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20 Hydroelectrolytic Disorders
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Therapy aims to increase potassium levels, minimize
ongoing losses, and treat the underlying disease to prevent
complications. KCl administration (potassium chloride) is
the choicetherapy. KCl results in a rapid increase in plasma
potassium concentration. In addition, the persistence of the
Cl− ion in ECF limits the initial potassium entry into the
cells, thus promoting an increase in plasma potassium.
Finally, chloride supports metabolic alkalosis, often associated with hypokalemia. In cases of mild hypokalemia, KCl
is administered orally or intravenously, in more severe
cases.
Hyperkalemia
Hyperkalemia, dened as plasma K+ concentration
>5 mmol/L, may be due to reduced renal K+ excretion+,
increased cellularK+release, increased K+intake, and pseudohyperkalemia (Table 20.6). Increased dietary K+ intake
alone generally does not cause hyperkalemia because excess
K+ is rapidly excreted by the adaptive mechanism based on:
• Increased cellular potassium uptake, facilitated by
insulin
• Increased beta-2 adrenergic tone
• Increased urinary potassiumexcretion
Therefore, hyperkalemia from increased intake canoccur
in the presence of other clinical conditions, such as renal
impairment.
Pseudohyperkalemia represents an articial increase in
plasma potassium concentration due to potassium leakage
from cells during venous sampling. Thrombocytosis causes
hyperkalemia due to the potassium release by platelets
during coagulation. Pseudohyperkalemia should be suspected in asymptomatic patients with no obvious underlying cause.
The etiology of hyperkalemia is often multifactorial;
impaired renal function, medications, and hyperglycemia are
the primary causes.
The symptoms of hyperkalemia are due to the difference
in potassium concentration between ICF and ECF, which
inuence the resting membrane potential. Hyperkalemia
results in partial membrane depolarization. The progression
of the clinicalpicture is characterized by prolongedcellular
depolarization , which reduces membrane excitability and is
manifested by asthenia, which may progress to accid
paralysis and hypoventilation. In addition, cardiovascular
Table 20.6 Causes of hyperkalemia
Reduced renal excretion Chronic renal failure
Increased potassium
intracellular release
Increased intake Potassium supplements
Pseudohyperkalemia Hemolysis
Acute renal failure
Drugs:
– Inhibitors of the enzyme that
converts angiotensinogen
– Angiotensin receptor blockers
– Nonsteroidal anti-inammatory
drugs
– Potassium-sparing diuretics
– Heparin
– Lithium
– Calcineurin inhibitors
Reduced distal renal ow
Hypoaldosteronism
– Hyporeninemic
hypoaldosteronism
– Adrenal insufciency
– Adrenocorticotropic hormone
deciency
Tubular diseases
– Obstructive uropathy
– Hereditary tubular defects
– Amyloidosis
Insulin deciency/resistance
Metabolic and respiratory acidosis
Hypertonicity
– Hyperglycemia
– Mannitol
Drugs
– Beta-blockers
– Digitalis poisoning
– Somatostatin
– Arginine
– Succinylcholine
Increased tissue catabolism
– Hemolysis
– Widespread trauma
– Rhabdomyolysis
Hyperkalemic periodic paralysis
Intense physical exercise
Blood transfusion
Foods
– Tourniquet kept for an excessive
period
– Excessive patient muscle
contraction during sampling
– Too rapid aspiration of blood by a
ne needle
Thrombocytosis (platelet count >106)
symptoms, such as bradycardia, hypotension, and conduction disturbances up to the cardiac arrest can also occur.
Numerous electrocardiographic alterations may occur during hyperkalemia.
280
Hyperkalemia
ACE inhibitors)
hear
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M. Ciaccio et al.
Fig. 20.9 Diagnostic
algorithm of hyperkalemia.
(Copyright EDISES 2021.
Reproduced with permission)
Measure magnesium and supplement if it is low
[Na
<25 mmol/L
Reduced distal
renal flow
(AKI, CKD,
t failure, etc.)
