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Marc D.

Berg, MD ± DeVos Children¶s Hospital


Rita R. Ongjoco, DO ± Sinai Hospital of Baltimore

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R irst, does the patient have an acidosis or an
alkalosis
R Second, what is the primary problem ±
metabolic or respiratory
R Third, is there any compensation by the
patient ± respiratory compensation is
immediate while renal compensation takes
time

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R ët would be extremely unusual for either the
respiratory or renal system to
overcompensate
R The pH determines the primary problem
R After determining the primary and
compensatory acid/base balance, evaluate
the effectiveness of oxygenation

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R pH 7.35 to 7.45
R paCO2 36 to 44 mm Hg
R HCO3 22 to 26 meq/L

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R pH < 7.35 R paCO2 < 36 mmHg
x Acidosis (metabolic and/or x Respiratory alkalosis
respiratory) (alveolar hyperventilation)
R pH > 7.45 R HCO3 < 22 meq/L
x Alkalosis (metabolic and/or x Metabolic acidosis
respiratory) R HCO3 > 26 meq/L
R paCO2 > 44 mmHg x Metabolic alkalosis
x Respiratory acidosis
(alveolar hypoventilation)

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Ô
  
  
Ô
 
So
R paCO2 > 44 with a pH < 7.35 represents a
respiratory acidosis
R paCO2 < 36 with a pH > 7.45 represents a
respiratory alkalosis
R or a primary respiratory problem, pH and
paCO2 move in the opposite direction
x or each deviation in paCO2 of 10 mm Hg in either
direction, 0. 08 pH units change in the opposite
direction

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Ô
   

Ô
 
And
R HCO3 < 22 with a pH < 7.35 represents a
metabolic acidosis
R HCO3 > 26 with a pH > 7.45 represents a
metabolic alkalosis
R or a primary metabolic problem, pH and
HCO3 are in the same direction, and paCO2
is also in the same direction

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R The body¶s attempt to return the acid/base
status to normal (i.e. pH closer to 7.4)
Ô  Ô  
 
respiratory acidosis metabolic alkalosis
respiratory alkalosis metabolic acidosis
metabolic acidosis respiratory alkalosis
metabolic alkalosis respiratory acidosis

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è V  

Respiratory acidosis
R Acute ±
x the pH decreases 0.08 units for every 10 mm Hg
increase in paCO2;
x HCO3 p0.1
0.1--1 mEq/liter per p10 mm Hg paCO2
R Chronic ±
x the pH decreases 0.03 units for every 10 mm Hg
increase in paCO2;
x HCO3 p1.1
1.1--3.5 mEq/liter per p10 mm Hg paCO2

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è V  

Respiratory alkalosis
R Acute ±
x the pH increases 0.08 units for every 10 mm Hg
decrease in paCO2;
x HCO3 [ 0-2 mEq/liter per 10 mm Hg paCO2
R Chronic ±
x the pH increases 0.17 units for every 10 mm Hg
decrease in paCO2;
x HCO3 [ 2.1
2.1--5 mEq/liter per 10 mm Hg paCO2

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Metabolic acidosis
R paCO2 = 1.5(HCO3) + 8 (?2)
R paCO2 1-1.5 per 1 mEq/liter HCO3
Metabolic alkalosis
R paCO2 = 0.7(HCO3) + 20 (?1.5)
R paCO2 p0.5
0.5--1.0 per p1 mEq/liter HCO3

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R Acceptable ventilatory and metabolic acid-
acid-base
status
R Respiratory acidosis (alveolar hypoventilation) -
acute, chronic
R Respiratory alkalosis (alveolar hyperventilation)
- acute, chronic
R Metabolic acidosis ± uncompensated,
compensated
R Metabolic alkalosis ± uncompensated, partially
compensated

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R paCO2 is elevated and pH is acidotic
R The decrease in pH is accounted for entirely
by the increase in paCO2
R Bicarbonate and base excess will be in the
normal range because the kidneys have not
had adequate time to establish effective
compensatory mechanisms

