Acid-Base Regulation

-Dr.Ahmed Sami-Al-Hasan
MBBS(DMC),FCPS,MRCS(Edinburgh)
Assistant Professor,KGH
samidmc@gmail.com
01819431787
• Acid…….. H+ donor.eg,H2CO3.HCL
• Base……..H+ Receiver
• Conjugate Base…remaining part of an acid
after donation of Proton H+….eg.HCO3- is the
conjugate base of H2CO3
• Conjugate acid of a base…is the acid formed
by a base after accepting the proton
• Buffer…..a mixture of weak acid to its
conjugate base that tends to maintain the PH
or hydrogen ion conc of a soln. within normal
range inspite of addition of base or acid to the
soln.
• Ph……..negative logarithm of H+ conc. In a
soln.
 Some important values
• Normal blood Ph…7.35-7.45(Avg 7.4)
Normal H+ conc.35-45nmol/l
Clinically safe range of Ph 7.3 to 7.5
Death ….ph >7.8 or<6.8
PO2………90-110 mm of Hg(12-14.7 Kpa)
PCo2……35-45 mm of Hg(4.5-6 Kpa)
HCO3……25-30 mmol/L
ICF Ph……slightly lower than ECF
Changes of ECF Ph causes parallel change of Ph at ICF
 Importance of normal PH
• enzyme activity
• Maintain molecular and structural
configuration of biomolecule eg…protein
which has affinity for H
• Oxygen transport and chemical control of
respiration
• Maintain internal environment (ECF
composition)
 Acidosis
• Adding acid or
• Removing base
 Alkalosis
• Adding base
• Removing base
• Primary event-initiating event
• 2ndary event-compensatory process
• Endogenous source of metabolic acid and
base-common…lactic acid, keto acid
• Exogenous source…rare
• Loss of acid-base from body fluid
 Metabolic acid-base production
• Insulin deficiency-acid
• Hypoperfusion…acid
• Hypoxia….acid
• Diet….protein..more acid,fruit more base,
vegetable less acid
 Potential source of volatile acid
• Oxidation of glucose
• Oxidation of fatty acid
• Oxidation of AA
 Potential source of non volatile acid

• Oxidation of basic AA,Sulphur containing

AA,Phosphate containing substance
 Routes of acid base excretion
• Pulmonary-for volatile acid.Functional reserve
more.Unidirectional(only acid not base)
• Renal –both non volatile,volatile.functional
reserve less.Bidirectional(Both acid base)
 Defense of Ph
• First line
Body buffer system-acts within seconds to
min
Pulmonary- within mins to hrs by regulating
CO2 content
2nd line defense-Renal system by regulating
serum biocarbonate and excretion of acid
 Body buffer system
• Blood-bicarbonate,HB,Phosphate,Protein
• ECF/Plasma-HCO3,PO4,Pr
• ICF-Pr,HCO3,PO4
• Urine-Amonia,PO4,HCO3
• RBC-Hb,PO4.HCO3
• At ECF 86% buffer activity by HCO3 buffer
• At ICF 64% by non bicarbonate(mostly Pr)
buffer
• PH= Pk+ log (base/acid)
 K,H+
• Acidosis….excess H+ at ECF……. Enters into ICF
in exchange of K……hyperkalemia
• Alkalosis…..base deficit at ICF…..H+ comes out
of cell…….inexchange of K…K enters into
cell….hypokalemia

and VICE VERSA

 ECF-vs-ICF buffer
• HCO3………………..protein PO4
• Moderate capacity…….large capacity
• Response quick……slow response
• No effect of serum K…..effect on serum K
 Bicarbonate buffer
• High buffering capacity
• Wide range of activity
• Conjugate base(HCO3) conc.is 20 times more
than its acid(H2CO3).Body is net acid secretor
• Works with Hb buffer.
 BASE EXCESS
• Difference between patient’s HCO3 conc.and
standard HCO3 conc.
• Normal value= -2mmol/l to +2 mmol/L
• +ve base excess= high HCO3 conc
• -ve base excess=low plasma HCO3 Conc
Ph ~ HCO3/PCO2
 Simple acid base disorder
• Metabolic Acidosis
• Metabolic Alkalosis
• Respiratory Acidosis
• Respiratory alkalosis
Equation
 Complex Acid-base disorder
Double face

MA+RA
• MAlk+RAlk
• MA+Ralk
• Malk+RA
Triple face type….MA+MAlk+RA
MA+MAlk +RAlk
 Compensated ABD
• Equation
ABD Ph Primary compensa Mechanis Ph after Plasma
tion m compensa HCO3
tion after
compensa
MA D D HCO3 D PCO2 hyperven Near More
tilation normal decreased
MAlk I I HCO3 I PCO2 hypoventil Near More
ation normal increased
RA d I PCO2 I HCO3 Renal Near Increased
HCO3 normal
generatio
n
RAlk i D PCO2 D HCO3 Renal Near decreased
HCO3 normal
excretion
 After compensation
• So, S. HCO3 increased in metabolic alkalosis
and respiratory acidosis compensation
• Decreased in MA and resp.alkalosis
compensation.
 Paradoxical Aciduria
• Coexisting hypokalemia and metabolic
alkalosis
• GOO due to pyloric stenosis
 Complex ABD
• If 2nd (unaffected component) remains normal
or change inversely with respect to change of
primary component
• Overt or under compensation
• Normal Ph but abnormal PCO2 and or HCO3
 Anion gap
• Total cation=Total anion
• Na + K +UC = Cl + HCO3+ UA
• (Na+K)-(Cl+HCO3)=UA-UC

