Valve disease

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Author:
cmatthews
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227758
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Valve disease
Updated:
2013-07-22 17:03:19
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BC CRNA Cardio Valves
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Summer 2013
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  1. Describe the AV valves
    • Mitral (only normally bicuspid valve)
    • Tricuspid
    • Closure is “soft”
    • Papillary muscles attach to valves via chordae tendineae
  2. Do the papillary muscles close the AV valves?
    • NO!! Contraction of papillary muscle isn’t what closes the valves (it’s back flow)
    • When ventricles contract papillary muscles also contract, pulls veins of valves in towards ventricle so backflow doesn’t push into the atrium
  3. What happens if the papillary muscle ruptures?
    Pap muscle dysfunction (rupture or paralysis of papillary muscle) if that happens the valve would push back to the atria (leak or failure)
  4. Describe the Semilunar valves
    • Aortic
    • Pulmonary
    • Semilunar are heavier, more backflow is needed for longer period of time for them to close.
    • “Snap closure” (Pressure in Aorta and PA are high, the valves snap close)
    • No chordae tendineae (Need to be strong and heavy but still pliable to handle stress of high velocity flow)
    • Openings of semilunar are smaller than those of AV valves. Because of the openings are smaller, velocity of blood going through those valves is greater, so they are subject to more mechanical abrasion.
  5. Area of the Aortic Valve
    2.5 -3.5 cm2
  6. Area of the Mitral Valve
    4-6 cm2
  7. NORMALLY, What is the pressure gradient and flow direction across a valve?
    Normally there is a low pressure gradient and unidirectional flow across a valve
  8. Describe Stenosis
    • Narrowed orifice from fibrosis with calcification
    • --↓ cross-sectional area
    • --Valve cusps fuse limiting opening
  9. What does Poiseuille‘s law have to do with stenosis of a valve?
    • Stenosis increases resistance to flow.
    • Resistance is inversely related to radius to 4th power so if the average valve radius is decreased by ½ the resistance is increased 16 fold.
    • A given flow rate of across the valve, greater resistance, greater pressure across the valve that’s required to drive the flow.

         
  10. What does Ohm's law have to do w/stenosis of a valve
    If resistance increases, we know pressure gradient (delta P) has to also increase in order for flow to remain constant

    • Q = Δ P
    •        R
  11. Describe the basics of insufficiency
    • Leaflets don’t seal completely
    • Regurgitation of blood into proximal chamber
    • Concentric Hypertrophy
    • Pressure Overload (From AS or MS)
    • Eccentric Hypertrophy
    • Volume Overload (from MR or AR)
  12. If delta P needs to increase, it's volume or pressure overload?
    • It’s pressure overload.
    • Regurgitant there is a volume overload
  13. What happens when there is pressure overload and concentric hypertrophy?
    • The ventricle will become stiff, compliance will decrease and diastolic filling will decrease.
    • This leads to decrease in SV and increase in EDP.
    • Changes in ESV depend on changes in afterload inotropy.
  14. What is the historically most common cause of valvular heart disease?
    Rheumatic Fever but because of antibiotics the incidence has declined substantially
  15. Does Rheumatic fever only involve the heart?
    No, It is an inflammatory condition. Can evolve, not just heart, but skin and connective tissue. Usually complication of URI. Usually caused by group A beta strep.
  16. What population usually gets rheumatic fever?
    young adults and children
  17. What is the cause of rheumatic fever and valve disease?
    Thought to be due to a toxin that’s produced by the strep or some sort of autoimmune cross reactivity between the bacterial and the cardiac antigens.
  18. How long do the antibodies persist in the body?
    Antibodies can persist for a year or more after the infection and during that time damage can continue
  19. Where does the inflammation from rheumatic fever take place in the heart?
    Inflammation can occur in all 3 layers of the heart (pericardium, myocardium and endocardium) This will then turn into fibrosis and scar tissue. The most significant things that happen are d/t valvular problems.
  20. Does the valve injury from rheumatic fever show up early or late?
    LATE, the patient may not show valvular disease for about 20-30years after the acute rheumatic fever has subsided.
  21. Is rheumatic fever autoimmune?
    yes
  22. What is the cause of rheumatic fever?
    • Streptococcal infection – usually group A
    • Sore throat
    • Scarlet fever
    • Middle ear infection
  23. Which valve(s) is effected by Rheumatic fever?
    Because the MV receives more trauma than other valves (just doing it’s normal job) it’s most seriously affected and the AV comes in second. Because the right heart pressures are lower, those two valves are less susceptible to damage
  24. Describe the changes to the valve in rheumatic fever
    • What happens over time the lesions will occur on adjacent valve leaflets and edges of those leaflets get stuck together, scar tissue forms and the adjacent leaflets get fused.
    • So that causes the stenosis (Narrow valve orifice) but at same time, as they fuse, the leaflets can’t close.
    • Opening not as wide as it should be but also can’t close.
    • Often a combo of MS and MR.
  25. So about __% of patients that develop rheumatic heart disease will develop MS. Additional __% will develop Aortic valve disease (AR or AS) in addition to MS.
    40%; 25%

