Presentation abg

‫‪arterial blood gases interpretation‬‬
‫)‪(ABGs‬‬

‫محمد رضا رجبی‬
‫کارشناس بیهوشی‬
‫کارشناس ارشد مراقبت های ویژه‬

‫دانشگاه علوم پزشکی تهران‬

‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫1‬

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

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.


Getting an
arterial blood
gas sample


‫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.‬


‫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.‬


‫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.‬


Ulnar Artery

Radial Artery


ABG Sample Port

Blood
Pressure
Waveform


Arterial Blood Sample Port

Can you identify potential clinical
problems with this

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]

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)

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


Evaluate pH and determine acidosis or alkalosis
7.35 7.40 7.45

Acid Normal Base
Acidosis Alkalosis


• Evaluate pCO2 (respiratory)

35 40 45

Base Normal Acid


• Evaluate HCO3 (metabolic)

22 24 26

Acid Normal Base


• 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


Blood Gas Report

Acid-Base Information
•pH
•PCO2
•HCO3
Oxygenation Information
•PO2 [oxygen tension]
•SO2 [oxygen saturation]


PaO2 [oxygen tension]
SaO2 [oxygen saturation]

a = arterial


Pulse Oximeter Measures SaO2


pH and [H +]

+] (9-pH)
[ H in nEq/L = 10


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+]).


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.


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.

 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


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 -] )


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


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.


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.


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).


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


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]


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:


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.

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
BE -30 mmol/L MV 32L

Interpretation: Partly compensated metabolic acidosis.


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
BE 17 mmol/L MV 3.75L
Interpretation: Partly compensated metabolic alkalosis with
corrected hypoxemia.

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
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

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
BE -30 mmol/L MV 48L
Interpretation: Severe partly compensated metabolic
acidosis without hypoxemia.

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

Case No. 7 cont’d
ABG result after bicarb:

pH 7.27 BP 130/80 mmHg
BE -14 mmol/L MV 13.2L


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
BE -2 mmol/L MV 7L
SaO2 98%
Hb 13 g/dL


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
BE -17 mmol/L MV 7L
SaO2 99%
Hb 7 g/dL


Case No. 8 cont’d
What is going on?


Case No. 8 cont’d
If the picture doesn’t fit, repeat ABG!!

pH 7. 45 BP 130/90 mmHg
BE -2 mmol/L MV 7L
SaO2 96%
Hb 13 g/dL
Technical error was presumed.

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
HCO3 18 mmol/L
BE -5 mmol/L MV 18L
SaO2 88%

Interpretation: Compensated metabolic acidosis with
moderate hypoxemia. Dx: PE

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
HCO3 42 mmol/L
BE +16 mmol/L MV 10L
SaO2 86%
.
Interpretation: Chronic ventilatory failure (resp. acidosis)
with uncorrected hypoxemia

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
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

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



• Clues
– Confusion, restlessness
– Headache, dizziness
– Lethargy
– Dyspnea
– Tachycardia
– Dysrhythmias
– Coma leading to death



• Solutions
– Improve ventilation
• Ensure adequate airway; positioning,
suctioning
• Encourage deep breathing and coughing
• Frequent repositioning
• Chest physio/ postural drainage
• Bronchodilators
• Decrease sedation/analgesia
• Oxygen therapy


Respiratory Alkalosis

• Excessive CO2 loss due to hyperventilation
• Causes
– CNS injury: brainstem lesions, salicylate overdose, Reye’s
Syndrome, hepatic encephalopathy
– Aggressive mechanical ventilation
– Anxiety, fear or pain
– Hypoxia
– Fever
– Congestive heart failure



• Clues
– Light headedness
– Confusion
– Decreased concentration
– Tingling fingers and toes
– Syncope
– Tetany



• Solutions
– Decrease respiratory rate and depth
• Sedation/analgesia as appropriate
• Rebreather mask
• Paper bag
• Emotional support/encourage patient to slow
breathing
• Calm, soothing environment


Metabolic Acidosis

• Excessive HCO3 loss, or acid gain
• Causes
– Diabetic ketoacidosis
– Sepsis/shock
– Diarrhea (fluid losses below gastric sphincter)
– Renal Failure
– Poison ingestion
– Starvation
– Dehydration


Metabolic Acidosis

• Clues
– Stupor
– Restlessness
– Kussmaul’s respirations )air hunger(
– Seizures
– Coma leading to death


Metabolic Acidosis

• Solutions
– Replace HCO3 while treating underlying cause
– Monitor intake and output
– Monitor electrolytes, especially K+
– Seizure precautions


Physiologic Effects of Acidosis
 Reduced cardiac contractility
 Increased PVR
 Reduced SVR
 Impaired response to catecholamines
 Compensatory hyperventilation


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


Metabolic Alkalosis

• HCO3 retention, or loss of extracellular acid,
• Causes
– GI losses above gastric sphincter
• Vomiting
• Nasogastric suction
– Antiacids
– Diuretic therapy causing electrolyte loss


Metabolic Alkalosis

• Clues
– Weakness, dizziness
– Disorientation
– Hypoventilation
– Muscle twitching
– Tetany


Metabolic Alkalosis

• Solutions
– Control vomiting
– Replace GI losses
– Eliminate overuse of antacids
– Monitor intake and output
– Monitor electrolytes


Effects of Metabolic Alkalosis
 Decreased serum potassium
 Decreased serum ionized calcium
 Dysrhythmias
 Hypoventilation / hypoxemia
 Increased bronchial tone / atelectasis
 Left shift of the Oxygen curve


‫‪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 ‫‪‬‬


‫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


‫مواردی که باعث کاهش شکاف آنیونی می شوند‬
‫‪ ‬هیپرکالمی‬
‫‪ ‬هیپوآلبومینمی‬
‫‪ ‬هیپوناترمی‬


increase the anion gap
in the absence of metabolic acidosis

 renal failure
 volume depletion
 metabolic alkalosis
 some penicillins


How to Analyze an ABG
1. PO2 NL = 80 – 100 mmHg

2. pH NL = 7.35 – 7.45
Acidotic <7.35
Alkalotic >7.45

3. PCO2 NL = 35 – 45 mmHg
Acidotic >45
Alkalotic <35

4. HCO3 NL = 22 – 26 mmol/L
Acidotic < 22
Alkalotic > 26


Four-step ABG Interpretation
Step 1:

 Examine PaO2 & SaO2

 Determine oxygen status

 Low PaO2 (<80 mmHg) & SaO2 means hypoxia

 NL/elevated oxygen means adequate oxygenation


Step 2:

 pH acidosis <7.35
alkalosis >7.45


Step 3:

 study PaCO2 & HCO 3

 respiratory irregularity if PaCO2 abnl & HCO3 NL

 metabolic irregularity if HCO3 abnl & PaCO2 NL


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.


~ 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


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.


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.


 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.


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)


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


What is the hydrogen ion concentration?

[H+] = 10 (9-pH)

= 10 (9-7.3)

= 10 (1.7)

= 50.1 nEq/L


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


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.


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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