interpretation of arterial blood gases (abg) -...

29-3-2015 W Vincken - UZ Brussel - VUB 1

Interpretation ofArterial Blood Gases (ABG)

Prof. Dr. W. VinckenHead Respiratory Division

Universitair Ziekenhuis Brussel (UZ Brussel)

Vrije Universiteit Brussel (VUB)


ABG: puncture

Patient

At rest for 5-15’

Minimize anxiety/pain (hyperventilation)

A. radialis puncture at non-dominant side

Allen test

Strictly aseptic


ABG: puncture

Syringe

Glass > plastic (gas-permeable)

Polypropylene > polystyrol

Dry heparin

Max 5% of sample volume

Draw blood slowly up (avoid hemolysis)


ABG: puncture

Remove air bubbles before mixing/cooling

Mix sample thoroughly turn 5 x up and down slowly

and roll horizontally for 5’’

Immediate transport (within 10’)

If not: Store at 0-4°C in icewater

Do not store directly on ice (hemolysis)


Before interpretation of ABG

Make/take note of

FIO2: room air (0.21) or under O2 therapy

Body posture: sitting or supine

At rest or during exercise


ABG: parameters

Parameters of oxygenation

PaO2

SaO2

PA-aO2


ABG: parameters


PaO2

SaO2

PA-aO2

Parameters of

alveolar ventilation and acid-base status

PaCO2

pH

[HCO3-]

Base Excess (BE)


ABG: normal values


PaO2 100 mmHg* [105 – (age/3)]

SaO2 > 97 %

PA-aO2 <10 mmHg (up to 20 mmHg in elderly)

*7.5 mmHg = 1 kPa


ABG: normal values

Parameters of alveolar ventilation and acid-base status

PaCO2 40 mmHg (35 – 45 mmHg)

pH 7.4 (7.35 – 7.45)

[HCO3-] 24 mMol/L

Base Excess (BE) 0 mMol/L


Abnormal ABG: hyperoxemia

High PaO2

No pathophysiological substrate

(except mild hyperoxemia in extreme alveolar hyperventilation)

Usually indicates

sampling error (air in blood sample) or

high FIO2 (oxygen administration)


Abnormal ABG: hypoxemia

Low PaO2

Desaturation : low SaO2

Hypoxemia

calculate PA-aO2

Hypoxemia with

PA-aO2

= respiratory failure type I

= oxygenation (lung) failure

Hypoxemia with normal PA-aO2

= respiratory failure type II

= ventilatory (pump) failure



Hypoxemia: calculate theAlveolo-arterial PO2 gradient

PAO2 is calculated using the alveolar gas equation PAO2 = PIO2 – [PACO2 / R]

PAO2 = [(Pb- PH2O) x FIO2] – [PaCO2 / 0.8]

PAO2 = [(760 - 47) x 0.21] – [PaCO2 x 1.25]

PAO2 = 149 – [PaCO2 x 1.25]

PaO2 and PaCO2 are measured (ABG)

PA-aO2 (mmHg) = PAO2 - PaO2

Normal PA-aO2 < 5 – 10 mmHg (up to 20 mmHg in elderly)


Hypoxemia: 3 main causes

(1) Reduced PAO2

(2) Increased PA-aO2

(3) Reduced PvO2

PA-aO2 = PAO2 – PaO2

PaO2 = PAO2 – PA-aO2


Hypoxemia (1):due to reduced PAO2*

Reduced PIO2

Reduced Pb: high altitude

Reduced FIO2: inhalation of hypoxic gas mixtures

Increased PACO2 = hypercapnia =

Ventilatory failure or Type II Respiratory Failure


PAO2 = PIO2 – [PACO2 / R]

PAO2 = [( Pb- PH2O) x FIO2] – [PACO2 / R]

