Systole: Isovolumetric Contraction LV pressure rises above aortic pressure causing aortic valve opening and rapid ejection

n S1 = Mitral/Tricuspid Valve Closure o Start of Systole S2 = Aortic/Pulmonic Valve Closure o End of Systole (beginning of diastole) Diastole: Isovolumetric Relaxation LV pressure rapidly falls below LA casing mitral valve opening and rapid filling diastisis (less rapid) atrial systole S3 = during rapid filling phase in early/mid diastole S4 = Coincides w/ LA contraction (after depol.) [stiff ventricle] Pressure Volume (PV) Loop: Mitral valve closure Isovolumic Contraction Aortic Valve Opening Rapid Ejection & Reduced Ejection Aortic Valve Closure Isovolumic Relaxation Increased Decreased EDPVR Preload EDV moved to right EDV moved to left ----Contractility Increased Slope Decreased Slope ----Afterload ESV moves to Right ESV moves Left (Increased SV) ----Pressure Overload ECM & ----EDPVR shifts down Compliance Volume Overload ECM & ----EDPVR shifts up Compliance Frank-Starling = Preload SV & Preload SV LaPlace Relationship = Wall stress Pressure & radius of Ventricle; Wall Stress Wall thickness

Valvular Heart Disease Etiologies: Congenital (Bicuspid AV), Genetic (Marfans prolapsed or aortic insufficiency [AD of Fibrillin-1]; Bicuspid AV [25% familial]; Systemic Inflammatory disease [rheumatic heart disease, syphilis, rheumatic arthritis, ankylosing spondylitis]; Infective Endocarditis; Carcinoid) Aortic Regurgitation/Insufficiency Pathophysiology: o Both Volume & Pressure Overload (Ventricle Size Pressure to maintain SV) o Systole = Blood flows out of ventricle into aorta o Diastole = blood flows back into left ventricle (instead of aortic valve remaining closed) o LVEDV Engages Frank-Starling Maintain SV by pumping more blood out Causes: Valve Leaflets (IE & Rheumatic Heart Disease) or Dilation of Root of Aorta (Aortic aneurysm & syphilis) o Acute = Aortic Dissection or Endocarditis Acute AR: o Causes = IE, Aortic Dissection, & Trauma o Pathophysiology = Ventricle has no time to compensate volume overload LV Pressure LA Pressure Not enough time for LV to compensate Shift EDPVR Curve up LVEDP & LAP Volume Increase LV Doesnt Compensate ESV & EDP o Presentation = Critically ill (typically a surgical emergency) Murmur is short (LV pressure rises in diastole & eventually equals aortic pressure [no gradient, unlike chronic] Normal Pulse Pressure) Very Sick (pulmonary edema, SOB, fever/chills/weight loss (endocarditis), severe tearing chest pain (dissection) Hard to diagnose by PE (SV not as big, heart not as enlarged, no widened pressure or decrescendo murmur) Diagnosed based on echo o Treatment = often requires urgent surgical valve replacement o EDPVR = Shifts to the right (no time to shift up or down; steeper portion of EDPVR EDP) Chronic AR: o Pathophysiology = Compensated = LV Volume & LV Compliance Downward EDPVR Shift Pressure maintained near normal Asymptomatic) LV compensates by Dilation & Eccentric Hypertrophy (Volume Overload) LVEDV, SV remains constant, ESV remains constant, LVEDP remains same, LAP remains same; aortic pressure changes a lot

