Arterial Supply to the Head and Neck

1. Common Carotid Artery (CCA)

• Right CCA - arises from the brachiocephalic (innominate) artery
• Left CCA - arises directly from the arch of the aorta
• Both ascend in the carotid sheath (with the internal jugular vein laterally and vagus nerve posteriorly), covered inferiorly by sternocleidomastoid
• At the level of C6, the CCA can be compressed against the carotid tubercle (Chassaignac's tubercle)
• At the level of C4 (superior margin of the thyroid cartilage), it bifurcates into the Internal Carotid Artery (ICA) and External Carotid Artery (ECA)
• The carotid sinus (baroreceptor) is a dilation at the proximal ICA; the carotid body (chemoreceptor) sits at the bifurcation
• The CCA and ICA give no branches in the neck

2. External Carotid Artery (ECA)

Fig. 2.21 - Common carotid artery and branches of the external carotid artery (Color Atlas of Human Anatomy Vol. 2)

Anterior Branches (3)

Medial Branch (1)

Posterior Branches (3)

Terminal Branches (2)

Memory aid: "Some Anatomists Like Freaking Out Poor Medical Students" = Superior thyroid, Ascending pharyngeal, Lingual, Facial, Occipital, Posterior auricular, Maxillary, Superficial temporal

3. Maxillary Artery (Largest Terminal Branch of ECA)

Fig. 2.22 - Maxillary artery (Color Atlas of Human Anatomy Vol. 2)

Part I - Mandibular (behind neck of mandible)

• Deep auricular artery - TMJ, external acoustic meatus, tympanic membrane
• Anterior tympanic artery - tympanic cavity
• Middle meningeal artery - passes through foramen spinosum; largest artery to dura mater; frontal and parietal branches
• Inferior alveolar artery - enters mandibular canal; supplies teeth and bone of mandible; terminates as mental branch

Part II - Pterygoid (near masticatory muscles)

• Masseteric artery, deep temporal arteries (anterior + posterior), pterygoid branches - masticatory muscles
• Buccal artery - buccal mucosa; anastomoses with facial artery

Part III - Pterygomaxillary (pterygopalatine fossa)

• Posterior superior alveolar artery - maxillary sinus, upper posterior teeth
• Infraorbital artery - passes through inferior orbital fissure and infraorbital canal; supplies face; gives anterior superior alveolar arteries (upper anterior teeth)
• Descending palatine artery → greater palatine a. (hard palate) + lesser palatine arteries (soft palate)
• Artery of pterygoid canal - auditory tube, pharynx
• Sphenopalatine artery (terminal branch) - nasal cavity (posterior lateral nasal arteries, posterior septal branches)

4. Internal Carotid Artery (ICA)

5. Subclavian Artery Contribution

• Posterior spinal artery
• Anterior spinal artery
• Posterior inferior cerebellar artery (PICA)

• Anterior inferior cerebellar artery (AICA)
• Superior cerebellar artery (SCA)
• Pontine branches
• Posterior cerebral artery (terminal) - joins circle of Willis via posterior communicating artery

6. Circle of Willis (Summary)

• Anterior communicating artery - connects the two anterior cerebral arteries
• Posterior communicating artery (bilateral) - connects ICA to posterior cerebral artery

What is an Artery?

How an Artery is Formed (Development / Embryology)

1. Vasculogenesis

• Mesoderm cells are stimulated by FGF2 (fibroblast growth factor 2) to form hemangioblasts (a common precursor for blood vessels and blood cells)
• Hemangioblasts then respond to VEGF (Vascular Endothelial Growth Factor) and become angioblasts (vessel-forming cells)
• Angioblasts cluster together to form blood islands
• Small cavities open up within these blood islands
• Angioblasts flatten into endothelial cells that line these cavities
• These cavities fuse into networks of endothelial-lined channels - this forms the first primitive vessels

2. Angiogenesis

• New vessels sprout and branch from the already-existing primitive vessels
• Also regulated by VEGF (stimulates endothelial cell proliferation at budding points)
• Final vessel stabilization is achieved by PDGF and TGF-β

