This document discusses different types of heart murmurs, including:
- Pansystolic murmurs which occur throughout systole and are caused by mitral regurgitation, tricuspid regurgitation, or ventricular septal defect.
- Late systolic murmurs which begin in mid-late systole and are caused by mitral valve prolapse.
- Early diastolic murmurs which occur immediately after S1 and are caused by aortic regurgitation or pulmonary regurgitation.
- Mid-late diastolic murmurs which occur after S2 and are caused by mitral stenosis or tricuspid stenosis.
It also describes continuous murmurs caused by patent ductus arterios
This document discusses different types of heart murmurs, including:
- Pansystolic murmurs which occur throughout systole and are caused by mitral regurgitation, tricuspid regurgitation, or ventricular septal defect.
- Late systolic murmurs which begin in mid-late systole and are caused by mitral valve prolapse.
- Early diastolic murmurs which occur immediately after S1 and are caused by aortic regurgitation or pulmonary regurgitation.
- Mid-late diastolic murmurs which occur after S2 and are caused by mitral stenosis or tricuspid stenosis.
It also describes continuous murmurs caused by patent ductus arterios
This document discusses different types of heart murmurs, including:
- Pansystolic murmurs which occur throughout systole and are caused by mitral regurgitation, tricuspid regurgitation, or ventricular septal defect.
- Late systolic murmurs which begin in mid-late systole and are caused by mitral valve prolapse.
- Early diastolic murmurs which occur immediately after S1 and are caused by aortic regurgitation or pulmonary regurgitation.
- Mid-late diastolic murmurs which occur after S2 and are caused by mitral stenosis or tricuspid stenosis.
It also describes continuous murmurs caused by patent ductus arterios
• Holosystolic murmurs • mitral or tricuspid valve regurgitation or Ventricular septal defect (VSD)
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Pansystolic Murmurs of MR • Timing: no gap between S1 & the onset of these murmurs • Intensity: does not change with respiration • Location: heard best at the apex radiates toward the left axilla • Pitch: high pitched & “blowing” in quality • Clench the fists SVR ↑ severity of MR & its murmur will intensify (AS not)
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Pansystolic Murmurs of TR
• Location: best heard left lower sternal border
radiates to the right of the sternum • Pitch: high pitched & blowing in quality. • Inspiration negative intrathoracic pressure ↑ intensity
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Pansystolic Murmurs of VSD
• Location: heard best fourth to sixth left
intercostal spaces does not radiate to the axilla • Pitch: high pitched & thrill • Intensity: does not increase with inspiration. the smaller the VSD louder the murmur
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Late systolic murmurs • Begin in mid-to-late systole & continue to the end of systole (mitral valve prolapse) • Usually preceded by a midsystolic click • Maneuvers: • maneuvers that increase the volume of the LV (e.g., sudden squatting/ ↑ venous return) delay the occurrence of prolapse & cause the click and murmur • volume of blood in the LV ↓ (e.g., on sudden standing), prolapse occurs more readily & the click and murmur occur earlier in systole (closer to S1)
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Diastolic Murmurs • Early decrescendo murmurs & mid-to-late rumbling murmurs • Early diastolic murmurs AR/ PR • Mid-to-late diastolic murmurs MS/ TS or less commonly abnormally increased flow across a normal mitral or tricuspid valve
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Early Diastolic Murmurs of AR • Decrescendo • Rapid diastolic relaxation of the left ventricle pressure gradient develops immediately maximum intensity at its onset • As the aortic pressure falls the LV pressure increases the gradient between the two chambers diminishes murmur decreases in intensity • High-pitched murmur, • Best heard left sternal border patient sitting, leaning forward, and exhaling
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Early Diastolic Murmurs of PR • Usually because of PAH • Early diastolic decrescendo murmur • Best heard the pulmonic area may increase with inspiration.
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Mid-to-late diastolic murmurs of MS • After S2 & preceded by OS • The murmur is at its loudest then decrescendos or disappears • Whether the stenosis is mild or severe, the murmur intensifies at the end of diastole in patients in normal sinus rhythm • The more severe the stenosis, the longer murmur • Low pitched • Best heard best at the apex lies in the left lateral decubitus
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Mid-to-late diastolic murmurs of TR • Rare • Lower sternum, near the xiphoid processuss
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
Continuous Murmurs • PDA persistent pressure gradient between two structures during both systole & diastole
Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016
The Differences of Continous and To-and-Fro Murmur
A to-and-fro murmur is not continuous;
rather, there is a systolic component and a distinct diastolic component, separated by S2 Lilly Leonard S. Pathophysiology of heart disease. 6 th ed. Wolters Kluwer. 2016 MATUR NUWUN