 Asymptomatic phase Marked LV dilation w/ constant pressure Decompensated = Enlarged heart demands unable to be met Contractility Symptoms & EDP Myocardial dysfunction triggers symptoms Mortality becomes significant LVEDP & LAP; Significant ESV; EDP o PV Loop = Initial: Volume EDV (shift to right) Forward Output Slightly (due to regurg.) BP Slightly Afterload Slightly Compensation: Curve Shifts (from ventricle compliance) Volume Overload ECM Ventricle Competence EDV doesnt result in significant Pressure (due to PV shift) Some sympathetic vasoconstriction & Slightly Contractility ESV remains normal Decompensated: Contractility curve shifts Down ESV & EDV Loop shifts right & Pressure o Wiggers Diagram = Compensated: Aortic pressure falls in both systole & diastole Decompensated: LVEDP LA Pressure; Pulse Pressure (SV Systolic pressure); Diastolic pressure (due to regurgitation) o Presentation/Signs/Symptoms = Murmur occurs (early/immediate Diastole right after valve closes/S2) Decrescendo Murmur (loudest initially); Stenosis (murmur when valves open); Regurgitation (murmur hen valves closed) Backwards HF = Volume Overload (dyspnea, orthopnea) Forward HF = Diminished Output (Fatigue) Palpitations (normal rhythm due to Pulse Pressure) Angina = Diastolic Pressure & O2 requirements from dilated LV (coronaries perfused in diastole) o Severity = Size, Pressure Gradient across aortic valve in Diastole (BP regurg.), duration of diastole (tachycardia may be beneficial) o Treatment = Asymptomatic w/ preserved LV Fx= Nothing Asymptomatic (preserved LV Fx) + HTN = Vasodilators Asymptomatic w/ LV Dysfunction (ESV or EF) = Surgery referral Symptomatic = Referral for Surgery Mitral Regurgitation/Insufficiency Etiologies = Annulus (supporting fibrous structure), Posterior Leaflet (thinner), Anterior Leaflet (broader), Papillary mms, Chordae Tendinae Pathophysiology: o Only volume Overload (LA acts as low pressure route during LV ejection to mask LV dysfunction) o Systole = Blood ejected into aorta (normal) as well as LA (regurgitation) o Diastole = Blood ejected backwards into LA again fills LV LVEDV Engages Frank Starling maintain SV by pumping out more blood (b/c a fraction flowing back into LA) o LVEDV Engages Frank-Starling Maintain SV by pumping more blood out Diagnosis: May measure with Echo; Measure ERO (effective regurgitant orifice) estimate of size of ole or defect (pts w/ small ERO fine without valve replacement Acute MR: o Causes = Infectious Endocarditis Organic MR (Leaflet, chordae tendinae, or papillary mms rupture) Chronic: MV prolapse, rheumatic heart disease, dilation of annulus (Marfans) Acute: sudden tear in valve support structure or leaflets Functional MR (problem with LV annulus dilation; valve leaking due to LV problem [e.g., CM or altered geometry from previous MI]) Ischemic CM = due to MI involving posterior wall (annulus dilation or altered papillary mms geometry) If leaflets close above annula plane tenting leak/regurgitation o Pathophysiology = Ventricle has no time to compensate volume overload LV Pressure LA Pressure LAP, LVEDP No compensatory phase Volume manifests as ESV, LAP, LVEDP o Presentation = Very symptomatic

Pulmonary Edema, BP, HR Endocarditis (most common underlying cause): hole in valve or rupture or papillary mms; weight loss, fever, bacteria in bloodstream AMR (one of chords ruptures) Ischemic Disease (MI ruptures papillary mms) Very Sick with very high intra-pressures o Treatment = Chronic MR: o Pathophysiology = Compensation = LV Volume & LV Compliance Downward EDPVR Shift Pressure maintained near normal Asymptomatic) Decompensation = Demands of enlarged heart unable to be met Contractility Symptoms & EDP Big LA & LV LV has time to remodel Symptoms are gradual onset o Severity = Size, LA pressure, LA compliance (resistance to backward flow; LA compliance regurg.), SVR (resistance to forward flow; SVR Regurg.) o Presentation/Signs/Symptoms = Prolonged asymptomatic phase (compensated by LVEDV & LA Size) LA Compensation = Dilation w/ accommodating Volume w/ LAP LV Compensation = Dilation w/ hypertrophy LVEDV w/ near normal LVEDP Decompensation (LVEDP & LAP) = Symptoms (after myocardial Dysfunction Sets in) Holo-Systolic (pan-systolic Murmur) Severity increases when SVR (resistance increases to aortic root more blood flows into low pressure route into LA) S3 Murmur (Volume of Blood) CO (fatigue & Weakness) Volume Overload (dyspnea & Orthopnea) LA Dilation stretches myocytes Propensity for arrhythmias (i.e., atrial fib.) o PV Loop = Compensated MR: EDV, Afterload, ECM, Compliance PV curve shifts down Decompensated MR: ESV, EDP, LAP Marked by Contactility ESV Shift Curves to Right Pressure o Wiggers Diagram = Compensated MR: Regurgitation into LA LA Pressure through all of Systole Prominent v Wave = c & v waves merge together Murmur starts at closure of Mitral Valve (S1) & continues through systole to aortic closure (S2) Holosystolic Murmur o Treatment = Vasodilators useful but dont delay surgery (not clinically useful) & Surgery (symptoms or LV dysfunction) Mitral Valve Replacement (due to regurgitation from MV prolapse) one of 2 most common valve procedures in US

