Water, Electrolyte &
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Transcript of 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.
STEP-2Hypoxaemic State
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.
STEP-2Hypoxaemic State
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