“Acid Base Imbalance”author

Dr.Praveen PawalJr. medicine

m.l.b .medical college jhansi.u.p

ACID BASE IMBALANCE

Acid base balance is important for the maintenance of normal cellular functions. Precise regulation of pH in a narrow range of 7.35 to 7.45 is essential.

pH is vital for –

1. normal cellular enzymatic reactions.

2. normal ionic concentration

Change in pH can cause cardiac arrhythmias. Extreme range of pH (i.e. <7.2 or >7.55) are potentially life threatening.

The concept of pH was first introduced by Danish chemist Soren

Peder Lauritz Sorensen at the Carlsberg Laboratory in 1909. It is unknown what the exact definition of p is. Some references suggest the p stands for “Power”, others refer to the German word “Potenz” (meaning power in German), still others refer to “potential”. Jens Norby published a paper in 2000 arguing that p is a constant and stands for “negative logarithm”, which has also been used in other works. H stands for Hydrogen. Sorensen suggested the notation "PH" for convenience, standing for "power of hydrogen",using the logarithm of the concentration of hydrogen ions in solution, p[H]. Although this definition has been superseded ,p[H] can be measured if an electrode is calibrated with solution of known hydrogen ion concentration.

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.

Acidaemia – blood pH< 7.35 with increased H+ concentration.

Alkalaemia – 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.

Basic physiology of acid base regulation

The body maintains pH within a normal range inspite of dietary

intake of acid and alkali and endogenous acid production.

Normally, when food is metabolized, two types of acids are added

to ECF.

1. Volatile acid –

H2CO3 – 22,000 mEq/day

2. Non volatile acid

Sulphuric acid

Phosphoric acid – 1 mEq/kg/day

Regulation of acid base

The regulation of pH in a narrow range is the function of buffers, lung and kidney. The Henderson – Hasselbalch equation describes the correlation between metabolic and respiratory regulations, which maintains pH.

Buffers – Buffers are chemical systems which either release or accept H+. So, buffers minimize change in pH induced by an acid or base load and provide immediate defense, but have least buffering power.e.g. – bicarbonate, bone bicarbonate, proteins, phosphate, Hb.

Respiratory regulation – by excreting volatile acids, lungs regulate PaCO2. When amount of CO2 increases in body , it will stimulate

PaCO2 sensitive chemoreceptors at central medulla, with resultant

rise in rate and depth of breathing.

pH = 6.1+logHCO3

-

PaCO2×0.0301

This hyperventilation will maintain PaCO2 at normal range.

Respiratory regulation acts rapidly (in seconds to minutes) and has double buffering power as compared to chemical buffers.

Tissue CO2

Venous Blood

Cl-

CO2 + H2O H2CO3 H+ + HCO3-

HbH H+ + Hb HCO3-

HCO3-

O2

Alveolar capillary barrier

Cl-

O2 + HbH HbO2 + H+

H+ + HCO3- H2o + CO2

Lung

Renal regulation :- Role of kidney is to maintain plasma HCO3-

and thus pH. It’s the most powerful buffering system, starts

within hrs and takes 5-6 days for peak effect.

HCO3- regulation is done by -:

1. Reabsorption of filtered bicarbonate ion.

2. Production of new HCO 3- ion by formation of titratable acid

3. Excretion of NH 4+ in urine.

CO2 + H2O

HCO3- + H+

HCO3-

Bicarbonate resorption

Glutamine

HCO3- NH4

+HCO3-

Ammonia excretion

NH4 + Cl-

NH4Cl-

CO2 + H2O

HCO3- + H+

HCO3-

Titratable acid formation

H+

H2PO4-

Blood Kidney

H++ HCO3-

H2CO3

CO2

Proximal tubules

Collecting ducts

Distal tubules

Arterial Blood Gas Analysis

Arterial blood gas (AG) measurements are invaluable in assessing the adequacy of pulmonary gas exchange and the presence and severity of acid base disturbances.

Proper interpretation of PaO2, PaCO2 and pH values require

knowledge of the clinical state of the patient, the therapy given and other data like Hb concentration, cardiac output.

Sampling technique – of choice for routine analysis is direct radial artery puncture.

Perform modified Allen’s test.

Clean the site.

Use 21 guaze needle with syringe.

Flush syringe and needle with heparin.

Enter skin at 45° angle.

Obtain 2-4ml blood without aspiration. Avoid suction of syringe .

If sample contains any air bubble, tap it to the surface and push it out of the syringe. Air bubbles can lead to increase in PaO2 and

decrease in PaCO2.

Apply firm pressure at punctured site.

Note :

1. The determination of acid base status does not necessarily require sampling of arterial blood. The best reason to sample arterial blood is to determine the state of oxygenations. Venous blood is perfectly acceptable for acid base determination if oxygen is not in question.

2. The sum of PO2 and PCO2 should be less than 140mmHg if the

patient is breathing room air.

3. ABG and serum electrolytes should be performed simultaneously for correct interpretation of acid base disorders.

Normal ABG Values -:

Na+ 135-145meq/lt

K+ 3.5-5.5meq/lt

TCO2 21-30meq/lt

iCa 1.1-1.4mmol/lt

HCT 47+7% (male)

42+5% (female)

Hb 13.5-17.5 (male)

12-16 (female)

At 37°C

pH 7.35-7.45

PCO2 40±5mmHg

PO2 95±5mmHg

HCO3- 24±2 mEq/lt

BE etc ±2 mEq/lt

SPO2 97۬±2%

Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management

allows for optimal function of medications Acid/base status may alter electrolyte levels

critical to patient status/care

TCO2 :- Total CO2 content of plasma is the sum of the plasma

concentration of HCO3-, dissolved CO2 and H2CO3. The

contribution of CO2 and H2CO3 is small. Hence, total CO2 in

plasma and HCO3 concentration are often used interchangeably.

