Transcript Internal Medicine Board Review (from MKSAP 13)

Internal Medicine Board
Review (from MKSAP 13)
Cardiology
June 2006
Congenital Heart Disease
In the Adult
Acyanotic Congenital Heart Disease
(covered in MKSAP)
• Atrial Septal Defect
• Bicuspid Aortic Valve
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Most common congenital anomaly
More common in men
Early systolic ejection click and outflow murmur
Diagnosis with echo important because of
endocarditis risk
– Coarctation and bicuspid aortic valve are associated
Ventricular Septal Defect
Patent Ductus Arteriosus
Valvular pulmonary stenosis
Coarctation of the aorta
Cyanotic Congenital Heart Disease (covered in MKSAP)
• Most patients with unoperated cyanotic heart
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disease have developed Eisenmenger’s
syndrome.
Tetralogy of Fallot
– most have had complete intracardiac repair,
occasionally only aortopulmonary shunt.
– PI leading to right heart dilation is common
– Yearly mortality increases after 25 years due to
sudden death, QRS >180ms best predictor, apparent
interaction between long QRS and right heart dilation,
general agreement to replace pulmonary valve when
QRS>180.
• Transposition of Great Arteries
– most have had been repaired with atrial switch
(Mustard, Senning) procedure [now doing arterial
switch]
– Risk RV failure (survival depends on RV function), sick
sinus syndrome, atrial arrhythmias
• #70 26 y.o. female. Heart murmur as a child
did not outgrow it. Married. Would like a child.
Mild cough and SOB especially at high altitude.
BP 110/70, HR 86. O2 sat 99%. Nl JVP. Good
carotid upstroke. Lungs clear. RV lift. S1 normal
S2 wide fixed splitting. 3/6 early to mid peaking
systolic murmur LUSB. Echo RV enlargement,
RAE, and high pulm flow but no ASD on TTE.
PA 45. Valves normal. Next step?
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TEE
ABX prophylaxis no other treatment
Have family and then consider closure of the defect
Cardiac cath
Reassurance
# 70 TEE
• Most likely dx is ASD (wide and fixed splitting of S2)
• However partial anomalous pulmonary venous drainage
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is an alternative diagnosis and is suspected when TTE
does not show ASD. RV enlargement is consistent with
a hemodynamically significant shunt.
Mild elevation of PA pressure is not a contrindication to
closure
TEE is indicated to define the anatomy and exclude
anomalous pulmonary venous drainage
Referral for closure is indicated and if feasible prior to
pregnancy (CHF sometimes complicates pregnancy, risk
paradox embolus)
Closure percutaneous or sugical depending on anatomy
and center’s experience
– Most ostium secundum ASD can be closed percutaneously
– Others require surgical closure
--Closure of ASD and VSD indicated if pulmonary
to systemic shunt ratio of 1.7:1 or greater with
evidence of right or left ventricular volume
overload respectively.
Location of types of Atrial
Septal Defects
ASD second
Most common
Congenital defect
Encountered in adults
(bicuspid AV #1)
Majority are secundum
More on ASD’s
• In absence of pulmonary vascular disease shunt
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is left to right resulting in RV volume overload.
With advancing age diminished LV compliance
can lead to increase in shunt fraction with
consequent right heart failure
A.fib is common in older adults with ASD’s.
Frequency of A.fib and potential for paradoxical
embolism lead to high incidence of embolic
stroke.
Before repair prophylaxis for endocarditis is not
indicated for isolated ASD’s. Following closure 6
mos of prophylaxis for endocarditis.
• #18 24 y.o. female emigrated from Phillipines
eval for murmur. HR 82. O2 sat 97%. JVP
normal. Carotid pulses brisk with rapid upstroke.
Lungs clear. Sustained apical impulse in 6th
intercostal space. S1 normal. S2 physiologically
split with normal P2. A soft S3 is audible.
Continuous murmur with crescendo-decresendo
quality is heard throughout, loudest 3rd left
intercostal space. Diagnosis?
– Mitral regugitation
– Mitral stenosis and insufficiency
– Pulmonary stenosis and insufficiency
– Patent ducts arteriosus
#18 patent ductus.
• Patent ductus arteriosus
– In acyanotic adult with patent ductus
communication is usually small. Murmur soft
and confined to systole.
