Metabolic acidosis is caused by an excess production of acids or loss of bicarbonate in the body. It results in a primary decrease in blood pH (acidemia) with low bicarbonate levels. The kidneys compensate by retaining bicarbonate to raise the pH. Causes include diabetic ketoacidosis, lactic acidosis, renal tubular acidosis, diarrhea, and uremia. An increased anion gap metabolic acidosis occurs when unmeasured anions like ketones and lactate are produced in excess. The clinical features include respiratory changes like Kussmaul breathing, as well as neurological symptoms. Arterial blood gas analysis is used to diagnose and classify the type and

1. ACIS BASE AND ELECTROLYTES-1
PRESENTED BY -DR SMRUTI
UNDER THE GUIDANCE OF
DR VAIBHAVI MAAM,
DR RUTU MAAM

2. BASIC TERMINOLOGY
-ph signifies free h+ ion conc,ph is inversely
related to h+ ion conc
ACID: any substance that can donate h + ion or
when added to solution raises h + ion hence
lowering ph
BASE: any substance that can accept h+ ion or
when added to solution lowers h + ion hence
raises ph

3. • Acidaemia means ph <7.35 ,acid blood
• Alkalaemia means ph >7.45,alkaline blood
• Two main mechanisms – Respiratory and Metabolic:
Normal PaCO2 40 (35-45)mmhg
Respiratory acidosis:PaCO2 >45 mmhg and low ph
Respiratory alkalosis :PaCO2 <35mmhg and high ph
(hyperventilation)
Normal Hco3 24 (22-26mEq/lt)
Metabolic acidosis Hco3 <22mEq/lt and low ph
Metabolic alkalosis Hco3 >26mEq/lt and high ph

4. The respiratory buffer response :
• Carbon dioxide (CO2) is a normal by-product of cellular metabolism.
• Partial pressure of CO2 in arterial blood (paCO2) is determined by alveolar
ventilation.
• The excess CO2 combines with water to form carbonic acid.
• The blood pH changes according to amount of carbonic acid in the body i.e. the
depth and rate of ventilation.
• As blood pH decreases (acidosis), CO2 is exhaled (alkalosis as compensation).
• As blood pH increases (alkalosis), CO2 is retained (acidosis as compensation).
• The respiratory response is fast and activated within minutes.

5. The renal buffer response:
• The kidneys secrete Hydrogen ion (H+) and reabsorbs
bicarbonate.
• In response to metabolic acid formation.
• Bicarbonate is a metabolic component and considered a base.
• As blood pH decreases (acidosis), the body retains
bicarbonate (a base).
• As blood pH rises (alkalosis), the body excretes bicarbonate
(a base) in urine.
• This compensation is slow and takes hours to days to get
activated

6. COMPENSATION IN ACID BASE DISORDERS:
The pH is dependent on the paCO2 /HCO3-
(bicarbonate) ratio: HENDERSON-HASSELBALCH
EQUATION
A change in CO2 compensated by a change in HCO3-
and vice versa:
• The initial change is called the primary disorder.
• The secondary response is called the compensatory
disorder

7. SAME DIRECTION RULE:
EXAMPLE:metabolic acidosis leads to
low ph---i.e fall in hco3 will
stimulate respiratory centre causing
hyperventilation which leads to CO2
WASHOUT and decreased pAco2
*low hco3 leads to low paco2

8. PREDICTION OF COMPENSATION:
• DISORDER:
• METABOLIC ACIDOSIS
METABOLIC ALKALOSIS
RESPIRATORY ACIDOSIS
Acute :(6-24hrs)rise in hco3
Fall in ph
Chronic:(>24 hrs)rise in hco3
Fall in ph
RESPIRATORY ALKALOSIS
Acute :fall in hco3
rise in ph
Chronic :fall in hco3
Rise in ph
• EXPECTED COMPENSATION:
• Paco2 =1.5 *hco3 +8
Paco2=hco3+15
• Rise in PaCo2=0.75*rise in hco3
=0.1* rise in PaCO2
=0.01 *rise in PaCo2
=0.4 *rise in Paco2
=0.003*rise in Paco2
0.2 *fall in pAco2
0.01*fall in Paco2
0.04 *fall in pAco2
0.002*fall in paco2

9. Conditions causing acid-base
imbalance
• Respiratory acidosis
• Any condition causing the
accumulation of CO2 in
the body.
• Central nervous system
(CNS) depression due to
head injury
• Sedation, coma
• Chest wall injury, flail
chest
• Respiratory
obstruction/foreign body
• Respiratory alkalosis
• Due to decrease in CO2
Hyperventilation occurs
and CO2 is washed out
causing alkalosis.
• Psychological: Anxiety, fear
• Pain
• Fever, sepsis, pregnancy,
severe anemia

