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Nor Hidayah Zainool Abidin
Supervisor : Dr Hasmizy

 Definition of Maternal mortality rate: The maternal mortality rate (MMR)
is the annual number of female deaths per 100,000 live births from any
cause related to or aggravated by pregnancy or its management (excluding
accidental or incidental causes). The MMR includes deaths during
pregnancy, childbirth, or within 42 days of termination of pregnancy,
irrespective of the duration and site of the pregnancy, for a specified year

 Normal cardiovascular changes in pregnancy
 Definition of PPCM
 Epidemiology
 Etiology
 Diagnosis
 Presentations
 Management
 Outcome
 Conclusion
Outline
 Blood volume increases by 40% to 50%
 Red cell volume increase by only 15% to 20%
 Levels of clotting factors I, VII, VIII, IX, X, and XII, and the
fibrinogen count are elevated
 About 8 weeks after delivery  blood volume to return to
normal.
 Cardiac output increases by 30% to 40%
 Heart rate rises by 10 to 15 beats per minute by 28 to 32
weeks’ gestation.
 M-mode ECHO, increases in end diastolic chamber size
and total left ventricular wall thickness
Maternal cardiovascular changes

 An increased cardiac output might not be well tolerated by
pregnant women with valvular heart disease (e.g., aortic or
mitral stenosis) or coronary arterial disease.
 A severe decompensation in myocardial function can
develop at 24 weeks’ gestation, during labor, and especially
immediately after delivery
Clinical Implications

Cardiomyopathy
Dilated
Hyperthrophied
Restrictive
Viral myocarditis
 Endomyocardial biopsies  dense lymphocytic infiltrates and
variable amount of myocyte edema, necrosis and fibrosis.
Viral genomes have also been found in these specimen.
Abnormal immunologic activity in
the parturent.
 autoantibodies that act against cardiac tissue proteins in
serum
 The prolonged persistence of fetal progenitor cells in maternal
circulation postdelivery may also trigger a pathological
autoimmune response in mother.
 Causitive link has not been establish
Etiology

 Other causes
 Nutritional deficiency particularly selenium
 Familial clustering of PPCM suggest genetic component
 Excessive prolactin production
 As prolactin is linked to a rise in blood volume,
 decrease in angiotensin responsiveness
 reduction in renal excretion of sodium and water.
 maladaptive response to the hemodynamic stress of
pregnancy, stress activated cytokines
 Prolonged tocolytic therapy
 Using beta agonist eg salbutamol and terbutaline has been
known to cause pulmonary edema and may be associated
with PPCM
 Advance maternal age
 Reportedly occur in women panning wide range of age
group. But the incidence seems to be higher in parturent >
30 yo
 Multiparity and multiple gestation
factors
 Race
 African descent
 Pregnancy induced hypertension and preeclampsia
 Commonly cited as risk factor
 Some belief it’s a different entity as this disorders shows
good LV recovery at 6 months, unlike the recovery in
patient with PPCM 30%
factors
 Cardiac failure develops in the last month of
pregnancy or in the first 5 months postpartum
 No other identifiable cause of heart failure
 There is no recognizable heart disease before the last
months of pregnancy
 Together with ECHO findings LV systolic
dysfunction:
 EF < 45%
 M-mode FS < 30%
 End diastolic dimension > 2.7cm/m2
Diagnosis

PND
Chest pain
Nocturnal cough
Lungs crepitations
New murmurs
Elevated JVP
Hepatomegaly
Presentations
Differencials:
Severe preeclamsia
ACS
Pulmonary embolism

Symptoms Key points
Agitation May indicate hypoxemia
Vomiting Consider Myocardial ischemia as
atypical presentations are common in
pregnancy
Breathlessness Evaluate cardiac and respiratory
causes
Chest, back, interscapular and /or
epigastric pain
Consider Myocardial ischemia and
aotic disection
Recognizing the women with
cardiac disease that may develop
into emergency situation