Base excess :- is derived from whole blood buffer base, defined as sum of concentration of buffer anions (HCO3

- and Hb) in

whole blood. BE is defined as difference between the observed and normal values for whole blood buffer base. It is used to overcome the limitation of plasma HCO3

- as an index of acid base

status.

In human physiology, base excess refers to the amount of acid required to return the blood pH of an individual to the reference interval pH (7.35 - 7.45) with the amount of carbon dioxide held at a standard value(ie pCO2-40mmHg). The value is usually reported in units of (mEq/L). The normal reference range is somewhere between -2 to +2.

Another definition for base excess is the amount of acid or base that must be added to a litre of blood (ECF) to return the pH to 7.4 at a pCO2 of 40 mmHg.

Base excess can be calculated by the Van Slyke equation. Base excess is a positive figure, indicating metabolic alkalosis, while base deficit is a negative figure and indicative of acidosis (normal range- ( -2 to +2).

Base excess = 0.93 (HCO3 - 24.4 + 14.8(pH - 7.4))

Alternatively expressed:

Base excess = 0.93 HCO3 + 13.77 pH - 124.58

Van Slyke equation--

SO2 :- Percent of O2 attached to Hb

PaO2 :- Pressure with which O2 is dissolved in blood.

90%

60 mmHg

10%

PaO2

SO2

Oxygen Dissociation Curve – Sigmoid shaped curve

Hypoxia ;refers to any state in which tissue receive inadequate supply of o2 to support normal aerobic metabolism i.e., Hypoxaemia, Ischaemia

Hypoxaemia ; refers to any state in which o2 content of arterial blood is reduced that is impaired oxegenation, low haemoglobin .

Impaired oxegenation :-Refers to hypoxaemia resulting from reduced transfer of o2 from lungs to bloodstream.

Assessing severity of type 1 respiratory impairment

Mild Moderate Severe

Pao2(kPa) 8-10.6 5.3-7.9 <5.3

Pao2 60-79 40-59 <40

Sao2 90-94 75-89 <75

Other markers of severe impairment

High Fio2 requirement to maintain adequate Pao2 Lactic acidosis (indicating tissue hypoxia) Organ dysfunction (drowsiness, confusion,renal failure,

haemodynamic collapse, coma)

Common causes of type 2 respiratory impairment

Chronic obstructive pulmonary disease

Opiate /benzodiazepine toxicity

Exhaustion Inhaled forein body

Flail chest injury Neuromuscular disorders

Kyphoscoliosis Obstructive sleep apnoea

The ABG in different pattern of type 2 impairment Paco2 HCo3 PhAcute ↑ → ↓ Chronic ↑ ↑ →Acute on chronic ↑ ↑ ↓

A-a gradientThe A-a gradient is the difference between the po2 in alveoli (PAo2) and the Po2in aterial blood (Pao2). Pao2 is measured on ABG but PAo2 has to be calculated using the alveolar gas equation A-a gradient = PAo2- Pao2

It is normally less than 2.6 kpa (20 mmHg), although it increases with age and Fio2 .This means that :1.the normal range for Pao2 falls with age2.the A-a gradient is most accurate when performed on room air. Simplefied alveolar gas equationPAo2 (kpa) = (Fio2 x 93.8)-(Paco2 x 1.2)

OrPAo2 (mmHg) = (Fio2 x 713)-(Paco2 x 1.2)Assumes the patient is at sea level and has a body temperature of 37°

BASICS OF ACID BASE DISORDER AND COMPENSATION

Four primary acid base disorder are defined :-

1. If initial disturbance affects HCO3-

Metabolic acidosis HCO3-

Metabolic alkalosis HCO3-

2. If PaCO2 affected first

Respiratory acidosis ( PaCO2)

Respiratory alkalosis ( PaCO2)

pH Primary change Secondary change

Metabolic acidosis

Low HCO3 PaCO2

Metabolic alkalosis

High HCO3 PaCO2

Respiratory acidosis

Low PaCO2 HCO3

Respiratory alkalosis

High PaCO2 HCO3

Compensation – The body’s response to neutralize the effect of the initial insult on pH homeostasis is called compensation.

Rule of same direction :-

In simple acid base disorders, HCO3 and PaCO2 compensatory

change are in the same direction as the primary changes.

HCO3 leads to PaCO2

HCO3 leads to PaCO2

This will bring pH to near normal although not to normal.

If these changes are in opposite direction or the actual changes are not equal to expected, it suggests mixed disorder.

2-Metabolic alkalosis ( HCO3 )-

Rise in PaCO2 =0.75x Rise in HCO3

3-Respiratory acidosis PaCO2)--

Acute - Rise in HCO3 =0.1x Rise in PaCO2

Chronic - Rise in HCO3 = 0.4x Rise in PaCO2

4-Respiratory alkalosis PaCO2)---

Acute - Fall in HCO3 =0.2x Fall in PaCO2

Chronic - Fall in HCO3 = 0.4x Fall in PaCO2

1-Metabolic acidosis( HCO3 )–

Expected PaCO2 = (1.5 × HCO3-) +8

OR PaCO2 = HCO3- + 15

By calculating compensation, we can differentiate between simple and mixed disorder.If expected change = actual change, disorder is simpleIf actual change is more or less than predicted, disorder is mixed.Mixed disorder :- defined as independent coexistence of more than one primary acid base disorder. Most common is mixed metabolic acidosis and respiratory acidosis.