10. Conditions causing acid-base
imbalance
• Metabolic acidosis -due to
excess of acids or deficit of
base
• Increased acids
• Lactic acidosis (shock,
haemorrhage, sepsis)
• Diabetic ketoacidosis
• Renal failure
• Deficit of base
• Severe diarrhoea
• Intestinal fistulas.
• Metabolic alkalosis - caused
by excess base or deficit of
acids.
• Acid Deficit:
• Prolonged vomiting,
nasogastric suction,
diuretics
• Excess base:
• Excess consumption of
diuretics and antacids
• massive blood transfusion
(citrate metabolized to
bicarbonate)

11. ARTERIAL BLOOD GAS ANALYSIS:
• Important routine investigation to monitor the
acid-base balance of patients ,effectiveness of gas
exchange
• A vital role in monitoring of Postoperative
patients,
Patients receiving oxygen therapy,
Those on intensive support,
Patients with significant blood loss, sepsis, and
comorbid conditions like diabetes, kidney
disorders, Cardiovascular system (CVS) conditions

12. WHY TO ORDER BLOOD GAS ANALYSIS
AND ITS LIMITATIONS:
• Aids in establishing diagnosis
• Guides treatment plan
• Improvement in the management of acid/base; allows for
optimal function of medications
• Acid/base status may alter levels of electrolytes critical to the
status of a patient.
• Limitations of blood gas analysis :
Can not yield a specific diagnosis. (e.g. A patient with asthma
may have similar values to another patient with pneumonia).
Does not reflect the degree to which an abnormality actually
affects a patient.
Cannot be used as a screening test for early pulmonary disease

13. OBTAINING AN ARTERIAL SAMPLE:
• Order of preference: Radial > brachial
>femoral artery.
• Radial artery is preferred:
ease of palpation and access
good collateral supply
Collateral supply to the hand: Confirmed By
the modified Allens test

14. MODIFIED ALLENS TEST:
• Ask the patient to make a tight fist.
• Apply pressure to the wrist: Using the middle and index
fingers of both hands Compress the radial and ulnar
arteries at the same time
• While maintaining pressure: ask the patient to open the
hand slowly. Lower the hand and release pressure on the
ulnar artery only.
• Positive test: The hand flushes pink or returns to normal
color within 15 seconds
• Negative test: The hand does not flush pink or return to
normal color within 15 seconds,indicating a disruption of
blood flow from the ulnar artery to the hand -radial
artery should not be used.

15. SAMPLING:
• Arm of the patient
• palm up on a flat surface
• wrist dorsiflexed at 45°
• Puncture site :
• cleaned with alcohol or iodine
• allow the alcohol to dry before puncture, as the alcohol can cause
arteriospasm
• local anesthetic (such as 2% lignocaine)
• Radial artery should be palpated for a pulse
• A preheparinised syringe with a 23/25 gauge needle should be
inserted at an angle just distal to the palpated pulse.
• After the puncture, sterile gauze should be placed firmly over the site
and direct pressure applied for several minutes to obtain
hemostasis

16. ERRORS:
• Allow a steady state after initiation or change in oxygen therapy before
obtaining a sample
• a steady state is reached between 3 and 10 minutes.
• in patients with chronic airway obstruction, it takes about 20-30 minutes.
• Always note the percentage of inspired air (FiO2 ) and condition of the
patient
• Do not use excess heparin as • it causes sample dilution • Excess of
heparin may affect the pH.
• Avoid air bubbles in syringe.
• Avoid delay in sample processing.
• In case of delay, the sample should be placed in ice and such iced samples
can be processed for up to two hours without affecting the blood gas
values.
Accidental venous sampling. The venous sample report should not be
discarded and can provide sufficient information.

17. STEPS OF INTERPRETATION:
Step 1: look at paco2 and hco3 to determine if
they are in normal range
If abnormal go to step 2,if normal either no
disorder or in critical sick patients rule out
mixed acid base disorders(step 5)

18. • Step 2: is there acidosis or alkalosis
Look at ph(normal value between 7.35-7.45)
• Step 3:identify primary acid base disorder
• Ph<7.35acidaemia may be metaboliclow hco3/
respiratoryhigh Paco2
• Ph>7.45alkalaemia may be metabolichigh
hco3/respiratoryhigh pAco2
• Step 4: Calculate expected compensationwhether actual
value matches expected compensation,matching confirms
primary disorder

