Acid-Base Disorders: Clinical
Applications
J.B. Handler, M.D.
Physician Assistant Program
University of New England
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Abbreviations
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ABG- arterial blood gas
SIADH- syndrome of
inappropriate ADH
ADH- anti-diuretic hormone
Cr- creatinine
AVP- arginine vasopressin
N- nausea
HA- headache
OSM- osmolality
DI- diabetes insipidus
ACEI- angiotensin converting
enzyme inhibitor
HTN- hypertension
HF- heart failure
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Nl- normal
K- potassium
Mg- magnesium
AMI- acute myocardial
infarction
S04- sulfate
Ca- calcium
Nl- normal
DKA- diabetic ketoacidosis
Resp- respiratory
EF- ejection fraction
MR- mitral regurgitation
DM- diabetes mellitus
RRR- regular rate and rhythm
2
Acid-Base Disorders
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Bicarbonate buffer system
CO2 (dissolved) +H2O  H2CO3 weak acid
H2CO3  H + HCO3
HCO3: weak base; levels regulated by kidneys
and maintained for buffering (NaHCO3 is salt)
CO2 +H2O  H2CO3  H + HCO3 (+ Na)
pH=7.40, PCO2= 40mmHg, HCO3= 22-28 meq/L
Respiratory center/lungs regulate removal of CO2
Total venous CO2 = dissolved CO2 + (H2CO3) +HCO3 (90-95% of total CO2)
Therefore, Total venous CO2  HCO3
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Acid-Base Disorders
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Normal metabolism produces 1 meq/L (80 meq/D)
of non volatile (H ) acid together with volatile acid
(CO2) daily.
Body fluid pH is tightly maintained at 7.40
(normal range 7.38-7.42) by continuous removal
of H by kidneys and CO2 by lungs.
Labs: Arterial pH, PCO2, HCO3 (calculated from
arterial blood or measured in venous blood (total
CO2.)
HCO3  total venous venous CO2
CO2 +H2O  H2CO3  H + HCO3
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Types of Acid-Base Disorders
Respiratory and Metabolic
 Primary respiratory disorders effect PCO2.
 Primary metabolic disorders effect HCO3.
 Primary disturbances are accompanied by
compensatory changes that move the pH
back towards normal but do not fully
compensate/correct the primary disorder.
 Magnitude of compensation depends on
how long the disturbance is present.
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Acid Base Disorders
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Respiratory Acidosis: pH decreased, PCO2
increased, HCO3 increased (comp.), acute and
chronic forms.
Respiratory Alkalosis: pH increased, PCO2
decreased, HCO3 decreased (comp.), acute and
chronic forms.
Metabolic acidosis: pH decreased, HCO3
decreased, PCO2 decreased (comp.).
Metabolic alkalosis: pH increased, HCO3
increased, PCO2 increased (comp.).
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Respiratory Acidosis
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Primary defect is increased PCO2 as a result of
decreased alveolar ventilation.
CO2 +H2O  H2CO3  H + HCO3
Conditions associated with decreased ventilation:
severe COPD; asthmatic who tires; drug OD with
suppression of ventilatory drive, neuromuscular
diseases.
Symptoms: somnolence, confusion (CO2
narcosis), coma, resp. arrest.
HCO3 increases (over time), leading to
compensation.
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Expected Changes/Compensation
Respiratory acidosis
 Acute – the pH decreases 0.08 units for
every 10mmHg increase in PCO2; HCO3
0.1-1 mEq/liter per 10 mm Hg PCO2
 Chronic - HCO3 1.1-3.5 mEq/liter per 10
mmHg PCO2; pH will move towards
normal
– HCO3 generated by kidneys over days
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Case 1
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Little Billy got into some of dad’s pain
meds (hydrocodone). He suffers a
significant depression of mental status and
respiration. You see him in the ED 3 hours
after ingestion with a respiratory rate of 4.
A blood gas is obtained. It shows pH =
7.16, PCO2 = 70mmHg, HCO3 = 24
meq/L
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Case 1
What 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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Case 1
Uncompensated respiratory acidosis
 There has not been time for metabolic
compensation to occur. As the narcotic
toxicity took hold, this child slowed his
respirations significantly, PCO2 built up in
the blood, and an acidosis ensued.
 If compensation had occurred the pH would
have been higher as a result of an increase
in_____?
HCO3
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Treatment of Resp. Acidosis
Ventilatory support until the underlying
disorder can be corrected.
 Narcotic antagonists (if applicable) for OD:
Naloxone (Narcan) IV-has short half life;
may require repeated doses.
 Benzodiezepine antagonists: Flumazenil
given IV may reverse benzodiazepine (OD)
induced respiratory depression. Short
duration of action. Use with caution.
