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
is 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,
hyperosmolality, decrease ionized calcium plasma
concentration
Hypercapnic acidosis treat by sodium bicarbonate
is not recommended unless metabolic acidosis coexist
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
production (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
- CRRT
Drug-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
-
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Thanks for your attention ~~
Any question?