BLOOD

GASES
TERMS & DEFINITIONS:
▪ ACID – it is a substance that can yield a hydrogen ion (H) or hydronium ion when dissolved in water.
▪ BASE – is a substance that can yield hydroxyl ions (OH).
▪ pH – is defined as the negative log of the ionization constant; it is also the pH in which the protonated and
unprotonated forms are present in equal concentrations.
• reference value for arterial blood pH is 7.40
• Acidemia occurs when arterial blood pH <7.35.
• Alkalemia occurs when arterial blood pH >7.45.
• NOTE: reference value for blood plasma pH is 7.40.
▪ pKa - the negative log of the dissociation constant.
• Dissociation Constant = aka “ionization constant”
• NOTE:
• pH = pKa means solution is in equilibrium, and protonated and unprotonated species are present in equal conditions
• pH < pKa means majority of the components will largely be protonated
▪ BUFFER – is the combination of a weak acid or weak base and its salt, is a system that resists changes in
pH.
• In plasma, the bicarbonate–carbonic acid system, having a pK of 6.1, is one of the principal buffers.
TERMS & DEFINITIONS:
▪ Respiration – the process to supply cells with oxygen for metabolic processes and
remove the carbon dioxide produced during metabolism
▪ Partial pressure – it is the amount of pressure contributed by each gas to the total
pressure exerted by the mixture.
▪ Hypercapnia – is the increased blood PCO2
▪ Hypocapnia – is the decreased blood PCO2.
▪ Partial pressure of carbon dioxide (PCO2) is measured in blood as mmHg
▪ Concentration of dissolved carbon dioxide (cdCO2) – this includes undissociated
carbonic acid (H2CO3) and carbon dioxide dissolved in blood (represented by
PCO2)
▪ Concentration of total carbon dioxide (ctCO2): Includes bicarbonate (primary
component), carbamino-bound CO2, carbonic acid, and dissolved carbon dioxide
Major Buffer Systems:
Buffer:
✓ consists if a weak acid and a salt of its conjugate base
✓ it resists the change in pH upon adding acid or base
✓ the effectiveness depends in the pKa of the buffering system and the pH of the environment
✓ System that can resist change in pH; composed of a weak acid or a weak base and its
corresponding salt
Four buffer systems of clinical importance exist in whole blood:
✓ Bicarbonate-carbonic acid buffer system uses HCO3- and H2CO3 to minimize pH
changes in plasma and erythrocytes. It is the most important buffer system in plasma.
✓ Protein buffer system uses plasma proteins to minimize pH changes in the blood.
✓ Phosphate buffer system uses HPO4-2 and H2PO4 to minimize pH changes in plasma and
erythrocytes; This is also the primary buffer in urine and is involved in the exchange of
sodium ion in the urine filtrate
✓ Hemoglobin buffer system uses the hemoglobin in red blood cells to minimize pH
changes in the blood. It is the most important intracellular buffer; It plays a role in
buffering CO2 as it is transported to the lungs for excretion
NOTE!!

■ Bicarbonate-carbonic acid system:

➢most important buffer system in ECF
1. Carbonic (H2CO3) dissociated CO2 and H2O allowing CO2 to be
eliminated by the lungs and H+ as water
2. Changes in H2O modify the ventilation (respiratory) rate
3. Bicarbonate(HCO3-) concentration can be change by the kidneys.
 ✔
ACID-BASE BALANCE:
The pH of plasma is a function of two independent variables:
Partial pressure of carbon dioxide (PCO2) - which is regulated by the lungs or (respiratory
mechanism)
Concentration of bicarbonate (HCO2) - which is regulated by the kidneys (renal
mechanism).
Carbon dioxide is transported as bicarbonate, carbamino compound (bound to serum proteins
and hemoglobin), and dissolved carbon dioxide. Carbon dioxide, pH, and PCO2 are related
according to the Henderson-Hasselbalch equation:
ACID-BASE BALANCE REGULATION:
 CO2 —> diffusess into the plasma and RBCs
 In plasma, CO2 is physically dissolved or combined with amino grp of
proteins to form Carbamino cmpds. But most CO2 freely diffuses into the
RBCs and catalyed by Carbonic Anhydrase, combines with H2O to form
H2CO3, that dissociated into H+ and HCO3-

