1. Valve Defects /Cardiac Cycle
UNM School of Medicine
CV/Pulmonary/Renal Block 2012
Slides from Steve Wood, PhD (UNMSOM) and John Wood, PhD (KU Med. Ctr.)

2. LOCATING CARDIAC VALVE MURMURS
The diagram above shows the optimal locations for hearing specific murmurs. Mitral and tricuspid valve murmurs are best heard in the apical region with the tricuspid valve adjacent to the sternum and the mitral valve more lateral. Aortic and pulmonic valve murmurs are heard best at the level of the 2nd or 3rd intercostal space, with the aortic valve on the right side of the sternum and the pulmonic valve on the left side of the sternum.

3. TYPES OF MURMURS

4. INTENSITY OF A MURMUR FLOW
The intensity of the murmur is directly related to the magnitude of the flow across the defective valve, which is dependent on the pressure gradient across the valve driving flow.
In the example of aortic stenosis above, the intensity of the murmur is dependent on ΔP across the valve, which is PLV – Paorta.

5. Normal Cardiac Cycle and Heart Sounds
Refer to this normal cardiac cycle when studying the abnormal cycles in the following slides
View the PowerPoint in slide show mode in order for sound files to work (S1 and S2 in the
normal heart)
Click here for normal heart sounds

6. AORTIC INSUFFICIENCY
Aortic insufficiency (regurgitation) occurs when the aortic valve leaflets fail to close completely.
The murmur begins upon incomplete closure of the aortic valve (S2).
Backflow of blood occurs from the aorta to the left ventricle during ventricular diastole.

7. AORTIC INSUFFICIENCY: INTENSITY OF THE MURMUR
Dependent on the pressure difference across the aortic valve:
Aortic pressure - Left ventricular pressure
This pressure difference decreases throughout diastole as aortic pressure decreases and left ventricular pressure increases (due to filling).
This results in a diastolic decrescendo murmur.
Note the large pulse pressure due to rapid “runoff” of blood to circulation plus back into ventricle.
Blood begins filling ventricle before Mitral valve opens (back flow from Aorta).
∆P across valve

8. “As long as the ventricle is not in failure, end-systolic volume may only be increased a small amount (as shown in figure) due to the increased afterload (ventricular wall stress).  If the ventricle goes into systolic failure, then end-systolic volume will increase by a large amount and the peak systolic pressure and stroke volume (net forward flow into aorta) will fall. These changes just described do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular dilation (remodeling) that increases ventricular compliance.”

9. Aortic regurgitation 2
There can also be a systolic murmur due to large stroke volume and turbulent flow
During ejection
EDM – early diastolic murmur
AFM – Austin Flint murmur – mitral leaflet displacement & turbulent back flow

10. AORTIC INSUFFICIENCY: ARTERIAL PRESSURE
A key feature of aortic insufficiency is low diastolic pressure.
Because of the backflow of blood from the aorta to the left ventricle, blood volume in the arterial system decreases faster than normal during diastole, even though total peripheral resistance (TPR) is unchanged (and so the rate of venous runoff is unchanged).

11. AORTIC INSUFFICIENCY: ARTERIAL PRESSURE
Pulse pressure is increased in aortic insufficiency.
Left ventricular end diastolic volume (LVEDV) is increased since ventricular filling now results from two routes: from the left atrium as well as backflow from the aorta.
The increase in LVEDV above normal is equal to the amount of the regurgitation.
The greater LVEDV will increase stroke volume (SV) compared to normal, and this will produce a larger pulse pressure and higher arterial systolic pressure.

12. AORTIC STENOSIS
The aortic valve leaflets do not open completely (stiff valve), which reduces the size of the opening through which blood is ejected (increased resistance to flow).
The stenotic aortic valve increases the resistance to left ventricular ejection (greater afterload), even though total peripheral resistance is not changed.

13. AORTIC STENOSIS: INTENSITY OF THE MURMUR
The murmur is dependent on the pressure difference across the aortic valve:
Left ventricular pressure - Aortic pressure
The murmur begins upon aortic valve opening and continues throughout ventricular systole (until aortic valve closure, S2).
The pressure difference across the stenotic aortic valve is initially low as ejection begins, and rises as ventricular pressure increases above aortic pressure until it reaches a peak at the midpoint of ventricular systole. As ventricular pressure falls during the slow ejection phase, the pressure difference across the valve then decreases until aortic closure occurs.
This results in a systolic crescendo-decrescendo murmur.
∆P across valve

14. Aortic Stenosis Ejection Sound (ES): Ejection Murmur:
mobile Ao valve leaflets
– bicuspid AS
– easily confused with S1
Ejection Murmur:
begins with ES, not S1
ends before S2

15. “In moderate stenosis (as shown in the figure) or severe stenosis, the stroke volume may fall considerably because the end-systolic volume increases substantially more than the end-diastolic volume increases. The fall in stroke volume can lead to a reduction in arterial pressure. Stroke volume falls even further if the ventricle begins to exhibit systolic and diastolic dysfunction. Compensatory increases in end-diastolic volume will be limited by ventricular hypertrophy that occurs due to the chronic increase in afterload. This hypertrophy can lead to a large increase in end-diastolic pressure that is associated with reduced end-diastolic volumes.
The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure.”
in moderate stenosis (as shown in the figure) or severe stenosis, the stroke volume may fall considerably because the end-systolic volume increases substantially more than the end-diastolic volume increases. The fall in stroke volume can lead to a reduction in arterial pressure. Stroke volume falls even further if the ventricle begins to exhibit systolic and diastolic dysfunction. Compensatory increases in end-diastolic volume will be limited by ventricular hypertrophy that occurs due to the chronic increase in afterload. This hypertrophy can lead to a large increase in end-diastolic pressure that is associated with reduced end-diastolic volumes.
The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure.

