Perioperative Hemodynamic Management of Carotid Artery Surgery
Summary by Nicholas Olson, DO 8.28.24
https://www.clinicalkey.com/#!/content/playContent/1-s2.0-S1053077015007338?returnurl=https:%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1053077015007338%3Fshowall%3Dtrue&referrer=https:%2F%2Fpubmed.ncbi.nlm.nih.gov%2F
Main Takeaways:
Patients undergoing carotid artery surgery are often at elevated risk and may experience hemodynamic instability
Hemodynamic lability and instability is mediated by carotid baroreceptors which are affected differently by surgical approach (angioplasty and stenting vs. endarterectomy) and anesthetic type (regional vs. general)
Patients undergoing carotid artery surgery are at risk for stroke, perioperative ischemia, hyperperfusion syndrome, and intracerebral hemorrhage. Intraoperatively there are various modalities that can be used to monitor cerebral perfusion.
Summary:
Background:
This review article provides a summary on the pathophysiology behind hemodynamic instability and lability seen in patients with carotid artery disease, as well as a review of the differences in physiologic changes seen in carotid endarterectomy versus carotid artery stenting. As hypotension/hypertension is common during different phases of carotid surgery, this article covers both antihypertensive and vasopressor therapy utility to maintain stable hemodynamics. This article also gives an overview of complications following carotid intervention as well as diagnosing cerebral hyperperfusion syndrome. Additionally, this article summarizes various modalities used to monitor for cerebral ischemia in carotid surgery.
Pathophysiology of Perioperative Hemodynamic Instability in Carotid artery surgery:
Carotid baroreceptors modulate blood pressure and heart rate in response to acute blood pressure changes by adjusting parasympathetic and sympathetic activity. When plaques develop within the carotid artery, blood flow is reduced which decreases the sensitivity of the baroreceptor and decreases cerebrovascular autoregulation. If there is only unilateral carotid stenosis, overall functionality can be considered normal. Bilateral involvement is associated with increased hemodynamic instability both intraoperatively and postoperatively. In carotid endarterectomy, hemodynamic instability can be seen in 12 to 54% of patients which is associated with transection of afferent nerve endings. This can last hours to days but baroreceptor function normalizes in the late postoperative period. In carotid artery angioplasty and stenting, the mechanical manipulation of the carotid baroreceptor is associated with hypotension and bradycardia in 29-51% of patients, which is thought to be mediated by parasympathetics.
Perioperative Management of Blood Pressure:
Blood pressure in patients with carotid artery stenosis is often labile and ranges from hypertension to hypotension in the perioperative period. Intraoperatively, following placement of the carotid artery cross-clamp, a blood pressure target between a normal perioperative value and 20% above the preop. pressure is often targeted to maintain adequate cerebral perfusion. With the increased blood pressure, however, there is increased risk of myocardial ischemia and intracranial bleeding.
For patients undergoing carotid endarterectomy, severe hypertension (SBP >180mmHg) occurs in 37-66% of patients and typically peaks in the first several hours following surgery. Maintaining systolic blood pressure within 20% or <160mmHg is often target and help to decrease risk of hematoma, MI, or intracranial bleed. Following cross-clamp removal, elevated cranial norepinephrine levels have been seen which supports a central sympathomimetic mechanism contributing to post-operative hypertension. Agents commonly used to treat hypertension following carotid artery surgery include alpha2 receptor agonists, beta blockers, direct-acting vasodilators. Of note, beta blockers do not cause cerebral vasodilation unlike direct-acting vasodilators (nitrates, nicardipine, sodium nitroprusside) which have the potential for intracranial hypertension by increasing cerebral blood flow through vasodilatation.
During carotid endarterectomy, hypotension is seen in 5-8% of patient in the perioperative period, lasting typically for 24-48hrs. When performed under regional anesthesia, hypotension is more common in the postoperative period (possibly due to increased use of antihypertensives during the intraoperative period) as opposed to general anesthesia where this is often hypertension in the postoperative period. During carotid stenting upon inflation of the balloon, there is an increase in stretch receptor firing which leads to hypotension and bradycardia. To help mitigate the effects of this phenomenon it can be reasonable to administer an anticholinergic Persistent hypotension lasting for >1 hour and requiring vasopressor therapy occurs in 19.2% of patients.
Detection of Cerebral Ischemia:
The ability to detect cerebral ischemia will differ by the type of anesthesia utilized during carotid surgery. In regional anesthesia, consciousness and neurological function can be easily assessed. When under general anesthesia, additional monitoring can help identify when/if there is cerebral ischemia. SSEP monitoring is a sensitive monitor but carries high false-negative results; however, it is highly specific in predicting neurologic outcome after carotid endarterectomy. EEG is another sensitive method to detect cerebral ischemia; however, it requires experienced personnel. Bispectral index (BIS) carries a 30-60 second delay and has a low predictive value. Transcranial Doppler is noninvasive and can be useful to monitor cerebral blood flow in large intracranial arteries (e.g. the middle cerebral artery) and can be detect embolism intraoperatively. Near-infrared spectroscopy monitors frontal lobe oxygenation and provides information regarding the changes in cerebral oxygenation during carotid artery cross-clamping. A 20% reduction in baseline is often used as an indication for carotid artery shunt placement (sensitivity 80%, specificity 82%).
Cerebral Hyperperfusion/Reperfusion Syndrome:
Cerebral hyperperfusion occurs when there is a rise in blood flow velocity >100% of the baseline (preop) level in the MCA and is accompanied by clinical symptoms (severe ipsilateral headache that improves in the upright position, neurological deficits, seizures) which aren’t caused by ischemia. It occurs in 0-3% of patients having carotid endarterectomy (1% undergoing carotid stenting) can be accompanied by intracranial bleeding which is associated high a high mortality. With stenting, it typically occurs within 12 hours. With endarterectomy, the peak occurrence is on day 6. Associated risk factors include recent ischemic stroke, severe ipsilateral or contralateral carotid artery stenosis, severe post-op. hypertension, and prior contralateral carotid endarterectomy that occurred <3 months prior.
Discussion/conclusion:
Patients undergoing carotid endarterectomy or carotid artery stenting are likely to experience hemodynamic instability due to the dysregulation and subsequent manipulation of the carotid baroreceptors. This often improves in the late post-operative period; however, in the immediate post-op period there may be severe hypertension or hypotension.
Carotid artery stenting, unlike endarterectomy, causes mechanical stretch on the arterial wall which can lead to profound hypotension and bradycardia.
Patients undergoing carotid artery surgery are at risk for cerebral ischemia. While neurologic function can be assessed in patient’s having intervention under regional anesthesia, general anesthesia can mask these symptoms. Therefore, one should consider the use of additional monitoring for cerebral ischemia. SSEPs, transcranial Doppler, EEG, and near-infrared spectroscopy are modalities that can be used, although each has its limitations.
In nearly all patients undergoing carotid artery surgery, there will be increased cerebral perfusion. One possible complication of this can be cerebral hyperperfusion syndrome which occurs when there is a rise in blood flow velocity >100% of the baseline (preop) level in the MCA and is accompanied by clinical symptoms (severe ipsilateral headache that improves in the upright position, neurological deficits, seizures) in the absence of ischemia. This can also be accompanied by intracerebral hemorrhage.