([K+] serum > 5 mmol/L)
Evaluation of severe signs
and symptoms
NO
Pseudohyperkalemia
Assessment
NO
Assessment of increased dietary intake
NO
+
] urine
or transcellular shift
Serum [Aldosteron]
Normal
YES
Low
YES
YES
Tr eat
according
to etiology
Urgent therapy
No further
investigation
Diagnosis andTherapy
Similar to hypokalemia, hyperkalemia alterscardiac conduction and muscle strength. Initial efforts should focus on
determining the need for urgent intervention (Fig.20.9). The
absence of symptoms does not rule out severe hyperkalemia
because it is often asymptomatic.
The hyperkalemia severity is assessed based on symptoms, plasma potassium concentration, and electrocardiographic alterations. A careful medical history is essential to
identify the possible drugsintake that alter potassium excretion or induce its release from the cells. Urinary sodium,
serum aldosterone and renin levels, and acid–base balance
assessed by hemogasanalysis provide helpful information
for the differential diagnosis (Fig.20.8).
If the etiology is not initially evident and the patient is
asymptomatic, the presence of pseudohyperkalemia should
be evaluated.
Therapy depends on the degree of hyperkalemia,
which is determined by potassium concentration, muscle
Drugs,
amyloidosis, etc.
Primary adrenal
insufficiency,
Serum [Renin]
Normal Low
Hyperglycemia,
drugs
(heparin,
tubular disorders,
(e.g. beta-blockers)
drugs
signs, and electrocardiographic changes. Therapy aims to
block the effects of hyperkalemia on cell membranes,
increase potassium transfer within cells, and remove
excess potassium and the cause of hyperkalemia. This is
carried out using calcium gluconate, which reduces membrane excitability; insulin and glucose because insulin
stimulates potassium entry into cells and glucose prevents hypoglycemia; alkalinizing treatment with sodium
bicarbonate, especially in patients with severe hyperkalemia andmetabolic acidosis, because it favors the movement of potassium inside the cells; and treatment with
diuretics that favor the renal potassium excretion (the
sodium excreted as a result of the diuretic must be reintegrated through the physiological solution). Finally,
hemodialysis represents the quickest method to reduce
plasma potassium concentration but it should be reserved
for patients with renal insufficiency and for those with
severe, potentially fatal, hyperkalemia who do not
respond to other therapies.
20 Hydroelectrolytic Disorders
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281
Recommended Readings
Adrogue HJ, Madias NE (2000) Hyponatremia. N Engl J Med
342(21):1581–1589
Diercks DB, Shumaik GM, Harrigan RA (2004) Electro- cardio-
graphic manifestations: electrolyte abnorma- lities. J Emerg Med
27:153–160
Elmi G, Faustini-Fustini M, Zaccaroni S, Zoni R (2011) Italian J Med
5(4):288
Gumz ML, Rabinowitz L, Wingo CS (2015) An integrated view of
potassium homeostasis. N Engl J Med 373(1):60–72
Hoorn EJ, Zietse R (2017) Diagnosis and treatment of hyponatremia:
compilation of the guidelines. J Am Soc Nephrol 28(5):1340–1349
Viera AJ, Wouk N (2015) Potassium disorders: hypokalemia and hyper-
kalemia. Am Fam Physician 92(6):487–495
Blood Gas Analysis
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PaoloCarraro
21
Introduction
Blood gas analysis is the measurement of the pH of the blood
and the partial pressures of oxygen (pO2) and carbon dioxide
(pCO
). These laboratory variables are always associated
2
with the determination of hemoglobin or hematocrit, the
barometric pressure of local atmosphere, and several calculated variables.
With simplication, we could distinguish the two main
purposes of this examination: the evaluation of the state of
oxygenation and the acid–base balance.
Interpretation of the results requires adequate knowledge
of pathophysiology and a precise picture of the clinical condition of the patient in terms of symptoms presented, previous pathological conditions, and treatment in progress, both
pharmacological and ventilatory.
This prole of examinations is often also associated with
other determinations that complete the information on the
patient’s status: oximetry (commonly co-oximetry) that veries the fraction of oxygenated hemoglobin, reduced or inactivated by toxic situations, electrolytes, glucose and lactate
metabolites, and sometimes other substrates such as urea,
creatinine, and bilirubin.
It is well known that this topic is quite complex, but, here,
in particular, we treat the aspects of competence and management by a clinical laboratory, whereas the clinical aspects
related to the main pathological conditions will be visited in
a more synthetic way.
balance, although these two functions are intrinsically
connected.
