ABG by DJ

ABGArterial Blood Gas Analysis

(A Basic Approach)

Dr. Dharmendra Joshi (DJ)Dr. Basanta Sapkota

House Officers,Department of Emergency

Tribhuvan University Teaching HospitalMaharajgunj, Kathmandu, Nepal

“Life is a struggle, not against sin, not against the Money Power, not against

malicious animal magnetism, but against hydrogen ions."

- H.L. MENCKEN

Table of Contents

1. Definition2. Purpose3. Information provided by ABG4. Normal results5. Why ABG is ordered?6. Extraction and Analysis7. Step wise approach to ABG8. Acid Base Disorders

Pulse Oximetry ‘The 5th Vital Sign’

• Non-invasive• Instantaneous• Ubiquitous• SaO2 < 95% the usual cutoff

for normal versus ‘abnormal’• Limitations:

– Patient must have pulse– Detects only significant

decreases in PO2 – Does not comment on content

ABG: Definition:

• Blood gas analysis, also called Arterial Blood Gas (ABG) analysis, is an invasive test which measures the amount of oxygen (O2) and carbon dioxide (CO2) in the blood, as well as the acidity (pH) of the blood.

Most Dyspneic Patients Don’t Require ABG Analysis

• When cause of dyspnea is established– Asthma, CHF, restrictive lung disease, etc.

• When dyspnea is so severe as to warrant immediate mechanical ventilation– The decision to intubate and mechanically

ventilate is almost always one based on clinical, not laboratory, grounds.

Purpose:

• Evaluates how effectively the lungs are delivering O2 to the blood and how efficiently they are eliminating CO2 from it.

• Indicates how well the lungs and kidneys are interacting to maintain normal blood pH (acid-base balance).

• Assess respiratory disease and other conditions that may affect the lungs, and to manage patients receiving oxygen therapy (respiratory therapy).

Purpose: Contd…

• Provides information on kidney function too.• Determine the pH of the blood and the partial

pressures of carbon dioxide (PaCO2) and oxygen (PaO2) within it.

• Assess the effectiveness of gaseous exchange and ventilation, be it spontaneous or mechanical.

Purpose: Contd…

• Assess metabolic status of the patient, giving an indication of how they are coping with their illness.

• It would therefore seem logical to request an ABG on any patient who is or has the potential to become critically ill.

• This includes patients in critical care areas and those on wards who 'trigger' early-warning scoring systems.

Limitations of ABGs

• ABGs measure gas partial pressures (tensions)– Remember: PO2 is not the

same as content! A severely anemic patient may have an oxygen content reduced by half while maintaining perfectly acceptable gas exchange and therefore maintaining pO2

Limitations of ABGs: Contd…

• Technical issues– They hurt,– Sampling from a vein by mistake,– Finding an arterial pulse can be difficult in very

hypotensive patients,– Complications such as arterial thrombosis are

possible, but rare.

Information provided by ABG

• PaCO2• This is the partial pressure of carbon dioxide dissolved

within the arterial blood. • It is used to assess the effectiveness of ventilation. A high

PaCO2 (respiratory acidosis) indicates underventilation, a low PaCO2 (respiratory alkalosis) indicates hyper- or over ventilation.

• The normal range for a healthy person is 4.7-6.0 kPa or 35-45 mmHg although in chronic pulmonary diseases it may be considerably higher and still normal for that patient.

Information provided by ABG Contd...

• PaO2• This is the partial pressure of oxygen dissolved

within the arterial blood and will determine oxygen binding to haemoglobin (SaO2).

• It is of vital importance but is not used in determining patients' acid base status and normally low readings indicate hypoxaemia.

• The normal range: 9.3-13.3 kPa or 80-100 mmHg.


• SaO2 • Oxygen saturation measures how much of the

haemoglobin (Hb) in the red blood cells is carrying oxygen (O2).

• Although similar to SpO2 (measured by a pulse oximeter), it is more accurate.