Common mixed acid base disordersDisorders Common causes

1. Metabolic acidosis and Respiratory acidosis (low pH, HCO3, PaCO2)

a. Cardiac arrest (hypoventilation + lactic acidosis)b. Shock with respiratory failure

2. Metabolic acidosis and Respiratory alkalosis

(N.pH, HCO3, PaCO2)

a.Salicylate intoxication c.Gram negative sepsisb.Liver failure d.malarial pyrexiae. Diabetic ketoacidosis with respiratory disease

3. Metabolic alkalosis and Respiratory acidosis

(N.pH, HCO3, PaCO2)

a. COPD with diureticsb. Metabolic alkalosis with severe hypokalemia and

respiratory weakness leads to hypoventilation

4. Metabolic alkalosis and Respiratory alkalosis

( pH, HCO3, PaCO2)

a. Liver failure with vomiting b. Patient on ventilator with continuous nasogastric

aspiration

5. Metabolic acidosis and metabolic alkalosis

(near N.pH and HCO3)

a. Diabetic ketoacidosis with vomitingb. Vomiting with severe volume depletion causing

lactic acidosis

6. Respiratory acidosis Respiratory alkalosis

Do not co-exist

Evaluation and investigation of acid base disorder

1. History and clinical examination.

2. Primary investigation – S.Na+, K+, Cl-, HCO3-, anion gap, CBC,

urinary electrolytes, blood sugar, renal function test etc.

3. ABG is mandatory for diagnosis of acid base disorder.

Anion gap :- The charge difference between unmeasured anion and cation is termed the anion gap.

Unmeasured anions – anionic protein, phosphate, sulphate and organic acids.

Unmeasured cations – Ca++, Mg++, K+

AG = (Na+ K+) – (HCO3- + Cl)

Normally, AG = 12±2 mEq/lt

Albumin normally compromises most of the anion gap.

1gm/dl in S.alb – 2mEq/lt in AG

Uses

Useful for etiological diagnosis of metabolic acidosis

Diagnosis of mixed disorder

Step by step analysis

1.Is there an acid base disorder – look for PaCO2 and HCO3-

If normal – No acid base disorder, or

Mixed acid base disorder (specially in critically ill patients)

If abnormal – Acid base disorder present

2.Look at pH

pH < 7.35 – acidosis

pH >7.45 – alkalosis

3.Whether its primary acid base disorder

If pH < 7.35 Metabolic acidosis HCO3

Respiratory acidosis PaCO2

If pH > 7.45 Metabolic alkalosis HCO3

Respiratory alkalosis PaCO2

4.Calculate the expected compensation- If the actual value

matches with the expected compensation, it confirms diagnosis of

primary disorder.

5.How to determine the presence of mixed acid base disorder---

Check direction of change- In simple acid base disorder, HCO3

and PaCO2 change from normal in same direction. If changes are in

opposite direction, it suggests mixed disorder.

Compare expected compensation with actual value - if actual

value is either more or less as compared to the calculated

expected compensation, it suggest mixed disorder.

Check anion gap

Compare fall in HCO3 with increase in plasma anion gap

Rise in AG = Fall in HCO3-, it shows high AG metabolic

acidosis

If in AG exceeds fall in HCO3, it suggests coexisting metabolic

alkalosis.

If in AG is less than fall in HCO3, it suggests loss of HCO3-

(diarrhea) causing non AG metabolic acidosis.

6. Clinical correlation and establish the diagnosis

•Case studies

20 yrs,male Anurag working in printing press brought in emergency department at 4 PM on 1st July 2009 by his family members with history of consumption of dye used in printing press, before 4 hours after quarrel with his father.

At the time of admission pt was unconscious, his vitals were as follows -

BP-110/70 mm of Hg

PR-80/min

Temp-Normal

RR-10/min Spo2-67%

cyanosis-Present

Pupils-NSNR

Typical smell of aniline dye

On systemic examination –

Chest –B/L clear

All other systemic examination were WNL.

Management –

ABG was done along with routine blood investigation

ABGPh 6.95PCo2 23.9mm Hg

P02 45mmHg

Bicarb 5.3 mmol/lBE -27S02 55%

K 2.2 mmol/lNa 140 mmol/lCl 118 mmol/liCa+ 0.87Hb 11.9 gm /dl

Since PH=6.95 so acidosis.

HCO3=5.3, so primary disorder is metabolic acidosis

whether it is compensated or not?

Expected fall in PCO2

=(1.5 x HCO3)+8

= (1.5 x 5.3) +8

= 15.95

But actual value of Pco2= 23.9 which is more then expected.

So it mixed disorder i.e. metabolic acidosis with Respiratory acidosis with hypokalemia, and as Po2 is 45 mmHg and so2 is 55% so there is hypoxemia because of methemoglobinemia and repiratory depression due to hypokalemia leading to respiratory acidosis because of hypoventilation.

Anion Gap = (Na++ K+ )-(Hco3 + Cl-)

= (140+2.2) –(5.3+118)

= 142.2-122.3

= 19.9( Normal Value 10-12 mmol)

i.e. it is High anion gap metabolic acidosis.

To correct acid base disorder i/v soda bicarb along with supplemental K+ infusion done.

Amount of sodabicarb to be given was-

=(Desired HCo3- Actual Hco3) X 0.5X BW

=(15-5.3)x0.5x60

= 9.7x30=291 meq(14 amp of HCo3 )

1 ampule of sodabicarb contains 22 meq.

So total 14 ampules will be given, out which half amount i.e.7ampules given with in first 1-2 hours & next 7 during remaining 24 hours.

To correct hypoxia,100% o2 inhalation along with oral methylene blue in doses of 200 mg in divided doses to reverse methemoglobinemia was given.

Amount of K+ to be given is- Since our pts K is 2.2mEq so defficiency is approx 450-

600mEq. Maximum dose which can be given in 24 hrs should not be more then 240meq & the infusion rate should not be >20meq/hr.

1amp of KCl contains 20 meq of K. KCl should be mixed with isotonic saline.Dont mix this with

D-5% as diluent.

Kamlesh 40 yrs male admitted in emergency deptt. On 06 Sep. 09 at 10 AM as acute onset ascending LMN type of quadriplegla with difficulty in respiration without bladder and bowel involvement and without any sensory impairment .Pt had history of high grade fever with sore throat 8 days back for 2 days.

Pt diagnosed as a case of GB syndrome with respiratory muscles paralysis.

On examination at the time of presentation -

PR -90/min

BP -140/90 mm Hg

Temp –Normal

RR-8/min, accessory muscles of respiration are working .

