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ABGA: bedside application
Acid-base Gas exchange
ER: GI bleeding
Patient A
• BP 95/65 mmHg
• ABGA:
7.37- 34- 73- 20
Patient B
• BP 130/50 mmHg
• ABGA:
7.28-24- 73- 13
Pneumonia
Patient A
Ceftriaxone + Azythromycin
• D1:
7.32- 30- 60- 16
• D2:
7.38- 34- 73- 20
Patient B
Ceftriaxone + Azythromycin
• D1:
7.32- 30- 60- 16
• D2:
7.26- 24- 73- 12
• Vital signs
BP RR PR BT
• Vital signs
BP RR PR BT [ ? ]
pH
1909, SPL Sorensen, Carlsberg Lab, Denmark
Ion concentration & protein function
[H+] in the blood: 0.00000004 mEq/L
pH (pH) : pouissance hydrogen
(power of H+)
Clinical symptoms of abnormal pH
pH manifestations
7.80 Death
Convulsion
Arrhythmia Increased excitability
Irritability
7.40 Normal
Drowsiness
Lethargy Depressive effect
Coma
6.80 Death
pH homeostasis
• Metabolism: acids
• Homeostatic organ-systems
Lung Blood
buffer Kidney
Acids production
13,000 mEq/day
• Volatile acid:
98 % of daily acids
• Non-volatile acid:
1-2% of normal acid
pathologic acids
40-80 mEq/day
Volatile acids (carbonic acid, H2CO3)
CO2
Lung: moment-to-moment regulation
Fixed (Non-volatile) acids
1) Source: metabolism non-metabolic: NH4Cl
2) Via kidney, blood buffers
Blood buffers
• H+(liquid) + A- (sponge) HA (wet sponge)
• First line of defense against abrupt pH change
Bicarbonate buffer system - more than 50 % of total blood buffering
HCO3: Open system Hb: Closed system
Units Mean Normal Acidotic Alkalotic
2 SD
1 SD
pH - 7.40 7.35 - 7.45 <7.35 >7.45
7.38 - 7.42
PCO2 mmHg 40 35 - 45 <45 >35
38 - 42
HCO3- mEq/L 25 22 - 28 <22 >28
24 – 26
ABG: normal values
Don’t discard VBGA
• 7.26- 43- 48- 12.8- 64 %
Arterial blood Venous blood
pH 7.40 7.36
PCO2 40 46
PO2 90 40
HCO3- 24 26
Pre-analytical errors of ABGA
– Anticoagulant
Dilution effect: liquid heparin
Liquid heparin
Lyophilized heparin
– Air contamination
• PaO2 < 158 mmHg (room air PO2): inc
• PaCO2: dec (less marked than PaO2)
• Air bubbles should be expelled within 2 min
cf. PaO2 > 158 mmHg
(MV, Anesthesia): dec
Calaf et al. Tech Note 2004
D: air bubble at the cone E: air bubble at the plunger
– Analysis timing
Calaf et al. Tech Note 2004
ABGA results: immediate, and 30, 60 min at 4 °C
ABGA: glass syringe vs. plastic syringe
• Paradoxical change:
inc PaO2, dec PaCO2
• microbubble due to friction
iced sample: diffusion of ambient air thru plastic
• Best to analyse within 30 min
66/M. CLL. WBC 282,000/mm3
ABGA: 7.38- 47- 31- 29- 54% (O2 2 L/min)
2nd ABGA, < 1 min: PaO2 41 mmHg
3rd ABGA, centrifuged: PaO2 68 mmHg
ABGA: whole blood vs. plasma
44/F. AML
8. 24
WBC 172,000
PaO2-Whole blood 51 mmHg
SpO2 82 %
PaO2-Plasma
8. 24 8. 25
8. 25
43,500
81 mmHg
95 %
118 mmHg
O2 CO2 H+
Clark Electrode
Serveringhaus Electrode
Sanz Electrode
Arterial blood
Buffer pH = 6.840
----- XXXX Diagnostics ------
Blood Gas Report 248 5:36 Jul 22 2000t ID
2570 / 00
Measured 37.0o C
pH 7.463
pCO2 44.4 mm Hg pO2 113.2 mm Hg
Corrected 38.6o C pH 7.439
pCO2 47.6 mm Hg pO2 123.5 mm Hg
Calculated Data
HCO3 act 31.1 mmol / L HCO3 std 30.5 mmol / L BE 6.6 mmol / L
O2 CT 14.7 mL / dl O2 Sat 98.3 % ct CO2 32.4 mmol / L
pO2 (A - a) 32.2 mm Hg pO2 (a / A) 0.79
Entered Data Temp 38.6 oC
ct Hb 10.5 g/dl
FiO2 30.0 %
Internal consistency
• Indirect metabolic
assessment
• Rule of eights
• Modified Henderson
equation
• Acid-base map
External congruity
• Lab-lab congruity
• Pt-lab congruity
• FIO2-PaO2 congruity
• SaO2-SPO2 congruity
Modified Henderson Equation
• H = 24 x PaCO2/HCO3
• Linear relationship between H+ and pH in 7.20-7.50
Ex) 7.30-28-86-18
H: 50
24 x 28/18 = 37.3
HCO3
• calculated value
• arterial blood
• anaerobic
• immediate
handling/ice-stored
Total CO2
• measured value
• venous blood
• air-contaminated
• lag in
measurement/room
temperature exposure
Difference 2 mEq/L: Good congruity
> 5 mEq/L: Incongruous !
