Valve Defects /Cardiac Cycle

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 plusback 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.” http://www.cvphysiology.com/Heart%20Disease/HD009d.htm

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 http://content.nejm.org/cgi/content/full/359/10/e11

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 aorticvalve 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): • 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.” http://www.cvphysiology.com/Heart%20Disease/HD009b.htm

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. http://www.cvphysiology.com/Heart%20Disease/HD009c.htm

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

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:  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

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 • http://www.texasheart.org/education/cme/explore/events/eventdetail_5469.cfm • http://www.merck.com/mmpe/resources/multimedia/name/audio.html