The Minimalist approach to
acid/base disturbances
ABG’s so easy….a GEICO rep can do it
OBJECTIVES
Acid/Base terminology and definitions
Normal physiologic acid/base regulation
Acid/base disturbances
ABG interpretation
Case studies
Acid/Base terminology and
definitions
Acid/Base regulation / Control of(
H+)concentration
– Acid—proton (H+) donor increases (H+)
– Base—proton (H+) acceptor decreases (H+)
Ph is the logarithmic/exponential
representation of (H+) concentration in
eq/liter
What is log????
10 =10(1)
log 10= 1
100=10(2)
log 100=2
1000=10 (3) log1000=3
0.1= 10 (-1) log 0.1 = -1
0.01 = 10 (-2) log 0.01= -2
ph = - Log (H+)
ph = 6 (H+) = 10 (-6) eq/liter
eq/liter
ph = 7 (H+) = 10 (-7) eq/liter
0.0000001eq/liter
ph =
(H+) = 10(-8) eq/liter
0.00000001 eq/liter
0.000001
H20 <<<<< (H+) + ( OH-)
(H+) = 10(-7) eq/liter
Pure Water has a ph 7(chemical neutral)
Physiologic regulation of
extracellular ph
Normal physiologic ph = 7.4
Essential for normal enzymatic reactions
Control Mechanisms/ Normal
physiology
Buffer systems (immediate)
Respiratory
(seconds)
Renal
(hours-days)
Buffer solutions
Solution of two or more compounds
Prevent marked changes in ph when acid
or base is added
Bicarbonate Buffer
H20 + CO2 <<< H2CO3 <<( H+)+ HCO3-
Henderson/Haselbalch Equation
ph = 6.1 + log HCO3-/ CO2
HCO3-/CO2= 20
Ph= 7.4
Ph is dependent on HCO3(direct) and CO2(inverse)
HCO3 increases--- ph increases
HCO3 decreases ---- ph decreases
CO2 increases---- ph decreases
CO2 decreases--- ph increase
Physiologic Response to
chronic acid load
Bicarbonate Buffer system (immediate)
– HCL + NaHCO3 >>>H2CO3 (CO2) +NaCL
Pulmonary Control (seconds to minutes)
– Ventilation of newly created CO2 in buffer
system
Renal control
(hours to days)
– Secretes H+ to reabsorb and regenerate
HCO3 consumed by buffer
Pathophysiology/ Acid/Base
disturbances
Acidosis---any process that lowers ph
– Lowers HCO3- or raises PCO2
Alkalosis--- any process that raises ph
– Raises HCO3- or lowers PCO2
Definitions
Neutral
– Ph 7.35-7.45
Acidemia
– Ph < 7.35
Alkalemia
– Ph > 7.45
More Definitons
Isoelectric principle
– + ions (cations) = -ions (anions)
Anion Gap—(Na + K) – (CL + HCO3) nl
=15
– Measures minor/unmeasured anions
– Endogenous/exogenous anions
Acid/Base disturbances
Primary
Secondary- a response to a primary
disturbance
– Opposite direction from primary
– Compensation is partial and incomplete
Acid/Base disturbaces
Respiratory--- alteration in pCO2
Metabolic --- alteration in HCO3
Acute Respiratory AcidosisElevation in PCO2
CNS vs. pulmonary
– CNS – coma, stroke
– Pulmonary-asthma, COPD, pneumonia (very
late)
.08 ph drop for every 10mm increase in
PCO2
– Typical abg’s 7.32/50/62
7.24/60/47
No metabolic compensation/ HCO3
unchanged
Treatment- Fix the problem
Chronic Respiratory Acidosis
Chronic/slow PCO2 elevation
– COPD/sleep apnea/obesity
Compensatory metabolic alkalosis a major
component
– Kidneys increase H+ secretion –increase
HCO3
.02 ph drop / 10 mm increase in PCO2
– Typical abg’s 7.38/50 /50
Treat underlying condition
– Beware excess O2
7.36/60/55
Acute Respiratory Alkalosis/
decreased PCO2
CNS vs pulmonary
– CNS stress, drugs, anxiety, sepsis, toxins
– Pulmonary pneumonia/asthma/pulmonary
embolism
.08 ph increase 10 mm decrease in PCO2
– Typical abg’s 7.48/30/62
No metabolic compensation
Treat underlying condition
– Supplement O2
– Beware of paper bag
Chronic Respiratory Alkalosis
Extremely rare…some other time….
