presentation abg

arterial blood gases interpretation

(ABGs)

رضا رجبیمحمد کارشناس بیهوشی

ویژههای مراقبت ارشد کارشناس

تهرانعلوم پزشکی دانشگاه

11/2/2010 1 mohammad reza rajabi

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.


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.

شریان های براکیال،اولنار،فمورال،دورسالیس پدیس و : سایر نواحی

.تیبیا

در نوزادان می توان از شریان نافی استفاده کرد.

11/2/2010 mohammad reza rajabi 5

بزرگترین شریان در بازوست و به هنگام سوراخ کردن آن : شریان براکیال

.ممکن است به اعصاب و لیگامان های ناحیه صدمه وارد آید

.راحت و قابل لمس است و به راحتی کنترل می شود: شریان رادیال

لمس آن سخت بوده و اگر بیمار همکاری نکند به سختی می : شریان اولنا

.توان از آن خون گرفت

. شریان بزرگ و راحت در لمس و سوراخ کردن است:شریان فمورال

استفاده از آن توام با خطراتی نظیر هماتوم و .اسپاسم شریانی نادر است

.ترومبوس است

به ندرت از آنها استفاده میشود،کوچک : شریان دورسالیس پدیس و تیبیا

.هستند و هنگام خونگیری خطر تخریب گردش خون انتهایی وجود دارد


است، یک کتتر شریانی را در ABGاگر نیاز به اندازه گیری مکرر

در طول مدتی که بیمار کتتر شریانی دارد ، .شریان رادیال جایگذاری کنید

به طور (پارستزی)انتهاها را از نظر رنگ ،حرارت ،احساس گزگز شدن

.مکرر بررسی نمایید

هیچگونه تزریقی از طریق کتتر شریانی انجام نشود و این تذکر را روی

.پانسمان کتتر شریانی قید نمایید


Radial Artery

Ulnar Artery


Blood

Pressure

Waveform

ABG Sample Port


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] 11/2/2010 14 mohammad reza rajabi

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+]

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


A normal [H+] of 40

nEq/L corresponds to a

pH of 7.40. Because

the pH is a negative

logarithm of the [H+],

changes in pH are

inversely related to

changes in [H+] (e.g., a

decrease in pH is

associated with an

increase in [H+]).

pH [H+]

7.7 20

7.5 31

7.4 40

7.3 50

7.1 80

7.0 100

6.8 160



The left side of the

“H” is the

respiratory side

with the “normal”

values (35 – 45)

around the

“midline” of the

The right side of

the “H” is the

metabolic side with

the “normal”

values (22 – 26)

around 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 acidosis with corrected hypoxemia 11/2/2010 44 mohammad reza rajabi

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. 11/2/2010 51 mohammad reza rajabi

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 11/2/2010 53 mohammad reza rajabi

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 [Na+ ] – ([Cl- ] + [Hco3

- ] )

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.

سدیم،بیکربنات،کلر: کاتیون ها وآنیون های تعیین شده

پتاسیم،منیزیم،کلسیم: کاتیون های تعیین نشده

فسفات،آلبومین،سولفات،الکتات: آنیون های تعیین نشده



(هیپرکلرمی)شکاف آنیونی طبیعی

اسهال

اسیدوز توبولی کلیوی

شکاف آنیونی افزایش یافته

(نورموکلرمی)

کتواسیدوز

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.



~ PaCO2 – pH Relationship

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.


presentation abg

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