Electrolytes
particularly hypothalamus is signaling that you are thirsty, so
―are ions (minerals) capable of carrying an electric charge
Cations: electrolytes with positive charge that move toward
the cathode (- charged area)
Anions: electrolytes with negative charge that move toward
the anode (+ charged area)
They are essential components in numerous processes:
 Volume and osmotic regulation
 Myocardial rhythm (*hea rt bea t) & neuromuscular
excitability
 Cofactors in enzyme activation (*enha nces enzyme
rea cti on )
 Regulation of adenosine triphosphate (*ADP prod.)
 Ion pumps & acid-base balance (*pH; a ci di c bl ood –
a ci dos i s a nd a l ka l i ne bl ood- a l ka l os i s )
 Blood coagulation (*ca s ca de  Ca 2+ i s i nvol ved )
 Production & use of ATP (*energy formed ) from
glucose
WATER
Body is composed of 40-70% water, which declines with
age & obesity
*the more fa t you a re, the l es s er wa ter
Water Content
1. Intracellular fluid: 2/3 of total body water
2. Extracellular fluid: other 1/3, fluid found outside the
cell
a. Intravascular fluid  plasma; BV (where
blood flows), veins, arteries
b. Interstitial fluid  surrounds cells/ tissues
c. Transcellular fluid  CSF, serous fluid, etc.
● Distribution of water in fluid compartments is controlled by
maintaining the concentration of electrolytes and proteins in
the individual compartments
1. Active transport: mechanism requires energy to
move ions across cellular membranes
2. Diffusion: passive movement of ions across
membranes; movement of water molecules from
higher to lower concentration and is moved by
osmotic gradient
OSMOLALITY
● Is a physical property of a solution that is based on the
concentration of solutes (mOsm/kg)
● Measure the number of dissolve particles/substances in the
solution
● Normal plasma osmolality: 275 to 285 mOsm/kg
● Maintained by thirst (*↑ plasma osmolality  brain
your body have to dilute the dissolved particles in the blood
to normalize the range by drinking water or stimulating AVP)
and AVP (arginine vasopressin hormone): same as ADH (anti-
IHI hormone; ↑ADH: the lesser you will urinate because
water are conserved)
Regulation of Blood Volume
● RAAS (renin-angiotensin-aldosterone system)
Four other factors that affect Blood Volume
1. ANP (atrial natriuretic peptide) release
2. Independent volume receptors release AVP
3. ↑GFR (glomerular filtration rate) with ↑vol.
expansion
4. ↑ Na+ will cause ↑ Na+ urinary excretion
Determination of Osmolality
 Serum or urine may be used as sample
 Principle: Freezing point or vapor pressure
(colligative properties of solution)
 Method: OSMOMETRY (*depending on the principle
applied), below are the two kinds
a) Freezing point depression osmolality
b) Vapor pressure depression osmolality
 Calculated osmolality useful for determining true
osmolality and osmol gap
Osmolal gap: difference between the measure osmolality and
the calculated osmolality
RR for Osmolality
Serum 275 to 295 mOsm/kg
Urine (24 h) 300 to 900 mOsm/kg
Urine:Serum ratio 1.0-3.0
Random urine 50 to 1200 mOsm/kg
Osmolal gap 5 to 10 mOsm/kg
↑ Osmol gap = alcohol toxicity, ethylene glycol poisoning, so
on.
(Note: Os mol gap i ndirectly i ndicates the pres ence of os moti ca l l y
a cti ve substances other than Na+, urea or gl ucose, such as etha nol ,
metha nol , ethyl ene gl ycol , l a cta te or B-hydroxybutyra te)
 HYPONATREMIA  low serum/plasma Na+ levels, usually
less than 135 mmol/L

SODIUM
● Most abundant in the ECF (like plasma)
● Represents 90% of all extracellular cations and largely
determines the osmolality of the plasma (*sodium plays a
huge role in dictating plasma osmolality)

