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Kira - Mat Med > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Discuss arrythmias in pregnancy
-Pregnancy affect on arrythmia (2)
-Most common types of arrythmias (2)
-Presentation
-Investigations

A
  1. Pregnancy affect on arrythmias:
    -Increase in severity and frequency due to increased HR/SV/CO/Blood volume
    -Commonest complication in women with congenital heart defects
  2. Most common arrythmias
    -SVT most common
    -Atrial/Ventricular ectopics 50-60% of pregnancies
  3. Presentation
    -Symtpoms of arrythmias do not corelate well with arrythmias
    -Only 10% of women with arrythmia sx have an arrythmia
  4. Investigations
    -Look and exclude precipitating causes Hyperthyroid, anaemia, PE, infection
    -ECG
    -Holter monitor
    -Echo to exclude structural heart defect
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2
Q

How should different arrythmias be managed
-General principles (3)
-Atrial/Ventricular ectopic beats
-Sinus tachycardia
-Atrial fibrillation
-Supraventricular tachycardia
-Ventricular tachycardia

A
  1. General principles
    -Beta-blockers = first line
    -Digoxin for rate control
    -Avoid amiodarone - fetal tachycardia, neonatal hypothyroid, FGR
  2. Atrial/Ventricular ectopic beats
    -Reassurance
    -Avoid caffeine, smkoing, drugs
  3. Sinus tachycardia
    -Investigate for underlying causes
    -If no causes then no treatment required
  4. Atrial fibrillaiton (Rare. Seen with ASD or mitral valve disease)
    -Beta blockers, digoxin, cardioversion
    -Give thromboprophyaxis
  5. SVT
    -Vagal manouvers
    -Adenosine
    -Second line - digoxin, verapamil, flecanide, esmolol, cardioversion
  6. VT
    -Cardioversion if unstable
    -Flecanide if stable
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3
Q

Discuss myocardial infarction in pregnancy
-Incidence (2)
-Causes (3)
-Risk factors (7)
-Presentation (2)
-Managment (4)

A
  1. Epidemiology
    -1:10000
    -Responsible for 5-7% of maternal death
  2. Main causes
    -Atherosclerosis IHD causes < 50% of MI
    -Coronary thrombosis
    -Coronary artery dissection
  3. Risk factors
    -DM, HTN. Hyperlipidemia, smoking
    -Cocaine
    -Age
    -40% have no risk factors
  4. Presentation
    -Usually atypical - epigastric pain or nausea
    -Usually occurs in 3rd trimester, peripartum or postpartum
  5. Management
    -GTN, ASpirin, clopidogrel
    -Beta blockers, nitrates, CCB
    -Percutaneous coronary intervention
    -Offer CS if MI within 2 weeks of delivery
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4
Q

Discus management of pregnant women who have had previous myocardial infarction (5)

A
  1. Pre conception stress test and echo to assess LV function
  2. Stop statins - tetarogenic
  3. Low dose aspirin and beta blockers for secondary prevention
  4. Restrict physical activity
  5. Monitor for arrythmias and CHF
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5
Q

Discuss the association of familial congenital heart defects with risk of congenital heart disease in a fetus and percentages (10 points)

A
  1. If mother has a CHD then risk = 5%
  2. More likely to be outflow tract abnormality
  3. More likely if mother (5%) affected cf with father (2%)
  4. ASD - 4-5%
  5. VSD - 6-10%
  6. Siblings are affected - 3%
  7. Mafans or HCM - 50% (Autosomal dominant)
  8. Rubella infection
  9. Diabetes
  10. Maternal age over 40
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6
Q

Discuss maternal patent ductus arteriosus in pregnancy
-Describe pathology
-Clinical features
-Issues in pregnancy
-If corrected
-If not corrected

A
  1. Pathology
    -Persistant patent duct between decending aorta and pulmonary trunk or L pulmonary artery
  2. Clinical features
    -Mainly asymptomatic
    -Continuous machinery murmur, LVH
  3. Issues in pregnancy if corrected
    -Nil issues
  4. Issues in pregnancy if not corrected
    -Congestive heart failure, pulmonary HTN
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7
Q

Discuss maternal atrial septal defects in pregnant women
-Incidence
-Clinical features
-Issues in pregnancy
-Management in pregnancy
-Impact to fetus is unrepaired