* and normal PA-aO2


Hypoxemia (2):due to increased PA-aO2

= Failure of the lung as a gas exchanger

= Intrapulmonary mechanism/cause of hypoxemia

= Oxygenation failure or Type I Respiratory Failure


Ventilation/perfusion mismatchDiffusion limitationRightLeft shunt


Hypoxemia (2):Oxygenation failure

Ventilation/Perfusion mismatch(R>L shunt-like effect of regions with low V/Q ratio)

obstructive lung diseases (COPD, asthma, …)

parenchymal lung disease (pneumonia, atelectasis, ILD, …)

vascular lung disease


Diffusion limitation

(with exercise and reduced transit time of RBCs in pulmonary capillaries)

increased thickness of alveolocapillary membrane Interstitial lung diseases

reduced surface area of alveolocapillary membrane Emphysema



Anatomic RL shunt(leads to refractory hypoxemia)

intracardiac (ASD, VSD, …)

intrapulmonary (A-V malformations, fistulas)



Hypoxemia: consequences (1)

Desaturation → central cyanosis

Chemoreceptor stimulation ↑ Central respiratory drive

↑ Output respiratory muscles

↑ VE and ↑ WOB : dyspnea

↑ VA and hypocapnia & respiratory alkalosis


Hypoxemia: consequences (2)

Tissue hypoxia organ disfunction: CNS, CV, kidneys

anaerobic metabolism → lactic acidosis

Pulmonary vasoconstriction pulmonary hypertension

cor pulmonale & right heart failure

Increased renal erythropoetin production secondary polycythemia


Abnormal ABG: hypercapnia

High PaCO2 (> 45 mmHg)

Respiratory acidosis : low pH (< 7.35)

pH = pK + log [HCO3-] / 0.03 x PCO2


Hypercapnia: 4 main causes

(1) Increased VCO2

(2) Reduced VA (reduced VE and normal VD)

(3) Increased VD

(4) Severe V/Q mismatching

PaCO2 = VCO2 / VAVCO2 = CO2 production

VA = alveolar ventilation = VE - VD


Hypercapnia (1): increased VCO2

Exercise with extreme effort

Fever and other hypermetabolic states in patients unable to increase VE and VA , e.g., mechanically ventilated patient

PaCO2 = VCO2 / VA


Hypercapnia (2): reduced VA

Reduced VA = alveolar hypoventilation =Ventilatory failure or Type II respiratory failure

Any hypoxemia is secondary to hypercapnia,

i.e., the PA-aO2 is normal

Extrapulmonary mechanism/cause of hypoxemia:

Severe UAO

Failure of the ventilatory pump

PaCO2 = VCO2 / VA


Reduced respiratory drive (central controller)

CNS disorders

Drug (illicit or not) overdose

Metabolic disorders

Obesity-hypoventilation syndrome (Pickwick syndrome)

Central alveolar hypoventilation (Ondine’s curse, …)

Hypercapnia (2):Failure of the ventilatory pump (a)


Dysfunction of respiratory neuromuscular apparatus

Motor neurons (ALS, poliomyelitis, …)

Peripheral nerve (Guillain-Barré, phrenic neuropathy, …)

Myoneural junction (myastenia, drugs, …)

Muscle (myopathy, metabolic disorders, malnutrition, …)

Hypercapnia (2):Failure of the ventilatory pump (b)


Chest wall disorders including severe obesity

Kyphoscoliosis

TBC sequellae incl. thoracoplasty

Severe obesity

Hypercapnia (2):Failure of the ventilatory pump (c)


Hypercapnia: consequences Hypoxemia with normal PA-aO2

PaO2 decreases with 1.25 mmHg/mmHg PaCO2 increase

Respiratory acidosis: reduced pH

If persistent:

HCO3- retention by the kidneys

increased [HCO3-] and positive BE

the reduced pH will increase towards 7.4 (normal) but not overshoot it

Compensatory metabolic alkalosis Acutely, Δ HCO3

- = 0.1 x Δ PaCO2

Chronically, Δ HCO3- = 0.35 x Δ PaCO2


pH = pK + log [ HCO3-] / 0.03 x PCO2


Clinical signs of hypercapnia

CNS: cerebral vasodilatation increased cerebral Q

intracranial hypertension

headache, papilledema

asterixis

lethargy, confusion progressing to coma ‘carbonarcosis’