Regulation:
A. Intake of H2O in response to thi rst as
stimulated/suppressed by plasma osmolality
B. Excretion of H2O, largely affected by AVP release to
changes in either blood volume or osmolality or
blood pressure
C. Blood Volume status which affects Na+ excretion
through RAAS and AVP
*Ketonuri a (a ffect rera bs orpti on) - ketones i n uri ne
*Sa l t-losing nephropathy -tubules of nephrons (da ma ged ki dney)
Method: DIRECT & INDIRECT ISE (ion selective electrode) *Dehydra ti on – you onl y not l os s wa ter, but a l s o el ectrol ytes
Specimen: Serum, plasma or urine (24h) *↑H2O retenti on – di l uti on of Na + i n bl ood
Principle: POTENTIOMETRY *The Na + is l ow not because it i s really decreased, but beca us e the
H2O i s i ncrea s ed
RR for Sodium *Nephroti c s yndrome – edema tous s i pa ti ent
*SIADH (syndrome of i nappropriate ADH) - ↓ADH (di l uti on effect)
Serum, plasma 135 to 145 mOsm/kg *Ps eudohypona tremi a (fa l s e hypona tremi a )
Urine (24 h) 120 to 140 mmol/d, varies
with diet
CSF 136 to 150 mmol/L

HYPERNATREMIA  values over 145 mmol/L
*D.I. - ↓ADH ↑uri na ti on
*Profus e s wea ti ng – l os s of s odi um
*Ei ther Na + i s reta i ned or ↑ i nges ti on of s a l t
*Admi nistration of hypertonic solution (many electrolytes, heavy s p.
gra vi ty) bei ng us ed duri ng di a l ys i s , etc.
POTASSIUM
+
● 𝐾 is the major intracellular cation in the body, with a
concentration 20 times greater inside the cells than outside.
● Many cellular functions require that the body maintain a
low ECF concentration of potassium ions.
● 2% of body’s total 𝑲+ ions: circulates in plasma
FUNCTIONS OF POTASSIUM IN THE BODY
 Regulation of neuromuscular excitability: affects
resting membrane potential (RMP); nerves, muscle
 Contraction of the heart [lethal injection,
𝐾 + (specifically KCl) is the one to inject w/c stops the
heart]
 ICF volume
 𝐻 + concentration
*res ti ng membra ne potenti a l – l evel of mus cl e a t res t
Regulation:
● Renal function related to tubular reabsorption and
secretion is important in the regulation of potassium balance
Three factors that influence distribution of potassium ions
between cells & ECF are as follows:
1. 𝑲+ loss frequently occurs whenever 𝑁𝑎+ , 𝐾 + -
ATPase pump is inhibited by conditions such as
―hypoxia, hypomagnesemia, or digoxin overdose
2. Insulin promotes acute entry of 𝑲+ into skeletal
muscle and liver by increasing 𝑁𝑎 + , 𝐾 + -ATPase
activity
 3. Catecholamines such as epinephrine ( 𝐵 2- Hyperkalemia  plasma 𝐾 + levels is high or above the
stimulator), promote cellular entry of 𝑲 + whereas reference range
propranolol (B-blocker) impairs cellular entry of 𝐾 +
EXERCISE
 𝐾 + is released from muscle cells during exercise,
which may increase plasma 𝐾 + by 0.3 to 1.2 mmol/L
but can be reversed after several minutes

HYPEROSMOLALITY
 As with uncontrolled DM, causes water to diffuse
from cells, carrying 𝐾 + with water which leads to
gradual depletion of 𝐾 + if kidney function is normal

CELLULAR BREAKDOWN
 This releases 𝐾 + into ECF (e.g severe trauma, tumor
lysis syndrome & massive blood transfusions)

CLINICAL APPLICATIONS
Hypokalemia  plasma 𝐾 + concentration below the lower
limit of the reference range