A
  1. Incidence
    -Most common CHD in women
  2. Clinical features
    -Usually ASx. Can Have RBBB, ESM, RVH
  3. Issues in pregnancy
    -Increase in arrythmias
    -Increase in RH volume overload and enlargment
  4. Management in pregnancy
    -Avoid hypotension
    -Echo and ecg
  5. Impact to fetus if not repaired
    -SGA
    -Increased PET
    -Fetal mortality
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8
Q

List the maternal congenital cardiac anomalies associated with high risk or poor maternal outcome or death (6)

A
  1. Pulmonary HTN
  2. Eisenmengers syndrome
  3. Coarchtation of the aorta - uncorrected with proximal dilitation of the aorta
  4. Marfans syndrome with aortic root dilitation >4.5cm
  5. Severe symptomatic aortic stenosis
  6. Single ventricle with poor systolic function (fontans or non-fontans)
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9
Q

List the maternal congenital anomalies associated with moderate risk of pregnancy complications (5-15%) (4)

A
  1. Unrepaired cyanotic defects (TOF, TGA)
  2. Systemic R ventricle (Repaired TGA)
  3. Well functioning fontans circulation
  4. Palliated TOF with severe pulmonary regurg and RV dysfunction
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10
Q

List the maternal cardiac congenital anomalies associated with low risk of pregnancy complications (<1%) (4)

A
  1. Isolated ASD - repaired or not repaired
  2. Isolated VSD - repaired or not repaired
  3. TOF with normal RV function and competent Pulmonary valve
  4. Coartation repaired with normal proximal aortic size
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11
Q

Discuss maternal ventrical septal defect in pregnancy
-Incidence
-Complications
-Clinical features
-Management in pregnancy

A
  1. Incidence
    -Large are rare as symptomatic in early life and repaired
    -Associated with T21, TOF or isolated
  2. Complications
    -L to R shunt worsened with increased peripheral vascular resistance
    -Increase in thromboembolism
    -Increased Pulmonary HTN and Eisenmengers
  3. Clinical features
    -Usually Asx
    -PSM, prominant apex beat
  4. Management in pregnancy
    -Avoid pregnancy in Eisenmengers syndrome 50% maternal death rate
    -Consider thromboprophylaxis
    -Isolated VSDlow risk in pregnancy if small. If large fix pre pregnancy
    -Avoid hypotension in labour to avoid shunt reversal
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12
Q

Discuss maternal congenital aortic stenosis in pregnancy
-Most common type
-Significant parameters
-Signs of decompensation
-Management in pregnancy

A
  1. Most common type
    -Bicusip valve
  2. Significant parameters
    -AV area <1cm, Gradient >50mmHg
  3. Signs of decompensation
    -Tachycardia (HR increases to maintain BP with decreasing SV)
    -Fixed gradient
    -Angina
    -Heart failure
  4. Management in pregnancy
    -Consider termination if severe and symptomatic AS
    -Beta blockers if LV function is good to increase diastolic filling
    -Surgical balloon valvuloplasty in pregnancy if required before value replacement
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13
Q

Discuss maternal coarctation of the aorta in pregnancy
-Risk associated with coarctation during pregnancy (5)
-Presentation (3)
-Management (2)

A
  1. Risks
    -Usually corrected but correction doesn’t eliminate all risk (10% WHO II-III)
    -If uncorrect risk of maternal death >40%
    -HTN esp in upper body with uterine hypotension
    -Aortic rupture
    -Aortic dissection - risk remains even with correction
  2. Presentation
    -Difference in upper and lower limb pulses
    -CXR shows prominant aortic knob, indentation of proximal thoracic descending aorta
  3. Management
    -If uncorrected advise surgical correction pre-pregnancy or TOP
    -Assess for aneurysm or post stenotic dilitation
    -Strict BP control with beta blockers
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14
Q

Discuss maternal TOF in pregnancy
-Incidence (1)
-Pathophysiology
-Impact to pregnancy (3)
-Impact to fetus (3)
-Management in pregnancy (3)