So anion gap= UA-UC

or Na-(Cl+HCO3) or (NA+K)-(Cl+HCO3)
• UA…….plasma protein
(albumin),phosphate,lactate,keto acid ion
• UC……….Ca,Mg,gama globulin
• NORMAL VALUE
• 10-20 meq/l
 Increased anion gap
• Renal failure….fails to excrete acid(sulphuric
and phosphoric acid)…increased
sulphate,phosphate anion……increased anion
gap
• Lactic acidosis……..lactate accumulates which
is an anion
• Ketoacidosis…ketoacid ion…acetoacetate ,beta
hydroxybutyrate ……anion
• Intoxication by
alcohol,salicylate,aldehyde….weak organic
acid..anion
• Decreased UC,Hypo
magnesemia,hypocalcemia
• Anion gap within 20-30……metabolic acidosis…
lactic acidosis,ketoacidosis
• High anion gap metabolic Acidosis-
RF,LA,KA.Here Cl level normal.AG increases
due to fall of HCO3…normochloromic type
MA
• Normal Anion gap MA= Diarrhoea,RTA..Cl
increases..hyperchloremic type
 Decreased AG
• Decreased unmeasured
anion..hypoalbuminaemia
• Increased unmeasured cation…
hypercalcemia,hypermagnesimia
 Metabolic Acidosis
• Due to primary decrease in plasma HCO3
following gain of acid other than H2CO3 or
loss of base
• Etiology
• Normal anion gap-hyperchloraemic MA
loss of base through GIT-
diarrhoea,intestinal fistula,pancreatic and
billiary fistula,ileostomy
• RTA
• Hypoaldosteronism
• Aldosterone antagonist(K sparing diuretics)
• CAI
• Dilutional acidosis-
• Recovery phase of KA
• Rapid correction of chronic hypocapnia
• Increased anion gap
RF,LA,KA ,Intoxicationalcohol,salicylate
 Lab Value of MA
….low ph,low plasma HCO3,Low Pco2
Base excess negative plasma anion gap..normal
or high
 Lactic acidosis
• Hypoxia
• Shock,
• HF
• Resp failure
• Pulmonary edema
• Sepsis
• malignancy
 KA,LA lab value
• High plasma anion gap
• Other values like MA
 Metabolic Alkalosis
• Primary increase in plasma HCO3,gain of base
and loss of acid other than H2CO3
 etiology
• Loss of acid GIT- vomiting,excessive NG
suction
• Loss of acid through renal route- loop and
thiazide diuretic
• Hyperaldosteronism,cushing syndrome
• Chronic hypokalemia
• Rapid correction of chronic hypercapnia
• hypochloraemia
 Lab value
• Ph high high plasma HCO3,High PCO2
• Positive base excess(above 5 mmol/l)
• Plasma anion gap..increased
 Resp Acidosis
• Caused by decrease RR and CO2 retension
• Opioids,sedatives,Anaesthetics
• ARDS
• COPD
Co2 retension occurs
Renal compensation- increased excretion of H
ion and increased reabsorption of newly
synthesized HCO#
 Resp alkalosis
• Caused by increase RR and CO2 loss
• Pneumonia,hyperventilation,high altitude
• Renal compensation by decreased
reabsorption of HCO3 and decresed
excreation of H ion
 Some important values
• Normal blood Ph…7.35-7.45(Avg 7.4)
Normal H+ conc.35-45nmol/l
Clinically safe range of Ph 7.3 to 7.5
Death ….ph >7.8 or<6.8
PO2………90-110 mm of Hg(12-14.7 Kpa)
PCo2……35-45 mm of Hg(4.5-6 Kpa)
HCO3……25-30 mmol/L
ICF Ph……slightly lower than ECF
Changes of ECF Ph causes parallel change of Ph at ICF
• A 65 yr old gentleman admitted to surgical
emergency department with abdominal pain
several episodes of vomiting.Patient had a
H/O open cholecystectomy 25 years
back.Patients biochemical status as below-
Ph= 7.53 PCo2= 6.3 Kpa(48 mm Hg)
Bicarbonate= 39 mmol/l.The biochemical
disorder best explained by-
• A.Respiratory alkalosis noncompensated
• B.Acute Metabolic alkalosis
• C.Compensated Metabolic Alkalosis
• D.Mixed Acid base disorder
• E.Metabolic Acidosis Compensated
• Ans…………. B
• The following is the biochemical picture of a
patient high output enterocutanous fistula
following the postoperative complication of
gastrojejunostomy……ph= 7.24 HCO3=15
mmol/l Base excess= -6 mmol/l Pco2=5.8
kpa(44mm Hg) Po2= 12.9 kPa(97 mmof
Hg)..The biochemical picture is best expalined
by
• A.Acute respiratory acidosis
• B.Respiratory Acidosis compensated
• C. Metabolic Acidosis corrected
• D.Metabolic Acidosis non compensated
• E.Mixed Acid Base disorder
• Ans …..D
• A 62 yr old lady underwent Total hip
replacement.Within 24 hour of surgery she
developed severe chest pain and
breathlessness.Her biochemical pictures are as
follows-
ph…..7.12 HCO3…..29.5mmol/l
PCO2…..12.7 kPa(95) mm Hg) Po2…
4.7(35mm of Hg).The biochemical picture can be
best explained by…
• A.Respiratory failure compensated
• B.Respirator acidosis compensated
• C.Respiratory failure .acute
• D.Respiratory failure chronic
• Respiratory alkalosis…compensated
• Ans… c
• The following is the biochemical picture of an
ICU patient following one month of mechanical
ventilation….ph…..7.5 HCO3=18 mmol/L.PCO2 22
mm of Hg….This is explained by-a.Resp.alkalosis
corrected
• B. Resp alkalosis non corrected
• C.Resp. alkalosis partially corrected
• D. Acute Respiratory failure
• E.Respiratory acidosis non corrected
• C