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33 Cards in this Set
- Front
- Back
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Describe normal heart valve function:
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*Maintain forward flow and prevent reversal of flow.
*Valves open and close in response to pressure ∆s b/t cardiac chambers. |
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Abnormal Valve Function:
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*Valve Stenosis
-Obstruction to valve flow during that phase of the cardiac cycle when the valve is normally open. -Hemodynamic hallmark: “pressure gradient” is proportional to flow across a valve. *Valve Regurgitation, Insufficiency, Incompetence: -Inadequate valve closure --> back leakage. -A single valve can be both stenotic and regurgitant; but both lesions cannot be severe! *Combinations of valve lesions can coexist: -Single disease process (rheumatic fever, endocarditis). -Different disease processes (AS + MR). -One valve lesion may cause another (MS--> Pulm HTN--> TR insufficiency). -Certain combinations are particularly burdensome (AS & MR). |
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List components of Mitral Valve Competence: 5
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*Integrated function of several anatomic elements:
-Posterior LA wall -Anterior & Posterior valve leaflets -Chordae tendineae -Papillary muscles -Left ventricular wall where the papillary muscles attach |
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Mitral Valve Disease: Etiology:
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*Mitral Stenosis (pretty rare):
-Rheumatic - 99.9%!!! -Congenital (uncommon) -Prosthetic valve stenosis (uncommon) -Mitral Annular Calcification (age 85+) -Left Atrial Myxoma (tumor that obstructs flow) *Acute Mitral Regurgitation (more common than MS): -Infective endocarditis (staph aureus). -Ischemic Heart disease: Acute MI & Papillary m rupture. -Mitral valve prolapse: Chordal rupture. -Chest trauma *Chronic Mitral Regurgitation -Ischemic Heart disease: Papillary m dysfunction, Inferior & posterior MI. -Mitral Valve prolapse -Infective endocarditis (strep viridans). -Rheumatic -Prosthetic -Mitral annular calcification (age 85+) -Cardiomyopathy: LV dilatation, IHSS. |
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Mitral Regurgitation-Pathophysiology:
What's the 1˚ abnormality? compensatory mechanisms? |
*MR: Leakage of blood into LA during systole
*1˚ Abnormality – Loss of forward SV into LA *Compensatory Mechanisms: -Increase in SV (& EF): Forward SV (from RV) + regurgitant volume (from LA) -Left Ventricular Volume Overload (LVVO) --> LV (LA) dilatation. |
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Chronic Mitral Regurgitation - LVVO:
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*LVVO is the pathphysiology of regurgitation:
-LV dilatation (to pump more blood to account for backwards flow of 2L/min). -Eccentric hypertrophy. *Increased LA pressure (now 18). *Dyspnea. *Pulmonary HTN (from increased LA pressure). *Atrial arrhythmias (large heart is arrhythmogenic). *Low output state (end-stage). |
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Pathophysiology –Acute vs Chronic Mitral Regurgitation:
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*Acute MR
-Normal (noncompliant) LA. -Increased LA pressure. -large “V” waves seen in PCWP measurement. -Acute Pulmonary Edema. *Chronic MR -Dilated, compliant LA. -LA pressure normal or slightly increased. -Fatigue, low output state. -Prone to atrial arrhythmias- a. fib. *Most patients fall between these two extremes!! |
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Mitral Regurgitation: Physical Findings:
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*Hyperdynamic Left Ventricle:
-Brisk carotid upstrokes you can feel. -Hyperdynamic LV apical impulse. -May feel LA lift with your palm; may feel RV tap with tip of your finger. *Auscultatory Findings: -S1 – soft or normal. -P2 (pulmonic component of second sound): increased. -Holosystolic blowing murmur @ apex (1˚ finding!). MVP – mid-systolic click & late systolic murmur. IHSS – murmur INCREASES with Valsalva maneuver. Acute MR – descrescendo systolic murmur. -S3 gallop & diastolic flow rumble |
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Mitral Stenosis -Pathophysiology:
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*Restriction of blood flow from LA --> LV during diastole
*Normal MV area is 4-6cm^2. -Mild MS: 2-4cm^2. -Severe MS < 1.0cm^2. *MV Pressure gradient – -MV gradient is proportional to MV flow//MVA. -MV Flow = CO/DFP (diastolic filling period) *As HR increases, diastole shortens disproportionately and MV gradient increases. -Normal is 2/3 diastole, 1/3 systole -Important therapy tgt is mitigating increase in HR! |
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Relationship between MV gradient and Flow for different Valve Areas:
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*Cross hatched area indicates range of normal resting flow.