A
  1. Incidence
    -Most common cyanotic congenital heart defect
  2. Pathology
    -Large LSD
    -Over riding aorta
    -Pulmonary stenosis
    -R ventricular hypertrophy
  3. Impact to pregnancy
    -Not repaired
    -Increase R to L shunt and hypoxia
    -Increase CVA with paroxismal embolism crossing shunt
    -If repaired
    -Worsening RV function from pulmonary regurg from surgery
  4. Impact to fetus
    -If not repaired causes hypoxemia = SGA, pregnancy loss, polychythemia and clotting
  5. Management in pregnancy
    -VTE prophylaxis
    -Elective admission for bed rest and O2 therapy
    -Gentic testing for Di-Goerges syndrome (50% recurrence)
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15
Q

Discuss maternal transposition of the great arteries in pregnancy
-Pathophysiology of TGA
-Surgical corrections
-Risks in pregnancy
-Management

A
  1. Pathophysiology
    -RV feeds into the aorta
    -LV feeds into the pulmonary circulation
    -Without correction it is incompatible with life
  2. Surgical corrections
    -Switch so that systemic venous return goes to LV then PA
    and pulmonry venous return goes to RV then to system. This means RV acts as LV which it is not set up to do and can weaken over time
    -Fontan procedure: RV acts as single ventricle for pulmonary and systemic circulation. Needs adequate pre-load but not too much the heart can’t handle. O2 sats low
  3. Risks in pregnancy
    -Well tolerated if RV normal and no arrythmia
    -Worsening of existing arrythmias
    -Pregnancy may have long lasting impact of ventricle function
    -Oedema, ascities
  4. Management
    -Prenatal assessment of RV function, heart rythum and stress test to check can accommodate increased HR
    -Antenatal - serial echos to assess RV and valve function
    -Thromboprophylaxis
    -Bed rest
    -Delivery and peripartum care in an experienced center
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16
Q

What is the incidence in:
-Serious cardiac disease complications in pregnancy
-Maternal deaths from serious cardiac disease

A
  1. 1% of pregnancies
  2. 2.3 per 100,000
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17
Q

Discuss preconception workup for women with cardiac disease
-Assessment of maternal risk - significant predictors (5)
-When to advise avoiding pregnancy (4)
-Expectations for CHD impact to fetus (3)
-Expectations for CHD impacts to mother (2)
-Optimisation of caridiac function (4)

A
  1. Assess level of risk to mother
    -Presence of pulmonary HTN
    -NYHA class III or IV
    -Lesion affecting haemodynamics (LVEF <40% or L heart obstruction)
    -Presence of cyanosis
    -Hx of TIA, arrythmia, heart failure
  2. Avoid pregnancy when:
    -Pulmonary HTN and fixedpulmonary vascular resistance
    -Dilated aortic root >4.5cm
    -Severe L heart obstruction
    -Severe LV impairment EF <30%
  3. Expectations for fetus
    -Increased miscarriage
    -Increased risk of heart anomilies 3%
    -Increased IUGR
  4. Expectations for mother
    -Worsening symptoms during pregnancy
    -Worsening symptoms after pregnancy
    -Death
  5. Optimising cardiac function
    -Stop teragenic drugs
    -Stop smoking
    -Loose weight / avoid obesity
    -Consider surgery pre pregnancy
18
Q

Discuss antenatal considerations for women with cardiac disease. (8)

A
  1. Risk straisfy to enable level of care to be determined
  2. MDT care with cardiologist, paeds, neonates, obs, MW and GP
  3. Refer high risk women to tertiary centre
  4. Consider thromboprophylaxis
    -Mechanical heart valves, fontans, marked LV disfunction with LV dilitation, L to R shunt
  5. Assess for arrythmia - ECG
  6. Assess valves, LV function, pulmonary HTN, aortic root - echo
  7. Fetal surveillance with anomly scan, fetal echo, serial GS
  8. Elective admission for bed rest, oxygenation, VTE prophylaxis
19
Q

Discuss intrapartum care for women with cardiac disease
-Mode of delivery
-Monitoring
-Location
-Pain relief

A
  1. Plan timing, site and mode of delivery
  2. Mode of delivery
    -CS rarely reduces risk. Do for recent MI, Aortic root >4cm, serverly impaired LV function.
    -Instrumental if wanting to reduce second stage
    -High risk or cyanosis
  3. Monitoring
    -Manage labour in upright or l lateral position with continuous CTG
  4. Location
    -Consider delivery in ICU if high risk
  5. Pain relief
    -Consider epidural to reduce demands on heart
20
Q