– Most adults with large patent ductus have
Eisenmenger’s physiology and are not surgical
candidates.
– Closure is indicated if associated with a
murmur to prevent the complications of
endarteritis.
– Closure percutaneously with coil.
• PFO —patent foramen ovale.
– Persist in 20% of people.
– Can be associated with interatrial septal
aneurysm.
– Can be diagnosed by contrast echo.
– Risk for paradoxical embolism.
– The specific indications for closure of a
patent foramen ovale after a cerebral
embolic event remain unclear
• #43 26 y.o. man diagnosed with heart murmur
as a baby. Told he would outgrow it.
Participates in sports without problem. 120/80,
64. Lungs clear. Nondisplaced apical impulse.
Normal S1, physio split S2. Thrill in 3rd left
intercostal space and 4/6 holosystolic murmur
noted radiating to the right. Echo small
perimembranous VSD. Normal chamber size
and normal PA pressures.
– Refer to surgeon for closure
– Treat with amoxicillin 2 gm 1 hour before
dental procedures
– Refer for percutaneous closure
– Initiate lisinopril therapy
#43 Treat w/ amoxicillin 2 gm 1 hour before dental procedures
Ventricular Septal Defect
• In acyanotic adult VSD usually small
• Large VSD present in childhood with CHF or pulmonary
hypertension
• Most common location in adults is perimembranous near
tricuspid valve
• Indications for closure in adulthood are large shunt
fraction 1.7:1 or greater or left ventricular volume
overload (LV overload occurs because shunt is primarily
confined to systole and the RV serves as a reservoir for
the shunted blood The LV diastolic volume is increased
because the stroke volume includes both forward flow
and shunted flow)
• Exam with hemodynamic sig VSD may reveal displaced
apical impulse, mitral diastolic rumble, S3.
Endocarditis Risk and Prophylaxis
In Congenital Heart Disease
• Risk of endocarditis is substantial except in
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operated patients with pulmonary stenosis, ASD,
VSD, PDA. If residual VSD or PDA leaks present
postoperatively, risk persists.
Antibiotic prophylaxis is indicated for almost all
patients with unoperated congenital heart
disease (except isolated ASD)
ASD—before repair no prophylaxis indicated
unless other coexisting abnormalities.
Prophylaxis for first 6 mos post repair and
indefinitely if residual abnormalities.
#59
45 y.o. known Eisenmenger’s b/c of
unrepaired VSD. Increased lethargy, frontal
headache, and difficulty concentrating.
Previous PMD phlebotomized 1 unit every 3
mos. Cyanotic, 95/65, 95, 84%. Clubbing.
Clear lungs, nl JVP. Widely physio split S2,
loud P2. Holosystolic murmur at left
parasternal border. High pitched diastolic
murmur at upper left sternal border. Right
sided S4.
HCT 56%, MCV 72. WBC 5.6. PLT 110.
• Symptoms suggest hyperviscosity, they
may be caused by iron deficiency.
Microcytic erythrocytes are rigid and not
easily deformed. Thus viscosity increases
paradoxically at lower hematocrit.
Eisenmenger’s Syndrome and Erythrocytosis
• Seconday erythrocytosis is compensatory and
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usually not associated with symptoms.
Hyperviscosity syndrome can occur when HCT
>65. Phlebotomy is indicated only to treat
symptoms.
Be sure not iron deficient and not volume
depleted.
When phlebotomy is necessary, follow by
isovolumic saline repletion (in presence of CHF
use 5% dextrose)
• Pregnancy contraindicated. Maternal mortality
excceds 50% with death usually in early
postpartum period.
• # 89
• 35 y.o. female hypertensive. Told had
hypertension at age 20 as well but did not follow
up. BP 200/100. S1. S2 physio split. An early
systolic ejection sound is noted and early
peaking murmur noted in second right
intercostal space. Short diastolic murmur along
LSB. U/A normal.
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Measure TSH
Measure BP lower extremities
Order Echo
Order 24 HR urine test for metanephrine and
vanillylmandelic acid
– Obtain CXR
#89 Measure BP lower extremities
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• Coarctation of the aorta
– Radial femoral delay
– Lower blood pressure in the legs
– Rib notching (dilated intercostal arteries that
provide collateral blood flow)
– Repair indicated when there is proximal HTN
and a gradient exceeding 20 mm Hg
– Discrete coarctation is usually amendable to
percutaneous repair while longer segments
may require surgery
Cardiac Disease And
Pregnancy
• #11 25 y.o. pregnant female presents with heart
murmur noted second trimester. First
pregnancy. New murmur. No PMH.
