Define Systemic Vascular Resistance and list its determinants. Briefly explain the role of its determinants.

Definition of Systemic Vascular Resistance (SVR)

Systemic Vascular Resistance (SVR) is the total resistance to blood flow offered by the entire systemic vasculature, excluding the pulmonary circulation. It reflects the afterload that the left ventricle must overcome to eject blood into the arterial system. This resistance is critical in regulating blood flow to various tissues and maintaining systemic blood pressure. SVR is primarily generated in the small arteries and arterioles, which are often referred to as resistance vessels due to their ability to dynamically alter their diameter.

Determinants of Systemic Vascular Resistance and Their Roles

The regulation of SVR is complex, involving a dynamic interplay of physical, neural, and humoral factors. The major determinants include:

• Vessel Diameter (Radius): This is the most significant determinant of SVR. According to Poiseuille's Law, resistance is inversely proportional to the fourth power of the vessel radius (R ∝ 1/r⁴).
  • Role: Even minor changes in arteriolar diameter have a profound impact on SVR. Vasoconstriction (narrowing of blood vessels) dramatically increases resistance, leading to higher SVR. Conversely, vasodilation (widening of blood vessels) significantly decreases resistance and SVR. This regulation is primarily mediated by the smooth muscle in the tunica media of arterioles.
• Blood Viscosity: This refers to the thickness or "stickiness" of the blood, primarily influenced by hematocrit (red blood cell concentration) and plasma protein levels.
  • Role: Higher blood viscosity (e.g., in conditions like polycythemia or severe dehydration) increases internal friction within the blood and against the vessel walls, thereby increasing resistance to flow and elevating SVR. Conversely, lower blood viscosity (e.g., in anemia or fluid overload) reduces SVR.
• Total Vessel Length: The overall length of the systemic vascular network.
  • Role: Resistance is directly proportional to the length of the blood vessel. While vessel length does not change significantly in an adult in the short term, it can be a factor in conditions like obesity, where the development of new capillaries and vessels to perfuse increased tissue mass can incrementally increase total peripheral resistance over time.

Additional Regulators and Modulating Factors:

Beyond the primary physical determinants, SVR is continuously modulated by various physiological mechanisms:

• Neural Regulation (Autonomic Nervous System):
  • Role: The sympathetic nervous system plays a dominant role. Sympathetic stimulation releases norepinephrine (and epinephrine from the adrenal medulla), which acts on alpha-1 adrenergic receptors in vascular smooth muscle, causing widespread vasoconstriction and an increase in SVR. The parasympathetic nervous system has minimal direct influence on systemic vascular resistance.
• Humoral Factors (Hormones and Chemical Mediators):
  • Role: Various hormones and vasoactive substances circulate in the blood, influencing arteriolar tone. Examples include:
    • Angiotensin II: A potent vasoconstrictor, increasing SVR as part of the Renin-Angiotensin-Aldosterone System (RAAS), especially in response to decreased blood pressure or renal perfusion.
    • Vasopressin (Antidiuretic Hormone): A potent vasoconstrictor, particularly at high concentrations, increasing SVR.
    • Endothelin: A powerful vasoconstrictor produced by endothelial cells.
    • Nitric Oxide (NO): A potent vasodilator, produced by endothelial cells, which decreases SVR. Reduced NO bioavailability is implicated in hypertension.
    • Prostaglandins: Some prostaglandins are vasodilators (e.g., prostacyclin), while others are vasoconstrictors.
• Local Metabolic Factors:
  • Role: Tissues regulate their own blood flow in response to metabolic needs (autoregulation). Accumulation of metabolic byproducts such as adenosine, lactic acid, carbon dioxide, and hydrogen ions (from increased metabolism) leads to local vasodilation, decreasing resistance in that specific vascular bed to enhance blood flow and oxygen delivery. This local effect overrides systemic influences to ensure adequate tissue perfusion.
• Vascular Compliance: The distensibility of blood vessels.
  • Role: Stiffer, less compliant vessels (e.g., due to atherosclerosis or aging) tend to offer increased resistance to flow, contributing to higher SVR and increased pulse pressure.

Determinant	Primary Mechanism of Action	Impact on SVR
Vessel Diameter	Smooth muscle contraction/relaxation in arterioles	Inverse (vasoconstriction ↑ SVR, vasodilation ↓ SVR)
Blood Viscosity	Hematocrit, plasma protein concentration	Direct (higher viscosity ↑ SVR, lower viscosity ↓ SVR)
Total Vessel Length	Overall length of systemic vasculature	Direct (longer vessels ↑ SVR)
Neural Regulation	Sympathetic nervous system activity	Direct (sympathetic stimulation ↑ SVR)
Humoral Factors	Hormones (Angiotensin II, Vasopressin, NO, Endothelin)	Variable (vasoconstrictors ↑ SVR, vasodilators ↓ SVR)
Local Metabolic Factors	Accumulation of metabolic byproducts (CO2, H+, Adenosine)	Inverse (metabolic activity ↓ local SVR)
Vascular Compliance	Elasticity of arterial walls	Inverse (stiffer vessels ↑ SVR)