Discuss postpartum considerations for women with cardiac disease (9)

A
  1. Avoid ergometrine causes HTN adn big fluid shifts
  2. Avoid high dose bolus of synto can cause hypotension
  3. Monitor BP and fluid balance
  4. Avoid hypotension esp in outflow obstruction lesions
  5. Avoid HTN in those at risk of aortic dissection and rupture
  6. VTE prophylaxis
  7. Screen new born for cardiac anomilies
  8. Contraceptive advice
  9. Cardiology FU in 6 weeks
21
Q

How is risk classified for cardiac disease with the NYHA

A
  1. NYHA
    -Based on symptoms
    Class I - aSx
    Class II - mild sx at exercise none at rest. Mild oedema
    Class III - Noticiable limitation in ability to exercise. Comfortable only at rest
    Class IV - Unable to do physical activity. Sx at rest
22
Q

Discuss Marfans in pregnancy
-Pathophysiology
-Complictions (3)
-Management in pregnancy
-Preconception (2)
-Antenatally (2)
-Labour (2)
-Post natal (1)

A
  1. Pathophysiology
    -Autosomal dominant mutation in fibrillin -1 gene codes for microfibrils, substrate of elastin in connective tissue
    -Accounts for 50% of dissection in women <40yrs.
  2. Complications
    -Weakened aortic root and dilitation, mitral valve prolapse, mitral regurg
  3. Management in pregnancy
    -Prenantal counselling - condition in offspring
    -If aortic root >4cm get surgical correction prior to conception or TOP
    -Risk of maternal death 25% if aortic root >4cm
    -Serial echo every 6-8 weeks to check dilation of aortic root
    -Strict BP control and B blockade to reduce rate of aortic root dilitation
    -Restrict activity
    -Pain relief in labour. CS if aortic root >4cm
    -Risk of dissection persists 6-8 weeks PP
23
Q

Discuss hypertrophic cardiomyopathy
-Pathophysiology
-Complications
-Features
-Management in pregnancy

A
  1. Pathophysiology
    -Autosomal dominant
    -Myocardial thickening and hardening.
    -Can be obstructive or non-obstructive
    -Incidence 2:1000
  2. Complications
    -Sudden death if family hx, usually Asx VT, LV wall >3cm, Unable to increase BP during exercise, CHF, AF
  3. Features
    Chest pain, syncope, ESM (outflow obstruction), Pansystolic murmur, arythmia
  4. Management in pregnancy
    -Well tolerated in pregnancy as LV increases in size and SV maintained.
    -If symtpomatic prepregnancy have worse complications during pregnancy
    -High chance of fetal heritence (50%). Can’t see on fetal echo
    -Continue B-Blocker if symptomatic
    -Avoid hypotension
    -Pain management in labour
24
Q

Discuss peripartum cardiomyopathy
-Epidemiology (2)
-Definition
-Risk factors (5)
-Complications

A
  1. Epidemiology
    -Rare
    -Maternal mortality rare up to 20% (10-15%)
  2. Defintion
    -Idiopathic cardiomyopathy resulting in HF feom LV systolic dysfunction with no other cause found and no history of heart disease
    -Occurs between 35 weeks to 5 months PP
  3. Risk factors:
    -Multiparity
    -Multiple pregnancy
    -AMA
    -HTN in pregnancy
    -Afro-carribena race
  4. Complications
    -VTE, HF, Arrythmia
25
Q

Discuss peripatum cardiomyopathy
-Diagnosis
-Management
-Prognosis/recurrence

A
  1. Diagnosis
    -Diagnosis of exclusion
    -ECHO with LVEF <45%
    -CXR - large cardiac shadow and pulmonary oedema
  2. Management
    -Anticoagulation
    -Hydralazine and nitrates for vasodilation and decreased after load
    -Diuretics for pulmonary oedema
    -Caution with steriod for fetal lung maturation. Increases risk of fluid overload
    -Digoxin for arrythmias
    -ACEi for vasodilation PP
    -Short second stage with instrumental delivery. Opt for ELCS if haemodynamically unstable
    -No ergometrine or syntometrine for 3rd stage
    -Consider furosemide for prevention of immediate PP autologous infusion
  3. Prognosis and recurrence
    -Outcomes are variable
    -50% make full spontaneous recovery. Can be swift or take yrs
    -Up to 25% have recurrence in future pregnancy
    -Women with persistent cardiac dysfunction 6-12 months PP should be counselled against further pregnancy. 50% recurrence 25% death.
    -Recommend contraception
26
Q

