acid-base balance
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Transcript acid-base balance
Arterial Blood Gas Analysis
By Mohamed hamdy
Assistant lecturer of Anesthesia
Ain-Shams University
Egyptian Resuscitation Council
(ERC)Instructor
Interpretation of ABG Analyses
Systematic Approch
ABG Abnormalities
Why we do Arterial Blood Gas Analysis?
Oxygenation
Represented by PaO2
Ventilation
Represented by Pa Co2
Acid Base Status
Represented by pH, HCO3 and base deficit.
Hb, Hct, oxygen saturation
Electrolyte e.g. Na+, K+.
Because H+ react highly with cellular proteins resulting
in alteration in their function therefore avoiding acidemia
and alkalemia by tightly regulation H+ which is essential
for normal cellular function.
Calculation of Alveolar Gas Equation and A-a Gradient:
PAO2 = FiO2×(Bp-pH2O)-PaCO2/R.
=
21×(760-47)-40/0.8
= 100 mmHg.
A-a Gradient is alvealo-arterial O2 gradient.
A-a Gradient = PAO2 -PaO2
It is normally = Age/4+4.
It’s Value: concise D.D of hypoxemia.
e.g.:
Decrease FiO2
Hypoventilation
normal A-a Gradient
Ventilation perfusion mismatch
Rt to Lt shunting
Diffusion abnormality
increase A-a Gradient
Approach To Hypoxemia
PaO2
A-a Do2
N
pCO2
N
FIO2
Alv.
Hypo.
100%
O2
Corrects
No Correction
V/Q Mis.
Diffusion
Shunt
1) Arterial/alveolar ratio(a/A)
PaO2/PAO2
Normal value for the a/A ratio is 0.8, meaning that 80% of the
alveolar oxygen is reaching the arterial system
2) PaO2/ FIO2 ratio
Normal ratio is 550 (a person breathing FIO2 of 1.0 at sea level
should have a PaO2 of 550 to 600 mmHg)
3) A-a gradient (on 100% oxygen)
PAO2 - PaO2
Where PAO2 is calculated by the alveolar air equation previously
presented
PO2 and PCO2 in Blood
16
4) Arterial-alveolar PCO2 Gradient (a-A PCO2)
Arterial PCO2 - Alveolar PCO2
Where Alveolar PCO2 is measured by means of end–tidal PCO2
Normal gradient is an alveolar PCO2 2 mmHg less than arterial,
Acute increase reflects increase in physiologic dead space
Getting an ABG sample
Sample source and collection:•Arterial blood sample is common utilized clinically
but venous blood may be useful in determining acid
base status.
•Blood sample should be in heparin coated syringe.
•The sample should be analyzed as soon as
possible.
•Air bubble should be eliminated.
•The syringe should be capped and placed in ice.
Problem associated with obtaining ABG:
Arterial puncture may result in acute hyperventilation. To
minimize that: we should use local anesthetic with small
needle.
When would you withdraw ABG sample after beginning or stopping
O2 supplementation?
In absence of significant lung disease we should wait from 5-7
minutes before withdraw ABG sample while patient with
obstructive lung disease we should wait 25 min.
Interpretation of ABG
Normal blood gas values:
Arterial blood
Mixed venous
Venous
PH
7.37-7.47
7.30-7.40
7.30-7.40
PO2
80-100
35-40
30-50
PCO2
36-44
40-50
40-50
O2 saturation
>95%
60%-85%
60%-80%
HCO3
22-26
22-26
22-28
Base difference
(deficit excess)
-2 to 2
Measurement
What is PH?
PH is –ve log of H+ concentration.
Relationship between pH & [H+]
pH
[H+]
(nanomoles/l)
6.8
158
pH = pK’a + log ([HCO3] / 0.03 x pCO2) 6.9
125
7.0
100
7.1
79
7.2
63
7.3
50
7.4
40
7.5
31
7.6
25
7.7
20
7.8
15
Henderson-Hasselbalch Equation
or more simply: The Henderson
equation:
[H+] = 24 x ( pCO2 / [HCO3] )
STEPS for interpretation of ABG
STEP 1:
Determine if numbers fit:
H+ =
24 PCO2
HCO3
H+ = (7.8-PH)×100.
The Rt side of the equation should be within 10% of the Lt
Side. If not so:
Another ABG
Chemistry panel for HCO3 should be done.
