Aortic Stenosis in Pregnancy

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Aortic Stenosis in Pregnancy

• Brendan Astley MD
• Norman Bolden MD

Nov 2006
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18 year old G1P0 Spanish speaking female

• PMH- Heart condition since age 12 (no further
  follow-up)
• SOB and CP at rest and exertion worse over last
  two years
• PSH- none
• Medications- PNV
• Allergies- NKDA
• FH- unknown
• SH- no tobacco, EtOH or drug use

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Physical Exam

• Vitals BP 104/62 HR 79 temp 36.6 RR 18
• sat 100
• Height 410 Weight 99lbs. now 119lbs.
• Heart IV/VI systolic murmur cresendo-decresendo
  murmur with no diastolic component, heard best
  at R upper sternal border, radiation to carotids
  bilaterally, no JVD, no 3rd or 4th heart sound
• Airway nml, Mal I
• Lungs CTA Bil., no w/r/r
• Abd NT gravid uterus, soft
• Ext no edema good pulses distally

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• Labs B positive
• BNP 5.5
• WBC 8.71, Hg 12.5, Hct 36.8, Plts 256
• Na 136, K 3.9, Cl 108, CO2 21, BUN 5, Cr 0.5, Glu
  71
• Ca 8.5
• TSH 0.9, RPR, NR, HIV, VZ immune, RI, GC/ chlam,
  hep B all negative

• Plan Admit to antepartum unit (social admission)
  to facilitate consultations by Maternal/Fetal
  Medicine, Cardiology, NICU and Anesthesiology.

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Cardiology

• Murmur appreciated and echo performed on 9/15
  showing AS lt.6cm2, probable bicuspid valve and EF
  65.
• Pt followed for change in symptoms.
• Mid Oct. at about 35 wks. Gestation she complains
  of increased CP and SOB especially with exertion
  but also at rest.
• .1-1.4 pregnancies with clinically significant
  cardiac problems
• Mortality from these .5-2.7

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Cardio contd

• Echo shows peak gradient of 62mmHg and .58cm2
  orifice by the continuity equation.
• Velocity waveform is asymmetric which usually
  equates with less than severe stenosis.
• CXR- WNL, no cardiopulmonary disease
• CXR abnormalities may include enlarged aorta,
  cardiomyopathy and possibly pulm. edema

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Expected EKG changes with AS

• Left ventricular hypertrophy (LVH)
• There are many different criteria for LVH.
• Sokolow Lyon (Am Heart J, 194937161)
• S V1 R V5 or V6 gt 35 mm
• Cornell criteria (Circulation, 19873 565-72)
• SV3 R avl gt 28 mm in men
• SV3 R avl gt 20 mm in women
• Framingham criteria (Circulation,1990
  81815-820)
• R avl gt 11mm, R V4-6 gt 25mm
• S V1-3 gt 25 mm, S V1 or V2
• R V5 or V6 gt 35 mm, R I S III gt 25 mm
• Romhilt Estes (Am Heart J, 198675752-58)
• Point score system
• Left atrial abnormality (dilatation or
  hypertrophy)
• M shaped P wave in lead II
• prominent terminal negative component to P wave
  in lead V1

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? Suggestions for Anesthetic Plan

• Anesthesia for Vaginal Delivery
• Monitors for Vaginal delivery
• Anesthesia for C/S
• Monitors for C/S.
• Maternal-Fetal Medicine, Cardiology , NICU, and
  Anesthesia develop working plan.
• If possible, avoid C/S. If vaginal delivery,
  must avoid valsalva.

