Valvular Disease Flashcards
Primary or secondary valve HD:
-leaflets or anchoring and supporting structures are damaged (do not function properly)
primary valve dysfunction
AS: “adequate assessment of valvular stenosis” include these two
- flow rates across valve
- pressure gradient
(both via ECHO or Cath)
how does bradycardia/tachycardia effect regurgitant flow/fraction, ejection and myocardial O2 demand
brady - increased regurgitant flow/fraction
tachy - shortens ejection and inc O2 demand
- detrimental in aortic stenotic lesions
MVP medication tx
-even thou majority do not need tx due to asypmtomatic
beta blocker
- inhibit autonomic imbalance
- may INC EDV -> DEC degree of prolapse
MVP: characteristic murmur
midsystolic click and late systolic murmur
Class III of NYHA coincides with which stage of ACCF/AHA stage of HF
C. Structural HD with prior or current symptoms of HF
regurgitant fraction parameters of mild, moderate and severe
mild < 30%
moderate 30-60 %
severe > 60%
Magnitude of AR reduced by:
tachycardia
peripheral vasodilation
chronic ventricular overload
AS: preload/LVEDV goal; fluids
maintain sufficient preload
normovolemia
systemic eval of primary valvular dysfunction of status of LV loading includes 3 things
- LV overload
- pressure overloading (aortic stenosis)
- volume underloading (mitral stenosis)
Class II of NYHA coincides with which stage of ACCF/AHA stage of HF
B. Structural HD but w/o signs or Sx of HF
MR: common dysrhythmia
afib
aortic and mitral insuff: hemodynamic and HR goal
reduced afterload
faster HR - shortens time for regurgitation
MS: timeline of stenosis post RHD and appearance of Sx
2 years post RHD
Sx develop 20-30 years after initial rheumatic fever
(Primary(anatomic) or functional) MVP
-redundant and thickened leaflets
primary (anatomic) MVP
MR: Implications of PAP measurements of LVEDV in chronic vs acute
acute MR works well
chronic MR poor measure of LVEDV
MS: volatile anethetics implications
nitrous - narcotic w/ low volatile
AS: why is bradycardia not desirable
< 60 bmp
- prolonged filling time -> ventricular distension, which can further decrease CPP (esp. subendocardium)
MR: EF and end-systolic dimension correlate with no improvement w/ surgery
EF < 30%
LV end-systolic dimensions > 55 mm
causes of MR (excluding obvious ones)
myxomatous degeneration
ankylosing spondylitis
carcinoid syndrome
NY Heart Association Functional HD classification related to exercise tolerance: Describes Class IV
symptoms AT REST
MAC in MVP
low conc (0.5 MAC) can decrease regurge fraction at low dose
MR: PCWP waveform characteristic
presence of V wave
not necessarily how much regurge volume but
indicates LA compliance in relationship to regurge volume
AR: long term tx that may delay need for surgery in asymptomatic patients with good LV function
nifedipine or hydralazine
in AS: what happens with LVEDV in early vs late stage
AS: LVEDV normal till late stage
volume late; pressure early
MS orifice reduction
from 4-6 cm2 to < 1.5 cm2
TR: hypercarbia and hypoxemia may cause this to PAP
INC PAP (avoid this)
AR: choice of anesthetic techinque in severe ventricular dysfunction
opioid-based
summary of MVP IE prophylaxis
only give to those with underlying cardiac conditions associated with HIGH risk outcomes from infectious endocarditis
treatment of pulmonic stenosis
surgery to relieve obstruction
chronic vs acute MR
reduced CO (chronic) pulm edema (acute)
MR: regurgitant fraction measured by 2 ways
pulsed doppler echo
cardiac cath
MR: neuraxial recommendations
Not CI but potential exists for profound hypotension w/ SNS depression
AR: LV dysfunction associated S/S
dyspnea
orthopnea
fatigue
coronary ischemia
narrowing of valvular orifice
restricted flow when valve open
inc flow resistance and turbulence
… describes what valve disease
valvular stenosis
AR: volume of regurgitation depends on 3 things:
- time available for regurge flow (HR)
- pressure gradient (Ao valve) pressure btw aorta and LV depends on SVR
- degree of AO valve imcompetence
which lesions progress faster (stenotic or regurgitant lesions)?
stenotic
AR: muscle relaxer choices
use non-depolarizers (Succs = bradycaria risk)
pancuroniium is desirable = offsets vagolytic effects of narcotics
AS: any change in basic hemodamic (__, __, __, __) can cause irreversible myocardial deterioration
HR
Rhythm
LVEDV
CPP
Chronic MR: secondary PA HTN dt
intimal fibroelastosis
-permanent vascular damage, fibrous scaring of intima and media per google
AS: pulse pressure
narrow
(Primary(anatomic) or functional) MVP
-mild bowing and normal leaflets
functional MVP
normal variant
MR: hemodynamic goals
INC HR (normal or slightly higher) DEC afterload avoid HIGH PVR Preload: NORMAL to INC'd Contractility: maintain
how does anesthesia affect sympathetic tone and what implications for valvular HD
decreased sympathetic tone during anesthesia may cause severe myocardial dysfunction
MVP: hemodynamic conditions that DEC preload and incidence of MV eversion are due to:
INC contractility DEC SVR head up/sitting position NTG/Nipride hypovolemia
MS: pulm edema occurs when these pressure changes occur btw PVP and plasma oncotic pressures
PVP > POP
MVP: EKG changes
PVC
repolarization abnormalities
prolonged QT
presence of bicuspid valve more common to occur when during aging/life
early life
btw 30-50 yo
AR: surgical recommendation for asymptomatic
surgery recommended BEFORE permanent dysfunction even if not symptomatic.
