Transcript ACID BASE BALANCE

Prof. Mehdi Hasan Mumtaz
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—
Cl—
HCO-3
-HCO
CO2
CO2+H2O
HHB
+
+H
3
Hb
BICARBONATE REABSORPTION
BY KIDNEY
HCO3Na+
HCO3-
Na+
RENAL T. LUMEN
HCO3H+
STIMULATED BY
HCO3-
HCO3-
H2CO3
M. ACIDOSIS
CO2
+
H2 O
CELL
H2CO3
CD
CO2
H2O
BICARBONATE GENERATION IN
KIDNEY
BHCO3-
Na+
STIMULATED
PCO2
Na+
BH+
(BY RESP ACIDOSIS)
&
-HCO3
(M. ACIDOSIS)
HCO3-
HB
CELL
H2O
CO3
H2O
PATHOPHYSIOLOGIC
DISTURBANCES
Lungs
Disturbances of CO2=
R. Centre
Disturbance of H++HCO3 = Metabolic
Henderson - Hosselbalch
EQUATION
Proton Acceptor (Base)
PH=PK+Log = -------------------------------Proton Donor (Acid)
-HCO
(Metabolic)
PH=PK+Log = ---------------------------------H2CO3 or PCO2 x 0.03
(Respiratory)
3
ACID-BASE DISTURBANCE
-HCO3
PCO2 x 0.03
MEATBOLIC
ACIDOSIS
RESPIRATORY
ALKALOSIS
ACIDOSIS
ALKALOSIS
HCO3
---------------PCO2x0.03
HCO3
---------------PCO2x0.03
HCO3
---------------PCO2x0.03
HCO3
---------------PCO2x0.03 
RATIO



Defect
Correction
Metabolic acidosis =
HCO3
---------PCO2
HCO3
---------PCO2 
Respiratory acidosis =
HCO3
---------PCO2
HCO3 
---------PCO2 
Metabolic alkalosis =
HCO3 
---------PCO2
HCO3 
---------PCO2 
Respiratory alkalosis =
HCO3
---------PCO2 
HCO3 
---------PCO2 
CAUSES OF M. ACIDOSIS
1.
2.
3.
4.
5.
6.
7.
8.
9.
Glomeralar failure.
Hyperkalamic M. Acidosis
Keto-acidosis.
Lactic acidosis.
Variable
Intestinal loss.
R. Tubular failure.
Actazolamide therapy. Hyppkalamic Acidosis
R. Tubular acidosis.
Hyperchloraemic
Acidosis
Ureteric transplantation.
NH4Cl el therapy.
CAUSES M. ACIDOSIS
A.HYPERKALAEMIC M. ACIDOSIS
1, GLOMERULAR FAILURE
2, KETOACIDOSIS
3, LACTIC ACIDOSIS
CAUSES OF M.ACIDOSIS
B.HYPOKALAEMIC M.ACIDOSIS
1.RENAL TUBULAR
2.ACETAZOLAMIDE THERAPY
3.RENAL TUBULAR ACIDOSIS
CAUSES OF M. ACIDOSIS
C.HYPERCHLORAEMIC ACIDOSIS
1.ACATAZOLAMIDE THERAPY
2.RENAL TUBULAR ACIDOSIS
3.URETERIC TRASPLANTATION
4.AMMONIUM CHLORIDE
CAUSES OF M. ACIDOSIS
D.HYPERCHLORAEMIC
HYPOKALAEMIC M.ACIDOSIS
1.ACETAZOLAMIDE THERAPY
2.RENAL TUBULAR 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-1
Assessment of Acid-Base Balance
CLASSIFICATION
ALKALOSIS
ACIDOSIS
METABOLIC
ACUTE
RESPIRATORY
CHRONIC
ACUTE
METABOLIC
ACUTE
CHRONIC
RESPIRATORY
CHRONIC
ACUTE
CHRONIC
STEP-1
Assessment of Acid-Base Balance
Acute
Chronic
- Uncompensated.
- 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)
DIAGNOSIS
IF 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
PH
A
C
I
D
O
S
I
S
A
L
K
A
L
O
S
I
S
PCO2
Classification
K+
HCO3
Actual
Standard


