A C ID A N D B A S E

D IS TU R B A N C E

Marshell Tendean, MD, DPCP

Department of Internal Medicine
UKRIDA, Jakarta
Acid Base Physiology

Acid

Base
 The metabolic and respiratory
components that regulate systemic
pH are described by the Henderson-
Hasselbalch equation:
H : 24 x pCO2 /
HCO3
The kidneys regulate plasm a [H CO 3] through
three m ain processes:

(1)Proximal Tubule Rabsorption" of

filtered HCO3
(2)Formation of titratable acid (HPO4-)
(3)Coligent duct Excretion of NH4+ in
the urine

Net Acid Excretion :

Titratable acidity, NH4, - urinary HCO3
Normal Values

Arterial Venous

pH 7.40 <7.35
HCO3 24 24
pCO2 40 >40
pO2 >70 <60
H 40
 Four Main Acid-Base Disorders

Disord Primary Secondary Mechanism of

er Alteration Response Response
Metaboli in in plasma Hyperventilation
c plasma pCO2
Acidosis HCO3
Metaboli in Hypoventilation
c plasma HCO3 increase in
Alkalosis pCO2
Respirat in plasma in Increase in acid
ory pCO2 plasma HCO3 excretion;
Acidosis increase in
reabsorption of
HCO3
Respirat in in plasma Suppression of
ory acid excretion;
Respiratory Disturbance
Compensation
pCO2 in in
pH
HCO3
Acute Resp. 10 1
Acidosis
0.08
Chronic 10 3
Resp. pCO2 in pH in
Acidosis 0.03 HCO3
Acute Resp. 10 2
Alkalosis
0.08
Chronic 10 5
Resp.
Alkalosis 0.03
Approach to the Patient:Acid-Base D isorders

Obtain arterial blood gas (ABG) and electrolytes

simultaneously.
Compare [HCO3] on ABG and electrolytes to verify
accuracy.
Calculate anion gap (AG).
Know four causes of high-AG acidosis (ketoacidosis,
lactic acid acidosis, renal failure, and toxins).
Know two causes of hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
Estimate compensatory response (Table 47-1).
Compare AG and HCO3.
Compare change in [Cl with change in [Na +].
M etabolic acidosis :

Increase in endogenous acid

production (such as lactate and
ketoacids)
Loss of bicarbonate (as in diarrhea)
Accumulation of endogenous acids
(as in renal failure).
Classified into :
Anion Gap Asidosis
Non Anion Gap asidosis
Causes ofH igh anion G ap M etabolic Asidosis :

Lactic asidosis
Ketoasidosis
Diabetic
Alcoholic
Starvation
Toxins :
Ethylene glicol
Methanol
Salicylates
Proplene glicol
Pyroglutamic acid Renal failure acute
and chronic
N on G ap M etabolic Acidosis :
I. Gastrointestinal bicarbonate
loss
A. Diarrhea
B. External pancreatic or
small-bowel drainage
C. Ureterosigmoidostomy,
jejunal loop, ileal loop
D. Drugs
1. Calcium chloride
(acidifying agent)
2. Magnesium sulfate
(diarrhea)
3. Cholestyramine (bile acid
diarrhea)
II. Renal acidosis
A. Hypokalemia
1. Proximal RTA (type 2)
Drug-induced: acetazolamide,
topiramate
2. Distal (classic) RTA (type 1)
Drug induced: amphotericin B,
ifosfamide
B. Hyperkalemia
1. Generalized distal nephron
dysfunction (type 4 RTA)
a. Mineralocorticoid deficiency
b. Mineralocorticoid resistance
(autosomal dominant PHA I)
c. Voltage defect (autosomal
dominant PHA I and PHA II)
d. Tubulointerstitial disease
 N ongap m etabolic acidosis
For non-gap m etabolic acidosis, calculate the urine anion gap
U AG = U N A + U K U CL
If U AG > 0: renalproblem
If U AG < 0: nonrenalproblem (m ost com m only G I)