*cel l ular damage >> l eak out si K from cells to plasma >> i ncreased
*a rti factual – human error

Method: Ion Selective Electrode

Principle: based on POTENTIOMETRY
Specimen: Serum, plasma or urine may be acceptable for
analysis (Avoid hemolysis! = FALSE INCREASE because erythrocytes
have high potassium ions content)
NOTE: SERUM > PLASMA (serum have higher values)
Heparin: anticoagulant of choice (whereas serum/plasma
gives similar 𝐾 + levels)

RR for Potassium
Serum 3.5 to 5.1 mmol/L
Urine (24 h) 36 to 86 mmol/L

CHLORIDE
−
● 𝐶𝑙 is the major extracellular anion
● Its precise function in the body is not well understood;
however, it is involved in maintaining osmolality, bl ood
volume and electric neutrality (electroneurality)
*↓i nta ke: hydration ● Passively reabsorbed, in conjunction with sodium by the
*ma l absorption: parasite- Giardia Lambia proximal tubules
*l a xatives – i nduce diarrhea
● In most processes, chloride shifts secondarily to movement
of sodium or bicarbonate ions
● Completely absorbed by: GI TRACT
● Filtered out by: GLOMERULUS
CLINICAL APPLICATIONS ● ↑total CO2 concentrations  occur in metabolic alkalosis
● Chloride disorders are often a result of same causes that as 𝐻𝐶𝑂3 − is retained, often with ↑pCO2 due to
disturb 𝑁𝑎 + levels because 𝐶𝑙 − passively follows sodium compensation by hypoventilation
ions
Typical causes of metabolic alkalosis
HYPERCHLOREMIA (↑ 𝐶𝑙 − lvls)  occur when there is an  Severe vomiting
excess loss of 𝐻𝐶𝑂3 − as a result of GI loses, RTA, OR  Hypokalemia
metabolic acidosis  Excessive alkali intake
↑ 𝐶𝑙 − = ↓𝐻𝐶𝑂3 −
Method: ISE or enzymatic methods
−
HYPOCHLOREMIA (↓ 𝐶𝑙 lvls)  occurs when excessive Specimen: Serum/plasma (Li Heparin)
loss of 𝐶𝑙 − from prolonged: RR: venous, 22 to 28 mmol/L
a) Vomiting
b) Diabetic ketoacidosis MAGNESIUM
c) Aldosterone deficiency
● 4th most abundant cation in the body
d) Salt-losing renal diseases (pyelonephritis) nd
● 2 most abundant intracellular ion after potassium ions
Low serum level of 𝐶𝑙 − may also be encounted in conditions
● About 53% of 𝑴𝒈𝟐 + in the body : found in the bone
with high serum 𝐻𝐶𝑂3 − concentrations such as:
● 46% : muscle, other organs & soft tissue
a) Compensated respiratory acidosis
● <1% : present in serum and RBCs
b) Metabolic Alkalosis
 1/3: protein bound
↓ 𝐶𝑙 − = ↑ 𝐻𝐶𝑂3 −
 Remaining 2/3: 61% is free/ionized and 5% is
complexed with other ions
Method: Ion Selective Electrode
Specimen: Serum, plasma, urine or sweat
FUNCTION
Lithium heparin: anticoagulant of choice
 Essential co-factor of >300 enzymes (including those
important in glycolysis)
RR for Chloride
 Transcellular ion transport
Serum 98 to 107mmol/L  Neuromuscular transmission
Urine (24 h) 110 to 250 mmol/d, varies  Synthesis of carbohydrates, proteins, lipids & nucleic
with diet acids
 Release of and response to certain hormones
BICARBONATE
nd
● 2 most abundant anion in the ECF Regulation:
● Total CO2 comprises the bicarbonate ion 𝐻𝐶𝑂3 − , H2CO3 ● Henle’s loop is the major renal regulatory site, where 50%
and dissolved 𝐶𝑂2 − to 60% of filtered 𝑀𝑔2 + is reabsorbed in ascending limb
 𝐻𝐶𝑂3 − accounts for more than 90% at physiologic ● Related to that of 𝐶𝑎2 + and Na+
pH ● PTH increases the renal reabsorption of 𝑀𝑔2 + and
 Total CO2 measurement is indicative of 𝐻𝐶𝑂3 − enhances intestinal absorption of 𝑀𝑔2 +
measurement
● Important for buffering blood (maintains correct pH of
blood: 7.35 to 7.45)

