Noradrenaline in resuscitation of septic shock

An extensive elaboration of noradrenaline and its properties can be found elsewhere. This is a brief summary, to help one answer questions like  Question 21 from the first paper of 2009, which was all like "briefly outline what initial agent you will use to treat the circulatory disturbance and how would you initially titrate the dose of the agent". The circulatory disturbance was vasodilated shock, which you had to work out by manually calculating the SVRI.

In short:

Measurement of vasodilation

Vasodilation can be viewed in a number of ways; a practical approach (which does not involve the direct measurement of small vessel caliber) is to evaluate it using the index of systemic vascular reistance, which is the relationship of the systemic arterio-venous pressure gradient to the cardiac output. The basic principle is that flow is equal to the pressure gradient divided by resistance, and thus resistance is the pressure gradient divided by flow.

SVR = ([MAP-RAP] × 79.9) / CO


SVRI = ([MAP-RAP] × 79.9) / CI

A normal SVR is 700-1600 dyn.s/cm5

A normal SVRI is 1970-2390 dyn·sec/cm5·m2

The CICM examiners have actually expected their fellowship candidates to perform this calculation in a previous SAQ paper (specifically, Question 19 from the first paper of 2006).

Vasodilated shock states

Generally speaking, these states are characterised by decreased SVR and increased cardiac output.

Thelist below is not all-inclusive, but covers the most frequently encountered forms:

Low-SVR, high-cardiac-output states

  • Septic shock
  • Anaphyactic shock
  • Vasodilation due to pharmacological agents (eg. nitrates)
  • Vasodilation due to severe liver disease (which is also probably endotoxin mediated)

Low-SVR, low-or-normal-cardiac-output states

  • Neurogenic (spinal) shock
  • Vasodilation due to SIRS following a global hypoxic/ischaemic injury
  • SIRS due to cardiopulmonry bypass

Pathogenesis of vasodilation in septic shock

Sepsis is the default model for the vasodilated high-output shock state.

In sepsis, there are numerous mechanisms mediating the systemic loss of vascular resistance.

Question 21 from the first paper of 2009 asks the candidate to briefly mention some of these.

A brief answer would consist of a list, resembling this one:

Causes of vasodilation in septic shock

A more detailed explanation has not been examined thus far. For a more detailed overview, one has no specific source to site. Many articles come up in a search for "pathophysiology of septic shock", but none answer this specific question. Perhaps the single broadest overview is afforded by our very own L.I.G Worthley's "Shock: a review of pathophysiology and management: Part I and Part II.

The use of noradrenaline in septic shock

Noradrenaline is the prototypic vasopressor, and is discussed at length elsewhere.


Its beneficial effects in sepsis include the following:

  • Increased preload by venoconstriction
  • Reversal of decreased SVR by arterial vasoconstriction
  • Mildly increased cardiac output by its vestigial β-1 effects (it's hardly the primary goal)



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