Signs Key points
Tachypnea
Tachycardia
Irregular heart beat
Hypotension Consider systolic and/or diastolic
heart failure, right heart failure.
Sepsis, hypovolumia
Critical hypertension Apo may occur in the setting of PE
New heart murmur
Wheeze Cardiac asthma
Febrile Sepsis. Consider
endocarditis/myocarditis
Recognizing the women with
cardiac disease that may develop
into emergency situation
 Challenging
◦ Due to rarity of clinical situation
 Guidelines are not well defined and
recommendation based on case reports
rather than prospective trials
 Counselling and education
 Optimization of cardiac function
 Maintenance of clinical skills by staff
 Early antenatal referral of high-risk women
 Recognition of the severity of the disease
 Stratification of risk
 History
 Assessment of functional status
Key planning issue
•Birth location, timing, mode of
delivery and staffing
Risk Description
Low risk (maternal mortality
< 1 %)
Minor and asymptomatic valve disease. NYHA
class 1
High risk (maternal
mortality up to 50%)
Unstable disease
Poor functional class (NYHA class 2)
Pulmonary hypertension
Previous acute episodes of cardiac
decompensation
Ischemic heart disease
Significant reduce EF < 40%
Multidiciplinary approach
Anaesthesiologis
t
obstetricia
n
cardiologi
st
Aims of
treatments
Alleviating
symptoms
Slowing
progression of
LV dysfunction
Improving
survival
Medical therapy
Optimization of fluid
status
Improvement of
myocardial O2
supply-demand ratio
Afterload reduction
Medical therapy for PPCM similar in non pregnant patients
 Nonpharmaceutical therapies
◦ Low-sodium diet: limit of 2 g sodium per day
◦ Fluid restriction: 2 L/day
◦ Light daily activity: if tolerated (eg, walking)
b-blocker Carvedilol
(starting dose 3.125 mg twice a day, target dose
25 mg twice a day)
Extended-release metoprol
(starting dose 0.125 mg daily, target
dose 0.25 mg daily)
Vasodilator Hydralazine (starting dose 10 mg 3 times a day,
target dose 40 mg 3 times a day)
Digoxin (starting dose 0.125 mg daily, target dose 0.25 mg
daily)
Monitor serum levels
Thiazide
diuretic
Hydrochlorothiazide (12.5-50 mg daily)
(with caution)
May also consider loop diuretic with caution
Low-molecular-weight heparin if ejection fraction
<35%
Antepartum management of peripartum cardiomyopathy
Angiotensin-
converting enzyme
(ACE) inhibitor
Captopril (starting dose 6.25-12.5 mg 3 times a day,
target dose 25-50 mg 3 times a day)
Enalapril (starting dose 1.25-2.5 mg 2 times a day,
target dose 10 mg 2 times a day)
Ramipril (starting dose 1.25-2.5 mg 2 times a day,
target dose 5 mg 2 times a day)
Lisinopril (starting dose 2.5-5 mg daily, target dose
25-40 mg daily)
Angiotensin-
receptor blocker (if
ACE inhibitor not
tolerated)
Candesartan (starting dose 2 mg daily, target dose 32
mg daily)
Valsartan (starting dose 40 mg twice a day, target dose
160 mg
twice a day)
Consider nitrates or hydralazine if woman is intolerant
to ACE
inhibitor and angiotensin-receptor blocker
Loop diuretic Furosemide intravenously or by mouth–dosing
considerations should be made on the basis of
creatinine clearance
Glomerular filtration rate >60 mL/min per 1.73 m2:
furosemide 20-40 mg every12-24 h
Postpartum management of peripartum cardiomyopathy
Loop diuretic Furosemide intravenously or by mouth–dosing
considerations
should be made on the basis of creatinine
clearance
Glomerular filtration rate >60 mL/min per 1.73
m2:
furosemide 20-40 mg every12-24 h
Glomerular filtration rate <60 mL/min per 1.73
m2:
furosemide 20-80 mg every 12-24 h
Vasodilator Hydralazine (starting dose 37.5 mg 3 or 4 times a
day, target dose
40 mg 3 times a day)
Isorbide dinitrate (starting dose 20 mg 3 times a
day, target dose
40 mg 3 times a day)
Aldosterone
antagonist
Spironolactone (starting dose 12.5 mg daily,
target dose
25-50 mg daily)
Eplerenone (starting dose 12.5 mg daily, target
dose 25-50 mg daily)
b-blocker as above Warfarin if ejection fraction <35%
 Airway
 Assess for Intubation
 Breathing
◦ Oxygen
◦ Monitor SaO2
◦ ABG every 4-6 h until breathing is stable
 Circulation
◦ Start cardiac and blood pressure monitoring
◦ Insert arterial catheter
◦ Central venous access
◦ In antepartum women, obtain fetal monitoring
ICU admission
Furosemide Dosing considerations should be made on the
basis of creatinine clearance
Glomerular filtration rate >60 mL/min per 1.73 m2:
furosemide 20-40 mg intravenously every 12-24 h
Glomerular filtration rate <60 mL/min per 1.73 m2:
furosemide 20-80 mg intravenous every12-24 h
In severe fluid overload, consider furosemide infusion
Vasodilator Nitroglycerin infusion 5-10 μg/min, titrate to clinical
status and
blood pressure
Nitroprusside 0.1-5 μg/kg per minute, use with
caution in
antepartum women
Positive inotropic
agents
Milrinone 0.125-0.5 μg/kg per minute
Dobutamine 2.5-10 μg/kg per minute
◦ IV IG has been shown to improve EF in
acute dilated cardiomyopathy
◦ A biologically active derivative of prolactin