Q: Metabolic acidosis, alkalosis에는 왜 acute, chronic 분류가 없나?
acidosis
alkalosis
respiratory
metabolic
acute ? chronic
acute ? chronic
metabolic
respiratory
Acute changes in PaCO2
Immediate changes in pH
Approximate PaCO2-pH Relationship
PaCO2 [HCO3-]P*
(mm Hg) pH (mmol3/L)
80 7.20 28
60 7.30 26
40 7.40 24
30 7.50 22
20 7.60 20 [HCO3
-]p = plasma bicarbonate concentration
Causes of Respiratory Acidosis
• Central: drugs (anesthetics, morphine, sedatives, antihistamine), stroke, infection, central hypoventilation syndrome
• Airway: asthma, COPD, airway obstruction
• Neuromuscular: poliomyelitis, kyphoscoliosis, myasthenia, muscular dystrophies
• Miscellaneous: obesity, permissive
Respiratory Acidosis
Drowsy
Confusion
Headache
Flapping tremor
Renal compensation in RAc
Acute: HCO3- ↑ = 0.1 × PCO2 ↑
Chronic: HCO3- ↑ = 0.35 × PCO2 ↑
Causes of Respiratory Alkalosis
1. Hypoxia
2. Pulmonary disease: pulmonary edema, pneumonia, pulmonary embolism, ILD
3. CNS-mediated
- hyperventilation syndrome
- CNS infection, hemorrhage, tumor
- medical conditions: sepsis, liver failure, pregnancy
- trauma, heat exposure
- medicine: salicylate, nicotine, xanthine, progesterone
4. Mechanical ventilation
Renal compensation in RAk
Acute: HCO3- ↓ = 0.2 × PCO2 ↓
Chronic: HCO3- ↓ = 0.5 × PCO2 ↓
Respiratory alkalosis
(Hypocapnia)
Cerebral vasospasm
Confusion headache
Paresthesia
tetany
Brain in respiratory acid-base disturbance
• More vulnerable to acid-base change than anticipated
by blood pH: faster movement of CO2 than HCO3-.
• Brain is significantly affected by
(1) acute changes in pH
(2) rapid correction of acidosis or alkalosis
pH = Acidemia
PaCO2 = Normal or low metabolic acidosis (MAc)
HCO3- = Low
pH = Alkalemia
PaCO2 = Normal or high metabolic alkalosis (MAk)
HCO3- = High
Metabolic acid-base disorders
Anion Gap?
ECF
state?
Anion Gap (AG)
• AG = Na – (Cl- + HCO3-) = 12 2
– 1 g/dL albumin = 2.5 mEq/L anion
– corrected AG = AG - 2.5 x (4.5-alb)
MAc- high AG
• Lactic acidosis
• Ketoacidosis
• Renal failure: acute, chronic
• Toxins: ethylene glycol, methanol, salicylate,
propylene glycol, pyrolglutamic acid
80/M. Distal CB stone
Liver abscess with septic shock
High lactate does not always mean
lactic acidosis
62/F
• 8년전 Coronary Artery Bypass Graft 받음
• Effort-related dyspnea AR/MR 진단
• AVR/MVR
• 의식상태 양호
인공호흡기 없이 호흡
WBC: 17500 12500
CRP: 7.1 5.8
• 임상 으로 호전되고 있으나 lactic acid가 증가되어 있슴
• 약물: lactic acidosis 유발 가능한 약물 없슴
• RAk 및 glucose 정상화 후
• Resp alkalosis에 의한 hyperlactemia
알칼리증과 당대사: 3번 과정을 촉진
6번 과정의 NADH+H+생성↑
pyruvate 생성 증가
lactate로의 전환 증가
신부전의 경우 gluconeogenesis 및 glycogenolysis 과정의 효소 장애
lactate level 증가
• 혈당에 의한 hyperlactemia
High AG is significant
• Even when HCO3- appears normal.
