Valvular Heart Disease Flashcards
Pressure vs time graph: atrial contraction
- Raises left atrial and left ventricular pressure
- “a” wave on pressure tracings, LV volume curve
- “A” wave on mitral valve flow
- S4 occurs at or just after peak flow velocity
- Associated with cardiac diseases reducing LV compliance or attenuate LV filling during early diastole
- Get increased amount of filling with atrial contraction → increased amount energy expended → sound
Pressure vs time graph: Isovolumic contraction
- LV pressure rises
- Mitral valve forced shut after LV pressure > LA pressure
- Closure of mitral valve = “C” wave on LA tracing
- Responsible for S1
- When LV pressure > aortic pressure → open aortic valve (end of isovolumic contraction)
Pressure vs time graph: ejection
- Aortic and ventricular pressures track together
- Left atrium is filling
- Initial decline of pressure (“x”) during relaxation
- Slow rise in pressure
- Peaks at “V” wave near end-systole
- LV pressure falls
- When LV Pressure < atrial pressure → aortic valve closes
- S2
Pressure vs time graph: diastolic rapid filling
- LV actively relaxes
- LV pressure < LA pressure → creates suction
- Result: rapid blood flow into LV; decreases pressure in LA (“y”)
- Rapid increase in LV volume (70% filling)
- “E” wave in mitral valve flow
- S3 due to increased volume of blood flow during rapid filling from high output state or volume overload; or due to conditions that increase LA V-wave pressure
Pressure vs time graph: Diastasis
Passive filling
• LA and LV pressures in equilibrium
• Minimal LV filling
• Length of diastasis depends on heart rate
Causes of heart murmur production
o Turbulent flow
o Abnormal vortices of flow
o Audible vibrations
o High pressure gradient = high flow velocity → high pitched murmur
o Low pressure gradient = low flow velocity → low pitched murmur
Types of heart murmurs
Systolic murmurs
1) Mid-systolic ejection murmur
• Produced by flow leaving ventricle
• Begins after LV Pressure > aortic pressure
• Increases intensity as ejection velocity increases
• Diminishes before end of systole
2) Holosystolic regurgitant murmur
• From backward flow from high to low pressure chamber
• Pressure gradient maintained throughout systole
• Constant intensity throughout
• Ex. Mitral regurgitation
Diastolic murmurs 1) Regurgitant murmur • Backward flow across incompetent semilunar valve • Decrescendo shape o Pressure gradually drops in vessels during diastole o Reduces pressure gradient • Ex. Aortic insufficiency 2) Filling murmur • Obstruction of filling of ventricles • Low pitched • Dual component: loudest when filling velocity is highest (early diastole and atrial systole) • Ex. Mitral stenosis
Causes of Aortic Valve insufficiency (aortic regurgitation)
Primary cusp abnormality
• Rheumatic → fibrosis and commissural fusion
• Degenerative
• Endocarditis → direct leaflet destruction
• Congential (bicuspid)
Primary aortic root abnormality
• Ascending aortic aneurysm (dilates valve)
• Aortic dissection (acute problem)
Pathophysiology of Aortic Valve insufficiency (aortic regurgitation)
o State of volume overload
o Increased afterload and preload → increased wall stress end- systole and end-diastole
o LV can’t compensate with increased ventricular ejection because afterload doesn’t fall
o Result: Frank-Starling Mechansim:
• LV chamber enlargement
• Filling curve shift to the right and downward → improved ventricle filling due to increased chamber compliance
• Initiated by mechanical stretch signal:
• Matrix metalloproteinases dissolve fibrous skeleton and reorient
• Myocytes elongate = eccentric hypertrophy (increase number of contractile units in series)
-Chronic compensated: systolic and diastolic wall stress about normal
-Chronic decompensated:
• LV volume increases
• Increased fibrosis → less compliance
• Systolic performance declines → heart failure
Hemodynamics of Acute Aortic insufficiency