Asymptomatic. Mild displaced apical impulse
and lower extrem edema. S1 and S2 normal, S3
at apex. 2/6 early to mid peaking systolic
murmur at left sternal border. Likely cause of
murmur?
– Bicuspid aortic valve with mild to mod AS
– Congenitally abnl pulmonary valve with mod
stenosis
– Physiologic murmur related to pregnancy
– Bicuspid aortic valve with moderate
regurgitation
#11 physiologic murmur
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– PHYSICAL FINDINGS AND PREGNANCY--
• S3 audible in more than 80% of normal pregnant women
• Early peaking ejection systolic murmur audible in 90%-pulmonary outflow murmur
• Increased blood volume during pregnancy
– (CO increases by 30 to 50% during pregnancy and to
about 80% above baseline during labor and delivery)
• Apical impulse displaces
• Lower extremity edema common
• Abnormal findings---S4, loud 3/6 systolic
murmur, diastolic murmur, fixed splitting of S2.
• In general, fixed obstructive lesions (MS, AS) poorly
tolerated in pregnancy—increased blood volume.
Regurgitant lesions well tolerated—decreased SVR
• #20 28 y.o. pregnant female referred for eval of
persistent dyspnea secondary to MS. 30 weeks
pregnant and dyspnea persists after metoprolol,
lasix, and digoxin. HR 70. Echo severe MS,
mean grad 14, valve area 1 cm2. Trivial MR. RV
systolic 50 mmHg. Crackles and edema. What
do you recommend?
– Surgical mitral valvotomy
– Urgent delivery fetus then reassessment of maternal
cardiac status
– TEE followed by percutaneous mitral balloon
valvuloplasty
– Diagnostic catheterization
– Fetal Echocardiogram
# 20 TEE followed by percutaneous mitral balloon
valvuloplasty
• Percutaneous valvuloplasty treatment of choice
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in pregnant women with severe MS whose sx
can’t be controlled with meds.
TEE to eval Mitral valve aparatus and eval for LA
thrombus
Abdominal shielding to limit radiation to fetus
(Avoid during first trimester)
Cardiac surgery can be performed during
pregnancy but should be avoided unless
absolutely necessary (best time 24-28 weeks)
(Maternal mortality 1-5%, fetal 15-38%)
• #30 28 y.o. female 29 weeks pregnant referred
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for progressive dyspnea. h/o rheumatic fever
and mitral stenosis. 4 wk increase dyspnea. No
palpitations. Elevated JVP. HR 100. Parasternal
impulse present. Opening snap and grade 2
diastolic rumble….EKG sinus tach, LAE, RAD.
What do you recommend?
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Digoxin
Metoprolol
Warfarin
Ramipril
amlodipine
• #30 metoprolol
– to slow HR, increase diastolic filling time.
– If sx persist then diuretic
– Note: ACE I, ARB contraindicated in
pregnancy
• #38 35 y.o. female 39 weeks pregnant
comes to office increasing dyspnea. No
prior PMH. First pregnancy. JVP 13,
diffuse apical impulse, apical systolic
murmur. S3 and S4. Crackles. EKG tachy.
• Diagnosis?
– Severe AS
– Severe TR
– ASD
– Peripartum cardiomyopathy
– Pulmonary embolism
#38
Peripartum Cardiomyopathy
• 1:1,300 to 1:15,000 pregancies in US, higher
in certain parts of Aftrica
• Risk increased in: African Americans,
multiple gestations, multiparous, women age
>30 years, h/o peripartum cardiomyopathy
• Usually occurs during last trimester
pregnancy or in first 6 mos post partum
(Most commonly diagnosed in first post
partum month)
• 50% of women with peripartum
cardiomyopathy will have improvement in LV
function within 6 mos after delivery.
