ARTERIAL BLOOD GAS LECTURE

1. Normal ABG values:

A. pH: 7.35-7.45
B. PaCO2: 35-45
C. PaO2: 80-100 mg
D. HCO3: 22-26
E. O2 Saturation: 95-100%
F. Base excess or deficit: + or – 3 mEq/L
G. Anion Gap: < 12 mEq

2. pH: Must be maintained between a very narrow range. This is done

by increasing/decreasing acids and bases as needed.

Decreased pH: acidosis

Increased pH: alkalosis

a. Acids: are molecules that can release hydrogen ions. There are
two groups of acids:

1. Carbonic acid (H2CO3): the most important acid in the

body and is equal to CO2. It is a weak acid that leaves the
body through respirations. Increased RR = decreased CO2.
Decreased RR = increased CO2.

2. Noncarbonic/fixed/inorganic acids: are not eliminated by

the lungs but are buffered by body proteins or extracellular
buffers such as bicarb (HCO3). They are then excreted by
the kidneys. Examples include:

a. HCL: Hydrochloric acid: Strong acid

b. H2PO4: Phosphoric acid: weak
c. Sulfuric acid
d. Lactic acid: formed by the incomplete oxidation of
glucose
e. Ketoacids: formed by the incomplete oxidation of fats
b. Bases: are molecules that can accept or combine with H+ ions.
The most important base is HCO3 (Bicarb).
1. HCO3: weak
2. NH3: ammonia: weak
3. Hydroxides: strong. This is not found in the body unless
there are many antacids consumed.

c. How we maintain acid-base balance:

1. Respirations: Blow off CO2 to remove acids. Works within

1-2 minutes of decrease in pH.

2. Proteins: The largest buffer system in the body. In acidosis,

calcium will jump off albumin (increasing serum Ca) and
allow H+ to bind with albumin to correct (Increase) the pH.

3. Bicarbonate: can combine with an acid to make it weaker or

with a base to make it stronger.

4. Potassium-Hydrogen exchange: In acidosis, hydrogen will

move into the cell and potassium will move out of the cell
causing an increase in pH and potassium. In alkalosis:
hydrogen will move out of the cell and potassium into the
cell thus decreasing the pH and potassium levels.

5. Renal Control mechanisms: The kidneys will excrete acid or

alkaline urine depending on what the body needs to rid itself
of. It has several mechanisms to perform this task:

a. Acidosis: H+ will be excreted and HCO3 will be held

onto. (proximal tubule)

b. Phosphate buffer system. Excessive acidosis will result in

PO4 (Phosphate) combining with H+ to form H2PO4
which is then excreted in the urine.

c. Ammonia buffer system: H= combines with ammonia

(NH3) to form Ammonium ion (NH4). NH4 combines
 with Chloride to form ammonium chloride which is then
excreted in the urine.

d. Hydrogen-potassium exchange in the urine. Acidosis:

excrete hydrogen and hold onto potassium. Alkalosis:
excrete potassium and hold onto hydrogen.

e. Aldosterone: increased aldosterone causes sodium to be

reabsorbed by the kidneys and potassium & hydrogen to
be excreted. This causes metabolic alkalosis and
hypokalemia. Decreased aldosterone causes the
opposite. Potassium and hydrogen are retained and
metabolic alkalosis occurs.

3. PaCO2: This is the respiratory component. CO2 makes carbonic

acid. The more CO2 you have the more acidic your blood. High CO2
levels are called hypercapnea and are compatible with respiratory
acidosis.

a. Hypercapnea: CO2 > 45. Causes include:

1. Impaired respiratory center: Drug OD, head injury

2. Pulmonary conditions: Bronchitis, pneumonia, p.
edema, respiratory distress syndrome
3. Chest wall abnormalities: Paralysis of respiratory
muscles, chest injuries, deformities, obesity
4. Other: Paralytic drugs, air high in CO2 content

S/S:

1. H/A, weakness, confusion, tremor, paralysis,

stupor, coma
2. Acidic urine (It takes at least one day for the
kidneys to compensate and increase the bicarb
level to compensate for the high CO2 content in
the blood)
3. Cerebral artery vasodilatation: Increased ICP,
papilledema if severe
 4. Warm, flushed skin, weakness, tachycardia if less
severe due to peripheral vasodilatation.
5. Hypercapnea in the lungs results in pulmonary
vascular vasoconstriction (increased PHPT).