Peripheral vasodilatation full bounding pulses with

warm, cherry-red skin


Abnormal ABG: hypocapnia

Low PaCO2 (< 35 mmHg)

Respiratory alkalosis: high pH (> 7.45)



Hypocapnia: 1 main mechanism

Increased VA = alveolar hyperventilation

PaCO2 = VCO2 / VA


Hypocapnia ~ alveolar hyperventilation: causes

Stimulation of chemoreceptors Hypoxemia

Metabolic acidosis

Pulmonary J-receptor stimulation Interstitial/parenchymal lung diseases

Tissue hypoxia Anemia, CO- , sulf- or metHb

Sepsis, hypotension, shock (also stimulation of baroreceptors)

Fever, thyrotoxicosis, strenuous exercise

Psychogenic : hyperventilation syndrome = diagnosis of exclusion


Hypocapnia: consequences

Respiratory alkalosis: increased pH

If persistent: HCO3

- excretion by the kidneys

reduced [HCO3-] and negative BE (= base deficit)

increased pH will decrease towards (but not below) 7.4

Compensatory metabolic acidosis Acutely, Δ HCO3

- = 0.2 x Δ PaCO2



pH = pK + log [ HCO3-] / 0.03 x PCO2


Abnormal ABG: acid-base disorders

Acidosis: low pH

Respiratory

Metabolic

Alkalosis: high pH

Respiratory

Metabolic


Metabolic acidosis

pH due to HCO3- and negative BE (base deficit), due to

Acid [H+] accumulation (and buffering by HCO3-)

renal failure

diabetes mellitus: ketoacidosis

tissue hypoxia/hypoperfusion (shock): lactic acidosis

intoxications: ASA, antifreeze, methanol, paraldehyde

Loss of HCO3-

diarrhea

pH = pK + log [ HCO3-] / 0.03 x PCO2


Metabolic acidosis

If persistent, the pH (hence increase in [H+]) leads to:

chemoreceptor stimulation

increased central respiratory drive

increased VE and VA: hyperventilation

hypocapnia

the low pH rises towards normal (not exceeding 7.4)

“compensatory respiratory alkalosis”

Δ PaCO2 = 1 à 1.3 x Δ HCO3-

pH = pK + log [ HCO3-] / 0.03 x PCO2

pH = pK + log [ HCO3-] / 0.03 x PCO2


Metabolic alkalosis

pH due to HCO3- and positive BE, due to

HCO3- accumulation

Excessive ingestion of alkali

Drug intake: diuretics, corticosteroids

Cushing syndrome

Hypokalemia

Loss of acid

Loss of gastric acid: prolonged vomiting, nasogastric suction

Via kidneys

pH = pK + log [ HCO3-] / 0.03 x PCO2


Metabolic alkalosis

If persistent, the pH (hence reduction in [H+]) leads to:

reduced chemoreceptor stimulation

reduced central respiratory drive

reduced VE and VA: hypoventilation

hypercapnia

the increased pH will decrease towards normal (but not below 7.4)

“compensatory respiratory acidosis”

