• Cardiac failure occurs when the heart is unable to pump sufficient blood to meet metabolic demands of body tissues
  
  • underlying cause may be cardiac or non-cardiac 

Common causes

Cardiac

• Left-to-right shunt (see Increased left-to-right shunt) 
• Arrhythmia
• Hypoplastic left heart syndrome
• Critical aortic stenosis
• Coarctation
• Interrupted aortic arch

Non-cardiac

• Sepsis
• Hypoxia 
• Anaemia
• Polycythaemia
• Fluid overload
• AV malformation
• Pulmonary hypertension

• Tachycardia
• Tachypnoea
• Hepatomegaly
• Excessive weight gain
• Hypotension
• Murmur
• Abnormal femoral pulses
• Weak femoral pulses (in obstructive left heart lesions – femoral pulses may not be absent if duct is still patent)

• Blood gases including lactate
• Baseline bloods including FBC, U&E, LFT
• Blood culture
• Chest X-ray – look for cardiomegaly and pulmonary oedema
• Pre and postductal saturations
  
  • postductal saturations can be considerably lower than preductal in aortic arch defects and PPHN (a difference of >2% is significant)
• ECG
• Echocardiogram

Resuscitation

Airway

• Routine intubation not indicated
• Intubate and ventilate babies presenting collapsed or with obvious cyanosis in association with cardiac failure 
• If apnoea occurs secondary to a prostaglandin infusion, intubate baby but do not alter infusion

Breathing

• See Ventilation: Conventional guideline
• Ventilate with PEEP 5–6 cm 
• Adjust ventilation to maintain:
  
  • PaCO₂ 5–6 kPa
  • pH >7.25

Circulation

• Vascular access with 2 IV cannulae or umbilical venous catheter (UVC) (see Umbilical venous catheterisation and removal guideline)
• Prostaglandin infusion to maintain ductal patency (see Prostaglandin infusion guideline)
  
  • open duct with dinoprostone (prostaglandin E₂, prostin E₂), see Neonatal Formulary. Start at 5–10 nanogram/kg/min, may be increased to 50 nanogram/kg/min, but only on cardiologist advice
• Monitor blood pressure invasively

Cardiac output

• Signs of poor cardiac output include: 
  
  • tachycardia 
  • low BP
  • acidosis 
  • high lactate
  • poor peripheral perfusion with cold extremities
• When cardiac output low:
  
  • ensure adequate intravascular volume 
  • correct anaemia
  • discuss with regional cardiac centre for choice of inotropes

• Discuss further management and transfer with regional cardiac centre
• Babies who respond to a prostaglandin infusion may not need transferring out-of-hours
• Appropriately skilled medical and nursing staff are necessary for transfer

Intubation

• Intubate if:
  
  • continuing metabolic acidosis and poor perfusion
  • long-distance transfer necessary
  • inotropic support needed
  • apnoea
  • recommended by cardiac team

Baby may go home or return to a paediatric ward or NNU, possibly on a prostaglandin infusion whilst awaiting surgery or for continuing care after a palliative procedure (e.g. septostomy)

Management plan

• Regardless of outcome, obtain a management plan from cardiac centre, defining: 
  
  • acceptable vital signs (e.g. saturations)
  • medication, including dosage
  • follow-up arrangements

Recognition and assessment

Definition

• Any lesion causing increased pulmonary blood flow 
• Usually presents when pulmonary resistance falls after 48 hr
• Size and type of lesion will influence time of presentation 

Differential diagnosis

• AVSD
• Partial AVSD
• VSD
• Truncus arteriosus 
• PDA

Investigations

• Chest X-ray looking for fluid overload
• Echocardiogram

Management

• If in cardiac failure, give immediate dose of diuretic
• May require maintenance diuretics (discuss with cardiologist)
  
  • usually furosemide 1 mg/kg twice daily (oral/IV) and amiloride 100 microgram/kg twice daily (oral)
• Discuss with cardiac centre for definitive management and follow-up