*The vertical line represents the threshold for developing pulmonary edema. *Pressure gradient increases as flow increases: -To a small degree with normal valve area(4-6cm2). -To greater degrees with smaller valve areas. -In severe stenosis, a significant gradient is present at rest. They can't really increase their CO. |
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Mitral Stenosis-Pathophysiology
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*MV gradient --> Increased LA pressure.
*Pulmonary HTN: -Can be passive. -Can be reactive- called a "2nd stenosis." *RV Pressure Overload (bottom figure): -RVH. -RV failure. -Tricuspid regurgitation. -Systemic Congestion --> peripheral edema, JVD, etc. *Paradoxes of MS: -Disease of Pulm Arteries & RV. -LV is unaffected (protected). -As RV fails, pulmonary symptoms diminish. |
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Mitral Stenosis- Clinical Symptoms:
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*There are symptoms related to severity of decrease in MV area (MVA):
-Dyspnea -orthopnea *And there are symptoms UNRELATED to severity of decrease in MVA: -Atrial fibrillation can occur at any time or severity of MS. -Systemic thromboembolism due to LA stasis--> arm, leg, stroke. *There are end-stage symptoms due to Pulmonary HTN AND RV failure: -Fatigue, low output state. Can't increase CO. -Peripheral edema and hepato-splenomegaly. -Hoarseness: recurrent laryngeal nerve palsy. |
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Mitral Stenosis: Physical Findings:
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*Body habitus – thin, asthenic, female.
*Low BP. *LA lift & RV tap. *Auscultatory findings: -S1: variable intensity; increased early, progressively decreases. -OS: opening snap, variable intensity. -A2-OS interval: varies inversely with severity of MS; shortens as MVA diminishes. -Low-pitched diastolic rumble @ apex (HALLMARK; patient in left decubitis position; use bell). -Duration of murmur correlates with severity of MS -Pre-systolic accentuation -Increased P2 |
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Mitral Valve Disease – Echo findings:
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*Mitral Stenosis:
-Thickened, deformed MV leaflets. -2D: MVA can be measured. -Doppler Gradient. -Can assess LAE, RVH, PHTN, TR,MR, LV function. *Mitral Regurgitation (shown in picture): -Determine etiology – leaflets, chordae, MVP, MI. -Doppler severity of MR jet. -LV function. |
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Mitral Valve Disease : Treatment:
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*Mitral Stenosis
-Medical Rx for Class I & II MS (pt is not limited in ADLs): -HR control – Digitalis & BB. Goal is to blunt HR increase during exercise. -Anticoagulation: Indicated in Afib, age >40yrs, LAE, MR, or prior embolic event. -Surgical Rx -Class III &IV patients with MS: -Mitral Valve Surgery: Open commissurotomy or MV replacement. -Interventional Rx Class II-III: Balloon Mitral Valvuloplasty: Commissural fusion. Best with pliable, noncalcified leaflets, No MR or LA thrombus. *Chronic Mitral Regurgitation -Medical Rx for mild to moderate MR with vasodilators, diuretics, anticoagulation. -Surgical Rx –ideally before LV systolic function declines. -MV replacement. -MV ring & CABG. -MR repair: associated with improved long-term LV function: MVP, ruptured chords, infective endocarditis, papillary muscle rupture. |
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Balloon Mitral Commissurotomy:
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D shows the state of the art balloon catheter. Patient can go home the next day. This is the most common intervention for MS.