    So for someone who has history, recurrence of acute rheumatic fever, that will cause more cardiac damage. Why we prophylaxis w/penicillin at least until early adult hood and the reason for that is that the exposure and susceptibility to strep has decreased
  26. Symptoms of ARF Jones Criteria (MAJOR)
    • Carditis
    • Polyarthritis
    • Sydenham chorea (involuntary movements)
    • Erythema marginatum(skin rash w/ advancing edge & clear center)
    • Subcutaneous nodules
  27. Symptoms of ARF Jones Criteria (Minor)
    • Migratory arthralgias
    • Fever
    • Increased acute phase reactants
    • --ESR
    • --CRP
    • --Leukocytosis
    • Prolonged PR interval
  28. Describe the acute phase of acute rheumatic fever
    • Carditis can be  associated w/tachycardia, decrease LV contractility, a pericardial friction rub.
    • Transient murmur of MR or AR.
    • May also be a mid-diastolic murmur at the apex. And those murmurs are d/t transient turbulent flow across those inflamed leaflets
  29. In order to diagnose acute rheumatic fever, what do we need to have?
    Dx: need evidence of strep infection and either 2 major criteria or 1 major + 2 minor
  30. What type of strep causes ARF?
    Group A beta strep
  31. If murmur occurs between 1st and 2nd heart sound it’s a __________ murmur
    systolic
  32. If a murmur occurs between 2nd and next 1st heart sound,it’s a _____ murmur
    diastolic
  33. In the pre-op Eval of your patient with valvular disease, what are you assessing and identifying?
    • Assessment of:
    • Severity of cardiac disease
    • Degree of impaired contractility
    • Presence of major organ system disease
    • Identification of:
    • Compensatory mechanisms (to maintain CO, increase in SNS and hypertrophy)
    • Current drug therapy
    • Prosthetic valve
    • *Important to get some information w/regard to exercise tolerance. Gives idea of what cardiac reserve is.
  34. These are the New York Heart Association Functional Classification, Describe each one

    Class I
    Class II
    Class III
    Class IV
    • Class I: asymptomatic
    • Class II: Symptoms with ordinary activity but comfortable at rest
    • Class III: Symptoms with minimal activity butcomfortable at rest
    • Class IV: Symptoms at rest
  35. For patients with heart disease, If myocardial contractility is impaired, get  dyspnea, orthopnea, easily fatigued.
    If they have compensatory mechanism of SNS (tachycardia, diaphoresis, anxiety) if that’s the case, that can precipitate ___________.
    CHF
  36. What are the causes of MS?
    • Rheumatic Fever (50% of patients)
    • Congenital
    • Calcification (elderly)
    • Endocarditis (in about 1% of cases of MS)
  37. What % of patients w/MS have RF?
    50%
  38. What % of pts w/MS have Endocarditis?
    1%
  39. What is the pathology of MS?
    • Thickening & calcification of leaflets
    • Fusion of commissures
    • Thickening & shortening of chordae tendineae
  40. What is the pathophysiology of MS?
    • ↓ Mitral valve orifice
    • ↑ Left atrial pressure
    • ↑↑LAP → ↓ SV
    • Occurs with ↑ HR
    • And/or AF
    • → ↑ pulmonary venous pressure → pulmonary edema
  41. When does MS become HD significant?
    when valve area is less than 2cm2.
  42. When the MS is mild, usually LV filling and SV are preserved at rest. Why?
    • Reason is because of increase in LAp.
    • Problem arises if stress induced tachycardia, less time for ventricular filling, so SV will decrease.
    • It’s also a problem if patient is no longer in SR and in A. fib because loss of effective atrial contractions will also decrease SV.
  43. In MS, what happens w/gradual progression of disease? What tips the patient into decompensation?
    • If the increase in LAp is more gradual, at least for a time the lymphatic drainage from lungs can increase and hold off development of pulmonary edema.
    • What will tip things over into decompensation, is things like A. fib. SNS stimulation (pain, sepsis, even pregnancy).
  44. Why does AF occur in MS?
    AF will frequently develop in patient, because of chronic pressure overload of LA, get LA enlargement. When LA dilates, it’s stretches the conduction fibers and the conduction system in atria is thrown off and so A fib will develop.
  45. Why is A. Fib such a problem w/MS?
    So A fib causes a problem w/CO in two ways, loss of atrial kick and the second is the tachycardia (usually has fast ventricular rate) so a decreased diastolic filling time. Vicious  cycle continues and further increases LAp
  46. Why do patients w/history of AF need to be anticoagulated?
    • Also, because atria are dilated, blood can stagnate (esp. in AF) pt is predisposed to thrombus formation.
    • Patients are frequently anti-coagulated in this circumstance
  47. Why is there vasoconstriction in MS?
    MS (Vasoconstriction is reflex) SNS stimulation can cause an increase in afterload so we end up w/combo of decreased preload and increased afterload that together contribute to LV dysfunction
  48. In the normal pressure volume loop, the EDV is ____  and the ESV is _____.
    • EDV = 120ml
    • ESV = 50ml
  49. Mitral Stenosis:

    __ EDV + __ ESV → __ SV
    ↓↓ EDV + ↓ ESV → ↓ SV


    • w/mod to severe MS, the ↓ in ventricular filling means a ↓ preload so the EDV and EDP are ↓.
    • That causes a ↓SV because of frank starling.
    • So ↓CO and ↓Aortic pressure. Because that (interdependence of loops) decrease in Aorta is a ↓afterload. Results the ↓ESV slightly.
    • But not enough to overcome the ↓EDV.
    • So net effect is a ↓ SV.
  50. With MS , blood passes through stenotic MV, from LA to LV, as pressure in LA rises above ___mmHg, there isn’t a large pressure gradient forcing blood into LV.
    30
  51. Describe the murmur heard in MS
    • Weak w/low frequency. Hard to hear.
    • NOT heard in 1st 1/3 of diastole!
  52. Why don't you hear MS murmur in the beginning of diastole?
    • During the early part of diastole, period of ventricular filling (not much blood in LV) can’t get through MV (stenotic) so 1st 1/3 of diastole, hard to hear not much blood reverberating around in ventricle.
    • Only after the ventricle is partially filled the blood can reverberate and produce rumbling sound.
  53. clinical presentation depends on how severe the MS is. What types of s/s would you see?
    • Early s/s: dyspnea, decrease in exercise capacity.
    • Then if the patient has severe MS, they will be dyspnic at rest
    • Show signs of pulmonary congestion, nocturnal dyspnea, pulmonary HTN, right heart failure, hepatomegaly, ascites, and peripheral edema
  54. If MS is really severe, the enlarged PA or LA can actually cause compression of ______
    recurrent laryngeal nerve (patient will sound hoarse)
  55. Why do you hear an opening snap early in diastole in MS?
    • On auscultation, opening snap heard in early diastole.
    • Actually caused by vibrations of stenotic valve that still has somewhat mobile leaflets, if calcified, not mobile at all, no opening snap.
  56. Which matters more, the duration or intensity of the murmur in MS?
    • It’s actually the duration of that murmur in diastole, not how intense it is that relates to the severity.
    • The longer it takes for blood to get to LA to LV the longer the stenosis and the longer the murmur.
  57. In MS, the rumbling diastolic murmur heard best at either ________ or ______
    Apex or Axilla
  58. What would you see on the CXR in MS?
    • Left Atrial Enlargement (may be seen as straightening of left heart border and elevation of left main stem bronchus)
    • Mitral calcification
    • Pulmonary edema or vascular congestion
  59. What would you see on the EKG of a patient w/MS?
    • broad and notched P wave (LA enlargement)
    • A. fib is seen in 1/3 of patients w/severe MS.
  60. What is the mean valve gradient (mmHg) and Mitral valve area (cm2) in MILD MS?
    • mean valve gradient = 6 mmHg
    • Mitral valve area = 1.6-2 cm2
  61. What is the mean valve gradient (mmHg) and Mitral valve area (cm2) in Moderate MS?
    • mean valve gradient = 6-10 mmHg
    • Mitral valve area  = 1-1.5 cm2
  62. What is the mean valve gradient (mmHg) and Mitral valve area (cm2) in SEVERE MS?
    • mean valve gradient = >10mmHg
    • Mitral valve area = <1 cm2
  63. In MS, the patient will usually become symptomatic if orifice size is decreased by __%.
    50%.
  64. If the area is less than __cm2 there is usually an associated transvalvular gradient of ________mmHg at rest and dyspnea on exertion.
    1; 10-20
  65. What is the normal transvalvular gradient across the MV?
    5mmHg
  66. Area less than 1cm2 is referred to as critical MS. If the pressure gradient across the valve is greater than 10, likely MS is severe, any additional stress (ex: Fever  or stress) could precipitate ____________
    pulmonary edema
  67. What is the treatment for MS?
    • Diuretics (for pulm. edema)
    • Beta blocker
    • Calcium channel blocker
    • Digoxin
    • Anticoagulation
    • Mechanical correction (Valve repair/replace)
  68. What is the target INR for a patient w/MS in A. fib?
    2.5-3
  69. Describe percutaneous valvuloplasty as MS treatment
    Balloon catheter advanced from fem vein to RA across atrial septum (create small septal defect) then pass the catheter through the narrow MV and balloon inflates and cracks the valve open.
  70. After percutaneous valvuloplasty for MS, what % of patients will have an  ASD?
    About 5% of these patient w/have persistent ASD as a result.
  71. After percutaneous valvuloplasty for MS, The estimated event free survival 7yrs after is _______%.
    67-76%.
  72. Why are BB, CCB, and digoxin good for a patient w/MS and A. fib?
    to slow ventricular rate to improve ventricular filling
  73. When would you perform mechanical correction of MS?
    Mechanical correction of MS if symptoms persistent or significant pulmonary HTN
  74. What is the overall goal for anesthesia in a patient w/MS?
    Goal: prevent or treat events that can ↓ CO or produce pulmonary edema
  75. Describe the intraoperative events with significant impact for the patient w/MS
    • ST or AF with rapid ventricular rate
    • Marked ↑ in central blood volume (Over-transfusion or Trendelenberg position)
    • Drug-induced ↓ SVR
    • Hypoxemia & hypercarbia(Exacerbates pulmonary HTN & Evokes right heart failure)
  76. Why is trendelenburg a bad position for the patient w/MS?
    Causes an autotransfusion
  77. What effect does pregnancy have on MS?
    In parturient, the patient having uterine contractions, just that can cause autotransfusion and precipitate CHF (Depending on how severe the MS is)
  78. Why is drug induced decrease in SVR bad for a patient w/MS?
    • For patient w/MS that rapid drop in afterload may not be tolerated. Because the way we compensate for decrease SVR and hypotension w/increase in HR and patient w/MS don’t’ want that because decreases diastolic filling time.
    • But a lot of our drugs will decrease SVR.
    • If we want to choose a drug treating decrease SVR (choose phenylephrine) increase tone but not increase HR.
  79. HD goals for a patient w/MS during anesthesia.
    Preload: 
    Afterload: 
    Contractility:
    Rate:
    Rhythm:
    MVO2:
    • Preload: Maintain, avoid hypovolemia; Not too full
    • Afterload: Maintain; Prevent pulmonary vasoconstriction (hypoxia, hypercarbia); Not
    • too tight
    • Contractility: Maintain;Usually intact. RV dysfunction may be a problem with long-standing pulmonary HTN; Not too strong
    • Rate: Maintain at low end of normal.  Avoid tachycardia; Slow
    • Rhythm: Keep ventricular response controlled in AF; Regular
    • MVO2: Not a problem
  80. What are the pros and cons of giving a sedative pre-op to a patient w/MS?
    • Pro = ↓ anxiety and associated SNS stimulation & tachycardia
    • Con = patient may be more sensitive to respiratory depressant effects
  81. What are our concerns regarding the chronic medications a patient w/MS is on? (aka what do we tell the patient to take or not take, etc. in pre-op)
    • Continue meds for HR control
    • Check & treat K+ (Don't want hypokalemia w/Digoxin)
    • Weigh risk/benefit of discontinuing anticoagulation
  82. What medications would we use or avoid during induction of anesthesia for a patient w/MS?
    • No ketamine
    • Others OK 
    • Select muscle relaxant to avoid CV side effects
    • ETOMIDATE is best!
    • Give Propofol SLOWLY!
    • Avoid HISTAMINE releasing drugs (esp. NMBlockers)
  83. For our patient w/MS & the maintenance of anesthesia, it's about how well we control HD, not what we use for anesthetics. Describe how you do this.
    • Minimize effects on HR, contractility, SVR, PVR
    • Low concentrations of volatile
    • Avoid nitrous oxide if pulmonary HTN present
    • Select muscle relaxant to avoid CV side effects (Slow, careful reversal & Avoid ↑ HR from antimuscarinic)AVOID Pancuronium.
    • Avoid “light” anesthesia (SNS stimulation)
    • Careful fluid replacement
  84. What kind of monitoring do we want for our patient w/MS?
    • Depends on:
    • --Complexity of surgical procedure
    • --Physiologic derangements from MS
    • If patient is asymptomatic w/no pulmonary congestion. Standard monitoring is fine unless procedure dictates more.
    • MS undergoing a major procedure especially if large amount of blood loss is expected. TEE A-line PA line
  85. What kind of care would we provide post-op to our patient w/MS?
    • Continue to monitor for pulmonary edema & RHF
    • Avoid SNS stimulation (Pain & Hypoventilation)
  86. What is the etiology of MR
    • Myxomatous degeneration (MVP)
    • Endocarditis
    • Rheumatic fever
    • Hypertrophic obstructive myopathy
    • Annulus calcification
    • Laundry list of other things (endocarditis, congenital, cardiomyopathy, systemic lupus, RA, and carcinoid syndrome)
  87. The leaflets so enlarged, they become redundant, and bow in the LA during systole rather than opposing each other and closing together. What does this describe
    Myxomatous degeneration and Mitral Valve prolapse
  88. In the case of rheumatic fever there can be excessive shortening of leaflets and hypertrophic obstructive myopathy. Referred to as ________
    • abnormal systolic anterior motion
    • (of the anterior mitral leaflet that prevents normal closure.

