ACID BASE DISORDERS

Importance of Acid-Base Disorders

Among the most common clinical problems
encountered in hospitalized patients, especially ICU
patients
Lead to significant physiologic effects
Proper management may be life-saving
Principles of A-B homeostasis and disturbances
Recognition of A-B disorders
Specific disorders: common etiologies,
pathogenesis, clinical features, general principles of
management
Interpretation of ABG and electrolyte results

Normal Arterial Blood Values
pH: 7.35 - 7.45
pCO
2
: 35 - 45 mmHg
HCO
3
: 22 26 mmol/L
pO
2
, O
2
saturation, base excess/deficit

Chemistry panel:
Sodium: 135 - 145 mmol/L
Potassium: 3.5 - 5 mmol/L
Chloride: 96 109 mmol/L
Total CO
2
: 23 -30 mmol/L
Glucose, BUN, Creatinine

Maintenance of blood pH
pH = 6.1 + log [HCO
3
]
(pCO
2
)(0.0301)

pH [HCO
3
]
pCO
2

pH [HCO
3
]
pH 1/ pCO
2


Regulation of pCO
2

CO
2
production pCO
2
elimination

glucose metabolism ventilatory forces

neural drive
bellows apparatus
airways
Bellows apparatus:
Upper airwayobstruction critical hinder elimination of
c02
Prob in bellows apparatus severe chest defects
tendency to retain c02
Depends on diff stimuli: co2 level, 02 level,

Regulation of plasma HCO
3
-
Via kidneys:
Reabsorption of filtered HCO
3

Formation of titratable acid
Excretion of NH
4
+
in urine
** Maintenance of the ratio of HCO
3
to pCO
2
via compensatory
responses by the kidneys and lungs

Anion Gap
AG = Na
+
- (Cl
-
+ HCO
3
)
Normal: 10 - 14
e.g. AG = 140 - (105 + 24) = 140 129 = 11

Normal values:
[Na+]: 135-145 mEq/L
[K+]: 3.5-5.0 mEq/L
[Cl-]: 96-109 mEq/L
[total CO2]: 24-30 mEq/L


Anion gap:
Represents those unmeasured anions in the
plasma
Increase in AG is due to increased in the
amount of unmeasured anions, and less
commonly due to a decrease in unmeasured
cations

Determinants:

Unmeasured Anions Unmeasured Cations
Albumin (15mEq/L) Calcium (5 mEq/L)
Organic Acids (5 mEq/L) Potassium (4.5 mEq/L)
Phosphate (2 mEq/L) Magnesium (1.5 mEq/L)
Sulfate (1 mEq/L)
---------------------------- ---------------------------
Total UA (23 mEq/L) Total UC (11 mEq/L)

AG = UA UC = 12 mEq/L


METABOLIC ACIDOSIS
Pathogenesis
May be due to:
Increased endogenous acid production (e.g.
lactate and ketones)
Loss of bicarbonate (e.g. diarrhea)
Decreased excretion of endogenous acids
(e.g. renal failure)

Common Causes of Metabolic Acidosis

HIGH ANION GAP NORMAL ANION GAP
Lactic Acidosis Diarrhea
Ketoacidosis Isotonic saline infusion
ESRD Early renal insufficiency
Methanol ingestion RTA
Ethylene glycol ingestion Acetazoleamide
Salicylate toxicity Ureteroenterostomy

Notes:
Normal AG acidosis = hyperchlorimic acidosis = seen in
diarrhea
High anion gap = prod of endogenous acids to some
anions not measured

METABOLIC ALKALOSIS
Pathogenesis
Due to net gain of HCO
3
or loss of volatile acid
(usually HCl secondary to vomiting)
2 stages:
GENERATIVE STAGE: loss of acid
MAINTENANCE STAGE: failure of
kidneys to compensation by excreting
HCO
3
, because of volume contraction,
low GFR, or depleted K
+
or Cl
-


Clinical effects
increases the affinity of hemoglobin for oxygen --
--- decrease tissue unloading
Decreases ventilation
Decreases ionized calcium ----- neuromuscular
hyperirritability
Supraventricular and ventricular arrhythmias