• The normal levels are 97% and above, although levels above 90% are often acceptable in critically ill patients.


• pH• The pH measures hydrogen ions (H+) in blood.• The pH of blood usually between 7.35 to 7.45.

A pH of less than 7.0 is called acid and a pH greater than 7.0 is called basic (alkaline). So blood is slightly basic.


• HCO3 (Bicarbonate)• HCO3 is a chemical (buffer) that keeps the pH of blood

from becoming too acidic or too basic & indicates whether a metabolic problem is present (such as ketoacidosis).

• A low HCO3- indicates metabolic acidosis, a high HCO3

- indicates metabolic alkalosis.

• HCO3- levels can also become abnormal when the kidneys

are working to compensate for a respiratory issue so as to normalize the blood pH

• Normal range: 22–26 mmol/l


• Base Excess (BE)• The base excess is used for the assessment of the metabolic

component of acid-base disorders, and indicates whether the patient has metabolic acidosis or metabolic alkalosis.

• A negative base excess indicates that the patient has metabolic acidosis (primary or secondary to respiratory alkalosis).

• A positive base excess indicates that the patient has metabolic alkalosis (primary or secondary to respiratory acidosis).

• Normal range: -3 to +3 mmol/l


• Other informations:• Some electrolytes (e.g., Na+, K+, Ca++)• Lactate• Other assorted calculated results.

SpO2 SaO2

• SpO2 and SaO2 are often used interchangeably, but they are not same.

• When O2 saturation is measured by pulse oximeter..... SpO2

• When O2 saturation is measured by CO- oximeter..... SaO2

• SpO2 is also called functional arterial O2 saturation and SaO2 as fractional arterial O2 saturation.

• Only true CO-oximeter can determine an accurate value for SaO2

SpO2 Vs SaO2 Contd...

• SpO2 == HbO2

HbO2 + Hb

• SaO2 == HbO2

HbO2+ Hb+COHb+MetHb+SfHb+COSfHb SaO2 == SpO2[1-SaCO]… (Nellcor equation)Non functional Hb is 2-3%In heavy smoker it may be up to 15%

Normal Results

• pH: Measurement of acidity or alkalinity, based on the hydrogen (H+) 7.35-7.45

• partial pressure of oxygen (PaO2): The partial pressure oxygen that is dissolved in arterial blood. 80-100 mm Hg

Normal Results Contd…

• partial pressure of carbon dioxide (PaCO2): The amount of carbon dioxide dissolved in arterial blood. 35-45 mm Hg

• oxygen content (O2CT): 15-23%

• oxygen saturation (SaO2): The arterial oxygen saturation. 94-100%

Normal Results Contd…

• Bicarbonate (HCO3-): The calculated value of

the amount of bicarbonate in the blood. 22-26 mEq/L

• The base excess indicates the amount of excess or insufficient level of bicarbonate. -2 to +2mEq/L (A negative base excess indicates a base deficit in blood)

Why ABG is ordered?

• Blood gas tests are ordered for patients with symptoms of an O2/CO2 or pH imbalance, such as difficulty breathing or shortness of breath & also if known to have a respiratory, metabolic, or kidney disease or experiencing respiratory distress to evaluate oxygenation and acid/base balance.

• Patients who are “on oxygen” (have supplemental oxygen) may have their blood gases measured at intervals to monitor the effectiveness of treatment.

Why ABG is ordered? Contd...

• Head or neck trauma, injuries that may affect breathing.

• Prolonged anesthesia – particularly for cardiac bypass surgery or brain surgery – during and for a period after the procedure.

Buffers

• There are two buffers that work in pairs:H2CO3 NaHCO3

Carbonic acid base bicarbonate

• These buffers are linked to the respiratory and renal compensatory system.

