Cardiac Murmurs

abnormal sound that is heard secondary to turbulent blood flow.

Characteristics

of Murmurs:
Timing
Intensity
frequency
location

3
Grade 4
Grade 5
Grade 6

known heart murmur presents with complaints of substernal chest pain,

which increases with exertion, and shortness of breath which is starting to limit his lifestyle. No risk factors for coronary artery disease.
On Physical Exam you find the following:
Delayed carotid upstroke
A sustained apical pulse
Prominent A wave in the neck
PMI is sustained but not displaced laterally
and you hear

as the valve area is reduced from 3 to 4

cm2 to 1.5 to 2 cm2. However, an additional reduction in t he valve area from half its normal size to a quarter of it’s normal size produces severe obstruction to flow and progressive pressure overload on the left ventricle.

this overload. The increased muscle mass allows the ventricle to

generate the increased force necessary to propel blood past the obstruction. The hypertrophied myocardium has decreased coronary blood flow reserve and can cause systolic and diastolic failure.
Patients may present with symptoms:
Angina: 35% of patients with severe AS present with chest pain and half will die in 5 years.
Syncope: 15% of patients with severe AS present with syncope and half will die in 3 years.
CHF: 50% of patients with severe AS present with CHF and half will die in 2 years.

history of rheumatic fever presents with progressive shortness of breath

and dyspnea on exertion and is progressively getting worse. He has also developed intermittent complaints of palpatations.
On exam:
Increased respiratory rate
Normal PMI
RV lift
Increased JVP
Crackles on lung exam
You hear this upon auscultation

ventricle is spared and tends to be small and under

filled. There is significant elevation in the left atrial pressures leading to left atrial enlargement which then gets transmitted to the pulmonary circulation leading to pulmonary edema and pulmonary hypertension. The left atrial enlargement can lead to atrial fibrillation and loss of atrial kick and decreased filling of the left ventricle. Systemic embolic events are seen in approximately one-third of patients with atrial fibrillation and mitral stenosis and maybe the presenting event before the diagnosis of mitral stenosis is made.

complaints of slowly progressive dyspnea on exertion and an uncomfortable

awareness of pulsations in the neck and chest.
On Exam you find the following:
-Abnormal brisk pulses
-Wide pulse pressures
-Quincke’s pulse
-Head bobbing
-Pistol shot sounds
On auscultation you hear this:

high frequency, and decrescendo in shape.
Systolic aortic flow murmur
Austin flint

murmur

aortic dissection or aortic valve endocarditis usually presents with significant

shortness of breath and the murmur maybe minimal and peripheral manifestations maybe diminished. This causes the abrupt introduction of a large volume of blood into a non-compliant ventricle increasing the LV end diastolic and pulmonary venous pressures leading to significant dyspnea. A murmur maybe minimal because the abrupt increase LV diastolic pressure rapidly diminishes the aortic to LV diastolic gradient.

changes occur over time. The chronic volume overload causes stretching

and elongation of myocardial fibers (eccentric hypertrophy). Eventually, the LV cannot compensate and you have LV dilatation and congestive heart failure.

the emergency room with complaints of severe chest tightness (10/10)

and acutely short of breath. He has PND and orthopnea. He is hypotensive, tachycardic and in respiratory distress. His EKG reveals an inferior and posterior wall myocardial infarction.
On Exam:
Vital signs are unstable
Crackles are noted bilaterally
PMI is still relatively normal
Ausculatory findings reveal this:

the murmur maybe short and confined to early systole, because

the LA pressures are elevated.

In chronic MR, the murmur is typically holosystolic starting after S1.

ventricle with an increase in end diastolic volume. At the

same time, there is new pathway for LV ejection into a low pressure system into the LA. The left ventricle initially is hypercontractile because it can eject blood back into the LA and out the aortic valve. Forward stroke volume is actually decreased.
In acute MR, the LA cannot accommodate the increased volume and builds up in the lungs leading to respiratory distress.

dilate, the LV will constantly be volume overloaded and eventually

weaken. Both of these will eventually lead to congestive heart failure.

a routine physical exam. He was referred to cardiology because

of a murmur and wanted clearance to play sports. He has a family history of sudden cardiac death.
On cardiac exam:
PMI is markedly sustained with a palpable a wave.
On auscultation you hear this:

will be sustained with a triple apical beat secondary a

palpable a wave
There is a harsh mid systolic murmur radiating throughout the precordium.
There is usually also a holosystolic murmur c/w MR
Maneuvers have specific affects on this murmur

transmission to first-degree relatives in 50% of cases. The most

common location of ventricular hypertrophy is subaortic, septal, and anterior wall hypertrophy.
Traditionally, dynamic left ventricular outflow tract obstruction has been considered as the cause of symptoms in patients, but it should be remembered that diastolic dysfunction, ischemia, MR, and arrhythmia’s are also important in producing symptoms.

a common finding on Holter monitoring. Sustained ventricular tachycardia and

fibrillation are the most likely mechanisms of syncope and sudden death in these patients.
Cardiac output may decrease as much as 40% if atrial fibrillation occurs, and these patients tend to rely on their atrial kick.