Describe the changes to cardiac function in pregnancy
-Cardiac output
-Stroke volume
-Heart rate
-Blood pressure
-CVP
-PCWP
-SVR and PVR
-Serum colloid osmotic pressure

A
  1. Cardiac output
    -Increases secondary to increased SV and HR (mostly SV)
    -20% increase by 8/40. 40% increase by 22/40
  2. Stroke volume
    -Increases due to increased myocardial mass and end diastolic volume
  3. Heart rate
    -Increases by 10-20bpm
  4. Blood pressure
    -Decreases due to vasoldilation. Lowest at 22-24/40
    -Returns to pre-pregnancy levels by term
    -Falls PP then peaks at day 3-6
  5. Central venous pressure
    -No change
  6. Pulmonary capillary wedge pressure
    -No change
  7. SYstemic and pulmonary vascular resistance
    -Decrease
  8. Serum colloid osmotic pressure
    -Decreases. Increases risk of pulmonary oedema
27
Q

What are the cardiac output changes for:
-Intrapartum (2) and cause (1)
-Post partum (2) and causes (3)

A
  1. Intrapartum
    -Increase CO by 15% in first stage
    -Increase CO by 50% in second stage
    -Drive by autologous transfusion with every contraction of 300-500mL
  2. Postpartum
    -Immediate increase of CO by 60% following delivery
    -Casued by relief of IVC, Contraction of uterus with return of blood to circulation, transfer of extravascular fluids
    -CO returns to normal after 1 hr
28
Q

What are the normal cardiaology examination findings for pregnant women (7)

A
  1. Bounding pulse
  2. Ejection systolic murmur
  3. Loud first heart sound
  4. Splitting of second heart sound
  5. Sinus tachycardia
  6. Ectopic beats
  7. Peripheral oedema
29
Q

What are the normal ECG changes in pregnant women (5)

A
  1. Atrial and ventricular ectopic beats
  2. Q wave and inverted T wave in lead III
  3. ST segment depression and T wave inversion in inferior and lateral leads
  4. QRS axis deviation to the left
  5. Reduced PR interval
30
Q

Discuss pulmonary hypertension
-Diagnostic criteria (3)
-Causes
-Pregnancy outcomes

A
  1. Diagnostic crieteria
    -Elevated pulmonary arterial pressure
    -Diagnosis made by doppler USS
    -Need to determine if fixed pulmonary vascular resistance with CCB
  2. Causes
    -Idiopathic
    -Chrnoic thromboemboli
    -Congenital heart disease with L->R shunt
    -Lung disease - COPD, CF. insterstial lung disease
    -Connective tissue diseases - SLE, scleroderma
  3. Pregnancy outcomes
    -TOP 7% mortality
    -Mortality 17-33% depending on cause
    -Most women die PP
31
Q

How should women with Pulmonary Hypertension be managed during pregnancy
-Antenatal (6)
-Intrapartum
-Postpartum

A
  1. Antenatal
    -If fixed PVR advise against pregnany
    -Continue PAH therapies - phosphodiesterases, prostanoid analogues and nitrous all safe in pregnancy
    -Stop endothelial receptor antagonisits - teratogenic
    -Consider CCB
    -Anticoagulate
    -Bed rest
  2. Intrapartum
    -Avoid hypovolemia
    -Avoid increasing systemic vasodilation (regional blocks and synto can do this)
    -If Vaginal delivery instrumental for shortened second stage
  3. Postpartum
    -Manage in ICU
    -Increase risk of dying PP
    -Counsel for contraception
32
Q

Discuss mitral valve prolapse in pregnant women
-Incidence (2)
-Features (3)
-Clinical significance (2)
-Management in pregnancy (3)