The State ofOxygenation
Blood oxygenation varies with the barometric pressure,
composition of the inhaled air, ventilatory volume, composition of the air at the alveolar level, state of the pulmonary
alveoli, efciency of blood circulation, and composition of
the blood, in particular the amount of hemoglobin. To understand the gradient of gas exchanges, the composition of
ambient air at sea level must be considered, as shown in
Table21.1. From this, the extent of the possible increase in
oxygenation can be deduced by enriching the air with O2.
Indeed, if hypothetically pure humidied oxygen is administered (irrespective of however irritating to the mucous membranes), then it is possible to reach the partial pressure
theoretically tending to 750mmHg with the aim of forcing
insufcient oxygenation for circulatory or parenchymal pulmonary disorders. Figure21.1 shows the physiological pressure gradients that push oxygen from ambient air to the
blood and then to the tissues. It is a schematic representation
that has great limitations but can help us understand the
physiology of oxygenation, at least under normal conditions,
by breathing ambient air at sea level.
The variable of greatest clinical interest for this evaluation is represented by oxygen saturation (sO2), normally provided by all blood gas analysis instruments. It is a parameter
Elements ofPathophysiology
As already mentioned, with blood gas analysis, we can actually obtain information on two particular pathophysiological
balances, namely, the state of oxygenation and the acid–base
P. Carraro (*)
Laboratory Medicine, Aziende ULSS3 Serenissima, Venice, Italy
e-mail: paolo.carraro@aulss3.veneto.it
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
M. Ciaccio (ed.), Clinical and Laboratory Medicine Textbook, https://doi.org/10.1007/978-3-031-24958-7_21
Table 21.1
their typical partial pressure at sea level at a barometric pressure of
760mmHg
Nitrogen 78 593
Oxygen 21 159
Argon and other gases 1 8
CO
H
Relative composition of the main gases in ambient air and
Percentage Millimeters of mercury (mmHg)
2
O vapor 0–7
2
0,03 0,2
283
284
O2voltage in mmHg
-
ACID -BASE BALANCE
Ventilation
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Fig. 21.1 A schematic representation of the partial
pressure gradients of oxygen, from the inhaled air to the
venous blood, in millimeters of mercury. This scheme
refers to a healthy subject, at sea level, in the absence of
therapeutic oxygen supplementation
that can be calculated from pO2 and hemoglobin by means of
an empirical equation of the hemoglobin dissociation curve,
with correction factors related to pH, body temperature, and
carbon dioxide (CO2). The limitation of this estimate is not
considering the effect of diphosphoglycerate (for example,
in transfusions) or the presence of pathological hemoglobin.
For these reasons, in the intensive eld, it is preferred not to
routinely use this type of calculation but to rely on the evaluation of an oximeter.
With this analyzer, fractions of hemoglobin are directly
measured by the spectrophotometric method and more accurate measurements are obtained, through the formula: oxyhemoglobin/(oxyhemoglobin + reduced hemoglobin) %.
Values of sO2 <95% are generally considered to indicate
hypoxemia and the widespread, dened condition of
“desaturation”.
