ACID-BASE

DISORDERS
TALAGA TRINIDAD
VILLAMOR VIZCARRA
ACID-BASE CHEMISTRY
ACID
A substance that can donate protons-
Hydrogen ion

A substance that accept protons-

Hydrogen ions BASE
➢ The acidity of body fluids is
quantified in terms of the
hydrogen ion concentration.

➢ pH or the negative logarithm

(base 10) of the hydrogen ion
concentration expresses the
degree of acidity. (H+ ion
conc. and pH are inversely
related.)

➢ Alterations in blood pH serve

as the basis for the diagnosis
of acid–base disorders.
➢ dissociation of acid–base pairs is an equilibrium reaction.

➢ the relationship between hydrogen ion concentration or pH and the relative

concentrations of the acid and base can be described mathematically in terms
of the dissociation constant for the acid–base buffer pair.
REGULATION OF ACID- BASE
HOMEOSTASIS

Three processes maintain acid–base balance:

1. extracellular buffering,
2. ventilatory regulation of carbon dioxide
elimination,
3. renal regulation of hydrogen ion and
bicarbonate excretion.
I. EXTRACELLULAR BUFFERING
➢ The principal extracellular buffer is the carbonic acid/bicarbonate
(H2CO3/HCO3–) system.
➢ Carbonic acid represents the respiratory component of the buffer pair. Blood
conc. is ∝ PCO2, which is determined by ventilation.
➢ Bicarbonate represents the metabolic component because the kidney may alter
its concentration by reabsorption.
II. RESPIRATORY
REGULATION

➢ Increasing minute ventilation by increasing respiratory rate

will increase CO2 excretion and decrease the blood PCO2.

➢ Decreasing minute ventilation decreases CO2 excretion and

increases blood PCO2.
III. RENAL
REGULATION
ACID-BASE
DISTURBANCES
ACIDEMIA ALKALEMIA
measured pH value in blood <7.35 measured pH value in blood >7.45

COMPENSATION
ACIDOSIS
HCO3
the process that
decreases pH
PaCO2

ALKALOSIS
HCO3
the process that
increases pH
PaCO2
CLINICAL ASSESSMENT OF ACID-
BASE STATUS
➢ A blood gas is measured to determine not only a patient’s acid–base status but
also their oxygenation.
➢ Arterial blood reflects how well the blood is being oxygenated by the lungs (an
accurate measurement of PaO2), whereas venous blood reflects how much
oxygen tissues are using.
ARTERIAL BLOOD GAS BLOOD GAS MIXED VENOUS BLOOD

7.40 (7.35-7.45) pH 7.38 (7.33-7.43)

80-100 mm Hg PO2 35-40 mm Hg

95% SaO2 70-75%

35-45 mm Hg PCO2 45-51 mm Hg

22-26 mEq/L 24-28 mEq/L

HCO3
 pH 7.35-7.45
Normal
Compensated Disorder
Mixed Disorder

Acidemia <7.35 Alkalemia >7.45

PRIMARY PRIMARY

Respiratory Acidosis Metabolic Acidosis Respiratory Alkalosis Metabolic Alkalosis

ANALYSIS OF ARTERIAL BLOOD GASES

STEPS IN ACID-BASE DIAGNOSIS
1. Obtain ABGs and electrolytes simultaneously.
2. Compare [HCO3–] on ABG and electrolytes to verify
accuracy.
3. Calculate SAG.
4. Is acidemia (pH <7.35) or alkalemia (pH >7.45)
present?
5. Is the primary abnormality respiratory (alteration in
PaCO2) or metabolic alteration in HCO3?.
6. Estimate compensatory response
7. Compare change in [Cl–] with change in [Na+]
 PATHOPHYSIOLOGY
● Too much acid buildup in the body fluids which is causing the
HCO3 (Bicarbonate) to DECREASE.
pH = HCO3
● Which can result from 3 CATEGORIES:
○ Increased acid production in the body
■ Ex. DKA
○ Decreased acid secretion
■ Ex. Kidney Failure
○ Loss of Bicarbonate-rich body fluids
■ Ex. Diarrhea
NORMAL VALUES FOR ABGs:
pH 7.35-7.45
HCO3 22-26
PaCO2 35-45