Respiratory Buffer Response

• H2CO3 level

• Blood pH

• Rate & depth of ventilation (Lungs)• Activation of the lungs to compensate for an

imbalance starts to occur within 1-3 minutes

Renal Buffer Response

• The kidneys excrete or retain bicarbonate(HCO3

-).• If blood pH decreases, the

kidneys will compensate by retaining HCO3

-

• Renal system may take from hours to days to correct the imbalance.

Extraction

• Usually extracted by a phlebotomist, nurse, respiratory therapist or Doctor.

• Commonly from the radial artery because:

- it is easily accessible, - can be compressed to

control bleeding,- has less risk for occlusion.

Extraction Contd...

• The femoral artery (or less often, the brachial artery) is also used, especially during emergency situations or with children.

• Blood can also be taken from an arterial catheter already placed in one of these arteries.

Extraction and analysis:

• IF ULNER/RADIAL ARTERY IS USED ---MODIFIED ALLEN’S TEST

• MODIFIED ALLEN’S TEST1. INSTRUCT PATIENT TO CLENCH HIS

FIST,2. USING YOUR FINGER APPLY

OCCLUSIVE PRESSURE ON BOTH RADIAL & ULNER ARTERY,

3. WHILE APPLYING OCCLUSIVE PRESSURE TO BOTH ARTERY, HAVE THE PATIENT RELAX HIS HAND.BLANCHING OF PALM &FINGER SHOULD OCCUR,

MODIFIED ALLEN’S TEST Contd…

4. RELEASE THE OCCLUSIVE PRESSURE ON ULNER ARTERY & NOTICE FLUSHING OF HAND WITHIN 7-10 SEC.THIS DENOTE THAT ULNER ARTERY SUPPLY IS ADEQUATE &IT’S SAFE TO PRICK RADIAL ARTERY. IF IT DOES NOT OCCUR IT MEANS ULNAR ARTERY SUPPLY IS NOT SUFFICIENT & RADIAL ARTERY IS NOT SAFE TO PRICK.

Extraction and analysis: Contd...

1. The syringe is pre-packaged and contains a small amount of heparin, to prevent coagulation or needs to be heparinised, by drawing up a small amount of heparin and squirting it out again.

2. Once the sample is obtained, care is taken to eliminate visible gas bubbles, as these bubbles can dissolve into the sample and cause inaccurate results.


3. The sealed syringe is taken to a blood gas analyzer. If the sample cannot be immediately analyzed, it is chilled in an ice bath in a glass syringe to slow metabolic processes which can cause inaccuracy.

4. Samples drawn in plastic syringes should not be iced and should always be analyzed within 30 minutes.

5. The machine used for analysis aspirates this blood from the syringe and measures the pH and the partial pressures of oxygen and carbon dioxide. The bicarbonate concentration is also calculated.


6. Results usually available for interpretation within five minutes.

7. After the blood has been taken, apply pressure to the puncture site for 10-15 minutes to stop the bleeding, and then places a dressing over the puncture.

8. Observe the patient for signs of bleeding or circulation problems.

Contraindication for arterial puncture

I. INFECTION AT SITE.II. ALLEN’S TEST NEGATIVE.III. ON ANTICOAGULANT THERAPY.IV. SEVERE PERIPHERAL VASCULAR DISEASE.V. DISTAL TO SURGICAL SHUNT.

Step wise approach to ABG

• Step 1: Acidemic or Alkalemic? • Step 2: Is the primary disturbance respiratory or

metabolic? • Step 3. Asses to PaO2. A value below 80mm Hg

indicates Hypoxemia. For a respiratory disturbance, determine whether it is acute or chronic.

• Step 4. For a metabolic acidosis, determine whether an anion gap is present.

• Step 5. Assess the normal compensation by the respiratory system for a metabolic disturbance .

Step 1: Acidemic or Alkalemic?

• Assess the pH –acidotic/alkalotic • If above 7.5 – alkalotic • If below 7.35 – acidotic

Step 2: Is the primary disturbance respiratory or metabolic?