CO2 + H2O —> H2CO3 —> H+ + HCO3-

 To maintain electroneutrality, chloride shifts into the cell (Chloride shift

aka :HAMBURGER SHIFT”)
 ✔
ACID-BASE BALANCE REGULATION:
LUNGS:

CO2 diffuses into the alveoli and is eliminated through ventilation; excretion of
CO2 allows rapid and very sensitive adjustments in blood pH
As the lungs eliminate CO2 to resist accumulating H+, the proportion between
HCO3- and H2CO3 readjusts to 20:1.
By regulating the rate of CO2 excretion, lungs can maintain the ratio at or
about 20:1 = minimizing pH changes
NOTE:
• RESPIRATORY ALKALOSIS: Slow or non-removal of CO2 by the lungs results in
INCREASE in H+ conc.
• RESPIRATORY ACIDOSIS: Rapid or fast elimination of CO2 results in DECREASED H+
conc.
H + HCO3 = H2CO3 → H2O + CO2(eliminated)
+ -
 ✔
ACID-BASE BALANCE REGULATION:
KIDNEYS:

main role: to reabsorb HCO3- from the PCT

• If not reabsorbed = cause a markedly increased H+
most important function: EXCRETION OF ACID (in the form of ammonium and
titrable acid) = generation of alkali or reabsorption of HCO3- from the glomerular
filtrate (PCT) and adding to the blood
H+ are also excreted by direct excretio and through indirect disposal in the form of
ammonium ions

H+ + HCO3- = H2CO3 → H2O + CO2(eliminated)

ACID-BASE BALANCE:
✔

The average normal ratio of HCO3 to CO2 is 20:1.

So any change in the bicarbonate concentration or the dissolved carbon dioxide concentration would
result in a change in blood pH.
ACID-BASE BALANCE:
Through mechanisms that involve the lungs and kidneys, the body
controls and excretes H+ in order to maintain pH homeostasis.
Imbalances between the rate of acid formation and excretion can occur
and can lead to alterations in consciousness, neuromuscular irritability,
tetany, coma, and death
❑ Acidosis - pH below the reference range
Alkalosis - pH above reference range
NOTE!!!!

The average normal ratio of cHCO3⁻ to cdCO2 is 20:1.

ACID-BASE BALANCE:
HENDERSON-HASSELBACH EQUATION:
 expresses acid-base relationship and relates the pH of a solution to the dissociation
properties of the weak acid
 indicates that pH depends on the ratio btween HCO3– and pCO2.
 NOTE: When the kidneys and the lungs are functioning properly, a 20:1 ratio off
HCO3- to H2CO3 will be maintained, and this is expressed by the equation.
 ✔
✔
✔
PARAMETERS IN THE ASSESSMENT OF ACID-BASE BALANCE:
pH:
NORMAL: 7.35-7.45
ACIDOSIS: <7.35
ALKALOSIS: >7.45
NOTE:
pH decreases by 0.015 each celsius above 37o
effectiveness of a buffer depends on the pKa of the buffering system and pH of the environment
major causes of external acidosis: Orgnic acidosis, diarrheal loss of bicarbonate, and acidosis(exotoxins)
pCO2 (VENTILATION OF LUNGS):
this is the pressure of carbon dioxide dissolved in arterial blood
NORMAL: 35-45mmHg
RESPIRATORY ACIDOSI: <35mmHg
RESPIRATORY ALKALOSIS: >45mmHg
NOTES:
pCO2 is an index or efficiency of gas exchange and not a measure of CO2 concentration in plasma
the lungs regulate pH through retention or elimination of CO2
an increasing ratio of heparin can cause marked artifactua rise on pCO2
Increased is seen in: Alcohol and Illicit drug use
 ✔
✔
✔
PARAMETERS IN THE ASSESSMENT OF ACID-BASE BALANCE:
HCO3– (METABOLIC - KIDNEYS):
NORMAL: 21-28 mEq/L
METABOLIC ACIDOSIS: <21mEq/L
METABOLIC ALKALOSIS: >28 mEq/L
NOTE:
HCO3 is under renal control by regulating pH through acid excretion and reabsorption of HCO3
pO2 (Degree of Oxygenation)
NORMAL: 80-100 mmHg
MILD HYPOXEMIA: 61-79 mmHg
MODERATE HYPOXEMIA: 41-60mmHg
SEVRE HYPOXEMIA: 40mmHg or less
NOTE:
pO2 reflects the availability of gas in blood
pO2 is the pressure of oxygen dissolved in arterial blood
pO2 is 60-70% lower in venous blood after oxygen if released in the capillary tissues
 ✔