LAB VALUES EXPECTED IN METABOLIC ACIDOSIS:

pH <7.35
HCO3 <22
PaCO2 <35 or normal
 CAUSES of METABOLIC ACIDOSIS
1. HIGH ANION GAP METABOLIC ACIDOSIS
2. NORMAL ANION GAP METABOLIC ACIDOSIS

● Anion Gap
○ Measurement of the balance between cations and anions
○ Important diagnostic tool for metabolic acidosis
[ Na ] + [ K ] - [ Cl ] + [ HCO3 ]
○ Normal Range: 10-14 mEq/L
 CAUSES of METABOLIC ACIDOSIS
1. HIGH ANION GAP METABOLIC ACIDOSIS
• > 14 mEq/L anion gap
• Conditions that cause the body to produce too much acid
and not enough bicarbonate
• Ex. DKA, lactic acidosis, aspirin toxicity, renal failure,
high-fat diet

2. NORMAL ANION GAP METABOLIC ACIDOSIS

• Loss of Bicarbonate in the body
• Ex. diarrhea, renal tubular acidosis
SIGNS & SYMPTOMS
 TREATMENT
1. SODIUM BICARBONATE
MOA ROA AND SIDE EFFECTS EFFICACY, COMMENTS
DOSAGE SAFETY AND
ECONOMICS
Reacts with H+ PO & IV; Metabolic Pregnancy -Recommended
ions to form 325mg- 650mg; 2- alkalosis, Category: C to raise arterial
water & CO2. it 5 mEq/kg IV Hypokalemia, pH to 7.2
acts as a buffer infusion over 4-8 Hypernatremia, -if IV NaHCO3 is
against acidosis hr Hypocalcemia administered, the
by raising blood goal is to increase,
pH not normalize (pH
7.2 and HCO3 8-
10 mEq/L)
 TREATMENT
2. TROMETHAMINE
MOA ROA AND SIDE EFFECTS EFFICACY, COMMENTS
DOSAGE SAFETY AND
ECONOMICS
Corrects acidosis IV; 1-5 mmol/kg Alkalosis, Pregnancy No evidence
by acting as a over 1 hr respiratory Category: C exists that it is
proton acceptor; depression, beneficial or
releases
bicarbonate hyperkalemia more
buffer to correct efficacious than
acidosis by NaHCO3
combining with
hydrogen ions
 TREATMENT
3. ORAL ALKALI REPLACEMENT

DRUG mEq of Alkali DOSAGE FORM COMMENTS

Shohl’s Solution 1 mEq bicarbonate Solution; Increase absorption

(Sodium Bicitrate/ 500mg Na citrate, of aluminum
Citric Acid) 334 mg citric acid/ 5
mL

Potassium Citrate 3.9 mEq bicarbonate 325 mg tablet Can cause bloating
because of CO2
production

Potassium 25 mEq 25- 50 mEq

Bicarbonate/ bicarbonate/tablet Effervescent tablet
Potassium Citrate
 TREATMENT
3. ORAL ALKALI REPLACEMENT

DRUG mEq of Alkali DOSAGE FORM COMMENTS

Potassium Citrate/ 2 mEq bicarbonate Solution; 1100 mg K

Citric Acid citrate, 334 mg citric
acid/ 5 mL

Sodium Citrate/ 2 mEq bicarbonate Syrup & Solution;

Potassium Citrate/ 550mg K citrate,
Citric Acid 500mg Na citrate,
334mg citric
acid/5mL
 PATHOPHYSIOLOGY
● Caused by excessive loss of of acids (H+) or increased amount of
bicarbonate produced in the body that leads to an alkalotic state in
the body.
pH = HCO3
● Maintained by abnormal renal function that prevents the kidneys
from excreting excess bicarbonate

● Respiratory response is to increase PaCO2 by HYPOVENTILATION

 LAB VALUES EXPECTED IN METABOLIC ALKALOSIS:
pH > 7.45
HCO3 > 26
PaCO2 > 45 or normal

MOST COMMON CAUSES OF METABOLIC ALKALOSIS:

“ ALKALI “
1. Aldosterone Production Excessive (Hyperaldosteronism)
2. Loop Diuretics
3. AlKali Ingestion of food ( Baking Soda, Milk and Antacids)
4. Anticoagulant ( Citrate)
5. Loss of fluids (vomiting)
6. Increased sodium bicarbonate administration
SIGNS & SYMPTOMS
TREATMENT
TREATMENT
RESPIRATORY ALKALOSIS
PATHOPHYSIOLOGY
• A decrease in PaCO₂ that leads to an increase in pH
• PaCO₂ decreases: Ventilatory CO₂ excretion exceeds metabolic CO₂
production
• Causes: Increase in neurochemical stimulation via central or
peripheral mechanisms, or physical increases in ventilation via
voluntary or artificial means
• Earliest compensatory response is to chemically buffer excess
bicarbonate by releasing hydrogen ions from intracellular proteins,
phosphates, and hemoglobin.
• Prolonged (>6 hours): The kidneys attempt to further compensate
by increasing bicarbonate elimination.
CLINICAL PRESENTATION
• Usually asymptomatic: Adverse neuromuscular, cardiovascular,
and GI effects.
• Decreased cerebral blood flow: Light-headedness, confusion,
decreased intellectual functioning, syncope, and seizures
• Cerebral hypoxia: Nausea and vomiting
• Severe: Cardiac Arrhythmias
• Alteration of electrolytes; serum Cl is usually increased; serum K,
P, and ionized Ca are usually decreased.
TREATMENT
• Often unnecessary: Few symptoms and only mild pH alterations
(ie, pH <7.50)
• Direct measures can be effective
Ex: Treatment of pain, hypovolemia, fever, infection, or salicylate
overdose
• A rebreathing device: Help control hyperventilation
• Mechanical ventilation: Decreasing the number of mechanical
breaths per minute, using a capnograph and spirometer, or
increasing dead space
RESPIRATORY ACIDOSIS
PATHOPHYSIOLOGY
• An increase in PaCO₂ and a decrease in pH
• Disorders: Restrict ventilation or increase CO₂ production, airway
and pulmonary abnormalities, neuromuscular abnormalities, or
mechanical ventilator problems.
• Early compensatory response for acute respiratory acidosis is
chemical buffering
• Prolonged (>12–24 hours): Proximal tubular HCO₃ − reabsorption,
ammoniagenesis, and distal tubular H+ secretion are enhanced
-> An increase in serum HCO₃ − concentration that raises pH to
normal
CLINICAL PRESENTATION
Neuromuscular symptoms: Altered mental status, abnormal behavior,
seizures, stupor, and coma.
Hypercapnia: Mimics a stroke or CNS tumor by producing headache,
papilledema, focal paresis, and abnormal reflexes.
CNS symptoms: Increased cerebral blood flow and are variable,
depending in part on the acuity of onset.
TREATMENT
• Provide adequate ventilation if CO₂ excretion is acutely and
severely impaired (PaCO₂ >80 mm Hg [>10.6 kPa]) or if life-
threatening hypoxia is present (arterial oxygen tension [PaO₂ ] <40
mm Hg [<5.3 kPa]).
• Ventilation: maintaining a patent airway, clearing excessive
secretions, administering oxygen, and providing mechanical
ventilation
• Treat underlying cause aggressively: Administration of
bronchodilators for bronchospasm or discontinuation of respiratory
depressants such as narcotics and benzodiazepines
TREATMENT
• Bicarbonate administration is rarely necessary and is potentially
harmful
• Chronic respiratory acidosis is treated essentially the same as
acute respiratory acidosis with a few important exceptions.
• Oxygen therapy should be initiated carefully and only if the PaO2 is
less than 50 mm Hg (<6.7 kPa) because the drive to breathe
depends on hypoxemia rather than hypercarbia.
MIXED ACID BASE
DISORDERS
 DIAGNOSIS
- one must know how each of the four simple disorders
alters the following:
i. pH
ii. PaCO2
iii. HCO3-
- Mixed disorder is suspected if blood gases do not
decrease within the range of expected responses for
a simple acid–base disturbance
- History and Physical examination
 MIXED RESPIRATORY ACIDOSIS AND
METABOLIC ACIDOSIS
- Characterized by failure of compensation.
- Absence of compensatory mechanisms = decrease pH
Respiratory disorder prevents the compensatory
decrease in PaCO2 expected in the defense against
metabolic acidosis.

