What will happen when the common carotid artery get occulated at the b

What will happen when the common carotid artery get occulated at the both sides ?

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Bilateral Common Carotid Artery Occlusion: What Happens?

The common carotid artery (CCA) is the parent trunk that divides into the internal carotid artery (ICA) and external carotid artery (ECA). Bilateral CCA occlusion is a rare but catastrophic event whose outcome depends critically on collateral pathways and the integrity of the circle of Willis.

1. Normal Blood Supply Context

Each CCA arises differently:

Right CCA - from the innominate (brachiocephalic) artery at the sternoclavicular notch
Left CCA - directly from the aortic arch

They ascend to ~C4 level and bifurcate into ICA (brain) and ECA (face/scalp). The ICA is the main supplier of the anterior two-thirds of the cerebral hemisphere via the MCA and ACA.

2. The Role of the Circle of Willis (Key Determinant)

This is the single most important factor in survival and outcome.

As Goldman-Cecil Medicine states: "In persons with an intact circle of Willis, the entire intracranial circulation can be supplied by a single patent internal carotid artery or vertebral artery."

However, only ~25% of individuals have a fully complete circle of Willis. Most people have anatomical variants - hypoplastic communicating arteries, absent A1 segments, or fetal PCA origins.

3. Three Main Collateral Pathways Available

If both CCAs occlude, the brain attempts compensation via (from Localization in Clinical Neurology, 8e):

Collateral Source	Mechanism
Circle of Willis	Vertebrobasilar system supplies anterior circulation via posterior communicating arteries
Extracranial-intracranial anastomoses	ECA branches (if patent at origin) - ophthalmic artery retrograde filling
Leptomeningeal anastomoses	Terminal surface branches of ACA, MCA, PCA interconnect

Important: If the bifurcation of the CCA remains patent, retrograde flow from the ECA can maintain ICA flow. As Adams & Victor's Neurology states: "If the bifurcation is patent, few, if any, symptoms may result because retrograde flow from the external carotid maintains internal carotid flow and perfusion of the brain."

4. What Actually Happens - Clinical Outcomes

Scenario A: Good Collateral Compensation (intact circle of Willis + patent bifurcation)

The patient may be relatively asymptomatic or have only mild, intermittent symptoms
Vertebrobasilar system compensates through posterior communicating arteries
ECA retrograde flow can sustain ICA perfusion

Scenario B: Partial Compensation (incomplete circle + bilateral occlusion)

Transient ischemic attacks (TIAs) - recurring episodes of focal neurological deficits
Amaurosis fugax (transient monocular blindness) - a horizontal shade sweeping up/down the visual field, lasting minutes, from ophthalmic artery low flow
Jaw claudication - from low flow in external carotid branches (also a feature of unilateral CCA occlusion, per Harrison's 22e)
Cognitive impairment and gait apraxia from chronic hypoperfusion (watershed ischemia)

Scenario C: Poor Collateral Supply (catastrophic bilateral occlusion)

This is the worst outcome, seen when communicating arteries are hypoplastic bilaterally. Per Adams & Victor's Principles of Neurology: "If one ICA had been occluded at an earlier time, occlusion of the opposite one may rarely cause bilateral cerebral infarction, in the circumstances of inadequacy of the posterior communicating arteries of both sides."

Bilateral catastrophic failure produces:

Bilateral hemisphere infarction - anterior two-thirds of both hemispheres
Stupor or coma (from bilateral MCA + ACA territory loss)
Bilateral hemiplegia
Bilateral hemisensory loss
Aphasia (dominant hemisphere) + anosognosia (non-dominant hemisphere)
Potentially cortical blindness if fetal PCA configuration is present (PCA arising from ICA rather than basilar)
Death in severe cases from massive cerebral infarction and herniation

5. Common Causes of Bilateral CCA Occlusion

Per Harrison's Principles of Internal Medicine 22E:

Takayasu's arteritis - the classic cause of bilateral CCA occlusion at their origin (a large-vessel granulomatous vasculitis)
Severe atherosclerosis (rarely bilateral)
Post-radiation arteriopathy (after head and neck radiation therapy)
Trauma
Aortic dissection extending into arch branches

Summary Table

Condition	Effect
Intact circle of Willis + patent bifurcation	Asymptomatic or minimal deficits
Partial circle + bilateral occlusion	TIAs, jaw claudication, amaurosis fugax, watershed ischemia
Absent/hypoplastic communicating arteries	Bilateral massive hemispheric infarction, coma, death
External carotid collaterals	Can sustain brain perfusion if ICA bifurcation patent

The bottom line: bilateral CCA occlusion is potentially fatal if collateral pathways fail. The outcome is entirely dictated by the anatomy of the circle of Willis, patency of the bifurcation, and speed of collateral recruitment. In clinical practice, it is most classically associated with Takayasu's arteritis affecting the aortic arch branches.