SPO2 -74%

Pt immediately intubated and put on ventilator on SIMV+PSVmode.Pt ABG was done within half hour which was-

pH-7.328 i.e. acidosis

pCO2 =48.6 i.e. respiratory acidosis (primary disorder due to CO2 retention because of respiratory muscle paralysis ie TYPE II respiratory failure-acute).

Now wheather it is compensated or not ?

For acute respiratory acidosis rise in HCO3- should be

= 0.1 X Rise in pCO2

= 0.1X (48.6-40)

= 0.1 X 8.6

= 0.86

So expected value of HCO3- should be –

HCO3- = 24+0.86

= 24.86

= 25

And actual value of HCO3- is 25 which is equal to expected valve.

So it is compensated respiratory acidosis because of type II respiratory failure.

Case 3 Date :02/04/09

Patient Name : Smt Kranti 26yrs FemaleCase of type 1 DM diagnosed 4 months back had discontinued medication from 1 month.Came here withC/C - 1-Fever x 2 day 2-Pain in knee joint x 2 days 3-Breathlessness x 2 day PR- 110/min BP -100/ 70mm Hg RR 30/min Dehydration++ Investigations--- RBS >500 mg Ketone: large Sugar : ++++S.creat. :1.10 mg/dl TLC : 24,100/cmm

02/04/09

Ph 6.99PCo2 10.5 mmHgP02 111 mmHgBE -29 mmol/LHCo3 2.6Tco2 45SO2 95Na+ 138 mmol/LK+ 4.2 mmol/LiCa+ 1.06 mmol/LHb 12.6 g/dl

ABG

Since PH=6.99 so acidosis.

HCO3=2.6, so primary disorder is metabolic acidosis

whether it is compensated or not?

Expected fall in PCO2

=(1.5 x HCO3)+8

= (1.5 x 2.6) +8

= 11.9

But actual value of Pco2= 10.5 which is less then expected.

So it mixed disorder i.e. metabolic acidosis with Respiratory alkalosis.

Management

DKA with severe metabolic Acidosis with respiratory alkalosis.1-IV Antibiotics2-HCO3 Deficity Calculated ---=O.5 X (BW) (actul HCO3- DesiredHCO3)

=0.5 x 40x 12.3= 247 Meq/L (11 amp of sodabicarb) out of which half is given with in 2 hr & rest to be given over 24 hrs IV.3-Inj insulin R accordingly to RBS.4-IVF : NS ISO -M

03/04/09

Ph 7.462PCo2 30.1 mmHgP02 107mmHg

BE

-2 mmol/L

HCo3 21.6Tco2 15So2 96Na+ 138.6 mmol/LK+ <2.0 mmol/LiCa+ 1.0 mmol/LHb 12.1 g/dl

Next day ABG was repeated pt had mild(metabolic Acidosis with Respiratory alkalosis) with hypokalemia may because of i/v NAHCO3 & insulin both of which causes intracellular shift of potassium .Hypokalemia was corrected. Pt improved.

Case 4

Pt Pyarelal 20 yrs old admitted here on 31st August 2009 with complain of snake bite in night with features of respiratory muscles paralysis. Pt was immediately intubated and put on mechanical ventilation. After resumption of spontaneous breathing pts ABG was done on next day at 3:52 PM to decide wheather to wean off from ventilator or not. Pt’s ABG was -----

Ans

Pts pH is normal i.e.7.42PCO2 is normal i.e. 39.9HCO3 is within normal range i.e.26PO2 is 75 mm HgIt means pt’s ABG is normal except decrease PO2 .So pt can be weaned of from ventilator after assessing the clinical condition and supplemental O2 should be given by maskOn assessing it was seen that pt was properly breathing with full effort and depth, RR is 16/min, pt was weaned off from ventilator in the evening and put on T-Tube breathing with supplemental oxygen, pt survived.

Case 5

Pt Ramchandra 29 yrs/male admitted here with complain of 10-12 loose motions per day with passage of blood along with fever for 3 days, for 1 day he also c/o decreased amount of urine. For all these he was admitted here and managed on the lines of acute gastroenteritis with ARF. On next day of admission he develops breathlessness with deterioration in his condition for which ABG was done which shows-

Analysis of ABGPt is pH is 7.46 ie alkalosis, pCO2 is 19.So it is Respiratory alkalosis.For acute Resp. alkalosis---Fall in HCO3- =0.2 X Fall in PaCO2

= 0.2 x (40-19) =0.2 X 21=4.2so expected HCO3 = 24-4.2

= 19.8but actual HCO3=13.5 which is less then the expected.So it is mixed disorder with metabolic acidosis due to hypoperfusion , renal failure, lactic acidosis due to sepsis and loss of HCO3 during diarrhea with Resp. alkalosis due to hyperventilation because of sepsis.

Case 6

58 years old male Gyasi admitted to Hospital with C/C -- 1-Fever chills and rigor x 8 days2-Altered sensorium x 4 hrs3-Breathlessnes x 4 hrs4-Decreased urine outputO/E : Pt unconscious PR- 90/min BP -70 systolic RR- 28 /min INVESTIGATION: Sr creatnine: 13.50 mg /dl

Hb:4.80 g/dl TLC :27,200/cmm

P-90 L-03QBC-Negative

ABG Na + 139K+ 5.3Tco2 0.65Hb 5.0PH 6.798Pco2 10Po2 120HCO3 1.5BE -30SO2 93%

Since pH=6.798 so acidosis.

HCO3=1.5, so primary disorder is metabolic acidosis

whether it is compensated or not?

Expected fall in PCO2

=(1.5 x HCO3)+8

= (1.5 x 1.5) +8

= 10.25

actual value of PCO2= 10.25 which is equal to expected.

So it is severe metabolic acidosis with hyperkalemia .Pt has hyperkalemia ,pH <7.1 & S.bicarbonate is <10 so NAHCO3 is given i/v.