ACID-BASE DISORDERS:
✔

Acidemia:
blood pH is less than the reference range,
reflects excess acid or H concentration.
Alkalemia:
pH greater than the reference range or excess base.
A disorder caused by
Compensated: when the body tries to restore acid-base homeostasis whenever an imbalance occurs.
NOTE:
• For disturbances of the respiratory component, the kidneys compensate by selectively excreting
or reabsorbing anions and cations. The kidneys are slower to respond (2–4 days), but response is
long term and potentially complete.
• The lungs can compensate immediately, but the response is short term and often incomplete.
Fully compensated – this implies that the pH has returned to the normal range (the 20:1 ratio has
been restored)
Partially compensated – this implies that the pH is approaching normal.
ACID-BASE DISORDERS:
GENERALLY:
❑ Metabolic Alkalosis
❑ Metabolic Acidosis
❑ Respiratory Alkalosis
❑ Respiratory Acidosis
❑ Non-respiratory acidosis:
• may be caused by the direct administration
of an acid-producing substance, such as
ammonium chloride or calcium chloride, or
by excessive formation of organic acids as
seen with diabetic ketoacidosis and
starvation.
• Compensation: HYPERVENTILATION
ACID-BASE DISORDERS:
Note:

Metabolic acid:
base disorders primarily involve bicarbonate concentration.
Respiratory acid:
base disorders primarily involve dissolved carbon dioxide
concentration.
 ✔

ACID-BASE DISORDERS:
✔

A. Metabolic Acidosis: (Primary bicarbonate deficit)

the bicarbonate concentration decreases, causing a decrease in the 20:1 ratio between HCO3⁻ and CO2, which results in a decrease in the
blood pH.
may be caused by organic acid production or when ingestion exceeds the excretion rate. Disorders include diabetic ketoacidosis due to the
production of:
• acetoacetic acid and p-hydroxybutyric acid;
• lactic acidosis due to the production of lactic acid;
• poisonings such as salicylate, ethylene glycol, and methyl alcohol;
• reduced acid excretion due to renal failure or tubular acidosis;
• loss of bicarbonate due to diarrhea or excessive renal excretion.
maybe caused by the following reasons:
• Direct administration or ingestion of acid-producing substances (i.e., ammonium chloride, calcium chloride, salicylates, ethanol).
• Production of organic acids as seen with diabetic ketoacidosis (increased levels of acetoacetic acid and β-hydroxybutyric acid and
lactic acid in lactic acidosis).
• Reduced excretion of acids as seen in renal tubular acidosis.
• Excessive loss of bicarbonate from diarrhea or drainage from a biliary, pancreatic, or intestinal fistula.
•
ACID-BASE DISORDERS:
✔

A. Metabolic Acidosis: (Primary bicarbonate deficit)

Laboratory findings in metabolic acidosis
1. ctCO2 decreased
2. PCO2 normal
3. pH decreased
Respiratory compensatory mechanism:
• A decreased pH triggers hyperventilation that lowers PCO2 and results in an increase in pH.
• This increases the ratio between HCO3- and CO2 to 20:1, which increases the blood pH.
Laboratory findings in compensation:
ctCO2 decreased
PCO2 decreased
pH normal
 ✔