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Respiratory Alkalosis
Primary defect is decreased PCO2 as a
result of increased alveolar ventilation.
 CO2 +H2O  H2CO3  H + HCO3
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Respiratory Alkalosis
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Hyperventilation: anxiety, panic attacks, sepsis,
CNS insult, cirrhosis, salicylates (overdose),
progesterone, mechanical over ventilation, etc.
Symptoms- lightheadedness, paresthesias, tetany.
Treatment- Address the underlying cause; most
cases of anxiety-hyperventilation syndrome are
self-limitedrespiratory muscle fatigue.
– When acute anxiety is a factor, re-breathing into a paper
bag may be useful (short term fix only).
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Expected Changes/Compensation
Respiratory alkalosis
 Acute – pH increases .08 units for every
10 mmHg decrease in PCO2 ; HCO3 0-2
mEq/liter per 10 mm Hg PCO2
 Chronic - HCO3 2.1-5 mEq/liter per 10
mm Hg PCO2
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Metabolic Acidosis
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Primary measured defect is decreased HCO3
(combines with increased H ions to buffer) with
resultant drop in pH.
CO2 +H2O  H2CO3  H + HCO3
Compensatory response is decreased PCO2.
Excess fixed acids (endogenous) in blood-most
common acid-base disorder.
Calculation of anion gap is important:
Na- (HCO3+CL)  6-12 on newer chem. analyzers
which yield higher Cl levels (normal range 98-107
meq/L) than older analyzers.
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Expected Compensation
Metabolic acidosis:
 PCO2 1-1.5 (mmHg) per 1 mEq/liter
HCO3
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Increase Anion Gap Acidosis
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pH decreased, HCO3 decreased, Cl normal.
Examples: Lactic Acidosis (cardiogenic shock or
arrest). Lactate prod. due to inadequate tissue
perfusion or hypoxia.
DKA-Hyperglycemia with metabolic acidosis;
increased production of ß-hydroxybutyric &
acetoacetic acids (ketoacidshyperketonemia).
Toxins- Ethylene glycol, salicylates, methanol.
Uremia (severe renal failure)- endogenous acids.
pH < 7.25 common, with HCO3 <16meq/L
Anion gap > 12meq
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Composition of Body Fluids
(meq/L)
Fluid
Na
Sweat 30-50
Gastric 40-80
Duodenum 60-120
Bile
145
Pancreas 140
Diarrhea 120-140
Cl
30-50
100
90
100
75
90
K
5
10
5-10
5
5
20
HCO3
0
0
0-10
15-20
115
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Normal Anion Gap Acidosis
(NAGA)
Hallmark is acidosis, decreased HCO3 and
hyperchloremia.
 GI HCO3 losses from pancreatic or small
bowel contents.
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– Example: massive (secretory) diarrhea with
volume contraction (NaCL and K loss as
well); HCO3 secretion in small/large intestine is
accompanied by Cl generation/absorption
(countertransport); volume contraction leads to
NA and Cl retention in the kidney.
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Renal Tubular Acidosis (NAGA)
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Hyperchloremic metabolic acidosis without anion
gap. Chloride levels are increased.
– Distal RTA-deficiency in H secretion by distal nephron;
cannot acidify urine; enhanced K secretion
(hypokalemia).
– Proximal RTA- Inability of proximal tubule to
adequately reabsorb filtered HCO3.
– Hyporeninemic hypoaldosteronemic RTA:
hyperchloremic acidosis with hyperkalemia. Impaired
Na reabsorption, K + H secretion.
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If suspected: nephrology consult
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Metabolic Acidosis: Sx and Rx
Decreased pH leads to hyperventilation,
PCO2 resultscompensatory.
 Additional symptoms reflect underlying
disorder.
 Treatment is specific for the underlying
disorder. Example:
Diabetic ketoacidosis (DKA) treated with
insulin, electrolyte replacement and volume
expansion (details in Endocrine module).
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Case 2
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JR has had intermittent vomiting and severe
diarrhea for 4 days. He has been unable to keep
fluids down and has not urinated in 8 hours. He
has a cardiomyopathy with compensated HF.
PE: P-90, BP-90/70 with postural changes. He
appears lethargic and cool to touch with a
prolonged capillary refill time. His arterial blood
gas reveals: pH=7.30, PCO2=28mmHg,
HCO3=14meq/L.
Na-136meq/L, K-3.0meq/L, Cl-110meq/L
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Case 2
What 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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Case 2
Compensated metabolic acidosis
 The prolong history of fluid loss through diarrhea
has caused a metabolic acidosis. The mechanisms
probably are twofold. First there is lactic acid
production from the hypovolemia and tissue
hypoperfusion. Second, there may be significant
bicarbonate losses in the stool accompanied by
generation/absorption of chloride. The body has
compensated by “blowing off” the CO2 with
increased respirations.