Metabolic
Uncompensated
Compensated
<7.3
7.3-7.4
N
30-40 


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

Primary change

Except


Primary change

PRACTICAL EXAMPLES
PH
7.26 7.38 7.20 7.36 7.60 7.56
PCO2 56
76
40
25
25
44
HCO3 24
24
9
15
24 38
STEP-2
Hypoxaemic State
Below 60 years of age:
 Normal PO2
= 97mmHg.(13 Kpa)
 Acceptable range
= >80mHg.(10.6Kpa)
 Mild hypoxiaemia = <80mmHg.(10.6Kpa)
 Moderate hypoxiaemia = <60mmHg.(8)
 Severe hypoxiaemia = <40mmHg.(5.3)
STEP-2
Hypoxaemic State
Above 60 years of age:
 Subtract 1mmHg from minimal 80mmHg
for every year over 60; this means
acceptable range:
•
•
•
•
60 years = >80 mmHg. =>10.6 Kpa
70 years = >70 mmHg. => 9.3 Kpa
80 years = >60 mmHg. = > 8.0 Kpa
90 years = >50 mmHg. = > 6.6 Kpa
New Born:
 Acceptable = 40-70 mmHg.= 5.3-9.3 Kpa
STEP-2
Hypoxaemic State
Oxygen Therapy
FIO2 x 5 = Expected PO2.
Uncorrected Hypoxaemia = PO2<Room Air Acceptable Limit.
Corrected Hypoxaemia = PO2 > Room Air Acceptable Limit.
<100mmHg.=13.3 Kpa
Excessively Corrected Hypoxaemia = PO2>100mmHg(13.3Kpa)
< minimal predicted.
OXYGENATION STATUS
FIO2 ----PIO2
PAO2 = PIO2-PACO2
PaO2
P(A-a)O2=PAO2-PaO2
PaO2/PAO2=0.67
-----------------------------------------------------DO2 520—720ml/min/m2
VO2 110—160 ml/min/m2
Lactate
PRACTICAL EXAMPLES
PH
PCO2
HCO3
BE
PO2
FIO2
AGE
7.24
32
14
-13
100
21
40
7.42
28
18
-5
50
40
50
7.54
29
24
+3
65
21
45
7.16
83
29
-3
30
40
40
7.36 7.48
83 33
48 24
+15 +1
45 75
21 50
80 70
PRACTICAL EXAMPLES
PH
PCO2
HCO3
BE
PO2
FIO2
AGE
7.24
28
12
-15
90
21
40
7.46
26
18
-4
70
21
75
7.40 7.48 7.48 7.55
56 33 33 20
34 24 24 18
+7 +1 +1 -3
55 50 160 45
21 50 50 21
60 30 30 40
STEP-3
Assessment of Tissue Oxygenation
1. Cardiac Status.
2. Peripheral Perfusion Status.
3. Blood Oxygen Transport Mechanism.
Depends on:
 Vital Signs
 Physical Examination.
STEP-3
Assessment 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/ ketones
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
Respiratory
Lung Functions will Help
Alkalosis
METABOLIC
Look at K+ & ClK+  Cl- 
H/o vomiting
Pyloric stenosis
If K+  find cause.
H/o bicarb therap.
RESPIRATORY
- H/o H. Injury
- L. Infection
- IPPV
PRACTICAL EXAMPLES
PH PCO2
7.25 40
7.29 35
7.58 40
7.52 42
7.35 37
HCO3 Na
20
130
20
135
37
145
35
130
18
136
K Cl UREA G
5.5 100 95 120
4.5 118 40 90
4.3 100 40 100
2.7 85 58 100
2.9 117 25 90
BUFFER BASE/BASE DEFICIT
“Sum of the Buffer anions;
44--55 meq/l
PREDICTED RESPIRATORY PH?
PCO2 -- PH RELATIONSHIP
 PCO2 20mmHg =  0.1PH.
 PCO2 10mmHg =  0.1PH
BASE EXCESS/ DEFICIT
Predicted Respiratory PH
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.
METABOLIC COMPONANT
METABOLIC PH CHANGE =
Measured PH -- Predicted Respiratory PH
DETERMINATION OF
METABOLIC COMPONENT
Determine predicted PH
Determine difference between measured and
predicted PH
Move two decimal point to the right
Multiply by 2/3
Base excess if measured Ph > predicted PH
Base deficit if measured PH<predicted PH
EXAMPLE
PH 7.04 PCO2 76
Predicted PH= 76-40=36 =.36=1/2*36