Treatment of Hypercapnea:

1. Improve ventilation
2. Intubate and ventilate
3. Pulmonary toilet
4. Tx the cause (ie: hold sedation)

b. Hypocapnea: PaCO2 < 35. Associated with respiratory

alkalosis and can occur suddenly without
compensation. Caused by hyperventilating. Causes
include:

1. Anxiety
2. Panic attacks
3. Fever
4. O2 deficiency
5. Early salicylate toxicity
6. Encephalitis
7. Anesthesia
8. Treatment for IICP
9. Metabolic acidosis (compensatory)

Signs and symptoms include:

1. Light-headedness
2. Dizziness
3. Tingling & Numbness of the fingers and toes,
seizures
4. Sweating
5. Palpitations
6. Air hunger, dyspnea
7. Possible Chvostek and trousseaus if calcium drops
8. Tetany and convulsions (Hypocalcemia)

Tx:
 1. Rebreathe air from a paper bag or cupped hands
2. Calm the patient

4. PaO2: An indirect measure of the oxygen content of arterial blood.

PaO2 is a measure of the tension (pressure) of oxygen dissolved in the
plasma. This pressure determines the force of O2 to diffuse across the
pulmonary alveoli membrane. It is decreased in:

a. O2 diffusion difficulties: pneumonia, shock lung, CHF

b. Premature mixing of venous blood with arterial blood:

c. Under ventilated and overperfused pulmonary alveoli:

Pickwickian syndrome, obese patients who cannot breathe
properly when in the supine position or patients with
significant atelectasis.

5.HCO3: Bicarb is the metabolic component. Bicarb = base, so the

more bicarb the more Alkalotic the patient.

a. Bicarb > 26 is compatible with metabolic alkalosis. Causes:

10.Excessive alkali: ingestion of NaHCO3, TPN with

acetate, IVF with lactate, citrate in blood
transfusions.
11. Loss of H-: vomiting, GI suction, binge-purge,
hypokalemia, diuretics, hyperaldosteronism

Signs and symptoms of metabolic alkalosis:

Asymptomatic or s/s volume depletion or
hypokalemia. There rarely are CNS s/s
Because HCO3 ions enter the CSF more slowly than
H+ ions.

1. Mental confusion
2. Hyperactive reflexes
3. Tetany
4. Hypoventilation (Compensatory)
 Treatment:

Treat the cause (give Cl-, K, antiemetics, etc)

c. Bicarb < 22 is compatible with metabolic acidosis.

Causes include:

1. Lactic acidosis: MI, shock, seizures, cardiac arrest

where tissues to continue to metabolize without O2
and the byproduct is lactic acid.
2. Ketoacidosis: uncontrolled DM, fasting, low
carbohydrate diets, excessive ETOH, vomiting and
dehydration.
3. Salicylate toxicity: ASA OD
4. Methanol/Ethylene glycol toxicity: AKA wood
alcohol. Can be absorbed through the skin, GI
tract or lungs. As little as 30cc can be fatal.
Causes metabolic acidosis, severe optic nerve and
CNS toxicity. Organ damage occurs after 24 hours
when it converts to formaldehyde and formic acid.
Ethylene is a component of antifreeze and
solvents. Lethal dose is about 100 cc. Converts to
oxalic and lactic acid.
5. Decreased renal function. CRF is the most
common cause of chronic metabolic acidosis
because it interferes with H+ secretion and HCO3
retention.
6. Increased HCO3 loss: loss of GI secretions which
are high in HCO3 such as occurs with severe
diarrhea, small bowel-pancreatic or biliary fistula
drainage, ileostomy drainage and intestinal
suctioning.
7. Hyperchloremic acidosis: When Cl- ions are
increased then HCO3 ions are decreased causing a
metabolic acidosis. Causes include chloride
containing meds such as ammonium chloride or
hyperal.
 Signs and symptoms of metabolic acidosis: Will see
s/s of the causal disorder:

1. Weakness, fatigue, malaise, h/a

2. anorexia, n/v, abd pain
3. Decreased LOC, stupor, coma
4. Skin dry, warm, flushed
5. Cardiac irritability, decreased contractility,
decreased Cardiac output with pH < 7.0
6. Increased RR (compensatory)
7. Acidic urine

6. Base excess or deficit. Base deficit (-) indicates metabolic

acidosis. Base excess (+) indicates metabolic alkalosis or
compensation to a prolonged respiratory acidosis. This number is
calculated by the pH, PCO2, and the Hct. It represents the amount of
buffers in the blood including HCO3, proteins and phosphate.

