Peripheral Vascular Resistance (PVR) is the opposition to blood flow caused by friction between the blood and the inner walls of the systemic blood vessels. While friction occurs throughout the circulatory system, most resistance is generated by the small arteries, known as arterioles. Arterioles act like adjustable nozzles, determining how hard the heart must pump to move blood through the body. PVR regulates blood pressure and ensures that blood flow, or perfusion, reaches all tissues and organs effectively.
Defining Vascular Resistance and Its Calculation
The physical principles governing PVR are analogous to Poiseuille’s Law, which describes fluid flow resistance in a tube. Resistance is directly proportional to the vessel’s length and the blood’s viscosity. Since vessel length and blood thickness change little in a healthy adult, these factors are not the body’s primary control mechanisms for resistance.
The radius of the blood vessel is the most powerful determinant of vascular resistance. Resistance is inversely proportional to the radius raised to the fourth power. This means that halving the vessel’s radius increases resistance sixteen-fold. This exponential relationship highlights why muscular arterioles are the main regulators of resistance, as their diameter can be rapidly adjusted.
In a clinical setting, PVR is referred to as Systemic Vascular Resistance (SVR). It is calculated using a modified version of Ohm’s Law, which treats blood flow as current, pressure difference as voltage, and resistance as SVR. The calculation is SVR = (Mean Arterial Pressure – Right Atrial Pressure) / Cardiac Output.
Mean Arterial Pressure (MAP) is the average pressure driving blood through the systemic circulation. Right Atrial Pressure, also known as Central Venous Pressure (CVP), is the pressure where blood returns to the heart. Cardiac Output (CO) is the volume of blood the heart pumps per minute. The resulting SVR value is expressed in the specialized unit of dynes \(\cdot\) sec \(\cdot \text{cm}^{-5}\), with a normal range between 800 and 1200 units.
Physiological Control of Vessel Diameter
The body actively regulates arteriolar diameter to manage PVR and ensure adequate tissue perfusion. This complex regulation involves rapid neural signals and slower-acting hormonal and local chemical factors. The smooth muscle lining the arterioles is normally in a state of partial contraction, known as vascular tone, which provides a baseline resistance the body can adjust.
Neural Control
The sympathetic nervous system provides the primary neural control over arteriolar diameter. Sympathetic nerve fibers release norepinephrine, which acts on alpha-adrenergic receptors in the smooth muscle to cause vasoconstriction, or narrowing. This widespread constriction is a rapid mechanism used to increase PVR and maintain blood pressure, such as when a person quickly stands up.
The sympathetic system’s constant output maintains the background vascular tone, as the parasympathetic nervous system has limited direct influence on most systemic vessels. This continuous activity allows resistance to be increased (vasoconstriction) or decreased (vasodilation) by adjusting the rate of nerve firing. A decrease in sympathetic output leads to vasodilation, which lowers PVR and increases blood flow.
Hormonal and Local Control
Circulating hormones provide systemic control, while local metabolites offer fine-tuned regulation specific to individual tissues. Powerful vasoconstrictors, such as Angiotensin II, are part of the Renin-Angiotensin-Aldosterone System, a hormonal cascade that raises PVR and blood pressure. Other circulating hormones, like epinephrine from the adrenal medulla, cause either constriction or dilation depending on the receptor type present in the vascular bed.
Local Metabolic Control
Local metabolic control is an intrinsic mechanism linking blood flow directly to tissue needs. When metabolism increases, local metabolites like carbon dioxide, lactic acid, and potassium ions are produced. These chemical signals act directly on the arteriolar smooth muscle to cause vasodilation, overriding systemic signals.
This vasodilation increases blood flow to the active tissue to supply oxygen and remove waste. Nitric oxide, a potent vasodilator released by endothelial cells, also regulates local PVR by relaxing the smooth muscle.
Peripheral Resistance and Systemic Blood Pressure
Peripheral vascular resistance is directly linked to systemic blood pressure: Mean Arterial Pressure = Cardiac Output x SVR. This equation demonstrates that for a given heart output, blood pressure is determined solely by the resistance in the blood vessels. Changes in PVR have significant cardiovascular implications.
High PVR
Chronic high PVR, or vasoconstriction, is a primary feature of systemic hypertension. The constant high resistance forces the left ventricle to work harder to eject blood, a workload known as afterload. Over time, this increased afterload can lead to ventricular hypertrophy, where the heart muscle thickens as it strains against the high pressure.
This thickening eventually impairs the heart’s ability to fill and pump efficiently, contributing to heart failure. The persistently elevated resistance causes long-term structural changes in the heart and blood vessels. Managing PVR is therefore a major focus in treating cardiovascular disease.
Low PVR
Conversely, a sudden drop in PVR can lead to hypotension, or low blood pressure. While a modest reduction in PVR is beneficial, promoting efficient flow, a significant drop indicates a loss of vascular tone. This condition is seen in distributive shock, such as septic shock, where inflammatory mediators cause widespread, uncontrolled vasodilation.
When PVR drops too low, the circulatory system effectively becomes too large for the available blood volume, and the pressure gradient necessary to push blood through the organs disappears. Despite the heart potentially pumping normally, the lack of resistance causes blood pressure to plummet, leading to inadequate tissue perfusion and organ malfunction. The immediate clinical goal is to administer medications that cause vasoconstriction to restore PVR and blood pressure.