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Tags: vascular

Aortic cross clamping

Open surgical procedures of the thoracoabdominal aorta carry the highest mortality rate among elective procedures
overall 30-day mortality ranging from 8% to 35%

Traditionally, aortic aneurysms are treated by open repair: following direct surgical exposure of the aorta, it is cross-clamped proximately and distally to the aneurysm, and the aneurysm is then opened and replaced by a prosthetic graft

In the elective case, prior to aortic cross-clamping, a dose of unfractionated heparin is given intravenously to reduce the risk of thrombosis
A recent systematic review has questioned the evidence supporting the beneficial effect of heparin in open AAA surgery and recommended the need for further research.

Repair of juxta- and suprarenal aortic aneurysms, compared with infrarenal aortic aneurysms, involves a more extensive mobilization of the viscera to achieve adequate exposure of the abdominal aorta. Furthermore, reimplantation of branch vessels or creation of an oblique anastomosis to accommodate branch vessel ostia is sometimes required. This added complexity can prolong the period of renal ischemia during aortic clamping – potentially increasing operative morbidity and mortality as well as the postoperative risk of renal dysfunction.

Haemodynamic Δ

When the cross-clamp is applied, perfusion to the lower half of the body is entirely reliant upon collateral circulation and there is a sudden increase in arterial pressure proximal to the clamp

↑ afterload & LV wall tension → ↑ myocardial workload & ↑ oxygen demand.
In normal circumstances, this would be met by an ↑ coronary blood flow & oxygen supply, but in patients with CAD it can cause myocardial ischaemia and impaired cardiac output

Management of this iatrogenic physiological change relies on vasodilatation

Factors affecting haemodynamic changes w/ cross-clamp:

Supraceliac clamping:

Infraceliac clamping:

↑SVR
↑BP

blood flow could shift from capacitance vessels distal to the occlusion toward areas proximal to the cross-clamp

↑preload ∵ volume shift from splanchnic vasculature into IVC

The reason for this drainage of blood from the splanchnic system is in part due to the recoil of the splanchnic vasculature once the transmural pressure decreases below the natural recoil of the venous system, leading to a collapse of the respective venous system.

↑ SVC blood flow
↓ IVC blood flow

↑ catecholamine & angiotensin → vaso- & venoconstriction → blood flow shift to body proximal to aortic clamp

If the cross-clamp is applied to the infraceliac aorta, the data on changes in the preload and cardiac output are inconclusive

haemodynamic Δ minimal w/ infra-renal clamping

In patients with occlusive disease of the aorta, the hemodynamic responses to aortic cross-clamping are less pronounced than in patients with aneurysmal disease; ∵ aortic collateral vascularisataion

Anrep effect

The sudden increase in arterial blood pressure and left ventricular pressure may lead to acute compression of subendocardial blood vessels and subsequent ischemia. This may cause a decrease in myocardial contractility. It is presumed that vascular autoregulation can regulate subendocardial blood distribution and increase the blood flow to the affected areas, which in turn increases the otherwise compromised contractility of the heart

compromised in IHD patients ∵ compromised autoregulation
→ limited ability of subendocardial tissue to adapt to ischaemia
→ ↓ contractility

Vasodilators may facilitate Anrep effect ∵

PPV

PPV unreliable for intra-renal clamping ∵blood flow shifts from infrasplanchnic to splanchnic vasculature

aortic pressure distal to clamp ∝ pressure proximal to clamp

The perfusion to the tissue and organs distal to the aortic cross-clamp depends on collateral vasculature and even more on perfusion pressure rather than on cardiac output. The clinical significance of these findings is that in order to maintain at least some blood flow to the tissues and organs below the aortic clamp site, the aortic pressure proximal to the clamp should be kept as high as the heart can tolerate to minimize ischemic injury to those organs.

O2 consumption

O2 consumption ↓ distal to level of clamp ∵ ↓ O2 supply
O2 uptake ↓ in muscles proximal to clamp ?∵ ↓ capillary nutritive blood flow from arterio-venous shunting & ↑ sympathetic discharge

Duration

↑ duration of aortic occlusion → ↑SVR & ↓CO gradually
?∵ fluid shift from intravascular to interstitial compartment

aortic cross-clamp duration of greater than 90 min is independently associated with a higher mortality

Haemodynamic Δ after unclamping

A second physiological insult occurs when the aortic cross-clamp is removed

SVR ↓ by 3/4 resulting in potentially profound hypotension.
↓ BP may be compounded by

severity of hypotension ∝ cross-clamp time

Preparation prior to unclamping
the aims should be to achieve adequate volume resuscitation and cardiovascular stability, correct acid-base and electrolyte disturbances and normalize the temperature. Increased minute ventilation during the period of cross-clamping may help to minimizes the effects of the ensuing metabolic acidosis

These measures in conjunction with a gradual release of the cross-clamp can reduce the degree of hypotension observed

Vasoconstrictors and positive inotropes may be required even after fluid replacement

In refractory hypotension, the cross-clamp may have to be reapplied

The gradual unclamping of the common iliac arteries one at a time, over a few minutes may also be helpful.