Δ PaCO2 = 0.6 x Δ HCO3-

pH = pK + log [ HCO3-] / 0.03 x PCO2

pH = pK + log [ HCO3-] / 0.03 x PCO2


Arterial Blood Gases : main use

Note sampling conditions

Careful sampling and handling

Detection of Respiratory Failure

Detection of Acid-Base disturbances


Interpretation of ABG

Oxygenation

Look at PaO2 and SaO2

Calculate PA-aO2

Alveolar ventilation

Look at PaCO2

Acid-Base status

Look at pH, HCO3- and BE


Thank you for listeningHope you learned something,

or at least enjoyed it

Prof. Dr. W. Vincken

Head Respiratory Division

UZ Brussel, VUB


Interpretation of ABG

10 examples


Interpretation of ABG : example 1

PaO2 mmHg 69

SaO2 % 91

PA-aO2 mmHg calculate

PaCO2 mmHg 60

pH 7.2

HCO3- mEq/L 24

BE mEq/L 0



PaO2 mmHg 69

SaO2 % 91

PA-aO2 mmHg 149 – 60x1.25 – 69 = 5

PaCO2 mmHg 60

pH 7.2

HCO3- mEq/L 24

BE mEq/L 0



PaO2 mmHg 69 Hypoxemia

SaO2 % 91 Desaturation

PA-aO2 mmHg 5 Normal

PaCO2 mmHg 60

pH 7.2

HCO3- mEq/L 24

BE mEq/L 0



Oxygenation

Reduced PaO2 and SaO2 69/91%

= mild hypoxemia and arterial desaturation

Normal PA-aO2 5

= hypoxemia is due to

Ventilatory failure = Failure of the respiratory air pump, or

Reduced PAO2 , or

Reduced PvO2






PaCO2 mmHg 60 Hypercapnia

pH 7.2 Acidosis

HCO3- mEq/L 24 Normal

BE mEq/L 0 Normal





PA-aO2 mmHg 5 Normal Type II RF

PaCO2 mmHg 60 Hypercapnia Respiratory

pH 7.2 Acidosis Acidosis

HCO3- mEq/L 24 Normal Acute

BE mEq/L 0 Normal



PaO2 mmHg 69

SaO2 % 91


PaCO2 mmHg 60

pH 7.37

HCO3- mEq/L 34

BE mEq/L + 10



PaO2 mmHg 69

SaO2 % 91

PA-aO2 mmHg 149 – 60x1.25 – 69 = 5

PaCO2 mmHg 60

pH 7.37

HCO3- mEq/L 34

BE mEq/L + 10






PaCO2 mmHg 60

pH 7.37

HCO3- mEq/L 34

BE mEq/L + 10







pH 7.37 Minimal acidosis

HCO3- mEq/L 34 Increased

BE mEq/L + 10 Positive


Interpretation of ABG : example 2PaO2 mmHg 69 Hypoxemia


PA-aO2 mmHg 5 Normal Type II RF

PaCO2 mmHg 60 Hypercapnia Respiratory

pH 7.37 Minimal acidosis Acidosis

HCO3- mEq/L 34 Increased Chronic

BE mEq/L + 10 Positive Compensatory

metabolic

alkalosis



PaO2 mmHg 99

SaO2 % 98


PaCO2 mmHg 30

pH 7.50

HCO3- mEq/L 24

BE mEq/L 0



PaO2 mmHg 99

SaO2 % 98

PA-aO2 mmHg 149 – 30x1.25 – 99 = 12.5

PaCO2 mmHg 30

pH 7.50

HCO3- mEq/L 24

BE mEq/L 0



PaO2 mmHg 99 Normal

SaO2 % 98 Normal

PA-aO2 mmHg 12.5 Normal

PaCO2 mmHg 30 Hypocapnia

pH 7.50 Alkalosis


BE mEq/L 0 Normal



PaO2 mmHg 99 Normal

SaO2 % 98 Normal


PaCO2 mmHg 30 Hypocapnia Respiratory

pH 7.50 Alkalosis Alkalosis


BE mEq/L 0 Normal



PaO2 mmHg 99

SaO2 % 98

PA-aO2 mmHg 12.5

PaCO2 mmHg 30

pH 7.42

HCO3- mEq/L 20

BE mEq/L - 4



PaO2 mmHg 99 Normal

SaO2 % 98 Normal


PaCO2 mmHg 30

pH 7.42

HCO3- mEq/L 20

BE mEq/L - 4



PaO2 mmHg 99 Normal

SaO2 % 98 Normal



pH 7.42 Minimal alkalosis

HCO3- mEq/L 20 Reduced

