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Acid-base and related complications in hemodialysis in CKD
Dr. Vishal Golay
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Basic terminology
• pH – signifies free hydrogen ion concentration. pH is inversely related to H+ ion concentration.
• Acid – a substance that can donate H+ ion, i.e. lowers pH.
• Base – a substance that can accept H+ ion, i.e. raises pH.
• Anion – an ion with negative charge.
• Cation – an ion with positive charge.
• Acidemia – blood pH< 7.35 with increased H+ concentration.
• Alkalemia – blood pH>7.45 with decreased H+ concentration.
• Acidosis – Abnormal process or disease which reduces pH due to increase in acid or decrease in alkali.
• Alkalosis – Abnormal process or disease which increases pH due to decrease in acid or increase in alkali.
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Endogenous sources of acid
Daily production ~ 1 mEq of H+/kg/day
Sulfuric acid ( from sulphur containing AA) Organic acids (from intermediary
metabolism) Phosphoric acid ( hydrolysis of PO4
containing proteins) Hydrochloric acid (from metabolism of
cationic AA-Lysine, Arginine, Histidine)
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pH in humans is tightly regulated between 7.35-7.45.
Renal regulatory responses
Respiratory regulatory responses
Chemical
Buffers
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Buffers
Buffers are chemical systems which either release or accept H+ and minimize change in pH induced by an acid or base load.
First line of defense blunting the changes in [H+] A buffer pair consists of: A base (H+ acceptor) & an acid (H+ donor)
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Buffers continued……
Extracellular buffers:
• HCO3¯/H2CO3
• HPO4²¯/H2PO4¯• Protein buffers
Intracellular buffers:•Hemoglobin•Proteins•Organophosphate compounds•Bone apatite
Examples:
HPO42- + (H+)↔H2 PO4
-
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-
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Respiratory regulation
2nd line of defense
10-12 mol/day CO2 is accumulated and is transported to the lungs as Hb-generated HCO3 and Hb-bound carbamino compounds where it is freely excreted.
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-
Accumulation/loss of CO2 changes pH within minutes
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Respiratory regulation contd…..
Balance affected by neurorespiratory control of ventilation.
During Acidosis, chemoreceptors sense ↓pH and trigger ventilation decreasing pCO2.
Response to alkalosis is biphasic. Initial hyperventilation to remove excess pCO2 followed by suppression to increase pCO2 to return pH to normal
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Renal Regulation
Kidneys are the ultimate defense against the addition of non-volatile acid/alkali.
HA + NaHCO3↔H2 O + CO2 + NaA Addition of Acid causes loss of HCO3¯
Kidneys play a role in the maintenance of this HCO3¯ by: Conservation of filtered HCO3 ¯
Regeneration of HCO3 ¯
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Net Acid Excretion(NAE)
Kidneys balance nonvolatile acid generation during metabolism by excreting acid.
Each mEq of NAE corresponds to 1 mEq of HCO3¯ returned to ECF.
NAE has three components: 1. NH4⁺ .
2. Titrable acids (acid excreted that has titrated urinary buffers)
3. Bicarbonate. NAE= NH4⁺ + TA-HCO3¯
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What goes wrong in CKD?
Generally a metabolic acidosis develops due to:
1. Failure of NAE to match with the endogenous acid production.
2. Failure to recapture filtered HCO3-
There is an absence of renal compensation in ESRD making interpretation simpler.
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Metabolic acidosis in ESRDIn addition to CKD
per se: DKA Alcoholic
ketoacidosis Lactic acidosis Toxin ingestion Catabolic state High protein intake Large salt and
water intake
between dialysis
GI alkali loss Hemofiltration with
NaCl replacement Ammonium chloride
ingestion
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Metabolic alkalosis in ESRD Vomiting Nasogastric drainage Exogenous alkali supplementation
(NaHCO3, KHCO3, CaCO3, Lactate, Acetate, Citrate, Glutamate, Propionate)
Alumimium hydroxide + Na Polysterine sulfonate coadministration
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Respiratory disorders in ESRD Respiratory acidosis-hypoventilation Respiratory alkalosis-hyperventilation
It is important to remember that respiratory acid-base disorders are
dangerous in ESRD as there is no renal compensation.
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Blood gas analysis in ESRD
Laboratory evaluation in patients with ESRD should include not only
HCO3 measurement but also pH and CO2.
Example: Even with a HCO3¯ in the normal
range, the patient maybe having a dangerously high pH and low PCO2 due to respiratory alkalosis.
