Valvular Heart Disease
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Valvular Disease Progression
- 1.Hemodynamic burden (volume overload or pressure overload)
- 2.CV compensation
- 3.Eventual cardiac muscle dysfunction, CHF, or sudden death
- Aortic or Pulmonic Stenosis
- Incompetence of the mitral or tricuspid valve
- Stenosis of the mitral or tricuspid valve
- Incompetence of the aortic or pulmonic valve
- Heart Rate control: Beta-blockers, Ca channel blockers, and digitalis
- BP & Afterload Control: ACE inhibitors and vasodilators
- Heart Failure Control: Diuretics, inotropes, and vasodilators
Broad/Notched P waves (P mitrale): LA enlargement typical of mitral valve disease
Anticoagulation in Patients with Prosthetic Heart Valves
- Warfarin discontinued 3-5 days preoperatively
- IV heparin/LMWH is administered until surgery
Antibiotic Prophylaxis Conditions
- 1. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair.
- 2. Previous infective endocarditis
- 3. Congenital Heart Disease: Unprepared cyanotic disease (palliative shunts and conduits), Completely repaired heart defects with prosthetic material/device 6 months after placement, repaired congenital heart disease with residual defects ay the site or adjacent to the site.
- 4. Cardiac transplantation recipients who develop cardiac valvulopathy.
- 5. Dental procedures that manipulate the gingival tissues or periapical regions of teeth or oral mucosa perforation
- 6. For invasive procedures (incision/biopsy) on the respiratory tract or infected skin, skin structures, or musculoskeletal tissue
- 7. NOT for GI or GU procedures.
- Info: Rheumatic heart disease is most common cause, Symptoms begin when the orifice size has decreased at least 50%. AFib in 30% of cases
- Path: Mechanical obstruction to the LV diastolic filling, increased LA pressure, increased pulmonary pressure, pulmonary edema
- Leads to: CHF, pulmonary HTN, and RV failure
- Anesthesia: Prevent decreased CO or pulmonary edema, sudden SVR decrease may not be tolerated since an increase in HR ay decrease CO. Avoid ketamine due to increase in HR.
- Afib tx: Cardioversion or B-blockers, Ca channel blockers, or digoxin.
- Info: Papillary muscle dysfunction, mitral annular dilation or rupture of chordae tendinae
- Path: decreased forward LV stroke volume and CO, LA volume overload, and pulmonary congestion and/or cardiogenic shock
- Regurgitation fraction: 1.Size of the valve, 2.HR/ventricular ejection, 3.Pressure gradients across the mitral valve (LV compliance and impedance to LV ejection)
- Tx: Symptomatic patients received ACEi or Beta-blockers and biventricular pacing
- Anesthesia: Prevent Bradycardia, Prevent increase in SVR, minimize drug induced myocardial depression, monitor regurgitant flow
Mitral Valve Prolapse
- Prolapse of one or both mitral leaflets into the LA w/ or w/o regurgitation
- S/S: Mid-systolic click and late systolic murmur
- Anesthesia: Same principles as mitral valve regurgitation. Prevent Bradycardia, Prevent increase in SVR (also significant decrease in SVR @ induction), minimize drug induced myocardial depression, monitor regurgitant flow. Minimize sympathetic activation, maintain fluid balance
- Risk Factors: Degeneration/ calcification of the aortic leaflets (stenosis) and presence of a bicuspid aortic valve
- Severe: Gradients over 50mm Hg and area under 0.8cm2.
- Info: uncreased LV pressure needed to maintain forward SV.
- Anesthesia: Maintain normal sinus rhythm, avoid brady/tachy-cardia, avoid hypotension, optimize IV fluid volume to maintain venous return and LV filling. (avoid decreased SVR). Bradycardia require prompt tx w/ glyco, atropine, or ephedrine. Tachycardia tx w/ esmolol. SVT tx w/ cardioversion.
- Info: Decreased CO due to regurgitation of SV from the aorta into the LV during diastole.
- Magnitude determined by: 1. time for the regurgitant flow to occur (HR), 2.Pressure gradient across the aortic valve. (Decrease: tachycardia and peripheral vasodilation)
- Steps: LV volume overload, LV hypertrophy, LVEDV increase, pulmonary edema
- S/S: diastolic murmur along the left sternal border
- Tx: vasodilators and inotropic drugs
- Anesthesia: Avoid bradycardia, avoid increases in SVR, minimize myocardial depression
- Info: Often caused by annular dilation secondary to RV enlargement or pulmonary HTN.
- Path: Hemodynamic consequence of RA volume overload
- Anesthesia: Maintain IV fluid volume and CVP, avoid increased pulmonary artery pressure (hypoxemia and hypercarbia), PPV and vasodilating drugs may be deleterious is they decrease venous return.
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