• Delivery is recommended
• Unless obstetric reasons for c-sec mode of
delivery should be vaginal because of
lower hemodynamic burden
• Because risk of recurrence of peripartum
cardiomyopathy is common repeated
pregnancy is “contraindicated”—pt’s with
persistent LV dysfunction and pts with h/o
serious episode should be counseled to
avoid repeat pregnancy
Cardiomyopathy and Pregnancy
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Notes on medical therapy
NO ACEI, ARB during pregnancy. (in animals
fetal hypotension and death. Also early delivery,
low birth weight, oligohydramnios, neonatal
anuria and renal failure)
Digoxin and hydralazine are considered safe
during pregnancy and breast feeding.
Diuretics can be used if sx not controlled by
decreased salt and central venous pressue
elevated. Most experience with thiazides and
lasix. (diuretics impair uterine blood flow and
placental perfusion).
Metoprolol, atenolol, labetalol have been used
safely in pregnancy—fetal monitoring
recommended for risk of intrauterine growth
retardation and fetal bradycardia.
• #58
• 35 y.o. female who has progressive dyspnea
days after delivery. EF 20%. Treated ACEI,
diuretic, B-blocker. Sx resolve. 12 mos after
delivery asymptomatic and EF 50% off meds.
She comes to you for counseling re: repeat
pregnancy.
– Advise her that she may proceed
– Resume ACE I during pregnancy
– Advise her not to become pregnant b/c of risk of
recurrent peripartum cardiomyopathy that may be
fatal
– Evaluate for another cause of cardiomyopathy b/c
diagnosis of peripartum cardiomyopathy is now in
question
#58 Advise her not to become pregnant b/c of risk of
recurrent peripartum cardiomyopathy that may be fatal
• Because recurrence of peripartum
cardiomyopathy is common, repeated
pregnancy is contraindicated.
• Regarding cardiomyopathy in general and
pregnancy:
– Avoid pregnancy is LVEF is less than 40% or
NYHA functional class is higher than II.
– Bed rest is often required and close cardiac
and obstetric monitoring mandatory
– Treating CHF is more difficult in pregnant than
in nonpregnant women.
• #104 28 y.o. female with aortic and mitral
mechanical prosthesis. INR therapeutic. Prepregnancy consult.
– Discontinue warfarin and treat with ASA and
dipyridamole during first trimester
– Continue warfarin through pregnancy and start
heparin 5000 U SQ TID plus ASA
– d/c warfarin and treat with enoxaparin 30 mg SQ BID
through pregnancy
– d/c warfarin and initiate dose adjusted unfractionated
heparin SQ during first trimester and resume
treatment with warfarin for rest of pregnancy until
shortly before delivery
– Use clopidogrel and ASA for first trimester and
warfarin for rest of pregnancy until shortly before
delivery
initiate dose adjusted unfractionated heparin SC during first
trimester and then resume treatment with warfarin
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Anticoagulation and Pregnancy
• During pregnancy increased risk of thombosis
or embolism
• Pregnant women with mechanical heart valve
have a 10% risk for development of
prosthetic valve thrombosis or another life
threatening complication
• Data are limited on safety of various
anticoagulation regimens and controversy
persists
Anticoagulation and Pregnancy
• Heparin does not cross the placenta
• 12-24% incidence of thromboembolic
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complications including valve thrombosis in high
risk pregnant patients treated with SQ
unfractionated heparin
Efficacy of dose adjusted SQ heparin not
established. Dose should be adjusted so that PTT
is at lesat 2-3 times control value 6 hours after
adminstered.
Heparin may not provide sufficient
anticoagulation for very high risk patients (cagedball or tilting disk--Bjork Shiley--mechanical
prosthesis)
Prolonged heparin can lead to thrombocytopenia,
osteoporosis, alopecia
• Warfarin crosses the placentafetal
anticoagulationrisk of spontaneous
abortion, prematurity, fetal deformity,
stillbirth, retroplacental hemorrhage and
intracranial hemorrhage.
• Historic reports 30% (more recent data 410%) risk warfarin embryopathy— bone
and cartilage abnormalities, nasal
hypoplasia, optic atrophy, blindness,
retartdation, seizures--with use in first
trimester.
– risk highest if exposure during 6th to 12th wk.
– Low risk if less than 5 mg QD warfarin dose.
• Warfarin does not enter breast milk
Current Recommendations
for anticoagulation
during pregnancy
C-section if labor occurs during warfarin
anticoagulation due to risk of fetal intracranial
hemorrhage.
