2. In a survey conducted at a university teaching hospital, 70%
of the participating physicians claimed that they were well
versed in the diagnosis of acid-base disorders and that they
needed no assistance in the interpretation of arterial blood
gases (ABGs).
These same physicians were then given a series of
ABG measurements to interpret, and they correctly
interpreted only 40% of the test samples.
11/2/2010 mohammad reza rajabi 2
3. A survey at another teaching hospital revealed that incorrect acid-
base interpretations led to errors in patient management in one-
third of the ABG samples analyzed
This can cause trouble in the ICU, where 9 of every 10 patients
may have an acid-base disorder.
11/2/2010 mohammad reza rajabi 3
4. Getting an
arterial blood
gas sample
11/2/2010 mohammad reza rajabi 4
5. شریان های مورد استفاده در نمونه گیری خون شریانی:
شریان رادیال ،شریان انتخابی جهت نمونه گیری است.
سایر نواحی: شریان های براکیال،اولنار،فمورال،دورسالیس پدیس و
تیبیا.
در نوزادان می توان از شریان نافی استفاده کرد.
0102/2/11 mohammad reza rajabi 5
6. شریان براکیال: بزرگترین شریان در بازوست و به هنگام سوراخ کردن آن
ممکن است به اعصاب و لیگامان های ناحیه صدمه وارد آید.
شریان رادیال: راحت و قابل لمس است و به راحتی کنترل می شود.
شریان اولنا: لمس آن سخت بوده و اگر بیمار همکاری نکند به سختی می
توان از آن خون گرفت.
شریان فمورال:شریان بزرگ و راحت در لمس و سوراخ کردن است.
اسپاسم شریانی نادر است.استفاده از آن توام با خطراتی نظیر هماتوم و
ترومبوس است.
شریان دورسالیس پدیس و تیبیا: به ندرت از آنها استفاده میشود،کوچک
هستند و هنگام خونگیری خطر تخریب گردش خون انتهایی وجود دارد.
0102/2/11 mohammad reza rajabi 6
7. اگر نیاز به اندازه گیری مکرر ABGاست، یک کتتر شریانی را در
شریان رادیال جایگذاری کنید.در طول مدتی که بیمار کتتر شریانی دارد ،
انتهاها را از نظر رنگ ،حرارت ،احساس گزگز شدن (پارستزی)به طور
مکرر بررسی نمایید.
هیچگونه تزریقی از طریق کتتر شریانی انجام نشود و این تذکر را روی
پانسمان کتتر شریانی قید نمایید.
0102/2/11 mohammad reza rajabi 7
14. Blood Gas Report
Acid-Base Information
pH-measures the bloods acidity
Normal range 7.35- 7.45
Overall H+ from both respiratory and metabolic factors
PCO2 partial pressure of carbon dioxide in the blood
Normal range 35-45 mmHg
Snapshot of adequacy of alveolar ventilation
•HCO3
the amount of bicarbonate in the blood
Normal range 22- 26 mEq/L
Oxygenation Information
•PO2 [oxygen tension]
•SO2 [oxygen saturation]
11/2/2010 mohammad reza rajabi 14
15. ABGs
An arterial blood gas (ABG) is a sample of arterial blood
that reports:
pH: 7.35 -7.45 (H ion concentration)
PaCO2: 35-45 mm Hg. ( ventilatory effectiveness)
HCO3: 22 to 26 mEq/L (metabolic effectiveness)
PaO2: 80-100 mm Hg (oxygenation of blood)
SaO2 = 95% - 100% (% of hemoglobin saturated)
11/2/2010 mohammad reza rajabi 15
17. Acid-Base Balance within the body
CO2 + H2O H2CO3 H+ HCO3-
Normal bicarbonate: 22 – 26 mEq/L
Normal base excess: -2 mEq/L - + 2 mEq/L
Normal Carbon Dioxide: 35 – 45 mmHg
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18. Evaluate pH and determine acidosis or alkalosis
7.35 7.40 7.45
Acid Normal Base
Acidosis Alkalosis
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19. • Evaluate pCO2 (respiratory)
35 40 45
Base Normal Acid
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20. • Evaluate HCO3 (metabolic)
22 24 26
Acid Normal Base
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21. • Determine level of oxygenation