16. AORTIC STENOSIS: ARTERIAL PRESSURES
Because of the high resistance to ejection in the stenotic aortic valve, the rate of ejection of blood is decreased.
As a result, aortic pressure rises more slowly than normal and the pulse pressure is reduced.
The time for left ventricular systole will be prolonged (while the time for left ventricular diastole is shortened). This causes paradoxical splitting of S2.
A hallmark of aortic stenosis is a large pressure difference between the left ventricle and aorta during ventricular systole.

17. AORTIC STENOSIS: CHRONIC CHANGES
The increased afterload due to high resistance of the stenotic aortic valve will lead to left ventricular hypertrophy over time (left axis deviation).
The Po line will shift upward and to the left due to the hypertrophy, and the diastolic filling curve will shift upwards due to decreased compliance of the ventricle.
Left atrial pressures will be increased due to decreased ventricular compliance, which may result in atrial hypertrophy.
Aortic stenosis may severely restrict increases in cardiac output (i.e., exercise).

18. Mitral regurgitation
Murmur depends on pressure difference across the mitral valve
P = LV – LA pressure
P remains large and relatively constant during ejection resulting in a holosystolic murmur.
LA pressure increases due to backflow across incompetent valve

19. These changes described do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure, nor do they include the ventricular dilation (remodeling) that increases ventricular compliance.

20. Mitral Regurgitation or Insufficiency
Inspection:
apex beat displaced to 7LICS
outward excursion of stethoscope head during systole
Auscultation:
murmur is holosystolic
– heard best over LV
sound is S3
Chronic Mitral Regurgitation
Chronic mitral regurgitation is usually a well tolerated lesion with minimal hemodynamic impact. However, when the valve's competence is suddenly disrupted by endocarditis or chordal or papillary muscle rupture, or left ventricular function is compromised by ischemia or hypertension, severe disability ensues.
In this patient with chronic MR, the bell of the stethoscope is resting gently on the point of maximal left ventricular impulse where we observe the following:
the apex beat is displaced to the 7th left intercostal space
there is outward excursion of the stethoscope during systole
the outward excursion is associated with a blowing murmur
the inward return of the stethoscope is associated with a thudding sound
The auscultatory complex can be mimicked by saying "wow-duh." The blowing murmur ("wow") occupies all of systole (holosystolic) and obscures the first and second heart sounds.
The thudding sound ("duh") is separated from the murmur by a pause, and is therefore mid diastolic.
Typically mitral regurgitant flow persists throughout all of systole, reflecting the driving force of the pressure difference between the left ventricle and atrium that is initiated as the left ventricular pressure rises at the onset of systole and greatly exceeds left atrial pressure throughout systole.
Although the regurgitant stream is directed toward the left atrium, the murmur of MR is best heard over the left ventricle, because the dorsal location of the left atrium is remote from the stethoscope.
[©2002 Blaufuss Multimedia]

21. Mitral Stenosis
Murmur intensity depends on pressure difference across mitral valve.
P = LA – LV
Highest at the beginning,
resulting in diastolic
decrescendo murmur with a rise in pressure
(crescendo) just before systole as atria contracts

22. Mitral Stenosis Loud S1: Opening Snap:
 elevated LA pressure and stiff leaflets
Opening Snap:
 mitral valve opens earlier than normal ( LA pressure)
 fused leaflets abruptly halt mitral valve opening, causing OS
Add / Remove sounds
The sound recording (phonocardiogram) from the cardiac apex is displayed with intracardiac pressures from the left ventricle (LV) and left atrium (LA). Obstruction of the mitral valve results in an atrioventricular pressure gradient (shaded area) throughout mid and late diastole, an elevated left atrial pressure and a reduced rate of ventricular filling (neither a rapid filling wave nor an a-wave are seen in the ventricular diastolic pressure.) The mitral valve closes late (late, loud S1) when ventricular pressure exceeds atrial pressure, and opens early (OS) when ventricular pressure falls below the elevated atrial pressure. The mid-diastolic murmur (MDM) corresponds with the atrioventricular pressure gradient. The elevated left atrial pressure, augmented by the left atrial a-wave, allows atrial emptying to proceed beyond the start of systole, and this turbulent flow in the face of rising ventricular pressure results in the crescendo presystolic murmur (PSM).
You may selectively add and remove the opening snap and mid-diastolic murmur by clicking on the buttons under the tracing.
[©2002 Blaufuss Multimedia]

23. ↓ SV =↓ afterload = small ↑ SV but not enough to compensate.
The changes described above and shown in the figure do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure.

24. Online resources