STEP 2:
STEP 3:
Determine if:
Acidemia (PH<7.37) OR Alkalemia(PH >7.44) is present.
Identify primary disturbance:
PH
Increase
Decrease
Alkalosis
Acidosis
Look at PCO2
Increased
Metabolic
Alkalosis
Decrease Increased
Respiratory
Alkalosis
Respiratory
acidosis
Decreased
Metabolic
acidosis
STEP 4:
Look at the direction of the change of HCO3/PCO2:
•If it is in the same direction it is either simple or mixed change.
•But if it is in the opposite direction so it is mixed change.
STEP 5:
Calculate rate of change of Hco3 and co2
(Expected compensation)
Response
Expected change
Metabolic acidosis
↓Paco2
1.2×(24-HCO3 measured)
Metabolic alkalosis
↑Paco2
0.7×(HCO3-24)
Acute respiratory acidosis
↑Hco3
0.1×(PaCO2-40)
Chronic respiratory acidosis
↑ Hco3
0.4×(PaCO2-40)
Acute respiratory alkalosis
↓ Hco3
0.2×(40-PaCO2)
Chronic respiratory alkalosis
↓ Hco3
0.4×(40-PaCO2)
Disturbance
Determine the Anion Gap
The Anion Gap
[(Na+) + (K+)] – [(Cl-) + (HCO3-)]
The normal A.G is 12meq ± 4.
Normal A.G (Hyperchloremic Acidosis)
↑ GIT loss of HCO3 as in: diarrhea, high output fistula
↑ renal HCO3 loss as in: RTA(I, II)
TPN.
↑ CL containing acids.
Wide Anion Gap Acidosis (↑ endogenou non-volatile acid)
Keto Acidosis
Uremia
Lactic Acidosis
Salicylism
Toxins : Methanol,Paraldehyde,Ethylene glycol
All anions and cations
ANIONS
Proteins 15
Organic acids 5
Phosphates 2
Bicarbonate 24
Sulfates 1
CATIONS
Calcium 5
Magnesium 1.5
Potassium 4.5
Sodium 140
Chloride 104
TOTAL 151
Na+
+
UC
TOTAL 151
=
Na+ – (Cl-) + (HCO3-) =
(Cl-) + (HCO3-) + UA
UA – UC
Very low or even –Ve A.G
Calculation of AG in urine:
Urine AG = ( Na+ + K+) – CLIn a patient with a hyperchloraemic metabolic acidosis:
•A negative UAG suggests GIT loss of bicarbonate (eg diarrhoea)
•A positive UAG suggests impaired renal distal acidification (ie
renal tubular acidosis).
STEP 6:
If there is metabolic acidosis calculate the A.G
Anion Gap = Na+ - (Cl- + HCO3-) = 12meq ± 4.
• Corrected A.G = observed A.G + 2.5 (normal
albumin - measured albumin).
If the anion gap ↑ proceed to step 7.
STEP 7:
If the anion gap metabolic acidosis is present we should evaluate
for additional metabolic disorder because the elevation of anion gap
above normal ∆ AG = (AG-12) should be buffered by HCO3.
Adding ∆AG to current HCO3 will yield the corrected Hco3 which should be
normal value 24 meq/l unless there is another disorder present.
Corrected HCO3 = current HCO3 (measured) +∆A.G
(Normal value 24 meq/l)
•If corrected HCO3 >24 → metabolic alkalosis is also present
•If corrected HCO3 <24 → a non gap metabolic acidosis is also present
•If corrected HCO3 = 24 → it is pure gap metabolic acidosis.
Final step:
Be sure that the interpretation of blood gas is consistent and
correlated with the clinical picture of the patient.
Case 1
A 75-year-old man presents to the ED after a
witnessed out of hospital VF cardiac arrest.
Arrived after 10 minutes, CPR had not been
attempted.
The paramedics had successfully restored
spontaneous circulation after 6 shocks.
On arrival the man is comatose with a GCS of 3
and his lungs are being ventilated with 50%
oxygen via ET tube.
He has a ST with rate of 120 min-1 and a blood
pressure of 150/95 mmHg.
ABG Analysis reveals:
FiO2
pH
PaCO2
PaO2
HCO3 BE
0.5
7.10
6.0 kPa (45 mmHg)
7.5 kPa(56 mmHg)
14 mmol l-1
- 10 mmol l-1
Case 2
A 65-year-old man with severe COPD
has just collapsed in the respiratory
high-care unit.
