water, electrolyte &

Water, Electrolyte &

Prof. Mehdi Hasan Mumtaz

Acid-Base Balance

BALANCE

Water Balance

Electrolyte Balance.

Acid Base Balance.

Nutritional Balance.

TOTAL BODY WATER 42L

IVS

ISS

ICS

5L

14L

23L

FLUID THERAPY

CELL

CAPILLARY

EG

OSMOLALITY

Na+

COP

INTRACELLULAR INTERSTITIAL VASCULAR

FLUIDS

IVS ISS ICS

1L 5% Dextros 5/42 X 1000 = 120ml

14/42 X 1000 = 333ml

23/42 X 1000 = 547ml

1L Nacl 0.9% 5/19 X 1000 = 263ml

14/19 X 1000 = 737ml -

1L Colloid containing solution

5/5 X 1000 = 1000ml - -

ACID-BASE BALANCE

Terminology.

Physiologic Compensation By Body.

Pathophysiologic Disturbances.

Practical Approach To Assessment.

Biochemical Reports & Case Histories.

DEFINITION OF TERMINOLOGY

ACID- STANDARD BICARBONATE.

BASE - BUFFER BASE & BASE DEFICIT.

ALKALI

BUFFERING & BUFFER.

PH.

24 x PCO2 (mmHg)

H+(nmol/L)=- -----------------------------

HCO3 (meq/L)

(40nmol/L)

PRODUCT OF METABOLISM

H++ - Anaerobic Metabolism.

CO2 - Aerobic Metabolism.

PHYSIOLOGIC COMPENSATION

HYDROGEN IONS. Incoporation in water.

H++HCO3 H2C3O CO2 + H2O. Loss from body.

• Kidney – regeneration of HCO3. Intestine.

CO2. Chemoreceptors in hypothalamus.

HCO3. HCO3 generation by erythrocytes. HCO3 re-absorption in renal tubules. HCO3 generation in renal tubules.

BICARBONATE GENERATION BY ERYTHROCYTES

Cl—

HCO-3

CO2

Cl—

-HCO3 +H+

CO2+H2O

HHB

Hb

BICARBONATE REABSORPTION BY KIDNEY

RENAL T. LUMEN

STIMULATED BY

HCO3-

M. ACIDOSIS

HCO3-

Na+

Na+

HCO3-

H2CO3

CO2

+H2O

HCO3-

CELL

CD

H2O

HCO3-

H+

H2CO3

CO2

BICARBONATE GENERATION IN KIDNEY

STIMULATED

PCO2

(BY RESP ACIDOSIS)

&

-HCO3

(M. ACIDOSIS)

B-

Na+

Na+

CELL

H2O

HCO3-

H+

H2O

CO3

B-

HB

HCO3-

PATHOPHYSIOLOGIC DISTURBANCES

Lungs

Disturbances of CO2=

R. Centre

Disturbance of H++HCO3 = Metabolic

Henderson - HosselbalchEQUATION

Proton Acceptor (Base)PH=PK+Log = --------------------------------

Proton Donor (Acid)

-HCO3 (Metabolic)PH=PK+Log = ----------------------------------

H2CO3 or PCO2 x 0.03(Respiratory)

ACID-BASE DISTURBANCE

-HCO3

PCO2 x 0.03MEATBOLIC RESPIRATORY

ACIDOSIS ALKALOSIS ACIDOSIS ALKALOSIS

HCO3----------------PCO2x0.03

HCO3----------------PCO2x0.03

RATIO

HCO3

----------------PCO2x0.03

HCO3

----------------PCO2x0.03

Metabolic acidosis =

Respiratory acidosis =

Metabolic alkalosis =

Respiratory alkalosis =

Defect

HCO3----------PCO2

HCO3----------PCO2

HCO3 ----------PCO2

HCO3 ----------PCO2

Correction

HCO3----------PCO2

HCO3 ----------PCO2

HCO3 ----------PCO2

HCO3 ----------PCO2

CAUSES OF M. ACIDOSIS

1. Glomeralar failure.

2. Keto-acidosis.

3. Lactic acidosis.

4. Intestinal loss.

5. R. Tubular failure.

6. Actazolamide therapy.

7. R. Tubular acidosis.

8. Ureteric transplantation.

9. NH4Cl el therapy.

Hyperkalamic M. Acidosis

Variable

Hyppkalamic Acidosis

Hyperchloraemic Acidosis

SCREENING TESTS METABOLIC ACIDOSIS

BLOOD GLUCOSE.