Indicates a mixed acid-base disorder
• If pH is alkalotic:
MAc + Alkalosis (metabolic/respiratory)
62/M. Alcoholic LC
• AGBA: 7.40- 40 -85- 25- 96
• Na 135, Cl 80, K 2.8
• AG= 135- (80+25)= 30 [High AG!]
AG = 30 - 12= 18
HCO3-= 25 - 24= 1
PI) vomiting for the last few days
Dx) metabolic acidosis + metabolic alkalosis
Non-AG acidosis
• Gastrointestinal bicarbonate loss: diarrhea, external
pancreatic/small bowel drainage [GI acidosis]
• Renal disease: proximal RTA, distal RTA, generalized
distal nephron dysfunction [Renal acidosis]
• Drug-induced hyperkalemia (with renal insufficiency):
K-sparing diuretics, trimethoprim, pentamidine, ACEI, ARB, NSAID, cyclosporin/tacrolimus [Medication acidosis]
• Others: rapid saline infusion
Non-AG acidosis
Urinary Anion Gap = Urine [Na++ K+- Cl- ]
Positive Negative
Renal cause Extra-renal cause
Urine pH
> 6 < 5.5
(Type I, RTA)
Hypokalemia
Hyperkalemia (Type IV RTA) (Type II RTA)
Low or negative AG
• Severe hypoalbuminemia: nephrotic
syndrome
• Multiple myeloma, paraproteinemias
(cationic proteins)
• Bromism (dextromethorphan bromide)
• Lithium (cation)
Useful parameters for assessment of MAc/MAk
• Anion gap (AG)
• Total CO2 (TCO2)
• Base excess (BE)
Total CO2= [HCO3- ] + [dissolved CO2 ]+ [H2CO3]
= [HCO3
- ] + 0.03 x PCO2
Total CO2
“You are seeing [HCO3- ] without arterial puncture.”
COPD A
7.35-60-54-33
2 mo ago
Na 138
K 4.1
Cl 102
TCO2 31
COPD B
7.35-60-54-33
2 mo ago
Na 138
K 4.1
Cl 102
TCO2 24
Azotemia A
Cr 3.0
2 mo ago
Na 138
K 5.4
Cl 102
TCO2 23
Azotemia B
Cr 3.0
2 mo ago
Na 138
K 5.4
Cl 102
TCO2 17
73/M. DM, CKD, HTN, s/p CABG
CC. Sore throat
Previous admission
TCO2 22.4
BUN/Cr 19/1.5
Day 1
TCO2 17.1
BUN/Cr 107/6.3
Base excess (BE)
Change in [strong acid] or [strong base] required to restore pH to 7.4 at 40 mm Hg of PaCO2 on 37℃
• BE = 0 +/- 3 mmol/L: WNL BE > +10, < -10 mmol/L: metabolic component in acid-base imbalance • Trend of BE
73/M. DM, CKD, HTN, s/p CABG
CC. Sore throat
CPCR D4
D2
D1
85/F. COPD, thyroid cancer with lung metastasis
Lasix
Acetazolamide
Causes of Metabolic Alkalosis
• ECF contraction
– GI: vomiting, gastric aspiration, villous adenoma
– Renal: diuretics, posthypercapnic state, hypercalcemia/hypoparathyroidism
– Recovery form lactic acidosis/ketoacidosis
– Nonabsorbable anions (penicillin, carbenicillin)
– Magnesium deficiency
– K depletion
– Bartter’s syndrome, Gitelman’s syndrome
High renin
renal artery stenosis
accelerated HTN
renin-secreting tumor
estrogen therapy
• ECF expansion MAk
Low renin
primary aldosteronism
adrenal enzyme defects
Cushing’s syndrome
licorice
Metabolic alkalosis & CO2 retention
• If PaCO2 > 55- 60
mmHg in MAk, suspect
primary respiratory
insufficiency.
