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ABG'S
ABG samples provides precise measurement of Acid-Base balance and lungs
ability to oxygenate the blood and remove CO2
Accurate interpretation of ABG requires knowledge of pt total clinical picture
including any TX receiving
Mixed venous blood sample evaluates overall tissue oxygenation
venous samples only give metabolic rates so little value, exposed to peripheral
vascular beds
normal ABG values:
Ph 7.35-7.45, PaO2 80-100 mmHg, PaCO2 35-45 mmHg, HCO3 22-26, BE +-2
Prior to ABG draw, review for: low platelet count or increased bleeding time
(meds etc)
Preferred site of ABG arteriotomy: radial artery.
collateral circulation of the hand, via modified Allens test must be evaluated prior
to a radial stick
Modified Allens test: have pt make tight fist, RT compress both radial and ulnar
artery, instruct pt to open hand and relax, RT release ulnar
Positive Allens test: hand pinks w/in 10-15 seconds after release of ulnar artery,
means circulation is adequate for puncture site
try other arm then try brachial if Allen test is negative
insert indwelling arterial catheter if frequent ABG's
Pressure should be applied for 3-5 mins or longer if clotting problem after Stick.
ABG and VGB samples used to: acid-base balance (Ph, PaO2 PaCO2, HCO3
BE), oxygenation status (PaO2, SaO2, CaO2, PvO2), and adequate ventilation
(PaCO2)
PaO2: O2 in plasma of arterial blood, reflects ability of lungs to transfer O2 into
blood
Hypoxemia: PaO2 less than normal predicted range, at any age, for pt breathing
room air or PaO2 <65mmhg, severe <40mmHg (any age) in pt with increased
FIO2
Hypoxia: inadequate tissue oxygenation
hypoxemia may result in hypoxia in pts with <CO, but they are not synonymous
most common cause of hypoxemia is >V/Q mismatch, in pts with lung disease
increased V/Q mismatch: decrease in V/Q matching, perfusion is good, but
ventilation is not, mucus plugging, secretions, bronchospasm, in specific portions
of the lung
causes of hypoxemia: >V/Q mismatch, diffusion defects, >CO2 from
hypoventilation, Drug OD (>CO2), <PIO2 (altitude), equip failure
SaO2: norm >95%, O2 saturation, actual amount of O2 bound to Hb expressed
as a %
Oxyhemoglobin disassociation curve shows the effects of O2 loading and
unloading in relationship to Hb
Left shift in HbO2 disassociation curve >Ph, >SaO2, >Hb affinity, <temp, <CO2,
<fetal Hb, <2,3 DPG, (increased affinity makes unloading at tissue more difficult)
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Right shift in HbO2 disassociation curve:
<Ph, <SaO2, <Hb affinity, >temp, >CO2, >fetal Hb, >2,3 DPG, (decreased affinity
makes unloading at tissue easier)
Ph and Hb affinity for O2: as Ph changes Hb affinity for O2 is directly affected
(Bohr effect), Ph up, Hb affinity also up, Ph down Hb affinity also down
2,3 DPG:
organic phosphate in RBC, stabilizes deoxygenated Hb, reducing its affinity for
O2, without it Hb would never unload O2 at the tissue
>2,3DPG:
Alkalosis, chronic hypoxemia, anemia
<2,3DPG
acidosis
Shunt: V/Q is equal to 0, perfusion with no ventilation, alveoli blocked, refractory
to O2
decreased V/Q mismatch: shunt effect, perfusion in excess of ventilation, nonrefractory to O2, partial obstruction, hypoventilation, COPD, interstitial disease
increased V/Q matching: ventilation in excess of perfusion, deadspace effect,
regional hyperventilation, often seen in PPV and <CO
Deadspace: ventilation no perfusion, increased PaO2 with a decreased CO2
(usually less than 40) emboli
P(A-a)O2: norm 10-15 mmHg on room air, or 25-65on 100%, predicted
dependent on age and FIO2, increase is resp defect, every increase of 50 is 2%
shunt above normal of 2-3%
First sign of hypoxemia is short of breath especially on exertion
clinical manifestations of hypoxemia are tachycardia, tachypnea, hypertension,
cyanosis, confusion
severe hypoxemia may result in tissue hypoxia, met acidosis, bradycardia,
hypotension, coma
lungs remove CO2 by ventilation
kidneys role in acid-base balance is what remove small quantities of acid, restore
buffer capacity of fluids by replenishing HCO3