19. • Step 5:Determine presence of mixed acid base
disorder:
• A. Direction of changes:
• As per rule of direction hco3 and pao2 changes from
normal in same direction,if opposite s/o mixed
disorder
• B. Compare expected comensation with actual
value,if actual is more or less compared to
expectedmixed disorder

20. • Anion gap : In certain mixed disorders ph,paco2 and hco3
are normal and only clue may be increased anion gap
D. Compare fall in Hco3 with increase in plasma anion gap :
1.In high anion metabolic acidosis rise in plasma anion
gap(ag-12) matches with fall in serum hco3 (24-
hco3),(rise in ag=fall in hco3)
2.If increase in anion gap exceeds fall in hco3 (rise in
ag>fall in hco3),s/o coexisting metabolic alkalosis
3.If increase in anion gap is lesser than fall of hco3 (rise in
anion gap<fall in hco3,eg in diarrhoea non anion gap
metabolic acidosis

21. EXAMPLES OF ACID BASE DISORDERS:
• Case 1:A 15 yr old boy is brought from examination hall in apprehensive
state with complain of tightness in chest:
Ph 7.54,hco3 21 meq/l,pAco2 =21mmhg
ANALYSIS: ph is high so pt has alkalosis,low paCo2 is suggestive of
respiratory alkalosis,hco3 is also s/o compensationfollows same direction
rule
FALL IN HCO3 =0.2*FALL IN PACO2=0.2*(40-21)=3.8
EXPECTED HCO3=24-3.8=20.2 which almost matches actual hco3 s/o
simple acid base disorder

22. • Case 2:A patient with poorly controlled iddm missed his
insulin for 3 days,ph 7.1,hco3 8 meq/lt,paco2 20mmhg,Na 140
meq/lt,Cl 106mEq/lt and urinary ketones+++
Analysis: ph is lowacidosis,low hco3 s/o metabolic
acidosis,pAco2 is also low s/o compensation
Expected compensation i.e fall in pAco2 will be
pAco2=hco3*1.5+8=20
Anion gap=Na-(Cl+Hco3)=140-(106+8)=26high anion gap
metabolic acidosis due to dka

23. • Case 3:A patient with severe diarrhoea complains of difficulty
in breathing
Ph 7.1 hco3 14meq/lt,paCO2 44mmhg and K 2.0meq/lt
Ph is low so patient has acidosis, low hco3 is s/o metabolic
acidosis,pAco2 is expected to reduce due to compensation, but
here it is high =s/o respiratory acidosis
Very low k+causes weakness of respiratory musclesrespiratory
acidosis
Thus pt has mixed disorder

24. • Case 4: ABG of pt with shock on ventilatory support since last 4
hours is ph 7.48,HCO3 14 meq/lt,PaCO2 22mmhg
pH is high so patient has alkalosis, low PaCo2 is s/o respiratory
alkalosis,if setting of ventilator is high rr and high tidal
volumerespiratory alkalosis
HCO3 is also low s/o compensation
Expected HCO3=0.2 * fall in paco2 =0,2* (40-22)=3.6mEq/lt
Thus expected hco3=24-3.6=20.4,but actual hco3 is low suggests
presence of additional metabolic acidosis (shock can cause lactic
acidosis)

25. • Case 5:Known case of COPD develops sever vomiting
• Ph 7.4 hco3 36meq/lt paco2 60mmhg
• Ph is normal either no disorder/has mixed acid base disorder
But hco3 and paco2 s/o presence of mixed disorders
High hco3 metabolic alkalosis(can occur due to vomiting)
High Paco2respiratory acidosis(can occur due to copd)
thus normal ph is end result of opposite changes and hence pt has
mixed disorder

26. AS BOTH PCO2 AND
HCO3 ARE IN
OPPOSITE
DIRECTION IT IS
MIXED DISORDER-
RESPIRATORY
ACIDOSIS+
METABOLIC
ACIDOSIS
TO CALCULATE
EXPECTED
COMPENSATION OF
HCO3=RISE IN
PACO2*0.1=1.6
HCO3=1.6+24=24.6
BUT IT IS 20.4

27. PRIMARY METABOLIC
ACIDOSIS
AS HCO3 IS LESS THEN
NORMAL AND PACO2 HAS
ALSO DECREASEDSAME
DIRECTION MEANS SIMPLE
ACID BASE DISORDER
PACO2=HCO3+15=28.3 WHICH
IS CLOSE TO ACTUAL VALUE
HENCE THERE IS
COMPENSATION