,

Amount of sodabicarb to be given ---- =(Desired HCO3- Actual HCO3) X 0.5X BW =(10-1.5) x 0.5 x 50 =212 (about 12 amp of SBC to be given ,out of which half of dose should be given in 1st hr & rest over next 24 hrs ).

Management --- BT II⨀ AntibioticAntimalarialAntihyperkalemic

Peritoneal Dialysis was plannedPatient expired before intervention was done.

Case 7

Name : Vandana 23 yrs ,Female k/c/ o pul koch’s four times defaulter(CAT II) Came her with C/C --- Breathlessness at restO/E : Pt nutrition was poor and malnourished

PR- 100/minBP- 100/70 mmHg

Chest : B/L crepts X-ray : Rt side pnemothorax localised with extensive b/l infiltration. TLC -8900 P-83 L-14 E-2Sr.crt : 1.0mg/dl Sr .billirubin : 0.64mg/dlSPO2 : 66 %

Na+ 134K+ 3.5Tco2 27ica 0.86HCt 37Hb 12.6Ph 7.516Pco2 31.8Po2 36Hco3 25.2BE 3 m mol/LSo2 65 %

ABG

Since Ph is 7.516, so alkalosis.

pCO2 is 31.8,so it is respiratory alkalosis.

Now expected fall in HCO3 should be----

= 0.4 x Fall in Pco2

= 0.4x8.2=3.3

So expected HCO3 should be=24-3.3=21.7

But actual value of HCO3 is—25.2

So it mixed disorder ie respiratory alkalosis(due to Type 1 respiratory failure) with metabolic alkalosis( may be due to chronic use of steroids).

Management ----High flow oxygen TherapyIV AntibioticsATT as advised by DOTS.

Case 8

Biharilal 60 yrs male. Admitted as case of Pul koch’s with Syst HTN was taking ATT & Amlong H.C/C : 1- low grade fever 2- ↓ Appetite 3- LethargyO/E: PR-92/min regular BP :150/90 mm Hg Chest :: B/L crepts ++ Dehydration ++

pH: 7.449So alkalosisHCO3 is 26.8Primary disorder is metabolic Alkalosis.So expected rise in Paco2= 0.75X Rise in HCO3

= 0.75X2.8 = 2.1So expected paco2= 40+2.1 = 42.1so it is mixed disorder ie metabolic alkalosis with ECF volume depletion due to thiazide diuretics and Respiratory alkalosis due to hyperventilation with hyponatrimia with hypokalemia.

As our pts S.Na is 110 meq/l ie severe hyponatremia. First rule out the causes of pseudohyponatremia. Then

we calculate serum osmolality,which is hypoosmolar in our pt.

Now we assess renal status which is normal in our pt ,after this we assess volume status of our pt which is depleted.

Now urine Na should be assesed.In our case it should be more then 20 to lebel it as diuretic induced hyponatremia.

First we stop the diuretic. Now we supplement fluid & salt which can be done

with i/v isotonic saline 0.9% at rate appropriate for the estimated volume depletion.

The targeted rate of Na correction should not be greater then 0.5 to 1 meq/l/hr & it should not exceed 8 meq/l on any day of treatment.

Na requirement=(Desired Na-Actual Na)x0.5xBW(kg)

0.9%NaCl per liter = 154 meq of Na 3%NaCl per liter = 514 meq of Na

Date : 06/08/09

Name : Gori Bai Age: 50 yrs Female

MRDNO: 14592

C/C: Loose motion 15- 18 times x4 days

B.P-80/60 mmHg

Investigations:

Hb-12.3

TLC 24100 cmm P- 78 L -18

Plt- 1.65

S.Billirubin- 0.77 mg/dl

S.Creatinine -2.29 mg/dl

Na+ 124.8 mmol/l

K+ 2.78 mmol/l

07/08/09

PH 7.27PCo2 17.9

P02 101 BECF -20 HCo3 6.6Tco2 7So2 97Na+ 124 K+ 2.78 iCa+ 0.25 Cl- 108

ABG

Since pH is 7.27 so it is acidosis.

HCO3 is 6.6, so it is metabolic acidosis.

Now whether compensated or not?

Expected PCO2=(1.5 X HCO3-)+8

=(1.5 X 6.6) +8

= 9.9 +8

= 17.9

=18

Actual PCO2=17.9

So it is compensated metabolic acidosis

Anion Gap = (Na++ K+ )-(HCO3 + Cl-)

= (124+2.78) –(6.6+108)

= 126.78-114.6

= 12( Normal Value 10-12 mmol)

i.e. it is Normal anion gap metabolic acidosis.

To correct acid base disorder i/v Soda bicarb is given.

Amount of sodabicarb to be given was-

=(Desired HCo3- Actual Hco3) X 0.5X BW

=(15-6.6)x0.5x60

= 8.4x30=252 meq(ie 12 ampules of Sodabicarb over 24 hrs).

Case10 History A 25 year old man, with no significant past medical history.Presents to the emergency department with a 2-day history of fever, productive cough and worsening breathlessness. Examination  He is hot and flushed with a temperature of 39.3ºC. He does not appear distressed but is using accessory muscles of respiration.There is diminished chest expansion on the left with dullness to percussion, bronchial breathing and coarse crakles in the left lower zone posteriorly. 

Pulse 104 beats/minRespiratory rate 28 breaths/minBlood pressure 118/70 mmHgSaO2 89%

H+ 31.8 nmol/LPh 7.50PCo2 3.74 kPa

28.1 mmHgP02 7.68 kPa

57.8 mmhgBicarb 23.9 mmol/LBE -0.5 mmol/LSP02 88.7%Lactate 1.2K 3.7 mmol/LNa 138 mmol/LCl 99 mmol/LiCa+ 1.2 mmol/LHb 15 g/dl

Answer:-

This patient has moderate type 1 respiratory impairment.Hyperventilation is an appropriate response to the hypoxaemia and sensation of dyspnoea and has resulted in a mild alkalaemia (remember that metabolic compensation does not occur in response to acute respiratory acid-base disturbance).The correct management for his condition is supplemental oxygen to correct the hypoxaemia and appropriate antibiotics to treat the infection.In a patient such as this, with moderate hypoxaemia and no ventilatory impairment, monitoring by pulse oximetry is more appropriate than repeated than repeated ABG sampling. Indications for further ABG analysis would include signs of exhaustion or hypercapnia or a further significant decline in Sao2 .

