Systemic Vascular Resistance (SVR) is a measurement of the total opposition blood encounters as it flows through the body’s vast network of blood vessels outside of the lungs. This resistance acts like friction, requiring the heart to generate sufficient force to push blood through the circulatory system. SVR is a fundamental metric for understanding how the cardiovascular system operates and directly relates to a person’s blood pressure.
The Physical Mechanism of Systemic Resistance
The primary control point for systemic resistance is within the body’s smallest arteries, known as the arterioles. These microscopic vessels are often referred to as resistance vessels because they contain a thick layer of smooth muscle in their walls. This muscle can contract or relax, which effectively changes the internal diameter, or lumen, of the vessel. The majority of the opposition to blood flow is generated in this precise location of the circulatory system.
The relationship between a vessel’s diameter and the resistance to flow is highly disproportionate. Even a small reduction in the radius of an arteriole causes a large increase in resistance. For instance, reducing the diameter of a vessel by half can decrease the blood flow to one-sixteenth of its original volume. This mechanism allows the body to make subtle adjustments to the smooth muscle tone for powerful control over blood flow and pressure throughout the body.
While diameter is the most dynamic factor, other physical properties also contribute to resistance. The length of the entire vascular system factors into the equation, although this parameter remains relatively constant in adults. Another factor is the viscosity, or thickness, of the blood, which is mainly determined by the concentration of red blood cells. Conditions that increase the number of red blood cells lead to thicker blood, which elevates SVR.
Calculating and Interpreting Systemic Vascular Resistance
SVR is not measured directly but is a calculated value derived from three hemodynamic measurements. The calculation follows a hydraulic version of Ohm’s law, where resistance equals a pressure gradient divided by flow. The pressure difference is determined by subtracting the Central Venous Pressure (CVP, pressure at the end of the system) from the Mean Arterial Pressure (MAP, pressure at the beginning).
The flow component of the calculation is the Cardiac Output (CO), which represents the volume of blood pumped by the heart per minute. This results in a formula where SVR equals the pressure gradient (MAP minus CVP) divided by the Cardiac Output. This formula quantifies the opposition the heart is working against to circulate blood.
A value for SVR is typically expressed in units of dynes-seconds per centimeter to the fifth power (dynes⋅sec⋅cm⁻⁵), with a normal range generally falling between 700 and 1500 of these units. A high SVR value signifies widespread vasoconstriction, or narrowing of the blood vessels, indicating that the heart must work harder to push blood forward. Conversely, a low SVR value indicates widespread vasodilation, or relaxation of the vessels, which can lead to low blood pressure because the flow is encountering insufficient opposition.
Biological Systems That Regulate SVR
Neural Control
The body employs control systems to continuously adjust SVR and maintain stable blood pressure. A primary pathway involves the sympathetic nervous system, often associated with the “fight-or-flight” response. When activated, the sympathetic nervous system releases chemical messengers like norepinephrine. These bind to receptors on the smooth muscle of the arterioles, causing them to constrict and rapidly increase SVR.
Hormonal Control
Hormonal control provides a slower but powerful regulatory mechanism, managing SVR over minutes or hours. One potent vasoconstrictor is the hormone Angiotensin II, a component of the renin-angiotensin-aldosterone system. Angiotensin II signals the arteriolar smooth muscle to increase its tone, resulting in a sustained elevation of SVR and helping to raise blood pressure.
Vasodilators
Working in opposition to these constricting forces are potent vasodilators that decrease SVR. A major example is Nitric Oxide (NO), a gas produced by the cells lining the blood vessels, called the endothelium. Nitric Oxide causes the surrounding smooth muscle to relax, leading to vasodilation and a reduction in resistance. Medications such as Angiotensin-Converting Enzyme (ACE) inhibitors disrupt the production of Angiotensin II, effectively reducing its constricting effect and lowering SVR to treat high blood pressure.
Clinical Implications of Abnormal SVR
Abnormal SVR values are associated with several serious health conditions. A chronically high SVR is the underlying cause of many cases of hypertension (high blood pressure). This persistent narrowing of the arterioles forces the left side of the heart to pump against greater pressure, increasing the heart’s workload over time. This sustained stress can eventually lead to heart muscle thickening and, ultimately, heart failure.
Conversely, an acutely low SVR is a defining characteristic of several life-threatening forms of shock. In conditions like septic shock or anaphylactic shock, the body releases massive amounts of inflammatory substances that cause widespread, pathological vasodilation. This sudden drop in SVR means that blood pressure plummets to low levels, making it impossible to maintain adequate perfusion of oxygen and nutrients to the organs. Medications that increase SVR, called vasopressors, are often used to raise the resistance and restore blood pressure to sustain organ function.