What is the blood supply to the brain and how is it managed in cases of compromised cerebral blood flow?

Blood Supply to the Brain: Anatomical and Physiological Overview

Primary Arterial Supply

The brain receives its blood supply through four major arteries: two internal carotid arteries (ICAs) anteriorly and two vertebral arteries posteriorly, which together deliver approximately 985 mL/min of blood flow under normal conditions. 1

Quantitative Flow Distribution

• Internal carotid arteries: Each ICA delivers approximately 290 mL/min to the anterior circulation, supplying the frontal, parietal, and temporal lobes 1
• Vertebral arteries: Each vertebral artery contributes approximately 80 mL/min, forming the basilar artery that supplies the posterior circulation including the brainstem, cerebellum, and occipital lobes 1
• External carotid arteries: Contribute approximately 125 mL/min each and can serve as collateral pathways in cases of significant stenosis 1

Circle of Willis and Collateral Circulation

The circle of Willis at the base of the brain provides critical anastomotic connections between the anterior and posterior circulations, allowing for collateral flow when one vessel becomes compromised 2. The vertebral arteries connect with the carotid vasculature through multiple anastomoses, including connections via the inferior spinal artery near the skull base 3.

Microvascular Architecture and Capillary Perfusion

The capillary bed represents the functional unit where oxygen and glucose delivery occurs, with arteries and veins serving primarily as conduits to support capillary function. 2

Capillary Flow Dynamics

• Red blood cell (RBC) velocity in cerebral capillaries ranges from 0.1-1.0 mm/s with an RBC flux of approximately 40-50 cells per second 2
• Capillary hyperemia occurs within 2-3 seconds of neural activation, actually preceding arteriolar dilation, challenging the traditional view that upstream vasodilation drives initial perfusion changes 2
• Mural cells (pericytes) actively control capillary diameter and regulate local blood flow in response to metabolic demands 2

Cerebral Blood Flow Regulation

Autoregulation Mechanisms

Cerebral blood flow is maintained constant at approximately 50 mL/100g/min through autoregulation, independent of systemic blood pressure fluctuations within the range of mean arterial pressure 60-150 mmHg. 4

Neurovascular Coupling

The brain has evolved a specialized "neurovascular unit" consisting of neurons, glia (astrocytes, microglia, oligodendrocytes), and vascular cells (endothelium, smooth muscle cells, pericytes) that work in concert to match blood flow to metabolic demand 2.

Neural activation triggers release of vasoactive substances including nitric oxide (NO), prostaglandin E2 (PGE2), adenosine, and potassium ions within 2-3 seconds, causing local vasodilation. 2

Metabolic and Chemical Regulation

• CO2 reactivity: CBF changes by 3% for every 1 mmHg change in arterial PCO2, making this the most potent physiologic regulator 2
• Oxygen sensitivity: Hypoxia causes vasodilation while hyperoxia causes vasoconstriction 4
• Metabolic coupling: Regional CBF increases 50-100% in response to functional activation in normal tissue 2

Management of Compromised Cerebral Blood Flow

Critical Flow Thresholds

Understanding specific CBF thresholds is essential for clinical decision-making in acute ischemia:

• >20 mL/100g/min: Tissue remains viable with reversible neurological deficits; immediate revascularization not required 2
• 10-20 mL/100g/min: Ischemic penumbra with reversible deficits if aggressive revascularization is performed promptly 2
• <10 mL/100g/min: Correlates with eventual infarction; represents irreversibly injured core 2
• <15 mL/100g/min: Significantly increased risk of hemorrhagic transformation, edema, and herniation following reperfusion 2

Acute Ischemic Stroke Management

For acute ischemic stroke, MRI with diffusion-weighted imaging (DWI) is the imaging procedure of choice, demonstrating 77% sensitivity within 3 hours of symptom onset compared to only 16% for CT. 2

Pharmacological Interventions

• Aspirin 325 mg orally within 24-48 hours of stroke onset is recommended for most patients (Class I, Level A evidence) 2
• Aspirin should NOT be given within 24 hours of intravenous thrombolysis (Class III recommendation) 2
• Clopidogrel's role in acute stroke treatment remains uncertain (Class IIb, Level C) 2

Blood Pressure Management

Induced hypertension may improve regional CBF through collateral flow augmentation, but must be carefully titrated. 2

• In select patients with acute stroke, a systolic blood pressure threshold (mean 156 mmHg) has been identified below which deficits worsen and above which they improve 2
• This approach is most beneficial in patients with multiple stenotic or occluded arteries 2
• Caution: Fluid resuscitation with normal saline bolus increases systemic blood pressure and stroke volume but does not significantly increase cerebral blood flow velocity in acute ischemic stroke 5

Chronic Cerebrovascular Disease

Collateral Compensation Assessment

In patients with significant carotid stenosis (>50%), determining whether compensatory blood flow has developed is critical for surgical decision-making. 1

• Patients with compensated stenosis show 118% of normal total brain blood flow (1174 mL/min) versus 86% (844 mL/min) in uncompensated patients 1
• 70% of patients with compensated flow remain asymptomatic compared to only 37% without compensation 1
• All potential collateral vessels, including the external carotid artery, may contribute to brain perfusion when major vessels are compromised 1

Imaging for Arteriopathy

• MR angiography (MRA) is preferred for noninvasive assessment of intracranial arteriopathies, though it is susceptible to flow-related artifacts that may simulate stenosis 2
• CT angiography (CTA) provides useful assessment of intracranial vessels in arteriopathies and thromboembolic disease 2
• Conventional cerebral angiography remains the gold standard for definitive vascular imaging, with low complication rates in experienced centers 2
• Very high-resolution MRI can directly image vessel walls, showing thickening or enhancement in arteriopathies 2

Cerebral Venous Thrombosis

Direct cerebral venography via microcatheter insertion through the internal jugular vein allows visualization of intraluminal thrombus and measurement of venous pressure. 2

• Normal venous sinus pressure is <10 mmH2O 2
• Increased venous pressure correlates with extent of parenchymal changes and is maximal in acute thrombosis 2

Common Pitfalls and Caveats

Autoregulation Loss

Below CBF of 15 mL/100g/min, autoregulation fails, making the brain vulnerable to both hypoperfusion with low blood pressure and hemorrhagic transformation with reperfusion 2. This represents a critical therapeutic window requiring careful blood pressure management.

Anatomic Variants

Anatomic variants including sinus atresia/hypoplasia, asymmetrical sinus drainage, and prominent arachnoid granulations can mimic venous thrombosis on imaging 2. When noninvasive imaging is inconclusive, conventional angiography may be necessary for definitive diagnosis.

Xenon CT Considerations

When using xenon CT for CBF measurement, head motion is the major limitation requiring inflatable restraints 2. Lowering xenon concentration to 28% reduces patient agitation and sedation to <5% of cases 2.

Perfusion Imaging Interpretation

Loss of normal CO2 reactivity (failure to decrease CBF by 3% per 1 mmHg PCO2 reduction) indicates irreversible cerebral injury and predicts poor outcome 2. This can be assessed through double xenon CT studies with ventilation manipulation.