 Mitral Stenosis  Typically caused by rheumatic carditis from rheumatic fever  Valve leaflets fuse, stiffen  Chordae tendineae contract, shorten 

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Presentation transcript:

 Mitral Stenosis  Typically caused by rheumatic carditis from rheumatic fever  Valve leaflets fuse, stiffen  Chordae tendineae contract, shorten  Valve opening narrows  Compromises blood flow from left atrium to left ventricle  Resulting in rise in L atrial pressure, L atrium dilitation, increased pulmonary artery pressure, R ventricular hypertrophy

 Mitral Regurgitation (Insufficiency)  Failure of closure of mitral valve during systole due to fibrotic and calcific changes  Blood leaks from L atrium to L ventricle along with normal blood flow  Results in increased volume to be ejected during next systole  Leading to dilation of L atrium and ventricles with hypertrophy  Rheumatic fever primary cause

 Mitral Valve Prolapse  Enlargement of valvular leaflets which prolapse into L atrium during systole.  Usually benign in nature but may progress to pronounced mitral regurgitation.  Most are asymptomatic  Most common in women between 20 and 54 years of age  Genetic  Auscultation of midsystolic click with late systolic murmur audible at apex.

 Aortic stenosis  Aortic valve orifice narrows and obstructs L ventricular outflow during systole  Leading to increased resistance to efection or afterload  Resulting in ventricular hypertrophy  Predominately caused by congenital malformation/disease  Most common valvular disorder in countries with aging populations  Caused by atherosclerosis and degenerative calcification  80% men

 Aortic regurgitations (insufficiency)  Aortic valve leaflets do not close properly during diastole  Leads to regurgitation of blood from the aorta back into L ventricle during diastole  L ventricle dilates with eventual hypertrophy  Asymptomatic  When patient becomes symptomatic, symptoms due to L ventricular failure  Bounding arterial pulse, widened pulse pressure, high-pitched blowing decrescendo diastolic murmur  Causes: infective endocarditis, congenital anatomic aortic valvular abnormalities, htn, Marfan syndrome  75% are men

Nonsurgical Drug therapy Diuretics Beta Blockers Digoxin Nitrates Calcium Channel Blockers Prophylactic antibiotic therapy Anticoagulants Antidysrhythmics Rest

 Surgical Management  Reparative procedures  Improved function of valve  Less problem with complications  Balloon valvuloplasty  Patients selected for this are typically older, high risk for surgical complications or have refused operative treatment  Benefits short lived  Postop precautions consistent with those for cardiac catheterization  Direct Commissurotomy  Requires open heart surgery and cardiopulmonary bypass  Removal of thrombi, cutting loose of fused leaflets, debridement of calcium from valve

 Mitral Valve Annuloplasty  Reconstruction of valve for acquired mitral insufficiency  Valve replacement  Xenograft  Porcine or bovine  Risk for clot formation minimized  No need for long term anticoagulant therapy  Typically used for the older patient  Prosthetic valve  More durable  Used in younger patients  Must have long term anticoagulation  See chart 38-9 for patient education

 Microbial infection involving endocardium  Found in Iv drug abusers, patients having had valve replacements, bacteremia, structural cardiac defects  Mortality high – early detection key  > 90% develop murmurs  Heart failure most common complication  See chart Key features of infective endocarditis  Interventions = antimicrobials, rest balanced with activity, supportive care for heart failure

 Most common procedure = orthotopic transplantation  Donor must be comparable body weight, ABO compatible  Heart must be transplanted within 6 hours of harvesting  See criteria for candidate selection pg 774  Biggest factor to remember is that vagus nerve will no longer function  Atropine, digitalis and carotid sinus pressure ineffective

 Require life long immunosuppressants  Long term complications  Coronary artery vasculopathy  Organ rejection  See Key Points at end of chapter 38

 Acyanotic  Do not cause deoxygenation  Skin and mucous membrane color is usually pink  Atrial septal defect  Left to right shunt  Opening between L and R atria  Surgical closure or patch of defect  Ventricular septal defect  Left to right shunt  Increased pulmonary blood flow  May have spontaneous closure  Surgical patching may be required  Prophylactic antibiotics for prevention of endocarditis

 Coarctation of the aorta  Narrowing of the descending aorta restricting blood flow leaving heart  Progressive, leading to chf  BP difference of 20mm between upper and lower extremities  Upper pulses full, lower pulses weak  CVA secondary to htn in upper circulation  Endocarditis prophylaxis  Surgical resection and patch of coarctation

 Cyanotic heart defects  Heart conditions that couse blood to contain less oxygen than required  Skin and mucous membranes usually pale to blue  Tetrology of Fallot  4 defects that combine to allow blood flow to bypass lungs and enter L side of heart  R to L shunt  Unoxygenated blood enters body circulation leading to cyanosis  Defects:  Pulmonic stenosis  R ventricular hypertrophy  Ventricular septal defect  Overriding aorta  Acidosis occurs  TET spells: hypercyanosis = transient periods of increased R to L shunting of blood

 Transposition of the great vessels  Aorta arises from R ventricle, pulmonary artery arises from L ventricle  This is inconsistent with life  Other anomalies exist that increase mixing of blood between the two separate circulations to promote oxygenation  R to L shunting of blood occurs

 Aneurysm – permanent dilation of an artery to at least 2 times its normal diameter  Fusiform = affects entire circumference of artery  Saccular = outpouching affecting only a distinct portion of artery  True aneurysm = arterial wall weakened by congenital or acquired problems  False aneurysm = occurs as a result of trauma or injury to all 3 layers of the artery wall  Abdominal aortic aneurysms (AAA) account for 75% of all aneurysms  Atherosclerosis is most common cause  AAA more common in men than women  S/S related to pressure on surrounding structures or rupture  Rupture is life threatening

 Interventions  Nonsurgical to monitor growth of affected area and maintain BP at a normal level  Surgical management is the excision of the aneurysm from the area with the placement of a woven Dacron graft  Pre and post op care consistent for those undergoing surgery with general anesthesia