has been found to be possible mediator
for PPCM. Hence bromocriptine (prolactin
inhibitors) has been used experimently to
treat PPCM
 Management of - Thromboembolic
complications
◦ Heparin sodium, alone or with oral warfarin
(Coumadin) therapy
 Consider endomyocardial biopsy; if proven viral
myocarditis,
 consider immunosuppresive medications (eg,
azathioprine, corticosteroids)
• IV IG has been shown to improve EF in acute dilated
cardiomyopathy
 Consider cardiac magnetic resonance imaging
 Perform endomyocardial biopsy to detect viral
myocarditis (if not previously completed)
 Assist devices:
◦ Intra-aortic balloon pump
◦ Left ventricular assist devices
◦ Extracorporeal membrane oxygenation
Refractory to therapy
• A biological active derivative of prolactin has been found to be possible mediator
for PPCM
Bromocriptine (prolactin inhibitors) has been used experimently to treat PPCM
 Normal delivery is recommended in
compensated PPCM.
 LSCS should only be undertaken if there are
obstetric indications
 Predelivery consultation with an
anaesthesiologists
 Preservation of myocardial contractility
 Optimization of preload
 Reduction of afterload
 Maintainance of sinus rhythm
 Aviodance of extreme blood pressure and
heart rate
 Avoidance of dramatic fall in peripheral blood
resistance due to limited cardiac reserve
 Aim to minimize cardiovascular work
 Avoid aortocaval compression
 Cardiovascular monitoring system
 Plan the management of 3rd stage labour.
Avoid syntocinon with ergometrine
 Careful attention to fluid management during
labour
 Avoid prolonged second stage with lower
threshold for the use of forceps or vacuum
assisted delivery.
 Routine intraoperative monitoring
 ECG, pulse oxymentry, capnography
 Invasive blood pressure
 CVP
 Pulmonary artery catheterization – poor
cardiac function
 Early administration of labour analgesia
◦ To blunt haemodynamic reflex of uterine
contraction and associated pain response
 Central neuraxial blockade for vaginal
delivery
◦ CSE
◦ Epidural
 Close haemodynamic monitoring
◦ invasive monitoring pressures
 Vasoactive agents may be required
 Early measures for early intervention should
be instituted if any derangement occurs
 Various case reports uses
◦ Continuous spinous anaesthesia
◦ Epidural anaesthesia
◦ Low dose sequential combined spinal-epidural
anaesthesia
◦ Opioid base anaesthesia
 Choice of anaesthetics influenced by
◦ Parturent’s haemodynamic and respiratory status
◦ Urgency of surgery
 LSCS  preferably be a planned during office
hours to ensure availability of staff and
optimal perfomance
 Joint management between consultant cardiac
and obstetric anaesthetists
◦ Expertise with invasive lines, heamodynamic
monitorign including TEE and cardiac intervention
 To be done in GOT instead of MOT due to
advantage of adequate equipments,
personnel and geographical proximity to ICU
for ease of transfer
◦ Often indicated in severely ill parturent
with tachypnoea, orthopnea and poor
cardiac status
◦ Urgent delivery of fetus is warranted in
fetal distress
 Techniques
◦ Opioid based general anaesthesia in the form of
modified RSI with cricoid pressure and tracheal
intubation
◦ Target control infusion of propofol and remifentanyl
together with rocurorium
◦ Sulfentanyl 50mcg, thiopentone 100mg, lignocaine
100mg with suxamethonium
◦ Ethomidate 20mg, fentanyl 500mcg with
suxamethonium
 Prevent rapid onset of sensory and
sympathetic block
◦ not advisable to give single shot spinal anaesthesia
 May result in catastrophic fall in systemic
vascular resistance in parturent with limited
cardiac reserve
 However reduction in afterload may improve
cardiac function whilst reducing myocardial
work
 Deterioration in cardiac function , APO and
arrythmias are causes of death.
◦ Planning of mx of this complications should be
done antenatally
 Loop diuretics may be given upon delivery to
reduce volume overload from autotransfusion
 Thromboprophylaxis should be considered
postpartum
 Breastfeeding is frequently possible.
 Active contraception
 Inform regarding increased risk of cardiac
disease later in life.
 Early follow up with cardiologist - to review
cardiac status and function and to optimize
medications
 Related to degree of LV dysfunction and LV dimension
at diagnosis
 A more severe LV dysfunction at diagnosis is associated
with higher risk for persistent LV dysfuntion
 FS < 20% and LV end diatolic dimension of > 6cm
 Recovery is more likely with LV EF of >30% at diagnosis
 PPCM patient may still have decreased contractile
reserve even though they have regained normal resting
left ventricular size.
 This can be detected with dobutamine chalenge test.
Prognosis
Mortality rate
14% in patients whose heart size return to normal
85% inpatient who maintained to have
cardiomegaly beyond 6 months
Overall mortality rate ranges 6-56%
Most death occur within 3 months postpartum
Heart failure
Arrythmias
Thromboembolic disease
Prognosis