• Assess the paCO2 level.• pH decreases below 7.35, the paCO2 should rise.• If pH rises above 7.45 paCO2 should fall.• If pH and paCO2 moves in opposite direction – primary

respiratory problem. • Assess HCO3 value.• If pH increases the HCO3 should also increase.• If pH decreases HCO3 should also decrease.• They are moving in the same direction, primary problem is

metabolic.

Step 3. For a respiratory disturbance, determine whether it is acute or chronic.

• Acute respiratory disturbances change pH 0.08 units for every 10 mmHg deviation from normal.

• Therefore, in acute respiratory acidosis, the pH will fall by 0.08 x [(PCO2 - 40)/10]

• In acute respiratory alkalosis, the pH will rise by 0.08 x [(40-PCO2)/10]

Step 3. Contd…

• Chronic respiratory disturbances only change pH 0.03 units for every 10 mmHg deviation from normal

• Therefore, in chronic respiratory acidosis, pH will fall by 0.03 x [(PCO2 - 40)/10]

• In chronic respiratory alkalosis, the pH will rise by 0.03 x [(40-PCO2)/10]

Appropriateness of Respiratory Response to Metabolic Acidosis

• Predicted Change in PCO2 = (1.5 x HCO3) + 8

• If patient’s PCO2 is roughly this value, his or her response is appropriate.

• If patient’s PCO2 is higher than this value, they are failing to compensate adequately.

Respiratory acidosis

pH PaCo2 HCO3 -

normal

Respiratory Alkalosis

normal

Metabolic Acidosis

normal

Metabolic Alkalosis

normal

Base Excess

• Is a calculated value estimates the metabolic component of an acid based abnormality.

• It is an estimate of the amount of strong acid or base needed to correct the metabolic component of an acid base disorder (restore plasma pH to 7.40 at a PaCO2 40 mmHg)

Formula

• With the base excess is -10 in a 50kg person with metabolic acidosis mM of HCO3 needed for correction is:

= 0.3 X body weight X BE = 0.3 X 50 X10 = 150 mM

Step 4. For a metabolic acidosis: Anion Gap Determination

• Calculation of AG is useful approach to analyze metabolic acidosis

• AG = (Na+ + K+) – (Cl- + HCO3-)

*A change in the pH of 0.08 for each 10 mm Hg indicates an ACUTE condition.

* A change in the pH of 0.03 for each 10 mm Hg indicates a CHRONIC condition.

REMEMBERHigh Anion Gap – causes:

• K etoacidosis • U remia • S epsis • S alicylate & other drugs• M ethanol• A lcohol (Ethanol)• L actic acidosis• E thylene glycol

In other way!!!

Reduced anion gap

• Increased ‘unmeasured’ cations • Rare• Hypermagnesaemia • Lithium toxicity• Xs protein

– Myeloma– Waldenstrom’s macroglobulinaemia – (Ig’s are strong cations)

Normal anion gap

• Disorders of bicarbonate homeostasis• Hyperchloraemia causes the acidosis• GI losses

– Vomitting – Diarrhoea

• Renal losses– Renal tubular acidosis– Acetazolamide

• Iatrogenic NaCl

Step 5. Assess the normal compensation by the respiratory system for a metabolic disturbance

• A patient can be uncompensated or partially compensated or fully compensated,

• pH remains outside the normal range,• pH has returned within normal range- fully

compensated though other values may be still abnormal,

Step 5 Contd...

• Be aware that neither the system has the ability to overcompensate,

• 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.

• The body’s attempt to return the acid/base status to normal (i.e. pH closer to 7.4).

Compensation:

• Primary Problem Compensation • respiratory acidosis metabolic alkalosis• respiratory alkalosis metabolic acidosis• metabolic acidosis respiratory alkalosis• metabolic alkalosis respiratory acidosis

Is there appropriate compensation?

Is it chronic or acute?