A
  1. Incidence
    -Most common cardiac abnormality in pregnancy
    -Incidence 15%
  2. Features
    -Usually asymptomatic
    -Can have symtpoms of heart failure, arrythmias, fatigue
    -Mid systolic click or late murmur on ascultation
  3. Clinical significane
    -Both MVP and MR are well tolerated in pregnancy
    -If no MR seen with women who have MVP then little clinical significance
  4. Management in pregnancy
    -Assess with echocardiogram
    -Surgical correction if severe MR prior to pregnancy
    -If signs of HF during pregnancy manage with reducing afterload - hydralazine, nitrates, digoxine and diuretics
33
Q

Discuss mitral stenosis in pregnancy
-Aietology (1)
-Features of severity (2)
-Correlation with mortality
-Pathophysiology in pregnancy
-Symtpoms

A
  1. Aietology
    -50% of MS caused by rheumatic heart disease
  2. Features of severity
    -NYHA III/IV
    -Valve area <1cm
  3. Correlation with mortality
    -Mild MS mortality <1%
    -Severe MS with associated pulmonary HTN mortality 30-60% (Pregnancy is contra-indicated)
  4. Pathophysiology in pregnancy
    -Increased HR = decreased diastolic filling = decreased SV = decreased CO
    -Increased LA filling = increased pulmonary vascular resistance = pulmonary oedema and arrythmias
    -Increased blood volume = increased LA pressure
  5. Symptoms of MR
    -Arrythmias - AF and associated sx (dyspnoea, palpitations, syncope
    -Pulmonary oedema, frothy pink sputum, cough, haemoptysis
    -Malar rash
34
Q

How should mitral stenosis be managed in pregnancy
-Pre-natal (3)
-Antenatal (7)
-Intrapartum (5)

A
  1. Pre-pregnancy
    -Echo to assess severity and full cardiology work-up
    -If severe advise against pregnancy
    -Offer surgical correction prior to pregnancy in severe cases
  2. Antenatal
    -Serial echos
    -Aim for reducing volume overload
    -Avoid increased HR by beta blockade and restricted activity
    -Treat AF with beta blockers and digoxin, LMWH
    -Treat pulmonary oedema with diuretics
    -Consider balloon valvoplasty in pregnancy if medical managment failing
    -Serial GS for fetus
  3. Intrapartum
    -Can aim for vaginal delivery
    -Avoid lithotomy or supine positions
    -Epidural OK
    -Avoid ergo/syntometrine in 3rd stage
    -Control pain to decrease HR
35
Q

Discuss artificial valves in pregnancy
-Types and features (2)
-Considerations for anticoagulation (6 points)
-Considerations for prophylactic antibiotics (2)

A
  1. Types
    -Bioprosthetic - pregnancy may accelerate failure. Don’t require anticoagulation
    -Mechanical - don’t require replacement. Very prothrombotic - require life long anticoagulation
  2. Considerations for anticoagulation
    -Mechanical valves need coagulation
    -Risk of thrombus is 45%
    -Risk of maternal mortality is 1-4%
    -Warfarin is mainstay of anticoagulation but increased risk of embryo (not dose dependant) and fetal toxicity (dose dependant)
    -Mitral valve highest risk of thrombus
    -LMWH is an alternative but not as good but safe for fetus.
  3. Considerations for antibiotic prophylaxis
    -Not routinely required for women with cardiac disease but give if suspicion of infection or previous infective endocarditis
    -Regimen = Amoxicillin + Gentamycin
36
Q

Discuss the three possible regimens for anticoagulation in women with mechanical heart valves.
-Risk of thrombosis
-Risk of fetal anomilies
-Risk of pregnancy loss
-Postpartum plan for anticoagulation

A
  1. Wafarin throughout pregnancy until 38 weeks then switch to LMWH or unfractionated heparin for delivery
    -Risk of thrombosis - 4%
    -Risk of fetal anomily - 6%
  2. Replace Wafarin with LMWH from 6-12 weeks then restart warfarin until 38 weeks then switch to LMWH or unfractionated heparin
    -Risk of thrombosis 9%
    -Risk of fetal abnormality low
  3. LMWH through out pregnancy with low dose aspirin adjunct
    -Risk of thrombosis 25%
    -No risk of fetal abnormality (LMWH doesn’t cross the placenta)
  4. Risk of pregnancy loss
    -All 3 regimens have a 30% risk of pregnancy loss
  5. Postpartum plan for anticoagulation
    -Restart heparin post delivery
    -Switch to warfarin at day 3 with bridging LMWH
37
Q