↓SVR
↓BP

The blood vessels in the previously ischemic areas are severely dilated because of the accumulation of adenosine, lactate, and CO2 during the time of ischemia. This increases the capacity of these blood vessels to levels above baseline, thus promoting a shift in blood flow and volume into those previously under-perfused areas. This shift in blood flow and the increase in vascular capacity in the areas below the clamp site may lead to central hypovolemia. Simultaneously, vasodilating compounds such as adenosine and lactate are washed out of the previously ischemic areas into the circulation, leading to additional vasodilatation, thus reducing blood pressure. Infusion of fluid and increase in intravascular volume prior to the release of the aortic cross-clamp can help to attenuate the development of central hypovolemia and to avoid significant hypotension

vasopressors promote this redistribution of blood volume
∵ nonischemic areas proximal to clamp more reactive to vasopressors than the ischemic & acidotic regions distal to the clamp site

Reactive hyperemia is an important component of the response to aortic unclamping. This might be explained by an induced arterial vasodilation distal to the clamp during the time of ischemia, resulting from smooth muscle relaxation and thus facilitating higher flows in that area after removal of the aortic clamp

CO may ↑ / ↓ / unchanged
LVEDP ↓
myocardial perfusion ↑

The blood flow in areas proximal to the cross-clamp site reduces to levels close to the time before clamping relatively quickly

The gradual release of the aortic cross-clamp and its partial or complete reapplication if significant hypotension develops has been recommended.
This avoids the abrupt changes in vascular resistance and the shift in blood flow and volume, thus attenuating the development of central hypovolemia and hypotension. The release of vasoactive and cardiodepressant metabolites from the ischemic areas will also be less abrupt. In addition, the production of oxygen-free radicals is reduced if the clamp is removed slowly.
i.e. postconditioning

Post-conditioning can be performed under control of blood pressure. The cross-clamp can be slowly released from the aorta without a significant decrease in blood pressure. If the blood pressure does drop, then the aorta can be completely or partially reclamped, allowing a smaller amount of flow to the lower body.

Humoral effects during clamp

Acidosis

The degree of acidosis and increase in the lactate concentration depend on the duration of aortic clamping and the underlying disease of the patient

sodium bicarbonate does not affect the degree of post-unclamping hypotension. This might be due to the correction of acidosis in the blood rather than in the tissue, including the arterial walls. Unclamping of the aorta also leads to a transient ↑ in CO2 washout as well as ↑CO2 production due to ↑ oxygen consumption in the now reperfused tissues, which can aggravate both vasodilatation and hypotension

RAAS

↑ Renin & angiotensin during aortic cross-clamping
→ contribute to ↑BP during clamping

suprarenal clamping: ∵ ↓ perfusion pressure in afferent arterioles.
infrarenal clamping, the cause for the observed increase in renin and angiotensin concentrations is less clear.

Catecholamines

↑ adrenaline & noradrenaline

Multifactorial

ROS

During ischemia, the metabolism of adenosine triphosphate produces adenosine, hypoxanthine, xanthine oxidase, purines, and free oxygen radicals

The concentration of hypoxanthine in particular increased threefold in humans after infrarenal aortic clamping, because of high levels of hypoxanthine in femoral venous blood

Hypoxanthine can cause cellular damage during reperfusion by producing cytotoxic ROS that lead to tissue damage

Decreasing or delaying the oxygen delivery during reperfusion (postconditioning) has been shown to reduce the extent of ischemia-reperfusion injury in animal models

Phosphate

hypoPO4 post-op
↑ phosphate compound synthesis after restoration of blood flow
→ shift in phosphate from extracellular to intracellular compartment

regular check until 48h post-op

Prostaglandins, neutrophils, complement

↑ prostaglandin & thromboxane

↑ leukocyte & neutrophil ∵ inflammatory response
↓ lymphocyte ∵ entrapment in end organs e.g. lungs

↑ anaphylatoxins C3a & C5a

Endotoxins, cytokines

↑ endotoxins & cytokines e.g. TNF & IL-6 ∵ ischaemia trigger

↓ perfusion / reperfusion of intestine ↑ intestinal permeability
→ ↑ endotoxins → ↑ cytokines

TNF a/w acute lung injury after acute intestinal ischemia and reperfusion

Effect on organ systems

Lung

resp complications common

↑PVR from cross-clamping of thoracic aorta. This might at least in part be explained by the increase in the blood volume circulating through the pulmonary vasculature that is associated with clamping of the thoracic aorta.

