Do you want a Fluid Bolus Why give

Do you want a Fluid Bolus?

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

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 -1000 mls.

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?

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)?

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

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. )

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

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

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.

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

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.

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)? ?

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

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.

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 >3 L given. Hypernatraemia. Cheap • Hartmanns – The best compromise.

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