3. Wall Formation

• After the initial endothelial tube is formed, surrounding mesenchymal cells differentiate and wrap around it to form the muscular and connective tissue layers of the arterial wall
• The cardiovascular system is the first organ system to become functional - the heart begins beating on day 21-22 of embryonic life

Structure of an Artery (Wall Layers)

Fig. 13.14 - Structure of an elastic artery (Histology: A Text and Atlas)

Fig. 13.16 - Photomicrographs of elastic (a) and muscular (b) artery walls

Layer 1 - Tunica Intima (innermost)

• Single layer of endothelial cells (flat, elongated, oriented along blood flow direction)
• Rests on a basal lamina and thin subendothelial connective tissue
• Endothelial cells are joined by tight junctions and gap junctions
• Contains Weibel-Palade bodies (store von Willebrand factor and P-selectin)
• Separated from tunica media by the internal elastic membrane

Layer 2 - Tunica Media (middle - thickest)

• Made of circularly arranged smooth muscle cells (appear spiral in cross-section)
• Contains collagen fibers, elastic fibers/lamellae, and proteoglycans
• Smooth muscle cells synthesize collagen, elastin, and ECM molecules
• Number of elastic lamellae relates to blood pressure (more lamellae = higher pressure)
• Bounded on its outer side by the external elastic membrane (prominent in muscular arteries)

Layer 3 - Tunica Adventitia (outermost)

• Loose connective tissue (collagen + elastic fibers)
• Contains fibroblasts and macrophages
• Contains vasa vasorum - small blood vessels that supply nutrients/oxygen to the arterial wall itself
• Contains nervi vasorum - sympathetic nerve fibers that release norepinephrine to cause vasoconstriction

Types of Arteries

Functions / Uses of Arteries

Artery vs. Vein - Key Differences

How Arteries Control Blood Pressure and Blood Flow

The Core Principle: Ohm's Law for Blood Flow

Blood Flow (Q) = Pressure Gradient (ΔP) ÷ Vascular Resistance (R)

Mechanism 1 - Elastic Recoil (Windkessel Effect)

• During systole (heart contraction), blood is ejected at high pressure into the aorta. The elastic walls stretch and store energy like a balloon.
• During diastole (heart relaxation), no blood is ejected from the heart. The elastic walls recoil, converting stored energy back into forward blood flow.
• This converts the pulsatile pump output of the heart into a more continuous, smooth flow through the smaller vessels.
• Without this, blood pressure would drop to zero between heartbeats.

Mechanism 2 - Neural Control (Baroreceptor Reflex)

Fig. 23-1 - Baroreceptor control of arterial pressure (Medical Physiology, Boron & Boulpaep)

How it works:

1. Baroreceptors (stretch receptors) in the carotid sinus and aortic arch detect arterial wall stretch (= pressure change)
2. Signals travel via afferent nerves to the medullary cardiovascular center
3. The medulla adjusts sympathetic and parasympathetic outflow:

• Postganglionic sympathetic fibers run alongside blood vessels and innervate both muscular arteries and arterioles
• They release norepinephrine, which binds α1 receptors on smooth muscle → vasoconstriction
• Severing the spinal cord above T1 causes a severe fall in BP because the sympathetic outflow to vessels is cut

Mechanism 3 - Local (Intrinsic) Control

A. Myogenic Mechanism

• Vascular smooth muscle cells (VSMCs) respond directly to stretch from increased pressure
• Increased transmural pressure → VSMCs stretch → vasoconstriction (protects capillaries from pressure damage)
• Decreased pressure → vasodilation (increases flow when supply falls)
• Important in: brain, heart, skeletal muscle, kidneys (autoregulation)

B. Metabolic Mechanism

• Active tissues produce metabolic byproducts that act directly on VSMCs to cause vasodilation, matching blood flow to metabolic demand:

• This is how exercising muscle or an active brain automatically receives more blood

C. Endothelial Mechanism - Nitric Oxide (NO)

• Endothelial cells lining arteries are not passive tubes - they actively release vasoactive substances
• Shear stress from flowing blood → endothelial cells release Nitric Oxide (NO)
• NO is synthesized from L-arginine by NOS3 (endothelial nitric oxide synthase)
• NO diffuses into adjacent smooth muscle → activates soluble guanylyl cyclase → produces cGMP → smooth muscle relaxation → vasodilation