Ph: hydrogen ion concentration in blood, reflects acid-base balance
Bases: solutions capable of accepting H+
PaCo2: respiratory component of acid-base balance, identifies degree of
ventilation in relation to metabolic rate
hypercarbia most often results from hypoventilation, CO2 >45
hypocarbia is usually caused by hyperventilation, CO2 <35
CO2: most reliable measurement of pt ventilation
HCO3: bicarb, norm is 22-26 mEq/L, primary metabolic component of acid-base
balance, regulated by renal system, usually requires 12-24 hrs for compensatory
response
BE+-:
base excess base deficit, standard deviation of HCO3 that takes buffering of
RBC's into account. Calculated with Ph, CO2 and Hematocrit and is a more
complete analysis of metabolic buffering capability
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Base excess: positive value indicates either base has been added or buffer
removed, larger the number the more sever the metabolic component
o allows analysis of pure metabolic components of acid-base balance,
changes in met components alter acid-base, respiratory components do
not
o Changes in CO2 do not effect
o Metabolic changes alter
Simple respiratory acidosis is inadequate ventilation, elevated CO2
o common causes of resp acidosis acute upper airway obstruction, severe
diffuse airway obstruction (acute or chronic), massive pulm edema
o Common non-respiratory problems that cause resp acidosis: drug OD,
spinal cord injury, neuromuscular diseases, head trauma, trauma to
thoracic cage
o How is acute resp acidosis compensated: none, renal changes are to slow
o How is chronic resp acidosis compensated: kidneys increase absorption of
HCO3
o How is uncompensated resp acidosis identified: ⬆Ph,⬇CO2, with normal
HCO3 and normal BE
o What is partially compensated resp acidosis: ⬆HCO3, but Ph is not yet
w/in normal limits
what is fully/completely compensated resp acidosis: ⬆HCO3 enough to bring Ph
within normal range
How is degree of compensating determined in resp acidosis: acute-HCO3⬆1 for
every 10-15 ⬆in CO2, chronic- HCO3⬆4 for every 10 ⬆CO2
neuromuscular disease or
obstructive disorder w/resp
short of breath and ⬆RR
acidosis, pt will RR will be what
Drug OD or impaired resp center
pt w/ resp acidosis pt RR will be
reduced
what
what effect does acute elevation of anesthetic, confused, semi-conscious and
CO2 and acidosis have on CNS
eventually coma
in acute resp acidosis how high
does CO2 get for Pt to reach coma around 70 mmHg
because ⬆CO2 causes systemic
vasodilation, what cardiac
manifestations should be
expected?
because ⬆CO2 causes cerebral
vasodilation, what might be
expected
warm flush skin, bounding pulse, arrhythmias
⬆ICP, retinal venous distension, papilledema,
headache
when HCO3 levels are up, what
happens to chloride levels
resp Alkalosis
if ⬆ result of renal compensation, then chloride will
be ⬇
abnormal condition in which there is an increase in
ventilation relative to the rate of CO2
PaCO2 below expected level indicating ventilation is
exceeding the normal level, hyperventilation
hyperventilation caused by pain, hypoxemia (PaO2
55-60), acidosis, anxiety
How to identify resp alkalosis in
ABG
what are the common causes of
resp alkalosis
how do the kidneys compensate
excrete HCO3
for resp alkalosis
What is the expected
compensation for acute resp
none, ⬆Ph, ⬇PaCO2, normal HCO3
Alkalosis
What is the expected
compensation for partially
⬆Ph, ⬇HCO3
compensated resp Alkalosis
What is the expected
compensation for fully
normal Ph, ⬇HCO3
compensated resp Alkalosis
Expected compensation is not
present for HCO3 in resp alkalosis, complicating metabolic disorder is also present
what should suspect
Clinical S&S associated w/ resp
tachypnea, dizziness, sweaty, tingling in fingers and
alkalosis
toes, muscle weakness and spasms
HCO3 or BE falls below normal, caused when
simple met acidosis
buffers are not produce in enough quantity (high
Gap), or when buffers are lost (normal Gap)
normal 11 (8-16 mEq/L), when fixed acids
accumulate in the body, H+ reacts to HCO3 causing
Anion Gap
it to ⬇,leading to a ⬇ anion gap