URINE/ BLOOD KETONES.

SERUM CHLORIDE.

SERUM POTASSIUM

RESPIRATORY ACIDOSIS

Acute Respiratory Failure. Erythrocyte

Chronic Respiratory Failure. Renal Generation.

METABOLIC ALKALOSIS

Administration of HCO3.

K+ depletion – Generation by kidney.

Pyloric Stenosis.

RESPIRATORY ALKALOSIS

Hysterical Over-breathing.ICP.Brain Stem Injury.Hypoxia.Pulmonary Oedema.Lobar Pneumonia.Pulmonary Collapse.Excessive Artificial Ventilation.

BALANCE OF ACID-BASE

NORMAL VALUES

PCO2

30-50mmHg or 4-6.6kPa. >50mmHg respiratory

or 6.6kPa acidosis <30mmHg respiratory

or 4kPa alkalosis

PH 7.30 – 7.50 >7.50 alkalaemia. <7.30 acidosis

BALANCE OF ACID-BASE

RELATIONSHIP

PCO2 and PH.

PCO2 & ventilation.

PO2 and normal range.

PO2 and FIO2.

PCO2, and temperature.

TERMINOLOGY

ACIDAEMIA - PH<7.30

ALKAEMIA - PH>7.50.

ACIDOSIS - Base Deficit Present.

ALKALOSIS - Base Excess Present.

HOW TO ASSESS BLOOD GASES?

STEP-1 Assessment of Acid-Base Balance.

STEP-2 Assessment of Hypoxaemic State.

STEP-3 Assessment of Tissue Oxygenation State.

STEP-1Assessment of Acid-Base Balance

CLASSIFICATION

ACIDOSIS ALKALOSIS

METABOLIC RESPIRATORY METABOLIC RESPIRATORY

ACUTE CHRONIC

ACUTE CHRONIC

ACUTE CHRONIC

ACUTE CHRONIC

STEP-1Assessment of Acid-Base Balance

Acute - Uncompensated.Chronic - Compensated.

-Fully.- Partially.

COMPENSATED PH 7.30-7.50

DIAGNOSIS.

DIAGNOSIS

SEQUENCE.

PH.

PCO2.

HCO3.

PH Normal 7.4

Compensated 7.3-7.5

PCO3 Normal 40mmHg (5.3kPa)

Compensated 30-50mmHg (4-6.6 kPa)

DIAGNOSISIF PH LOW – acidosis. Look at PCO2. If PCO3 high - respiratory acidosis If PH low - acidosis Look at PCO2 If it is normal or low. Look at HCO3. It is low – metabolic acidosis.

IF PH HIGH - alkalosis Look at PCO2. If it is low - respiratory alkalosis If PH high - PCO2 normal or high. Look at HCO3. High - metabolic alkalosis.

NOW LOOK FOR COMPENSATION

Classification

PH PCO2 HCO3 K+

Actual Standard

Metabolic

Uncompensated

Compensated

<7.3

7.3-7.4

N

30-40

Except

Respiratory

Uncompensated

Compensated

<7.3

7.3-7.4

>50

>50

N

N

Metabolic

Uncompensated

Compensated

>7.5

7.4-7.5

N

40-50

Respiratory

Uncompensated

Compensated

>7.5

7.4-7.5

<30

<30

N

N

A

C

I

D

O

S

I

S

ALKALOSIS

Primary change Primary change

STEP-2Hypoxaemic State

Below 60 years of age: Normal PO2 = 97mmHg.

Acceptable range = >80mHg. Mild hypoxiaemia = <80mmHg. Moderate hypoxiaemia = <60mmHg. Severe hypoxiaemia = <40mmHg.


Above 60 years of age: Subtract 1mmHg from minimal 80mmHg

for every year over 60; this means acceptable range:• 60 years = >80 mmHg.• 70 years = >70 mmHg.• 80 years = >70 mmHg.• 90 years = >50 mmHg.

New Born: Acceptable = 40-70 mmHg.


Oxygen Therapy

FIO2 x 5 = Expected PO2.

Uncorrected Hypoxaemia = PO2<Room Air Acceptable Limit.

Corrected Hypoxaemia = PO2 > Room Air Acceptable Limit. <100mmHg.