- Sudden volume overload in LV
- Limited ability to dilate to accommodate → total stroke volume rises only a little and net forward stroke volume falls
- HR increases to compensate for decreased SV
- Increased LV diastolic pressure, causes increase in LA pressure
- End-systole: central aortic pressure falls rapidly
- Due to aortic regurgitation
- LV pressure falls to zero, but fills rapidly
- Combined flow from LA and aortic insufficiency
- Rise in LV pressure
- Reaches equilibrium with LA before end-diastole (c)
- Forces mitral valve shut as LV pressure > LA
- No further blood flow across mitral valve
- LA does not empty completely → increase in pressure as blood returns from lungs
- LA contraction against closed mitral valve
- No effective forward flow during atrial systole
- No flow until next diastole
- Murmur
- High-pitched decrescendo (g)
- Begins end-systole, rapidly declines to nothing
- Amplitude proportional to pressure gradient
- Also, a systolic ejection murmur (h) from turbulent flow across aortic valve
- Acute treatment: surgical correction
Hemodynamics of Chronic Aortic insufficiency
- Gradual development allows accommodation and LV remodeling
- Large chamber with low diastolic pressures
- Normal heart rate
- Near normal effective CO
- Near normal net forward stroke volume
- Aortic pressure declines from end-systole to end-diastole at greater rate than normal
- But no equilibrium between aorta and LV occurs
- LV systolic pressure is elevated from large stroke volume
- LV diastole pressure near zero
- LA pressure near normal
- Mitral valve flow normal
- Very large pulse pressure (aorta pressure rises and fall rapidly)
- Murmur
- Throughout diastole
- Decrescendo-type
Hemodynamics of Chronic Decompensated Aortic insufficiency
- Heart larger but decreased systolic function
- Increased end systolic volume
- Similar stroke volume but elevated diastolic filling pressures
- Symptomatic dyspnea
Progression of aortic insufficiency
o Long period = asymptomatic (chronic compensated)
o If LV function is normal, then low (1-2%/year) conversion to symptomatic limitation/LV dysfunction
o If LV dysfunction (LV EF 25% per year
o Once symptoms: mortality rate is >10% per year
Treatment of aortic insufficiency
Prevent symptoms with exercise:
o Induces vasodilation → reduces ejection impedance
o Increases heart rate → reduces diastolic time so less time for insufficiency to occur
Treatment BEFORE symptoms arrive
o Optimally preserves LV function
o Monitor LV size and insufficiency severity by echocardiography
o Usually = valve replacement, sometimes repair
o Successful surgery → regression of hypertrophy
Causes of Aortic stenosis
o Calcific degeneration of valve: nodules of Ca2+ → stiffening
o Rheumatic heart disease: fusion of leaflets
o Congenital heart disease (bicuspid valve)
• Asymmetric leaflets
• Increase stress and deterioration → calcification
Pathophysiology of Aortic stenosis
o Mechanical shear stress (most important)
o Genetic predisposition
o Injury-inflammation cycles:
• More severe response in those with lipid abnormalities or coronary artery disease risk factors
• Atherosclerosis (but no evidence of benefits from statins)
• Multiple pathways for production of Ca2+ (ex. Osteoblasts)
Progression of Aortic stenosis
Symptoms develop when about 25-33% of normal opening
Normal:
valve area of 3.5-4.0 cm2
mean gradient: 0 mmHg
Mild:
valve area of 1.5-2.0 cm2
mean gradient: 40
symptoms: angina, dyspnea, and exertional syncope; most symptomatic
Severe:
valve area of 50
symptoms: angina, dyspnea, and exertional syncope; most symptomatic unless sedentary
Symptoms of aortic stenosis