BE mEq/L - 4 Negative


Interpretation of ABG : example 4PaO2 mmHg 99 Normal

SaO2 % 98 Normal



pH 7.42 Minimal alkalosis Alkalosis

HCO3- mEq/L 20 Reduced Chronic

BE mEq/L - 4 Negative Compensatory

metabolic

acidosis



PaO2 mmHg 60

SaO2 % 88


PaCO2 mmHg 32

pH 7.49

HCO3- mEq/L 24

BE mEq/L 0



PaO2 mmHg 60

SaO2 % 88

PA-aO2 mmHg 149 – 32x1.25 – 60 = 49

PaCO2 mmHg 32

pH 7.49

HCO3- mEq/L 24

BE mEq/L 0





PA-aO2 mmHg 49 Increased

PaCO2 mmHg 32

pH 7.49

HCO3- mEq/L 24

BE mEq/L 0



Oxygenation reduced PaO2 and SaO2 60/88%

= hypoxemia and arterial desaturation

Increased PA-aO2 49 = hypoxemia is due to

Oxygenation failure

Failure of the lung as a gas exchanger

Intrapulmonary disease

Ventilation/perfusion mismatch

Diffusion limitation

Right>Left shunt







pH 7.49 Alkalosis


BE mEq/L 0 Normal





PA-aO2 mmHg 49 Increased Type I RF




BE mEq/L 0 Normal



PaO2 mmHg 60

SaO2 % 88

PA-aO2 mmHg 49

PaCO2 mmHg 32

pH 7.42

HCO3- mEq/L 18

BE mEq/L - 6






PaCO2 mmHg 32

pH 7.42

HCO3- mEq/L 18

BE mEq/L - 6


Interpretation of ABG : example 6PaO2 mmHg 60 Hypoxemia





HCO3- mEq/L 18 Reduced Chronic

BE mEq/L - 6 Negative Compensatory

Metabolic

acidosis



PaO2 mmHg 92

SaO2 % 94


PaCO2 mmHg 40

pH 7.27

HCO3- mEq/L 16

BE mEq/L - 7



PaO2 mmHg 92

SaO2 % 94

PA-aO2 mmHg 149 – 40x1.25 – 92 = 7

PaCO2 mmHg 40

pH 7.27

HCO3- mEq/L 16

BE mEq/L - 7



PaO2 mmHg 92 Normoxemia

SaO2 % 94 Normal


PaCO2 mmHg 40

pH 7.27

HCO3- mEq/L 16

BE mEq/L - 7




SaO2 % 94 Normal


PaCO2 mmHg 40 Normocapnia

pH 7.27 Acidosis






SaO2 % 94 Normal


PaCO2 mmHg 40 Normocapnia Acute

pH 7.27 Acidosis Acidosis

HCO3- mEq/L 16 Reduced Metaboli

c




PaO2 mmHg 100

SaO2 % 97


PaCO2 mmHg 30

pH 7.37

HCO3- mEq/L 16

BE mEq/L - 7



PaO2 mmHg 100

SaO2 % 97

PA-aO2 mmHg 149 – 30x1.25 – 100 = 12

PaCO2 mmHg 30

pH 7.37

HCO3- mEq/L 16

BE mEq/L - 7




SaO2 % 97 Normal


PaCO2 mmHg 30

pH 7.37

HCO3- mEq/L 16

BE mEq/L - 7




SaO2 % 97 Normal



pH 7.37 Minimal acidosis




Interpretation of ABG : example 8PaO2 mmHg 100 Normoxemia

SaO2 % 97 Normal


PaCO2 mmHg 30 Hypocapnia Compensatory

Respiratory

alkalosis

pH 7.37 Minimal acidosis Acidosis

HCO3- mEq/L 16 Reduced Metabolic




PaO2 mmHg 95

SaO2 % 96


PaCO2 mmHg 40

pH 7.50

HCO3- mEq/L 32

BE mEq/L + 8



PaO2 mmHg 95

SaO2 % 96

PA-aO2 mmHg 149 – 40x1.25 – 95 = 4

PaCO2 mmHg 40

pH 7.50

HCO3- mEq/L 32

BE mEq/L + 8




SaO2 % 96 Normal


PaCO2 mmHg 40

pH 7.50

HCO3- mEq/L 32

BE mEq/L + 8




SaO2 % 96 Normal


PaCO2 mmHg 40 Normocapnia

pH 7.50 Alkalosis






SaO2 % 96 Normal


PaCO2 mmHg 40 Normocapnia Acute


HCO3- mEq/L 32 Increased Metabolic




PaO2 mmHg 83

SaO2 % 91


PaCO2 mmHg 50

pH 7.43

HCO3- mEq/L 32

BE mEq/L + 8



PaO2 mmHg 83

SaO2 % 91

PA-aO2 mmHg 149 – 50x1.25 – 83 = 4