    (this is in MR section)
  89. In MR, the annulus itself can become calcified, can happen w/normal aging. Which patient populations is this common in?
    More common among HTN patients as well as diabetic and those w/end stage renal disease (shows the complexities of multiple comorbidities coming together)
  90. Calcification (stenosis) causes MR how?
    Calcification (stenosis) interferes w/the approximation of the leaflets and so regurgitation results.
  91. In the 90s, what drug was associated w/development of MR and as a result that combination withdrawn from market as a result
    weight loss drug (Fen Phen)
  92. Describe the murmur for MR and where it is heard best
    • With MR there is backflow of blood through MV into the LA during systole (v. ejection) results in high frequency blowing type murmur. Swishing, similar to AR but this occurs during systole (AR during diastole).
    • Murmur of MR is best heard over the apex of the heart.
  93. Describe the pathophysiology of MR
    • Part of the LV SV is ejected → LA during systole
    • ↑ L atrial volume
    • ↓ CO
    • Volume-related stress on LV
    • So in order to eject more, frank starling kicks in again, so LV SV increases
  94. The severity of MR and the ratio of forward flow to backward flow will be dictated by 5 factors:
    • Size of mitral orifice
    • Systolic pressure gradient between LV and LA.
    • Systemic vascular resistance (opposing forward flow from LV)
    • LA compliance
    • Duration of regurgitation w/systole (in essence the systolic ejection time)
  95. What is the equation for the regurgitant fraction?
    • RF = Volume of MR
    •       Total LV Stroke Volume
  96. The regurgitant factor will increase when ?
    the resistance to Aortic outflow is increased. Blood flows via path of least resistance, goes back into LA
  97. Name some things that will increase the regurgitant factor
    • If pressure in Aorta is high (high systemic BP) Can also occur from AS.
    • How high the LA pressure goes up w/MR will depend on how compliant the LA is. (The pressure volume relationship is what compliance is)
  98. In ACUTE MR what happens?
    • The pressure in LA will rise significantly when exposed to higher regurgitant volume (little change in compliance of LA).
    • One of the things that’s helpful the high pressure in LA sort of opposes regurgitant flow, keeps more of the blood from coming from LV to LA BUT pressures reflected back into pulmonary circulation, so pulmonary congestion and edema result
  99. Describe what happens in chronic MR.
    LA has enlarged and is more compliant so LAp is not as elevated. Pulmonary congestion s/s are less common. The LV enlargement and the eccentric hypertrophy result from chronic volume overload.
  100. What are the mild, moderate, and severe  regurgitant fractions (%)?
    • Mild: 20-30
    • Moderate: 30-50
    • Severe: >50
  101. Severity of MR is dependent on what FIVE things?
    • Systolic Ejection Time
    • Regurgitant Orifice Area
    • Pressure Gradient
    • LA compliance
    • Increased SVR
  102. Describe what you would see in acute MR
    • Normal LA size & compliance
    • High LA pressure
    • High pulmonary venous pressure
    • Pulmonary congestion & edema
  103. Describe what you would see in chronic MR
    • ↑ LA size & compliance
    • More normal LA & pulmonary venous pressures
    • ↓ Forward CO
    • Patient w/chronic MR, overtime will develop symptoms of low forward flow. Low CO. Fatigue, weakness, A. fib.
  104. In MR: ___ EDV + ___ ESV → ___SV (although net SV into the aorta may be decreased)
    ↑ EDV + ↓ ESV → ↑↑ SV (although net SV into the aorta may be decreased)
    • see prominent V wave in acute MR.
    • Prominent enough to merge w/ preceding C wave. (C wave in LA trace is start of ventricular contraction and v wave at end of ventricular contraction)