Aortic Stenosis Etiology: o Degenerative (older people senile aortic stenosis) o Rheumatic (anyone & any valve) o Congenital (bicuspid typically younger people, at risk for Aortic stenosis & regurgitation) Pathophysiology: o Left Ventricle pressure increases tremendously o Afterload does not directly depend on BP (exception; BP can be normal/low but afterload b/c interventricular pressure w/i left ventrical increases) o Pressure Overload o Concentric Hypertrophy (pressure overload) o Rheumatic valve-thick leaflets w/ commissures w/ central area that leaks Wiggers Diagram: o Systole = LVP much higher than aortic (stenosis) Pressure gradient all through systole o Instantaneous Gradient, Peak instantaneous gradient (max value), Peak-Peak Gradient (difference in highest LV & highest aortic pressures)

Peak LV & Peak Aortic pressures do not occurrence at same time (peak-peak gradient no physiological significance but correlates w/ severity of aortic stenosis) Mean gradient (gradient averaged through systole) Peak Instant. & Mean gradients measured non-invasively & invasively Non-invasive (echo, doppler velocity) Invasive (Catheters in LV & root of aorta; pull-back gradient to calculate LVP; simultaneous gradient using 1 catheter in aortic root and 1 in LV to calculate both)

PV Loop: o Significant afterload (interventricular pressure) PV Loop strikes slope at higher level ESV o Ventricle Hypertrophies Pressure Overload Ventricular Compliance EDPVR Curve moves upward o ESV Slight EDV shift in curve EDP for same volume Presentation/Signs/Symptoms: o Murmur occurs when valve is open (systole) Crescendo-Decrescendo Murmur = Diamond shaped murmur (LV pressure rises & then drops) Murmur doesnt start right at S1 (must pass isovolumetric contraction before you hear murmur) Ejection Systolic Murmur = Reaches peak intensity & dwindles before S2 o Delayed & Diminished Carotid Pulse = Aortic Pressure peaks later (delayed peak) than LV pressure & doesnt rise as much; max amplitude lower than normal o S4 = Ventricle Stiff (pressure overload & Hypertrophy) o Mid (Ejection) Systolic Murmur (Crescendo-Decrescendo) o Later Stages = diminished/absent aortic component of S2 (severe calcifiv\cation of valve) o Severe AS Signs = Delayed/diminished carotid pulse, late peaking murmur (higher pressure gradient from LV), Absent A2 (calcified) o Symptoms = Angina (survival 5 yrs; O2 demand from mms mass or wall stress; EDP O2 supply); Syncope (survival 3 yrs; exertional; CO cant b/c of fixed stenosis; SVR LV baroreceptor mediated vasodilation); HF (survival 2 yrs; w/ systolic dysfx 6 months; EDP Diastolic HV; Contractility (systolic dysfx) later stages) o ECG = Left ventricular hypertrophy, significantly voltage in precordial leads; T-wave inversion; abnormal repolarization (LV mass) Treatment: o Main Method = Fix Stenotic Valve (AVR vs. valvuloplasty) Consider fixing when there are symptoms or signs of myocardial dysfx Valvuloplasty: Percutaneous (try to separate leaflets w/ balloon through aortic