PaCO2 mmHg 50

pH 7.43

HCO3- mEq/L 32

BE mEq/L + 8




SaO2 % 91 Borderline


PaCO2 mmHg 50

pH 7.43

HCO3- mEq/L 32

BE mEq/L + 8


Interpretation of ABG : example 10PaO2 mmHg 83 Normoxemia



PaCO2 mmHg 50 Hypercapnia Compensatory

Respiratory

acidosis


HCO3- mEq/L 32 Increased Metabolic



Definition of Respiratory Failure

Abnormal Arterial Blood Gases

Hypoxemia with PaO2 < 60 mmHg

without or with

Hypercapnia with PaCO2 > 50 mmHg

Without ABGs No Diagnosis of RF


Classification of Respiratory Failure According to type of onset/duration

Acute Respiratory Failure

Chronic Respiratory Failure

Acute on Chronic Respiratory Failure


Classification of Respiratory Failure According to type of ABG abnormality

Respiratory Failure Type I Hypoxemia with (due to) increased PA-aO2

Normocapnia or hypocapnia

Respiratory Failure Type II Hypoxemia with (due to) hypercapnia

Normal PA-aO2


Type I RF ~ Oxygenation Failure Failure of the lung as a gas exchanger (O2 and CO2)

Increased PA-aO2

Type II RF ~ Ventilatory Failure Failure of the respiratory system as an air pump

Normal PA-aO2

Mixed Failure

Classification of Respiratory Failure According to type of ABG abnormality


Oxygenation Failure

Reduced PaO2 (hypoxemia)

Increased PA-aO2

Reduced PaCO2 (hypocapnia)

Increased pH (respiratory alkalosis)

If persistent: compensatory metabolic acidosis (renal bicarbonate excretion) Acutely, Δ HCO3

- = 0.2 x Δ PaCO2



Oxygenation Failure

Abnormal Chest X-Ray

Diffuse pulmonary diseases

Localised pulmonary diseases

Normal Chest X-Ray

Anatomic R>L shunts

Asthma (except for hyperinflation)

Pulmonary embolism/vascular disease


Ventilatory Failure

Increased PaCO2 (hypercapnia)

Reduced pH (respiratory acidosis)

Reduced PaO2 (pro rata hypoxemia)

Normal PA-aO2

If persistent: compensatory metabolic alkalosis (renal bicarbonate retention) Acutely, Δ HCO3

- = 0.1 x Δ PaCO2



Classification of Respiratory Failure

Type I Type II

Acute Hypoxemia with

increased PA-aO2

Hypocapnia

Respiratory alkalosis

Hypoxemia with

normal PA-aO2

Hypercapnia

Respiratory acidosis

Chronic Hypoxemia

Hypocapnia

Compensated respiratory alkalosis

Due to HCO3- excretion

and metabolic acidosis

Hypoxemia

Hypercapnia

Compensated respiratory acidosis

Due to HCO3- retention

and metabolic alkalosis


Classification of Respiratory Failure

Type I Type II

Acute PaO2

PA-aO2

PaCO2

pH

Low

High

Low

High

Low

Normal

High

Low

Chronic PaO2

PA-aO2

PaCO2

pH

HCO3-

BE

Low

High

Low

High normal

Low

negative

Low

Normal

High

Low normal

High

positive


Thank you for listeningHope you learned something,

or at least enjoyed it

Prof. Dr. W. Vincken

Head Respiratory Division

UZ Brussel, VUB

interpretation of arterial blood gases (abg) -...

Documents