The Acid–Base Balance
The pH of the blood and, therefore, of the main metabolic
environments of the body is close to 7.38, with an extremely
low oscillation tolerance. In fact, we speak of acidemia
already below 7.35 and alkalemia above 7.45, whereas those
that exceed the limits of 7.10 and 7.70, respectively, are generally considered critical values. The buffer system of the
blood most involved in its homeostatic maintenance is that of
bicarbonate–carbonic acid, although there is buffering competition between hemoglobin, albumin, phosphates, and
other substances. The physiological importance of bicarbonates, as shown in Fig. 21.2, is due to the intervention of
organs, such as the lungs, which can modulate their effectiveness by intervening to compensate for any variations:
variations in ventilation (volume of air displaced per minute)
can either increase or decrease the content of carbon dioxide
in the blood, considered the acid component of the buffer;
even the kidneys carry out control function by acting on the
urinary elimination of bicarbonates, the mainalkaline component. All this happens under physiological conditions but
can be accentuated in pathology, for example, if there is an
increase in organic acids due to a metabolic disease or an
introduction of acids or strong bases following an intoxication. However, we must also consider the limits of these
compensations in the sense that the lungs, in case of metabolic acidosis, can certainly eliminate more CO2 in an
150
Air
Fig. 21.2 The equilibrium equation of a bicarbonate buffer. Above are
shown the effects of its displacement on pH; below the points of action
of possible renal and ventilatory compensation
100
Alveolus
O H
2
Blood pH
Acidosis Alkalosis
CO2+ H
Possible compensation actions
95
Arterial blood
2CO3
Venous blood
H++ HCO
Kidney function
extremely short time but within a quantitative limit that normally stands at around 15mmHg. Renal function in retaining or eliminating bicarbonates is also limited, in particular,
by a certain slowness of effectiveness requiring 2 or 3days to
reach full capacity. It is precisely these limitations, however,
that allow us to distinguish the alterations of balance in acute
and chronic forms, whether compensated or not. Then, we
must consider the pathologies that can affect the two control
organs, namely, the kidneys and the lungs, producing imbalances that must be carefully interpreted. Finally, we must
also keep in mind the interactions between the control of
oxygenation and that of the acid–base balance: in particular,
it is low oxygenation that induces, for example, an increase
in ventilation as a compensatory attempt, determining an
alkalotic tendency that the kidneys will tend to control by
increasing the elimination of bicarbonate. It is therefore clear
how these balances have rendered blood gas analysis the fundamental examination for understanding the state of vital
functions, resulting in those who know how to correctly
interpret the pathophysiological state of a patient, to reinforce this consideration and also to observe the mechanisms
by which the body controlsthese functions. In practice, we
are equipped with biological “sensors” that are highly similar to the electrodes used in the instruments, located at the
brainstem and at the level of the carotids, which are able to
detect even small variations in pH and pO2 by rapidly activating, both nervously and hormonally, the corrective actions.
Instrumentation
A blood gas analyzer can be considered the paradigm of the
instrument intended for point-of-care testing: since its debut,
with the rst models set up by Astrup in 1954 and by John
P. Carraro
45
3
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285
Severinghaus in 1957, the utmost attention was paid to simplicity of use. In highly synthetic terms, we can say that in
the past the instruments were composed of four electrodes
(one of which was a reference and three were selective) that
required frequent replacement of the membranes and a uidic system to movethe sample of untreated blood into the
measuring chamber; in addition buffered solutions to calibrate the pH, and two gas mixtures for the calibration of pO2
and pCO2 were required. Subsequent developments anticipated automation and miniaturization technologies that preceded laboratory analyzers by many years. In practice, these
were the rst so-called “point-of-care testing” devices
suitable to be used even by operators with limited skills for
laboratory diagnostics.
The heart of modern instruments is still based on the rst
one in 1957 that employed selective electrodes: the glass
membrane electrode for pH, the Clarke electrode for oxygen,
and the Astrup electrode for carbon dioxide. During the subsequent evolution, the measurement of hemoglobin soon
appeared as a necessity to calculate oxygen saturation and
other derived parameters and became available by conductivity or the colorimetric method. Between the 80s and 90s
several other ion-selective electrodes for the most important
species were also integrated, and later alsobiosensors based
on the immobilization of enzymes for some substrates;
nally colorimeters endowed of different wavelengths to
measure the different states of hemoglobin on whole blood,
after ultrasonic hemolysis, have been introduced. Based on
thisadvancement, the analyzer has became asmall laboratory, At the end of the 90s, was automatic, did not need manual calibration procedures, had reduced maintenance, and
was able to analyze small volumes of blood.
The subsequent evolutions can be essentially summarized
through four innovations:
• Abolition of the use of gas mixtures for the calibration of
O2 and CO2 through the development of containers for
calibration liquids capable of maintaining stable dis-
solved gas contents
• Prolongation of the life of individual electrodes, some-
times without the need to periodically replace the
membranes
• Miniaturization of the electrodes and their integration into
a single cartridge containing various solutions, uidics,
and the measuring cell (so-called “cartridge” instruments)
• Automation of quality control procedures, including
operational decisions resulting from the results obtained
• Full connectivity for connection to the computer systems
of the department, hospital, and laboratory
The different characteristics of the instruments currently
on the market can be deduced from the greater or lesser ability to integrate these innovations into equipment that are progressively less demanding to manage.
