ventricle into the left atrium during systole

Arises due to complication of mitral valve prolapse, LV dilatation, infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture or ischemia after MI, rupture of chordae tendinae, hypertrophic cardiomyopathy, senile calcification, myxomatous degeneration

Features:
Holosystolic, high pitched blowing murmur 
Radiates toward axilla 
Displacement of PMI (volume overload)
S3

Physical Exam
Increased by maneuvers that increase TPR-squatting, hand grip

pathophys: increased left atrial volume and presurre
Reduced CO
Volume overload in LV

Complications: more prone to atrial fibrillation and mural thromboembolism

Question 5

Tricuspid Regurgitation

Answer 5

Holosystolic murmur Loudest at tricuspid area radiating to right sternal border

Physical Exam:
Increased by maneuvers that increase RA return (inspiration)

Commonly caused by RV dilation, RF and infective endocarditis

Question 6

Mitral Stenosis

Answer 6

Narrowing of mitral valve orifice
usually due to chronic rheumatic valve disease
congenitl stenosis, severe senile calcification, endocarditis with large vegetations

Clinical:
Opening snap followed by diastolic rumble with last second crescendo
Decrease between S2 and Opening snap correlate with increased severity
Gets louder before S1 (unless a .fib-irregularly irregular)

Volume overload leads to dilatation of the left atrium (increased pressure) resulting in pulmonary congestion with edema and alveolar hemorrhage (hemosidern laden macrophages), pulmonary hypertension and eventual right sided heart failure,
Possible hemoptysis due to collateralization between pulmonary and bronchial veins

At risk: atrial fibrillation with associated risk for mural thrombi
Severity of stenosis dictates severity of symptoms

Physical Exam: Increased by maneuvers that increase LA return (expiration)
Left Lateral Decubitus position

Question 7

PDA

Answer 7

Continous machine like murmur
Loudest at S2

Often due to congenital rublela or prematurity

Best heard at left infraclavicular area

Question 8

VSD

Answer 8

Holosystolic, harsh sounding murmur

Loudest at tricuspid area accentuated with hand grip maneuver due to increased afterload

Question 9

S3 sound

Answer 9

Ventricular gallop
Commonly head in patient with left ventricular systolic failure or restrictive cardiomyopathy

caused by blood rushing into a partially filled ventricle

Use bell at apex of heart and have patient lie in left lateral decubitus position

Exhaling makes it louder-decreased volume of lungs and bringing heart closer to chest wall

Can be heard physiologically in adolescents

Question 10

S4 Sound

Answer 10

Atrial gallop
Before S1

Heard immediately after atrial contraction phase as blood is forced into stiff ventricle

Extensive left ventricular hypertrophy due to hypertension, aortic stenosis, and hypertrophic cardiomyopathy

heard with bell over cardiac apex in left lateral decubitus

Intensifies durign experiation