Metabolic acidosisIs characterized by fall in plasma HCO3,

fall in pH (<7.35).

PaCO2 is reduced secondarily by hyperventilation, which

minimizes the fall in pH.

HCO3- with acidemia.

Classified into high anion gap and normal anion gap

acidosis.

Causes of high anion gap metabolic acidosis :-1. Lactic acidosis 2. Ketoacidosis - Diabetic

AlcoholicStarvation

3. Toxins - Propylene glycolEthylene glycolMethanolPyroglutamic acidSlicylates

4. Renal failure – Acute and chronic

Causes of normal anion gap acidosis :-

Diarrhoea CA inhibitors Ureterosigmoidostomy Proximal RTA Distal RTA NH4Cl infusion

Clinical features –

A. Manifestation of underlying disorder

B. Manifestation of metabolic acidosis

1. Pulmonary – Kussmaul’s breathing

2. CVS – Cardiac arrhthmias, response to inotropes, secondary hypotension (particularly when pH <7.2)

3. CNS – Headache, confusion, lethargy, dizziness, coma

4. Others – Anorexia, nausea, vomiting, muscular weakness, rickets in children and osteomalacia in adults.

Treatment

1. Treatment of underlying disorder. It is most important and may be the only required treatment for mild to moderate acidosis.

2. Alkali therapy – reserved for selected patients.

3. Correct volume and electrolyte deficits

Indications for alkali therapy

1. When blood pH <7.15-7.2. Such a severe acidosis is life

threatening.

2. When HCO3 falls below 10mEq/lt. Low HCO3 needs prompt

treatment because -

a. Small additional fall in HCO3 can cause a large fatal drop in

pH.

b. Respiratory compensation requires heavy muscular work. Such

compensatory hyperventilation for prolonged period can cause

fatigue of respiratory muscles, and the patient may develop

superimposed respiratory acidosis.

3. Treatment of hyperkalemia with metabolic acidosis.

Bicarbonate is mainly required in normal AG acidosis but is

controversial in increased AG acidosis.

Goal of treatment

The aim of treatment is to return blood pH to a safer level of

about 7.2.

Bicarbonate must be increased to 10 mEq/lt.

Amount of HCO3 required =

(Desired HCO3 – Actual HCO3) × 0.5 × Body weight (in kg)

Except in cases of extreme acidaemia, NaHCO3 should be

administered as an infusion over a period of several minutes to

few hrs.

i.e. 50-100mEq of NaHCO3 over 30-45min during initial 1-2hr of

therapy.

Precaution during NaHCO3 administration

1. NaHCO3 is highly irritant, so establish proper large IV line.

2. Avoid IV bolus.

3. Correct hypokalemia as intracellular K+ shifting can cause life

threatening hypokalemia.

4. NaHCO3 should be given with caution in circulatory overload.

5. Avoid mixing of calcium with NaHCO3, to avoid precipitation

6. Avoid mixing of NaHCO3 with inotropes.

Disadvantage and risk of NaHCO3 therapy

1. Hypernatremia and volume overload, specially in CHF and

renal failure patients.

2. CNS acidosis and hypercapnia.

3. Hypokalemia and hypocalcemia.

4. Overshoot or rebound alkalosis in organic acidosis- due to

conversion of accumulated organic anions into bicarbonate.

5. Stimulation of phosphofructokinase activity, enhances lactate

production and worsens acidosis.

METABOLIC ACIDOSIS IN SPECIFIC SITUATION

[ I ] Increased Anion Gap Acidosis

1. Lactic acidosis

It is the most serious and most common cause of metabolic

acidosis in hospitalized critically ill patients. The most common

cause of lactic acidosis is shock (cardiogenic or septic)

Type A - Characterized by impaired tissue oxygenation.

Type B - No hypoxia but mitochondrial respiration is

impaired.

Causes of lactic acidosis

Type A Type B

Shock (Cardiogenic or septic)

Respiratory failure

Carbon monoxide or

Cyanide poisoning

Severe anaemia

Diabetes mellitus

Hepatic failure

Severe infection

Toxins – Ethanol, Methanol

Drugs - Biguanides

Diagnosis – Diagnose lactic acidosis in increased AG acidosis, by exclusion of ketoacidosis, intoxication, renal failure. Serum lactate levels confirm the diagnosis.

Normal S. lactate level – 1mEq/lt

Lactic acidosis – 4-5mEq/lt

Commonly goes upto - 10-30mEq/lt.

Treatment

Goal of therapy is adequate tissue oxygenation and treatment of

the underlying cause.

Tissue oxygenation can be improved by high inspired oxygen

fraction, ventilator support, repletion of ECF volume, after load

reducing agents and inotropic support by dopamine and

dobutamine. Avoid vasoconstricting drugs like noradrenaline, as

they can worsen tissue hypoxia. Administration of NaHCO3 is

started late (pH <7.1) and discontinued early. Early bicarbonate

hemodialysis is effective.

2. Diabetic ketoacidosis

Due to overproduction of acetoacetic acid and -hydroxybutyric

acid due to relative or absolute insulin deficiency.

Cornerstone of treatment is insulin administration, with

replacement of water, Na+ and K+. Alkali should not be

administered routinely as insulin and supportive therapy regenerate

bicarbonate from resolution of retained ketone bodies.

Bicarbonate is indicated in patients where pH<7.1, the goal of

therapy is to raise pH to relatively safe level of 7.2. HCO3 is also

indicated in severe hyperkalemia.

