G4vi / 22A20 / 20A07: Describe the physiological control of systemic vascular resistance (SVR)

22A20: Exam Report

Describe the physiological control of systemic vascular resistance (SVR)

22% of candidates passed this question.

A definition or description of SVR that recognised the importance of radius in small arteries/arterioles as the major determinant attracted marks.

Resistance is ΔP/flow; where ΔP is not only MAP and flow is volume/time.

The systemic vascular resistance is the resistance of several circuits in parallel, which have both common and independent factors in their regulation.

As they are in parallel the sum of reciprocals is used, 1/SVR = 1/R1 + 1/R2 to determine the overall value.

A detailed explanation of the Hagen-Pouiselle law was not required, attracted few marks and wasted writing time. The remainder of the answer focus was on the factors that control the radius of these vessels.

As a question regarding control, an approach that included sensors, integrators and effectors tended to yield a more comprehensive answer with resultant higher marks. Other useful structures included divisions into intrinsic/local factors (including endothelial input and autoregulation), neural control (reflexes and central controller) and hormonal control.

As the question was regarding physiological control, no marks were awarded to pharmacological manipulation of SVR. Given the potential scope of the question, detailed descriptions of how noradrenaline exerts its effect were not required beyond receptor level although stating ‘sympathetic nervous system activation results in vasoconstriction’ were too simplistic to attract full marks.

20A07: Exam Report

Describe the physiological control of systemic vascular resistance (SVR).

21% of candidates passed this question.

This question invited a detailed discussion of the physiological control mechanisms in health, not pathophysiology nor drug-mediated effects. The central and reflex control mechanisms that regulate SVR over time are distinct from the local determinants of SVR.

There was often confusion between dependent and independent variables. Cardiac output is generally depended upon SVR, not vice versa, even though SVR can be mathematically calculated from CO and driving pressures.

The question asked about systemic vascular resistance and did not require a discussion of individual organs except for a general understanding that local autoregulation versus central neurogenic control predominates in different tissues.

Emotional state, temperature, pain and pulmonary reflexes were frequently omitted. Peripheral and central chemoreceptors and low-pressure baroreceptors were relevant to include along with high pressure baroreceptors. 

G4vi / 22A20 / 20A07: Describe the physiological control of systemic vascular resistance (SVR)


  • SVR can be defined using Darcy’s law
    • R = ΔP / Q
    • Where R is resistance, DP is pressure gradient, Q is flow
  • SVR is the resistance (pressure drop) generated in blood flowing through the systemic arterial circulation
  • Normal SVR
    • SVR = (Mean aortic pressure – RAP) / CO
    • E.g. SVR = (100 mmHg – 0 mmHg)/ 5L per minute
    • SVR = 20 mmHg/L/min or 20 Wood units
    • Or x 80 to give: 1600 dynes-sec/cm5
  • Arterioles
    • 100 – 200 μm in diameter
    • Main site where resistance develops
    • Can dilate or constrict their diameter by 50%

Factors which affected SVR:

  • Described by Hagen Poiseuille equation:
    • R = 8ηl / πr4
    • Where:
      • L = length of vessel (relatively constant)
      • η = viscosity of blood (affected by HCt, lipid + protein content of blood, temp)
      • r = radius > most important factor
    • Radius of vessels regulated by systemic and local factors

Systemic factors:

  • Hormonal
    • Vasoconstriction > ­­↑ ­SVR
    • Caused by: angiotensin II, vasopressin, adrenaline
  • Neural
    • ↑ ­SNS output > vasoconstriction (via α1 adrenoreceptors on vascular smooth muscle > Gq GPCR > ↑ IP3 + DAG) > ↑ SVR
    • ­↑ SNS output in response to:
      • Hypovolaemia e.g. haemorrhage (detected by baroreceptors)
      • Hypothermia (detected by peripheral and central thermoreceptors)
      • Hypoxia (detected by peripheral and central chemoreceptors)

Local / regional factors

  • Intrinsic myogenic autoregulation (contraction of vascular smooth muscle in response to stretch from ↑ perfusion pressure)
  • Metabolic autoregulation (vasodilation in response to ↑ tissue demand mediated by K+, adenosine, ↑ CO2, ↑ H+ > leads to ↓ SVR)
  • Flow or shear-associated regulation (↑ NO > vasodilation)
  • Prostacyclin and NO release from endothelium (vasodilation)
  • Endothelin release from endothelium (vasoconstriction)
  • Thromboxane released by platelets (vasoconstriction)

Author: Madeline Coxwell Matthewman