Transcript Slide 1

Anesthetic management of
peripartum cardiomyopathy
by Dr/ Amr Maher mahmo
Lecturer of anesthesia
 It is a form of heart failure affecting females in their
last months of pregnancy or early puerperium.
(1)
 The role of anesthesiologist is important in the perioperative and the intensive care unit.
 Diagnostic criteria for PPCM:
 Development of heart failure within last month of pregnancy or
six months postpartum.
Absence of any identifiable cause for heart failure
Absence of any heart disease before last month of pregnancy.
Echocardiographic criteria of left ventricular dysfunction:
Ejection fraction < 45%
Left ventricular fractional shortening < 30%.
Left ventricular end-diastolic dimension > 2.7 cm/m2 BSA
Risk factors:
 Black race, family history.
Advanced maternal age.
 Multiparity, multiple gestations.
Obesity, malnutrition.
Gestational hypertension, preeclampsia, cesarean section.
 Poor antenatal care, breast feeding.
 Alcohol, cocaine and tobacco abuse.(1)
 Incidence:

1 in 4,000 live births.

This wide variation may be explained by the influence of genetic
and environmental factors, as well as different reporting patterns
and diagnostic criteria used.(1)
Etiology:-
Myocarditis:• It is not known whether it is an association or a cause.
• Only diagnosed by histological examination of endometrial
biopsy.
• also, the vasopressor therapy in PPC may lead to a
Histological changes resembling myocarditis.
Viral infection
• During pregnancy, there is a degree of depressed
immunity that may lead to viral infection. Viral infection has been
implicated as a cause of myocarditis that would lead to
cardiomyopathy.
• On the other hand, it has been argued that viral cardiomyopathy
should not be included as a cause of PPCM. But rather a separate
entity.
Autoimmune theory:
• Studies hypothesized, that fetal cells may escape to the systemic
circulation triggering immune response.
• Higher rates of PPCM with twin pregnancies and its familial
predisposition supports this theory.
 Inflammatory cytokines:
• In PPCM patient, higher concentrations of inflammatory
cytokines like TNF α, CRP, IL-6 were found. CRP levels
correlated inversely with left ventricular ejection fraction
(LVEF).(1)
Selenium deficiency:
•Significantly low selenium concentrations in PPCM patients
was found, still, this might be a mere incidental association
rather than a cause.

Exaggerated hemodynamic response
•
In pregnancy, there is physiologic changes in the C.V.S. (1)
It has been postulated that PPCM may be an exacerbation of
this normal phenomenon.

Prolonged tocolytic therapy
•
Usually tocolysis causes tachycardia and vasodilation, so it
may actually unmask existing heart disease rather than play an
etiologic role.
 Diagnosis
the S&S are basically the same S&S of heart failure.
 We have to exclude other causes of heart failure as valvular and
ischemic heart diseases.
 Symptoms
• Dyspnea on exertion, cough, orthopnea and paroxysmal nocturnal
dyspnea, resembling left sided heart failure.
• Non specific symptoms include palpitations, fatigue, malaise and
abdominal pain.
• Embolic manifestations may be present, as mural cardiac thrombi
commonly occur. The patient may complain of chest pain,
hemoptysis and hemiplegia, rarely myocardial infarction may be the
presentation due to coronary embolism.