The class of portable instruments has recently been
enriched with some new models: they are based on a
handheld (in some cases pocket) card containing uidics,
electrodes, and calibrators that allow maximum portability even in rescue vehicles and in the absence of gravity.
Less miniaturized models are close in concept to bench
tools but retain the logic of a disposable board. Their analytical reliability is precisely based on guaranteeing new
materials to each test, whereas their criticisms concerns
the sampling method and the small volume of blood used.
For this reason, they require targeted training and methods of use strictly in accordance with the recommended
procedures.
The Main Variables Measured andCalculated
pH: The concentration of H+ ions is not directly measurable
and is therefore deduced by the electrochemical method.
This theoretical limitation justies the use of the conventional scale that denes pH as –log [H+].
pCO2 and pO2: Both of these are measurements of the par-
tial pressure of the analyzed species, a fraction of the total
pressure given by the atmospheric pressure under conditions
in which the measurement is obtained. The traditional unit is
millimeters of mercury (mmHg), and according to the
International System (SI), it is kilopascals (KPa). For conversion, consider that 1mmHg=0.133kPa.
Total CO2 Concentration: This depends on the solubility constant of the gas and is therefore calculated with a
formula starting from pCO2, assuming a temperature of
37°C.
Bicarbonates: They are estimated with an accurate formula
starting from pCO2 and pH, always at 37°C.
Base Excess (BEecf ): This is the estimated excess of bases
for extracellular uid compared to the standard theoretical
conditions of pH of 7.40 and pCO2 equal to 40mmHg. It is
also referred to as BE “in vivo.”
Base Excess in the Blood or BE (B): This refers to the
same standard theoretical conditions but also takes into
account the buffering effect of hemoglobin, and it is also
called excess of bases “in vitro.” The estimates obtained with
the calculation of the excess of bases have several limitations, not considering the variables of other blood buffers,
proteins, and the volume of circulating and interstitial uids.
Nevertheless, they provide an immediate estimate of the possible dose of bicarbonates needed to bring the pH back into
the normal range.
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P. Carraro
Total Hemoglobin: In blood gas analyzers, total hemoglobin can be determined with a simplied colorimeter, deducted
by calculating the hematocrit measured by the conductivity
method or by an oximeter at multiple wavelengths. The latter
method provides accurate results.
Fractions of Hemoglobin: An oximeter allows analysis of
hemolyzed blood without the addition of any reagent, by
comparing the absorbance at different wavelengths, chosen
on the basis of the behavior expected by different species:
the percentages of carboxyhemoglobin (COHb), metahemoglobin, oxygenated hemoglobin, and reduced hemoglobin are thus determined. Obviously, interfering with this
measure are conditions such as the presence of turbidity,
abnormal stains, and sulfo-hemoglobin that cannot be estimated with this method.
Oxygen Saturation (sO2): This is a fraction of oxyhemo-
globin with respect to the overall ability of hemoglobin to
bind oxygen. Clinically, it is one of the most important variables and is calculated from pO
and total hemoglobin, with
2
corrections caused by variations in temperature, pH, and
pCO2. The calculation formula is deduced with empirical
models on the basis of a normal oxygen dissociation curve
and therefore cannot consider the content of diphosphoglycerate (DPG, low in transfused blood) and other factors.
However, it remains a much more accurate measurement
than the transcutaneous led pulse oximetric method that is
often used in the clinic, in particular if a two-wavelength
estimation model is used.
Oxygen Tension at 50% Hemoglobin Saturation
(p50): This is the partial pressure of oxygen at which a
hemoglobin saturation of 50% is obtained. It represents an
estimate of the dissociation curve of hemoglobin evaluated at
the critical point of 50%. It allows estimating the afnity of
oxygen toward the patient’s hemoglobin. It can be calculated
only on venous blood.
The Pre-Analytical Phase
adjustments in the administration of oxygen. A measure after
20–30 minutes of stable conditions is therefore recommended, if possible.
An anxious state, frequently present in patients in the
emergency room, or concerns about the pain of thepuncture,
can affect the outcome of the examination through moderate
hyperventilation, thus resulting in a decrease in CO2 and so
with a tendency toward respiratory alkalosis.
An accurate measurement also requires that the request
for the examination be accompanied by clinical information
about body temperature, spontaneous or assisted ventilation,
and oxygen ow to supplement the inhaled air [fraction of
inspired oxygen (FIO2)]. The instrument allows correcting
the results based on this information.
