ICU Primary Snippet – Physiological Control of SVR

Written by Dr Madhuri Anupindi 

Describe the physiological control of systemic vascular resistance (SVR)

Systemic vascular resistance = change in pressure/blood flow

• Blood flow = volume/time
• Hagen-Pouiselle law: resistance = (8 x length of vessel x viscosity of blood)/(πr⁴)
• Therefore, radius of the vessel is most significant determinant of systemic vascular resistance

The vascular system has both in series and in parallel components which comprise systemic vascular resistance

• For components in series: total resistance = sum of all the individual resistances
  • Small arteries and arterioles make up approx. 70% of total resistance  greatest effect
  • Large arteries need significant decrease in their radius to have an effect on total resistance as normally contribute only around 1% of total resistance
• For components in parallel: total resistance = inverse of the sum of the inverse of the individual resistances
  • Parallel arrangement of vessels therefore reduces resistance to blood flow  capillaries which have smallest diameter therefore make up only very small amount of total vascular resistance

** Primary way SVR is controlled is via changing the radius of the arterioles**

Factors that control the radius of arterioles:

Systemic control:

• Peripheral and central chemoreceptors
  • Hypoxia  ↑sympathetic activity  ↑SVR
  • Hypercapnoea ↑sympathetic activity  ↑SVR
  • Acidosis  ↑sympathetic activity  ↑SVR
• Arterial baroreflex:
  • High-pressure baroreceptors
    • Receptors in the carotid sinus (innervated by sinus nerve of Hering – branch of glossopharyngeal) and aortic arch (innervated by aortic nerve – branch of vagus)  synapse in nucleus tractus solitarius
    • Carotid baroreceptor responds to both increase and decrease in wall stretch while aortic arch baroreceptor responds only to increase in wall stretch
    • ↑Arterial wall stretch  ↑action potential causing receptor firing  ↑stimulation of nucleus tractus solitaries  inhibition of sympathetic vasomotor outflow  ↓SVR (opposite occurs with decreased wall stretch)
  • Low-pressure baroreceptors
    • Receptors in pulmonary arteries, large veins, walls of RA and RV – primarily activated in response to volume
    • ↑Volume  ↑ wall stretch  ↑receptor firing  activate vasomotor centre  ↑HR (in response to stretch of SA node – Bainbridge reflex), ↑ANP release  ↓renin, ADH, aldosterone release  vasodilatation, ↓Na/H20 reabsorption  (opposite occurs with decreased volume)
  • Autonomic central control (arterial baroreflex/chemoreceptors are also part of this)
    • The baseline of sympathetic tone acting on alpha receptors causing vasoconstriction – vascular beds are variably responsive to changes in sympathetic neural activity
      • Arterioles of muscle, splanchnic, renal and skin are more responsive to sympathetic activation compared to cerebral or coronary arterioles non-essential vascular beds can be vasoconstricted to preserve flow to vital organs
      • ↑Sympathetic activation  activates RAAS and activates adrenal medulla to release catecholamines  ↑SVR
    • Inhibition/reduction of sympathetic activation  vasodilatation  ↓SVR
  • Hormonal control
    • Anti-diuretic hormone
      • ↑Osmolarity, ↓volume, ↑angiotensin II  ↑ADH (synthesised in hypothalamus, stored and then released from posterior pituitary)  ↑water reabsorption via V2 receptor, ↑vascular resistance via V1 receptor  ↑SVR
    • Renin-angiotensin-aldosterone
      • ↓renal perfusion pressure  ↑renin – converts angiotensinogen – angiotensin I  converted by ACE to angiotensin II  ↑sympathetic activity, aldosterone, ADH, release of norad/adrenaline  ↑SVR
    • Catecholamines (cause similar effect as sympathetic nerve activation but effects are longer lasting)
      • Exercise, hypoglycaemia, pain, ↑stress  release of adrenaline and noradrenaline  vasoconstriction  ↑SVR
    • Temperature:
      • ↑temperature  vasodilatation (opposite occurs with decreased temperature)

Local control

• Myogenic control
  • ↑Pressure in vessel  smooth muscle stretched  depolarisation of smooth muscle  voltage gated calcium channels open  ↑intracellular calcium  myosin light chain phosphorylation  vasoconstriction
  • Myogenic control more sensitive depending on the organ e.g. very responsive in cerebral circulation
• Metabolic control
  • ↑Metabolic demand of tissue  ↑Release of substances such as CO₂, lactate, ATP, adenosine, nitric oxide, potassium  dilatation of arterioles
• Flow control

Local vasodilatation in distal arterioles  ↑flow in that local proximal arteriole  ↑shear stress  release of vasodilatory substances  vasodilatation in proximal arteriole