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Clinical implications of acid-base disturbances in ESRD
Metabolic acidosis: Initially hyperchloremic but becomes high
AG as ESRD sets in. Associated with:
Insulin resistance GH/IGF-1 axis suppression Mineral bone disease Protein degradation and muscle wasting Increase risk of mortality ITT studies show delay in progression of CKD
with Rx
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Metabolic alkalosis: Nausea, lethargy and headache Soft tissue calcification Cardiac arrhythmia Sudden death Reflection of a low protein intake in dialysis
patients. Poses risk for dangerous alkalosis with minimal
hyperventilation.
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Respiratory alkalosis: Dizziness, confusion, seizures (if acute). Cardiovascular compromise (specially if ventilated). Reflects underlying diseases which have a poor
outcome.
Respiratory acidosis: Anxiety, dyspnea, confusion, hallucinations, coma. Sleep disturbances, loss of memory, daytime
sleepiness, tremor, myoclonus, asterixis.
Poor compensation may cause dramatic changes in Ph
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Principle of dialytic correction Correction is by adding HCO3
- instead of the removal of H+.
This regulation is un-physiologic and determined by the physical principles of diffusion and convection.
Gain of HCO3- in dialysis is determined by the
transmembrane concentration gradient
Dialysis prescription (fixed) Endogenous acid production (variable)
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Bicarbonate fluctuations during HD
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Alkali source in HD
1950’s-1960’s: HCO3¯ was the alkali source. Initially 26mM/L→ later 35mM/L pH was adjusted to 7.4 to prevent CaCO3
ppt. by aeration with CO2/O2 gas mixture. Central solution preparation was not
possible.
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1960’s -1980’s: Acetate became the chief alkali used. Aim was to create a positive balance of acetate
(3-4mM/L) which is later metabolized to HCO3¯. A value of 37mEq/L was set by trial and error. It was inefficient (avg. predialysis HCO3¯ was
<18mM/L) and needed large acetate levels which accumulated as dialysis became more efficient
Toxicity: hypotension, CO2 loss (decreased ventilatory drive and hypoxemia).
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Bicarbonate HD (since 1990’s) Proportioning systems enabled use of HCO3¯. Acetic acid in the “acid concentrate” reacted with
HCO3¯ to generate acetate which prevented a rapid rise of pH.
Thus the final dialysis solution composition became: HCO3¯ =30-40mM/L Acetate=2-4mM/L pH=7.1-7.3
This raised the avg. predialysis HCO3¯ by 3-4mM/L
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Other modes of alkali delivery Sorbent cartridge hemodialysis. Hemofiltration. Acetate-free biofiltration.
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Acid-base balance during HD
Transmemb. HCO3¯ gradient over time
Dialysiance of HCO3¯
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Factors determining HCO3¯ during HD
Postdialysis HCO3¯ : Determined by the dialysis prescription.
Predialysis HCO3¯ : Endogenous acid production between Rx (diet,
catabolic state)-This may cause variations as large as 6mEq/L
Rate of fluid retention-”dilution acidosis” . 1 L ot fluid retained can affect preHD HCO3¯ by >1mEq/L.
The avg. preHD HCO3¯ values in stable patients on 3/wk HD is 19-25mEq/L.
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Management of low HCO3¯ with HD
Target for a preHD HCO3¯ of >22mEq/L (following the KDIGO-CKD 2012 guidelines).
Some reasonable targets are: Intradialytic gain of 6-10mM/L of HCO3¯
Target post HD HCO3¯ of 30-34mM/L (risky in some) using a higher bath HCO3 of ~36-40mM/L
A more reasonable target would be a post-HD HCO3¯ of approx. 27mM/L once acidosis is controlled.
Only definite way is to measure pre and post HD HCO3¯ levels.
Always look for causes if target not achieved (eg. nutrition, fluid intake, RRF with loss of HCO3¯, loss in stool etc.)
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Acid-base balance in special situations
Daily hemodialysis (nocturnal HD or short daily HD):
These modalities quickly normalizes HCO3¯.
Pre and post HD variations can be <1mM/L.
Thus, a lower bath HCO3¯ of 28-32mM/ should be used.
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Acid-base balance in special situations
Critical care settings: Always evaluate the acid-base status before HD. They are high risk for alkalosis. If the pre HD HCO3¯ is >28mM/L or there is
respiratory alkalosis, use a bath with lower HCO3 (eg. 20-28mM)
Respiratory alkalosis=normalize pH and not HCO3¯.
Severe preHD metabolic acidosis (HCO3¯ <10mM/L): excess correction can paradoxically cause CSF acidification and lactic acidosis).
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Kussmaul’s respiration (deep and rapid)
Cheyne-Stokes respiration•Brain injury•CO poisoning•Metabolic encephalopathy
Biot’s breathing•Medullary injury•Chronic opioid use
Apneustic respiration•Damage to upper pons
Ataxic respiration•Damage to the medulla oblongata
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THANK YOU