3.7: Blood Supply to the Brain

The brain, despite comprising only about two percent of total body weight, requires approximately 15-20 percent of the body's cardiac output to sustain its high metabolic demands. This continuous blood supply is essential for delivering oxygen and glucose to neurons while also removing metabolic waste products. Any disruption in cerebral circulation, even for a few minutes, can lead to irreversible neuronal damage, highlighting the brain’s dependence on an uninterrupted blood flow.

Arterial Blood Supply

The brain receives blood from two primary sources: the internal carotid artery and the vertebral artery. These arteries are branches originating from the common carotid and subclavian arteries, respectively, as illustrated in Figure 6. The internal carotid artery further bifurcates into the anterior and middle cerebral arteries. These arteries are instrumental in supplying the frontal and parietal regions of the cerebrum, facilitating essential cognitive and sensory functions. Concurrently, the vertebral arteries unite to form the basilar artery, a crucial conduit for blood supply to the posterior brain structures. From the basilar artery, branches such as the posterior cerebral artery emerge to nourish the temporal and occipital lobes of the cerebrum. Additionally, the posterior inferior cerebellar arteries supply critical regions of the cerebellum and spinal cord.

The cerebral arterial circle, or the circle of Willis, is of particular significance; it is an intricate junction where the vertebral (basilar) and internal carotid arteries converge. They mainly include posterior cerebral artery, a branch of the basilar artery, and anterior cerebral artery and posterior communicating artery, branches of the internal carotid artery. This circular arrangement facilitates interconnection between major cerebral vessels, ensuring the provision of collateral circulation to vital cerebral structures. In the event of vessel occlusion, the circle of Willis acts as a safeguard, maintaining adequate blood flow to prevent ischemic symptoms. This remarkable anatomical feature exemplifies the brain's innate capacity to adapt and preserve its function even under challenging circumstances.⁷

Figure 6 | Blood Supply to the Brain | ⁸ This illustration shows the major blood vessels supplying the brain. The major arteries, including the carotid and vertebral arteries, are depicted as they branch into smaller vessels, forming the cerebral arterial circle (Circle of Willis).

Venous Return

Figure 7 | Dural Sinuses and Veins | ⁹ Blood drains from the brain through a series of sinuses that connect to the jugular veins.

Following its journey through the brain, the deoxygenated blood follows a specific return route to systemic circulation. This journey is facilitated by an interconnected system of dural sinuses and veins, illustrated in Figure 7, which ensures the seamless transition of blood from the CNS back into the circulatory system. The dural sinuses converge and ultimately give rise to the jugular veins. The jugular veins serve as conduits that ensure the efficient return of blood to the heart, completing the cycle of oxygenation and nourishment.

Cerebral Hemodynamics

The brain is a remarkable structure within the landscape of physiological intricacies, constituting merely 2 percent of the body's mass. Approximately 15 to 20 percent of the total cardiac output is devoted to sustaining the brain's constant metabolic demands, as neurons require ample oxygen and glucose to maintain their activities.

The cranial enclosure houses a complex interplay of brain, CSF, and blood. However, this space is limited. Cerebral perfusion pressure (CPP) operates as a stabilizing force throughout this arrangement, maintaining a delicate balance as long as CSF circulates freely. CCP is determined by the difference in mean arterial pressure and the intracranial pressure (ICP). Mean arterial pressure ranges from 70 to 100 mm Hg whereas ICP varies from 7-15 mm Hg. Therefore, CPP is approximately 60 to 80 mm Hg.

The average blood flow rate is about 50 ml per 100 g of cerebral tissue per minute. Cerebral blood flow (CBF) exemplifies a delicate equilibrium. CPP and cerebral vascular resistance (CVR) jointly govern CBF. CBF = CPP/CVR relationship offers insights into the finely calibrated balance. The cerebral vessels modulate their caliber to maintain constant blood flow, especially within a mean arterial pressure range of 50 to 150 mm Hg.

If the volume of any component, whether brain tissue, CSF, or blood, starts to increase, compensatory mechanisms come into play to prevent drastic shifts in ICP. In a scenario where a lesion develops within the brain, compensatory mechanisms engage initially, such as CSF moving to the spinal subarachnoid spaces, helping to mitigate the impact. However, these mechanisms have limitations. As ICP rises, the brain's venous channels become compressed while arterial vessels dilate to sustain CBF. This interplay between resistance and dilation strives to uphold CPP but can eventually lead to the formation of edema. As edema progresses, ICP escalates further, resulting in a cycle that intensifies over time. This interplay between rising ICP and cranial rigidity sets the stage for a complex dynamic.

Variations in factors such as carbon dioxide and hydrogen ion concentrations prompt adjustments in perfusion (autoregulation). For example, metabolic variations such as elevated carbon dioxide levels, diminished pH, and decreased oxygen levels lead to localized vasodilation. Local neuronal activity acts as an architect, influencing the regional distribution of blood. Neural orchestration via the sympathetic and parasympathetic systems elicits mild vasoconstriction and vasodilation. A marginal elevation in CBF during sleep, attributed to heightened arterial carbon dioxide levels, attests to the regulation of CBF.¹⁰

The impact of various anesthetics on CBF regulation is complex and multifactorial, influenced by factors such as dosage, patient characteristics, and concurrent use of other medications. Different anesthetics can affect CBF regulation differently due to their distinct mechanisms of action and pharmacological properties. Inhalational anesthetics such as isoflurane have been shown to decrease cerebral metabolic rate and CBF in a dose-dependent manner. However, they can also disrupt cerebral autoregulation, which is the brain's ability to maintain constant blood flow despite changes in blood pressure. Disruption of cerebral autoregulation may lead to fluctuations in CBF and potentially contribute to adverse neurological outcomes. Intravenous anesthetics like propofol and barbiturates also impact CBF regulation. Propofol, for example, can cause dose-dependent decreases in CBF and cerebral metabolic rate. However, propofol may help preserve cerebral autoregulation within certain dosage ranges. Barbiturates have been used for cerebral protection during neurosurgical procedures due to their ability to decrease cerebral metabolic rate and intracranial pressure. Opioids, including fentanyl and morphine, are often used as adjuncts to anesthesia. While opioids generally do not have a significant direct effect on CBF regulation, they can cause respiratory depression, which may indirectly impact CBF through changes in arterial blood gasses and blood pressure. Local anesthetics primarily affect peripheral nerves and have minimal direct effects on CBF regulation.¹¹