Harrison's Principles of Internal Medicine 22E, p. 2143
Adams and Victor's Principles of Neurology 12E, pp. 2224-2227
Goldman-Cecil Medicine, p. 3922 (Circle of Willis section)
Localization in Clinical Neurology 8E, p. 1350 (Collateral Circulation)

Do they increase BP and increase heart rate

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Bilateral CCA Occlusion: Effect on BP and Heart Rate

Short answer: YES - both BP and HR increase. This is due to loss of baroreceptor inhibition, producing "Baroreflex Failure Syndrome."

Understanding the Normal Carotid Sinus Baroreceptor Role

The carotid sinus is located in the wall (adventitia) of the carotid bulb - the dilation at the CCA bifurcation. It is a stretch-sensitive baroreceptor. When blood pressure rises:

The sinus wall is stretched
Baroreceptor afferents fire more frequently via the carotid sinus nerve (branch of CN IX - glossopharyngeal)
Signals travel to the nucleus tractus solitarius (NTS) in the medulla
This inhibits sympathetic outflow and activates parasympathetic (vagal) output
Result: HR falls, BP falls - a "brake" on the cardiovascular system

This diagram from Lippincott's Pharmacology summarizes the reflex:

What Happens When Both CCAs Are Occluded (or Bilateral Carotid Sinus Denervated)

When the CCA is occluded bilaterally, the carotid sinuses receive no pulsatile blood flow and no stretch. The baroreceptors go silent. This removes the tonic inhibitory brake on the cardiovascular system.

The result, per Cummings Otolaryngology (Head & Neck Surgery):

"Bilateral baroreceptor dysfunction causes unopposed sympathetic outflow and results in marked fluctuations in blood pressure and a sustained tachycardia."

This is clinically called Baroreflex Failure Syndrome and causes:

Effect	Mechanism
Increased BP (hypertension)	Unopposed sympathetic vasoconstriction + increased cardiac output
Increased HR (tachycardia)	Loss of vagal tone + sustained sympathetic cardiac stimulation
BP lability (wild fluctuations)	No baroreceptor damping of moment-to-moment pressure swings

As Guyton & Hall states: "A primary purpose of the arterial baroreceptor system is to reduce minute-by-minute variation in arterial pressure to about one-third of what would occur if the baroreceptor system were not present." Remove it, and BP swings wildly.

The Carotid Body Component (Additional Effect)

At the same bifurcation sits the carotid body - a chemoreceptor sensitive to:

Low O₂ (hypoxia)
High CO₂ (hypercapnia)
Low pH (acidosis)

With bilateral CCA occlusion, if the brain becomes ischemic (reduced O₂ delivery), the carotid body may also be stimulated, further driving sympathetic activation and raising BP and HR even more.

Timeline of Events After Bilateral Baroreceptor Loss

Per Cummings (from the surgical experience of bilateral carotid body tumor excision - the closest clinical model):

Time	Event
0-24 hrs	Initial BP/HR instability begins
24-72 hrs	Sustained tachycardia and hypertensive episodes fully manifest
Weeks-months	Gradual compensation from aortic arch baroreceptors and possible neural regrowth

Important Nuance: Baroreceptors Do Reset Over Time

Guyton & Hall points out that baroreceptors reset over 1-2 days if exposed to chronically altered pressure. So in chronic bilateral CCA occlusion (e.g., in Takayasu's arteritis), the aortic arch baroreceptors may partially compensate, and BP/HR instability may improve over weeks - but it remains abnormal and labile.

Treatment of Baroreflex Failure Hypertension/Tachycardia

From Cummings Otolaryngology:

Acute: Sodium nitroprusside or labetalol (IV) to control hypertensive surges
Chronic: Clonidine (alpha-2 agonist) - reduces norepinephrine release AND stimulates parasympathetic outflow to slow HR

Summary

What is lost	What happens
Carotid sinus stretch (baroreceptor unloaded)	No inhibitory impulses to medulla
No NTS activation	Sympathetic tone goes unopposed
Parasympathetic withdrawn	Heart rate increases (tachycardia)
Vasoconstriction + increased CO	Blood pressure increases (hypertension)
No moment-to-moment buffering	Wild BP fluctuations

So to directly answer your question: Yes - bilateral CCA occlusion causes both increased BP and increased HR through loss of baroreceptor-mediated inhibition, leading to unopposed sympathetic outflow. This is the syndrome of Baroreflex Failure.

Cummings Otolaryngology Head & Neck Surgery, p. 127-128
Lippincott Illustrated Reviews: Pharmacology, p. 128
Guyton & Hall Textbook of Medical Physiology, pp. 228-229

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