 Maternal safety in the future
 LV function generally considered to be the most
important prognostic factors
 Dobutamine stress ECHO may help further define
risk of subsequent pregnancy
 All PPCM subsequent pregnancy should be consider
high risk and should be manage in tertiary hospital
with multidiciplinary team.
Subsequent pregnancy

 Obstetric Anaesthesia and Analgesics, Practical
Issues, Alex SIA, YK Chan & Stephen Gatt, pg 236-
242, 2012.
 Peripartum Cardiomyopathy, Review and
guidelines, Johnson Et Al, American Journal of
Critical Care, vol 21, March 2012.
 Harrison Principle of Internal Medicine Textbook
References:

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Recommendation for safety standards and monitoring during anaesthesia
 

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Peripartum cardiomyopathy

  • 1. Nor Hidayah Zainool Abidin Supervisor : Dr Hasmizy
  • 2.   Definition of Maternal mortality rate: The maternal mortality rate (MMR) is the annual number of female deaths per 100,000 live births from any cause related to or aggravated by pregnancy or its management (excluding accidental or incidental causes). The MMR includes deaths during pregnancy, childbirth, or within 42 days of termination of pregnancy, irrespective of the duration and site of the pregnancy, for a specified year
  • 3.   Normal cardiovascular changes in pregnancy  Definition of PPCM  Epidemiology  Etiology  Diagnosis  Presentations  Management  Outcome  Conclusion Outline
  • 4.  Blood volume increases by 40% to 50%  Red cell volume increase by only 15% to 20%  Levels of clotting factors I, VII, VIII, IX, X, and XII, and the fibrinogen count are elevated  About 8 weeks after delivery  blood volume to return to normal.  Cardiac output increases by 30% to 40%  Heart rate rises by 10 to 15 beats per minute by 28 to 32 weeks’ gestation.  M-mode ECHO, increases in end diastolic chamber size and total left ventricular wall thickness Maternal cardiovascular changes
  • 5.   An increased cardiac output might not be well tolerated by pregnant women with valvular heart disease (e.g., aortic or mitral stenosis) or coronary arterial disease.  A severe decompensation in myocardial function can develop at 24 weeks’ gestation, during labor, and especially immediately after delivery Clinical Implications
  • 7. Viral myocarditis  Endomyocardial biopsies  dense lymphocytic infiltrates and variable amount of myocyte edema, necrosis and fibrosis. Viral genomes have also been found in these specimen. Abnormal immunologic activity in the parturent.  autoantibodies that act against cardiac tissue proteins in serum  The prolonged persistence of fetal progenitor cells in maternal circulation postdelivery may also trigger a pathological autoimmune response in mother.  Causitive link has not been establish Etiology
  • 8.   Other causes  Nutritional deficiency particularly selenium  Familial clustering of PPCM suggest genetic component  Excessive prolactin production  As prolactin is linked to a rise in blood volume,  decrease in angiotensin responsiveness  reduction in renal excretion of sodium and water.  maladaptive response to the hemodynamic stress of pregnancy, stress activated cytokines
  • 9.  Prolonged tocolytic therapy  Using beta agonist eg salbutamol and terbutaline has been known to cause pulmonary edema and may be associated with PPCM  Advance maternal age  Reportedly occur in women panning wide range of age group. But the incidence seems to be higher in parturent > 30 yo  Multiparity and multiple gestation factors
  • 10.  Race  African descent  Pregnancy induced hypertension and preeclampsia  Commonly cited as risk factor  Some belief it’s a different entity as this disorders shows good LV recovery at 6 months, unlike the recovery in patient with PPCM 30% factors
