Fluids & Vasopressors – knowing when to stop & start in septic shock patients
Sepsis is one of the top 10 causes of death in the US. There are approximately 750,000 cases of sepsis annually, of which more than 215,000 will result in death. Sepsis is also one of the most common causes of admission into critical care and one of the most common causes of death in critical care.
Once identified the first line interventions needed in the care bundle (taking a blood culture, giving antibiotics and oxygen) are acknowledged to be safe, simple, and immediate actions.
The remaining element of the bundle has been much more problematic to deliver optimally i.e. the fluid administration. This is the element that would most benefit from closer attention. Historically it was assumed that the low blood pressure seen in sepsis and raised lactate was a consequence of simple hypovolemia and as such would be resolvable by aggressive fluid administration to achieve a target central venous pressure of 8 mmHg. Accordingly large volumes of fluids were and still are given to improve arterial pressure. This has been the corner-stone component of the standard sepsis bundle. However, we now know that sepsis is not a simple volume-depleted state and almost half of septic patients are found to be poorly responsive to fluids. If fluids are administered in large volumes to a non fluid responsive patient the fluid is destined move quickly from the blood stream and become lodged peripherally causing oedema and even cardiac diastolic dysfunction.
Not surprisingly recent multicentre clinical trials (ProCESS, ARISE and PROMISE) have demonstrated that aggressive fluid resuscitation does not improve the outcome of patients with severe sepsis. If given in excess, any fluid, whether a starch, colloid, simple crystalloid or balanced salt will likely result in major consequences for the patient. It is not just a matter the choice of fluid.
In sepsis tissue perfusion is compromised by the arterial and venous vasodilation that occurs secondary to the infection induced systemic inflammatory response. The inflammation increases the size and hence capacitance of the arterial and venous vasculature and venous return and blood pressure fall. Furthermore, there is evidence that administered fluids may in fact directly effect the circulation and in effect be vasodilators in their own right. So fluids have the potential to worsen the circulatory insult they are administered to solve.
Clearly a more physiological approach to fluid administration is necessary. Advanced hemodynamic monitoring is required to achieve careful administration of fluids in patients with sepsis. Hemodynamic monitoring can be used to assess fluid response. Septic patients can then be triaged into those who will benefit from more fluid by increasing their stroke volume and those who require earlier co-treatment with vasopressors to resolve the underlying venous capacitance/tone issues.
Logically, the purpose of fluid resuscitation is to cause a clinically significant increase in stroke volume - so stroke volume is the parameter that must be continuously monitored to know if the fluid is having the desired effect. It is fundamentally important that it is now possible to continuously monitor, with appropriate precision and accuracy, changes in stroke volume following fluid administration. This can be achieved invasively via an arterial line and now also non invasively using finger photoplethysmography. Importantly, both options are now available in a single monitor platform - the LiDCOrapidv2 monitor. The critical decision to continue fluids, or to consider early use of a vasoconstrictor, can be made after an initial fluid challenge is made either via a reversible passive leg raise (PLR), or balanced salt infusion of 500 mls. If the patient remains hypotensive (MAP < 65 mmHg) and non fluid responsive i.e. does not increase SV by > 10%, then noradrenaline can be administered. It is not well known that noradrenaline can be given via a peripheral venous line, this avoids the delays inherent with the insertion of a central venous catheter. The availability of continuous stroke volume and blood pressure monitoring with the LiDCOrapidv2, before invasive line placement, fits well with the septic patient pathway, where fluids will be administered as a first line intervention and you quickly want to know if the patient is responding appropriately, or is one of the 50% who will likely require vasoconstriction. The LiDCO monitor is designed to allow both non invasive and invasive options to be available to users – so transitions can easily be made from non invasive to arterial line and later back to a period of non invasive monitoring if required.
Advances in hemodynamic monitoring mean that septic patients can now be assessed throughout their clinical pathway for their response to first line fluid administration. Better informed judgments can be made regarding the timing of adjunctive norepinephrine. An appropriate and individualized conservative fluid +/- vasopressor approach can be devised earlier and even instituted prior to central catheter insertion, limiting the hypotensive period while simultaneously avoiding the deleterious effects of overly aggressive fluid administration that occurs today to inappropriate CVP endpoints. Knowing and monitoring when to stop/limit (fluids) and when to start (vasoconstrictors) through the monitoring of stroke volume changes is key.