Blood Sampling Materials
Blood gas analysis syringes must contain lyophilized heparin balanced for electrolytes normally measured at the same
time (in particular calcium and possibly magnesium). Many
commercial preparations allow a ready solubility and therefore a lower concentration. While using balanced heparins, it
is not appropriate to obtain concentrations above 40IU per
ml, as interference would no longer be controllable; it is better to keep the concentration below 20IU/ml. Two different
types of syringes should be used: for arterial samples from a
direct puncture, you can use a model with a vented rib with
which the ow of blood leads to lling the syringe that is
prepared with the piston already extended. In fact, when the
blood reaches the rubber seal, the air passage is interrupted
and the seal becomes airtight. The needle can now be locked
by inserting it into a rubber block or it can be replaced, with
normal safety procedures, with a cap, after ejection of each
air bubble. Attention should be paid to the potential interference on some parameter due to the lubricant used, usually
declared by the manufacturer.
After normal disinfection, the skin should be dry, particularly if small amounts of blood or capillary blood are taken.
In fact, traces of benzalkonium chloride have a tensioactive
action on membranes interfering with the determination of
sodium, potassium, and calcium.
Patient Preparation
In emergency or intensive care conditions, it may be necessary to immediately carry out an examination. However, it
must always be evaluated whether these are instantaneous
determinations of variables that can change even in a few
minutes. As a rule, therefore, it is required that the patient be
under basal conditions, in particular that the patient should
not be conditioned by changes in breathing, ventilation, and
Site ofArterial Sampling
Several arteries can be used. The rst choice is the radial
artery, which is located on the side of the thumb of the wrist;
due to its small size, the use of this artery requires a specic
skill. Alternative sites for access are the brachial artery or
femoral artery, but they have several disadvantages as they
can be more difcult to detect because they are less super-
ab
21 Blood Gas Analysis
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Fig. 21.3 The Allen test for the verication of the normal arterial ow of the radial and ulnar arteries. (a) Manual occlusion of both the arteries.
(b) Resumption of regular ow while compressing only the radial artery
287
cial than the radial artery, may present collateral circulation
problems, and are surrounded by structures that could be
damaged by a defective technique.
Modied Allen Test
This is a test to assess collateral circulation of the palm of the
hand, which must be performed before taking an arterial
sample.
5–15seconds. In this situation, only the radial artery
supplies arterial blood to that hand and does not have
to be punctured.
Performing Radial Artery Sampling
1. Place the patient on his/her back, lying down or sitting in
an armchair with armrests. Avoid hyperventilation by
reassuring the patient. Keep your wrist in extension.
2. Locate the radial artery by performing the Allen test for
1. Ask the patient to clench his/her st; if the patient is
unable to do this, then personally close the patient’s hand
tightly.
2. With the thumbs, apply occlusive pressure on the ulnar
artery and radial artery to hinder the ow of blood to the
hand (Fig.21.3a).
3. By applying this occlusive pressure to both the arteries,
the patient should relax his/her hand and check whether
the palm and ngers are “pale.” If this does not occur,
then the occlusion of the arteries exerted with the ngers
is not complete, and, so, it is necessary to repeat the
maneuver.
4. Release the occlusive pressure on the ulnar artery only to
determine whether the test is positive or negative
(Fig.21.3b):
Positive: The ulnar artery has good blood ow if blood
ow to the hand is restored within 5–15seconds.
Negative: Ulnar circulation is inadequate or nonexistent if the blood ow to the hand is not restored within
collateral circulation.
3. If you cannot nd the radial artery at the chosen site,
then repeat the test on the other side.
4. Disinfect the sampling site on the patient with the induction products and allow it to dry. Pull the plunger of the
syringe to the required level of lling (usually 2ml).
5. With the index nger, locate the wrist, inform the patient
of the imminent puncture, and, holding the syringe like a
pen between the thumb, index, and middle ngers, insert
the needle with an inclination of 30–45°, avoiding contaminating the area where the needle enters the skin.
6. Advance the needle into the radial artery until blood
appears, and, then, wait for spontaneous lling. Do not
pull back the plunger of the syringe. The gasket of the
plunger has no hold until it is wet with blood, so you
should not suck but wait for the lling due to blood
pressure.