  • 11.  Cardiac failure develops in the last month of pregnancy or in the first 5 months postpartum  No other identifiable cause of heart failure  There is no recognizable heart disease before the last months of pregnancy  Together with ECHO findings LV systolic dysfunction:  EF < 45%  M-mode FS < 30%  End diastolic dimension > 2.7cm/m2 Diagnosis
  • 12.
  • 13. PND Chest pain Nocturnal cough Lungs crepitations New murmurs Elevated JVP Hepatomegaly Presentations Differencials: Severe preeclamsia ACS Pulmonary embolism
  • 14.  Symptoms Key points Agitation May indicate hypoxemia Vomiting Consider Myocardial ischemia as atypical presentations are common in pregnancy Breathlessness Evaluate cardiac and respiratory causes Chest, back, interscapular and /or epigastric pain Consider Myocardial ischemia and aotic disection Recognizing the women with cardiac disease that may develop into emergency situation
  • 15.  Signs Key points Tachypnea Tachycardia Irregular heart beat Hypotension Consider systolic and/or diastolic heart failure, right heart failure. Sepsis, hypovolumia Critical hypertension Apo may occur in the setting of PE New heart murmur Wheeze Cardiac asthma Febrile Sepsis. Consider endocarditis/myocarditis Recognizing the women with cardiac disease that may develop into emergency situation
  • 16.  Challenging ◦ Due to rarity of clinical situation  Guidelines are not well defined and recommendation based on case reports rather than prospective trials
  • 17.  Counselling and education  Optimization of cardiac function  Maintenance of clinical skills by staff  Early antenatal referral of high-risk women
  • 18.  Recognition of the severity of the disease  Stratification of risk  History  Assessment of functional status Key planning issue •Birth location, timing, mode of delivery and staffing
  • 19. Risk Description Low risk (maternal mortality < 1 %) Minor and asymptomatic valve disease. NYHA class 1 High risk (maternal mortality up to 50%) Unstable disease Poor functional class (NYHA class 2) Pulmonary hypertension Previous acute episodes of cardiac decompensation Ischemic heart disease Significant reduce EF < 40%
  • 22. Medical therapy Optimization of fluid status Improvement of myocardial O2 supply-demand ratio Afterload reduction Medical therapy for PPCM similar in non pregnant patients
  • 23.  Nonpharmaceutical therapies ◦ Low-sodium diet: limit of 2 g sodium per day ◦ Fluid restriction: 2 L/day ◦ Light daily activity: if tolerated (eg, walking)
  • 24. b-blocker Carvedilol (starting dose 3.125 mg twice a day, target dose 25 mg twice a day) Extended-release metoprol (starting dose 0.125 mg daily, target dose 0.25 mg daily) Vasodilator Hydralazine (starting dose 10 mg 3 times a day, target dose 40 mg 3 times a day) Digoxin (starting dose 0.125 mg daily, target dose 0.25 mg daily) Monitor serum levels Thiazide diuretic Hydrochlorothiazide (12.5-50 mg daily) (with caution) May also consider loop diuretic with caution Low-molecular-weight heparin if ejection fraction <35% Antepartum management of peripartum cardiomyopathy
  • 25. Angiotensin- converting enzyme (ACE) inhibitor Captopril (starting dose 6.25-12.5 mg 3 times a day, target dose 25-50 mg 3 times a day) Enalapril (starting dose 1.25-2.5 mg 2 times a day, target dose 10 mg 2 times a day) Ramipril (starting dose 1.25-2.5 mg 2 times a day, target dose 5 mg 2 times a day) Lisinopril (starting dose 2.5-5 mg daily, target dose 25-40 mg daily) Angiotensin- receptor blocker (if ACE inhibitor not tolerated) Candesartan (starting dose 2 mg daily, target dose 32 mg daily) Valsartan (starting dose 40 mg twice a day, target dose 160 mg twice a day) Consider nitrates or hydralazine if woman is intolerant to ACE inhibitor and angiotensin-receptor blocker Loop diuretic Furosemide intravenously or by mouth–dosing considerations should be made on the basis of creatinine clearance Glomerular filtration rate >60 mL/min per 1.73 m2: furosemide 20-40 mg every12-24 h Postpartum management of peripartum cardiomyopathy
