Pathophysiology of valve disease

Dr. Roldan  pathophysiology of valve disease

aortic valve 

• tricuspid leaflets
• aortic regurgitation = diastolic (ARD) starts at S2
• acute - endocarditis, aortic dissection, trauma, valve implant malfunction
• chronic - Bicuspid aortic valve, Aortic root/annular dilatation, Previous endocarditis, Rheumatic disease, Connective tissue diseases
• aging, infection, inflammation

• large pulse pressure > 100 mm Hg
• systolic murmur may also be hearddue to large stroke volume - 3-4 left IC space
• increased with hand grip maneuver (increases diastolic P)

• aortic stenosis = systolic (ASS)  starts after S1

• only chronic
• crescendo - decresendo as turbulent flow increases then decreases
• 2nd right intercostal space with pt. leaning forward  (increases periph. vasc. resist.)
• causes
• < 70 y/o = congenital bicuspid valve
• > 70 y/o = degenerative (calcified, sclerosed)
• 
  

mitral valve

• bicuspid leaflets
• MI can damage papillary muscles = regurgitation
• mitral stenosis = diastolic (MSD) starts after S2
• rheumatic fever > 95%
• high risk for stroke (LA clot)

• mitral regurgitation = systolic  (MRS) starts at S1 - best heard at apex

murmurs memory tool:  hARD ASS MSD MRS

tricuspid valve

• 3 leaflets
• allow tivial nl regurg (lower closing pressures)
• the trivial to mild regurgitation % refers to percent of the population who show this, not the % regurgitation.

pulmonic valve

• 2 leaflets (SEMILUNAR)
• allow trivial nl regurg (lower closing pressures)
• the trivial to mild regurgitation % refers to percent of the population who show this, not the % regurgitation.

PRESSURE VOLUME LOOPS

AS - compensated

AS - decompensated

AR - compensated

AR Chronic Compensated  (dilated LV)

• similar to elite athletes

AR -decompensated  - systolic failure

MR acute compensated

• Incomplete closure 
• of mitral valve
• Flow regurgitates 
• back into the LA
• LA pressure
• LA size
• LV size
• LV end-diastolic 
• pressure

MR chronic compensated

MR chronic decompensated

MS 

• "happy left ventricle" = low EDP
• "sad right ventricle" = pressure overload RV failure

Summary Figure (looks like great MCQ for exams)

Pressure–volume loops in patients with valvular heart disease. A, normal; B, mitral stenosis; C, aortic stenosis; D, mitral regurgitation (chronic); E, aortic regurgitation (chronic). LV, left ventricular.

(Reproduced, with permission, from Jackson JM, Thomas SJ, Lowenstein E: Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:239.)

Dr. Andrews

MS

• Acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks after an episode of group A streptococcal pharyngitis
• Pathogenesis
• Antibodies directed against the M proteins of streptococci have been shown to cross react with self antigens in the heart
• CD4+ T-cells specific for streptococcal peptides also react with self proteins in the heart, and produce cytokines that activate macrophages

Infective Endocarditis

• Infection characterized by colonization of the heart valves or 
  

  mural endocardium by a microbe
• Leads to vegetations
• Most cases caused by bacterial infections – bacterial endocarditis
• Acute infective endocarditis
• Infection of a previously normal heart valve by a highly virulent organism
  • that produces necrotizing, ulcerative, destructive lesions
• Subacute infective endocarditis
• Organisms of lower virulence
• Organisms cause insidious infections of deformed valves
• Janeway lesions (nontender, macular lesions most commonly involving the palms and soles). Janeway lesions occur more frequently in endocarditis caused by Staphylococcus aureus. Janeway lesions are caused by septic emboli. Subcutaneous abscesses are found on histologic examination.