REGULATION
Most 𝑯𝑪𝑶 𝟑 − (85%) in the kidneys is reabsorbed: PROXIMAL
TUBULES
15% is being reabsorbed: DISTAL TUBULES

CLINICAL APPLICATIONS
● Acid-base imbalances cause changes in 𝐻𝐶𝑂3 − and CO
levels
● ↓HCO-  may occur from metabolic acidosis as 𝐻𝐶𝑂3 −
 CALCIUM
+
● 99% of 𝑪𝒂𝟐 in the body: part of bone
● Remaining 1%: mostly in the blood & other ECF

The other 1%:

 45% is free, ionized (closely regulated to maintain
muscle contractility)
 40% bound to protein (albumin)
 15% bound to anions

● Three hormones― parathyroid hormone, vit.D & calcitonin

are important for maintaining 𝐶𝑎2 + concentration
Hormone: Effect on Calcium:
PTH increased calcium
VIT.D increased blood calcium
CALCITONIN decreases calcium level in the blood

PTH
bone >> activates bone resorption >> osteoclasts break down bone
>> release calcium into ECF >> blood = ↑Ca
* cons erves ca l ci um by i ncrea s i ng the tubul a r rea bs orpti on
* s ti mul a tes rena l producti on of a cti ve vi ta mi n D

Vit.D
renal reabsorption >> calcium retention = ↑Ca
*cholecalciferol: obta ined from diet or exposure of s kin to a ctivation
of a bs orba bl e s unl i ght to ki dney
* enha nces the PTH effect on bone res orpti on

Calcitonin
calcitonin >> inhibit action of Vit. D & PTH (hormone produced by
thyroid gland) = ↓Ca
*a ppa rentl y not s ecreted duri ng norma l regul a ti on of i oni zed
ca l cium conc. in the bl ood, i t i s s ti l l be excreted i n res pons e to
hyperca l cemi c s ti mul us

● ↓ ionized 𝐶𝑎2 + concentrations in the blood can cause

neuromuscular irritability which may become clinically
apparent as irregular muscle spasms called tetany.
*teta ny – a s ymptom i n whi ch na gka ka roon ng i nvol unta ri l y
*a nta cids – hyperacidity contra cti on of mus cl es
*enemas – counter react

Method: 3 most common colorimetric ―calmagite, formazan

dye and methylthymol blue
Specimen: Serum, plasma, urine (AVOID HEMOLYSIS!)

RR for Magnesium
Serum (colorimetric) 0.66 to 1.07 mmol/L
(1.7 to 2.4 mg/dL)
Figure 11.5 Hormonal response to hypercalcemia and
hypocalcemia; PTH: 25-OH; Vit.D: 25-hydroxyvitamin D; 1,25
(OH)2 vit D, dihydroxyvitamin D

*ta ke note of the a dult normal values

PHOSPHATE
● Predominant intracellular snion
● 80% : bone
● 20% : soft tissues
● <1% : plasma
● Found in all living cells ― DNA, RNA, ATP, CPK, PEP, etc.