Anticoagulation and pregnancy …
Low Molecular Weight Heparin
• Currently data insufficient to support use LMWH
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during pregnancy.
It does not cross placenta and no teratogenic
effects reported.
6th ACCP conf supports use of LMWH throughout
pregnancy except 24 hrs before delivery when
recommendation is IV unfractionated heparin.
However FDA changed labeling to state
enoxaparin not recommended for prosthetic
valves during pregnancy.
More notes on Anticoagulation and pregnancy…
• Dipyridamole should not be used during
pregnancy (no data on clopidogrel or
ticlopidine)
• Information limited on IIbIIIa inhibitors
during pregnancy
• 81 mg ASA safe during pregnancy—
recommended for patients with shunts,
cyanosis, or biologic-valve prosthesis
– (A low dose of ASA may also decrease the
incidence of preeclampsia.)
• Thombolytic therapy has been used in
pregnancy in emergency
• #68 26 y.o. female 30 weeks pregnant
murmur noted during pregnancy.
Asymptomatic. Slight elevated JVP.
Parasternal lift. S1 normal. S2 prominent,
fixed split. Grade 2 mid peaking ejection
murmur LSB. Echo secundum ASD with
RV enlargement. 8 weeks later in labor.
What do you recommend?
– Full anticoagulation in postpartum period
– Hemodynamic monitoring during delivery
– ABX propylaxis during delivery
– Early post partum ambulation
– Delivery by c-section
• #68 Early post partum ambulation
– Decrease risk of DVT paradoxical
embolism
• #47 26 y.o. 30 weeks pregnant murmur
during pregnancy and intermittently in
past. Asymptomatic. Slight elevation JVP
with an A wave. Parasternal lift is noted.
S1 normal S2 prominent, fixed, split.
Grade 2 mid peaking ejection systolic
murmur at LSB. What is most likely Dx?
– Physiologic murmur of pregnancy
– ASD with volume overload
– Pulmonary valve stenosis
– Aortic regurgitation
– Mitral stenosis
# 47 ASD with volume overload
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• Other notes on congenital heart
disease in pregnancy
• Congenital heart disease is the most common
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form of structural heart disease that affects
women of childbearing age in US
Pregnant cyanotic women have a high risk of
fetal loss. Cyanosis is a recognized handicap to
fetal growth, resulting in low birth weigh infants
The incidence of congenital heart disease in
offspring of women with congenital heart
disease is about 5 %.
• #91 20 y.o. female in first trimester
progressive dyspnea. Acyanotic woman
with parasternal lift and loud P2. No S3 or
S4. No murmur. EKG tall P waves II, III, F
and tall R in V1 and RAD. What is most
likely dx?
– Severe pulmonic valve stenosis resulting in RV
pressure overload
– Primary pulmonary hypertension
– Large ASD causing RV enlargement and pulm
HTN
– Severe mitral stenosis
• #91 Primary pulmonary hypertension.
– ASD and VSD that result in severe pulm
HTN cause cyanosis.
– In pulm stenosis P2 would be
diminished or absent.
– Need to exclude secondary causes
pHTN.
Severe pulmonary
hypertension in pregnancy
• PA pressure >70% systemic
• Whether secondary or primary carries 3050% risk of maternal death.
• If pulmonary hypertension identified
counsel against pregnancy
• Termination of pregnancy should be
considered.
• #98 20 y.o. in first trimester of pregnancy
progressive dyspnea. You diagnose
severe pulm HTN. TEE excludes shunt.
What is associated with lowest risk of
maternal mortality?
– Termination of pregnancy
– Initiation of prostacyclin therapy
– Intiation of bosentan therapy
– Initiation of anticoagulation
– Initiation of ACEI therapy
#98—termination of pregnancy
Cardiac contraindications to pregnancy
“
”
Severe pulmonary HTN
is an absolute
contraindication to
pregnancy . 30-50%
risk maternal death.
Indications for C-section in women with
Cardiovascular Disease
• Obstetric reasons
• Anticoagulation with warfarin
• Controversial Reasons
– Fixed obstructive cardiac lesion
– Pulmonary hypertension
–
Unstable
aortic
lesion
____________________________
• Vaginal delivery is the preferred mode of
delivery in most women with heart
disease.
