abg interpretation

Overview.

Indications of ABG.

Contraindication.

Parameters and reference ranges.

Other useful information from arterial blood gases.

Factors influencing blood gas results.

Primary acid-base disturbances.

Mixed acid–base disorders

Interpretation of ABG.

An arterial blood gas (ABG) test measures the

acidity (pH) and the levels of oxygen and carbon

dioxide in the blood from an artery.

Blood may be collected from one of the following

arteries:

•Radial artery in the wrist

•Femoral artery in the groin

•Brachial artery in the arm

ABGs provide the following information:

•Oxygenation

•Adequacy of ventilation

•Acid-base levels

Respiratory failure - in acute and chronic states.

Any severe illness which may lead to a metabolic

acidosis - for example:

Cardiac failure.

Liver failure.

Renal failure.

Hyperglycaemic states associated with diabetes

mellitus.

Multiorgan failure.

Sepsis.

Burns.

Poisons/toxins.

Ventilated patients.

Sleep studies

An abnormal modified Allen test (Assessment of collateral

circulation).

Local infection or distorted anatomy at the potential

puncture site (eg, from previous surgical interventions,

congenital or acquired malformations, or burns).

The presence of arteriovenous fistulas or vascular grafts.

Known or suspected severe peripheral vascular disease of

the limb involved.

severe coagulopathy.

Anticoagulation therapy with warfarin, heparin and

derivatives, aspirin is not a contraindication for arterial

vascular sampling in most cases.

Use of thrombolytic agents, such as streptokinase or tissue

plasminogen activator.

digital occlusion of

radial and ulnar

artery

clenching of hand

About 30 sec

ulnar artery

occlusion released.

The test is then

repeated, but this

time the radial

artery is released

while the ulnar

artery remains

compressed .

Positive Modified Allen Test (Normal) :

if the hands flushing within 5-15 sec it indicate that the ulnar artery

has good blood flow.

Negative Modified Allen Test (Abnormal):

if the hands does not flushing within 5-15 sec it indicate that the

ulnar circulation is inadequate , in this situation the radial artery

supplying arterial blood to that hand should not be punctured.

Analyte arterial blood gases venous blood gases

pH 7.35 - 7.45 7.32 – 7.43

PaCO2 35-45 mmHg

4.7- 6.0 kPa

41 – 50 mmHg

PaO2 75-100 mmHg

11-13 kPa

25 – 40 mmHg

Base excess

(BE)

−2 to +2 mmol/L

total CO2

(tCO2 )

23-30 mmol/L

100-132 mg/Dl

HCO3 22–26 mEq/L 23 – 27 mmol/L

The venous oxygen is lower than

the arterial oxygen. The PCO2 will

be higher in venous than arterial

blood.

Arterial blood is bright red colour,

but venous blood is dark maroon in

colour.

Arterial blood gases more painful

and have more complication.

Notes :

age and altitude dependent

Kilopascals: to convert pressures to kPa, divide

mmHg by 7.5

mmHg change in PaCO2 above or below 40 mmHg

results in 0.008 unit change in pH in the opposite

direction

change in [HCO3-] of 10 mEq/L will result in a

change in pH of approximately 0.15 pH units in the

same direction

The Base Excess

The metabolic component of the acid–base balance is

reflected in the base excess.

This is a calculated value derived from blood pH and

PaCO2.

It is defined as the amount of acid required to

restore a litre of blood to its normal pH at a PaCO2 of 40

mmHg.

The base excess increases in metabolic alkalosis and

decreases (or becomes more negative) in metabolic

acidosis.