Excessively Corrected Hypoxaemia = PO2>100mmHg < minimal predicted.

STEP-3Assessment of Tissue Oxygenation

1. Cardiac Status.

2. Peripheral Perfusion Status.

3. Blood Oxygen Transport Mechanism.

Depends on:

Vital Signs

Physical Examination.

STEP-3Assessment of Tissue Oxygenation

BP. Pulse Pressure. Heart Rate ECG. Skin Color & Condition. Capillary Fill. Senosrium. Electrolyte Balance. Urine Out Put.

If Above 1,2 Good Only 3 Interfering. Arterial Oxygen Tension Po2. Blood Oxygen Content. Hb Oxygen Affinity.

SUMMARY

ASSESS ACID/BASE STATUS.

ASSESS HYPOXAEMIC STATE

ASSESS TISSUE OXYGENATION.

TRY TO FIND OUT THE CAUSE.

SEE FOR THE NEED OF HCO3.

SUMMARY

Acidosis Metabolic

Look at

1. Blood urea

If and K+ G.F.

2. Blood Glucose ket

If and K+ ketoacidosis.

3. PO2

If K+ Lactic acidosis

4. Serum HCO3.

If only H/o Therapy

5. If K+ think of NH4Cl

therapy + G. Transplantation

6. If Cl- K+ Think of actazolamide

therapy and R. Tubul

Acidosis.

7. If Cl-N K+ Proximal Tubul

Failure.

OTHERWISE THINK ABOUT

GIT INVOLVEMENT

SUMMARY

Lung Functions will Help

Respiratory

METABOLIC

Look at K+ & Cl-

K+ Cl- H/o vomiting

Pyloric stenosis

If K+ find cause.

H/o bicarb therap.

Alkalosis

RESPIRATORY

- H/o H. Injury

- L. Infection

- IPPV

BASE EXCESS/ DEFICIT

“mEq of HCO3 that is excess/ deficit

per litre of E. C. Water”

PREDICTED RESPIRATORY PH?

PCO2 -- PH RELATIONSHIP

PCO2 20mmHg = 0.1PH.

PCO2 10mmHg = 0.1PH

BASE EXCESS/ DEFICIT

1. Calculate difference between measured PCO2 and 40mmHg. Move decimal 2 places to left.

2. If PCO2 > 40 subtract ½ difference from 7.4.

3. If PCO2 < 40 add the difference to 7.40.

PH 7.21 PCO2 90 90-40 = 50 = 0.50 = 0.50x ½ = 0.25 7.40-0.25 =7.15

PH 7.47 PCO2 18 40-18 = 22= 0.22 7.40 + 0.22 =7.62 Predicted Resp PH.

DETERMINATION OF METABOLIC COMPONENT

10mEq/L variance from buffer base

PH change of c-15 units.

Move decimal 2 places to right i.e. 15

ratio 15:, 2:3=2/3

Measured PH - Predicted PH (resp)

- metabolic PH change.

DETERMINATION OF METABOLIC COMPONENT

1. Determine PCO2 variance. I.e. PCO2 -40mmHg PCO2.

Move decimal 2 point to left.

2. Determine Predicted Resp. PH.

3. Measured PH – Predicted PH difference move decimal 2 places to rt. X 2/3=base excess/deficit.

Base Excess = measured PH> predicted PH.

Base Deficit = measured PH> predicted PH.

APPROXIMATE Na+ & K+

CONCENTRATION IN BODY FLUID

Plasma Gastric Biliary Pancratic S. Intestine

Na+

K+

140

4

60

10

40

5

110

5

Ileal Ileost0my Diarrhoea Sweat

120

5

130

15

60

40

60

10

DOES TRADITIONAL BLOOD GAS ANALYSIS SERVES THE PURPOSE?

PH

PCO2

PO2

HCO3

WHAT INFORMATION DOES IT GIVE?

OXYGEN UPTAK

CO2 PRODUCTION

ACIDITY/ ALKALINITY

WHAT INFORMATION IS REQUIRED FOR THERAPY?

UPTAKE - O2 uptake in lungs.

TRANSPORT - from lungs to capillaries.

RELEASE - from capillaries to tissues.

HOW TO WE GET?