Respiratory Acidosis

– Acute: for every 10 increase in pCO2 -> HCO3 increases by 1 and there is a decrease of 0.08 in pH MEMORIZE

– Chronic: for every 10 increase in pCO2 -> HCO3 increases by 4 and there is a decrease of 0.03 in pH


– Acute: for every 10 decrease in pCO2 -> HCO3 decreases by 2 and there is a increase of 0.08 in pH MEMORIZE

– Chronic: for every 10 decrease in pCO2 -> HCO3 decreases by 5 and there is a increase of 0.03 in pH

Assess the PaCO2

• In an uncompensated state – when the pH and PaCO2 moves in the same direction: the primary problem is metabolic.

• The decreasing PaCO2 indicates that the lungs acting as a buffer response (blowing of the excess CO2)

• If evidence of compensation is present but the pH has not been corrected to within the normal range, this would be described as metabolic disorder with the partial respiratory compensation.

Assess the HCO3

• The pH and the HCO3 moving in the opposite directions, primary disorder is respiratory and the kidneys acting as a buffer response: are compensating by retaining HCO3 to return the pH to normal range.

pH PaCO2 HCO3-

Resp.Acidosis Normalbut<7.40

Resp.Alkalosis Normalbut>7.40

Met. Acidosis Normalbut<7.40

Met. Alkalosis Normalbut>7.40

Fully Compensated

Partially Compensated

pH PaCO2 HCO3-

Res.Acidosis

Res.Alkalosis

Met. Acidosis

Met.Alkalosis

HOW TO KNOW THE DISORDER pH PaCO2 HCO3ˉ


Acute < 7.35 > 45 Normal

Partly Compensated < 7.35 > 45 > 26

Compensated ~ Normal > 45 > 26


Acute > 7.45 < 35 Normal

Partly Compensated > 7.45 < 35 < 22

Compensated ~ Normal < 35 < 22

Metabolic Acidosis

Acute < 7.35 Normal < 22

Partly Compensated < 7.35 < 35 < 22

Compensated ~ Normal < 35 < 22

Metabolic Alkalosis

Acute > 7.45 Normal > 26

Partly Compensated > 7.45 > 45 > 26

Compensated ~ Normal > 45 > 26

Evaluating Oxygenation

• What is a ‘normal’ PO2?– Oxygenation gradually deteriorates during life,– Several calculations available for determining ‘normal’

based on patient age.

• PaO2 = 104.2 - (0.27 x age)• i.e., 30 year old ~ 95 mmHg 60 year old ~ 88 mmHg• Note: Some patients with previous (and now resolved) severe pulmonary

diseases may never recover their full lung function, so any sense of ‘normal’ needs to be tempered with historical information

Evaluating Oxygenation in ABGs• Determine the A-a gradient• A-a Gradient =• [(Patm - PH2O) x FiO2] - (PCO2/RQ) - PaO2 • Patm = 760 mmHg• PH2O = 47 mmHg• FiO2 = 0.21 on room air at sea level• PCO2 is taken from the blood gas measurement• RQ can be assumed to be 1 (possible range from 0.7

to 1.0)

Evaluating Oxygenation with ABGs

Check A-a Gradient

No Yes

Is the patient hypoxic?

Hypoventilation

Normal Elevated

Check A-a Gradient

No defect CompensatedDefect. i.e., patient is hyper-ventilating or onsupplemental O2