  • 26. Loop diuretic Furosemide intravenously or by mouth–dosing considerations should be made on the basis of creatinine clearance Glomerular filtration rate >60 mL/min per 1.73 m2: furosemide 20-40 mg every12-24 h Glomerular filtration rate <60 mL/min per 1.73 m2: furosemide 20-80 mg every 12-24 h Vasodilator Hydralazine (starting dose 37.5 mg 3 or 4 times a day, target dose 40 mg 3 times a day) Isorbide dinitrate (starting dose 20 mg 3 times a day, target dose 40 mg 3 times a day) Aldosterone antagonist Spironolactone (starting dose 12.5 mg daily, target dose 25-50 mg daily) Eplerenone (starting dose 12.5 mg daily, target dose 25-50 mg daily) b-blocker as above Warfarin if ejection fraction <35%
  • 27.  Airway  Assess for Intubation  Breathing ◦ Oxygen ◦ Monitor SaO2 ◦ ABG every 4-6 h until breathing is stable  Circulation ◦ Start cardiac and blood pressure monitoring ◦ Insert arterial catheter ◦ Central venous access ◦ In antepartum women, obtain fetal monitoring ICU admission
  • 28. Furosemide Dosing considerations should be made on the basis of creatinine clearance Glomerular filtration rate >60 mL/min per 1.73 m2: furosemide 20-40 mg intravenously every 12-24 h Glomerular filtration rate <60 mL/min per 1.73 m2: furosemide 20-80 mg intravenous every12-24 h In severe fluid overload, consider furosemide infusion Vasodilator Nitroglycerin infusion 5-10 μg/min, titrate to clinical status and blood pressure Nitroprusside 0.1-5 μg/kg per minute, use with caution in antepartum women Positive inotropic agents Milrinone 0.125-0.5 μg/kg per minute Dobutamine 2.5-10 μg/kg per minute
  • 29. ◦ IV IG has been shown to improve EF in acute dilated cardiomyopathy ◦ A biologically active derivative of prolactin has been found to be possible mediator for PPCM. Hence bromocriptine (prolactin inhibitors) has been used experimently to treat PPCM
  • 30.  Management of - Thromboembolic complications ◦ Heparin sodium, alone or with oral warfarin (Coumadin) therapy  Consider endomyocardial biopsy; if proven viral myocarditis,  consider immunosuppresive medications (eg, azathioprine, corticosteroids) • IV IG has been shown to improve EF in acute dilated cardiomyopathy
  • 31.  Consider cardiac magnetic resonance imaging  Perform endomyocardial biopsy to detect viral myocarditis (if not previously completed)  Assist devices: ◦ Intra-aortic balloon pump ◦ Left ventricular assist devices ◦ Extracorporeal membrane oxygenation Refractory to therapy • A biological active derivative of prolactin has been found to be possible mediator for PPCM Bromocriptine (prolactin inhibitors) has been used experimently to treat PPCM
  • 32.  Normal delivery is recommended in compensated PPCM.  LSCS should only be undertaken if there are obstetric indications  Predelivery consultation with an anaesthesiologists
  • 33.  Preservation of myocardial contractility  Optimization of preload  Reduction of afterload  Maintainance of sinus rhythm  Aviodance of extreme blood pressure and heart rate  Avoidance of dramatic fall in peripheral blood resistance due to limited cardiac reserve
  • 34.  Aim to minimize cardiovascular work  Avoid aortocaval compression  Cardiovascular monitoring system  Plan the management of 3rd stage labour. Avoid syntocinon with ergometrine  Careful attention to fluid management during labour  Avoid prolonged second stage with lower threshold for the use of forceps or vacuum assisted delivery.
  • 35.  Routine intraoperative monitoring  ECG, pulse oxymentry, capnography  Invasive blood pressure  CVP  Pulmonary artery catheterization – poor cardiac function