Hypophosphatemia  low level of phosphate

Can be caused by: SAD-C-AIVH
 S epsis
 A lcoholism
 D KA
 C OPD
 A sthma
 I nflammatory bowel disease
 V it.D deificiency
Specimen: Serum, plasma, urine (IONIZED SAMPLES)
 H yperparathyroidism

Hyperphosphatemia  high levels of phosphate

Can be caused by:
 Renal disease (common in neonates)
 Intense exercise (can be seen)
 Neoplastic disorders
 Intravascular hemolysis

Specimen: Serum, plasma, urine (INORGANIC PHOSPHORUS:

Avoid hemolysis!)
 LACTATE
↑AG
● Is a by-product of emergency mechanism tha t produces a
 Uremia/renal failure which leads to 𝑃𝑂4 − and 𝑆𝑂42
small amount of ATP when oxygen delivery is severely
retention
diminished
 Ketoacidosis (as seen in cases of starvation/diabetes)
 Methanol, ethanol, ethylene gl ycol or salicylate
Method: Enzymatic methids
poisoning
Specimen: Serum & plasma
 Lactic acidosis
Venous stasis = ↑lactate levels (AVOID TOURNIQUET
 Hypernatremia
APPLICATION IF POSSIBLE)
 Instrument error

RR for Lactate ↓AG

Venuous 0.3 to 2.0 mmol/L (2.7 to 18  Hypoalbuminemia (decreased in unmeasured
mg/dL) anions)
Arterial 0.3 to 1.6 mmol/L (2.7 to  Severe hypercalcemia (increased in unmeasured
13.5 mg/dL) cations)

↑LACTATE = acidosis & cellular death

Anion Gap
● AG is the difference between unmeasured anions &
unmeasured cations
 No actual “gap” but useful for determining an
increase in one of more of the unmeasured anions or
a QA issue with the instrument
 Two equations used, with different RR
 ACID-BASE BALANCE REFERENCE RANGES
Total CO2/ctCO2 or HCO3-/ bicarbonate concentration
Maintenance of H+
= 22 to 26 mmol/L
Acid  substance that can donate hydrogen ions when
Partial Carbon Dioxide (PCO2)
dissolved in H2O
= 35 to 45 mmHg
Base  substance that can donate hydrogen ions
4 KINDS OF ACID-BASE DISORDERS:
1. Respiratory Acidosis
2. Metabolic Acidosis
Buffer Systems: Regulation of 𝐻 + and the Henderson- 3. Respiratory Alkalosis
Hasselbalch Equation 4. Metabolic Alkalosis
*buffer consists of a weak acid and a salt of its conjugate
base, and it allows a solution to resist changes in pH upon *↑7.45 – ALKALOSIS *RESPIRATORY- N: HCO3-
adding acid or base *↓ 7.35 – ACIDOSIS *METABOLIC- N: pCO2

R espiratory is
O pposite
M etabolic must be
REGULATION OF ACID-BASE BALANCE: LUNGS & E qual (*same direction)
KIDNEYS (TRANSPORT OF CARBON DIOXIDE)
● The end product of most aerobic metabolic processes, *ang titignan na Equal is yung pH and bicarbonate conc.
easily diffuses out of the tissue where i t is produced and into e.g ↑pH ↑HCO3  METABOLIC ALKALOSIS
the plasma and RBCs of the surrounding capillaries. *check for pH and partial CO2 ang titignan na Opposite
● Dissociation of H2CO3 causes the development of a e.g ↓pH ↑pCO2  RESPIRATORY ACIDOSIS
concentration gradient due to the increase in red blood cells.
● Beyond reabsorption of bicarbonate, the other major METABOLIC ACIDOSIS
function of the kidneys’ buffering capacity is excreting Expected Lab Findings:
hydrogen ions. Bicarbonate is DECREASED
pH is DECREASED
Assessment of Acid-Base Homeostasis Partial CO2 is NORMAL

