QOTM – BP management in sepsis

This month’s questions:
1. In patients on escalating doses of vasopressors (and/or inotropes) should we routinely be inserting a femoral arterial line to correlate with radial arterial pressures, and if so and they differ which pressure do we target? Is anyone doing this already
2. Is there ever any benefit in using inotropes as part of the management of septic shock? Do they do more harm than good? Should we instead restrict ourselves to vasopressors and fluid optimisation?

A

I must admit that I have not seen combined femoral and radial arterial lines utilised in cases outside of cardiac ICU, but anecdotally there does seem to be an increase in people championing their use in instances of escalating vasopressors (particularly at recent ICU meetings and conferences). If anything, it has certainly made me more wary of situations we often get caught in, ramping up pressors on someone who is deteriorating and it becomes unclear as to whether we are mitigating or contributing to this decline. Although I have little experience of this in the septic population, I think in the presence of clinical signs of vasoconstriction I would be tempted to try it, and in the presence of a significant difference would target treatments and therapies to a femoral blood pressure over a radial.

As for the use of inotropes in septic shock, I guess the million dollar question is what are we trying to achieve? A MAP, a specified flow, a change in surrogates of end organ perfusion, an improvement in VTI/Ejection Fraction/other echocardiographic parameters……..

Most people would agree that septic shock (at least early on and pre-large volume of IV fluids) is primarily a vasoplegic insult with some element of hypovolaemia, and therefore it seems ‘sensible’ to correct these disturbances and I would therefore advocate this as the main stay of treatment provided physiological stability and/or improvement is achieved. That is not to say I do not believe inotropes have a place but:

1. Diastolic failure is apparently the more common cardiac complication in sepsis and the benefit of inotropes is even less clear than systolic failure

2. Large scale studies- e.g. LEOPARDS haven’t as far as i’m aware demonstrated a benefit from the use of inotropes in this population

3. A lot of our inotropes are inodilaters, and given that there are reports of a greater association between diastolic pressures and capsular organ dysfunction (especially of the kidney) than other BP parameters, I would be concerned about sacrificing this for a potentially less important systolic pressure.

I would be interested to see what others think…………….

B

Thanks for the QOTM, the papers and the reply/nudge.
I was unaware of the increasing concern regarding mismatch between Radial and femoral lines. It would make sense, and I can personally remember a couple of cases where a-lines have needed replacing to another site, only to find the measurements are significantly different. However, without a strong feeling regarding the incidence of this phenomenon or the pathophysiological significance of which figure to follow it would be difficult to create an algorithm or treatment plan that incorporates routine femoral “back up” checking. Perhaps the most pragmatic approach would be to do exactly as you suggested: “consider the possibility of radial overvasoconstriction in cases where vasoconstrictor requirement is escalating without response”. In these situations I would agree that the femoral pressure is probably more reflective of what is happening at a core organ level.
With regards to inotropes I think you have again hit the nail on the head- what exactly are the parameters we are looking to chase? Additionally, I think the ICU literature repeatedly falls foul of the homogenisation of the ICU population. I don’t think individual ICU patients fit any grouping and this is why most studies that recruit broad categories of patient always seem to end up as negative studies, whereas those that have some aspect of clinician-led or nurse led management (i.e. patient specific not population specific interventions) all seem to show positive outcomes.
Towards this end my approach to inotropes in septic shock would be as follows:
1. No routine use of inotropes in this population. Mainstay of treatment is as you described.
2. In the event of deterioration / escalation / evidence of non-response I would widen my investigations to include assessment of cardiac function – e.g. CO monitoring, ECHO, mixed venous saturations, trop/ecg etc.
3. If there was a hint of cardiac dysfunction then do a very gentle trial of inotrope with further assessment to determine response.

I think this gives the best balance between considering all options in someone who is not heading the right way, but avoiding the routine use of something with a lot of potential downsides and no real evidence of benefit.

However, I suspect there is a large amount of evidence that I am unaware of. I too would be interested in others feelings on this.

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