Exertional angina • Subendocardial ischemia • Increase in O2 demand due to: • LV hypertrophy • Increase in systolic pressure • Prolongation of ejection time • Reduced perfusion from suboptimal capillary structure and elevated diastolic pressures Exertional syncope • Inadequate rise in CO → underfilling of vasculature • Bezold-Jarisch reflex • Due to high pressures in LV • Results in decreased contractility and HR, further vasodilation Dyspnea on exertion • Diastolic dysfunction • Systolic failure
Treatment of aortic stenosis
Medical Treatment
o Avoid heavy exertion and competitive sports if moderate or greater AS severity
o Maintain sinus rhythm
o Alert patient for symptoms to watch out for
o Follow up echocardiogram in asymptomatic patients
• Mild: every 3-5 years
• Moderate: every 1-2 years
• Severe: every year
o Symptomatic patients → surgery
Surgical treatments
o ALL symptomatic patients should be considered
o Best outcome: with normal LV function
o Asymptomatic patients, consider surgery if:
• During other CV surgery
• With symptoms and hypotension during exercise stress test
• With LV dysfunction (LV EF <50%)
• Marked LV hypertrophy
• Critical reduction in valve area
Hemodynamics of Aortic stenosis (as increase in severity)
Systolic pressure drop (shaded region)
• Area of region = mean pressure across the aortic valve
• Increases as stenosis becomes more severe
• Shape changes (aortic pressure rate of increase rises more slowly)
Murmur
• Diamond shaped ejection murmur
• Mild stenosis: peaks in mid-systole
• More severe: prolonged (peaks later in systole)
• Pitch usually increases as well
Second heart sound
• Calcification of valve → stiffens leaflets, less motion → decreased sound intensity
Compensatory LV changes with aortic stenosis
o Pressure overload → concentric LV hypertrophy
o Myocytes increase number of contractile units in parallel
• Thicker, more powerful cells
o Maintains near normal end-systolic wall stress
o Energy efficiency is improved (reduced Vmax, lower dP/dt)
o Downside:
• Coronary flow is impaired
• Decreased active relaxation rate
• Decreased extent of relaxation
• Filling pressures go up
Compensatory LA changes with aortic stenosis
o Elevated LV pressures → elevates LA pressures → LA hypertrophy
o Atrial contraction more powerful → higher velocity → S4
Types of dyspnea
• Exertional
• Orthopnea
o Develops in recumbent position; relieved if elevate head
o Due to heart’s inability to handle fluid that pooled in lower extremities and now gets returned back to central circulation
• Paroxysmal nocturna
o Same mechanism as orthopnea
o More severe and prolonged
• Pulmonary edema
o Most severe
o Flooding of alveoli
Describe the sequence of events that take place in the alveoli as left atrial pressure rises
• LA pressure rises due to:
o Aortic stenosis → diastolic myocardium abnormalities
o Aortic insufficiency → volume overload
o Mitral valve disease → stenotic obstruction of forward flow or leaflet insufficiency
• Results in increased pulmonary venous pressure
• Increases pulmonary capillary pressure → increase in interstitial lung fluid (capillary leakage and increased total volume in lungs)
• Increased lung stiffness
• Closure of some dependent airways
• Result: reduced tidal volume and increased effort
• Need more breaths/minute at higher effort level → SOB
• Eventually: alveoli collapse and flood → no gas exchange
Common causes of mitral stenosis
• Common cause: rheumatic fever
o Fusion of mitral apparatus
Pathophysiology of mitral stenosis
o LV inflow obstruction
Symptoms:
• Dyspnea from high filling pressures
• Hemoptysis: hemorrhages in pulmonary vasculature from increased pressures
• Fatigue from decreased CO
LA is enlarged
• Atrial fibrillation → sluggish blood flow
• Thrombus formation with embolism
RV and RA may become enlarged and dysfunctional later in disease
Hemodynamics of mitral stenosis
o Diastolic pressure gradient from reduced valve opening
o LV pressure normal
o Aortic pressure normal
o LA pressure continually elevated
o Results in severe pulmonary HT
• With increased pulmonary vascular resistance → RV hypertrophy
Heart sounds
1) Increased amplitude of S1