Causes of nongap metabolic acidosis - DURHAM

D iarrhea,ileostom y,colostom y,enteric fi

stulas
U reteraldiversions or pancreatic fi
stulas
RTA type Ior IV,early renalfailure
H yperailm entation,hydrochloric acid adm inistration
Acetazolam ide,Addisons
M iscellaneous post-hypocapnia,toulene,sevelam er,cholestyram ine
ingestion
III. Drug-induced hyperkalemia (with renal insufficiency)
A. Potassium-sparing diuretics (amiloride, triamterene,
spironolactone)
B. Trimethoprim
C. Pentamidine
D. ACE-Is and ARBs
E. Nonsteroidal anti-inflammatory drugs
F. Cyclosporine and tacrolimus
IV. Other
A. Acid loads (ammonium chloride, hyperalimentation)
B. Loss of potential bicarbonate: ketosis with ketone excretion
C. Expansion acidosis (rapid saline administration)
D. Hippurate
E. Cation exchange resins
Primary Metabolic Disturbance:
Calculate anion gap : Na (Cl + HCO3)
Normal = 12 +/- 2
If gap is >20 then there is primary metabolic acidosis
regardless of pH or bicarb.
Helps narrow differential with a anion gap or non-
anion gap metabolic acidosis
A fall in serum albumin by 1 g/dL from the normal
value (4.5 g/dL) decreases the AG by 2.5 meq/

Delta gap = (actual AG 12) + HCO3

Adjusted HCO3 should be 24 (+_ 6) {18-30}
If delta gap > 30 -> additional metabolic alkalosis
If delta gap < 18 -> additional non-gap metabolic acidosis
If delta gap 18 30 -> no additional metabolic disorders
 Look for an osmolar gap in patients with an
anion gap metabolic acidosis, and the etiology
is unknown.
It occurs in these two intoxications:
1. Methanol
2. Ethylene glycol
Calculate Osmolar gap:
Step 1: osm = 2 (Na+) + (gluc/18) + (BUN/2.8)
+ (BAL/5) norm = 285-295 mOsm/L
Step 2: Measured - calculated should be < 10-15
Treatm ent M etabolic Acidosis
Treatment of metabolic acidosis with alkali should be
reserved for severe acidemia except when the
patient has no "potential HCO3" in plasma. Potential
[HCO3] can be estimated from the increment () in
the AG (AG = patient's AG 10).
Consequently, patients with a normal AG acidosis
(hyperchloremic acidosis), a slightly elevated AG
(mixed hyperchloremic and AG acidosis), or an AG
attributable to a nonmetabolizable anion in the face
of renal failure should receive alkali therapy, either
PO (NaHCO3 or Shohl's solution) or IV (NaHCO 3), in
an amount necessary to slowly increase the plasma
[HCO3] into the 2022 mmol/L range.
 In general, severe acidosis (pH <
7.10) warrants the IV administration
of 50100 meq of NaHCO3 , over 30
45 min, during the initial 12 h of
therapy.
The goal is to increase the [HCO3] to
10 meq/L and the pH to 7.20, not to
increase these values to normal
 M etabolic alkalosis
Calculate the urinary chloride to diff
erentiate saline
responsive vs saline resistant
M ust be offdiuretics in order to interpret urine chloride