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Anesthesia for Vaginal Delivery

• Neuroaxial anesthesia
• Continuous Spinal
• Single shot spinal not reasonable for prolonged
  labor
• Reliable block
• Intrathecal narcotics avoid the sympathectic
  block with ensuing hypotension
• Intrathecal narcotics not effective for second
  stage of labor.
• Small doses of intrathecal LAs added to narcotics
  improve analgesia while limiting hemodynamic
  consequences.
• Chance for spinal headache

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Anesthesia for Vaginal Delivery

• Neuroaxial anesthesia
• Epidural
• Prostitratable to produce minimal hemodynamic
  changes, adequate anesthesia possible for vaginal
  or C-section, if performed properly no spinal
  headaches
• Conshigher failure rate compared with spinal

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Anesthesia for Vaginal Delivery

• IV Narcotic analgesia (PCA)
• Proswould offer patient some analgesia (most
  still report 8-10/10 pain despite Fentanyl PCA)
• Cons Respiratory Depression (mother and fetus),
  Sedation (mother and fetus), N/V, decreased beat
  to beat variability on fetal heart rate tracing.
• Cons.Would not effectively control the pain from
  second stage of labor and therefore would not
  attenuate the increase in HR associated with
  delivery.

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Stages of Labor

• 1st stage 2 phases
• latent phase encompasses the onset of pain to the
  first noticed change in cervical dilation
• Maximal dilation phasebegins around 3 cm
• 2nd stage Maximal cervical dilation 10cm until
  delivery of fetus
• 3rd stage After delivery of fetus until
  delivery of placenta

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Board Questions??

• During the first stage of labor, the pain of
  uterine contractions is transmitted via spinal
  cord segments..
• AT6 to L1
• BT6 to L5
• CT10 to L1
• DT10 to S1
• ET10 to S5
• Answer is.C

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Anesthesia for C-section

• General anesthesia
• Prosgood airway control, minimal hemodynamic
  changes compared to epidural/spinal boluses to
  start case, can treat hemodynamic changes rapidly
  with close monitoring
• Conspossible difficult airway, aspiration risks,
  tachycardia and/or hypertension on induction or
  emergence, caution with volatile agents and
  hypotension or myocardial depression

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Hospital Course

• Induced to L D at 35 weeks.
• Arterial line placed
• Swan-Ganz catheter placed
• Early epidural also placed by anesthesia
• Continuous Telemetry monitoring
• Pitocin was started on the night of 11/7 and by
  morning she was well dilated and contracting
  regularly

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PCWP/CVP readings

• 11/7
• 1950hrs PCWP 10-11, CVP 5-7, good UOP
• 2330hr PCWP 10-13
• 11/8
• 0100 PCWP 7-9complains of CP
• 0300CVP 15-16, trop .15
• 0500 PCWP 11-15, CO 5L/min
• 0800 trop lt.1 (nml)
• Wedge maintained in above normal range
• Delivery at 1130am

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Hospital Course contd

• No symptoms of AS during induction course.
• Ready for delivery in AM with forceps
• No valsalva by mother and epidural working well
  with slow dosing.
• PCWP and urine output maintained throughout
  delivery with fluids and gentle epidural dosing.

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Hospital Course contd

• After forceps delivery pt transferred to
  Step-Down on esmolol drip due tachycardia.
• Drip stopped in CCU 11/8 and gentle diuresis
  started with Lasix.
• Stable vital signs throughout hospital stay.
• Day 3 post-forceps delivery patient transferred
  home with 6 week follow-up with cardiology for
  possible valve replacement.

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Physiologic Changes during pregnancy

• Beginning to change at 5 weeks10 fold increase
  in uterine blood flow at term
• Cardiovascular Blood volume 35, CO
• 40-50, SV 30, HR 15-20
• Cardiovascular SVR 15, sys and diastolic BP
  10mmHg
• Pulmonary Changes O2 consumption 20, RR
  15, MV 50, TV 40, alv vent. 70
• ERV 20, FRC 20

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Aortic Stenosis

• In the past Rheumatic Valvular degeneration was
  the primary cause
• Congenitally bicuspid valves become calcified and
  cause stenosis most commonly now(1-2 of
  population)
• Senile degeneration can also occur
• 30 of patients older than 85 have significant
  changes
• Risk for sudden death with AS increases when
  grad. gt50mmHg and orifice less than .8cm2

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Normal Anatomy
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Aortic stenosis Anatomy
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AS 2D echo

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Symptoms

• Rheumatic AS patients may remain asymptomatic for
  40 years
• Bicuspid valve patients will develop symptoms
  between 15-65 years of age
• Calcifications of the valve usually occur after
  age 30
• THE TRIAD.