• When stenotic but pliable valve
• Snaps shut → increase in sound amplitude
• With calcification → decreased mobility → decreased amplitude
2) Opening snap
• Early in diastole
• Opening of valve = rapid filling stretches leaflets out
• Snap occurs when taunt leaflets reach peak of opening
• Calcification decreases snap
3) Diastolic rumble
• Low-pitched (relatively small gradient)
• Two part murmur:
• Mid-diastolic: initial part; occurs after opening snap (diastolic flows greatest)
• Decrease in murmur sound in mid-diastole (lower flow gradient)
• Late diastolic/ pre-systolic part: due to atrial contraction, only occurs with sinus rhythm
• ***Murmur amplitude is proportional to CO
Treatments of mitral stenosis
o Balloon valvuloplasty o Open surgical commisuratomy o Mitral valve replacement o Anticoagulation o Prevention of pulmonary HT
Progression of mitral stenosis
Minimal: Valve area: > 2.5 cm2 Mean gradient: 0 mmHg Peak PA pressure: WNL mmHg Symptoms: none
Mild: Valve area: 1.5-2.5 cm2 Mean gradient: 10 mmHg Peak PA pressure: >50 mmHg Symptoms: dyspnea with minimal exertion, orthopnea, paroxysmal nocutrnal dyspnea, fatigue
Severe + pulmonary HT:
Valve area: 10 mmHg
Peak PA pressure: >70 mmHg
Symptoms: decreased dyspnea, increased fatigue, increased fluid retention
Causes of Mitral Insufficiency
o Leaflet substance loss (ex. Due to rheumatic heart disease) o Excess substance • Too large → mitral valve prolapse with myxomatous degeneration o Loss of annular contraction o Leaflet destruction o Chordal rupture (flail valve) o Papillary muscle dysfunction o Annular stretch from LA enlargement
Pathophysiology of Mitral Insufficiency
o State of increased preload and reduced afterload for LV
o Dilation (eccentric remodeling and hypertrophy) → Increased LV volume at end diastole
o More complete EF → Decreased volume at end systole
o Supranormal LV function when well compensated
o Deterioration → progressive increases in both end diastolic volume and end systolic volume
Hemodynamics of Acute Mitral Insufficiency
(ruptured chordae tendinea or papillary muscle, or endocarditis)
• Small LA can’t accept large volume of blood → increase in LA pressure (v wave)
• LA pressure lowest during isovolumic relaxation (p)
• LA pressure not at zero = preserves LA/LV pressure gradient in diastole
• LV rapid filling → S3
• Fast equilibrium of LA and LV; pressures rise further after atrial contraction (q)
• End systolic volume is reduced in compensation to increased contractility
• Murmur: systolic, peaks early in systole, diminishes before end-systole
Hemodynamics of Chronic Mitral Insufficiency
- LV is enlarged, more compliant
- Diastolic pressures near normal
- Sinus rhythm
- Prominent a wave from atrial contraction (s)
- Systolic atrial pressures increase (t) from regurgitation
- Produces large gradient between LA and LV
- Causes rapid filling of LV
- Prominent S3
- Rapid equilibrium occurs in mid-diastole
- Murmur: holosystolic
- Constant amplitude since gradient is maintained
Hemodynamics of Chronic Decompensated Mitral Insufficiency
- Weakened LV can’t contract as well
- End-systolic volume increases
- Forward stroke volume is reduced
- Increased regurgitant volume present
- Normal EF from favorable loading conditions
- But decreased LV function
- LA and LV pressures high
Pulmonic stenosis
Cause:
o Congenital (almost all)
o Rheumatic disease or carcinoid syndrome
Pathophysiology:
o Pressure overload
o In utero: stimulates myocyte hypertrophy and hyperplasia
• Allows longer/better compensation
• Valve grows proportionately with body = degree of stenosis remains stable
• Calcification is rare
o Acquired: poorly tolerated, high wall stress
Symptoms:
o Fatigue from reduced CO
o Dyspnea with exertion
• Poor CO → poor perfusion of chest muscles → lactic acidosis → dyspnea
Treatment
o Patients with moderate or severe gradients (>50 mmHg)