valve); for people who cant undergo surgery or temporary measure o Avoid Atrial fib. (stiff ventricles more dependent on atrial kick during diastole), Exercise (fixed CO), in preload or afterload (i.e., vasodilators, nitroglycerin, diuretics) o Statins (since AS similar to atherosclerosis) o AV Replacement due to AV stenosis from calcific degeneration due to aging (one of 2 most common valve surgeries in US) Mitral Stenosis Etiology: Mostly rheumatic heart disease; some congenital MS or Infectious Endocarditis; pediatric congenital stenosis Pathophysiology: o Sudden worsening w/ atrial fib. or increased demands (e.g., labor) HR or Blood flow requirements Doesnt happen in AS b/c HR shortens Diastole (MS more dependent on prolonged Diastole) Exercise, high-output conditions (pregnancy, fever, anemia, thyrotoxicosis), atrial fib w/ RVR) o Disease of Plateaus (dont decline as rapidly as patients w/ AS) o LA is affected chamber b/c there is pressure gradient btw LA & LV LA volume & LA pressure (LV is unaffected) LAP Pulmonary circulation Dyspnea, orthopnea, pulmonary edema (can cause pulmonary HTN Pressure overload of RV RV HF) o Problem = Diastolic filling PV Loop: o Not that useful for MS b/c LV is not affected Mainly takes place in atrium o Less blood coming into LV SV EDV Afterload Slight shift of curve to the left Presentation/Signs/Symptoms: o Diastolic Murmur (mid-diastolic rumble) May decrease in intensity at end of Diastole Pre-Systolic Accentuation = May have accentuation when atria Contracts (only occurs when pt is in normal rhythm & has an atrial contraction; if in atrial fib. this cannot happen)

o o o o

Opening Snap (during time w/ opening of mitral valve due to tensing of chordae) Mild MS = Mid-diastolic Murmur that disappears later during Diastole (due to pressure gradient btw LA & LV disappearing during diastole) Pre-systolic accentuation Severe MS = Gradient remains all throughout Diastole Murmur is present throughout Diastole w/ presystolic accentuation Valve opens earlier b/c LA pressure is higher Snap Occurs earlier Signs = Loud S1 (closure of Mitral valve due to pressure gradient opens wider & remains open for greater distance at end of diastole snap closed at beginning of systole), Opening Snap, Mid-Diastolic Rumble, presystolic accentuation in sinus rhythm Severe Stenosis: Shorter S2-OS Interval (higher LA pressure) & longer duration of mid-systolic murmur Symptoms = LA Pressure (Dyspnea & diminished exercise tolerance), PA Pressure (Pulmonary HTN [all develop passive pulmonary HTN but not all develop reactive], RVH, RV failure hepatomegaly, JVP, ascites), underfilled LV, CO, LA size (can cause atrial fib & risk for clot), Hemoptysis (LAP bronchiole veins rupture), Hoarseness (pressure on recurrent laryngeal nerve by enlarged LA or enlarged pulmonary artery) ECG = Evidence of LA enlargement & RVH (late stages) V1 = P wave deep and wide w/ small positive component & wide/deep neg. component V5 & V6 = Right Axis Deviation & Prominent S Waves (from RVH)