7.Anion gap: Compares the amount of positive ions (Cations Na+)

with the amount of negative ions (anions such as Cl- and HCO3-).
There appear to be more positive cations than negative anions,
because some of the negative anions are not measured.

The difference between the number of cations (+) and anions (-) is
called the anion gap.

The gap of unmeasured anions includes sulfates, phosphates and

organic acids.

A normal anion gap is < 12 mEq

The anion gap is helpful in determining how much of an acidotic state

the client has and if it is improving or worsening. The higher the gap,
the worse the metabolic acidosis.
 8. Directions for interpreting ABG’s:

Normal values: pH = 7.35-7.45

PaCO2 = 35-45

HCO3 = 22 – 26

1. Look at your pH first. Is the patient normal, acidotic or Alkalotic?

2. Look at your PaCOs (acid). Is it normal, high or low. High would be

compatible with acidosis. Low with alkalosis. The PaCO2 will go in the
opposite direction of the pH if the problem is respiratory.

3. Look at your HCO3 (base). Is it normal, high or low. If it is high it is

compatible with alkalosis, if it is low it is compatible with acidosis. The
HCO3 will go in the same direction as the pH if the problem is metabolic.

4. ROME: Respiratory opposite the pH, Metabolic equal (same) direction as

the pH.

9. Explain the difference between an uncompensated, partially

compensated and compensated acid base imbalance.

When a problem originally happens, it is uncompensated. For example: A

COPD patient retains CO2 and develops a respiratory acidosis:

pH = 7.32 PaCO2 = 48 HCO3 = 24. Only the pH & paCO2 are abnormal.

The kidneys will begin to excrete H+ and hold onto bicarb in an attempt to
compensate causing a partially compensated ABG:

pH = 7.34, PaCO2 = 48, HCO3 = 28 All are abnormal

Eventually the kidneys will be successful in holding on to the “right”

amount of bicarb = compensated abg’s:

pH = 7.36, PaCO2 = 48, HCO3 = 32 pH is normal, PaCO2 & HCO3 are

abnormal.
How do I know which one caused the problem. The body will not
overcorrect the acid-base imbalance, which means the pH will be closest to
the problem. A pH of 7.36 is closest to acidosis, right? So, to create an
acidosis, you need either more acid (CO2) than usual or less base (HCO3)
than usual. The abg’s above have more acid and more base. Only more acid
can cause a acidosis. So this is a compensated respiratory acidosis.

Case Study 1: Mr. J is a 65 y/o male with a long history of chronic

bronchitis and a 3 pack a day smoking habit for 50 years. He is taken
to radiology and is returned to the room. You are checking on him
when you find him obtunded and difficult to rouse. His respirations
are 6 per minute and you note his oxygen has been turned up to 6
liters (Orders read 2 l/m). The following are the results from his
ABGs:

pH= 7.29, PaCO2 = 90, PaO2 = 150, HCO3 = 24, O2 = 98%

1. Respiratory Acidosis

2. O2 is set too high, he has lost his hypoxic drive. Therefore he is

hypoventilating and retaining CO2

3. A person’s O2 level does not need to be higher than 100. High O2

levels can be toxic to the lungs

4. Chronic hypoxia is interpreted by the kidneys as anemia and they

secrete erythropoietin to produce more RBC’s. With higher RBC to
Oxygen ratio, the O2 saturation will decrease.

5. ROME means that a respiratory acid base imbalance goes in the

opposite direction as the pH and a metabolic imbalance goes in the
same (equal) direction as the pH.