o Balloon valvuloplasty is procedure of choice
o Alternative: surgery
Pulmonic valve insufficiency
Causes:
o Usually with other congenital abnormalities or secondary to balloon valvuloplasty or surgery
o Commonly from dilation of pulmonary artery
Pathophysiology:
o Isolated pulmonic insufficiency rare
o Usually not a significant problem because pulmonary system at low pressures
o Likely makes RV dysfunction progress faster if occurs with existing pathology
Tricuspid Stenosis
Causes:
o Almost all acquired from rheumatic valve disease
o Alternatively: Carcinoid disease
Pathophysiology:
o Similar to mitral stenosis but smaller pressure gradient
o Reduces CO response to exercise
o If severe: reduces CO at rest and increases RA pressure
• Venous congestion
• Fluid retention → edema and fatigue
o If untreated → progressive fatigue and symptoms of low CO
• Progressive fluid retention
• Liver congestion
• Edema
• Eventually → cardiac cachexia
Treatment
o Valvular commissurotomy
o Valve replacement
Tricuspid insufficiency
Causes: o Most commonly from annular enlargement and RV dysfunction o Trauma o Carcinoid and rheumatic disease o Congenital causes
Pathophysiology
If mild to moderate:
• Well tolerated for decades
If severe:
• Changes similar to chronic mitral insufficiency
• RA and RV enlargement
• Increased central venous pressure
• Eventually → RV failure
• Well tolerated if normal RV systolic pressures
• If pulmonary HT, RV fails at faster rate
Symptoms
o Fatigue
o Fluid retention
Treatment
o Valve repair
o Sometimes valve replacement
Explain the effect of infective endocarditis on valve function, signs of endocarditis and principles of prevention as defined by national guidelines
Pathophysiology
o Diseased valve with disrupted endothelial surface
o Sterile fibrin platelets thrombus forms on valve (vegetation and endothelial damage)
o Valve infected
• Local tissue destruction → valve regurgitation, abscess, pericarditis, fistula formation
• Embolic events → cerebral, systemic, pulmonary
• Immune complexes → arthritis, nephritis
Typical endocarditis organisms o Strep viridans o Strep bovis o Strep faecalis o Other strep o Staph coagulase + and – o Gram negative, fungal and culture negative
Diagnose: using Duke Criteria (because non-specific symptoms of fever, fatigue, heart failure)
o Blood cultures
o Evidence of valve involvement (new regurgitation, echo)
o Predisposition (ex. Certain cardiac conditions or injection drug-use)
Treatment
o Some cured by antibiotics with modest valve damage
o Others need valve surgery
AV Repair/Replacement
Repair:
• Annular dilation repair (associated with aortic aneurysm)
• Bicuspid valve without calcium → make seal
• Perforation (typically from endocarditis) → patch leak
Replace Valve:
Porcine valve
o Aortic valve from pig mounted on stent of polypropylene or wire
o Non-thrombogenic, no long-term anticoagulation
o Poor hemodynamics, progressive calcification and tissue failure
Stentless Porcine Valves
o Intact porcine valve or entire aortic root
o Better hemodynamics
Homografts
o Cyropreserved human aortic roots
o Procedure of choice for endocarditis complicated by abscess
o Technically challenging, hard to judge durability
Autografts
o Replaces aortic valve with patient’s own pulmonic valve; inserts bioprosthesis for pulmonic
o Long and difficult operation
o Long-term = degeneration
Mechanic valves
o Both single and double leaflet types
o Double leaflet typically have better flow profile
• St. Jude = most commonly implanted mechanical valve
o Excellent durability
o Risk of thrombosis → must take warfarin
• Pathologic processes of late failure of tissue-derived valves:
o Fibrous thickening of leaflets
o Tissue overgrowth with leaflet retraction
o Collagen disruption
o Leaflet tears
o Leaflet calcification
o Infection
** degeneration = greatest cause of failure for bio valves
**tissue overgrowth and thrombosis = for mechanical valves