Notes:
Dec tissue unloading 02 stays with the hgb, due to
shift of o2 hgb dissociation curve
Can lead to hypoxemia not breathing properly



Management
Identify and correct the underlying stimulus for
HCO
3
generation


Remove the factors that sustain HCO
3

reabsorption (e.g. ECF contraction or hypoK
+
)
Acetazoleamide
Dilute 0.1N HCl or NH4Cl
Hemodialysis

RESPIRATORY ACIDOSIS

Etiology and pathogenesis
may be due to severe pulmonary disease (e.g.
advanced COPD), respiratory muscle fatigue, or
abnormalities in ventilatory control (e.g. stroke)

Clinical effects
depends on severity and acuteness
may be dyspneic or tachypneic
Systemic vasodilation especially cerebral
vasodilation ----- increased ICP ----- pseudotumor
cerebri
Myoclonic jerks, asterixis, tremors, restlessness,
coma

Management
Depends on severity and rate of onset
May be life-threatening
Measures to reverse underlying cause
Restoration of adequate alveolar ventilation
Avoid rapid correction of hypercapnea

RESPIRATORY ALKALOSIS

Etiology and pathogenesis
Develops when a sufficiently strong ventilatory
stimulus causes CO
2
output in the lungs to
exceed its metabolic production in the tissues
May be due to stimulation of CNS (e.g. pain,
anxiety), peripheral chemoreceptors (e.g.
hypoxemia 2
o
to pneumonia), chest receptors
(e.g. PTE).

Clinical effects
Panic, weakness, and sense of impending doom
Paresthesias about the hands and feet
Trousseaus and Chvosteks signs
Possible tetany, seizures

Notes:
Trousseau and chvostek relative hypoxemia

Management
Directed toward alleviation of underlying disorder
Change in dead space, tidal volume and
respiratory frequency, if on MV
Re-breathing from paper bag during symptomatic
attacks of hyperventilation syndrome
notes:
If not on mechanical ventilation = give paper bag, to
retain the c02

Interpretation of Acid - Base Disorders
Determine if sample is arterial or venous.
Compare HCO
3
on ABG and electrolyte panel to
verify accuracy
Determine if pH or pCO
2
are normal or abnormal.
If any of above are abnormal determine primary
A-B disturbance
Compute for expected compensation to
determine presence of mixed disorders.
Calculate the Anion Gap
RULE: If AG > 20 high AG metabolic acidosis is present
regardless of the pH or HCO
3
.
Compare the change in AG (AG) with change in
HCO
3
(HCO
3
).
RULE: If change (i.e. increase) in AG is < change( i.e.
drop) in HCO
3
, there is combined high AG met acidosis
and normal AG (hyperchloremic) acidosis.
RULE: If AG is > HCO
3
, there is combined high AG
metabolic acidosis and metabolic alkalosis.

Notes:
The [total CO2] is the sum of the measured [CO2]
+ [HCO3-]. Thus the [HCO3-] from the blood gas and the
[total CO2] from the electrolyte panel usually are within 2
mEq/L. Otherwise the measurements are in error or were
taken at different times.
If pH and pO2 are normal, check AG: if normal
then normal A-B


Prediction of Compensatory Responses on Simple
Acid - Base Disorders
Primary Acid-
Base Disorder
Expected Range of
Compensation
Limits of
Compensation
Metabolic
Acidosis
PCO2 =
1.5[HCO3
-
] + 8
PCO2 =
12-14 mm Hg
Metabolic
Alkalosis
PCO2 =
0.6 mm Hg for each 1
mEq/L [HCO3
-
]
PCO2 =
55 mm Hg
Respiratory
Acidosis
[HCO3
-
] =
1(acute) 4 (chronic)
mEq/L for each 10 mm
Hg PCO2
[HCO3
-
] =
45 mEq/L
Respiratory
Alkalosis
[HCO3
-
] =
2 (acute) -5 (chronic)
mEq/L for each 10 mm
Hg PCO2
[HCO3
-
] =
12-15 mEq/L