    • No true isovolumetric contraction phase (no straight line, rounded) because the blood begins to flow across MV and into LA before the Aortic valve opens.
    • MR will decrease LV afterload because total outflow resistance is decreased. Causes an increased SV and a decreased ESV volume.
    • So a increased SV but not all is going into Aorta. No true isovolumetric relaxation phase. As ventricle starts to relax, the MV is never completely closed. Blood can flow back into the LV from LA. (As long as LV is higher than LA pressure)
    • Width of SV increases but ejection into Aorta is decreased.
  105. What would you hear in Chronic MR
    • Apical holosystolic (pansystolic) murmur radiating to axilla
    • S 3 reflecting increased volume returning to LV during diastole
  106. What would you see on the CXR and EKG w/chronic MR?
    LAE, LVH
  107. Which is better surgical or medical treatment for MR?
    • Surgical repair (preferable) or replacement
    • Early surgery to prevent muscle dysfunction

    Repair better for younger patient and replacement better for older w/extensive disease
  108. For MR, Survival may be prolonged if surgery before EF is less than ___%
    60%
  109. Operative mortality____% for repair &
    _____% for replacement
    • 2-4% 
    • 5-7%
  110. For MR, If EF is less than ___%, there won’t be improvement w/surgery
    30%
  111. What medications can we give to treat the patient w/MR (in general)
    • Vasodilators in acute MR (No benefit to long term use in asymptomatic patient w/chronic)
    • ACEI
    • Beta blockers
    • Digoxin
    • Diuretics

    *Pacing (BiV)

    Symptomatic patient: meds/pacing help decrease functional MR and improve exercise intolerance
  112. What is our overall goal in anesthesia for our patient w/MR?
    Goal = to prevent and treat events that lead to decreased CO
  113. What are some intraoperative considerations for our patient w/MR?
    • Prevent bradycardia (ideal HR = 80-100)
    • Prevent ↑ SVR
    • Minimize drug-induced myocardial depression
    • Monitor magnitude of regurgitant flow with PA line (V wave) or ECHO
  114. What are the HD goals for out patient w/MR?
    Preload:
    Afterload:
    Contractility:
    Rate:
    Rhythm:
    MVO2:
    • Preload: Usually slightly increased; however: preload reduction may reduce regurgitant flow; Full
    • Afterload: Decrease with anesthetics, vasodilators; Forward
    • Contractility: Maintain’ may be depressed, titrate myocardial depressants carefully; Strong
    • Rate: Slightly increased; Fast (80-100bpm)
    • Rhythm: If AF present, control ventricular response; Regular
    • MVO2: Compromised if MR coexists with ischemic heart disease
  115. What is important to keep in mind regarding preload and afterload w/MR?
    • Need adequate volume for forward flow. Excessive volume could dilate LV and MV annulus and make the MR worse.
    • Decrease afterload slightly, avoid sudden decrease that could make the regurgitation worse
  116. What are our concerns during induction of anesthesia in our patient w/MR?
    • ↓ Dose of sedative-hypnotic to
    • Minimize change in SVR
    • Avoid bradycardia (relative tachycardia 80-100 bpm)
  117. What are our concerns during maintenance of anesthesia in our patient w/MR?
    • Volatiles helpful because of ↓ SVR & Negative inotropy (minimal)
    • Opioids  (Pros = minimal myocardial depression & Cons = bradycardia
    • MR – Pancuronium may be a good choice
  118. What are our concerns during laryngoscopy in our patient w/MR?
    • Laryngoscopy, SNS time and acute increase in afterload as a result.
    • Attenuate carefully, opioid vs. propofol bolus (opioid minimal myocardial depression but high dose fentanyl but could get bradycardia)
  119. What is our plan for fluid management and Monitoring for our patient w/MR?
    • Fluid management: Maintain intravascular volume to maintain CO (preload)
    • Monitoring: Consider PA catheter to monitor v wave if regurg is severe
  120. What % of the population has Mitral Valve Prolapse?
    2% of the population
  121. What are some causes of Mitral Valve Prolapse?
    • Inherited (Autosomal dominant)
    • Connective tissue diseases (Marfans or Ehlers-Danlos [defect in collagen synthesis])
    • SLE
    • thyrotoxicosis
    • myocarditis

    more common in women, esp. thin lean bodies.
  122. Is mitral valve prolapse symtomatic?
    NO, Usually asymptomatic & benign

    • (but can have chest pain and palpitations)
    • Patient may have anxiety and orthostatic symptoms. Dyspnea, fatigue, and sometimes arrhythmias that require Beta-blockade
  123. What would you expect hear upon auscultation of your patient w/mitral valve prolapse?
    Mid-systolic click (and late systolic murmur)
  124. What is the patho behind mitral valve prolapse?
    • the leaflets become enlarged normal collagen replaced by abnormal connective tissue.
    • Either primary anatomic form or connective tissue disease (more likely in elderly).
    • Inherited normal variant or connective tissue disease or more elderly patient
  125. What is treatment of mitral valve prolapse dictated by?
    • Is MR present? (may or may not be)
    • Treatment is dictated by amount of regurgitation if they have it.
  126. What is the anesthetic managment of a patient w/mitral valve prolapse?
    • Evaluation for MR
    • Avoid:
    • Hypovolemia
    • Increased sympathetic tone
    • Decreased afterload (phenylephrine better than ephedrine

    Avoid events that enhance LV filling, avoid SNS that will increase contractility.
  127. What is the etiology of AS?
    • Degeneration & calcification (“senile AS”)
    • Calcification of congenital bicuspid valve
    • Can also be from rheumatic heart disease

    AS is often caused by age related changes. Similar risk factors as there are to ischemic heart disease, (HTN, hyperlipidemia)
  128. Usually only what valve is bicuspid?
    • Mitral valve
    • (can have abnormal bicuspid AoV that will cause AS)
  129. Which type of AS is common in those 65 years and older?
    • Most patient present after age 65 have age related form.
    • Young patients have congenital valve w/ calcifications.
  130. ____% of patient who have RF related AS are likely have MV disease as well
    95%
  131. Pathology of AS
    • “Wear & tear” of valve motion
    • Common pathology with atherosclerosis
    • Turbulence across valve disrupting endothelium & collagen matrix

