Acute circulatory failure is encountered in shock, regardless of its origin, when
physiological compensatory mechanisms are overwhelmed. The initial tachycardia and reflex
vasoconstriction of shock aims to maintain sufficient arterial pressure and tissue
perfusion pressure. Beyond these mechanisms of compensation for relative and/or absolute
hypovolaemia, arterial hypotension and tissue hypoperfusion appear, expressed clinically
by functional signs (e.g. asthenia) and physical signs (arterial hypotension,
consciousness disorders, mottling, oliguria, etc.).
It has been observed that organ failure induced by circulatory insufficiency is
associated with a poor prognosis in septic shock. In daily clinical practice, acute
circulatory failure is most often characterised by haemodynamic failure as reflected by
arterial hypotension and/or tachycardia. Early treatment of acute circulatory failure is
a recognised prognostic factor in trauma patients and patients with septic shock (2,3),
leading to a reduction in mortality.
The first line of treatment for circulatory failure is usually early vascular filling due
to relative and absolute hypovolaemia. The choice of fluids depends on the clinical
situation, although for septic shock crystalloids are recommended as first-line therapy.
Although early vascular filling is the first line of treatment, overfilling, also known
as "induced" vascular filling, is alone recognised as a factor associated with excess
mortality in various situations of acute circulatory failure. It is now accepted that
early administration of inotropic and/or vasopressor agents, i.e. before the end of
vascular filling, is necessary to restore arterial pressure and therefore limit the
consequences of tissue hypo perfusion. In order to determine the choice between continued
vascular filling and the administration of vasopressor and/or inotropic agents,
predictive indicators of vascular filling requirements have been developed. These aim to
determine whether or not vascular filling will increase cardiac output or one of its
surrogates such as the subaortic time velocity integral (SATI).
Numerous indicators have been described for more than 30 years in intensive care units.
Dynamic criteria are those that have the best predictive performance compared to static
indicators. Their time-consuming implementation requires an invasive approach for most of
these criteria due to their technical nature and the need to respect sometimes
restrictive validity criteria.
The technological development of ultrasound scanners has allowed their liberal use and
the validation of dynamic ultrasound criteria predictive of the response to vascular
filling (respiratory variations of the sub-aortic velocity time integral, S wave, index
of distensibility of the inferior vena cava, index of collapsibility of the superior vena
cava, central venous pressure). The mechanism underlying superior vena cava
collapsibility is complex, involving variations in intra-thoracic pressure as well as the
inherent movements of the lung parenchyma. These pathophysiological mechanisms have not
yet been described.
A recent study has demonstrated the interchangeability between delta PP and respiratory
variations in subclavian vein diameter in intensive care patients and in the operating
theatre.
The advantages of the transthoracic ultrasound approach to assessing respiratory
variations in subclavian vein diameter are its rapidity of implementation, ease of use,
non-invasive nature and reproducibility.