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The triad

• Any one of these symptoms being present is
  ominous and the patients life expectancy is less
  than 5 years
• ANGINA
• SYNCOPE
• CHF

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Angina

• This is the initial symptom in 50-70 of
  patients. Most commonly occurring with exertion
• May be present without CAD b/c of
• Increased myocardial O2 consumption, with
  increased myocardial thickness and increased
  afterload
• Also increased LVEDP impairing flow to
  subendocardial layers

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Syncope

• First symptom in 15-30 of patients
• Once this occurs the average life expectancy is
  3-4 years
• Origin of syncope is controversial, however it
  may be related to uncompensated decrease in SVR
  with exercise

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CHF

• Due to diastolic dysfunction (increased LV
  thickness) or systolic dysfunction (increased
  afterload or decreased myocardial contractility)
• Once LV failure occurs the average life
  expectancy is 1-2 years
• All AS patients are at increased risk of sudden
  death, as previously stated and.
• Only 18 of patients are alive 5 years after the
  peak systolic gradient is gt50mmHg or the orifice
  lt0.7cm2

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Pathophysiology

• Stage 1 asymptomaticmild stenosis
• Normal stroke volume maintained as gradient
  between LV and aorta increases
• Higher gradient results in concentric LV
  hypertrophy

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Pathophysiology

• Stage 2 moderate stenosissymptomatic
• Dilation as well as hypertrophy occur in this
  stage
• Decreased EF may be noted (due to decreased
  contractility)
• Increased LVEDP and LVEDV leads to increased
  myocardial work and O2 consumption.at risk
  myocardium

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Pathophysiology

• Stage 3 critical AS
• Valve area is less than .5cm2/m2 and EF decreases
  further with further increases in LVEDP
• Pulmonary edema when LA gt25-30 mmHg
• RV failure will develop if sudden death does not
  occur first

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Calculation of Stenosis

• Gorlin equation AV area (cm2)
• CO (L/min)/
• Mean pressure gradient1/2
• This is the simplified version of the Gorlin
  equation (Hakki equation)

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Continuity equations

• AV areaLVOT velocity/AV velocity x LVOT area
  ---LVOT calculation can have errors because its
  an area squared.
• AV area CO/(HR x systolic ejection period x 44.3
  x gradient in mmHG1/2) ---Gorlin equation weak
  under low CO states
• Hakki equationbased on the fact that HR x sys
  ejection period x 44.3 1000 therefore AV Area
  CO/ sq root of gradient (mmHg)

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PA Cath

• Because of increased LVEDP stretching the mitral
  annulus a prominent v wave can be observed with
  disease progression. LA hypertrophy develops and
  the A wave becomes prominent
• Example to follow on next slide

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Arterial line

• Pulsus parvus (narrow pulse pressure)
• Pulsus tardus (delayed upstroke)
• These features make the wave appear overdampened

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Hemodynamic profile

• AS increase LV preload and SVR
• Decrease HR
• Keep contractile force and PVR constant
• Preload because of Decreased LV compliance as
  well as Increased LVEDP preload augmentation is
  needed
• (caution with nitro)

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Hemodynamics continued

• Heart rate no extremes of HR
• Increase HR decreased coronary perfusion
• Sinus rhythm important for added EF
• Contractility
• avoid B-blockers they can increase LVEDP and
  decrease CO

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Hemodynamics continued

• SVR most of afterload is due to stenotic lesion,
  therefore its fixed.
• If SBP is decreased the patient can develop
  subendocardial ischemia
• Early alpha-adrengic agonists needed as treatment
• PVR this stays normal until very late in the
  disease process