    Endothelin and fibrous damage results and causes calcifications.Now also thinking common etiology w/atherosclerotic valvular disease, cellular proliferation, lipid accumulation, etc
  132. Describe the pathophysiology of AS
    • Flow across the AV is impeded during systole. If valve opening is decreased by more than 50% it takes a significant increase in LVP to drive the blood into the aorta.
    • This usually develops over time (don’t get acute AS) & the LV compensates by developing LV concentric hypertrophy.
    • So hypertrophy serves an important role, decreases wall stress, but it also decreases LV compliance.
    • So later the LA also has to hypertrophy in order to fill the now non-compliant LV.
    • In AS, left atrial contraction probably is responsible for more than that normal.
  133. Why is atrial kick so important in AS?
    25% of atrial kick so loss of atrial kick (A. fib) can cause marked deterioration.
  134. In AS, if valve opening is decreased by more than ___% it takes a significant increase in LVP to drive the blood into the aorta.
    50%
  135. In AS: ___ESV + __ EDV → ___ SV
    ↑↑ ESV + ↑ EDV → ↓ SV
    •  Significant ↑ESVbecause LV emptying is impaired d/t high afterload from resistance in valve, ↓SV , because ↑ESV, the excess residual volume added to the incoming venous return causes ↑ EDV which means ↑preload that activates frank starling to try and help the ventricle overcome (in part) resistance to flow in AS.
  136. What kind of murmur would you see in AS?
    • HARSH systolic murmur.
    • Systolic Murmur heard best in the aortic area
    • There may also be a thrill (vibrations that can be felt by hand in chest and lower neck)
  137. What is the clinical presentation of AS?
    • Angina: ↑ myocardial oxygen demand & ↓ myocardial oxygen supply
    • Syncope: Inability to ↑ CO with exertion & Vasodilation from exertion → ↓ BP → ↓ cerebral perfusion
    • DOE
    • SEM (mid-systolic ejection murmur?)
  138. Describe the correlation between clinical symptoms and median survival for AS
    • Angina: 5 years
    • Syncope: 3 years
    • CHF: 2 years
    • AF: 6 months
  139. In AS, about __% will succumb to death in 3 years
    75%
  140. Angina associated w/AS is  an imbalance myocardial oxygen supply/demand. Describe how this happens?
    • Demand is increased in 2 ways: ventricular hypertrophy, larger mass that needs to be perfused.
    • Increase in systolic ventricular pressure increases wall stress but we also have a decrease in oxygen supply. Because of the increased diastolic pressure in LV. There is decreased coronary perfusion.
    • Hypertrophy makes it difficult to get adequate CO at rest
  141. Why do we see syncope (especially upon exertion) with AS?
    • see is syncope w/exertion in particular. Hypertrophy makes it difficult to get adequate CO at rest, outflow is fixed, can’t compensate for needs required w/exertion
    • With exertion get normal vasodilation which will decrease BP, vasodilation, can’t get more blood out to perfuse brain (and other places) so the patient becomes syncopal and looses consciousness.
  142. What do you see on the CXR and EKG for a patient w/AS?
    With a CXR see prominent ascending aorta and EKG may show LV hypertrophy
  143. What is the important thing to remember regarding a patient w/AS? (pre-op)
    • May be asymptomatic, listen for murmur!
    • Check H&P and see if anyone else did, esp. in elderly
  144. What is mild AS (by ECHO)?
    • Mean transvalvular pressure gradient (mmHg) < 20
    • Peak transvalvular pressure gradient (mmHg) < 36
    • Aortic valve area (cm2)1.0 – 1.5
  145. What is moderate AS (by ECHO)?
    • Mean transvalvular pressure gradient (mmHg) 20-50
    • Peak transvalvular pressure gradient (mmHg) >50
    • Aortic valve area (cm2) 0.8-1
  146. What is severe AS (by ECHO)?
    • Mean transvalvular pressure gradient (mmHg) >50
    • Peak transvalvular pressure gradient (mmHg) >80
    • Aortic valve area (cm2) <0.8
  147. What is the treatment for asymptomatic AS?
    • Asymptomatic AS
    • Slow rate of progression over 20 years
    • Only 20% of patients will progress to severe or symptomatic
    • Caution with meds that can result in hypotension (Vasodilators, Diuretics, & NTG)
    • Current research is looking at statins
  148. What is the treatment for Severe AS?
    • AVR (Valve replacement indicated if symptoms develop or evidence of LV dysfunction)
    • Valvuloplasty not as effective as in MS (Immediate relief of outflow but Restenosis in 50% of patients within 6M)
    • Again need to be careful w/anything that will decrease SVR
  149. What is the goal of anesthesia for a patient w/AS?
    Goal = to prevent hypotension & any hemodynamic change that will ↓ CO
  150. What are some intraop considerations for a patient w/AS?
    • Maintain NSR (need atrial kick)
    • Avoid bradycardia (if too slow, overdistention of LV and too fast then less time for ventricular filling)
    • Avoid hypotension (decrease coronary blood flow and cause ischemia, results in further deterioration of LV function, avoid so you don't have to treat!)
    • Optimize intravascular fluid volume to maintain venous return & LV filling
  151. What should we do if our patient w/AS gets hypotensive?
    • treat aggressively!
    • Otherwise get cardiogenic shock & cardiac arrest CPR unlikely to be effective.
    • Impossible to create adequate SV across a stenotic valve w/compressions
  152. What are the HD goals for our patient w/AS?
    Preload
    Afterload
    Contractility
    Rate
    Rhythm
    MVO2
    • Preload: Maintain venous return; Full
    • Afterload: Maintain coronary perfusion gradient; Tight
    • Contractility: Usually not a problem, may require inotropic support if hypotension persists; Not too strong
    • Rate: Avoid bradycardia (↓CO) and tachycardia (ischemia and no ventricular filling); Not too fast or too slow
    • Rhythm: Sinus; may need cardioversion or
    • beta blockers; Regular
    • MVO2: Avoid tachycardia and hypotension
    • (ischemia is constant risk)
  153. What are our concerns during induction for a patient w/AS?
    • ** Don’t ↓ SVR**
    • Etomidate = drug of choice.
    • NO propofol!!!! (not even slowly!!)
    • Opioid --Use opioid (don’t want to slow HR too much so reasonable dose)
  154. What is our anesthetic management during maintenance of anesthesia for a patient w/AS?
    • Avoid myocardial depression
    • Avoid ↓ SVR
    • Muscle Relaxant – minimal CV side effects
  155. What should we do regarding fluid management and monitoring for a patient w/AS?
    • Fluid Management: Maintain normal intravascular volume
    • Monitoring: EKG – select leads to monitor LV Invasive monitoring may be advised (A-line, PA catheter, & TEE)
  156. Can we do regional anesthesia in a patient w/AS?
    • Neuraxial blockade contraindicated (↓ SVR) 
    • Regional: In severe AS it’s absolutely contraindicated
    • Decrease SVR w/profound sympothectomy!
  157. What are the two types of etiology for AR?
    • Abnormal valve leaflets
    • Dilation of Aortic Root
  158. What kinds of things can cause abnormal valve leaflets leading to AR?
    • Congenital (bicuspid valve)
    • Endocarditis
    • Rheumatic fever
  159. What can lead to dilation of Aortic Root and cause AR?
    • Aortic aneurysm (Inflammation & Connective tissue disease-Marfan syndrome)
    • Aortic dissection
    • Annuloaortic ectasia
    • Syphillis
  160. What is the pathophysiology behind aortic insufficiency?
    • Abnormal flow of blood from aorta → LV during diastole
    • LV must pump regurgitant volume + normal volume from LA
    • Compensation depends on Frank-Starling to augment SV
  161. Factors that influence severity of AR are the same as MR, name them!
    • Size of regurgitant orifice
    • Pressure gradient across the AV
    • Duration of diastole (MR it was systole)
  162. Describe how the Frank-Starling law applies to the patient w/AR
    In contrast to MR, w/AR the entire stroke volume is injected into Aorta. Because all the volume goes into the aorta, there is an increase in Systolic BP and an increase in afterload. Ultimately, the LV then has to pump regurgitant volume as well as normal volume from LA (Frank Starling kicks in) LV compensates for hypertrophy now for the added volume (rather than the added pressure)
  163. What kind of hypertrophy do you get in AR?
    ECCENTRIC