Valvular Heart Disease
#15
• 21 y.o. female, murmur on screening exam. No
PMH. Runs 3-8 miles daily for cross country. No
syncope. SOB with windsprints. No FH sudden
death. HR 52. BP 98/60. 2/6 cresendo
decresendo murmur loudest LUSB. Which would
suggest need for echo?
– Murmur decreases in intensity with valsalva
– SOB with unusual exercise
– Soft S3
– Murmur peaks in intensity in the latter half of
systole
– A split S1
#15 Murmur peaks in intensity in the latter half of
systole
• Late-peaking suggests LV outflow
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obstructionfurther testing.
Murmur of dynamic subvalvular LV outflow
obsturction (hypertrophic cardiomyopathy)
increase with valsalva.
AS and PS and MR and TR diminish during
valsalva.
Intensity of innocent flow murmurs also diminish
during valsalva.
Flow murmurs peak in the first half of systole
An S3 is common in children and young adults
Echo for evaluation of murmurs
Murmurs….
• VSD: pansystolic, palpable thrill may be
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associated
PDA: continuous, machinery-like
Increase with Inspiration
– TR, TS, PS (right sided murmurs)
• Increase with Handgrip
– Mitral regurgitation
• Aortic Stenosis
– Decrease with handgrip, decrease with standing,
decrease during valsalva
• Hypertrophic Obstructive Cardiomyopathy
– Decrease with handgrip, increase with standing,
increase during valsalva
• 63 y.o. male farmer. 3/6 holosystolic
murmur at apex heard throughout and
louder at left sternal border. LV displaced
laterally. HR 94. BP 136/80.
ASYMPTOMATIC. Echo--myxomatous
degeneration MV with partial flail posterior
leaflet. LV enlarged. LV EF 52%.
– Surgery if LV dilated 8 weeks after ACEI
– Surgery if MIBI normal
– Surgery if TEE shows repairable valve
– Surgery despite lack of symptoms
– Surgery contraindicated based on presence of
LV dysfunction
Chronic severe MR w/ LV dysfunction
--Surgery despite lack of symptoms
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• Indications for surgery in chronic
severe mitral regurgitation
Symptoms
Left ventricular systolic dysfunction
(EF<60%, endsystolic diameter>45mm)
Atrial fibrillation
Pulmonary hypertension
• Intervention for chronic severe MR should
be considered earlier if successful mitral
valve repair is likely
Chronic Mitral regurgitation
• Organic: Myxomatous degeneration,
rheumatic, infective endocarditis …
• “Functional”: Dilated cardiomyopathy,
ischemic (prior MI)
• Chronic left ventricular volume overload
• Forward CO preserved by LV dilation at
expense of increased wall stress
Chronic Mitral regurgitation
• Vasodilators improve hemodynamics in
acute MR, role in chronic MR not
adequately studied. Thus routine use in
asymptomatic pts not recommended. If
HTN present, then vasodilator. And, in pts
with functional MR complicating
cardiomyopathy, afterload reduction is
indicated.
• In anorectic drug (fenfluramine and
dexfenfluramine) induced MR (or AR)
regurgitation appears to regress in the
first year after discontinuation of
exposure.
• # 51. 54 y.o. female evaluated for exertional dyspnea.
Orthopnea for mos. Rheumatic fever as a child. No
palpitations. HR 86, BP 124/76. JVP 14. Bibasilar rales.
Regular rhythm, diminished S1, widely split S2. 3/6
holosystolic murmur at apex radiating to axilla. 2/6
holosystolic murmur at LLSB increases with inspiration.
2/6 decresendo diastolic rumble at apex. EKG sinus,
RVH, BAE. Echo-- BAE, normal LV size and fxn. RVE,
normal fxn. Mitral leaflets thickened and restricted.
Minimal leaflet Ca++ and mild to mod subvalvular
thickening. Mean grad 11 and valve area 0.9 cm2.
Severe MR and TR noted. RV systolic 62 mmHg. Best
course of action?