Other Defect

Normal

Elevated

~ PaCO2 – pH Relationship

80 7.20

60 7.30

40 7.40

30 7.50

20 7.60

pH < 7.35Acidosis

pH > 7.45Alkalosis

pCO2 > 45Respiratory

HCO3 < 22Metabolic

pCO2 < 35Respiratory

HCO3 > 26Metabolic

PaCO2 ↑10→HCO3 ↑3.5

PaCO2 ↑10→HCO3 ↑1

PaCO2 ↓10→HCO3 ↓4

PaCO2 ↓10→HCO3 ↓2

PaCO2 ↑7→HCO3 ↑10

Urine Cl < 10 Cl ResponsiveAnion Gap < 12

Non-Anion GapAnion Gap > 12

Anion Gap

Urine Cl > 10 Cl Unresponsive

Interpreting ABGs

Osm Gap > 10Methanol

Ethylene Glycol

Osmolar Gap < 10Ketoacidosis

Lactic acidosis Uremia

Aspirin/salicylate tox

DiarrheaRenal tubular acidosis

AcetazolamideTotal parenteral nutrition

Ureteral diversionPancreas transplant

CNS depressantsNeuromuscular disorder

Thoracic cage abnormalitiesObstructive lung disease

Obesity/hypoventilation syndromeMyxedema coma

Anxiety/painSepsis

CNS (stroke)Aspirin OD

Chronic liver diseasePulmonary embolism

PregnancyHyperthyroidism

Loss of body fluids:Vomiting

Nasogastric suctioningDiuretic use

Excess body fluids:Exogenous steroidsCushing’s syndromeHyperaldosteronismBartter’s syndrome

=Na - (Cl+HCO3)

Acute

Chronic

PaCO2 ↓15→HCO3 ↓10

Compensation:If: ΔPCO2/ΔHCO3

=CO2/HCO3ratioThen it IS comp.

Acute

Chronic

(2xNa) + (Glu/18) + (BUN/2.8) = calculated serum osmoles

HCO3 loss Extra H+

ABG Vs VBG

Arterial Blood Gas

• PAINFUL• Arterial injury• Thrombosis with distal

ischemia• Hemorrhage/hematoma• Aneurysm formation• Median nerve damage• Infection• Needle stick injury• Reflex sympathetic dystrophy

Venous Blood Gas

• Samples can be drawn simultaneously at time of veni puncture

• Should be done without tourniquette

• More difficult to obtain in pulseless patients

• Controversy regarding level of agreement with arterial values

ABG Vs VBG

1. To measure pH, bicarb, or base excess, especially in hemodynamically stable patients, a VBG is equivalent and there is no need for an ABG.On average for pH the difference is about 0.02 - 0.03. So for average DKA patient, no ABG is needed.

2. A VBG is a good screening tool for hypercarbia, with a venous PCO2 < 45 mmHg having about 100% sensitivity. However, VBG cannot tell about the degree of hypercarbia reliably. If an absolute number needed, ABG is the way to go.

ABG Vs VBG Contd...

3. For hypoxia, or workup requiring calculations of oxygen tension, ABG is done (hypoxic arrest, calculating A-a gradients)

4. Studies are raising the concern for increased mortality in patients who have hyperoxia after return of circulation after cardiac arrest. These patients need ABG’s to guide the vent settings. The increased mortality in these patients has even been seen within the first hour.

Acid Base Disorders

1. Respiratory Acidosis2. Respiratory Alkalosis3. Metabolic Acidosis4. Metabolic Alkalosis


• Lower pH and an increased PCO2 and is due to respiratory depression (not enough oxygen in and CO2 out).

• pH decrease (<7.35)• PCO2 increase (>45mmHg)• Any condition that results

in hypoventilation can cause respiratory acidosis.

Causes of respiratory acidosis

CNS depression – sedatives, narcotics, CVA

Neuromuscular disorders – acute or chronic

Acute airway obstruction – foreign body, tumor, reactive airway

Severe pneumonia, pulmonary edema, pleural effusion

Chest cavity problems – hemothorax, pneumothorax, flail chest

Chronic lung disease – obstructive or restrictive

Central hypoventilation, OSA

Respiratory Acidosis: Signs&Symptom

• Respiratory : Dyspnoea, respiratory distress and/or shallow respiration.

• Nervous: Headache, restlessness and confusion. If co2 level extremely high drowsiness and unresponsiveness may be noted.