(arterial samples only)
• Normal = 80 – 100 mmHg
• Mild hypoxemia = 60 – 80 mmHg
• Moderate hypoxemia = 40 – 60 mmHg
• Severe hypoxemia = less than 40 mmHg
11/2/2010 mohammad reza rajabi 21
22. Blood Gas Report
Acid-Base Information
•pH
•PCO2
•HCO3
Oxygenation Information
•PO2 [oxygen tension]
•SO2 [oxygen saturation]
11/2/2010 mohammad reza rajabi 22
27. pH and [H +]
+] (9-pH)
[ H in nEq/L = 10
11/2/2010 mohammad reza rajabi 27
28. A normal [H+] of 40 pH [H+]
nEq/L corresponds to a
pH of 7.40. Because 7.7 20
the pH is a negative 7.5 31
logarithm of the [H+],
7.4 40
changes in pH are
inversely related to 7.3 50
changes in [H+] (e.g., a 7.1 80
decrease in pH is 7.0 100
associated with an 6.8 160
increase in [H+]).
11/2/2010 mohammad reza rajabi 28
29. The left side of the The right side of
“H” is the the “H” is the
respiratory side metabolic side with
with the “normal” the “normal”
values (35 – 45) values (22 – 26)
around the around the
“midline” of the “midline” of the
The “midline” of the “H” is a line which runs
between the “normal” values for carbon dioxide
and bicarbonate.
11/2/2010 mohammad reza rajabi 29
30. Hydrogen Ion Regulation
The body maintains a narrow pH range by 3
mechanisms:
1. Chemical buffers (extracellular and intracellular)
react instantly to compensate for the addition or
subtraction of H+ ions.
2. CO2 elimination is controlled by the lungs
(respiratory system). Decreases (increases) in pH
result in decreases (increases) in PCO2 within
minutes.
3. HCO3- elimination is controlled by the kidneys.
Decreases (increases) in pH result in increases
(decreases) in HCO3-. It takes hours to days for
the renal system to compensate for changes in pH.
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31. Respiratory acidosis metabolic alkalosis
Respiratory alkalosis metabolic acidosis
I. Buffers kick in within minutes.
II. Respiratory compensation is rapid and starts within
minutes and complete within 24 hours.
III. Kidney compensation takes hours and up to 5 days
11/2/2010 mohammad reza rajabi 31
32. CENTRAL EQUATION OF
ACID-BASE PHYSIOLOGY
The hydrogen ion concentration [H+] in extracellular fluid is
determined by the balance between the partial pressure of
carbon dioxide (PCO2) and the concentration of bicarbonate
[HCO3-] in the fluid. This relationship is expressed as
follows:
[H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )
11/2/2010 mohammad reza rajabi 32
33. NORMAL VALUES
Using a normal arterial PCO2 of 40 mm Hg and a normal
serum [HCO3
- ] concentration of 24 mEq/L, the normal
+
[H ] in arterial blood is
24 × (40/24) = 40 nEq / L
11/2/2010 mohammad reza rajabi 33
34. PCO2/[HCO3- ] Ratio
Since [H+] = 24 x (PCO2 / [HCO3-]), the stability of the
extracellular pH is determined by the stability of the
PCO2/HCO3- ratio.
Maintaining a constant PCO2/HCO3- ratio will maintain a
constant extracellular pH.
11/2/2010 mohammad reza rajabi 34
35. PCO2/[HCO3- ] Ratio
When a primary acid-base disturbance alters one
component of the PCO2/[HCO3- ]ratio, the compensatory
response alters the other component in the same direction
to keep the PCO2/[HCO3- ] ratio constant.
11/2/2010 mohammad reza rajabi 35
36. COMPENSATORY CHANGES
When the primary disorder is metabolic (i.e., a change in
[HCO3 - ], the compensatory response is respiratory (i.e.,
a change in PCO2), and vice-versa.