3. Alcoholic ketoacidosis

It occurs after abrupt discontinuation of alcohol consumption

and is usually due to vomiting, prolonged starvation and volume

depletion. Correction of hypoglycemia with dextrose infusion

will stimulate insulin secretion and inhibit glucagon secretion

and thereby promote regeneration of bicarbonate from

metabolism of retained ketone bodies. Correction of

hypovolemia will prevent ketoacidosis. Supplement thiamine

with glucose to avoid development of Wernicke’s

encephalopathy.

4. Salicylate (Aspirin) poisoning

It is characterized by respiratory alkalosis or mixed metabolic acidosis with respiratory alkalosis. Respiratory alkalosis is caused by direct stimulation of respiratory center by salicylates whereas accumulation of lactic and keto acids cause metabolic acidosis.

Treatment –

Gastric lavage

Correction of hypovolemia by saline

Forced alkaline diuresis

Increase in pH converts salicylates to more impermeable salicylic acid and thus prevents CNS damage.

Thus, unless blood is already alkalinzed by respiratory alkalosis,

give NaHCO3 infusion – 88mEq/4amp of NaHCO3 in 1 lt of

D5% and infuse at rate of 10-15 ml/kg/hr. (25ml of 7.5%

NaHCO3 contains 22mEq NaHCO3).

Bicarbonate haemodialysis can be done in patients with serum

concentration of salicylates > 80mg /dl, refractory acidosis, severe

CNS symptoms, progressive clinical deterioration, pulmonary

edema, renal failure.

5. Renal failure

At gfr <20ml/min, inability to excrete H+ with retention of anions

– PO43-, SO4

2+ results in increased anion gap acidosis. The

unmeasured anions replace HCO3- which is consumed as a buffer.

Hyperchloremic metabolic acidosis (normal anion gap) develops

in milder cases (gfr = 20-50ml/min). Correction of severe acidosis

with alkali therapy in renal failure patients carries risk of volume

overload. In such patients, dialysis can be used.

II ] Normal anion gap acidosis

The hallmark of this disease is low HCO3 of metabolic acidosis

with hyperchloremia so that anion gap remains normal

1. GI loss of bicarbonate

Diarrhea or pancreatic damage can result in HCO3 loss due to

increased secretion and decreased absorption. Hyperchloremia

occurs because the ileum and colon secrete HCO3- in one to one

exchange for Cl- by counter transport. The resultant volume

contraction causes further increased Cl- retention by kidney in

setting of decreased HCO3.

Correction of hypvolemia and hypokalemia are the most important

measures. Correction of acidosis with NaHCO3 is required only in

selected patients with severe acidosis.

2. Renal tubular acidosis

a. Classic distal (type 1) RTA

Characterized by hypokalemic, hyperchloremic metabolic acidosis

and is due to selective deficiency of H+ secretion in distal tubules.

Despite acidosis, Urinary pH is always above 5.5

Nephrocalcinosis, nephrolithiasis and bone disease are important

clinical complications.

Supplementation of bicarbonate (1-3mEq/kg/day) is essential.

Potassium salt is given to correct hypokalemia.

b. Proximal (type 2) RTA

characterized by hypokalemic, hyperchloremic metabolic acidosis

due to a selective defect in proximal tubular ability to reabsorb

filtered HCO3.

During early stage, when HCO3 is >18 mEq/lt, urine is alkaline but

can be acidic when plasma HCO3 <15-18 mEq/lt.

Treatment is to treat the underlying disorder. If alkali therapy is

needed, dose is quite large (10-15mEq/lt). Supplement potassium

adequately to avoid hypokalemia. Thiazide diuretics can also be

helpful.

c. Type IV RTA

It is characterised by a disturbance in distal nephron function that

impairs renal excretion of both H+ and K+, so there is

hyperchloraemic normal anion gap acidosis with hyperkalemia.

Magnitude of hyperkalemia and acidosis are disproportionately

severe for the observed degree of renal insufficiency. In Type IV

RTA, mild to moderate chronic renal failure is almost always

present. Urine pH can be <5.5.

Urinary ammonium excretion is depressed.

Urinary anion gap to assess hyperchloremic metabolic acidosis –

Metabolic acidosis

NH4Cl excretion by the kidney

Urinary anion gap reflects the ability of the kidney to excrete

NH4Cl.

Urinary anion gap = Na+ + K+ - Cl-

80 - NH4+

Normally urinary anion gap is zero or positive with a value of 30-50

(mmol/lt). It is useful to differentiate between gi and renal cause of

hyperchloremic acidosis. If the cause is gi HCO3 loss, urinary anion

gap is negative because of increased NH4Cl excretion by kidney. In

RTA, with impaired NH4Cl excretion, urinary AG is positive.

In contrast to urinary NH4+ excretion, measurement of urine pH

cannot reliably distinguish acidosis of renal or extrarenal origin.

An acidic urine pH does not necessarily indicate increase in net acid

excretion. With a significant reduction in the availability of

ammonium to serve as a buffer, only a small amount of distal H+

secretion will lead to a maximal reduction in urine pH. In this

setting, pH of the urine is acidic but the quantity of H+ excretion is

insufficient of meet daily acid production.

By contrast, alkaline urine doest not necessarily imply a renal

acidification defect. In conditions where availability of NH4+

is not

limiting, distal H+ secretion can be massive and yet the urine

remains relatively alkaline due to buffering effects of NH4+.

METABOLIC ALKALOSIS

pH > 7.45

High HCO3

The most useful factors to determine etiology of metabolic alkalosis

are –

ECF volume

Blood pressure

Urinary chloride concentration

Serum potassium

Urinary chloride differentiates metabolic alkalosis into two major

groups.