While the base excess may give some idea of the metabolic

nature of a disorder,

InterpretationBEPaCo2pH

Acidemia

<7.35

High

(>45)

Positive

(>+2)

1ry respiratory acidosis with renal compensation

Normal

(-2-+2)1ry respiratory acidosis

Negative

(<-2)

Mixed respiratory and metabolic acidosis

Normal

(35-45)

Negative

(<-2)Primary metabolic acidosis

Low

(<35)

Negative

(<-2)

Primary metabolic acidosis with respiratory

compensation

InterpretationBEPaCo2pH

Alkalemia>7.35

High

(>45)

Positive

(>+2)

1ry metabolic alkalosis with respiratory compensation

Normal

(35-45)

Positive

(>+2)

Primary metabolic alkalosis

Low

(<35)

Positive

(>+2)

mixed respiratory and metabolic alkalosis

Normal

(-2-+2)

Primary respiratory alkalosis

Negative

(<-2)

Primary respiratory alkalosis with renal

compensation

Alveolar-arterial oxygen gradient :

is a measure of the difference between the alveolar

concentration of oxygen (A) and the arterial

concentration of oxygen(a) .

It is used in diagnosing the source of hypoxemia

The alveolar–arterial oxygen gradient :

P(A–a)O2 = PAO2 – PaO2

PaO2 = arterial oxygen tension

PAO2 = alveolar oxygen tension

PAO2 = FiO2(PB – PH2O) – (PaCO2 / 0.8)

FiO2 = fraction of inspired oxygen

PB = barometric pressure (760 mmHg at sea level)

PH2O = water vapour pressure (47 mmHg at 37° C)

*R = Respiratory quotient = 0.8 (usual)

Normal value <15 mmHg

Estimating A-a gradient:

Normal A-a gradient = (Age+10) / 4

A-a increases 5 to 7 mmHg for every 10% increase

in FiO2

Hypoxia

V/Q Mismatch

Hypoventilation

Shunting

Low Fi02

Hypoxia (PaO2)< 95 mm Hg

A-a gradient A-a gradient

> 15 mmHg < 15 mmHg

(Lung disease) (Normal lungs)

*(V/Q) imbalance High PaCO2 Low PaCO2

* Shunting

* Hypoventilation * Low FiO2

Give 100% O2

PaO2 does not improve

* Shunt

PaO2 increases :

* V/Q imbalance

Anion gap :

The anion gap is the difference between primary

measured cations (sodium Na+ and potassium

K+) and the primary measured anions (chloride

Cl- and bicarbonate HCO3-) in serum.

Its used to identify the cause of metabolic

acidosis

Calculation:

With potassium :

= ([Na+] + [K+]) − ([Cl−] + [HCO3−])

Without potassium (daily practice):

= Na+ − (Cl- + HCO3−)

The reference range of the anion gap is 3-11 mEq/L

Delayed processing of the sample may yield a falsely low

PaO2, as the delay allows leucocytes to consume oxygen.

This can be avoided by prompt transport of the sample on

ice.

Air bubbles introduced when performing the arterial

puncture can also cause a falsely high PaO2 and a

falsely low PaCO2.

This can be avoided by gently removing air bubbles within

the specimen immediately after collection without agitating

the sample.

Body temperature can also affect arterial blood gas

tensions.

This is relevant in febrile or hypothermic patients, so

body temperature should be recorded at the time of

collection.

pH

7.35 – 7.45

Acidosis

<7.35

Metabolic

Hco3 <24

Respiratory

Pco2 >40

Alkalosis

> 7.45

Metabolic

Hco3 >24

Respiratory

Pco2 < 40

Metabolic : change in HCO3 and pH in the same

direction .

Respiratory : change in HCO3 and pH in the opposie

direction .

.

One Way To Remember This Relationship Is To Use The

Acronym ROME :

Respiratory Opposite Metabolic Equal

Respiratory acidosis is a medical emergency in which

decreased ventilation (hypoventilation) causes increased

blood carbon dioxide concentration and decreased pH.

Types of Respiratory Acidosis :

acute respiratory acidosis :

the PaCO2 is elevated above the upper limit of the reference range

(over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH

<7.36).

chronic respiratory acidosis:

the PaCO2 is elevated above the upper limit of the reference range,

with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to

renal compensation and an elevated serum bicarbonate (HCO3−

>30 mm Hg).