7. Take out the needle and syringe, place a cotton tablet
over the site, and exert rm pressure long enough to stop
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P. Carraro
the bleeding. Check whether the bleeding has stopped
after 2–3minutes. Five minutes or more may be necessary for patients suffering from hypertension or clotting
alterations or for those taking anticoagulants.
8. Cover the needle by closing the safety cover or pricking
the rubber block.
9. With the syringe facing upward, expel the air bubbles,
remove the needle and close with the cap, and then rotate
the sample in your hands to mix the anticoagulant.
10. Immediately transport the sample to the laboratory in a
refrigerated bag or directly to the decentralized instrument, if present in the department.
An illustrative video is also accessible on the site from which
this information was obtained, subject to free registration
(http://www.nejm.org/doi/full/10.1056/NEJMvcm0803851).
The vented rib syringe described here is absolutely unsuitable for venous or arterial sampling from the infusive line. In
these cases, in fact, the piston prevents the suction of blood
or even allows a retrograde ow of air to the blood sample.
Finally, inthe case of sampling from arterial infusive lines
under pressure, must be carried out by personnel trained for
this purpose to avoid accidents and possible dilution or contamination of the sample.
Capillary blood sampling is a valid alternative to the puncture of an artery to obtain a blood sample that is highly similar
to an arterial one. Necessary conditions include correct peripheral perfusion as the subdermal blood may not be representative of the central one; this happens mainly in patients with
severe hypotension, sepsis, and under conditions of peripheral
vasoconstriction. So, you can proceed only if the skin is rosy
and warm, heating the part to about 42°C.Squeezing the skin
should be absolutely avoided, and, therefore, the puncture must
be deep enough to provide the necessary amount of blood.
Venous sampling does not replace arterial sampling. It
can only be used to provide pH, pCO2, electrolytes, metabolites, carboxyhemoglobin, and meta-hemoglobin. The degree
of oxygenation of peripheral venous blood does not provide
reliable information and should not appear in the report. It
should also be considered that a venous sampling for blood
gas analysis requires more attention than does a standard
sampling, completely avoiding the application of the tourniquet or removing it, after the puncture, at least 1 minute
before blood collection; this is to avoid spurious increases in
pCO2 and therefore lowering of pH.
Other particular types of sampling are that from a “shunt,”
usually used during dialysis sessions, and the sampling of
mixed blood, obtained from a catheter in the pulmonary
artery. The laboratory report must indicate these particular
types of sampling, and the common reference values for arterial or venous blood should not be applied.
Transport andStorage
Some literature reports unanimously show a signicant
effect on the pO2 of transport by the pneumatic tube system. Probably it is due tobalancing of the gas with any air
bubbles present, favored by shaking and pressure changes
in the tube. These effects can be greatly reduced by systematically eliminating air bubbles after sampling and
calibrating the pneumatic system to reduce acceleration
and jolts.
Of great importance is the storage time before the examination. The main variables of the progressive decrease of
CO2 and O2 (due to both loss and metabolic consumption)
are as follows: the initial concentrations and therefore the
gradient toward the environment, the amount of hemoglobin, the number of leukocytes, time and temperature, and
the dissociation curve of hemoglobin. From another point
of view, it should be considered that refrigeration also
blocks the cellular pump of potassium, leading to an
increase in its concentration. For these reasons, storage at
room temperature should be preferred for the shortest possible time, no later than 30minutes after collection. If waiting or transport does not allow this limit to be respected,
then the sample must be refrigerated and analyzed within
2hours. For this purpose, the aforementioned Clinical and
Laboratory Standards Institute (CLSI) document recommends ice near the fusion, in order to obtain a temperature
of just over 0°C.
Analysis
All samples should be mixed for at least 1minute by rotation
between the hands and by means of a low-speed rotary agitator. Only in the case of freshly performed sampling is a
shorter mixing time allowed, whereas a longer time is
required in critical or dialysis subjects who normally have a
high sedimentation rate.
Many analyzers suck up the sample and then introduce an
air bubble into the syringe: this must be promptly removed if
it is necessary to repeat the analysis.