ACID-BASE DISORDERS:
✔

B. Metabolic Alkalosis: (Primary bicarbonate excess)

the bicarbonate concentration increases, causing an increase in the 20:1 ratio between HCO3⁻ and CO2, which results in an increase in the
blood pH.
Maybe caused by the following reasons:
• Excess administration of sodium bicarbonate or through ingestion of bicarbonate-producing salts, such as sodium lactate, citrate, and
acetate.
• Excessive loss of acid through vomiting, nasogastric suctioning, or prolonged use of diuretics that augment renal excretion of H+ can
produce an apparent increase in HCO3–.
• Hypokalemia and chloride deficit stimulate the reabsorption of HCO3– in the distal tubules.
may be caused by ingestion of excess base, decreased elimination of base, or loss of acidic fluids. Disorders include:
• ingestion of excess alkali (antacids);
• intravenous administration of bicarbonate;
• renal bicarbonate retention; prolonged diuretic use;
• loss of hydrochloric acid from the stomach after vomiting, intestinal obstruction, or gastric suction;
• glucocorticoid excess as in dishing syndrome;
• mineralocorticoid excess as in hyperaldosteronism
ACID-BASE DISORDERS:
✔

B. Metabolic Alkalosis: (Primary bicarbonate excess)

Laboratory findings in metabolic alkalosis
1. ctCO2 increased
2. PCO2 normal
3. pH increased
Respiratory compensation mechanism:
• The pH increase slows breathing (hypoventilation), thus increasing the amount of CO2 retained by the lungs.
• This increased CO2 retention causes an increase in H2CO3, which results in more dissolved CO2 in the blood.
• The carbonic acid lowers the pH. This decreases the ratio between cHCO3⁻ and cdCO2 to 20:1, which decreases the blood pH.
Laboratory findings in compensation
1. ctCO2 increased
2. PCO2 increased
3. pH normal
 ✔
ACID-BASE DISORDERS:
✔

C. Respiratory Acidosis: (Hypercapnia)

Inability of a person to exhale CO2 through the lungs (hypoventilation) causes an increase of PCO2.
The increased PCO2 causes an increase in the concentration of dissolved carbon dioxide, which forms carbonic acid in the
blood. This decreases the 20:1 ratio between HCO3⁻ and CO2, which decreases the blood pH
May be caused by the following:
• Ineffective removal of CO2 from the blood as seen in lung disease.
• Airway obstruction as seen in chronic obstructive pulmonary disease (COPD). Destructive changes in the airways and
alveolar walls increase the size of the alveolar air spaces, resulting in a reduction of the lung surface area available for
gas exchange. As a result, CO2 is retained in the blood, causing chronic hypercarbia (elevated pCO2).
• Drugs such as barbiturates, morphine, and alcohol will cause hypoventilation which subsequently increase blood
pCO2 levels.
• Decreased cardiac output, as observed with congestive heart failure, will result in less blood being presented to the
lungs for gas exchange and, therefore, an elevated pCO2
Respiratory acidosis may be caused by chronic obstructive pulmonary disease, such as:
• chronic bronchitis and emphysema
• ingestion of narcotics and barbiturates
• severe infections of the central nervous system such as meningitis
ACID-BASE DISORDERS:
✔

C. Respiratory Acidosis: (Hypercapnia)

Laboratory findings in respiratory acidosis
1. ctCO2 normal
2. PCO2 increased
3. pH decreased
Renal compensatory mechanism:
• The kidneys increase sodium-hydrogen exchange, ammonia formation, and bicarbonate retention.
• The increased bicarbonate concentration aids the return of the 20:1 ratio, which raises the blood pH
Laboratory findings in compensation
1. ctCO2 increased
2. PCO2 increased
3. pH normal
ACID-BASE
✔ DISORDERS:
C. Respiratory Alkalosis: (Hypocapnia)
Decreased PCO2 results from an accelerated rate or depth of respiration, or a combination of both. Excessive
exhalation of carbon dioxide (hyperventilation) reduces the PCO2, causing a decrease in the concentration of
dissolved carbon dioxide, which forms less carbonic acid in the blood. This increases the 20:1 ratio between
cHCO3⁻ and cdCO2, which increases the blood pH
may be caused by:
• hypoxia, anxiety, nervousness, excessive crying, pulmonary embolism, pneumonia, congestive heart
failure, salicylate overdose
ACID-BASE
✔ DISORDERS:
C. Respiratory Alkalosis: (Hypocapnia)
Laboratory findings in respiratory acidosis
1. ctCO2 normal
2. PCO2 decreased
3. pH increased
renal compensatory mechanism corrects respiratory alkalosis by excreting bicarbonate.
Laboratory findings in compensation
1. ctCO2 decreased
2. PCO2 decreased
3. pH normal
OXYGEN METABOLISM:

❑ Oxygen is transported bound to hemoglobin present in red blood cells and in a physically dissolved state.
❑ Three factors control oxygen transport:
1. PO2
2. free diffusion of oxygen across the alveolar membrane
3. affinity of hemoglobin for oxygen.
❑ Note: Release of oxygen to the tissues is facilitated by an increase in H+ concentration and PCO2 levels at the
tissue level.
❑ Note:
Under normal circumstances, the saturation of hemoglobin with oxygen is 95%.
When the PO2 is >110 mmHg, greater than 98% of hemoglobin binds to oxygen
When a person's oxygen saturation falls below 95%, either the individual is not getting enough oxygen or does
not have enough functional hemoglobin available to transport the oxygen.
❑ Clinical significance of PC>2 levels in blood:
▪ Increased values (>95%) are observed with supplemental oxygen.
▪ Hypoxemia: Causes include decreased pulmonary diffusion, decreased alveolar spaces due to resection or
compression, and poor ventilation/perfusion (due to obstructed airways—asthma, bronchitis, emphysema,
foreign body, secretions)
 MORE SUMMARIES
FOR EASIER LIFE!! ☺
• Reference ranges for arterial blood
gas analysis

• pH: 7.35-7.45
• ctCO2: 22-26 mmol/L
• PCO2: 35-45 mm Hg
SAMPLE COLLECTION AND HANDLING:
ANTICOAGULANT: HEPARIN
Must use anaerobic collection for blood pH and blood gas studies
If blood is exposed to air:
• CO2 and PCO2 – decrease
• pH increase
• PO2 increase
If testing prolonged (>20mins) blood should be kept in cracked ice to prevent
glycolysis, which leads to:
• CO2 and PCO2 – increase
• pH decrease
• PO2 decease
 ✔
HOW TO EVALUATE BLOOD GAS THE EASY
✔

WAY:
Look at the pH, determine if acidosis or alkalosis
Compare pCO2 and HCO3⁻ to “NORMALS”
pCO2 going opposite pH = RESPIRATORY
HCO3⁻ going the same direction as pH =
METABOLIC
If pH is normal, full compensation occurred
If main compensatory mechanism kicked in, but
pH still out of normal range, partial compensation
has occurred
EFFECTS OF BLOOD pH TO PLASMA ELECTROLYTES:
pH of blood can alter the levels and movements of electrolytes
ACIDOSIS: RBCs also buffer the excess hydrogen ions by exchanging these for
cellular potassium, producing a mild hyperkalemia
 Can also cause Hypercalcemia
ALKALOSIS: increased bicarb in plasma causes shifting of plasma potassium into
cells, creating hypokalemia
 Can also cause Hypocalcemia
REMEMBER!!!:
The body’s cellular and metaolic activities are pH-dependent = body will try to return
to normal pH if there is an imbalance occuring
FULL COMPENSATION = pH returns to normal
PARTIAL COMPENSATION =. pH nears normal range
Lungs can compensate immediately but the response is short-term and incomplete
Kidneys are slow in its response but long-term and complete
METHODS:

 SAMPLE COLLECTION:
 SX: arterial blood
 Anti-CoA: 0.05 Heparin/mL of blood
 NOTES:
• Syringe: 1-3mL, pre heparinized
• Newborn: collection through indwelling umbilical artery catheter
• Excess heparin should be avoided = causes false decrease in blood pH
• Use of liquid heparin can cause erroneous results = excessive amt can dilute or possibly contaminate the
sample if equilibrated with room air
• perform ALLEN TEST
• 45-90o angle of the needle
• No Bubbles trap
• Mix adequately
• Keep syringe capped before analysis
METHODS:

 SAMPLE CONSIDERATIONS:
 must be processed immediately (less than 30mins)
 Transport: Place in ice water to prevent cellular metabolsm and accumulation of acidic by-
products
 blood samples should be chilled (if there is a delay)=prevents O2 consumption of RBCs and
release of acidic metaabolites
 On standing:
• pH and pO2: DECREASE
• pCO2: INCREASE
 Excess Heparin = Downward shift of blood pH
 Glycolysis = decrease blood pH
METHODS:

 SOURCE OF ERRORS:
 Transport and storage
 Type and Heparin Concentration
 Speed of SYringe filling
 Maintenance of sample Anaerobiosis
 Inadequate mixing of sample
 Blood collection Device
 Sample condition (leukocytosis and thrombocytosis)
FACTORS AFFECTING BLOOD GASES AND MEASUREMENTS:

 TEMPERATURE
• the electrode sample chamber be maintained at constant temperature for all measurements
• NOTE: Each degree o fever in the patient = pO2 will fall 7% and pCO2 will rise 3%
 ELEVATED PLASMA PROTEIN CONCENTRATIONS
• pO2 test is affected by build-up of proteins on the surface of the membrane
 BACTERIAL CONTAMINATIONS
• Bacterias consume oxygen and cause low values of pO2
 IMPROPER TRANSPORT OF SPECIMEN
• if not transported on ice water: pO2 changes more rapidly than pH and pCO2
LACTIC ACIDOSIS:

 Definition: the excessive accumultion of lactic acid in plasma due to:

 Over production
 defective removal by the renal and hepatic systems
 underutilization
 Definition: inability of mitochondria to process the amount of pyruvate with which it is presented
 produced from pyruvic acid by the action of lactate dehydrogenase and NAD
 usually seen in cases of tissue hypoxia
 characterized bu elevated anion gap and low blood pH
 Two Forms:
• L-Lactate: most common cause of Lactic Acidosis
• D-Lactate
 Method: ENZYMATIC
• L-Lactate Dehydrogenase
• Lactate Oxidase: most common
LACTIC ACIDOSIS:

 Causes:
• Sepsis
 septic shock: >2mmol/L
• Cancer
• Seizure
• Heart Failure
• Liver & Kidney diseases
• Uncontrolled DM
• Hemorrhage
• Poisoning
• HIV infection
• Vitamin Deficiency
• Treatment Overdose
LACTIC ACIDOSIS:

 Reference range:
• Venous Blood Lactate: 5-20mg/dL (0.6-2.2 mmol/L)
• Arterial Blood Lactate: 3-mg/dL (0.3-0.8 mmol/L)
 Interpretation of results:
• Indication of sepsis: >19mg/dL (>2mmol/L)
• Diagnostic level: >45 mg/dL (>5mmol/L)
 Patient and Sample Preparation:
• Avoid exercise
• Blood should be drawn without tourniquet
• SX req: Gray-top or any Anti-glycolytic tube for plasma sample
LACTIC ACIDOSIS:

 Types of Lactic Acidosis:

① Type A-Hypoxic Lactic Acidosis:
 related with decreased oxygenation (with tissue hypoxia)
 Causes: Shock,MI, Severe CHF, Seizures, Pulmo edema, hypovolemia

② Type B-Metabolic Lactic Acidosis

 mostly associated with diseases and high demand of cellular oxygen (NO TISSE HYPOXIA)
 Causes: Severe Infection, Cancer, Leukemia, Liver and Renal dse, DM, Intoxication, Inborn errors of
matabolism
CSF LACTATE:

 Aids in the diagnosis of meningitis

 assists in the differentiation off bacterial meningitis and viral meningitis