Causes of Respiratory Acidosis :

Respiratory centre depression (↓RR ).

• drugs (anaesthesia, sedative, narcotics )

• Trauma

• Increasing ICP

• Stroke

• Encephalitis

• Central apnea

• Supplemental O2 in chronic Co2 retention (i.e COPD)


Neuromascular disorders (↓TV ):

• Myasthenia gravis

• Gullain-Barre syndrome

• Poliomyelitis

• Muscular dystrophies

• Myopathies

• Chest wall disease (obesity, kyphoscoliosis )


Airway obstruction (↓FEV ).

Mechanical hypoventilation (inadequate mechanical

ventilation).

Symptoms of Respiratory Acidosis

Treatment of Respiratory Acidosis

Treatment is aimed at the underlying disease, and

may include:

• Bronchodilator drugs to reverse some types of airway

obstruction

• Noninvasive positive-pressure ventilation (sometimes

called CPAP or BiPAP) or a breathing machine, if

needed

• Oxygen if the blood oxygen level is low

• Treatment to stop smoking

Respiratory alkalosis is a condition marked by low levels

of carbon dioxide in the blood due to breathing

excessively

Types of respiratory alkalosis

Acute respiratory alkalosis:occurs rapidly. For every 10 mmHg drop in PCO2 in arterial

blood, there is a corresponding 2 mEq/L drop in bicarbonate ion due

to acute compensation. During acute respiratory alkalosis, the person

may lose consciousness where the rate of ventilation will resume to

normal.

Chronic respiratory alkalosis:

is a more long-standing condition. For every 10 mmHg drop in

PCO2 in arterial blood, there is a corresponding 5 mEq/L drop in

bicarbonate ion. The drop of 5 mEq/L of bicarbonate ion is a

compensation effect which reduces the alkalosis effect of the drop in

PCO2 in blood. This is termed metabolic compensation.

Causes of Respiratory Alkalosis :

Respiratory centre stimulation :

• CNS disorders

• Hepatic failure

• Gram negative sepsis

• Drugs (theophylline, catecholamine, psychotropic )

• Pregnancy

• Anxiety

• Pain

Mechanical hyperventilation (excessive mechanical

ventilation)

Causes of Respiratory Alkalosis :

Hypoxemia:

• Pulmonary disease (pneumonia, oedema, PE, ILD)

• Sever anaemia

• Heart failure

• High altitude

Symptoms of Respiratory Alkalosis

Treatment of Respiratory Alkalosis :

Treatment is aimed at the condition that causes

respiratory alkalosis.

Breathing into a paper bag -- or using a mask that

causes you to re-breathe carbon dioxide -- sometimes

helps reduce symptoms.

metabolic acidosis is a condition that occurs when the body produces

excessive quantities of acid or when the kidneys are not removing enough

acid from the body

blood pH is low (less than 7.35) due to increased production of hydrogen ions

by the body or the inability of the body to form bicarbonate (HCO3-) in the

kidney

Raised anion gap Normal anion gap

(hyperchloraemia)

Accumulation of acids :

•Ketoacids in diabetic

ketoacidosis (DKA).

•Lactic acid, eg shock, infection.

•Drugs/toxins, eg salicylates,

ethylene glycol, methanol,

paracetamol

• chronic renal failure

(accumulation of sulfates,

phosphates, urea

Loss of bicarbonate or ingestion

of acid :

•Gastrointestinal tract (GIT)

causes, eg longstanding

diarrhoea, pancreatic fistula.

•Renal tubular acidosis.

•Addison's disease.

•Drugs, eg carbonic anhydrase

inhibitors.

Symptoms of Metabolic Acidosis

Management of Metabolic Acidosis

General measures:

Put the patient in the resuscitation area, or transfer to a high-

dependency area as soon as feasible.

Put the patient on an ECG monitor, SaO2 monitor and BP/HR

monitor.

In patients who are clinically unwell and have deteriorating SaO2

levels or conscious levels, consider intubation and assisted

ventilation, after taking senior A&E/medical/anaesthetic advice.