Causes of met acidosis with high
metibolicy produced acid gains or ingestion of acids
anion gap can be divided into two
categories what are they
lactic acidosis (hypoxia, sepsis), ketoacidosis
High anion gap met acidosis from
(diabetes, starvation, lack of glucose), renal failure
metabolicy acid gains
(retained sulfuric acid)
High anion gap metabolic acidosis salcylate poisoning (aspirin), methanol, ethylene
from ingestion of acids
glycol
normal anion gap metabolic
acidosis (hyperchloremic acidosis) diarrhea or pancreatic fistula
from loss of HCO3 is caused by
normal anion gap met acidosis
from failure to reabsorb HCO3 is renal failure
most often caused by
normal anion gab met acidosis
ammonium chloride or IV nutrition
from ingestion may be caused by
what signs may be present w/renal
⬆blood urea, nitrogen and creatinine, ⬇urine output
disease
How does the body compensate
⬇CO2(hyperventilation)
for met acidosis
If normal or ⬆PaCO2 is present
resp defect is also present (combination resp/met
w/met acidosis what should RN
acidosis)
suspect
What is the predicted
if PaCO2 is not at predicted level, resp abnormality
compensation of PaCO2 for met
is present
acidosis
what is the most common and
Kussmaul's breathing
obvious sign of met acidosis
what is Kussmaul's respiration
very rapid, very deep ventilation
dyspnea, headache, nausea, vomiting followed by
S&S and Pt complaints w/severe
confusion and stupor. Vasoconstriction, pulm
met acidosis
edema, arrhythmias (if severe enough)
simple met alkalosis
above normal HCO3
hyperkelemia, hypochloremia, ng suction (⬇acid),
most common causes of met alk vomiting (⬇acid), post hypercapnic disorder,
diuretics, steroids or to much bicarb therapy
how does body compensate for
hypoventilation to ⬆ PaCO2
met alkalosis
⬆ in PaCO2 enough to return Ph to normal
fully compensated met alk is
(hypercarbia may be present and may appear as
identified by
resp acidosis)
when to suspect a mixed acid
normal or near normal Ph w/severe abnormal HCO3
base disorder
or PaCO2
where should we look for clues of pt hx, physical exam, lab tests, knowing primary
mixed acid base disorders
disorders, expected compensations
expected compensation for acute
PaCO2⬆15-HCO3 ⬆
resp acidosis
expected compensation for chronic
PaCO2⬆10-HCO3 ⬆
resp acidosis
expected compensation for acute
PaCO2⬇5-HCO3 ⬇
resp alkalosis
expected compensation for chronic
PaCO2⬇10-HCO3 ⬇
resp alkalosis
expected compensation for met
acidosis
mixed/combined resp met acidosis
HCO3 ⬆1-PaCO2⬆
⬆PaCO2 ⬇HCO3
hypercapnia and low HCO3 work synergistically to
why is combined resp/met acidosis
significantly reduce Ph, often resulting in profound
so easy to identify
acidosis
common causes of resp/met
cardio pulm resuscitation, COPD and hypoxia,
acidosis are
poisoning and drug OD
heart stops-blood circulation stops, apnea causes
cardio pulm resuscitation and
resp acidosis, and hypoxia causes lactic acidosis
resp/met acidosis
(metabolic)
chronic COPD w/compensated resp acidosis
COPD and hypoxia w/resp met
suddenly gets met disturbance like hypotension or
acidosis
renal failure, causing hypoxia and lactic acidosis
mixed/combined met resp
⬆HCO3 w/below normal PaCO2-additive effects may
alkalosis
result in severe alkalosis
When met alk is super imposed on
resp alk, why does it become so when superimposed there is no compensation
severe
what clinical situation will you most hypoxemia, hypotension, neuro damage, to much
likely see met/resp alkalosis
mech vent, anxiety, pain, or any of above in combo
chronic COPD w/elevated HCO3, suddenly
What pts most often get combined
reduction in PaCo2 from mech vent will cause resp
met resp alkalosis
alk onto the met alk pt already has
Mixed met acidosis with resp
either abnormality usually compensates for the other
alkalosis are difficult to recognize
because
met acidosis with Paco2 lower
resp alk is also occurring simultaneously, Ph will be
than predicted for degree of
just above 7.4 (appearing to compensate for for resp
acidosis
alk)
what is the prognosis for met
poor, most likely seen in critically ill
acidosis on resp alkalosis