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
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.
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
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%
Multifactorial in origin
Clinical criteria
The use of ECHO to demonstrate LV systolic dysfunction is increasingly believed to be the central to diagnosing PPCM
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
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)
Acute decompensated heart failure
with invasive monitoring
Even with maximal therapy, intractable heart failure may need heart transplantation.
Immunosuppressant agent
IV IG has been shown to improve EF in acute dilated cardiomyopathy
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
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
Anaethetist primary responsibilty is to the parturent and there should not be undue hasten to deliver the fetus if maternal safety is compromised.
Anaethetist primary responsibilty is to the parturent and there should not be undue hasten to deliver the fetus if maternal safety is compromised.
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