intensive care conference: management of acid-base disorders with crrt -- 2011 international society...
TRANSCRIPT
Intensive care conference:management of acid-base disorders
with CRRT--2011 International Society of Nephrology
主講人 : R2 顏介立
Introduction
1. acid-base homeostasis challenge in ICU
2. Focus on CRRT (Continuous renal replacement therapies ) in critical patient
with AKI
3. hypercapnic acidosis and lactic acidosis
for example
CRRT (Continuous renal replacement therapies )
- called "go slow dialysis”- The major advantage of continuous therapy i
s the slower rate of solute or fluid removal per unit of time
- CVVHD (Continuous veno-venous hemodialysis )- CVVHF (Continuous veno-venous hemofiltration )- CVVHDF
CRRT (Continuous renal replacement therapies )
Hypercapnic acidosis
1. Cause- Increase CO2 production or decrease CO2 elimination
2. Physiological compensatory: lung: hypercapnia stimulate cental and paripheral
chemoreceptors=>increase ventilation
Hypercapnic acidosis
2. Physiological compensatory:kidney: 3-5 days (in animal model)
** but this mechanism is limited in AKI patient
Hypercapnic acidosis
3. Management- ALI/ARDS treatment: CO2 retention permission
=>low tidal volume(4-6ml/kg) and low pressure(<30)
=>maintain adequate oxygenation
=>PaCO2=66.5mmhg/ PH decrease to 7.2- Acidosis would “well tolerated” if fair tissue perfusion
and oxygen
Hypercapnic acidosis
3. Management- Hypercapnic acidosis controversies:Advantage:
improve arterial and tissue oxygenation,
reduce oxidative stress, anti-inflammatory effect
Disadvantage:
vasodilating effect, increase capillary permeability
(may worsen brain edema) =>ICH
may cause myocardial depression, pulmonary hypertension
Conclusion:
patient with advanced age and multiple comorbidities,
lung-protective stragegies may disadvantage
Hypercapnic acidosis
3. Management
sodium bicarbonate : - Worsen exisiting hypercapnia- Worsen heart failure due to volume expansion, hype
rosmolality, decrease ionized calcium plasma concentration
- Hypercapnic acidosis treat by sodium bicarbonate
is not recommended unless metabolic acidosis co-exist
Hypercapnic acidosis
3. Management -Intermittent hemodialysis:
rapid flux of bicarbonate => excess CO2=>
required hyperventilation
-CRRT:
much slower buffer delivery=>
correct combined respiratory and metabolic acidosis
by CRRT in case reports.
Hypercapnic acidosis
3. Management- Convective hemofiltration:
use hemofiltration with replacement fluid contain
NaOH can remove half of CO2 production
=>50% reduction in minute ventilation and keep
PaCO2 level 35-38 with stable blood PH- CVVHF may an effective adjunctive treatment
for acidosis in respiratory failure patient
=> avoid intubation and ventilator induced ALI or
infection
Lactic acidosis
1. pathophysiology: - Pyruvate: precursor of lactate
PDH
Lactic acidosis
2. Classification of lactic acidosis:- Type A: inadequate oxygen supply- Type B: dysregulation of metabolism rather than
hypoxia
B1: liver disease, malignancy
B2: drug induced: metformin, aspirin, propofol……
B3: congenital
- Sepsis induced lactic acidosis
Lactic acidosis
3. Clinical application of lactate:
- Lactate acidosis is related to high mortality- Lactate is a prognosis indicator surviving sepsis campaign regard lactate
level>4mmol/L need aggressive treatment protocols
- Treat underlying disease
Lactic acidosis
4. Treatment of lactic acidosis: - Treatment underlying disease
- Sodium bicarbonate: may worsen oxygen delivery, increase lactate produ
ction (especially when hypoxia=>induce glycolysis), decrease portal vein flow
- The surviving sepsis campaign recommended hold
sodium bicarbonate unless ph<7.15 -two randonmized trials
Lactic acidosis
4. Treatment of lactic acidosis- CRRT Type A lactic acidosis:
small observational studies showed efficient
management of severe type A lactic acidosis=>
CRRT vs sodium bicarbonate infusion
Lactic acidosis
4. Treatment of lactic acidosis- CRRTDrug-induced lactic acidosis: metformin
- shock and overdose
@ increase intestinal lactic acid production, impaired gluconeogensis, glycogenolysis, mitocondrial respiration and phophorylation=>mortality rate>30%
@metformin is sliminated by kidney and highly water
soluble
Lactic acidosis
4. Treatment of lactic acidosis- CRRT-Drug induced lactic acidosis Hemodialysis and CRRT=> Correct acidosis and remove metformin from plasma-NRTI-induced lactic acidosis-Summary: CRRT are useful in uncontrollable acidemia with multiple organ failure, and removal causative toxin
Anticoagulation
- heparin:
Heparin is the most commonly utilized anticoagulant @ risk of systemic bleeding and heparin-induced
thrombocytopenia
Anticoagulation
Citrate: - chelating ionized calcium=> anticoagulation @decrease risk of systemic bleeding @systemic calcium infusion- Citrate=>bicarbonate (carbonic anhydrase) @liver, skeletal muscle, kidney (high mitochondria)- Citrate toxicity=> in liver failure patient @ metabolic acidosis=> because bicarbonate loss and citrate can’t metabolize bicarbonate
@ ca2+ decrease but total plasma calcium increase
Conclusion
- Hypercapnic acidosis and lactic acidosis - Bicarbonate infusion vs addition bicarbonate
during CRRT
- Need further prospective controlled study
Thanks for your attention ~~ Any question?