Aortic Cross-Clamp

Dramatic physiological changes occur following clamping of the descending aorta:

• Exact haemodynamic responses vary depending on the level
  • Supra-coeliac clamping consistently redirects blood flow and has predictable responses
    Requires a potent vasodilator; e.g. GTN or SNP.
    • Compliant splanchnic circulation collapses and drains its large blood resevoir into the central circulation, greatly ↑ preload
  • Infra-coeliac clamping is inconsistent, but less dramatic
    Usually will not require vasoactives.
    • Complaint splanchnic circulation buffers the blood drained from the non-compliant renal circulation

Physiology of Clamping

Immediate effects:

• ↑ Afterload
  • ↑ Systemic BP
    By 7-10%.
  • May precipitate LV failure
  • Have a profound afterload-reducing agent available GTN, SNP, nicardipine.
• ↑ Preload
  Due to redistribution in blood volume:
  • ↓ Venous capacitance distal to clamp
    Ejection of blood from splanchnic beds.
  • ↑ Venous capacitance proximal to clamp
    • ↑ CVP
    • ↑ PCWP
    • ↑ LVEDP
• Contractility
  Effect varies depending on capacity to ↑ coronary flow in the setting of ↑ O₂ demand:
  • Adequate coronary supply
    ↑ Contractility as a response to ↑ in preload and afterload.
    
    • CO may ↑ 10-30%.
  • Inadequate coronary supply
    Diastolic dysfunction, ↑↑ LVEDP, ↓ CO.
• ↑ Myocardial oxygen consumption
  

Short-term effects:

• Myocardial ischaemia
  Will occur if the ↑ in LVEDP exceeds the rise in aortic root pressure.
• ↓ Global oxygen consumption
  Both distal and proximal to clamp.
  • ↑ MV PO₂
• ↓ Spinal perfusion pressure
  Due to combination of:
  • ↓ Spinal blood flow
  • ↑ CSF pressure
• ↑ Catecholamines
• ↑ Renin and angiotensin
• ↓↓ Renal blood flow
  • ↓ GFR
  • ↓ UO
  • Ischaemia-reperfusion injury
    Subsequent AKI.
  • 0.25mg/kg of mannitol is often given to maintain urine output, without much evidence

Long term effects:

• ↑ SVR
  Continues to ↑ with ↑ duration of cross-clamping.

Preparing for Clamping

Peri-clamping:

• Have potent vasodilator available
• Start vasodilator as the surgeon is placing the clamp
  Clamp is placed slowly to avoid aortic dissection.
• Aim SBP ~90mmHg

Post-clamping:

• Wean vasodilator as able

Aortic Unclamping

Immediate effects:

• ↑ ETCO₂
  Due to ischaemic washout.
  • Minimise washout by unclamping each lower limb separately
  • Also present:
    • Lactate
    • NO
• ↓ BP
  May be profound.
  • Due to:
    • ↓ SVR by 70-80%
      Distal circulation is profoundly vasodilated due to ischaemia.
    • Relatively volume deplete venous bed
• ↓ Preload
  Due to:
  • Central hypovolaemia
    Blood pooling into re-perfused tissues.
  • Venodilation
    Secondary to hypoxia.
• CO
  May ↓, ↑, or remain unchanged depending on relative effect of:
  • ↓ SVR
  • ↓ Preload
  • Ischaemic washout
    Generally ↓ inotropy.
• Acidosis
  Lactic acidosis due to re-perfusion of ischaemic tissues.

Short-term effects:

• ↑ Renin and angiotensin release

Long-term effects:

• Persistent ↓ GFR and RBF
  May remain ↓ for up to 6 months post-operatively.

Preparation For Unclamping

Preload:

• Give volume targeting slightly elevated filling pressures prior to release.
  • Vasodilators given prior to release allow extra volume without ↑ filling pressures
    Cease 5-10 minutes prior to unclamping.

Contractility:

• CaCl₂
  • Inotropy
  • Myocardial membrane stability
    In preparation for hyperkalaemic washout.
  • Blood product calcium chelation
• NaHCO₃
  In preparation for acidosis.
• Adrenaline
  Consider:
  • Adrenaline infusion
  • 10μg/ml push-dose available

Instability After Unclamping

Hypotension:

• Have the surgeon reapply the clamp
• Give more volume
• Consider unclamping strategies
  Limits degree of reperfusion:
  • Partial unclamping
    
  • Partial reclamping
    May be done for bleeding control as well.
  • Staged unclamping
    Selective reperfusion of different areas.
  • Slow unclamping

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References