Acid-Base Disorders: Acidosis and Alkalosis

METABOLIC ALKALOSIS
● When blood pH is less than the RR (7.35 to 7.45), it is
Expected Lab Findings:
academia/acidosis
Bicarbonate is INCREASED
Acidosis may be caused by:
pH is INCREASED
Primary metabolic or respiratory imbalance
Partial CO2 is NORMAL
Primary metabolic acidosis: the amount of acid exceeds the
capacity of the buffer systems, and there is a decrease in RESPIRATORY ACIDOSIS
bicarbonate Expected Lab Findings:
Bicarbonate is NORMAL
pH is DECREASED
Partial CO2 is INCREASED

● Body compensates for metabolic acidosis through RESPIRATORY ALKALOSIS

hyperventilation, which is an increase in the rate or deth of Expected Lab Findings:
breathing. Bicarbonate is NORMAL
*Arterial Blood Gas Analysis pH is INCREASED
Sample used: Arterial Blood to determine acid-base status of Partial CO2 is DECREASED
the patient
 Compensation Mechanism ● Respiratory alkalosis means pH is increased and pCO2 is
decreased >> but when compensated by kidney which is
● regulated by the help of kidney and lungs (*gagawa ng called RENAL COMPENSATION OR RENAL COMPENSATORY
paraan yung body natin para di tuluyang bumagsak yung pH
MECHANISM (kidney will try to excrete excess HCO3-) >>
natin) there will be ↓HCO3- ↓partial CO2 result (unchanged) >> pH
*note  NORMAL HCO3- RATIO IS 20:1 then be decreased = NORMALIZED 
● Metabolic Acidosis (Primary Bicarbonate Deficit) – patient
EXPECTED LABORATORY FINDINGS IN COMPENSATION
will experience symptoms TO RESPIRATORY ALKALOSIS:
*with diabetes people are common to have this as they have HCO3- is DECREASED
what we so-called “ketoacidosis” pH is now, NORMAL
pCO2 is DECREASED
● Metabolic acidosis is compensated by the lungs so pH will *goal of compensatory mechanism: to bri ng back your blood a t
be normalized  and this is called RESPIRATORY norma l pH
COMPENSATION OR RESPIRATORY COMPENSATORY
MECHANISM (again, to go back to normal level) >> may SUMMARY: EXPECTED LABORATORY FINDINGS
compensate through hyperventilation which lowers pCO2 >> Acid-Base Baseline/Original In compensation
results to increase in pH (*kasi nga acidosis deba so decreased si Disorder Finding
pH, itataas thru this para mag-normal :>)
Metabolic ↓ HCO3- ↓ HCO3-
EXPECTED LABORATORY FINDINGS IN RESPONSE Acidosis ↓ pH N: pH
TO METABOLIC ACIDOSIS:
N: pCO2 ↓ pCO2
HCO3- is DECREASED
Metabolic ↑ HCO3- ↑ HCO3-
pH is increased so now, NORMAL (*successful compensation)
Alkalosis ↑ pH N: pH
pCO2 is DECREASED
N: pCO2 ↑ pCO2
Respiratory N: HCO3- ↑ HCO3-
● Metabolic alkalosis is compensated by the lungs so pH will
Acidosis ↓ pH N: pH
be normalized  and this is called RESPIRATORY
COMPENSATION OR RESPIRATORY COMPENSATORY ↑ pCO2 ↑ pCO2
MECHANISM (again, to go back to normal level) >> may Respiratory N: HCO3- ↓ HCO3-
result to hypoventilation (*slow down breathing) which retains Alkalosis ↑ pH N: pH
or conserves more CO2 >> ↑pCO2 >> ↓pH >> bicarbonate or ↓ pCO2 ↓ pCO2
total CO2 will then be remain increased
EXPECTED LABORATORY FINDINGS IN RESPONSE Blood Gas Analyzers: pH, pCO2 and pO2
TO METABOLIC ALKALOSIS: ● Blood gas analyzers use electrodes (macroelectrochemical
HCO3- is INCREASED sensor) as sensing devices to measure pO2 and pH
pH is now, NORMAL ● The pO2 measurement is AMPEROMETRIC
pCO2 is INCREASED ● Potentiometry measures the electric otential between two
electrodes, in which a change in voltage indicates the
● Respiratory acidosis means that the patient tend to have concentration of each analyte
difficulty in exhalation of CO2 (HYPOVENTILATION) >> *basahin daw from this to pababa dahil baka kumuha here si
compensated by kidney and this is call ed RENAL ma’am vergeeee, kayang kaya na daw natin e2 (di mo sure
COMPENSATION OR RENAL COMPENSATORY MECHANISM char! GO GUYS OKI GAHAHAHA)
(tubular secretion/reabsorption wherein kidney will try to
increase HCO3- conc.) >> raises the blood pH then be Measurement of pO2
NORMALIZED  ● pO2 electrode is an amperometric electrode, often referred
EXPECTED LABORATORY FINDINGS IN COMPENSATION to as a ‘Clarke electrode.’
TO RESPIRATORY ACIDOSIS: ● Selectively allow O2 to diffuse into the electrolyte solution
HCO3- is INCREASED
pH is now, NORMAL Measurement of pH and pCO2
pCO2 is INCREASED (a.k.a. hypercapnia) ● Glass membrane sensitive to H+ is placed around an
internal Ag-AgCl (silver chloride) electrode to form a
measuring electrode
*again, we used arterial blood specimen in blood gas analysis
Anticoagulant of choice: HEPARIN (*di ilalagay sa test tube,
aspirated by syringe and spread it out a little bit to the barrel)
Manner of collection: arterial puncture, vertical puncture
collection
*syringe must be on ice bath or bring ice tubes when
assigned to collect but usually performed by physician or
trained health care worker on the said test as this is prone to
embolism
TYPES OF SENSORS
Spectrophotometric Determination of Oxygen
Saturation (Co-Oximetry)
● Actual percent oxyhemoglobin (O2Hb) can be determined
spectrophotometric using a CO-oximeter designed to directly
measure the various hemoglobin derivatives
● CO-oximeters should have four wavelengths― HHb, O2Ht,
COHb and MetHb
*5 wavelenghts can also measure sulfhgb as well as recognize
dyes and pigments, turbidity and abnormal proteins