= 18=.18=7.4-.18=7.22
Base Excess/deficit=7.22-7.04=0.18=
18*2/3=12
As measured PH is less than predicted,so
it is Base deficit
PaCO2/HCO3 Relationship
1. A.Respiratory acidosis.
Expected HCO3=24+0.1*(Paco2-40)
2. Chronic Respiratory acidosis.
Expected HCO3=24+0.35*(Paco2-40)
3. A.Respiratory alkalosis.
Expected HCO3=24-0.2*(40-Paco2)
4. Chronic respiratory alkalosis.
Expected HCO3=24-0.5*(40-Paco2)
EXPECTED PaCO2
METABOLIC ACIDOSIS
Expected PaCO2=1.5*(HCO3) + 8
METABOLIC ALKALOSIS
Expected PaCO2=40+0.6*(HCO3)
APPROXIMATE Na+ & K+
CONCENTRATION IN BODY FLUID
Plasma
Na+
K+
Ileal
120
5
Gastric
Biliary
Pancratic
S.
Intestine
140
4
60
10
40
5
110
5
Ileost0my Diarrhoea
130
15
60
40
Sweat
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
TRANSPORT
RELEASE
- O2 uptake in lungs.
- from lungs to capillaries.
- 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 CHALLENGES
Balancing 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 SATURATION
2. 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 monoxide
tHb
=
10.0 mmol/L
cO2Hb
=
07.7 mmol/L
cRHb
=
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
Hb – O2 affinity
cPO2 + tPO2
Capillary – tissue PO2
Hb – OXYGEN AFFINITY
sO2(%)
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.
pO2
The Oxygen Dissociation Curve (ODC) depicts the relationship between sO2 and pO2.
The blood oxygen
mL/100ml
ctO2/(mmol/L
Absorption curve
a
Depicts the
20
9
18
8
16
7
14
6
Relationship between ctO2
and pO2.
12
ctO2
10
v
5
4
8
3
6
2
4
1
2
pO2
0
2
4
20
6
40
PO2
8
60
10
12
80
kPa
mmHg
DEEP PICTURE CONTAINS
INFORMATION
on
OXYGEN UPTAKE
TRANSPORT
RELEASE
Deep Picture Contains
Information
OXYGEN UPTAKE
PaO2
= 9.2 – 15.5 Kpa
QSQT = 2-6%
Optimise Ventilation
Optimise Specific Lung Disease
Specific Lung Disease
(PAO2 – PaO2) = 5 - 15mmHg
Deep Picture Contains
Information
RELEASE
PO2 Gradient
- Optimise Ventilation
- Optimise Factors
O2 Dissociation Curve
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
CLINICAL SCENARIO
A 60 year old woman presents with
pneumonia ,shock and resp.distress.
ABG; Fio2 0.5
PH 7.15
PCO2 30/4
HCO3 10.3
PO2 105/14 BE
-18.3
a, Describe; Acid base status?
b, Is there problem with O2 transfer?
c, Is intubation likely to be necessary?
ANSWER
1, Metabolic Acidosis +Resp. Acidosis
2,Yes,A-a gradient is raised at 218.
Shunt or V/Q mismatch
3,Paco2 is very high than expected
Paco2 in metabolic acidosis showing
imminant respiratory arrest.
Clinical scenario
You are asked to see
a 15 y old asthmatic
male, having treatment
in A&E for thelast 3
hours,having ,low pco2
& now tachypnoic with
mild wheez.
PH
PCO2
HCO3
FIO2
PO2
BE
Na
CL
7.5
30
23.1
0.5
80
-1.5
143
105
7.39
30
17..9
0.5
175
-7.9
143
105
QUESTIONS
Calculate& interpret A-a gradient.?
Describe acid base status.?
Has his asthma improved ,reasons.?
What is the most likely explanation for
the unchanging hypocapnoea.?
BIOCHEMICAL REPORT
PH
7.4
PCO2 3.5
HCO3 18
FIO2 21
PO2
11.5
BE
-4
Glucose 10
Periphery cold
Na
K
Cl
HB
Hct
BP
HR
SPO2
140
2.9
94
14.5
48
90/76
132
98