The Race to the Bottom
The dangers of de-resuscitation
Jan De Waele
Notes/Discussions
Not giving excess fluid in the initial stages is much better than having to remove it, even if you do it well
Why remove fluid? To prevent or treat the toxic effects of fluid therapy
Non-invasive
Diuretics
- Effective but metabolic side effects, exacerbation of AKI, toxicity
- Advantage of continuous diuretic infusions with hourly target
Invasive
Ultrafiltration
- Able to control rate effectively
- Invasive support
Targeted therapy: compartmentalized fluid collections (pleural effusions, ascites, etc)
Invasive monitoring, biomarkers of fluid overload, vasopressor requirements
Method TBD by: extent of fluid overload, organ dysfunction attributable to fluid overload, organ function/hemodynamic instability
FACTT Trial: higher neurocognitive impairment with conservative fluid strategy?
“We don’t have a biomarker for euvolemia. What is euvolemia?”
Dry enough? When to stop CVVH? P.M. Honore
Notes/Discussions
We are trying to determine how much fluid is interstitial/intravascular
Bioimpedance key to monitor body water composition
Current methods to assessing volume status?
- Traditional examinations: physical findings, lab parameters, static measures (CVP, LVV, etc), dynamic measures (SVV/PPV, echocardiography, etc)
- ECW/ICW > 0.9, EVLWI > 12 mL/kg IBW
How to bring fluid back into the intravascular space?
- Reabsorption: Plasma oncotic pressure, high dose Albumin, hypertonic saline
- CRRT: 50-300 mL/hr; might be too slow for extreme hypervolemia, might not tolerate faster due to vascular refilling
- Albumin only contributes 17% of oncotic pressure
HTS infused over 30 min, 500 mL x 1 hr via CRRT then back to maintenance extraction rate
- This can be done at least 2x daily per speaker
- Neuro evaluation, q4h electrolytes, lactate, daily monitoring with PiCCO or echo
- TBD (use of HTS, Albumin, CRRT for volume removal)
(Too) permissive hypotension
Karim Brohi
Notes/Discussions
National traumatic hemorrhage data:
Initial death
Early death (cardiovascular collapse)
Late death (with but not of MSOF...TBI?)
In actively bleeding patient, change from perfusion model to a hemostatic one
Essentially, it is useless to attempt to target a blood pressure in these resuscitations; generally hemodynamic targets ended up getting significantly more volume without ever achieving target
Permissive hypotension: too long or too permissive = BAD
Too long: every minute hypoperfused is too long
Too low: for the brain? NO
- Low, high vs pressor resuscitation: low volume resuscitation better, all animals on pressors DIED
- Pig model: early resuscitation had higher early CI but massively increased ICP and decreased cerebral O2 delivery
- Problem is if it’s too low for the heart; early high cardiac biomarkers correlated with death by cardiovascular collapse in 24hrs; significant micro changes in cardiac myocytes, apoptosis
- Must maintain coronary perfusion pressure; MAP > 50 or palpable central pulse (prefer not with fluids if bleeding, but if no other option, maybe only option to maintain cardiac support)
“Blood is for bleeding, salt water is for cooking pasta.”