28. PH IS SUGGESTIVE OF
ALKALOSIS:
HCO3 IS HIGH WHICH IS S/O
METABOLIC ALKALOSIS BUT
PCO2 HAS NOT INCREASED
EXPECTED RISE IN
PACO2=0.75*RISE IN
HCO3=17.6+40=57.6
HENCE HERE THERE IS
ADDITIONAL RESPIRATORY
ALKALOSIS WITH
METABOLIC ALKALOSIS

29. ABG SHOWS ACIDAEMIA
HCO3 AND PACO2 ARE BOTH
IN OPPOSITE DIRECTION
EXPECTED PACO2
=HCO3+15=23.8 BUT IT IS >40
HENCE MIXED
METABOLIC+RESPIRATORY
ACIDOSIS,SERUM LACTATE
LEVEL IS HIGH S/O LACTIC
ACIDOSIS PT HERE WAS IN
SEPTICEMIA

30. METABOLIC ACIDOSIS:
• Pathophysiology:
1.Loss of base –Hco3 via gi tract/kidneys
(diarrhoea,proximal rta)
2.Overproduction of metabolic acids in body-
ketoacidosis/lactic acidosis
3.Ingestion or infusion of acids/potential
acids(salicyclates/NH4Cl)
4.Failure of H+ excretion by kidney(renal failure)

31. ETIOLOGY:
• Calculation of anion gap is helpful in narrowing
etiological diagnosis, Anion gap=Na-
(Cl+Hco3)=12+/-2 normal value
Normal Anion Gap: Increased anion gap:
1.Loss of Hco3-diarrhoea,ca
inhibitors,uterosigmoidostomy,
proximal rta
1.Metabolic disorders:lactic
acidosis,dka,alcoholic
ketoacidosis
2.Failure to excrete:distal rta 2.Addition of exogenous
acids:salicyclates/methanol
poisoning
3.Addition of h+ Nh4Cl infusion 3.Failure to
excrete:acute/chronic renal
failure

32. CLINICAL FEATURES:
• 1.Pulmonary changes:kussmaul’s breathing ,hyperventilation
more due to tidal volume>rr
• 2.Cardiovascular changes:high susceptabilty for cardiac
arrythmias,decreased response to inotropes,secondary
hypotension may occurdue to depressed myocardial
contractility and arterial vasodilation
• 3.Neurological changes:headache,confusion,lethargy and
drowsiness to coma
• 4.Rickets in children,osteomalacia in adults

33. DIAGNOSIS:
• In abg: low hco3,low ph,compensatory fall in pAco2 confirms diagnosis
• ANION GAP:NA-Cl +HCO3,blood sugar,serum K+,renal function
tests,serum lactate,level of salicyclates,urinary examination for
ph,ketones,oxalate crystals are useful investigations.
• URINARY ANION GAPABILITY OF KIDNEY TO EXCRETE
NH4CLUINARY NA+K-CL=80-NH4
• NORMAL UAG=0/+VE VALUE
• If cause of metabolic acidosis is gi hco3 loss uag is –ve increased nh4cl
excretion in response to acidosis.
• If cause is renal failure the UAG is +ve

34. TREATMENT:
• 1.SPECIFIC MANAGEMENT OF UNDERLYING
DISORDER
• 2.ALKALI THERAPY:BICARBONATE
ADMINISTRATION SHOULD BE RESERVED
ONLYFOR SELECTIVE PATIENTS WITH
ACIDAEMIA.
• 3.CORRECT VOLUME AND ELECTROLYTE
DEFICITS

35. INDICATIONS OF ALKALI THERAPY:
1.When blood ph drops below 7.15 to 7.20life threatening acidaemia
2.When HCO3 falls below 10mEq/lt needs prompt rx as
a. small additional fall in hco3 can cause large fatal drop in ph
b.Respiratory compensation requires heavy muscular workfatigue of
respiratory musclesfailure of ventilationPaco2 rises and patient
develops superimposed respiratory acidosis
3.Treatment of hyperkalemia with metabolic acidosis
4.Patients with acute normal anion gap i.e. diarrhoea need early bicarbonate
therapy and in lactic acidosis bicarbonate should be started late and
discontinued early
AMOUNT OF HCO3 REQUIRED=DESIRED HCO3-ACTUAL
HCO3*0.5*BODY WEIGHT IN KG

36. DISADVANTAGE OF ALKALI THERAPY:
• 1.Hypernatremia and volume overload especially in chf or
renal failure
• 2.CNS acidosis and hypercapnia
• 3.Hypokalemia and hypocalcaemia
• 4.Overshoot or rebound alkalosis in organic acidosis (i.e
ketoacidosis,lactic acidosis)due to conversion of accumulated
organic anions (lactate,acetoacetate)into bicarbonate
• 5.Stimulation of phosphofructokinase activity enhances lactate
production and worsens acidosis

