Systemic Vascular Resistance (SVR) represents the total opposition blood flow encounters as it moves through the body’s vast network of blood vessels, excluding the pulmonary circulation. This measurement reflects the degree of tension, or tone, in the muscular walls of the arteries and arterioles throughout the systemic circuit. SVR is a fundamental component of cardiovascular physiology, directly influencing the amount of pressure required for the heart to pump blood effectively and regulating overall blood pressure.
SVR: The Core Concept of Resistance
Systemic Vascular Resistance can be understood by applying a concept similar to Ohm’s Law in physics, where pressure is equivalent to the product of flow and resistance. In the circulatory system, this translates to Mean Arterial Pressure (MAP) being equal to Cardiac Output (CO) multiplied by SVR. This relationship demonstrates that if the volume of blood pumped by the heart remains constant, an increase in resistance will result in a higher blood pressure. Conversely, if the resistance drops, the heart must either increase its output or the blood pressure will fall.
The physical dimensions of the blood vessels determine the majority of this resistance. The vessel radius is the most powerful determinant of SVR, as even a small change in diameter has a dramatic effect on flow. Mathematically, resistance is inversely proportional to the radius raised to the fourth power, meaning halving the vessel radius increases resistance sixteen-fold. This explains why the body primarily manipulates the diameter of small arteries and arterioles to adjust resistance.
These muscular arterioles, sometimes called resistance vessels, are the body’s primary regulators of SVR and are the site of the greatest pressure drop in the circulation. The total length of the vessels also affects resistance, though this factor remains relatively constant in adults. Blood viscosity, which is its thickness, is a third factor. Conditions like polycythemia, where there is an abnormally high concentration of red blood cells, increase viscosity and thereby increase SVR, making the heart work harder.
Physiological Control of Vascular Resistance
The body employs rapid systems to adjust SVR by controlling the smooth muscle tone in the arteriolar walls. These regulatory mechanisms are divided into short-term neural control and longer-term hormonal control. The autonomic nervous system provides immediate adjustments through the sympathetic nervous system, which releases norepinephrine to cause widespread vasoconstriction. This reflex is constantly monitored by baroreceptors, specialized pressure sensors located in the carotid arteries and the aortic arch.
When baroreceptors sense a drop in blood pressure, they signal the brainstem to increase sympathetic outflow, which constricts the arterioles and raises SVR to normalize the pressure. The hormonal system offers a more sustained method of SVR control, most notably through the Renin-Angiotensin-Aldosterone System (RAAS). When the kidneys detect low blood flow or pressure, they release renin, initiating a cascade that produces Angiotensin II.
Angiotensin II is a potent vasoconstrictor that directly causes the smooth muscle in the arterioles to contract, sharply increasing SVR. Other hormones, such as vasopressin (ADH) released from the pituitary gland, also contribute to increased SVR by promoting vasoconstriction. Epinephrine from the adrenal medulla can also increase SVR, especially during acute stress, though its effect varies depending on the receptor type. These systems work in concert to ensure resistance is finely tuned to maintain adequate blood flow to all organs.
Clinical Implications of Abnormal SVR
Measuring SVR is a valuable tool in intensive care settings because it provides insight into the hemodynamic state and the underlying cause of abnormal blood pressure. The normal range for SVR in adults typically falls between 700 and 1500 dynes·s/cm⁵. Values outside this range indicate a significant physiological imbalance that requires clinical attention.
Pathologically high SVR means the blood vessels are excessively constricted, forcing the heart to pump against greater resistance. This condition significantly increases the heart’s afterload, which is the pressure the left ventricle must overcome to eject blood into the aorta. Chronic high SVR, often seen in severe hypertension, leads to ventricular hypertrophy, where the heart muscle thickens as it strains.
This increased strain over time can lead to heart failure because the muscle eventually becomes inefficient and unable to fully relax or fill. Low SVR, conversely, indicates widespread vasodilation, where the blood vessels are too relaxed.
This state is frequently observed in types of distributive shock, such as septic shock or anaphylaxis, where inflammatory mediators cause a massive relaxation of the arterioles. In low SVR states, the circulatory system essentially becomes too large for the available blood volume, causing blood pressure to drop precipitously. Even if the heart’s output is high, the lack of resistance means the pressure required to perfuse organs cannot be maintained. This inability to maintain adequate Mean Arterial Pressure results in poor blood flow to vital organs, leading to tissue damage and organ failure.