– Digoxin
– ASA
– Anticoagulation INR 2-3
– Percutaneous balloon mitral valvotomy
– Refer for mitral valve repair or replacement
# 51 mitral valve repair or replacement
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•
Interventions Mitral Valve
Percutaneous balloon mitral valvotomy:
– Pliable, non-calcified valve, </= 2+ MR, no other
cardiac intervention required
– (3 or 4+ MR, LA thrombus contraindications)
• Open commissurotomy
– Relatively pliable noncalcified valve, any amount MR,
no other cardiac intervention required
• MVR
– Calcified nonpliable valves
• In pregnant women, ballon valvotomy
associated with fewer fetal complications than
open commussurotomy
Mitral Stenosis
• Often due to previous rheumatic heart disease
• Normal MVA 4-5. Mod MS 1-1.5, Sev MS<1cm2.
• MS exacerbated by a.fib, exercise, stress, fever,
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pregnancy (b/c increased HR leads to shorter diastolic filling period)
Abx prophylaxis against endocarditis and
rheumatic fever (at least 10 yrs after last
episode or until age 40, lifetime in high risk (ie.
teachers), salt restriction, diuretics, negative
chronotropic (prolong filling period) agents.
Anticoagulation if a.fib or prior thomboembolus.
Echo if change in symptoms. Mild to mod pHTN
(PASP >40) may be indication for more frequent
follow up.
• #80
• 36 y.o. with substernal chest pressure. 2 mos
progressive fatigue, dysnea, palps. 2 hours
began CP to jaw, SOB. BP 110/90. HR 110 and
irregular. Elevated JVP, crackles, irregular,
accentuated P2. diastolic rumble at apex. EKG
a.fib, RBBB, RAD, ST elevation V2-5. Cause?
– CAD plaque rupture
– Coronary thromboembolism from LV thrombus
– Coronary thromboembolism from LA thrombus
– Coronary arteritis
– Coronary vasospasm
• # 80 Coronary embolism from LA
thrombus
• #75 28 y.o. female with palpitations
(heavy beat then pause) no associated sx.
HR 72 BP 108/68. Mid systolic
nonejection click. EKG sinus no
preexcitation. Echo posterior leaflet
prolapse with mild late systolic MR. Holter
multiple PVC’s. Next step?
– History and PE in 1-2 yrs
– TEE
– Lisinopril
– Echo in 6 mos
– Propafenone therapy
#75 History and PE in 1-2 years
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–Mitral Valve prolapse
• Most patients with MVP have a good
prognosis
• Patients with myxomatous disease are at
risk for valve degeneration with MR
• Endocarditis prophylaxis in patients with
MR or leaflet thickening
• MVP syndrome—palpitations and atypical
chest pain
#23
• 76 y.o. male to your office for yearly exam.
•
Over 6 mos decreased exercise tolerance—
dyspnea and CP uphill. No SOB at rest. No
syncope. CAD. Lipids. h/o stent. ASA. Lipitor.
HR 82. BP 142/82. 3/6 cresendo decresendo
systolic RUSB to carotids. Delayed upstroke of
pulse. Echo LVH, nl fxn. Peak aortic 86, mean
44. Mid RCA 70%. 0.7 cm2.
What is the best course of action?
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Refer AVR and CABG
Refer valvotomy and PTCI
DP MIBI
Exercise testing
No intervention
# 23 AVR plus CABG
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• # 116 71 y.o. male CHF. LV impulse
enlarged and lateral. Late peaking
cresendo decresendo systolic murmur.
Echo global LV dysfunction. EF 20-25%.
AV calcified decreased opening. Peak grad
26 mean 16. What test next?
– TEE
– Exercise stress test with EKG
– Dobutamine stress echo
– Adenosine MIBI
# 116 Dobutamine stress echo
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– Low gradient Aortic Stenosis
• Aortic valve gradients depend on flow
• Patients with LV dysfunction have increased
•
perioperative risk
An increase in aortic gradients in setting systolic
augmentation of LV suggests AS is severe. (AVR
better long term survival than med if severe AS and contractile reserve)
• Contractile reserve without an increase in
•
gradients suggest that stenosis is not severe.
Lack of contractile reserve suggest a poor
prognosis after AVR. (AVR worse long term survival than meds if
no contractile reserve)
More notes on Aortic Stenosis …
• Asymptomatic patients with severe AS
have a good prognosis
• Severe AS valve area <1.0cm2, mean
gradient >50 mmHg.
• Consider patient size. Valve area of
0.45cm2/m2 is severe.