1. Macroelectrode - have been used in blood gas

instruments since the beginning of the clinical
measurement of blood gases
2. Thick and thin film technology - is a further Quality Assurance
modification of electrochemical sensors PRE-ANALYTICAL CONSIDERATIONS
3. Optical sensors - are another form of technology Sources of error in the collection and handling of blood gas
that is used for blood gas specimens include the ff:
● Collection device
Calibration ● Form and concentration of heparin used for anti -
coagulation
Two different gas mixtures with known pCO2 and pO2 levels ● Speed of syringe filling
are used―
● Maintenance of the anaerobic environment
 One of the mixtures: is used to calibrate the lower ● Mixing of the sample to ensure dissolution and distribution
end, and the composition of this mixture is 0% O2 of the heparin and transport & storage time before analysis
and 5% CO2
 Second mixture: Used to calibrate the gases on the
upper end & the composition is 20% O2 and 10%
CO2
*sa inyo na yan (>___<) what u see, what u get basta ang
tinuro ko sa inyo is yung acid-base balance

Correction for Temperature

● When temperature-corrected results are reported, it is
critical that results also be reported with the 37 degree
Celsius (non-corrected) results

Calculated Parameters
● HCO3- measurement is based on the Henderson-
Hasselbalch equation and can be calculated when pH and
pCO2 are known
● Carbonic acid (H2CO3) concentration can be calculated
using the solubility coefficient of CO2 in plasma at 37°C
● ctCO2 is the bicarbonate + dCO2 (carbonic acid) +
associated CO2 with proteins
● Base excess is calculated from an algorithm uses the
patient’s pH, pCO2 and hgb