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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

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Intensive care conference:management of acid-base disorders with CRRT--2011 International Society of Nephrology

主講人: R2 顏介立


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
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 (Continuousveno-venous hemodialysis)

  • CVVHF (Continuousveno-venous hemofiltration)


Hypercapnic acidosis
Hypercapnic acidosis

1. Cause

  • Increase CO2 production or decrease

    CO2 elimination

    2. Physiological compensatory:


    hypercapnia stimulate cental and paripheral chemoreceptors=>increase ventilation

Hypercapnic acidosis1
Hypercapnic acidosis

2. Physiological compensatory:

kidney: 3-5 days (in animal model)

** but this mechanism is limited in AKI patient

Hypercapnic acidosis2
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 acidosis3
Hypercapnic acidosis

3. Management

  • Hypercapnic acidosis controversies:


    improve arterial and tissue oxygenation,

    reduce oxidative stress, anti-inflammatory effect


    vasodilating effect, increase capillary permeability

    (may worsen brain edema) =>ICH

    may cause myocardial depression, pulmonary hypertension


    patient with advanced age and multiple comorbidities,

    lung-protective stragegies may disadvantage

Hypercapnic acidosis4
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 co-exist

Hypercapnic acidosis5
Hypercapnic acidosis

3. Management

-Intermittent hemodialysis:

rapid flux of bicarbonate => excess CO2=>

required hyperventilation


much slower buffer delivery=>

correct combined respiratory and metabolic acidosis

by CRRT in case reports.

Hypercapnic acidosis6
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


Lactic acidosis
Lactic acidosis

  • pathophysiology: - Pyruvate: precursor of lactate


Lactic acidosis1
Lactic acidosis

2. Classification of lactic acidosis:

  • Type A: inadequate oxygen supply

  • Type B: dysregulation of metabolism rather than


    B1: liver disease, malignancy

    B2: drug induced: metformin, aspirin, propofol……

    B3: congenital

    - Sepsis induced lactic acidosis

Lactic acidosis2
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 acidosis3
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 acidosis4
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 acidosis5
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


Lactic acidosis6
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


    CRRT are useful in uncontrollable acidemia with

    multiple organ failure, and removal causative toxin


  • heparin:

    Heparin is the most commonly utilized anticoagulant

    @ risk of systemic bleeding and heparin-induced




  • 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


  • Hypercapnic acidosis and lactic acidosis

  • Bicarbonate infusion vs addition bicarbonate

    during CRRT

    - Need further prospective controlled study