• Echo follow up in asymptomatic AS
– Every 5 years mild
– Every 2 years moderate
– Every year severe (to detect development
asymptomatic LV dysfunction)
More notes on Aortic Stenosis …
• AVR in symptomatic patients with severe AS.
• Consider AVR in asymptomatic patients with
•
severe stenosis AND left ventricular dysfunction,
marked LVH, hypotension on exercise testing, or
moderate or greater valve calcification and a
rapid increase in aortic jet velocity.
Added risk for noncardiac surgery in severe
symptomatic AS (mortality rate as high as 10%)
– if elective AVR first,
– if not surgical (AVR) candidate percutaneous
valvuloplasty may be considered
• If severe AS but asymptomatic noncardiac
surgery can be performed with close
intraoperative monitoring with only slightly
increased risk.
• # 66 36 y.o. man to ICU with abrupt
hypotension and hypoxemia. Intubated.
38.1, 121, 88/30, pulm edema. Regular
with summation gallop. No murmur. TTE
inadequate. TEE bicuspid AV partially
destroyed with vegetations. Severe AI.
Normal LV fxn. You start abx. Which is
indicated?
– B-blocker
– Nitroprusside
– Intraaortic balloon pump
– Cath and coronary arteriography
– Transfer for surgery for emergent AVR
(#66 Nitroprusside)
• After load reducing therapy with or
without inotropic support to optimize
forward cardiac output
• IABP contraindicated in aortic regurg
• Depending on response to intensive
medical intervention patient may require
urgent surgery. If surgery can be deferred
to allow a period of therapy with ABX early
postop infection after AVR is less likely.
Notes on acute valve regurgitation
• Patients with acute severe AR or MR are
•
•
•
•
symptomatic and may present with cardiogenic
shock
Many physical findings of chronic severe
regurgitation are NOT present in patients with
acute severe regurgitation
Diagnosis is with echo
IABP useful in acute severe MR but
contraindicated in AR
Urgent or emergent surgical intervention is
usually indicated in acute mitral or aortic
regurgitation
• # 85 86 y.o. female evaluated for recent
abrupt onset dyspnea. She had a
bioprosthetic AV placed 16 years ago for
calcific AS. No fever. Harsh cresendo
decresendo systolic murmur at RUSB to
carotids. What is cause of SOB?
– Prosthetic valve failure
– Paraprosthetic leak
– Thrombus formation
– Mitral stenosis and mitral regurgitation
– Infective endocarditis
• #85 Prosthetic valve failure
After 16 yrs valve at risk for failure, cuspal
calcification and then fracture leading to acute
AR. Intuitively should expect diastolic murmur.
However murmur of AR may not be prominent
whereas the increase in stroke volume across
calcified bioprosthesis is more audible.
Thombosis not likely in bioprosthetic valve
placed years earlier.
• KEY POINT—In patients with prosthetic
valves and new/changed cardiac
symptoms, need to evaluate valve.
• #100 35 y.o. female for f/up AVR 3 mos
ago for congenital bicuspid aortic valve.
No a.fib or thromboembolism. Echo
shows normal mechanical aortic valve.
– Coumadin INR 2-3
– INR 2.5-3.5
– INR 2-3 plus ASA 100 mg
– INR 2.5-3.5 plus ASA 100 mg
– ASA 650 mg QD
#100 INR 2-3. Prosthetic Valves
Preoperative Cardiac
Evaluation
• ACC/AHA Guidelines.
– The need for preoperative testing is determined by:
• 1)Clinical predictors of the patient
(minor/intermediate/major).
• 2)Risk of the surgery (low/intermediate/high).
• 3)Patient’s functional status (</> 4 METS).
– Remember that all patients requiring emergent
surgery go to the OR immediately regardless of
cardiac risk.
• Don’t forget benefit of Beta-blockade to goal HR 60
Patient Clinical Predictors
Risk of Surgery
Functional Capacity
Shortcut to noninvasive testing in
preop patients if any two factors
are present
– Intermediate clinical predictors (class 1
or 2 angina, prior MI based on Q’s,
compensated or prior heart failure, diabetes,
or renal insufficiency)
– Poor functional capacity
– High risk surgery (emergency—may not
have a choice---,aortic repair, peripheral
vascular surgery, prolonged surgical
procedures with large fluid shifts or blood
loss)