On initial assessment he is found to be
apnoeic but has an easily palpable
carotid pulse at 90 min-1.
A nurse is ventilating his lungs with a
BVM and supplementary O2 (with
reservoir)
ABG Analysis reveals:
FiO2
pH
PaCO2
PaO2
HCO3 BE
0.85 (estimated)
7.20
(80 mmHg)
(147 mmHg)
40 mmol l-1
+ 14 mmol l-1
Case 3
A 75-year-old lady is admitted to the ED following a
VF cardiac arrest, which was witnessed by the
paramedics.
A spontaneous circulation was restored after 4 shocks,
but the patient remained comatose and apnoeic.
The paramedics intubated her trachea, and on
arrival in hospital her lungs are being ventilated with
an automatic ventilator using a tidal volume of 900
ml and a rate of 18 breaths min-1.
ABG Analysis reveals:
FiO2
pH
PaCO2
PaO2
HCO3-
BE
1.0
7.60
2.65 kPa (20 mmHg)
25.4 kPa (192 mmHg)
20 mmol l-1
-2 mmol l-1
Case 4
An 18-year-old male insulin dependent diabetic is admitted
to the ED.
He has been vomiting for 48 hours and because he was
unable to eat, he omitted his insulin.
He has a ST at a rate of 130 min-1 and his blood pressure is
90/65 mmHg.
He is breathing spontaneously with deep breaths at a rate
of 35 min-1 and is receiving oxygen 6 l min-1 via O2 mask.
His GCS is 12 (E3, M5, V4).
ABG Analysis reveals:
FiO2
pH
PaCO2
PaO2
HCO3-
BE
0.4
6.79
(14 mmHg)
(129.2 mmHg)
4.7 mmol l-1
- 29.2 mmol l-1
Case 5
His vital signs are:
Heart rate
120 min-1 – sinus
tachycardia – warm peripheries
Blood pressure 70/40 mmHg
Respiratory rate
35 breaths min-1
SpO2 on oxygen
92%
Urine output
50 ml in the last 6 hours
GCS
13 (E3, M6, V4)
ABG Analysis reveals:
FiO2
pH
PaCO2
PaO2
HCO3-
BE
0.4 (approx)
7.12
4.75 kPa (36 mmHg)
8.2 kPa
(62 mmHg)
12 mmol l-1
- 15 mmol l-1
Case 6
Which patient is more hypoxemic, and why?
Patient A: pH 7.48, PaCO2 34 mm Hg, PaO2 85 mm Hg, SaO2 95%,
Hemoglobin 7 gm%
Patient B: pH 7.32, PaCO2 74 mm Hg, PaO2 55 mm Hg, SaO2 85%,
Hemoglobin 15 gm%
Patient A: Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl
Patient B: Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml O2/dl
Patient A, with the higher PaO2 but the lower
hemoglobin content, is more hypoxemic.
Case 7
The PO2 in a cup of water open to the
atmosphere is always higher than the arterial
PO2 in a healthy person (breathing room air)
who is holding the cup.
True or False
Case 8
A patient is admitted to the ICU with reabeted vomiting the following
BLOOD GASES
pH: 7.40
PCO2: 38
HCO3: 24
PO2: 72
ELECTROLYTES, BUN & CREATININE
Na: 149
K: 3.o
Cl: 100
CO2: 24
BUN: 110
Creatinine: 8.7
What is(are) the acid-base disorder(s)?
The patient was both uremic (causing metabolic acidosis)
and had been vomiting (metabolic alkalosis).
Case 9
55 yrs old pt. who drink fifth of wesky per day has 2 wks
history of diarrhea , Anion gap is 20, HCO3 = 10, PH =
7.30, PO2 =0.90 mmHg, PCO2 = 30 mmHg.
What is(are) the acid-base disorder(s)?
Case 10
25 yrs pt. come to ER with fever, abd. pain , vomiting,
with the history of migrane PH = 7.33, PCO2 = 8mmHg,
PO2 = 80 mmHg, HCO3 = 4, Sodium = 140 mmol, K = 3
mmol, CL = 108 mmol.
What is(are) the acid-base disorder(s)?
“Life is a struggle, not against
pharama, not against the physics,
not against Anesthesia Exame,
but against hydrogen ions.“
M. Hamdy
Any Question?