• CVS: Tacycardia and dysrhythmias

Management of Respiratory Acidosis

• Increase the ventilation. • Causes can be treated rapidly include

pneumothorax, pain and CNS depression r/t medication.

• If the cause cannot be readily resolved, mechanical ventilation.


• Respiratory alkalosis, characterized by a raised pH and a decreased PCO2, is due to over ventilation caused by hyperventilating, pain, emotional distress, or certain lung diseases that interfere with oxygen exchange.

• pH increases• PCO2 decreases

Causes of Respiratory Alkalosis

Anxiety, pain, fever

Hypoxia, CHF

Lung disease with or without hypoxia – pulmonary embolus, reactive airway, pneumonia

CNS diseases

Drug use – salicylates, catecholamines, progesterone

Pregnancy

Sepsis, hypotension

Hepatic encephalopathy, liver failure

Mechanical ventilation

Hypothyroidism

High altitude

Respiratory Alkalosis: Signs/Symptoms

• CNS: Light Headedness, numbness, tingling, confusion, inability to concentrate and blurred vision.

• Dysrhythmias and palpitations• Dry mouth, diaphoresis and tetanic spasms of

the arms and legs.

Management of Respiratory Alkalosis

• Resolve the underlying problem• Monitor for respiratory muscle fatigue• When the respiratory muscle become

exhausted, acute respiratory failure may ensue

Metabolic Acidosis

• Metabolic acidosis is characterized by a lower pH and decreased HCO3

-; the blood is too acidic on a metabolic/kidney level.

• Causes include diabetes, shock, and renal failure.

• pH decreases (<7.35)• HCO3 decreases (<22mEq/l)

Causes of Metabolic Acidosis

• Renal failure• Diabetic ketoacidosis • Anaerobic metabolism• Starvation• Salicylate intoxication

Metabolic Acidosis: Signs/Symptoms

• CNS: Headache, confusion and restlessness progressing to lethargy, then stupor or coma.

• CVS: Dysrhythmias • Kussmaul’s respirations• Warm, flushed skin as

well as nausea and vomiting

Management of Metabolic Acidosis

• Treat the cause• Hypoxia of any tissue bed will produce

metabolic acids as a result of anaerobic metabolism even if the pao2 is normal

• Restore tissue perfusion to the hypoxic tissues• The use of bicarbonate is indicated for known

bicarbonate - responsive acidosis such as seen with renal failure

Metabolic Alkalosis

• Metabolic alkalosis is characterized by an elevated pH and increased HCO3

- and is seen in hypokalemia, chronic vomiting (losing acid from the stomach), and sodium bicarbonate overdose.

• pH increases (>7.45)• HCO3

- increases (>26mEq/l)

Causes of Metabolic Alkalosis

• Excess of base /loss of acid.• Ingestion of excess antacids, excess use of

bicarbonate, or use of lactate in dialysis.• Protracted vomiting, gastric suction,

hypchoremia, excess use of diuretics, or high levels of aldesterone.

Metabolic Alkalosis: Signs/Symptoms

• CNS: Dizziness, lethargy disorientation, siezures & coma.

• M/S: weakness, muscle twitching, muscle cramps and tetany.

• Nausea, vomiting and respiratory depression.

• It is difficult to treat.

Management of Metabolic Alkalosis

• Remove factors that sustain HCO3- reabsorption:

Restore plasma volumeRestore chloride lostReplace potassium in hypokalaemiaStop diuretics• Treat underlying cause.

• Valuable information can be gained from an ABG as to the patients physiologic condition

• Remember that ABG analysis if only part of the patient assessment.

• Be systematic with your analysis, start with ABC’s as always and look for hypoxia (which you can usually treat quickly), then follow the four steps.

• A quick assessment of patient oxygenation can be achieved with a pulse oximeter which measures SaO2.

It’s not magic understanding ABG’s, it just

takes a little practice!

Thank You!!!

Health & Medicine

ABG by DJ