Mixed acid-base disorder
When pH of a sick patient is around 7.40
suspect a mixed acid-base disorder
pH = 7.390
PaCO2 = 64 mmHg
PaO2 = 76 mmHg
HCO3- = 39 mEq/L
BE = 12
pH = 7.427
PaCO2 = 16 mmHg
PaO2 = 123.9 mmHg
HCO3- = 7 mEq/L
BE = -20.5
F/57. Cx ca with rectovaginal
fistula, hydronephrosis
67/M. COPD, Cor pulmomale
Lasix
Mixed acid-base disorder
• Compare AG and HCO3- :
AG > HCO3
- : coexisting MAk, RAc
AG < HCO3- : coexisting non-AG acidosis, RAk
70/M. DM, HTN
◈C.C vomiting (onset: 5 DA)
◈P.I
5년전부터 DM, HTN 으로 medication 하면서 지냄
(최근까지 insulin 은 사용하지 않고 OHA 복용함)
5일전 oral sore 발생. 물을 포함하여 거의 사하지 못함
이후 vomiting, weight loss 발생하여 응급실 통해 입원함
ABGA: 7.16-26-96-(-17.7)-9.0
Ca 8.7
Glucose 931
Cr 3.7
Protein 6.2
Albumin 3.6
Na 139, K 6.2, Cl 101, TCO2 6.5
AG = Na – ( Cl + HCO3) = 139 - (101 + 9) = 29 corrected AG = 12 - 2.5 x (4.5 – 3.6) = 10
AG acidosis (DKA) + MAk (vomiting)
AG = 29 - 10 = 19
HCO3 = 24 – 9 = 15
접수일자 접수 간 BE pH lactic acid Chloride Cr
810 17:14 -12 9.2 108 2.46
18:49 -14.1 7.2 6.5
20:12 -13 7.2 4.5
21:48 -13.1 7.25 3.3 1.85
811 0:01 -12.4 7.28 2.2
6:04 -11.3 7.33 3.6 113 2.03
12:04 -11.6 7.33 4.5
18:52 -13.1 7.31 3.8
19:47 -12.8 7.3 3.4
20:53 -11.6 7.32 2.2
22:26 -13 7.28 2.8
23:35 -11.9 7.27 1.8
812 5:29 -14.5 7.22 2.3 112 2.57
9:00 -13.4 7.26 3.1
11:13 -12.7 7.26 2.7
98/M, aspiration pneumonia
호
전
8/12
Na 139, Cl 112, TCO2 11.8 HCO3 12.0 mmEq/L Cr 2.57 mg/dL AG 15.0 mEq/L Albumin 2.0 (corrected AG: ca 7) AG = 15 - 7= 8 HCO3 = 12 AG acidosis + Non-AG acidosis (due N/S infusion)
접수일자 접수 간 BE pH lactic acid Chloride Cr NS total NS
20140810 17:14 -12 9.2 108 2.46 300
18:49 -14.1 7.2 6.5 700 1000
20:12 -13 7.2 4.5 1000 2000
21:48 -13.1 7.25 3.3 1.85 2000 4000
20140811 0:01 -12.4 7.28 2.2
6:04 -11.3 7.33 3.6 113 2.03
12:04 -11.6 7.33 4.5
18:52 -13.1 7.31 3.8 500
19:47 -12.8 7.3 3.4 500 1000
20:53 -11.6 7.32 2.2 1000 2000
22:26 -13 7.28 2.8 30 2030
23:35 -11.9 7.27 1.8 30 2060
20140812 5:29 -14.5 7.22 2.3 112 2.57 180 2240
9:00 -13.4 7.26 3.1 120 2360
11:13 -12.7 7.26 2.7
pH
0
2
4
6
8
10
lactic acid
100
105
110
115
120
125
Chloride
-16
-14
-12
-10
-8
-6
-4
-2
0
BE
0
0,5
1
1,5
2
2,5
3
Cr
Common settings associated with mixed disorder
ABG Analysis
Pre-existing disease
Acute disease
Drugs
Hb
WBC
BUN/Cr
Electrolytes
(past TCO2)
Albumin
CXR
PFT
ECG
Hb
WBC
BUN/Cr
Electrolytes
(past TCO2)
Albumin
CXR
PFT
ECG
Supplemental Info:
Vital signs
Hb
WBC
BUN/Cr
Electrolytes
(past TCO2)
Albumin
CXR
ABGA
pH
PaCO2
PaO2
BE
HCO3
ABGA
pH
PaCO2
PaO2
BE
HCO3
ABGA
pH
PaCO2
PaO2
BE
HCO3
ABGA
pH
PaCO2
PaO2
BE
HCO3
ABG
REPORT
pH
PaCO2
HCO3-
Acid Base
+ History
+ Previous ABGA/lab
pH = 7.25, PaCO2 = 70 mmHg
HCO3- = 31 mEq/L
Previous healthy, basal PaCO2 40 mm Hg
expected HCO3- = 24 + 0.1 x (70 - 40) = 27 mEq/L
Ans) Acute RAc + MAk superimposed
pH = 7.25, PaCO2 = 70 mmHg
HCO3- = 31 mEq/L
COPD, basal PaCO2 70 mm Hg
expected HCO3- = 24 + 0.35 x (70- 40)= 34.5 mEq/L
Ans) Chronic RAc + MAc superimposed
pH = 7.25, PaCO2 = 70 mmHg
HCO3- = 31 mEq/L
COPD, basal PaCO2 55 mm Hg
expected HCO3- = 24 + 0.35 x (55 - 40) + 0.1 x (70
- 55) = 29 + 1.5= 31.5 mEq/L
Ans) Acute on chronic RAc. No metabolic
component present