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Metabolic Alkalosis
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Hallmark: High HCO3 with increased pH.
Most common: Saline responsive metabolic
alkalosis, commonly seen with extracellular
volume contraction and hypokalemia.
Severe vomiting or continuous NG suction: HCl
and NaCl losses from stomach initiate the
alkalosis and volume contraction. Cl loss (and
total body stores) sustains the alkalosis because
renal Na reabsorption from volume contraction is
accompanied by HCO3 reabsorption (most
available anion with Cl depleted).
See Case 1 from “Fluid and Electrolyte Disorders”
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Metabolic Alkalosis
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Activation of the RAA system to maintain volume
results in hypokalemia (Na/K/H exchange in
distal tubule) and additional H losses.
Hypokalemic, hypochloremic metabolic
alkalosis with volume contraction.
Entire sequence is rapidly corrected by
administering 0.9% saline* (isotonic) with
supplemental KCL. The process will self
perpetuate until adequate amounts of Na/K/Cl
and H2O are available.
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*AKA- normal saline
Expected Compensation
Metabolic alkalosis
 PCO2 0.5-1.0 (mmHg) per 1 mEq/liter
HCO3
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Case 3
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A 27 y.o. male is brought to the ED by his
girlfriend after being found obtunded at home.
PE: P-100, BP-100/60, RR- 6
pH-7.26, PCO2-65mmHg, PO2- 68mmHg,
HCO3-31 meq/L
What is the primary disorder?
Has there been any compensation?
What is the correct treatment?
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Case 4
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Following an alcoholic binge, a 54 y.o man
presents to the ED with severe N & V x 3 days.
He has had only water in the last 36 hrs.
PE: P-110, BP- 90/70, 70 syst upright. ETOH on
breath, liver enlarged.
pH-7.52, PCO2-47mmHg, HCO3-35 meq/L,
Na-129 meq/L, K-2.7 meq/L, Cl-84 meq/L.
What is the primary disorder? Compensation?
Explain the electrolyte abnormalities. What is the
treatment plan for this man?
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Case 5
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A 16 y.o with Type 1 DM is brought to the ED
after collapsing at home. He is dehydrated,
disoriented, hypotensive and his breath has a
sweet odor.
PE: Ill appearing male c/o abdominal pain.
T- 99, P-120, BP- 90/60, RR- 24; skin turgor ,
mucous membranes dry; lungs- clear; heart- RRR,
no murmurs/gallops; abd: soft, non-tender. Urine
via catheter- small volume, Sp Gr, ++for glucose
and ketones. O2 sat- 97%
IV started, fluids running. Labs/ABG:
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Case 5 (cont.)
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pH-7.24, PCO2-25 mmHg, HCO3-10meq/L
Glucose- 700mg/dl, Na-124 meq/L, K-5.2
meq/L, Cl-98meq/L, Cr-1.0mg/dL, BUN24mg/dL
What is the primary disorder? Compensation?
What are the sources for abnormal acid production
(at least 2)? How do you explain the electrolyte
abnormalities?
Thoughts on management?
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Case 6
A 24 y/o med student becomes extremely
anxious prior to his board exams. He is
brought to the ED with light-headedness,
and muscle cramps. P-100, RR-25, BP120/70; remaining exam unremarkable.
 pH-7.52, PCO2-25mmHg, HCO3-24 meq/L
 What is the primary acid-base disturbance?
Has there been any compensation?
 What is the treatment for this patient?
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Case 7
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A hospitalized man (medical ward without
monitoring) is discovered by the nursing staff
unconscious with no pulse or respirations; a “code
99” is called. During the initial response, team
members start an IV, and initiate CPR. The initial
ABG reveals:
pH- 7.01, PCO2- 65mmHg, HCO3- 12 meq/L,
PO2- 43mmHg
Explain these findings. Management?
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Case 7 (cont)
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He is intubated, ventilated and given 100% O2.
There is initial delay in getting the defibrillator.
CPR is continued. An ABG obtained 3” later
reveals:
pH- 7.21, PCO2- 41mmHg, HCO3- 13 meq/L,
PO2- 280mmHg. Rhythm: V Fib- now ready to
defibrillate
Explain these findings. Management?
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Case 7 (continued)
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Following defibrillation, he stabilizes
hemodynamically. He is placed on a ventilator
with TV of 900cc, rate of 14; FiO2- .40
ABG 1 hour later:
pH- 7.50, PCO2- 26mmHg , HCO3- 22meq/L,
PO2- 160 mmHg
How do you explain these findings?
Management?
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