Signs
•
Blood pressure may be normal, elevated or low.
•
Tachycardia, gallop rhythm.
•
engorged neck veins and pedal edema
•
Clinically, the heart may be normal or there may be mitral
and/or tricuspid regurgitation with pulmonary crepitations(1)
 Investigations
• ECG….. No specific findings.
• chest x-ray…. May show cardiomegaly, pulmonary
venous congestion.
•Echocardiography…. It is the most important diagnostic tool, and
assess the severity and the prognosis of PPCM.
• Echo findings are :oincreases LVEDD, decreased LVFS and LVEF.
odilatation of all cardiac chambers with subsequent functional
mitral, tricuspid, pulmonary and aortic regurgitation.
• Dobutamine stress Echo is a better prognostic tool than the
ordinary Echo,(1) TEE and cardiac MRI are better tools in detecting
intramural thrombi than the ordinary Echo.
COMPLICATIONS
Thromboembolism
•Thrombi often form in patients with LVEF < 35% and associated
with mortality rate 50%.(1)
Arrhythmias
• all kinds of arrhythmias have been reported up to ventricular
tachycardia and heart arrest.(@)
 Organ failure
• Acute liver failure and hepatic coma d.t passive liver congestion
secondary to cardiac failure. Also, multiorgan failure may occur.
 Obstetric & perinatal complications
• There is increased incidence of abortion, premature deliveries,
intrauterine growth retardation, or intrauterine fetal deaths.
 Management
Non pharmacological measures
• As any heart failure, salt and water restriction (2-4 gm/day,, 2
L/day).
• Once the severe symptoms are improved, modest exercise
should be encouraged. (1)
Pharmacological measures
• As any heart failure; digoxin, diuretics, vasodilators and
anticoagulation are the mainstay. But we to consider the safety of
these drugs in pregnancy and lactation.
• Digoxin
 It is a class C drug, but presumed safe in low doses.
 In pregnant female, the serum level should monitored. (1)
 Some studies claimed that digoxin for 6 month decreases the
risk of recurrence of PPCM.
• Diuretics
 They are safe in pregnancy and lactation.
 Aim to reduce preload .
Continue diuretics
 Usually, loop diuretics are used and thiazides are used in milder
cases. spironolactone is very beneficial in heart failure, but better
avoided in pregnancy.
 Should be used with caution not to induce dehydration and
uterine hypoperfusion. Also, metabolic alkalosis may develop.
• Vasodilator
 They reduce the pre and after load in heart failure, and so
increase the C.O.
 Hydralazine and nitrates are the vasodilator of choice during
pregnancy.
 ACEI, and ARB are mainstay in heart failure but they class d, and
contraindicated in pregnancy due to teratogenicity. So, they are
considered after labour, but breast feeding has to be discontinued.
• calcium channel modulators
 Calcium channel blocker, though has –ve intropism, but has been
shown to improve the survival in cardiomyopathy patients. it also
reduces the level of inflammatory cytokines so they would play
important in PPCM.
 Levosemindane is especially valuable and used with success in
PPCM. but again, breast feeding should be avoided during its use.(1)
• Beta Blockers
 like CCB, BB now has important role in heart failure and they
are not contraindicated in pregnancy, though associated with low
birth weight.
 Both BB, and ACI have an additional role in immunosuppression
and prevent remodeling and reduce ventricular dimensions.
• Antiarrhythmic agents
 No antiarrhythmic agent is completely safe in pregnancy.
 Quinidine and Procainamide, has high safety profile, but
treatment should always start in a hospital because of the high
incidence of torsades de pointes.
 Amiodarone may cause hypothyroidism, growth retardation and
perinatal death, so it should be reserved for life threatening
arrhythmias only.
•
Anticoagulation therapy
 Anticoagulation therapy targets patients with LVEF less than
35%, bedridden, with atrial fibrillation, mural thrombi, obese,
or with history of thromboembolism.
 The therapy may persist for as long as six weeks in the
Puerperium.
 Heparin is used in the antepartum and heparin or warfarin is
used in the postpartum period as warfarin is contraindicated
in the antepartum period due to its teratogenicity.
 OBSTETRIC MANAGEMENT
•
induction of delivery should be considered if a patient’s condition
deteriorates despite maximal medical management.
• If the patient is compensated, normal vaginal delivery is
preferred, while if the patient is severely decompensated or there
is obstetric indications, cesarean section should be done.(1)
• In both cases, the patient should be admitted to ICU for early
detection of complications.
 ANESTHETIC MANAGEMENT
 Anesthesia for vaginal delivery:
 Controlled epidural analgesia under invasive monitoring is a
safe and effective method.
 Sympathectomy induced by epidural leads to afterload and
preload reduction that improves myocardial function in PPCM
patients.
Anesthesia for cesarean section:
Both general anesthesia (GA) and regional anesthesia (RA) have
been used.
 Regional anesthesia
• Single shot spinal anesthesia is not preferred, because of its rapid
hemodynamic changes and hypotension.
• Epidural anesthesia is used because of its better hemodynamic
stability.
• Continuous spinal anesthesia , with its lower failure rates, faster
onset, good muscle relaxation, less drug requirement,
postoperative analgesia facilities and better maintenance of
hemodynamics has also been successfully applied.
• In severely compromised patients, local infiltration with bilateral
ilioinguinal bloacks have been used.
 General anesthesia
• GA may be needed in emergency situations or when RA is
contraindicated, particularly in anticoagulated patients
• GA has the advantages of airway control and ventilation, and it
facilitates the use of transesophageal echocardiography
• GA has the disadvantage that it can cause maternal and fetal
cardiorespiratory depression, and the stress of rapid sequence
induction on decompensated heart could be dangerous. There is
also increased risk of LVF and pulmonary edema. GA does not
provide thromboprophylaxis like RA.
• Opioid-based anesthesia may be advantageous in compromised
cardiac conditions, but carries a high risk of fetal respiratory
depression.(1)
• in mild cases, noninvasive monitoring can be used. in severely
decompensated cases, the use of invasive monitoring is a must. This
includes the use of arterial line and may be pulmonary artery
catheter.
Postoperative management
• All PPCM patients should be managed in an ICU as they are prone
to develop LVF and pulmonary edema in this period. Also, to
monitor the possible complications.
• Postoperative pain can be managed by RA or parenteral opioidbased techniques.
 Prognosis
 Poor prognosis criteria
The worst prognosis is found in patients with:•Higher age and parity, multiple gestations.
•Black race.
•Later onset of symptoms (> 2 weeks) after delivery.
•Coexisting of medical illness.
•Delay of initiation of medical treatment.
•Intracardiac thrombi, conduction defects, or persistence of
ventricular dysfunction for more than 6 months.
 RISK OF RECURRENCE IN SUBSEQUENT PREGNANCY
 The highest risk of recurrence remains in patients with
persistent cardiac dysfunction and the lowest risk is in those
whose cardiac functions have been normalized, as evidenced by
dobutamine stress test