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R Causes
x Respiratory pathophysiology - airway obstruction,
severe pneumonia, chest trauma/pneumothorax
x Acute drug intoxication (narcotics, sedatives)
x Residual neuromuscular blockade
x CNS disease (head trauma)

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R paCO2 is elevated with a pH in the
acceptable range
R Renal mechanisms increase the excretion of
H+ within 24 hours and may correct the
resulting acidosis caused by chronic
retention of CO2 to a certain extent

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R Causes
x Chronic lung disease (BPD, COPD)
x Neuromuscular disease
x Extreme obesity
x Chest wall deformity

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R paCO2 is low and the pH is alkalotic
R The increase in pH is accounted for entirely
by the decrease in paCO2
R Bicarbonate and base excess will be in the
normal range because the kidneys have not
had sufficient time to establish effective
compensatory mechanisms

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R Causes x Drugs
x Pain x Sepsis
x Anxiety x ever
x Hypoxemia x Thyrotoxicosis
x Restrictive lung x Pregnancy
disease x Overaggressive
x Severe congestive mechanical
heart failure ventilation
x Pulmonary emboli x Hepatic failure

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R Normal paCO2, low HCO3, and a pH less
than 7.30
R Occurs as a result of increased production of
acids and/or failure to eliminate these acids
R Respiratory system is not compensating by
increasing alveolar ventilation
(hyperventilation)

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R paCO2 less than 30, low HCO3, with a pH of
7.3--7.4
7.3
R Patients with chronic metabolic acidosis are
unable to hyperventilate sufficiently to lower
paCO2 for complete compensation to 7.4

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R Causes
x Ketoacidosis - diabetic, alcoholic, starvation
x Lactic acidosis - hypoxia, shock, sepsis, seizures
x Toxic ingestion ± salicylates, methanol, ethylene
glycol, ethanol, isopropyl alcohol, paraldehyde,
toluene
x Renal failure - uremia

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R Causes x Diarrhea
x Carbonic anhydrase
x Renal tubular
inhibitors
acidosis
x Acid administration
x Post respiratory
(HCl, NH4Cl, arginine
alkalosis
HCl)
x Hypoaldosteronism
x Sulfamylon
x Potassium sparing
x Cholestyramine
diuretics
x Ureteral diversions
x Pancreatic loss of
bicarbonate

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R urther evaluation of the arterial blood gas
requires assessment of the effectiveness of
oxygenation of the blood
R Hypoxemia ± decreased oxygen content of
blood - paO2 less than 60 mm Hg and the
saturation is less than 90%
R Hypoxia ± inadequate amount of oxygen
available to or used by tissues for metabolic
needs

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R ënadequate inspiratory partial pressure of
oxygen
R Hypoventilation
R Right to left shunt
R Ventilation
Ventilation--perfusion mismatch
R ëncomplete diffusion equilibrium

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R Alveolar--arterial O2 tension difference
Alveolar
x A-a gradient
x PAO2-PaO2
x PAO2 = ëO2(PB - PH2O) - PaCO2/RQ*
R arterial--Alveolar O2 tension ratio
arterial
x PaO2/PAO2
R arterial--inspired O2 ratio
arterial
x PaO2/ëO2
x P/ ratio
*RQ=respiratory quotient= 0.8

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ABG A-a grad
PaO2 PaCO2 RA 100%
Low ëO2 N* N
Alveolar hypoventilation p N N
Altered gas exchange
Regional V/Q mismatch p/N/ p N/p
ëntrapulmonary R to L shunt N/ p p
ëmpaired diffusion N/ p N
Anatomical R to L shunt
(intrapulmonary or intracardiac) N/ p p
* N=normal

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R irst, does the patient have an acidosis or an
alkalosis
x Look at the pH
R Second, what is the primary problem ±
metabolic or respiratory
x Look at the pCO2
x ëf the pCO2 change is in the opposite direction of the
pH change, the primary problem is respiratory

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R Third, is there any compensation by the
patient - do the calculations
x or a primary respiratory problem, is the pH
change completely accounted for by the change
in pCO2
ż if yes, then there is no metabolic compensation
ż if not, then there is either partial compensation or
concomitant metabolic problem