The internal barometer should be periodically checked by
comparing it, for example, with a professional meteorological barometer (airports, weather stations) located at the same
altitude. Some Pmint of Care Testing (POCT) devices are no
longer equipped with a barometer, and their use is guaranteed by calibrators at the current pressure.
There is no uniform behavior of instrument manufacturers regarding the expression of certain analytes: potassium
can be corrected as serum potassium or expressed as plasma;
glucose is sometimes corrected to blood glucose, other times
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as plasma. It is information that can be obtained from
manufacturers.
The main analytical problem is the accidental aspiration
of a clot. This can lead to not only the complete blockage of
the instrument but also some interference on the electrodes if
whips or protein residues stop near the measuring cells. In
these cases, the instrument must be carefully sanitized before
proceeding to new examinations.
pH and pCO2 with selective electrodes are not susceptible to interfering substances. Other variables potentially
interferering aresome gases used in anesthesia, benzalkonium of disinfectant solutions on electrolytes, salicylates
and bromides on the chlorine electrode, electrolyte solutions can condition the hematocrit if measured by conductivity method and nally the presence of turbidity and
lipemia thatcan produce overestimation of hemoglobin. If
cord or newborn blood is measured, then a spurious
increase in COHb can occur in the presence of fetal
hemoglobin.
The Postanalytical Phase
Result Validation
Particular attention should be paid to critical pH values (generally if <7.1 or >7.6) and electrolytes. Even an internal
inconsistency between some parameters can lead to suspect
an analytical error: the CLSI suggests, for example, to evaluate as incongruent pH and normal bicarbonates with pCO2
less than 25mmHg or a sum of pO2 and pCO2 greater than
150in a subject breathing ambient air.
Particularly altered values can be obtained from patients
kept at low temperatures, as can happen in intensive care or
during cardioplegia in the operating room: in these subjects,
the results after correction should always be calculated.
Hemolysis, as a sampling artifact, is not normally recognized because it is not detectable by inspection but must be
carefully considered. Ionized calcium should be reported
with correction to pH 7.40 in cases of samples stored for
more than 30minutes.
Table 21.2 Biological variability and related desirable analytical performance of some variables of blood gas analysis(CV is coefcient of
variation)
Biological variability (%)
CV%
intra-
individual
pH 0.2 – 0.1 – –
pCO
2
Bicarbonate 4.0 4.8 2.0 1.6 4.9
4.8 5.3 2.4 1.8 5.7
CV%
interindividual Imprecision Bias
Desirable performance
(%)
Total
error
materials are the abnormal surface tension and conductivity
that can mask certain electrode drifts, with a matrix effect.
Oxygen solubility is also limited, and this carries the risk of
measurement artifacts if the liquid is exposed to air before or
during sampling. This type of problem, in particular when
different operators provide sampling using different procedures, may result in an apparent instability of the instrument
in internal quality control or even erroneous situations of
noncompliance in external quality assurance. Some commercial materials, to overcome these limitations, contain in
solution albumin, free hemoglobin, or even erythrocytes.
These materials can hardly be used in internal control when
integrated into the instrument, according to the recent market
trends. In an intensive environment, pO2 values above
400mmHg are often encountered, i.e., in a range of concentrations far from normal quality controls; for this reason, in
these situations, it is recommended to also adopt materials
with high oxygen values.
Alternative quality control procedures include those that
are based on electronic checks of the state of the instrument
and electrodes as well as data deriving from the signal
obtained with the washing solutions, uidic efciency, and
sample integrity. This methodology (called “alternative quality control”) must in any case be supported by external materials that are periodically analyzed, even with a lower
frequency.
The biological variability of blood gas analysis and the
resulting analytical performance targets available in the literature are summarized in Table21.2 (https://www.westgard.
com/biodatabase1.htm).
Quality Control
Blood gas analysis has some peculiarities, usually having to
substitute the use of materials other than fresh blood from
donors. In practice, as quality control materials buffered
aqueous solutions are often used, collected in glass ampoules
or in plastic and metal bags strictly waterproof gas and without contact with ambient air. The main limitations of these
The Report
There are some peculiarities regarding blood gas analysis
that require specic information on the report. First is the
type of blood taken. In the case of venous, shunt, or mixed
blood, it is not appropriate to indicate the oxygenation
parameters, which could be misleading or in any case do not
have the possibility of associating them with reference val-
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