DEEP PICTURE OF BLOOD GASES

O2 UPTAKE

MOUTH TO ALVEOLI

“Grahams’ Law”

of

diffusion

O2 UPTAKE

Alveoli to Hb

“Henrys’ Law”

of

diffusion

COMBINE BOTH LAWS

Mouth to Alveoli

Grahams’ Law of diffusion

Alveoli to Hb

Henrys’ Law of diffusion.

TRANSPORT TO CAPILLARIES

DO2

“ 520 - 720ml/min/m2 ”

O2 RELEASE TO TISSUE

VO2

“ 110 - 160ml/min/m2 ”

WIHAT IS DEEP PICTURE?

PCO2.

tHb.

oS2.

O2Hb.

ctO.

p50.

VO2.

O2 TRANSPORT

AMOUNT OF HB.

FRACTION OF OXYGENATED HB.

O2 TENSION.

MAJOR CHALLENGESBalancing O2 Supply

and

O2 Demand

O2 CARRYING CAPACITY

98% Bound to Hb.

2% in plasma.

Forms of hemoglobins.

Oxygenated – O2 Hb.

Deoxygenated – RHb.

Dyshaemoglobins. Carboxyhaemoglobin (CoHb). Methaemoglobin (MetHb).

tHb = cO2Hb + cRHb + cCoHb + cMetHb

DEGREE TO WHICH Hb CARRIES O2

Expressed in two Different Ways.

1. Fraction of Oxygenated Hb.

cO2Hb

O2Hb = -----------------------------------------------

cO2Hb + cRHb + cCoHb + cMetHb

FRACTIONAL SATURATION2. O2 Saturation.

cO2Hb

sO2 = --------------------------- X 100

cO2Hb + cRHb

DEGREE TO WHICH Hb CARRIES O2

“FUNCTIONAL SATURATION”

Relationship between Oxygenated Hb (O2Hb)

and Oxygen Saturation sO2)

O2Hb = sO2 x (1-CoHb – cMetHb)

Example:Patient exposed to carbon monoxidetHb = 10.0 mmol/L

cO2Hb = 07.7 mmol/LcRHb = 0.3 mmol/L cCoHb = 2.0 mmol/L

7.7 mmol/L 0.77

cO2Hb = --------------------------- = ---------- (7.7+0.3+2.0) mmol/L (or 77%)

7.7 mmol/L

sO2 = -------------------------- X 100 = 96.25%(7.7+0.3) mmol/L

OXYGEN CONTENT

ctO2 = tHb x O2Hb + pO2 x

DYSHAEMOGLOBINS

BLOOD TRANSFUSION

FIO2

OXYGEN RELEASE

cPO2 + tPO2

Capillary – tissue PO2

Hb – O2 affinity

Hb – OXYGEN AFFINITY

98%_____________________________

Normally the arterial blood is approximately 98%

saturated with oxygen.

75%_________________

After release of oxygen to the tissue, mixed

venous blood is approximately 75% saturated .

A left shift of th ecurve < > A right sift of the curve

Indicates impeded release of oxygen. Indicates facilitated release of O2.

The Oxygen Dissociation Curve (ODC) depicts the relationship between sO2 and pO2.

sO2(%)

pO2

The blood oxygen mL/100ml

Absorption curve

Depicts the

Relationship between ctO2

and pO2.

ctO2

20

18

16

14

12

10

8

6

4

2

0

9

8

7

6

5

4

3

2

1

2 4 6 8 10 12

20 40 60 80 mmHg

pO2

kPa

ctO2/(mmol/L

a

v

PO2

DEEP PICTURE CONTAINS INFORMATION

on

OXYGEN UPTAKE

TRANSPORT

RELEASE

Deep Picture Contains Information

OXYGEN UPTAKE

PaO2 = 9.2 – 15.5 Kpa

QSQT = 2-6%

(PAO2 – PaO2) = 5 - 15mmHg

Optimise Ventilation

Optimise Specific Lung Disease

Specific Lung Disease

Deep Picture Contains InformationRELEASE

PO2 Gradient

O2 Dissociation Curve

- Optimise Ventilation

- Optimise Factors

Deep Picture Contains Information

TRANSPORT

tHb = 11.7–14.6G/dl-F

= 13/8–16.4 G/dl-

M

O2Hb = 0.94 – 098

PO2.

CTO2.

Blood transfusion

RBC production

Optimise Ventilation

Dyshaemoglobins

water, electrolyte &

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