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Last Update: 03/27/2025 09:47 PM

Current Deck: ACG Part 2::Obstetrics

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SS_OB 1.35 Discuss the pathophysiology and anaesthetic management of the following medical conditions particular to pregnancy:
- Peripartum cardiomyopathy 
  • Dilated cardiomyopathy that occurs between the last month of pregnancy and 5 months postpartum
  • Significant associated morbidity and mortality
  • Diagnosis one of exclusion based on echo findings

Aetiology/pathophysiology:
  • Unknown cause, poorly understood mechanisms but likely related to an increase in oxidative stress -> normal mechanisms to protect the heart are disrupted -> proteases cleave protactim -> the cleaved prolactin segment induces apoptosis, endothelial dysfunction and downregulates cardioprotective factors in the cardiac myocyte
Diagnosis:
  • Difficult as they often present with symptoms of normal pregnancy
  • Bloods: NT-proBNP (compare to pregnancy-specific reference ranges)
  • ECG: tend to be non-specific and include: bundle branch block, ST-segment depression, T wave inversion, ectopy and bradyarrhythmias or tachyarrhythmias, prolonged QTc if EF <35%
  • CXR: Signs of heart failure, cardiomegaly, pulmonary congestion
  • Transthoracic echocardiography (TTE) is the gold standard diagnostic investigation for PPCM and LV dysfunction is the key finding. At presentation, mean LVEF is 30%.f LV dilatation occurs, functional mitral regurgitation may be observed on TTE. Right heart dysfunction identified at baseline is an independent predictor of poor outcome.
  • If presenting shocked consider:
    • Peripartum cardiogenic shock, amniotic fluid embolism, pulmonary embolism and myocardial infarction
Management:
  • supportive therapy
  • medical therapy
  • lifestyle modifications. 
  • If presenting pregnant:
    • Consider gestation, fetal viability, haemodynamic stability
    • MDT: Pregnancy-heart team: Core members include a cardiologist, obstetrician, obstetric anaesthetist, maternal fetal medicine specialist and critical care nursing and midwifery personnel
    • Once PPCM is suspected, the pregnancy heart team should formulate an individualised management plan for the antepartum period, for labour and delivery and the postpartum period.
Goals of management:
  • (i) Optimise preload: cautious fluid challenge if intravascular volume is reduced, i.v. diuretics if there is evidence of pulmonary congestion. If systolic arterial pressure is >110 mmHg, a vasodilator (e.g. glyceryl trinitrate infusion) should be considered, with close monitoring for signs of reduced placental perfusion. 
  • (ii) Optimise oxygenation: oxygen supplementation by face mask or by non-invasive ventilation may reduce respiratory distress. If ongoing hypoxaemia or an altered mental state is present, tracheal intubation and invasive ventilation may be required. 
  • (iii) Correct haemodynamic instability using inotropic, vasopressor, or both drugs: the choice of agent is determined by the individual patient’s condition, disease severity and the response to different medications. 
  • (iv) Urgent delivery (if pregnant) if haemodynamic instability persists despite optimal management. 
  • (v) Consider bromocriptine (dopamine agonist) therapy post-delivery with counselling regarding impact on lactation (see below). 
  • (vi) Consider anticoagulation therapy: caution if delivery is imminent.
Thromboprophylaxis:
  • PPCM associated with LV thrombosis and thromboembolic complications
  • Prophylactic anticoagulation is generally recommended
  • therapeutic anticoagulation is indicated in the presence of intracardiac thrombus, systemic thromboembolism or atrial fibrillation
  • low molecular weight or unfractionated heparin is recommended because urgent delivery may be needed
  • DOACs contraindicated in pregnancy and when breastfeeding
Mechanical support (VAD, IABP or ECMO):
  • If patient remains hemodynamically unstable despite maximal medical therapy
  • Type:
    • If oxygenation adequate: IABP or VAD
    • Severe respiratory failure but preserved cardiac function: VV ECMO (usually ARDS, not PPCM)
    • Cardiogenic shock + poor oxygenation: VA ECMO (complications including severe bleeding, infection and thrombosis, significant fetal mortality associated)
    • If unable to wean mechanical support within 10 days, switch to VAD or may need cardiac transplantation
Arrhythmias:
  • Common with PPCM, especially if LVEF <35%
  • Cardioversion and defibrillation safe in pregnancy, monitor fetal HR post
Delivery:
  • Risk stratification mWHO (bottom of document)
  • MDT: Pregnancy-heart team: Core members include a cardiologist, obstetrician, obstetric anaesthetist, maternal fetal medicine specialist and critical care nursing and midwifery personnel
  • Specialist centre with experts in cardiac and obstetric disease
  • Should be able to provide specialist ICU and mechanical support
  • Vaginal delivery preferable as it is associated with reduced rates of infection, blood loss and thrombotic events
  • Planned induction of labour for cessation of anticoagulation therapy
  • Monitoring: Additional monitoring for labour and delivery such as continuous SpO2, ECG, consider A-line, CVL unlikely to be needed for vaginal delivery unless vasopressors anticipated
  • assisted vaginal delivery technique, with forceps or ventouse, is often recommended to reduce maternal effort adn CVS fluctuations
  • Back up plan for emergency/LSCS
Neuraxial for labour:
  • epidural, combined spinal-epidural (CSE), dural puncture epidural all have pros and cons
  • Titrated, incremental epidural doses of local anaesthetic (e.g. bupivacaine 0.0625e0.125%) over 10e20 min with close monitoring of vital signs and observation
  • Once established can move to standard maintenance e.h. 0.0625% PIEB
  • Vasopressors should be the predominant treatment for hypotension after the initiation of neuraxial analgesia. 
LSCS and PPCM:
  • Neuraxial preferred
  • cautious, titrated, incremental doses of local anaesthetic until an adequate level of block is established
  • A ‘low-dose’ CSE technique (0.5-1ml 0.5% bupivacaine) has been recommended for establishing neuraxial anaesthesia in women with severe cardiovascular disease who do not have an in situ epidural
  • Haemodynamic management: cautious i.v. fluid boluses and consideration of inopressors (e.g. ephedrine and noradrenaline) over pure vasoconstrictors (e.g. phenylephrine)
  • If GA (anticoagulated, too unstable, patient refusal): A-line, consider CVL, slow careful induction and obtund laryngoscopy response with short acting opioids (alfentanil, remi)
Post-delivery:
  • Auto-transfusion may cause pulmonary oedema or acute decompensation
  • Increased risk of PPH and poorly tolerated, early active management recommended:
    • Oxytocin administered slowly via an infusion pump (e.g. 2 IU oxytocin over 10 min\
    • TXA
    • Pregnancy team advice on other uterotonics:
      • Carboprost increases pulmonary vascular resistance by >100% and has been associated with severe bronchospasm, hypoxaemia and death
      • Ergometrine increases systemic vascular resistance and coronary vasospasm through its effect on vascular smooth muscle
    • If surgical control fails - can trial other uterotonics
  • Likely to need HDU/ICU post-op if severe disease or complications