It is important to emphasize that compensatory responses
limit rather than prevent changes in pH (i.e., compensation
is not synonymous with correction).
11/2/2010 mohammad reza rajabi 36
38. Renal Compensation for primary respiratory disorders
Resp.Acidosis: PaCo2
Acute 1meq/L in [Hco3-] for each 10 mmHg in PaCO2
Chronic 3meq/L in [Hco3-] for each 10 mmHg in PaCO2
Resp.Alk: PaCo2
Acute 2meq/L in [Hco3-] for each 10 mmHg in PaCO2
Chronic 5meq/L in [Hco3-] for each 10 mmHg in PaCO2
11/2/2010 mohammad reza rajabi 38
39. Respiratory Compensation for primary renal disorders
Metabolic Acidosis: [HCO3]
1.2 mmHg in PaCO2 for each meq in [HCO3]
Metabolic Alk: [HCO3]
0.7 mmHg in PaCO2 for each meq in [HCO3]
11/2/2010 mohammad reza rajabi 39
40. Mixed Acid-Base Abnormalities
Case Study No. 3:
56 yo neurologic dz required ventilator support for several
weeks. She seemed most comfortable when hyperventilated
to PaCO2 28-30 mmHg. She required daily doses of lasix to
assure adequate urine output and received 40 mmol/L IV K+
each day. On 10th day of ICU her ABG on 24% oxygen & VS:
11/2/2010 mohammad reza rajabi 40
41. ABG Results
pH 7.62 BP 115/80 mmHg
PCO2 30 mmHg Pulse 88/min
PO2 85 mmHg RR 10/min
HCO3 30 mmol/L VT 1000ml
BE 10 mmol/L MV 10L
K+ 2.5 mmol/L
Interpretation: Acute alveolar hyperventilation
(resp. alkalosis) and metabolic alkalosis with corrected
hypoxemia.
11/2/2010 mohammad reza rajabi 41
42. Case study No. 4
27 yo retarded with insulin-dependent DM arrived at ER
from the institution where he lived. On room air ABG & VS:
pH 7.15 BP 180/110 mmHg
PCO2 22 mmHg Pulse 130/min
PO2 92 mmHg RR 40/min
HCO3 9 mmol/L VT 800ml
BE -30 mmol/L MV 32L
Interpretation: Partly compensated metabolic acidosis.
11/2/2010 mohammad reza rajabi 42
43. Case study No. 5
74 yo with hx chronic renal failure and chronic diuretic therapy
was admitted to ICU comatose and severely dehydrated. On
40% oxygen her ABG & VS:
pH 7.52 BP 130/90 mmHg
PCO2 55 mmHg Pulse 120/min
PO2 92 mmHg RR 25/min
HCO3 42 mmol/L VT 150ml
BE 17 mmol/L MV 3.75L
Interpretation: Partly compensated metabolic alkalosis with
corrected hypoxemia.
11/2/2010 mohammad reza rajabi 43
44. Case study No. 6
43 yo arrives in ER 20 minutes after a MVA in which he
injured his face on the dashboard. He is agitated, has mottled,
cold and clammy skin and has obvious partial airway obstruction.
An oxygen mask at 10 L is placed on his face. ABG & VS:
pH 7.10 BP 150/110 mmHg
PCO2 60 mmHg Pulse 150/min
PO2 125 mmHg RR 45/min
HCO3 18 mmol/L VT ? ml
BE -15 mmol/L MV ?L
. Interpretation: Acute ventilatory failure (resp. acidosis) and
acute metabolic acidosisreza rajabi corrected hypoxemia
11/2/2010 mohammad
with 44
45. Case study No. 7
17 yo, 48 kg with known insulin-dependent DM came to ER
with Kussmaul breathing and irregular pulse. Room air
ABG & VS:
pH 7.05 BP 140/90 mmHg
PCO2 12 mmHg Pulse 118/min
PO2 108 mmHg RR 40/min
HCO3 5 mmol/L VT 1200ml
BE -30 mmol/L MV 48L
Interpretation: Severe partly compensated metabolic
acidosis without hypoxemia.