Acid base imbalance pH CO2 or HCO3

Respiratory acidosis Decreased Increased CO2
Respiratory alkalosis Increased Decreased CO2
Metabolic acidosis Decreased Decreased HCO3
Metabolic alkalosis Increased Increased HCO3
6. Other conditions which can cause respiratory acidosis include:

A. Impaired respiratory center: OD, head

injury
B. Pulmonary conditions: Asthma,
emphysema, bronchitis, pneumonia,
pulmonary edema, ARDS
C. Chest wall abnormalities: paralysis,
trauma, deformities, obesity
D. Paralytic drugs
E. Air high in CO2
F. Sleep apnea

7. Signs and symptoms of Respiratory acidosis include:

a. headache, weakness, confusion, tremor, paralysis, lethargy,

stupor or coma

b. Acidic urine (will take one day to produce)

c. Cerebral artery vasodilatation (increased ICP, papilledema)

d. Warm, flushed skin; tachycardia

CASE STUDY 2: There has been a school bus accident. A 7 year old boy
c/o lightheadedness, numbness and tingling in his fingers and toes. His
arterial blood gases are:

pH: 7.55 PaCO2 = 28 PaO2 = 100 HCO3 = 25 O2 Sat = 100%

1. This patient has Respiratory alkalosis.

2. The patient has hyperventilated due to fear and anxiety and “Blown off”
their CO2.

3. Signs and symptoms of hypocapnea are:

a. Light-headedness, dizziness
b. Tingling and numbness of the fingers and toes
c. Sweating and palpitations
d. Air hunger, dyspnea
e. Chvostek and Trousseaus
f. Tetany and convulsions

4. Slow down the patient’s breathing, have them re-breathe CO2 from a
bag.

5. Other conditions which can cause this problem include: panic attacks,
fever, Oxygen deficiency, early salicylate toxicity, encephalitis,
anesthesia, and treatment for IICP.

6.Respiratory alkalosis causes the body to hold onto hydrogen ions to

correct the pH. The amount of ionized calcium decreases and the patient
experiences numbness, tingling, etc.
CASE STUDY 3: Mrs K is a 46 y/o female s/p abdominal surgery. She has
a nasogastric tube (NGT) to low-intermittent suction and is draining about
700 cc of gastric secretions every 12 hours. She has the following ABG
results and potassium level.

pH = 7.55 PaCO2 = 48 PaO2 = 100 HCO3 = 34 O2 Sat = 100% K = 2.8

1. Metabolic equal means that the pH and the HCO3 go in the same
direction if the problem is metabolic in nature.

2. This patient has metabolic alkalosis because their HCL acid is removed
by naso-gastric suctioning.

3. GI suctioning

4. Causes include excessive gain of alkali: ingestion of NaHCO3,

hyperalimentation with acetate, IVF with lactate, Citrate in blood
transfusions or d/t loss of H- ions such as occurs with vomiting, GI suction,
binge-purge, hypokalemia, diuretics, hyperaldosteronism

5. Signs and symptoms of metabolic alkalosis include: May be

asymptomatic or have s/s volume depletion or hypokalemia, mental
confusion, hyperactive reflexes, tetany, hypoventilation (compensatory).
Death occurs if > 7.55

6. Decreased hydrogen ions leads to hyperkalemia. Why? The body holds

onto hydrogen and rids itself or binds with potassium in an effort to lower
the pH and return it to WNL.
7. Treatment includes treating the cause, replacing chloride and potassium,
antiemetics and stop antacids.
CASE STUDY 4:

Mr. P has suffered a cardio-pulmonary arrest. He was “down” for 3 minutes

before CPR was initiated. He has now been intubated and given 100%
oxygen via an ambu bag when you obtain the following ABG’s:

pH = 7.28 PaCO2 = 32 PaO2 = 76 HCO3 = 16 O2Sat = 100%

1. This condition is known as metabolic acidosis

2. This condition can occur either d/t the following:

a. Lactic acidosis (anaerobic metabolism of glucose without O2)

b. Ketoacidosis: burning fats instead of carbs
c. Salicylate toxicity
d. Decreased renal function* (the most common cause for this
condition
e. Methanol/ethylene glycol toxicity
f. Hyperchloremic acidosis
g. HCO3 loss with severe diarrhea, intestinal suctioning/drainage

3. His CO2 is low because they have been hyperventilating him with 100 %
via ambu bag.

4. A venous CO2 is an indirect measurement of arterial HCO3. It is drawn

much more frequently than arterial blood gases and can therefore alert you
to acid-base imbalances.

5. Signs and symptoms of metabolic acidosis include: weakness, fatigue,

malaise, h/a, anorexia, n/v, abd pain, decreased LOC, stupor, coma, skin dry,
warm, flushed, cardiac irritability, decreased contractility, decreased CO.

6. The patient will increase their respiratory rate if at all possible to blow off
CO2 and correct the acidosis.

Case studies and quiz are under: Case studies: acid-base lecture