Pulmonary dysfunction after aortic clamping can also be attributed to the release of cells and compounds during reperfusion that are subsequently entrapped in the lungs.

Thromboxane and leukocyte may accumulate in the pulmonary tissue and, in combination with the increase in complement C3a and C5 activity after aortic clamping, lead to inflammatory processes and increase in microvascular permeability in the lungs, which can lead to noncardiogenic pulmonary edema

Dextran, heparin, pentastarches, and mannitol have been tested to avoid microparticle aggregation in the lungs, with some success
no convincing evidence yet

Kidney

Kidney injuries common
incidence: supra-renal > infra-renal clamping (30 vs 10%)

Renal insufficiency is a dreaded complication, as the mortality due to acute renal failure has been shown to be as high as 25% in abdominal aneurysms and as high as 50% in thoracoabdominal aneurysms

Cross-clamping the thoracic aorta leads to an 85–94% decrease in renal blood flow, glomerular filtration rate, and urine output

The etiology of renal failure after aortic surgery is almost always acute tubular necrosis induced by an ischemia-reperfusion insult associated with aortic cross-clamping
atheroemboli due to supra-renal clamping is another cause

kidneys respond differently to ischemia and reperfusion and that oxygen deprivation may continue despite reinstitution of the blood flow.

The renin–angiotensin system affects the renal blood flow during aortic clamping. Mainly, angiotensin II will increase the renal vascular resistance and sodium absorption directly by causing constriction of the vas afferens and indirectly by increasing aldosterone production.

The decrease in renal function during the time of severely reduced blood flow to the kidney can be seen as an energy conserving and a protective compensatory mechanism of the kidneys.

Spinal cord

see Spinal cord protection

During the time of aortic cross-clamping, the spinal cord perfusion relies on collateral blood flow.

The artery of Adamkewicz is one of the most distal feeding arteries to the spinal cord, and if this artery derives from that part of the aorta affected by the placement of the cross-clamp or repair itself, then the spinal cord is at the greatest risk for ischemia.

Intestine

depends on location of clamping, e.g. supra-mesenteric / supra-celiac

As part of the open aortic aneurysm repair, the inferior mesenteric artery (IMA) and the hypogastric artery are often sacrificed, putting the patient at risk of developing colorectal ischemia

other risk factors

Intestinal tonometry measuring intraluminal PCO2 as a surrogate of mucosal CO2 is a reliable predictor for the occurrence of intestinal ischemia and can be used intraoperatively.

The ischemic lesions of the colon are most often located in the sigmoid segment and usually result from inadequate collateral blood flow from the SMA and hypogastric arteries to the sigmoid colon

High mortality rates are associated with colonic ischemia when transmural necrosis is present

Summary in words

The temporary occlusion of the aorta and the subsequent reinstitution of blood flow to previously ischemic areas are the most critical steps during open aortic repair.

The occlusion of the aorta will increase afterload and arterial blood pressure.

Cross-clamping of the supraceliac aorta leads to blood volume shifts resulting in an increase in preload and cardiac output.

Clamping of the infraceliac aorta leads to less predictable shifts in blood volume and changes in cardiac output.

During aortic cross clamping, many vasoactive substances and mediators are released further altering blood flow and hemodynamic parameters.

Release of the aortic cross-clamp is followed by shifts in blood volume as well as the release of vasodilating substances such as lactate, adenosine, and CO2, leading to central hypovolemia and hypotension.

Reinstitution of blood flow after unclamping also triggers an ischemia-reperfusion response.

The complex hemodynamic, humoral and inflammatory changes occurring during aortic clamping and after unclamping of the aorta can ultimate contribute to frequently observed postoperative complications like pulmonary dysfunction and acute kidney injury.

Practice

  • To avoid overloading the heart during aortic clamping, fluid administration before aortic clamping should be kept to a minimum.
  • BP during aortic clamping should be kept as high as the heart can tolerate to maintain collateral perfusion to areas distal to the aortic cross-clamp.
  • To attenuate hypotension after unclamping, the clamp should be removed slowly from the aortic cross-clamp. A fluid bolus and vasopressors should be administered as well.
  • Slow and gradual removal of the aortic cross-clamp and reperfusion with normo-oxygenated rather than hyper-oxygenated blood may help reduce the severity of ischemia-reperfusion injury.

References

The Pathophysiology of Aortic Cross-Clamping