11/2/2010 mohammad reza rajabi 45
46. Case No. 7 cont’d
This patient is in diabetic ketoacidosis.
IV glucose and insulin were immediately administered. A
judgement was made that severe acidemia was adversely
affecting CV function and bicarb was elected to restore pH to
7.20.
Bicarb administration calculation:
Base deficit X weight (kg)
3
30 X 48 = 480 mmol/L Admin 1/2 over 15 min &
3 repeat ABG
11/2/2010 mohammad reza rajabi 46
47. Case No. 7 cont’d
ABG result after bicarb:
pH 7.27 BP 130/80 mmHg
PCO2 25 mmHg Pulse 100/min
PO2 92 mmHg RR 22/min
HCO3 11 mmol/L VT 600ml
BE -14 mmol/L MV 13.2L
11/2/2010 mohammad reza rajabi 47
48. Case study No. 8
47 yo was in PACU for 3 hours s/p cholecystectomy. She
had been on 40% oxygen and ABG & VS:
pH 7.44 BP 130/90 mmHg
PCO2 32 mmHg Pulse 95/min, regular
PO2 121 mmHg RR 20/min
HCO3 22 mmol/L VT 350ml
BE -2 mmol/L MV 7L
SaO2 98%
Hb 13 g/dL
11/2/2010 mohammad reza rajabi 48
49. Case No. 8 cont’d
Oxygen was changed to 2L N/C. 1/2 hour pt. ready to be D/C
to floor and ABG & VS:
pH 7.41 BP 130/90 mmHg
PCO2 10 mmHg Pulse 95/min, regular
PO2 148 mmHg RR 20/min
HCO3 6 mmol/L VT 350ml
BE -17 mmol/L MV 7L
SaO2 99%
Hb 7 g/dL
11/2/2010 mohammad reza rajabi 49
50. Case No. 8 cont’d
What is going on?
11/2/2010 mohammad reza rajabi 50
51. Case No. 8 cont’d
If the picture doesn’t fit, repeat ABG!!
pH 7. 45 BP 130/90 mmHg
PCO2 31 mmHg Pulse 95/min
PO2 87 mmHg RR 20/min
HCO3 22 mmol/L VT 350ml
BE -2 mmol/L MV 7L
SaO2 96%
Hb 13 g/dL
Technical error was presumed.
11/2/2010 mohammad reza rajabi 51
52. Case study No. 9
67 yo who had closed reduction of leg fx without incident.
Four days later she experienced a sudden onset of severe chest
pain . Room air ABG & VS:
pH 7.36 BP 130/90 mmHg
PCO2 33 mmHg Pulse 100/min
PO2 55 mmHg RR 25/min
HCO3 18 mmol/L
BE -5 mmol/L MV 18L
SaO2 88%
Interpretation: Compensated metabolic acidosis with
moderate hypoxemia. Dx: PE
11/2/2010 mohammad reza rajabi 52
53. Case study No. 10
76 yo with documented chronic hypercapnia secondary to
severe COPD has been in ICU for 3 days while being tx for
pneumonia. She had been stable for past 24 hours and was
transferred to general floor. Pt was on 2L oxygen & ABG &VS:
pH 7.44 BP 135/95 mmHg
PCO2 63 mmHg Pulse 110/min
PO2 52 mmHg RR 22/min
HCO3 42 mmol/L
BE +16 mmol/L MV 10L
SaO2 86%
.
Interpretation: Chronic ventilatory failure (resp. acidosis)
with uncorrected hypoxemia
11/2/2010 mohammad reza rajabi 53
54. Case No. 10 cont’d
She was placed on 3L and monitored for next hour. She
remained alert, oriented and comfortable. ABG was
repeated:
pH 7.36 BP 140/100 mmHg
PCO2 75 mmHg Pulse 105/min
PO2 65 mmHg RR 24/min
HCO3 42 mmol/L
BE +16 mmol/L MV 4.8L
SaO2 92%
.