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Aortic Valve Disease: Etiology:
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*Aortic Stenosis:
-Degenerative calcific (senile; this is most common cause. It's a gradual process.) -Congenital: Uni or bicuspid aortic valve--> calcifies ~2 decades earlier in life. -Rheumatic. -Prosthetic valve stenosis. *Acute Aortic Insufficiency: -Infective endocarditis (staph aureus) -Acute Aortic Dissection: -Marfan’s Syndrome (cystic medial necrosis) -Chest trauma *Chronic Aortic Insufficiency *Aortic leaflet disease -Infective endocarditis -Rheumatic -Bicuspid Aortic valve -Prolapse & congenital VSD -Prosthetic *Aortic root disease -Aortic aneurysm/dissectrion -Marfan’s syndrome -Connective tissue disorders (SLE, ankylosing spondylitis) -3˚ Syphillis -HTN causes some dilation of the aortic root. Most common cause of aortic insufficiency. -Annulo-aortic ectasia |
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Aortic Stenosis - Pathophysiology:
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*Normal AVA 2.5-3.0cm^2
-Severe AS <1.0cm^2 -Critical AS <0.7cm^2; <0.5cm^2/m^2 *Hemodynamic Hallmark -Big systolic pressure gradients. -AV grad proportional to AV flow//AVA. -AV flow = CO/SEP (systolic ejection period). -50-100mmHg gradients are common in severe AS. Can be totally asymptomatic. |
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Relationship between AV gradient and Flow for different Aortic valve areas:
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*Like Mitral Stenosis – as flow increases so does the gradient.
*Unlike Mitral Stenosis: -Resting flows are higher: -smaller AV area. -shorter SEP (systolic ejection period). -Larger gradients. -Significant (>50mmHg) gradient can be present at rest in asymptomatic individuals. |
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Pathophysiology of Aortic Stenosis- LV Pressure Overload:
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*Chronic LV Pressure Overload --> Concentric LVH
*“Stiff” noncompliant LV -Increased LVEDP. -Increased LV mass --> Increased MVO2. *Well tolerated for decades: -LV fails --> CHF. *Atrial fibrillation: -Poorly tolerated --> heart failure. -Loss of atrial “kick.” -Rapid HR. -Acute pulmonary edema and hypotension. |
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Aortic Stenosis: Natural History & Clinical Symptoms:
when do sx develop? risk factors? |
*Asymptomatic for many years
*Symptoms develop when valve is critically narrowed and LV function deteriorates: -Bicuspid AV 5th - 6th decade -Senile AS 7th-8th decades *Classic Symptom Triad -Angina pectoris – 5 years. -CHF in 1-2 years. -Syncope in 2-3 years. -Sudden Death (low risk if elderly and asymptomatic; kids are at risk even if asymptomatic). *Natural History Studies: -Gradient progression is variable; 6-10mmHg/yr. *Risk Factors: -Age > 70. -CAD, hyperlipidemia. -Chronic renal failure. *Pts with asymptomatic severe AS require close f/u. Echo every 6 months or yearly. |
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Aortic Stenosis: Physical Findings:
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*Parvus et Tardus: slow rising and prolonged.
*Systolic ejection murmur is classic murmur. "Diamond shaped" or "crescendo-decrescendo" murmur. *S4 gallop. *Paradoxical splitting of S2. |
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Aortic Insufficiency- Pathophysiology:
What's the 1˚ abnormality? compensatory mechanisms? |
*1˚ abnormality – LVVO.