Causes of Metabolic Alkalosis

Saline responsive

(Urine chloride <15 mEq/L)

Saline resistant

(Urine chloride > 20mEq/L)

ECF volume depletion

Vomiting / Gastric suction

Diuretics

Hypercapnia correction

No ECF vol. Depletion

NaHCO3 infusion

Multiple transfusion

Normal or increased ECF Vol

Hypertensive

Hyperaldosteronism

Cushing’s syndrome

Normotensive

Bartter’s syndrome

Severe K+ depletion

Clinical features

CNS - Neuromuscular excitability, paresthesia, light headache,

carpopedal spasm.

CVS - Hypotension, cardiac arrhythmias

Others - Weakness, postural dizziness, muscle cramps.

Respiratory - Compensatory hypoventilation may cause

hypoxia in patients with preexisting lung disease.

Treatment

A. Treat the underlying cause

B. Saline responsive alkalosis

1. adequate correction of volume, chloride and K+ deficit.

2. IV isotonic saline with KCl or isolyte G are given.

3. H2 inhibitors or PPI reduce gastric acid secretion and minimize

further H+ loss.

4. If alkalosis is due to diuretics, dose reduction may be needed.

KCl supplementation, spironolactone or carbonic anhydrase

inhibitors can be used.

5. In rare cases, diluted HCl can be given IV (0.1N HCl). It can

cause thrombophlebitis. So should be infused in large veins.

6. Dialysis can be useful in occasional patients with severe

metabolic alkalosis, volume overload and renal failure.

C. Saline resistant – Specific treatment of underling cause like

surgical treatment for pituitary tumour or adrenal adenoma, or

supportive treatment, like spironolactone, correction of

hypokalemia, sodium restriction.

Respiratory acidosis

PaCO2

pH < 7.35

In most cases, hypoxemia occurs earlier and is more prominent

than hypercapnia.

All patients with hypercapnia, who are breathing room air are

hypoxic.

In chronic hypercapnia, hypoxemia is the primary stimulus to

respiration. So, rapid and excessive correction of hypoxemia with

uncontrolled oxygen can cause extreme hypercapnia, which can

lead to neurological symptoms. .

Causes of Respiratory Acidosis

CNS depression

Drugs (anesthesia, sedative)

Infection, Stroke

Neuromuscular impairment

Myopathy, myasthenia gravis, polymyositis, hypokalemia

Ventilation restriction

Rib fracture, pneumothorax, haemothorax

Airway

Obstruction, asthma

Alveolar diseases

COPD, pulmonary oedema,

ARDS, pneumonitis

Miscellaneous

Obesity, hypoventilation

Clinical features

1. Features of underlying primary disorder’

2. CNS – anxiety, headache, dysopnea, psychosis, hallucination

and coma can be caused by acute severe hypercapnia. Chronic

hypercapnia can lead to sleep disturbances, personality changes,

tremors, myoclonic jerkes. Increased CSF pressure may cause

papilloedema.

CNS manifestations are more with respiratory acidosis and less

with metabolic acidosis.

Treatment

A. General measures

1. Treat the underlying cause promptly

2. Adequate oxygenation

3. If a patient of chronic hypercapnia develops sudden increase in

PaCO2, search for the aggrevating factor. Vigorous treatment of

pulmonary infection, bronchodilator therapy and removal of

secretions.

B. Oxygen therapy

Oxygen therapy is like a “Double edged Sword”. In acute

respiratory acidosis, major threat to life is hypoxia and not

hypercapnia. So O2 supplementation is needed. In chronic

hypercapnia, O2 therapy should be instituted cautiously and in

lowest possible concentration since hypoxia may be primary and

only stimulus to respiration.

C. Mechanical ventilation

In acute respiratory acidosis, early use of mechanical ventilator is

more appropriate. While in chronic respiratory acidosis, more

conservative approach is admirable, because of greater difficulty in

weaning such patients from ventilators.

Indications

1. Unstable, symptomatic or progressively hypercapnic (PaCO2 >

80mmHg) patients.

2. Signs of muscle fatigue apparent, start MV before respiratory

failure occurs.

3. Refractory severe hypoxia or apnea.

4. Depression of respiratory center (e.g. drug overdose)

In patients with chronically PaCO2 , rapid correction of

hypercapnia with MV may lead to post hypercapnic alkalosis,

which can be detrimental. So, correction of hypercapnia should be

done gradually.

D. Alkali therapy

Avoid alkali therapy except in patients with associated metabolic

acidosis, severe acidaemia (pH<7.15), severe bronchospasm, as

alkali therapy restores responsiveness of bronchial musculature to

agonists.

Respiratory alkalosis

PaCO2

pH (>7.45)

Etiology

Respiratory alkalosis is the most frequently encountered acid base disorder

Causes of Respiratory Alkalosis

1. Hypoxemia

a. Pulmonary disease : Pneumonia, interstitial fibrosis, emboli and oedema

b. CHF, hypotension or severe anaemia

c. High altitude residence

2. Pulmonary diseases

3. Direct stimulation of the medullary respiratory center

a. Psychogenic or voluntary hyperventilation, pain, pregnancy

b. Hepatic failure, gram negative septicemia

c. Salicylate intoxication

d. Rapid correction of metabolic acidosis

e. Neurological disorders, accidents, pontine tumour

Clinical features

Clinical features vary with severity, rate of onset and underlying

disorder. The mortality increase is in direct proportion to the

severity of hypocapnia. PaCO2 below 20-25 mmHg carries a grave

prognostic sign, specially in critically ill patients.

Common features are :-

Light headache, tingling of the extremities, circumoral anaesthesia,

cardiac arrhythmias, tetany or seizures.

Treatment

1. Treatment of underlying cause

2. Mild alkalosis with few symptoms needs no treatment.

3. As hypoxemia is the common cause of hyperventilation, O2

supplementation is essential along with etiological diagnosis and

treatment.

4. In absence of hypoxemia, hyperventilation needs reassurance and

rebreathing in a paper bag.

5. Pretreatment with acetazolamide minimizes symptoms due to

hyperventilation at high altitude.