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Aortic Cross-Clamping

Afterload

• Afterload: The force opposing the shortening of myocardial fibers.
• Components:
  • Traditionally considered external forces.
  • Includes intrinsic myocardial forces that oppose fiber shortening.

Extrinsic Afterload

• Three-Element Windkessel Model:
  • Components: Impedance, aortic compliance, peripheral vascular resistance.
  • Effective Arterial Elastance (Ea): A simple afterload descriptor, calculated as the ratio of end-systolic pressure (mean arterial pressure) to stroke volume. An increase in the Ea slope indicates an increase in afterload.

Intrinsic Afterload

• Wall Stress-Tension:
  • Influenced by ventricular pressure (P), radius (r), and wall thickness (h).
  • Determinants:
    1. Wall stress affects myocardial oxygen supply and demand. Increased wall stress increases demand and reduces supply, potentially causing ischemia.
    2. Ventricular radius impacts wall tension, where increased preload increases afterload and affects oxygen supply-demand balance.

Ventricular-Load Coupling

• Coupling Dynamics:
  • Parabolic relationship between left ventricular stroke work and afterload.
  • Stroke work increases with increased stroke volume and arterial pressure.
  • The descending limb indicates ventricular failure as stroke volume decreases with increasing afterload.
  • Contractility shifts the curve: higher contractility improves tolerance to afterload.

Key Factors

1. Increase in Left Ventricular Afterload:

   • Influenced by:
     • Clamp Level: Higher clamps increase afterload more significantly.
       • Thoracic Aorta Clamping:
         • Increases mean arterial and pulmonary pressures, decreases cardiac index.
         • Supracoeliac Clamping:
           • Increases mean arterial pressure, decreases ejection fraction, and causes myocardial ischemia.
         • Infrarenal Clamping
           • Minimal changes, no wall motion abnormalities.
     • Aortic Disease: Aortic occlusive disease shows less afterload increase due to collateralization.

2. Left Ventricular Function:

   • Normal ventricles handle afterload increases better but can fail with significant afterload.
   • Anrep Effect: Increased contractility following afterload increase, possibly due to increased coronary blood flow and autoregulation recovery.

3. Coronary Artery Disease and Myocardial Ischemia:

   • Increases in preload and afterload raise oxygen demand and limit supply.
   • Duration of Clamping: Longer durations worsen vascular resistance and reduce cardiac output.

4. Preload Increases:

   • Seen with higher clamps, resulting in increased left ventricular end-diastolic volumes and pressures.
   • Mechanisms:
     • Blood Volume Redistribution: Arterial recoil and venoconstriction.
     • Afterload-Induced Preload: Ventricular dilation to maintain stroke volume.

5. Wall Tension:

   • Increased ventricular radius raises wall tension and myocardial ischemia risk.

Management of Aortic Cross Clamping

• Manage left ventricular contractility, afterload, preload, ventricular dilation, myocardial ischemia, and clamp height.

Myocardial Preservation

• Goals: Decrease afterload, normalize preload, improve coronary blood flow and contractility.
• Methods: Bypass/shunt during thoracic clamping, vasodilators during lower clamping.

Specific Medications

Nitroglycerine

• Uses: Prevent/manage myocardial ischemia.
• Mechanism: Venodilator (low dose), arteriolar dilator (high dose).
• Advantages: Does not increase heart rate at low dosages.

Magnesium

• Advantages: Calcium channel blocker, alpha-1 blocker, arteriolar dilator, improves diastolic function, anti-arrhythmic, analgesic.

Volatile Anesthetic Agents

• Isoflurane: Significant vasodilation, not advisable as the sole vasodilator.
• Sevoflurane and Halothane: Increase myocardial blood flow, reduce platelet adhesion, induce pharmacological preconditioning.

Inotropic Support

• Essential during clamping, especially with inodilators, to manage hemodynamic effects.

Thoracic Epidural

• Reduces sympathetic outflow, increases venous capacitance, improves myocardial oxygen supply-demand balance.

Summary of Management

1. Anaesthesia Depth: Maintain with inhalation agents and thoracic epidural.
2. Fluid Management: Avoid increases in wall tension.
3. Heart Rate Control: Titrate beta-blockers.
4. Venous Return Manipulation: Patient positioning.
5. Vasodilators: Use for circulation and coronary supply-demand balance.
6. Inotropic Support: Continue during clamping.

Unclamping

Declamping Shock

• Cardiac Output: Increases in response to decreased afterload.
• Arterial Blood Pressure and Systemic Vascular Resistance: Reductions due to vasodilation and exposure to vasoactive substances.
• Myocardial Depression: Caused by cytokines and endotoxins from ischemic bowel.

Effects Above and Below the Clamp

• Proximal: Vasodilation, increased venous capacitance, myocardial ischemia risk.
• Distal: Reactive hyperemia, reduced venous return.

Other Contributing Factors

• Oxygen Radical Formation: Reperfusion injury.
• Inflammatory Response: Various mediators.
• Lung and Reperfusion: Pulmonary hypertension, increased alveolar ventilation, potential alveolar edema.
• Kidney: Renin-angiotensin system activation, importance of renal perfusion, hyperkalemia risk.

Management of Unclamping

• Preparation: Start 10 minutes before unclamping.
• Fluids: Administer colloids to increase PAWP/CVP.
• Vasopressors/Inotropes: Support blood pressure and cardiac function.
• Nitroglycerine: Low-dose to manage wall tension.
• Leg Elevation: Augment venous return.
• Maintain Mean Arterial Pressure: Use vasopressors to ensure adequate perfusion.

Summary of Unclamping Hypotension Causes

1. Hypovolemia from blood pooling.
2. Ischemia-mediated vasodilation.
3. Accumulation of vasoactive/metabolites.

Links

• Endovascular Abdominal Aortic Aneurysm Repair (EVAR)
• Cardiac surgery
• Aortic surgery
• Thoracic emergencies

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References:

1. Levin, A. (2010). The cardiovascular effects of aortic clamping and unclamping. Southern African Journal of Anaesthesia and Analgesia, 16(2), 62–71.(https://www.tandfonline.com/doi/full/10.1080/22201173.2010.10872666)

Summaries:

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© 2025 Francois Uys. All Rights Reserved.

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