  • 36.  Early administration of labour analgesia ◦ To blunt haemodynamic reflex of uterine contraction and associated pain response  Central neuraxial blockade for vaginal delivery ◦ CSE ◦ Epidural  Close haemodynamic monitoring ◦ invasive monitoring pressures  Vasoactive agents may be required  Early measures for early intervention should be instituted if any derangement occurs
  • 37.  Various case reports uses ◦ Continuous spinous anaesthesia ◦ Epidural anaesthesia ◦ Low dose sequential combined spinal-epidural anaesthesia ◦ Opioid base anaesthesia  Choice of anaesthetics influenced by ◦ Parturent’s haemodynamic and respiratory status ◦ Urgency of surgery
  • 38.  LSCS  preferably be a planned during office hours to ensure availability of staff and optimal perfomance  Joint management between consultant cardiac and obstetric anaesthetists ◦ Expertise with invasive lines, heamodynamic monitorign including TEE and cardiac intervention  To be done in GOT instead of MOT due to advantage of adequate equipments, personnel and geographical proximity to ICU for ease of transfer
  • 39. ◦ Often indicated in severely ill parturent with tachypnoea, orthopnea and poor cardiac status ◦ Urgent delivery of fetus is warranted in fetal distress
  • 40.  Techniques ◦ Opioid based general anaesthesia in the form of modified RSI with cricoid pressure and tracheal intubation ◦ Target control infusion of propofol and remifentanyl together with rocurorium ◦ Sulfentanyl 50mcg, thiopentone 100mg, lignocaine 100mg with suxamethonium ◦ Ethomidate 20mg, fentanyl 500mcg with suxamethonium
  • 41.  Prevent rapid onset of sensory and sympathetic block ◦ not advisable to give single shot spinal anaesthesia  May result in catastrophic fall in systemic vascular resistance in parturent with limited cardiac reserve  However reduction in afterload may improve cardiac function whilst reducing myocardial work
  • 42.  Deterioration in cardiac function , APO and arrythmias are causes of death. ◦ Planning of mx of this complications should be done antenatally  Loop diuretics may be given upon delivery to reduce volume overload from autotransfusion  Thromboprophylaxis should be considered postpartum
  • 43.  Breastfeeding is frequently possible.  Active contraception  Inform regarding increased risk of cardiac disease later in life.  Early follow up with cardiologist - to review cardiac status and function and to optimize medications
  • 44.  Related to degree of LV dysfunction and LV dimension at diagnosis  A more severe LV dysfunction at diagnosis is associated with higher risk for persistent LV dysfuntion  FS < 20% and LV end diatolic dimension of > 6cm  Recovery is more likely with LV EF of >30% at diagnosis  PPCM patient may still have decreased contractile reserve even though they have regained normal resting left ventricular size.  This can be detected with dobutamine chalenge test. Prognosis
  • 45. Mortality rate 14% in patients whose heart size return to normal 85% inpatient who maintained to have cardiomegaly beyond 6 months Overall mortality rate ranges 6-56% Most death occur within 3 months postpartum Heart failure Arrythmias Thromboembolic disease Prognosis
  • 46.   Maternal safety in the future  LV function generally considered to be the most important prognostic factors  Dobutamine stress ECHO may help further define risk of subsequent pregnancy  All PPCM subsequent pregnancy should be consider high risk and should be manage in tertiary hospital with multidiciplinary team. Subsequent pregnancy
  • 47.   Obstetric Anaesthesia and Analgesics, Practical Issues, Alex SIA, YK Chan & Stephen Gatt, pg 236- 242, 2012.  Peripartum Cardiomyopathy, Review and guidelines, Johnson Et Al, American Journal of Critical Care, vol 21, March 2012.  Harrison Principle of Internal Medicine Textbook References:

Editor's Notes

  1. Rare condition Heart failure is asscociated with reduced left ventricular (LV) systolic function that occur in the last month pre-delivery and in the first 5 months postpartum. likely the diagnosis of PPCM: Peripartum stage Signs and/or symptoms of heart failure Ejection fraction <45%
  2. Multifactorial in origin
  3. Clinical criteria The use of ECHO to demonstrate LV systolic dysfunction is increasingly believed to be the central to diagnosing PPCM
  4. Women with known underlying cardiac disease are at risk of critical cardiac compromise during and after pregnancy. Pregnancy itself is associated with cardiac decompensation. May occur in severe PE who develop PPCM
  5. Heart failure should be treated according to guidelines on heart failure and it can be divided into supportive (heart failure therapy, heart rhythm disturbances, cardiogenic shock) specific therapy (immunosuppressive therapy, interferon, immunoglobulin, immune-adsorptive therapy, immune-modulation)
  6. Acute decompensated heart failure with invasive monitoring Even with maximal therapy, intractable heart failure may need heart transplantation.
  7. Immunosuppressant agent IV IG has been shown to improve EF in acute dilated cardiomyopathy
  8. If the patient is haemodynamically stable vaginal delivery should be carried out. Urgent delivery irrespective of gestation duration should be considered in women with advanced heart failure and haemodynamic instability despite treatment. Caesarean section is recommended with combined spinal and epidural anaesthesia
  9. If GA required, obtund the response to intubation, carefully titrate anesthetics, monitor closely and have strategies in managing hypertension, hypotension, arrythmias, APO and cardiac arrest
  10. Anaethetist primary responsibilty is to the parturent and there should not be undue hasten to deliver the fetus if maternal safety is compromised.
  11. Anaethetist primary responsibilty is to the parturent and there should not be undue hasten to deliver the fetus if maternal safety is compromised.
  12. Fett et al reported half of women with subsequent pregnancy after PPCM experience worsening heart failure and long term systolic dysfunction Another half experience no deteroriation and regain normal left ventricular systolic function Even with normalization of left ventricular function, the risk of recurrence exist as multiparity is a risk factor associated with PPCM