Acute Metabolic Acidosis
Decreased HCO3
– Direct HCO3 loss via GI/kidneys
– Decreased HCO3 from H+ buffering
Metabolic Acidosis - defined by
the associated anion
Anion gap acidosis- increased minor
anions
– Endogenous/Exogenous
Non anion gap acidosis-hyperchloremic
– HCO3 loss from GI/kidneys
– Increased reabsorption of CL-
Acute metabolic acidosis
Compensatory respiratory alkalosis
Compensation is rapid but incomplete
PCO2 drop= HCO3 drop
– Typical abg
7.34/35/98 serum HCO3 =20
Treatment of Metabolic Acidosis
Define and treat the underlying condition
Watch for elevations in K+
Beware HCO3-
Pitfalls of HCO3- treatment
Paradoxical CNS and intracellular acidosis
Over correction alkalosis
Aggressive Na load
Indications for HCO3- therapy
HCO3 < 5
Ph <7.10
Cardiovascular instablity or irritability
More likely to use on ventilated patients as
CO2 is “blown off”
Anion Gap Acidosis MUDPILES
Methanol
Uremia
Diabetic (ketones)
Paraldehyde
Iron
Lactate
Ethylene glycol
Salicylate
Alternative Classification of
anion gap acidosis
Ketoacidosis
Lactic acidosis
Exogenous poisonings
Uremia
Ketoacidosis
Diabetic
alcoholic
Diabetic ketoacidosis
Insulin lack
– Hyperglycemia
– Fatty acid breakdown Ketone accumulation
Treatment
– Correct underlying disorder
– fluids
– insulin
– maintenance of electrolytes especially K+
Alcoholic Ketoacidosis
EtOH use followed by vomiting/starvation
– Excessive ketone accumulation
– Dehydration
– Hypo or normoglycemia
Treatment
– Fluids
– Maintenance of electrolytres
– Glucose
Lactic Acidosis
Type A tissue hypoxia/underperfusion
Type B abnormal lactate utilization
Treatment
Correct underlying cause
– Antibiotics
– Blood transfusion
– Goal directed sepsis therapy
– Fluids/pressors
Exogenous toxins
Alcohols
– Methanol/ethylene glycol
Salicylate
Alcohol poisoning
Ethanol not usually a major cause of
acidosis
MethanolEthylene Glycol
– Formate/Oxylate accumulation
– Increased osmolar gap
– Renal failure/oxylate crystals
Treatment for methanol/ethylene glycol
– Ethanol drip
– Dialysis
Clues to diagnosis for ethylene
glycol/methanol intox
History
– “sterno” or anti freeze ingestion
Altered mental status
Unexplained visual disturbances/coma
Unexplained anion gap acidosis
Renal failure
Diagnostic Aides
ABG/ HCO3
Serum osm
ETOH level
Osmolar gap
Oxylate crystals
Salicylate Toxicity
Altered mental status
Anion gap acidosis
Primary respiratory alkalosis as well
– Typical abg 7.35/20/110 serum HCO3 15
Treatment
– Alkalinazation of the urine
– K+ replacement
– Dialysis
Lab Evaluation of anion gap
Metabolic Acidosis
Ketones
Salicylate
Lactate
Etoh/serum osm
Osmolar gap = measured-calc serum osm
Non Anion Gap-Hyperchloremic
acidosis
GI or renal HCO3- loss
Compensatory CL- resorption
Usually associated with
hypo/hyperkalemia
Metabolic Alkalosis
Primary elevation in extracellular HCO3– H + losses from GI (vomiting)
– Excessive renal H+ excretion/ elevated HCO3
resorpbtion
– Exogenous ingestion
Respiratory compensation
– If HCO3 goes up by 10 pco2 goes up by 7
– Typical abg 7.47/47/100 HCO3 =34
Metabolic Alkalosis
Physical effects
– Tetany
– Neuromuscular hyperactivity
– Seizures
– Decreased K+/ionized Ca 2+
Treatment
– Correct underlying cause
– Acetazolamide---causes renal HCO3 loss
– Correct electrolytes
ABG interpretation
Step 1 obtain ABG/ HCO3- (electrolytes
SMA7/Istat)
Step 2 ph determination to determine
– ph 7.35-7.45 = nuetral
– ph < 7.35 = academia
– ph > 7.45 + alkalemia
Acidemia Flow chart to
determine underlying process
HCO3 low- primary process is metabolic
acidosis
pCO2 elevated- primary process is
respiratory acidosis
Metabolic Acidosis
What is the anion gap????
Is the respiratory compensation
appropriate
– Appropriate PCO2/HCO3 =1 HCO3 =15/
PCO2 =30
– PCO2/HCO3 > 1 resp alkalosis HCO3=15
PCO2= 20
PCO2/HCO3 < 1 resp acidosis
15 PCO2 =43
HCO3=
Respiratory Acidosis
Is the acidosis acute/chronic?
– Acute –ph down .08/10 mmPCO2 elevation
– Chronic ph down .03/10mm PCO2 elevation
– Acute on chronic 7.35/50/50
– Outside limits—second primary process
Alkalemia flow chart
HCO3 elevated- primary metabolic
alkalosis
pCO2 decreased- primary respiratory
alkalosis
Metabolic Alkalosis
Is the respiratory response appropriate?
– PCO2/HCO3 = .7 7.48/47/75 HCO3 =35
Respiratory Alkalosis
Acute—is the ph response appropriate
– Ph .08 up for every 10 mm decrease in PCO2
Nuetral ph
Look for mixed primary disturbances
– PCO2
– Anion gap
– HCO3
Case studies
Having FUN yet???/
Follow the flow charts!!!!!
Case #1
57 y.o acutely SOB
7.32/60/55
HCO3=32
SMA 7 and anion gap otherwise normal
Case #2
31 y.o homeless male unresponsive in
park
7.24/29/107
Na 140 K 5.4 Cl 97 HCO3 14 glucose
110
Renal function normal
Case #3
61 y.o with severe arthritis confused and
agitated
7.34/18/110
Na 142 K 2.9 CL 99 HCO3 12
Glucose/renal function wnl
Case #4
19 y.o. diabetic with vomiting
7.38/38/110
Na 140 K 2.8 CL 95 HCO3 24
Glucose 440 renal function wnl