  164. Backflow of blood from aorta into LV, there’s no true isovolumetric relaxation phase (on the L). Rather the LV begins to fill w/blood from Aorta before the MV opens. Once MV opens, the LV begins to fill w/blood from LA.
  165. Aortic Regurgitation:
    ___EDV +  ___ ESV → ___ SV  (although no net SV into aorta- may be decreased)
    ↑↑ EDV +  +/- nl ESV → ↑↑ SV  (although no net SV into aorta- may be decreased)

    +/- normal ESV (depends if LV in failure or not) if LV not in failure ESV is probably normal, if the LV is in failure then the ESV is increased
  166. Describe the murmur in AR
    Murmur between S2 and S1, blowing murmur, high pitch swishing quality heard most over LV.
  167. Describe the clinical presentation of acute AR
    • LV size is normal
    • LV is relatively non-compliant
    • Volume load of regurg → substantial ↑ LVEDP
    • Sudden ↑↑ LVEDP → ↑ LAP → pulmonary edema
    • Surgical emergency (need AVR)
  168. Describe the clinical presentation of chronic AR
    • LV undergoes compensation
    • Chronic dilatation → eccentric hypertrophy
    • ↑ LV compliance
    • ↓ aortic diastolic pressure
    • High SV (↑ SBP) + ↓ DBP = ↑ pulse pressure
    • ↓ coronary perfusion pressure
  169. What is a HALLMARK sign of AR
    Wide Pulse Pressure
  170. Why are we concerned about the coronary perfusion in AR?
    • Decrease coronary perfusion pressure because of decrease in aortic diastolic pressure, consequently a decrease in myocardial oxygen supply.
    • Decrease supply potentially increased demand (eccentric hypertrophy but some concentric hypertrophy as well) so angina can develop in absence of CAD.
  171. Describe the murmur heard in AR
    Diastolic murmur over the left sternal border
  172. In AR, you see peripheral signs of hyperdynamic circulation, what are they?
    • Widened pulse pressure
    • ↓ DBP
    • Bounding pulses
  173. With progression of AR, you see signs of LV failure. What are they?
    • Dyspnea
    • Orthopnea
    • fatigue