ACUTE AR - immediate surgery
MS: anticoagulants in minor surgery (dc or continue)
continue unless obvioulsy major blood loss anticipated
less common causes of MS
- carcinoid syndrome
- LA myxoma
- severe mitral annular calcification
- endocarditis
- cor triatriatum (congenital defect)
- rheumatic arthritis
- systemic lupus erythematosus
- congenital
- iatrogenic MS after MV repair
on PA chest what indicates cardiomegally
heart size is 50 % of internal width of thoracic cage
75% of symptomatic patients will die within __ years w/o valve replacement
3 years
which valves and dysfunctions produce pressure overload
mitral stenosis
aortic stenosis
TR: treatment
find cause of lesion
improve lung function
relieve LV failure
reduce PHTN
AS: LV consequences
- dec compliance
- remodeling
- dec. contractility of myocardium
valvular HD: cardiac cath
measure transvalvular gradients
estimate degree of regurgitation
visualize coronary arteries
determine intracardiac pressures
8 points on systemic eval of primary valvular dysfunciton
- category (stenosis, insuff, mixed)
- status of LV loading
- acute vs chronic evolution
- cardiac rhythm and effect on diastolic filling time
- LV function
- secondary pulm vasc and RV function
- HR
- periop anticoagulation
MS: PA catheter risks w/ presence of PHTN
PA rupture!
MVP: how does PPV affect VR
PPV blunts decrease in VR and helps prevent increase in degree of prolapse
MS: tx (HR)
prevent tachycardia (reduces filling time)
Most common feature of AR
WIDE PP
major complications of TAVI (transcatheter aortic valve implantation)
stroke, cognitive dysfunction, aortic dissection, bleeding, femoral/inguinal artery injury, perivalvular leaks
MR: preop sedation and anticholinergics use recommendations/guidelines
okay to use
MS: PHTN and RVF may be caused by
hypercarbia hypoxmia lung hyperinfilration increase in "lung water" (think inotropic and; pulm vasodilating drugs)
MVP prognosis
usually benign
can have complications: cerebral embolic events, infective endocarditis, severe MR, dysrhythmias, sudden death
chronic MR (which type of LVH: concentric or eccentric)
eccentric
-w/ progressive contractility impairment
AR: biphasic pulse, second peak dt strong LV contraction, occurs in significant AR, double pulse felt dt back flow in early diastole
Biseferien’s pulse
AR: RV and pulm vascular circuit usually spared in chronic AI until secondary (functional) MR occurs. This results in _______ (related to MV annulus change)
dilation of mitral valve annulus
-> gradual increase in LAP and PAP caused by MR eventually causes pulm HTN (functional/secodary MR definition)
compliance of LA in chronic vs acute MR
acute - non compliant LA
chronic - compliant LA
AS: avoid which muscle relaxors
histamine releasing (atricurium)
MR: induction recommendation
prevent DEC SVR and DEC HR
pancuronium maintains HR
MR: induction and paralytic recommendation
avoid bradycardia and significant increase in afterload
pancuronium maintains HR
treatment options in symptomatic MR
ACE inh or B-blocker (coreg)
biventricular pacing
improve sx and exercise tolerance
AS: what happens to pressure gradient btw LA and LV
- decreases (less filling into LV less pressure)
- ventricular filling dependent on normal atrial contraction
- loss of atrial systole = CHF, hypotension
functional MVP usually seen in this population
women < 45 yo
MS: reversal from NMB implications
avoid tachycardia from anticholinergic
give anticholinergics sloooowly
MR: consequences of dysrhythmia
loss of atrial kick
PULM congestion
LA/LV overload
LOW CO
AS: hemodynamic parameters (diastolic time, CPP) = decreases myocardial O2 supply
decreased
-diastolic time
+ dec CPP
“2 factors” of aortic stenosis (assuming she meant risk factors”
- degeneration and calcification of leaflets (aging process)
- presence of bicuspid valve (if only 2 leaflets, more work split btw 2 leaflets instead of usual 3)
AS: HR goal
NSR
70 - 80 BMP
which valves and dysfunctions produce volume overload
mitral regurgitation
aortic regurgitation
MS: drugs to avoid
avoid ketamine
avoid histamine producing NMBs
acute MR choice med class
vasodilator
-no benefit for long term in asymptomatic pts w/ chronic MR..
AR: maintenance anesthetic
and in Severe AR
N2O + volatile
or Opioid
Severe AR: high dose opioid (avoid brady)
most common valvular disease in elderly and
most common cause of obstruction to LV outflow
aortic stenosis