Pt’s ventilatory pattern has changed to more rapid and
shallow breathing. Although still acceptable the pH and
CO2 are trending in the wrong direction. High-flow
oxygen may be better for this pt to prevent intubation
11/2/2010 mohammad reza rajabi 54
55. Respiratory Acidosis
• Excessive CO2 retention
• Causes
– Airway obstruction
– Depression of respiratory drive
• Sedatives, analgesics
• Head trauma
– Respiratory muscle weakness resulting from muscle disease or
chest wall abnormalities
– Decreased lung surface area participating in gas exchange
11/2/2010 mohammad reza rajabi 55
56. Respiratory Acidosis
• Clues
– Confusion, restlessness
– Headache, dizziness
– Lethargy
– Dyspnea
– Tachycardia
– Dysrhythmias
– Coma leading to death
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62. Metabolic Acidosis
• Clues
– Stupor
– Restlessness
– Kussmaul’s respirations )air hunger(
– Seizures
– Coma leading to death
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63. Metabolic Acidosis
• Solutions
– Replace HCO3 while treating underlying cause
– Monitor intake and output
– Monitor electrolytes, especially K+
– Seizure precautions
11/2/2010 mohammad reza rajabi 63
64. Physiologic Effects of Acidosis
Reduced cardiac contractility
Increased PVR
Reduced SVR
Impaired response to catecholamines
Compensatory hyperventilation
11/2/2010 mohammad reza rajabi 64
65. Manifestations usually being when serum pH goes
below 7.2
Tachycardia (until pH less than 7.0, than bradycardia)
Kussmaul’s respirations
Dysrhythmias
CNS depression
11/2/2010 mohammad reza rajabi 65
66. Metabolic Alkalosis
• HCO3 retention, or loss of extracellular acid,
• Causes
– GI losses above gastric sphincter
• Vomiting
• Nasogastric suction
– Antiacids
– Diuretic therapy causing electrolyte loss
11/2/2010 mohammad reza rajabi 66
68. Metabolic Alkalosis
• Solutions
– Control vomiting
– Replace GI losses
– Eliminate overuse of antacids
– Monitor intake and output
– Monitor electrolytes
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69. Effects of Metabolic Alkalosis
Decreased serum potassium
Decreased serum ionized calcium
Dysrhythmias
Hypoventilation / hypoxemia
Increased bronchial tone / atelectasis
Left shift of the Oxygen curve
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70. Anion Gap
) ] -3 [Na+ ] – ([Cl- ] + [Hco
difference between the concentrations of the measured
cations and the measured anion
approximately 8 to 12 mEq/L in healthy individuals
فقط بعضی از آنیون ها و کاتیون ها در آزمایشگاه تعیین می شوند.
کاتیون ها وآنیون های تعیین شده : سدیم،بیکربنات،کلر
کاتیون های تعیین نشده: پتاسیم،منیزیم،کلسیم
آنیون های تعیین نشده: فسفات،آلبومین،سولفات،الکتات
0102/2/11 mohammad reza rajabi 07
71. شکاف آنیونی طبیعی (هیپرکلرمی) شکاف آنیونی افزایش یافته
(نورموکلرمی)
اسهال
کتواسیدوز
اسیدوز توبولی کلیوی اسیدوز الکتیک
نارسایی کلیوی مزمن
سالیسیالت ها
مسمومیت با متانول
مسمومیت با اتیلن گلیکول
0102/2/11 mohammad reza rajabi 17
72. مواردی که باعث کاهش شکاف آنیونی می شوند
هیپرکالمی
هیپوآلبومینمی
هیپوناترمی
0102/2/11 mohammad reza rajabi 27
73. increase the anion gap
in the absence of metabolic acidosis
renal failure
volume depletion
metabolic alkalosis
some penicillins
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77. Four-step ABG Interpretation
Step 3:
study PaCO2 & HCO 3
respiratory irregularity if PaCO2 abnl & HCO3 NL
metabolic irregularity if HCO3 abnl & PaCO2 NL
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78. Four-step ABG Interpretation
Step 4:
Determine if there is a compensatory mechanism working
to try to correct the pH.
ie: if have primary respiratory acidosis will have increased
PaCO2 and decreased pH. Compensation occurs when
the kidneys retain HCO3.
