FRCA Notes

Aortic cross-clamp physiology

The curriculum asks for knowledge on 'the pathophysiology of aortic cross-clamping and of renal protection strategies'.

'Describes the cardiovascular physiology... relevant to perioperative vascular surgery' is equally applicable.

Resources

  • Perhaps unsurprisingly, aortic cross-clamping causes profound physiological effects, owing to both:
    • Its application, impairing end-organ blood supply and affecting haemodynamics above the clamp
    • Its release, where metabolites from anaerobic metabolism are released into the systemic circulation

  • The nature and degree of the pathophysiological derangement depend on:
    • Site of clamp application
    • The duration of application
    • Patient's physiological reserve
    • Whether said application occurs in an elective or emergent fashion

Clamp application

  • The key consideration is the site of clamp application, with more proximal clamping having a more profound haemodynamic effect

  • One the clamp is applied, there is a large increase in SVR
    • This massively increases afterload
    • There is an increase in arterial pressure proximal to the clamp (MAP ↑50%)
    • Filling pressure (↑40%) and ejection fraction (↓40%) are also effected

  • In order to maintain cardiac output, there is:
    • Sympathetic stimulation, increasing heart rate and contractility
    • Increased preload from central veins, increasing contractility via Frank-Starling mechanism

  • There is a perfect storm for myocardial ischaemia, with:
    • Reduced coronary perfusion pressure (as CPP = AoDBP - LVEDP, the latter of which is elevated) and therefore myocardial oxygen supply
    • Increased myocardial oxygen demand on account of greater contractility
  • There is consequent myocardial RMWA in 33% (supra-renal clamp) to >90% (supra-coeliac clamp) of patients, even if normal hearts pre-operatively
  • Heart failure may occur too

  • The therapeutic aim of the anaesthetist is to reduce afterload by decreasing SVR through vasodilation:
    • Deepening depth of anaesthesia
    • Use of opioids
    • Direct vasodilators such as GTN or sodium nitroprusside

  • Vasodilation may facilitate fluid loading in anticipation of post-clamp hypotension
  • Vasodilators mayn't, however, improve cardiac output and can cause blood re-distribution, which may affect tissue perfusion

Clamp release

  • Release of the clamp causes a 70 - 80% decrease in SVR

  • This effect is compounded by:
    • Blood sequestration in the lower body, particularly the splanchnic circulation
    • Washout of anaerobic metabolites (H+, K+, adenosine, ADP, purines, hypoxanthine, xanthine oxidase) causes:
      • Ischaemia-reperfusion injury
      • Metabolic lactic acidosis leading to direct myocardial suppression
      • Peripheral vasodilation
  • These changes reduce LVEDV (preload) and coronary blood flow
  • The net effect of reduced SVR, reduced preload and myocardial flailing is hypotension

  • Methods to minimise the haemodynamic instability associated with clamp release are:
    • Optimising intravascular volume in the pre-release phase
      • Administration in the post-release phase is less effective
    • Hyperventilation to minimise acidosis caused by CO2 returning from the lower limbs
    • Gradual release of the cross-clamp by the surgeons
    • Use of vasoactive drugs
      • These drugs tend to be less effective following cross-clamp release as anaerobic metabolites reduce the sensitivity of adrenergic receptors in areas distal to the clamp
      • Vasoconstrictors may lower cardiac output and divert blood away from the central compartment
    • Ensure normal clotting by avoiding hypothermia and acidosis

  • Overall, management of cross-clamp application and release requires excellent surgeon-anaesthetist communication to anticipate and mitigate the physiological effect

  • Renal vasculature can be severely affected by cross-clamping regardless of level
    • Supra-renal clamping may lead to a 95% reduction in renal blood flow and consequent ATN
    • Infra-renal clamping decreases renal cortical blood flow leading to reduced GFR (67%) and reduce renal plasma flow (48%), which is maintained for up to 6 months post-operatively

Risk factors for post-operative renal impairment

Patient factors Procedural factors
Age >70yrs Perioperative use of diuretics
Diabetes mellitus Perioperative use of aminoglycosides
Cardiac failure Repeat IV contrast load within 7 days
Pre-operative eGFR ≤60ml/min (CKD stage 3a) Complex EVAR
ACE-I or ARA therapy
Perioperative dehydration


Pathophysiology

  • Spinal cord perfusion pressure (SCPP) = MAP (anterior spinal artery pressure) - CSF or venous pressure (whichever is higher)
  • Application of the cross-clamp reduces anterior spinal artery pressure and thus spinal cord perfusion pressure, increasing the risk of ischaemia
    • Compromise of the artery of Adamkiewicz (T12/L1), the most distal collateral supply to the anterior spinal artery, increases this risk further
  • Cross-clamping also increases venous pressure, further reducing SCPP

  • The pathogenesis of neurological impairment involves not only hypotension, but also hypoxia and reperfusion injury
  • Neurological damage is present in up to 40% although the risk of paraplegia is lower:  ≤1% (AAA) or 4 - 16% (TAA)
    • Level and duration of cross-clamping are key risk factors
    • Advanced age, diabetes, emergency surgery and perioperative hypotension are also risk factors for spinal cord ischaemia

Prevention & spinal cord protection

  • For a more comlpete resource see this 2016 BJA article, though in brief the techniques used to prevent neurological damage include:
    • Surgical technique e.g. sequential clamping of the aorta
    • CSF drainage to maintain SCPP
    • Maintenance of adequate MAP
    • Cooling techniques
    • Use of free radical scavengers, which reduces incidence of paraplegia in animal studies

  • Impaired visceral perfusion can occur regardless of the level of cross-clamp application
  • Blood flow is affected by:
    • Vessel ligation or temporary occlusion by the cross-clamp
    • Periods of perioperative hypotension
    • Reduced cardiac output e.g. arrythmias
    • Emboli or thrombosis

  • The most commonly affected area is the descending colon due to inferior mesenteric artery occlusion
  • Hepatic hypoperfusion may cause impaired lactate clearance
  • Overall incidence of visceral injury is 1 - 10%

  • Lung complications following cross-clamping are common
  • Inflammatory mediators released after the cross-clamp is removed increase pulmonary vascular resistance
  • The resultant pulmonary hypertension and increased vascular permeability can lead to:
    • Pulmonary oedema
    • Acute lung injury
    • Requirement for prolonged ventilation