Fig. 32-7 - Endothelial-derived NO leads to smooth muscle relaxation (Ganong's Review of Medical Physiology)

• Stimuli for NO release: shear stress, acetylcholine, bradykinin, VIP, substance P
• Mice lacking NOS3 are chronically hypertensive, proving tonic NO release is essential for normal BP
• Nitroglycerin (used in angina) works by mimicking NO → dilates coronary arteries

Mechanism 4 - Hormonal Control (Long-term)

Renin-Angiotensin-Aldosterone System (RAAS)

• When BP falls, the kidney releases renin → converts angiotensinogen to angiotensin I → ACE converts it to angiotensin II
• Angiotensin II causes direct vasoconstriction of arterioles → raises total peripheral resistance (TPR) → raises BP
• Angiotensin II also stimulates aldosterone release → increases Na⁺ reabsorption in kidney → increases blood volume → raises BP
• ACE inhibitors (e.g. ramipril) and angiotensin receptor blockers (ARBs) block this pathway to treat hypertension

Antidiuretic Hormone (ADH / Vasopressin)

• Released by posterior pituitary when BP falls or plasma osmolarity rises
• Acts on V1 receptors in vascular smooth muscle → arteriolar vasoconstriction → raises TPR
• Acts on V2 receptors in kidney → water retention → raises blood volume

Atrial Natriuretic Peptide (ANP)

• Released by atria when blood volume is too high
• Causes vasodilation and promotes Na⁺/water excretion → reduces blood volume and BP

Summary Table

Why is Blood Pressure Measured in Arteries, Not Veins?

Reason 1 - Arteries Have High, Measurable Pressure; Veins Do Not

Reason 2 - Arteries Are Pulsatile; Veins Are Not

• Systolic pressure (peak, during contraction) - ~120 mmHg
• Diastolic pressure (lowest, during relaxation) - ~80 mmHg
• Pulse pressure = Systolic - Diastolic (normally ~40 mmHg)

"The rhythmic contraction of the left ventricle, ejecting blood into the arterial tree, results in pulsatile arterial pressures. The peak left ventricular end-systolic pressure approximates the systolic arterial blood pressure; the lowest arterial pressure during diastolic relaxation is the diastolic blood pressure." (Morgan & Mikhail's Clinical Anesthesiology 7e)

Pulsatile waveforms persist from the aortic root all the way to peripheral arteries (Morgan & Mikhail's Clinical Anesthesiology)

Reason 3 - How the BP Measurement Actually Works

1. The cuff is inflated above systolic pressure → completely blocks blood flow → artery is occluded → no sound
2. As cuff pressure is slowly released and falls below systolic pressure → a spurt of blood squirts through with each heartbeat → creates turbulent flow → you hear Korotkoff sounds (tapping) through the stethoscope
3. The pressure at which sounds first appear = Systolic BP
4. As cuff pressure falls further, sounds change character (louder → muffled)
5. The pressure at which sounds disappear = Diastolic BP

"The sounds of Korotkoff are produced by turbulent flow in the brachial artery. When the artery is narrowed by the cuff, the velocity of flow exceeds the critical velocity and turbulent flow results." (Ganong's Review of Medical Physiology 26e)

• The artery having enough pressure to be occluded by the cuff then reopened
• Intermittent pulsatile blood flow producing identifiable sounds
• Neither of these things happens in a vein - veins have too little pressure to be meaningfully occluded and reopened, and produce no audible turbulent pulse

Reason 4 - Arteries Reflect the Heart's Actual Output

• Systolic BP reflects: stroke volume, ejection force of the heart, arterial stiffness
• Diastolic BP reflects: peripheral vascular resistance and arterial compliance
• Mean Arterial Pressure (MAP) = (SBP + 2×DBP) / 3 = best predictor of organ perfusion
• Pulse pressure = reflects stroke volume and large-artery stiffness

Reason 5 - Practical Accessibility

• It is large, superficial, and easily accessible
• It lies directly under the BP cuff
• Its pressure closely reflects central aortic pressure
• Korotkoff sounds are clearly audible over it

Summary: Arteries vs. Veins for BP