37. METABOLIC ALKALOSIS:ETIOLOGY AND
DIFFERENTIAL DIAGNOSIS: BASED ON URINARY
CHLORIDE CONCENTRATION
SALINE RESPONSIVE
(URINE CHLORIDE<15MEQ/LT)
SALINE RESISTANT
(URINE CHLORIDE >20MEQ/LT)
ECF VOLUME DEPLETION:
1.VOMITING/GASTRIC SUCTION
2.DIURETICS
3.HYPERCAPNIA CORRECTION
NORMAL/INCREASED ECF VOLUME
HYPERTENSIVE:
1.HYPERALDOSTERONISM
2.CUSHING SYNDROME
NO ECF VOLUME DEPLETION:
1.NAHCO3 INFUSION
2.MULTIPLE TRANSFUSION
NORMOTENSIVE:
1.BARTTERS SYNDROME
2.SEVERE K+ DEPLETION

38. TREATMENT OF METABOLIC
ALKALOSIS:
• A.Treatment of underlying cause
• B.In saline responsive alkalosis:
1.Adequate volume correction
2.Iv isotonic saline with kcl or isolite g are preferred infusions
3.Proton pump inhibitors
4.Diuretics induced-dose reduction,kcl
supplementation,spironolactone and carbonic anhydrase
inhibitors
5.Dialysis therapy
C. Saline resistant-specific rx of underlying cause

39. RESPIRATORY ACIDOSIS
• Occurs when effective alveolar venilation fails to keep pace
with rate of co2 production
• RENAL COMPENSATION:Kidney responds by increasinh
H+ secretion so that urine becomes acidic and plasma hco3
rises gradually
• Acute: every 10mmhg rise in paco2 causes 1 meq/lt rise in
hco3 and 0.1 fall in ph
• Chronic: every 10mmhg rise in paco2 causes 4 meq/lt rise in
hco3 and 0.03 fall in ph

40. CAUSES OF RESPIRATORY ACIDOSIS:
1.CNS depression :Drugs(sedative,anesthesia),infection,stroke.
2.Neuromuscular impairment :Myopathy,myasthenia
gravis,polymyositis,hypokalemia.
3.Ventilation restriction :Rib fracture,pneumothorax,hemothorax.
4.Airway:Obstruction,asthma.
5.Alveolar diseases :COPD,ARDS,pulmonary
oedema,pneumonitis.
6.Miscellaneous:Obesity,hypoventilation.

41. TREATMENT OF RESPIRATORY
ACIDOSIS:
A. General measures: patent airway,adequate
oxygenation,treatment of pulmonary infection,bronchodilator
therapy,removal of secretions can offer benefits in such
patients.
B. Oxygen therapy: in acute respiratory acidosis major threat
is hypoxia so oxygen is needed,
in chronic hypercapnia O2 therapy should be instituted
cautiously and in lowest possible concentration as it is only
primary stimulus to respiration and o2 therapy can lead to
further reduction in alveolar ventilation and aggravate
hypercapnia drastically.

42. • C. Mechanical Ventilatory Support:
In acuteearly use is appropriate
In chronicmore conservative approach is advisable because of
difficulty in weaning
Indications:1.Unstable,symptomatic/progressively
hypercapnic,paco2>80mmhg patients
2. If patients exhibits signs of muscle fatigue, start MV before
respiratory failure occurs
3.Refractory severe hypoxia or apnoea
4.Depression of respiratory centre (eg drug overdose)

43. RESPIRATORY ALKALOSIS:
• Occurs when respiratory disturbance causes excessive
pulmonary co2 excretion(hyperventilation) that exceeds
metabolic production of co2 by tissues
• Acuteevery 10mmhg fall in paco2 causes 2meq/lt fall in
hco3 and 0.1 rise in ph
• Chronicevery 10mmhg fall in paco2 causes 5meq/lt fall in
hco3 and 0.03 rise in ph
• Etiology:1.Benign:anxiety/pain induced,
2.Iatrogenic-mechanical ventilation,
3.Serious illness-sepsis,hepatic failure,brain tumor

44. TREATMENT OF RESPIRATORY
ALKALOSIS:
1.Treatment of underlying cause.
2.As hypoxemia is common cause-supplement O2
3.In absence of hypoxemia, hyperventilation needs reassurance
and rebreathing in paper bag
4.Pretreatment with acetazolamide minimizes symptoms due to
hyperventilation at high altitude

45. THANK
YOU