FRCA Notes

Ventricular Septal Defect

The curriculum wants us to demonstrate knowledge of 'common congenital heart defects – including VSD'.

Resources

  • Ventriculo-septal defects are the commonest form of congenital heart defect in children, representing 20- 30% of cardiac malformation

Class Maximum diameter compared
to normal aortic valve annulus		 Ratio of pulmonary (Qp) to
systemic (Qs) blood flow
Small <1/3 <1.5
Moderate 1/3-2/3 1.5-2.0
Large >2/3 >2.0


  • The magnitude and direction of blood flow in systole across a VSD are determined by:
    1. The size of the defect
      • A small defect limits left-to-right shunt as the resistance across the defect is higher
      • A large, non-restrictive defect with normal PVR may lead to a large left-to-right systolic shunt

    2. The PVR
      • A high PVR may lead to minimal net shunting, as the sum of resistance to blood flow from the LV may approximate that of the aortic resistance
      • If PVR exceeds SVR, then right-to-left shunting may ensue

Development of congestive cardiac failure

  • When blood is shunted left-to-right, there is a commensurate decrease in LV output
  • This leads to compensatory mechanisms to raise LVEDV to achieve a normal cardiac output in the presence of the shunt i.e. sympathetic nervous system + RAAS activation
  • LV volume overload ensures, and eventually high LA pressure and pulmonary congestion can occur
  • Over time, congestive cardiac failure occurs

Development of pulmonary hypertension

  • The presence of the intra-cardiac shunt transmits LV pressures to the pulmonary vascular bed during LV systole
  • In the absence of RVOT obstruction, pulmonary artery systolic pressures equalises with that of the aorta
  • Raising PA pressure may help differentiate VSD from ASD
  • The increased pulmonary blood flow leads to increased LA and LV blood volume with volume overload, hypertrophy and LA dilation
  • Over time, pulmonary oedema, reactive pulmonary vascular changes and pulmonary hypertension will develop
  • If left unrepaired, there will be raised RV pressure
  • If RV pressure exceeds LV pressure (or systemic arterial pressure) there will be shunt reversal and a fixed, severe pulmonary hypertension a.k.a. Eisenmenger's syndrome

Symptoms

  • Those with small, restrictive VSDs may be asymptomatic and have normal growth/development

  • Those with moderate-to-large VSDs are likely to demonstrate symptoms relating to raised pulmonary blood flow and cardiac failure:
    • Reduced growth/development/failure to thrive
    • Respiratory distress
    • Respiratory distress during feeding
    • Recurrent respiratory tract infections
    • Sweating
    • Lethargy
    • Poor exercise tolerance

  • Typically acyanotic as the blood ejected systemically is still oxygenated

Signs

  • Tachypnoea/dyspnoea and respiratory distress
  • Pansystolic murmur at the left sternal border
  • Precordial thrill
  • Hepatomegaly

Perioperative management of the patient with a VSD


History and examination

  • Full anaesthetic history including:
    • Full medical history inc. drugs and allergies
    • Birth history and perinatal complications
    • Presence of coalescing congenital abnormalities e.g. Trisomy 21, 13 or 18

  • History of recent respiratory tract infections which predispose to complications of CPB
  • Airway examination, especially if concurrent congenital syndromes
  • Look for potential venous access sites

Investigations

  • Bloods: FBC, clotting, U&E, LFT and G&CM
  • ECG: LA/LV/RV hypertrophy
  • TTE: VSD location, size, shunt direction, chamber size/function, PA pressure
  • CXR: cardiomegaly, pulmonary oedema

Monitoring and access

  • AAGBI
  • A-line
  • CVC if major surgery e.g. correction

Haemodynamic goals

  • The main goal intra-operatively is to avoid large decreases in PVR, as this can result in:
    • Increased pulmonary blood flow but reduced systemic blood flow
    • Hypotension, impaired coronary perfusion pressure and reduced end-organ perfusion

  • One should therefore avoid:
    • High inspired oxygen concentrations
    • Low CO2; permit high-normal EtCO2
    • Alkalosis
    • Anaemia
    • Air in lines

  • Opioid-heavy techniques can help facilitate this

  • Post-operative complications are almost exclusively cardiovascular in nature
  • Non-cardiac complications include SIRS-type responses and bleeding/coagulopathy
Cardiovascular complications
Cardiac tamponade
Low CO state
Dysrhythmias; tachycardia or heart block
Pulmonary hypertensive crisis
Presence of a residual VSD