    Usually the compensation of LA dilation and LVH will be enough to meet demands for years, asymptomatic. Progressive remodeling of LV and systolic dysfunction develops (Eventually) then decrease in CO, increase in Lap and so on w/all the pulmonary symptoms.
  174. How do you treat asymptomatic chronic AR?
    Clinical progression is slow so no tx
  175. How do you treat asymptomatic severe AR with good LV??
    • Afterload reduction when BP > 140
    • Calcium channel blockers
    • ACE inhibitors
    • Don’t prolong the compensated stage of chronic AR in the absence of HTN
    • If not HTN they are of no benefit
  176. How do you treat symptomatic AR?
    • AVR
    • If symptomatic or evidence of impaired LV function (EF less than 50) then surgical correction may be offered (AVR)
    • Patients that develop angina or HF are likely to die within 2 years unless they have some surgical replacement of their valve.
  177. What is the overall goal of anesthesia in AR?
    Goals = Maintain forward LV SV
  178. What are the intraoperative considerations for our patient w/AR?
    • HR > 80
    • Avoid ↑ SVR
    • Minimize myocardial depression
    • If LV failure occurs: Vasodilator to ↓ afterload and Inotrope to ↑ contractility
    • Modest ↑ HR and ↓ SVR
    • All the compensations patient develop may be tight balance. Careful anesthetic induced myocardial depression doesn’t tip balance away from compensation.
  179. Why should we avoid abrupt increase in SVR or bradycardia in AR?
    • Bradycardia increased diastole, increases regurgitation and that increases LV overload.
    • Avoid abrupt increase in SVR, could also precipitate LV failure.
  180. What are our HD goals in AR? 
    Preload
    Afterload
    Contractility
    Rate
    Rhythm
    MVO2
    • Preload: Normal to slightly ↑; Full
    • Afterload: ↓ with anesthetics or vasodilators (to ↓ regurgitation); Forward
    • Contractility: Usually adequate; Maintain
    • Rate: ↑ reduces ventricular volume and raises
    • diastolic aortic pressure; Fast
    • Rhythm: Usually sinus; not a problem; Regular
    • MVO2: Usually not a problem
  181. What are our concerns during induction of anesthesia for our patient w/AR?
    Avoid ↓ in HR or ↑ SVR
  182. What are our concerns during maintenance of anesthesia in our patient w/AR?
    • Volatiles good choice (↑ HR, ↓ SVR, minimal myocardial depression)
    • High dose opioid risks ↓ HR
    • Muscle relaxants with minimal CV effects
    • Treat bradycardia & Junctional rhythm with atropine
  183. What should we do regarding fluid management and monitoring in our patient w/AR?
    • Fluid Management: Maintain preload
    • Monitoring: Severe AR may require PA catheter or TEE for managing volume replacement, etc.
  184. Tell me everything Sue said about TS?
    • Rare in adult population
    • Etiology: Common cause is rheumatic heart disease & Usually other valves involved. Also
    • Carcinoid syndrome
    • Pathophysiology: ↑ right atrial pressure↑ pressure gradient between RA & RV
  185. Etiology of TR?
    • Usually functional rather than structural (Due to right atrial enlargement [from volume or pressure overload] Pulmonary hypertension)
    • Infective endocarditis (IV drug abuse)
    • Carcinoid syndrome
    • RHD
    • Often associated with mitral or aortic disease
  186. Pathophysiology of TR (short and sweet version)
    Right atrial volume overload
  187. What would you see clinically in someone w/TR?
    Patients may have hepatomegaly, ascites, peripheral edema.
  188. What would our anesthetic management be for someone w/TR?
    • Maintain CVP in high normal, facilitate RV preload and RV filling.
    • Avoid anything that would increase PAp. (hypoxemia and hypercarbia)
    • Avoid a decrease venous return
  189. What are the pulmonary valve diseases?
    • Pulmonic stenosis: Usually congenital & corrected in childhood
    • Pulmonic valvulotomy can relieve obstruction
    • Pulmonic regurgitation: From pulmonary HTN with annular dilatation
    • Rarely symptomatic
  190. What is the cause of IHSS (Hypertrophic Cardiomyopathy)?
    • Genetically determined
    • Heterogeneous ventricular hypertrophy
    • --Abnormal myocytes
    • --No obvious cause

    Morgan says it can occur spontaneously.
  191. What kind of hypertrophy develops in IHSS (Hypertrophic cardiomyopathy)?
    Characterized by abnormal myocardial cells. Myocardial hypertrophy that develops (“Papriori” meaning before or in absence of pressure volume overload) This hypertrophy is independent of pressure/volume
  192. What is the LV like in IHSS (Hypertrophic cardiomyopathy), how does it function?
    • LV is hyperdynamic (w/small chamber)
    • Diastolic dysfunction (↑ LVEDP)

    Thought this hypertrophied muscle, that tends to be located in upper part of intraventricular septum below the AV, is what causes the diastolic thickness and diastolic dysfunction.
  193. What kind of obstruction do you see w/IHSS? (Hypertrophic cardiomyopathy)
    There is an obstruction that results, it’s a narrowing in subAS area. What causes this is what’s referred to as systolic anterior motion (SAM) of the anterior mitral leaflet against that hypertrophied septum. The obstruction is dynamic (not always the same) not fixed. The obstruction will peak in mid to late systole. And the degree (how much it’s obstructed) can vary from systole to systole (beat to beat).
  194. What are some things that can increase the obstruction in IHSS (Hypertrophic cardiomyopathy)?
    • Things that will increase obstruction:
    • Increased contractility
    • decreased ventricular volume
    • decreased LV afterload.

    So this gets associated w/some MR because what happens w/this systolic anterior motion is that the mitral leaflets fail to coapt (come together) and regurgitation results.
  195. In IHSS, (hypertrophic cardiomyopathy)___% of patients get dynamic obstruction of LVOT because of that systolic anterior motion (the anterior mitral leaflet against the hypertrophied septum).
    25%
  196. What are some things we want to evaluate for in a patient w/IHSS?
    • Evaluate for potential of:
    • Significant dynamic obstruction
    • Malignant arrhythmias
    • Myocardial ischemia
  197. What is our anesthesia management like for a patient w/IHSS?
    • Volatiles provide some myocardial depression
    • Phenylephrine good choice as vasopressor

    If significant: some degree of myocardial depression is usually a good thing and the volatiles are good for that. If patient does become hypotensive, phenylephrine good choice because it doesn’t increase contractility but will increase SVR.
  198. What are our HD goals in a patient w/IHSS?
    Preload
    Afterload
    Contractiity
    Rate
    Rhythm
    MVO2
    • Preload: Full; one of the first treatments for hypotension
    • Afterload: Increased; treat hypotension aggressively with α adrenergic agonists (phenylephrine)
    • Contractility: Prefer depression
    • Rate: Normal range; Not too slow, not too fast; beta blockers decrease left ventricular outflow tract gradient and increase LVEDP
    • Rhythm: Sinus rhythm is crucial; atrial pacing may be helpful
    • MVO2: Not a problem

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