1. Do you want a Fluid Bolus?

2. Why give fluid – The theory? Increase preload, increase cardiac output, increase oxygen delivery.

3. Increase preload Adding to venous pool of capacitance vessels. Will it sit there or will it add to the effective circulating volume, which is usually only 500-1000mls.

4. Increase Cardiac Output? Does the critically ill patient have a right ventricle that obeys starlings law (decreased contractility in sepsis, diastolic dysfunction, increased afterload) Even if the rt ventricle CO increases does that cause increased systemic CO?

5. Increased Oxygen Delivery? Is delivery the problem? What happens to oxygen extraction in the critically ill? Is the benefit through increased cardiac output or increased microvascular flow by decreasing viscosity (haematocrit)?

6. Why you might be asked Decreased urine output Hypotension NG feed not running

7. Decreased Urine Output Pre-renal failure definitely exists. Hypovolaemia is not the only cause of pre-renal failure. Hypervolaemia increases renal vein pressure reducing GFR. Decreased urine output isn’t always renal failure (stress response etc.)

8. Hypotension BP = CO x SVR Fluid will increase CO only with the caveats described earlier. Remember it’s not pressure we want but perfusion.

9. NG feed not running Does every patient need ‘background’ fluid? Why would they? Do you take in 1ml/kg/hr? Bolus’ as required are physiological.

10. So what…..? Giving fluid when required gives patient benefit. BUT – If not required it leads to. –Tissue oedema Impaired oxygenation Anastamotic breakdown Heavy limbs – decreased mobilisation Decrease gut function Intra-Abdominal hypertension. –Increased venous pressures Decreased flow from LV – RV i.e. decreased perfusion leading to organ failures.

11. So the first question is… Is there evidence of hypovolaemia?

12. The second is…. If yes, is that a problem (evidence of organ hypoperfusion)? Just because there is ‘room for fluid’ that doesn’t mean it should be given.

13. It’s never that easy however… How do I know if there is hypovolaemia? –CVP is useless –The LIDCO is fine if you know what you’re doing and the patient is still, etc. –Other cardiac output monitors are available – Oesophageal Doppler, PICCO etc. –Straight leg raising is useful unless the patient has abdo pain. –Fluid challenge (trial of therapy)????

14. Fluid challenge Fine so long as you define your endpoint, and if it’s ineffective, you don’t repeat it.

15. Fluids in sepsis There is only 1 RCT looking at giving fluid bolus’ in sepsis – it showed an increased mortality! There is increasing evidence that after limited fluid resuscitation, vasopressors should be used early. Vasopressors are a more ‘specific’ therapy for the pathophysiology of sepsis – that patient is not hypovolaemic they are vasodilated and leaky.

16. Choice of fluid Starches – renal failure and increased mortality. Gelatins – Expensive, anaphylaxis risk, not effective colloids. Albumin – Expensive, poor colloid in sepsis, blood product. Blood – if bleeding fluid of choice. FFP – Excellent colloid full of ‘goodness’ but limited resource, expensive, blood product. Saline – Un-physiological – Hyperchloraemic acidosis if >3L given. Hypernatraemia. Cheap Hartmanns – The best compromise.

17. So in summary… It’s difficult to know what’s best. You may never know. I think in 20yrs we will be giving much less. However people will insist on measuring the CVP.