o Treatment: o Main Tx = Fix the Stenosis (Percutaneous valvuloplasty) o Medical Therapy = Diuretics (control pulmonary HTN), Prevent HR, Prevent clots w/ anticoagulation Mixed Lesions AS + MR Pressure Overload & Volume Overload Make it wors AR + AS Mitral Valve Prolapse Etiology: Annulus dilation, leaflet floppiness, or chordae rupture Pathophysiology: leaflet closes behind mitral annula plane (prolapse from floppy cords or leaflets) or valve dips back into LA (cord rupture Flail mitral leaflet) o Posterior leaflets are much easier to repair than anterior (mostly have to replace anterior prolaps) Echo Studies (severity of regurgitation) MVP-Valve Disorder: o Connective Tissue Disorder (either sporadic or familial [AD w/ low penetrance; e.g., Marfans w/ other issue involvement like AV]) o Other valves (mainly Tricuspid & sometimes AV) may be involved o Often Benign (does not need to be treated, just monitored) o Click & Murmur (mid-late systolic murmur w/ minimum or no mitral incompetence) o Severe Mitral Incompetence (often older men) = classic mitral incompetence murmur (Holosystolic), LV enlargement, HF symptoms, arrhythmias (atrial fib.), embolic phenomena (sudden death rare unless enlarged heart & HF) Symptoms are late finding & usually due to HF or atrial fib. Gradual progressive process (sudden symptoms in chordal rupture, atrial fib. or endocarditis) Irreversible LV damage may precede symptoms (use ultrasound) MVP-Syndrome: No significant mitral incompetence o Slight click & short murmur o Autonomic Dysfunction o Younger People (mainly young women) o Benign Prognosis o Symptoms = palpitations, arrhythmias, fatigue, exercise intolerance Tricuspid Valve Disease Functional Tricuspid Regurgitation (common) = RV enlargement or RV Failure (MS) o RV Failure = Due to pressure overload (pulmonary venous HTN) commonly from LV failure or from pulmonary arterial HTN Organic Tricuspid Regurgitation or Stenosis (rare) = o Diagnosed by Hx o Carcinoid Syndrome (carcinoid tumor of small bowel) = Liver metastasis from high levels of circulating serotonin & metabolites) Valve thickening & retraction (both tricuspid &pulmonic) o Drugs giving Carcinoid Type Presentation:

Serotonin Agonists (receptor 5-HT2B) fibrosis & sclerosis of leaflets fusion of mitral & tricuspid chordae Most not used anymore (ergotamine, fenfluramine, pergolide, cabergoline, MDMA/ecstasy) Carcinoid typically right-sided Valve histopathology identical to carcinoid o Trauma: prolapse of tricuspid due to rupturing of chords or devices in LV (defibrillator wires stuck in valve) Rheumatic Heart Disease Cords are thick, retracted, & scarred Latent Condition, immunologic rxn to strep throat, valve condition is autoimmune Rheumatic Heart Disease = Mitral stenosis or regurgitation; can also involve aortic or tricuspid Late Valve Fibrosis from the acute inflammation (10-30 yrs after acute rheumatic fever or multiple infections over time) Reduced by antibiotics & hygiene Children w/ recurrent Strep Low dose penicillin prophylaxis Marfans Syndrome Relatively common AD, connective tissue disorder involving Fibrillin-1 gene (regulator of TGF-B causes hypertrophy & fibrosis) Systemic disease & Mitral Prolapse o May have: MVP, aortic aneurysm, aortic dissection, aortic incompetence (aorta reason for decrease life expectancy) Tall, thin, long fingers, lax joints, lens displacement Bacterial Endocarditis TEE diagnostic for Endocarditis (looks like mass or bulk on leaflet [vegetation]) Clinical Presentation: o Acute = fulminant onset; high fever, shaking chills (e.g., catheter infected w/ Staph aureus) o Subacute = less virulent organisms attack damaged & predisposed valves (insidious onset w/ fatigue, night sweats, myalgias, weight loss) o Peripheral Symptoms (due to septic or immune complexes throughout the body) = Stroke/TIA, flank pain/renal failure, pulmonary embolism, mycotic aneurysm, Janeway lesions (abscesses on skin), Oslers Nodes (painful raised lesions), splenomegaly Modified Duke Criteria: Dx from blood cultures & echo that show vegetation (major & minor criteria) Valve Disorder Treatments Percutaneous Procedures o Usually not curative symptomatic relief o May sometimes provide long-term relief for pulmonary & mitral stenosis Valve replacements o Usually not curative symptomatic relief o May sometimes provide long-term relief for pulmonary & mitral stenosis Stenotic Lesions (symptom onset precedes HF/death usually) o Interventions postponed until symptomatic