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79. ~ PaCO – pH Relationship
2
0.08 change in PH for every 10 mmHg change in PaCO2
~ [HCO3] – pH Relationship
0.1 change in PH for every 1 meq/L change in bicarbonate
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80. Respiratory Compensation
The ventilatory control system provides the compensation
for metabolic acid-base disturbances, and the response is
prompt.
The changes in ventilation are mediated by H+ sensitive
chemoreceptors located in the carotid body (at the carotid
bifurcation in the neck) and in the lower brainstem.
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81. Respiratory Compensation
A metabolic acidosis excites the chemoreceptors and
initiates a prompt increase in ventilation and a decrease in
arterial PCO2.
A metabolic alkalosis silences the chemoreceptors and
produces a prompt decrease in ventilation and increase in
arterial PCO2.
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82. Recall that for acute respiratory disturbances (where renal
compensation does not have much time to occur) each
arterial PCO2 shift of 10 mm Hg is accompanied by a pH
shift of about 0.08, while for chronic respiratory
disturbances (where renal compensation has time to occur)
each PCO2 shift of 10 mm Hg is accompanied by a pH
shift of about 0.03.
11/2/2010 mohammad reza rajabi 82
83. CENTRAL EQUATION OF ACID-
BASE PHYSIOLOGY
The hydrogen ion concentration [H+] in extracellular fluid is determined by
the balance between the partial pressure of carbon dioxide (PCO2) and the
concentration of bicarbonate [HCO3-] in the fluid. This relationship is
expressed as follows:
[H+] in nEq/L = 24 x (PCO2 / [HCO3 -] )
where [ H+] is related to pH by [ H+] in nEq/L = 10 (9-pH)
11/2/2010 mohammad reza rajabi 83
84. Case report
Very sick 56 year old man being evaluated for a possible
double lung transplant
Dyspnea on minimal exertion
On home oxygen therapy
(nasal prongs, 2 lpm)
Numerous pulmonary medications
arterial blood gas sample is taken, revealing the following:
pH 7.30
PCO2 65 mm Hg
11/2/2010 mohammad reza rajabi 84
85. What is the hydrogen ion concentration?
[H+] = 10 (9-pH)
= 10 (9-7.3)
= 10 (1.7)
= 50.1 nEq/L
11/2/2010 mohammad reza rajabi 85
86. What is the bicarbonate ion concentration?
Remember that [H+] = 24 x (PCO2 / [HCO3 -] )
Thus,
[HCO3 -] = 24 x (PCO2 / [H+] )
[HCO3 -] = 24 x (65 / 50.1 )
[HCO3 -] = 31.1 mEq/L
11/2/2010 mohammad reza rajabi 86
87. What is the acid-base disorder?
Recall that for acute respiratory disturbances (where
renal compensation does not have much time to occur)
each arterial PCO2 shift of 10 mm Hg is accompanied
by a pH shift of about 0.08, while for chronic
respiratory disturbances (where renal compensation
has time to occur) each PCO2 shift of 10 mm Hg is
accompanied by a pH shift of about 0.03.
11/2/2010 mohammad reza rajabi 87
88. What is the acid-base disorder?
In our case an arterial PCO2 shift of 25 mm Hg (from 40 to 65
mm Hg) is accompanied by a pH shift of 0.10 units (from 7.40
to 7.30), or a 0.04 pH shift for each PCO2 shift of 10 mm. Since
0.04 is reasonably close to the expected value of 0.03 for an
chronic respiratory disturbance, it is reasonable to say that the
patient has a
CHRONIC RESPIRATORY ACIDOSIS.
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