Carotid hemodynamics — UH Anesthesiology

Take Home Point:

CEA is associated with impairment of baroreceptor sensitivity.
During carotid surgery cross-clamping, adequate perfusion pressure must be maintained across the circle of Willis to reduce the risk of development of ischemic neurologic deficits. SBP should be kept at normal preoperative value to 20% above that value.
Postoperative Severe Hypertension = SBP > 180 mmHg postoperatively. Treat with vasodilators (sodium nitroprusside, nitrates, or nicardipine)
Perioperative hypotension is commonly caused by anesthetic vasodilatory or myocardial depressive effect or due to the residual effect of antihypertensive administered during the cross clamping period. Treat with fluid replacement and vasopressors.
There is no evidence of superiority of particular anesthetic agents in reducing hemodynamic instability or improving outcome after carotid artery surgery.

Summary:

CEA-related Hemodynamic Instability in Symptomatic Patients

When a standard CEA is performed. a longitudinal arteriotomy is done to remove the calcified plaque, usuallyfollowed by patch angioplasty. CEA is associated with a surgical stripping of sensory nerve endings from the arterial wall, resulting in an impairment of baroreceptor sensitivity.
CEA surgery in symptomatic patients is associated with increased intraoperative and postoperative hemodynamic instability, related to dysfunction of the baroreceptors during a 7-to 10-day period after a transient ischemic attack or stroke.

Carotid Atheromas

The presence of a carotid atheroma reduces blood flow through the affected carotid artery, thereby decreasing cerebral perfusion. It also reduces baroreceptor sensitivity and affects cerebrovascular autoregulation, even in asymptomatic patients. If only 1 site is affected, the overall functioning still can be considered as normal. If both carotid arteries are involved, a bilateral baroreceptor dysfunction exists, making the patient more prone to intraoperative and postoperative hemodynamic instability.

Perioperative Hypertension

It is observed more frequently after eversion CEA when compared with conventional CEA.
During carotid surgery cross-clamping, adequate perfusion pressure must be maintained across the circle of Willis to reduce the risk of development of ischemic neurologic deficits. SBP should be kept at normal preoperative value to 20% above that value.

Postoperative Severe Hypertension

Definition – SBP >180mmHg postoperatively.
Typically peaks first hours after surgery.
Risk Factors- preoperative SBP greater than 160mmHg, peripheral vascular disease, intraoperative shunting, intracranial carotid artery stenosis, renal insufficiency, neurologic instability, and cardiac arrhythmia.
Complications --> postoperative bleeding, MI
Treatment --> Sodium nitroprusside, nitrates, or nicardipine.

Perioperative hypotension

Perioperative hypotension during CEA occurs in 5% to 8% of patients and usually lasts for 24 to 48 hours. Hypotension can be observed after unclamping and in the postoperative period. This phenomenon seems to be related to the more frequent administration of hypotensive agents to counter the hypertensive response during cross-clamping.
Anesthetic agents decrease peripheral vascular tone, and directly affect the myocardium.
There is no evidence of superiority of particular anesthetic agents in reducing hemodynamic instability or improving outcome after carotid artery surgery.
Treat hypotension with fluid replacement and vasopressors

Vasopressors of Choice

In hypotensive, anesthetized patients, the rise in mean arterial pressure after a bolus of phenylephrine (100-200 μg) was associated with decreased frontal lobe cerebral tissue oxygenation (rSO2), whereas the increase in mean arterial pressure with a bolus administration of ephedrine(5-20mg) did not influence rSO2.

Detection of Cerebral Ischemia

Cerebral Hyperperfusion Syndrome

Defined as arterial hypertension in combination with a spectrum of clinical symptoms ranging from severe, ipsilateral, migraine-like headache that typically improves in the upright position to transient, focal neurologic deficits or focal or general seizures in the absence of cerebral ischemia.
Rise in blood flow velocity in MCA > 100%, compared with baseline preoperative level.
Refer to pathophysiology of chronic vasodilation and autonomic dysfunction related hyperperfusion.