Get large-bore IV access (a central venous line may be needed) and

rehydrate aggressively. Use colloids if necessary.


Consider catheterisation to monitor urine output and obtain urine for

analysis.

If there is any possibility of drug or toxin ingestion, give initial

therapies such as activated charcoal/chelating agents/emetics,

dependent on the specific compound ingested and latest local

guidelines for poisoning.

Liaise with local or national toxicology/poisoning services if there has

been ingestion of a potentially dangerous substance.

Obtain specialist input (usually the on-call general medical team

initially) as soon as possible.


Correction of acidosis

Treatment of the underlying cause is the aim. Use of bicarbonate

infusions is not recommended, as it can lead to a fatal outcome. It

should be used only where advised in cases of poisoning.

Specific therapy for the underlying cause

This is the most important and efficient way to correct the acidosis

and improve the patient's outlook. Toxicological/general

medicine/renal medicine expertise should be engaged to offer specific

therapy for the identified underlying problem.

Complications of Metabolic Acidosis

The major problem is suppression of myocardial contractility and

unresponsiveness to catecholamines caused by the acidaemic state.

This may lead to a vicious cycle of hypoperfusion,

worsening lactic acidosis and further cardiac suppression, causing

multi-organ failure. If pH is <7.1-7.2 then cardiac arrhythmias are

likely.

Metabolic alkalosis is primary increase in HCO3− with or without

compensatory increase in Pco2; pH may be high or nearly normal

is a relatively frequent clinical problem that is most commonly due to

the loss of hydrogen ions from the gastrointestinal tract or in the urine

most common causes:

* Vomiting.

* diuretics .

* mineralocorticoid excess.

To differentiate between these conditions, it is usually

helpful to measure the urinary chloride concentration

In causes of metabolic alkalosis associated with a

reduction in the ECV, there will be a stimulus for avid

Na and Cl reabsorption to replenish extracellular

volume. In these setting urinary Cl should be expected

to be very low, < 25 meq/L.

If the urinary Cl is low, indicating a hypovolemic

state, then administration of NaCl and water to

replenish the extracellular volume should stop the

stimulus for aldosterone production and in turn should

lead to appropriate excretion of excess HCO3- and

improvement of hypokalemia. Thus, leading to

correction of the metabolic alkalosis. Such causes of

metabolic alkalosis are said to be saline responsive

In contrast, states of mineralocorticoid excess are

associated with an expanded volume and sometimes

hypertension. The urinary Cl will be high (> 40

meq/L).

In these patients, administration of saline would

further expand the extracellular volume and worsen

hypertension. It would not correct the alkalosis which

is primarily due to hypokalemia. Such causes of

metabolic alkalosis are said to be saline resistant.

Urine Cl < 25 meq/L

Saline Responsive

Urine Cl > 40 meq/L

Saline Unresponsive

Vomiting or nasogastric suction

Diuretics

Posthypercapnia

Cystic Fibrosis

Low chloride intake

Primary mineralocorticoid excess

Exogenous Alkali load

Barrter's or Gitelman's syndrome

Severe Hypokalemia (K< 2.0)

Causes of saline resistant metabolic alkalosis can

further be distinguished based on whether or not the

patient is hypertensive. Mineralocorticoid excess states

tend to be associated with hypertension while

exogenous alkali load, Barrters and Gitelman's

syndrome are associated with normal blood pressure.

Symptoms of Metabolic Alkalosis

Saline - Responsive metabolic alkalosis:

Re-expand volume with Normal Saline ( Primary Therapy).

Supplement with Potassium to treat hypokalemia (alkalosis

associated with severe hypokalemia will be resistant to volume

resuscitation until K is repleted) .

H+ blockers or PPIs if vomiting/NG suction to prevent further

losses in H+ ions.

Discontinue diuretics.

Acetazolamide if NS contraindicated due to CHF.

(Monitor for hypokalemia).

