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?