Discuss use of warfarin and LMWH in pregnancy
-Issues with warfarin (8)
-Issues with LMWH (3)
-Reversal of warfarin if acute bleeding
-Reversal of LMWH if acute bleeding

A
  1. Issues with warfarin
    -Requires monitoring with INR
    -Crosses the placenta
    -Embryopathy - 6-12/40 not dose dependant. 10-20% risk
    -Mainly cartilagenous problems
    -Increased miscarriage
    -Fetopathy 12-40 weeks. Dose dependent higher risk >5mg. Risk 5-10%.
    -Intracranial haemorrhage, low IQ, neurological dysfunction, SGA babies
    -Needs 2 week washout period for fetus prior to delivery.
  2. Issues with LMWH
    -Requires monitoring with anti-Xa (0.8-1.2)
    -With perfect use clot risk 1:20
    -Doesn’t cross placenta so safe in pregnancy
  3. Reversal of warfarin
    -Vit K and FFP
  4. Reversal of LMWH
    -protamine sulphate
38
Q

Discuss the WHO classification system for cardiac disease in pregnancy
-Class
-Examples of what’s included in each class
-Risk of cardiac even in each class
-Risk of pregnancy in each class

A
  1. WHO class I
    -Small or mild MVP pulmonary stenosis or patent ductus arteriosis; repaired ASD, VSD; ectopic beats
    -Risk of cardiac event 2.5-5%
    -Risk to pregnancy - No increase over baseline
  2. WHO class II
    -Repaired TOF, unrepaired VSD/ASD, arrythmias
    -Risk of cardiac event 5-10%
    -Risk of mortality low. Risk of morbidity moderate
  3. WHO classII-III
    -Hypertrophic cardiomyopathy, marfans without aortic disstension, LV disfunction EF >45%, repaired oc-arctation
    -Risk of cardiac event 10-19%
    -Risk of mortality intermediate, risk of morbidity moderate / severe
  4. WHO class III
    -Repaired Fontans, Moderate LV dysfunction (EF 30-40%), mechanical valves, Previous PP cardiomyopathy, severe Asx AS
    -Risk of cardiac event 19-27%
    -Risk of mortality and morbidity - severe
  5. WHO Class IV
    -Fontans with any complication, Severe sx AS, severe MS, Aortic diameter >4.5cm, Pulmonary HTN
    -Risk of cardiac event 40-100%
    -Risk of mortality extremely hig. Risk of morbidity severe
39
Q

Discuss the Sui model for risk of cardiac events
-4 predicting measures
-Points system and associated risk of cardiac events with these

A
  1. 4 predicitors in the model
    -NYHA class>II or cyanosis
    -Outlet obstruction of the L heart (Mitral area <2cm, Aortic area <1.5cm
    -Prior cardiac event
    -EF <40%
  2. Points system
    0 = risk of cardiac event 5%
    1 = risk of cardiac event 27%
    >1 = risk of cardiac event 75%
40
Q

Discuss rheumatic heart disease in pregnancy
-Risk factors (3)
-Pre-conceptions care (6)
-Antenatal care (4)
-Intrapartum care (5)
-Postnatal care (2)

A
  1. Risk factors
    -Previous strep A infection
    -Low SES
    -Maori and aboriginal populations
  2. Pre-conception care
    -Consider surgical management prior to pregnancy if required
    -Confirm Dx of RHD - Echo
    -Change any anti-HTN to pregnancy safe options
    -Assess cardiac risk if NYHA III/IV avoid pregnancy
    -Anaesthetic assessment
    -Check if needs to continue prophylactic Ben Pen (3-4 weekly IM)
  3. Antenatal care
    -Change warfarin to LMWH even if only first trimester 6-12 weeks
    -Anticoagulation if prosthetic valves/AF etc
    -MDT care
    -High alert for deterioration
  4. Intrapartum
    -Aim VB
    -Routine prophylaxis for endocarditis not recommended in labour
    -Avoid ergo
    -Consider diuretics immediately PP depending on heart condition
    -Early epidural
  5. Postnatal care
    -Consider anticoagulation
    -Avoid COC

Kira - Mat Med (14 decks)

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