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Toronto study

• 1986-2000 of 49 pregnancies in women with AS
• Mild AS (gt1.5cm2 or gradlt36mmHg)
• Mod AS (1.0-1.5cm2 or grad 36-63mmHg)
• Severe AS (lt1.0cm2 or grad gt63mmHg)
• All women had functional NYHA class I or II
  disease when enrolled
• 59 of patients, 29/49 had severe AS
• Silversides C.K., Colman J.M., Sermer M., Farine
  D., Sui S. C., Early and intermediate-term
  outcomes of pregnancy with congential aortic
  stenosis. American Journal of Cardiology
  20039111

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NYHA functional classification

• Class I Asymptomatic
• Class II Symptoms with greater than normal
  activity
• Class III Symptoms with normal activity
• Class IV Symptoms at rest

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Toronto study continued

• 10 of severe AS patients (3/29) had early
  cardiac complications (pulmonary edema or atrial
  arrhythmias)no complications in mild/mod groups
• One pt. had AVA .5cm2, peak gradient 112mmHg, she
  developed pulmonary edema at 12 weeks had
  emergent aortic valvuloplasty then had a Ross
  procedure 4 years after delivery
• The second pt. had gradient of 104mmHg she had
  postpartum hemorrhage, hypotension and subsequent
  pulmonary edema. Resection of her subaortic
  membrane was performed 17 months after delivery.
• The third pt had a bicuspid valve AVA .7cm2,
  gradient of 64mmHg, she had atrial arrhythmias
  during antepartum period. She underwent a Ross
  procedure 18 months postpartum.

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Ross procedure

• Pulmonary valve is removed and placed into Aortic
  valve position and a cadaver valve is placed into
  the pulmonary valve position
• Advantages include no anticoagulation required
  so their next pregnancy may not be as complicated
  and a longer duration of use for aortic valve
  should be possible, with a lower rate of
  infection post-op

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Toronto Study continued

• 8 mild/mod AS had cardiac surgery in follow-up
  and 41 of severe AS group had post-partum
  cardiac surgery10 with severe AS had cardiac
  complications during pregnancy
• 12 pregnancies complicated by preterm birth,
  resp. distress syndrome, IUGR
• Rate is similar general population
• No fetal or neonatal deaths
• Silversides CK, Colman JM, Sermer M, Farine D,
  Siu SC. Early and intermediate-term outcomes of
  pregnancy with congenital aortic stenosis. Am J
  Cardiol 200391(11)1386-9

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Brazilian study

• Study of 1000 women with heart disease followed
  between 1989-1999
• HD-- Rheumatic HD 55.7, Congenital HD 19.1,
  Chagas disease 8.5, arrhythmias 5.1 and
  cardiomyopathies 4.3
• A subset of patients who had moderate to severe
  AS experienced 68.5 maternal morbidityi.e. CHF
  angina
• 2 needed Aortic valve replacement
• 1 sudden death
• Avila WS, Rossi EG, Ramires JA, Grinberg M,
  Bortolotto MR, Zugaib M, et al. Pregnancy in
  patients with heart diseaseexperience with 1000
  cases. Clin Cardiol 200326(3)135-42

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Anesthetic management goals

• Maintain Normal Sinus Rhythm up to 20 of CO is
  provided by atrial kick in a normal patient and
  possibly up to 40 in AS pts.
• Maintain HR 70-90 Bradycardia decreases CO in pt
  with fixed stenotic lesion and tachycardia does
  not allow for diastolic filling of ventricles.
• Generous preload maintain at normal to high
  range.

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Anes. Management goals contd

• Close hemodynamic monitoring Arterial line and
  with moderate to severe stenosis- PA cath/TEE to
  help delineate hypovolemia from CHF. Be prepared
  for cardioversion urgently
• Lidco may be useful
• No Valsalva and minimize pain. These could affect
  preload and sympathetic response (HR, BP) and
  worsen her condition acutely.
• Narcotic based anesthetic preferred in unstable
  or severe AS patients (50-100mcg/kg IV)

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After Hospital stay

• Pt seen by cardiology follow up post-op and
  Cardiothoracic surgery
• She was recommended for valve surgery
• Cardiology has sent her letters warning of sudden
  death as this patient has no longer been coming
  to her appointments and is currently lost to
  follow upwith no valve replacement

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