HCl or NH4Cl in emergency. (HCl can cause

hemolysis, NH4Cl should not be used in liver disease)

Hemodialysis in patients with marked renal failure

Saline – Unresponsive metabolic alkalosis

(Mineraldocorticoid excess).

Surgical removal of mineralocorticoid producing

tumor.

Aldosterone inhibitor.

ACE inhibitor.

Discontinue steroids.

Potassium repletion (only intervention needed to treat

the alkalosis).

When a patient develops an acid-base imbalance, the body

attempts to compensate.

the lungs and the kidneys are the primary buffer response

systems in the body.

The body tries to overcome either a respiratory or

metabolic dysfunction in an attempt to return the pH into

the normal range.

Metabolic compensation occurs over 2-3 days reflecting

altered renal HCO3 production l secretion .

Respiratory compensation through ventilation control of

PaCo2 occurs immediately

A patient can be uncompensated, partially compensated, or

fully compensated

If the pH is between 7.35-7.45, the condition is fully

compensated.

If the pH is outside the range of 7.35-7.45, the condition is

only partially compensated

Metabolic acidosis Metabolic

alkalosis

Respiratory

acidosis

Respiratory

alkalosis

pH ↓ ↑ ↓ ↑

PaCO2 N

(uncompensated)

↓ (compensated)

N (uncompensated)

↑ (compensated)↑ ↓

HCO3ˉ ↓ ↑ N

(uncompensated)

↑ (compensated)

N (uncompensated)

↓ (compensated)

BE ↓ ↑ N/↑ N/↓

Clinical

features

Kussmaul-type breathing

shock, coma

Paraesthesia, tetany,

weakness

Acute: air hunger,

disorientation

Chronic:

hypoventilation,

hypoxia, cyanosis

Acute:

hyperventilation,

paraesthesia, light-

headedness

Chronic:

hyperventilation,

latent tetany

It is possible to have a mixed respiratory and

metabolic disorder that makes interpretation of an

arterial blood gas result difficult.

As a general rule, when a normal pH is accompanied

by an abnormal PaCO2 or HCO3ˉ then a mixed

metabolic-respiratory disorder exists.

Respiratory acidosis and metabolic acidosis :

A patient with acute pulmonary oedema after an

acute myocardial infarct

Respiratory alkalosis and metabolic alkalosis:

A patient with hepatic cirrhosis who is given

diuretics.

Respiratory acidosis and metabolic alkalosis :

A patient with long-standing chronic obstructive

pulmonary disease who is given diuretics for

concomitant heart failure.

Respiratory alkalosis and metabolic acidosis.

A patient with chronic renal failure who begins to

hyperventilate secondary to anxiety

Step 1 : Is The pH normal?

pH

Alkalemia

>7.45

Step 2 : Is the disturbance respiratory or metabolic?

Match The CO2 Or The HCO3 With The pH

ROME :

Respiratory Opposite Metabolic Equal

Step 3 : Is there appropriate compensation for the

primary disturbance?

pH is between 7.35-7.45 fully compensated

pH is outside 7.35-7.45 partially

compensated.

Step 4 : Are The pO2 And The O2 Saturation normal?

pO2 (<80 mmHg)

Hypoxia

SO2 (<95 %)

Hypoxaemic respiratory failure (type I respiratory

failure): PaO2 is less than 60 mm Hg (8 kPa) with a

normal or low PaCO2

Hypercapnic respiratory failure (type II respiratory

failure): PaCO2 is more than 50 mm Hg (6.5 kPa) and

indicates inadequate alveolar ventilation.

Respiratory failure may be acute or chronic:

Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore less than 7.3.

Chronic respiratory failure develops over several days or longer. There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased. Clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.

If the pH 7.30 , the PaCo2 is 50 , and the HCO3 is 24 ,

what is likely diagnosis ?



Uncompensated Respiratory Acidosis



Acute Respiratory Alkalosis



Compensated Metabolic Acidosis



Partially Compensated Metabolic Acidosis.



Compensated Metabolic Alkalosis

abg interpretation

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