*Severity of LVVO: -Size of regurgitant orifice. -Diastolic pressure gradient between Ao & LV. -HR or duration of diastole. -Patients do better with faster HR. Encourage them to do cardio exercise. You regurgitate less when exercising. *Compensatory Mechanisms: -LV dilatation & eccentric LVH. -Increased LV diastolic compliance. -Peripheral vasodilation; especially in the kidney. Helps to promote forward flow. |
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Chronic LV Volume vs Pressure Overload:
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*Could be on test?*
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Acute vs Chronic AR Pathophysiology and Clinical Presentation:
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*Acute Aortic Regurgitation
-Sudden AoV incompetence -Noncompliant LV -Acute Pulmonary Edema -Emergency AVR *Chronic Aortic Regurgitation -Long asymptomatic phase -Progressive LV dilatation--these folks have the biggest hearts! -DOE, orthopnea, PND -Frequent PVC’s |
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Chronic Aortic Regurgitation: Physical Findings:
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*Widened Pulse Pressure > 70mmHg (170/60)
*Low diastolic pressure <60mmHg *Hyperdynamic LV: -DeMusset’s signs -Corrigan’s pulse -Quincke’s pulsations -Durozier’s murmur *Auscultation: -Diminished A2. -Descrescendo diastolic blowing murmur @ LSB -Length of murmur correlates with severity. -Accentuated by hand-grip maneuver, squatting; these increase peripheral vascular resistance. -Austin-Flint murmur: diastolic flow rumble @ apex: -Due to interference with trans-mitral filling by impingement from aortic regurgitant jet. -DDx: mitral stenosis (increases intensity with amyl nitrite) |
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Aortic Valve Disease: Diagnostic Testing:
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*The echo is key
*cor bovinum: you got a big ass cow heart |
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Aortic Valve Disease: Treatment:
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*Aortic Stenosis
-Medical Rx: -A.fib – rate control; cardioversion -CHF -diuretics -Balloon Aortic Valvuloplasty -Surgical Rx- -AVR: for symptomatic pts with severe or critical AS -Operate before LV dysfunction -CABG for CAD -Ross Procedure *Aortic Insufficiency -Medical Rx: Vasodilator Rx -Surgical Rx – AVR -Acute AI – emergently; urgently for I.E. -Chronic AI with symptoms of CHF -Asymptomatic AI before LV dysfunction: ESV > 55mm |
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Balloon Aortic Valvuloplasty:
what's it for? when would you do it? Disadvantages? |
*For Severe Aortic Stenosis!
*Extremely high risk for AVR *Urgent/emergent need for noncardiac surgery *Patient with limited lifespan – cardiac or noncardiac *Patient refuses surgery *Younger patients with pliable. noncalcified valves. *Bridge to eventual SAVR/TAVR: -Low gradient, low EF -Severe heart failure *Disadvantages of BAV: -Re-stenosis within 6-12 mos is common. -Vascular access injury. -Risk of acute aortic insufficiency. |
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Aortic Valve Surgery: Ross Procedure:
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**"Not gonna tell you about the Ross procedure."**
Autotransplant of pulmonic valve to the aortic position Reimplantation of the coronary arteries Homograft valve in the pulmonic position Indications Younger patients No anticoagulation Requires similar sized aortic and pulmonic roots **"Not gonna tell you about the Ross procedure."** |
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Discuss.
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**Skipped this slide.**
*CXRay in MS: -Straightening Left Heart border -Elevated Left main bronchus (not well seen here) -“Double Density” of enlarged LA behind LV. -Pulmonary congestion. **Skipped this slide.** |
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Mitral Stenosis: Diagnostic Testing findings--
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*CXRay in MS:
-Straight Left Heart border -Elevated Left main bronchus -“Double Density” -Pulmonary congestion *EKG: -Normal SR: RAD,RVH,LAE -A.Fib: RAD, coarse fib waves (LAE), RVH LAE: left atrial enlargement RVH: right ventricular hypertrophy RAD: right atrial dilation SR: sinus rhythm |
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Transcatheter Aortic Valve Replacement:
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*Newer procedure than Balloon Aortic Valvuloplasty to treat AS.
*Balloon expandable stent/valve for symptomatic patients with severe/critical AS who are inoperable or have high surgical risk: COPD, porcelain aorta, prior LIMA underlying sternum. *Transfemoral or transapical approach. *Recent FDA approval; ongoing clinical trials for high risk patients. *Results: -High success: 95% -30 day mortality: 10% -One year mortality or re-hospitalization: 42.5% -In hospital stroke rate: 3.3% -Need for PPM: 5.9% -Major vascular injury: 6.7% -Procedural learning curve >135 cases predictor of improved survival. |