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x or a metabolic problem, calculate the expected
pCO2
ż if equal to calculated, then there is appropriate
respiratory compensation
ż if higher than calculated, there is concomitant
respiratory acidosis
ż if lower than calculated, there is concomitant
respiratory alkalosis

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R Next, don¶t forget to look at the effectiveness
of oxygenation, (and look at the patient)
x your patient may have a significantly increased
work of breathing in order to maintain a ³normal´
blood gas
x metabolic acidosis with a concomitant respiratory
acidosis is concerning

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V 
Little Billy got into some of dad¶s barbiturates.
He suffers a significant depression of mental
status and respiration. You see him in the
ER 3 hours after ingestion with a respiratory
rate of 4. A blood gas is obtained (after
doing the ABC¶s, of course). ët shows pH =
7.16, pCO2 = 70, HCO3 = 22

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†hat is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory acidosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic alkalosis

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Uncompensated respiratory acidosis
R There has not been time for metabolic
compensation to occur. As the barbiturate
toxicity took hold, this child slowed his
respirations significantly, pCO2 built up in the
blood, and an acidosis ensued.

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Little Suzie has had vomiting and diarrhea for 3
days. ën her mom¶s words, ³She can¶t keep
anything down and she¶s runnin¶ out.´ She
has had 1 wet diaper in the last 24 hours.
She appears lethargic and cool to touch with
a prolonged capillary refill time. After
addressing her ABC¶s, her blood gas reveals:
pH=7.34, pCO2=26, HCO3=12

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†hat is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory alkalosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic acidosis

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Compensated metabolic acidosis
R The prolong history of fluid loss through
diarrhea has caused a metabolic acidosis. The
mechanisms probably are twofold. irst there is
lactic acid production from the hypovolemia and
tissue hypoperfusion. Second, there may be
significant bicarbonate losses in the stool. The
body has compensated by ³blowing off´ the CO2
with increased respirations.

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You are evaluating a 15 year old female in the
ER who was brought in by EMS from school
because of abdominal pain and vomiting.
Review of system is negative except for a 10
lb. weight loss over the past 2 months and
polyuria for the past 2 weeks. She has no
other medical problems and denies any
sexual activity or drug use. On exam, she is
alert and oriented, afebrile, HR 115, RR 26
and regular, BP 114/75, pulse ox 95% on RA.

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Exam is unremarkable except for mild abdominal
tenderness on palpation in the midepigastric
region and capillary refill time of 3 seconds.
The nurse has already seen the patient and has
sent off ³routine´ blood work. She hands you
the result of the blood gas. pH = 7.21 pCO2=
24 pO2 = 45 HCO3 = 10 BE = -10 saturation =
72%

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†hat is the blood gas interpretation?
R Uncompensated respiratory acidosis with
severe hypoxia
R Uncompensated metabolic alkalosis
R Combined metabolic acidosis and respiratory
acidosis with severe hypoxia
R Metabolic acidosis with respiratory
compensation

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Metabolic acidosis with respiratory compensation
R This is a patient with new onset diabetes
mellitus in ketoacidosis. Her pulse oximetry
saturation and clinical examination do not reveal
any respiratory problems except for tachypnea
which is her compensatory mechanism for the
metabolic acidosis. The nurse obtained the
blood gas sample from the venous stick when
she sent off the other labs.

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R The ëCU Book ± Paul L. Marino, 1991,
Algorithms for acid-
acid-base interpretations, p415
p415--
426
R Textbook of Pediatric ëntensive Care 3rd Edition
± edited by Mark C. Rogers, 1996, Respiratory
Monitoring: ënterpretation of clinical blood gas
values, p355-
p355-361
R Pediatric Critical Care ± Bradley uhrman and
Jerry Zimmerman, 1992, Acid-
Acid-Base Balance
and Disorders, p689-
p689-696
R Critical Care Physiology ± Robert Bartlett, 1996,
Acid--Base physiology p165
Acid p165--173.

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