Saline responsive Saline-resistant UCL >10

UCL<10
Vom iting If hypertensive: Cushings,Conns,RAS,
renalfailure w ith alkaliadm inistartion
N G suction If not hypertensive: severe hypokalem ia,
hypom agnesem ia,Bartters,G ittelm ans,
licorice ingestion
O ver-diuresis Exogenous corticosteroid adm inistration
Post-hypercapnia
 Treatm ent M etabolic Alkalosis
This is primarily directed at correcting the
underlying stimulus for HCO3 generation.
If primary aldosteronism, renal artery stenosis, or
Cushing's syndrome is present, correction of the
underlying cause will reverse the alkalosis.
[H+] loss by the stomach or kidneys can be mitigated by
the use of proton pump inhibitors or the discontinuation
of diuretics.
The second aspect of treatment is to remove the factors
that sustain the inappropriate increase in HCO 3
reabsorption, such as ECFV contraction or K + deficiency.
K+ deficits should always be repaired.
Isotonic saline is usually sufficient to reverse the alkalosis
if ECFV contraction is present.
 If associated conditions preclude infusion of
saline, renal HCO3 loss can be accelerated by
administration of acetazolamide, a carbonic
anhydrase inhibitor, which is usually effective in
patients with adequate renal function but can
worsen K+ losses.
Dilute hydrochloric acid (0.1 N HCl) is also
effective but can cause hemolysis, and must be
delivered centrally and slowly.
Hemodialysis against a dialysate low in [HCO 3]
and high in [Cl] can be effective when renal
function is impaired.
 Respiratory Alkalosis
C au ses of R esp iratory A lkalosis

Anxiety, pain, fever

H ypoxia, CH F
Lung disease w ith or w ithout hypoxia pulm onary em bolus, reactive
airw ay, pneum onia
CN S diseases
D rug use salicylates, catecholam ines, progesterone
Pregnancy
Sepsis, hypotension
H epatic encephalopathy, liver failure
M echanicalventilation
H ypothyroidism
H igh altitude
Treatm ent Respiratory
Alkalosis
The management of is directed toward
alleviation of the underlying disorder.
If respiratory alkalosis complicates ventilator
management, changes in dead space, tidal
volume, and frequency can minimize the
hypocapnia.
Patients with the hyperventilation syndrome
may benefit from reassurance, rebreathing
from a paper bag during symptomatic
attacks, and attention to underlying
psychological stress.
 Respiratory Acidosis

C au ses of resp iratory acid osis

CN S depression sedatives, narcotics, CVA
N eurom uscular disorders acute or chronic
Acute airw ay obstruction foreign body, tum or, reactive airw ay
Severe pneum onia, pulm onary edem a, pleuraleff
usion
Chest cavity problem s hem othorax, pneum othorax, fl
ailchest
Chronic lung disease obstructive or restrictive
Centralhypoventilation, O SA
 Treatm ent Respiratory acidosis
Acute respiratory acidosis can be life-threatening, and
measures to reverse the underlying cause should be
undertaken simultaneously with restoration of adequate
alveolar ventilation.
Aggressive and rapid correction of hypercapnia should be
avoided, because the falling Pa co2 may provoke the same
complications noted with acute respiratory alkalosis (i.e.,
cardiac arrhythmias, reduced cerebral perfusion, and
seizures).
The Paco2 should be lowered gradually in chronic respiratory
acidosis, aiming to restore the Pa co2 to baseline levels and
to provide sufficient Cl and K+ to enhance the renal
excretion of HCO3.
Chronic respiratory acidosis is frequently difficult to correct.
 Pneumonics for pnuemonic lovers

Metabolic Metabolic Acute Metabolic Respiratory

Acidosis Acidosis Resp. Alkalosis Alkalosis
Anion Gap Non-Gap Acidosis CLEVERPD CHAMPS
MUDPILERS HARDUPS anything
causing
hypoventilati
on
Methanol Hyperaliment CNS Contraction CNS disease
Uremia ation depression Licorice Hypocapnia
DKA/Alcohol Acetazolamide Airway Endocrine Anxiety
ic Renal Tubular obstruction (Conn/Cushi Mech.
ketoacidosis Acidosis Pulmonary ng/Bartters) Ventilation
Paraldehyde Diarrhea edema Vomiting Progesterone
Isoniazid Uretero-Pelvic Pneumonia Excess Salicylates
Lactic shunt Hemo/Pneu alkali Sepsis
acidosis Post- mothorax Refeeding
Ethanol hypocapnia Neuromusc Post-
Renal Spironolacton ular hypercapnia