Metabolic disorder prevents the buffering and renal

mechanisms from raising the bicarbonate concentration as
expected in the defense against respiratory acidosis.
 MIXED RESPIRATORY ACIDOSIS AND
METABOLIC ACIDOSIS
- develops in patients with:
i. Cardiorespiratory arrest
ii. Chronic lung disease and shock
iii. Metabolic acidosis and respiratory failure
 TREATMENT:

• Oxygen delivery- to improve hypercarbia and hypoxia

• Mechanical ventilation may be needed to reduce
PaCO2.
• During the initial stage of therapy, appropriate
amounts of alkali should be given to reverse the
metabolic acidosis.
 MIXED RESPIRATORY ALKALOSIS
AND METABOLIC ALKALOSIS
- most common mixed acid–base disorder
- occurs frequently in critically ill surgical patients with
respiratory alkalosis caused by:
• mechanical ventilation
• hypoxia
• sepsis
• hypotension
• neurologic damage
• pain
• drugs
- with metabolic alkalosis caused by:
• vomiting or nasogastric suctioning
• massive blood transfusions
 MIXED RESPIRATORY ALKALOSIS
AND METABOLIC ALKALOSIS
- It can also occur in patients
i. with hepatic cirrhosis who hyperventilate,
receive diuretics, or vomit
ii. chronic respiratory acidosis and an
elevated plasma bicarbonate concentration
who undergo a rapid decrease in PaCO2.
 MIXED RESPIRATORY ALKALOSIS
AND METABOLIC ALKALOSIS
• Renal excretion of bicarbonate (to compensate for
respiratory alkalosis)- prevented by metabolic
alkalosis.
• Retention of PaCO2 (to compensate for metabolic
alkalosis)- prevented by primary respiratory alkalosis.
• The failure of compensation can result in a severe
alkalemia.
 TREATMENT:

• NaCl and KCl solutions- help correct the metabolic

component of a mixed respiratory and metabolic
alkalosis
• Readjust the ventilator or treat the underlying
disorder causing hyperventilation to correct the
respiratory component.
 MIXED METABOLIC ACIDOSIS AND
RESPIRATORY ALKALOSIS
● often seen in patients with:
○ advanced liver disease
○ salicylate intoxication
○ pulmonary-renal syndromes
● The respiratory alkalosis will decrease the Pa CO2 beyond
the appropriate range for the respiratory compensation
usually seen with metabolic acidosis.
● The plasma bicarbonate concentration also decreases below
the level expected in compensation for a simple respiratory
alkalosis.
● the defense of pHis enhanced; thus the pH can be normal
or close to normal, with a low Pa CO2 and a low (HCO 3).
 TREATMENT:

- Treatment of Mixed Metabolic Acidosis and Respiratory

Alkalosis should be directed at the underlying cause.
- Because of the enhanced compensation, the pH is usually
closer to normal than in either of the other disorders.
 MIXED METABOLIC ALKALOSIS AND
RESPIRATORY ACIDOSIS
- occurs in patients with COPD and chronic respiratory acidosis
who are treated with salt restriction, diuretics, and possibly
glucocorticoids.
- When diuretics are initiated, plasma HCO3- increases because of
increased renal HCO3- generation and reabsorption = metabolic
alkalosis.
- The elevated pH diminishes respiratory drive and may therefore
worsen the respiratory acidosis.
 TREATMENT:
- treatment is initiated to maintain PaO2 and PaCO2
● NaCl and KCl therapy
○ for renal excretion of retained HCO3- from diuretic induced
metabolic alkalosis.
○ should be used cautiously to avoid exacerbating any
underlying CHF
*observe patient’s response to discontinuation of diuretics and
administration of NaCl and KCl
*PaCO2 will normalize if simple metabolic disorder, while minimally
affected for mixed disorder.
JOURNALS
 Acid-Base Status Disturbances in Patients on
Chronic Hemodialysis at High Altitudes
Background
Acid-base disorders have been previously described in patients with chronic
hemodialysis, with metabolic acidosis being the most important of them; however, little
is known about the potential changes in acid-base status of patients on dialysis living at
high altitudes.

Methods
Cross-sectional study including 93 patients receiving chronic hemodialysis on
alternate days and living in Bogotá, Colombia, at an elevation of 2,640 meters (8,661
feet) over sea level (m.o.s.l.). Measurements of pH, PaCO2, HCO3, PO2, and base
excess were made on blood samples taken from the arteriovenous fistula (AVF) during
the pre- and postdialysis periods in the midweek hemodialysis session. Normal
values for the altitude of Bogotá were taken into consideration for the interpretation of
the arterial blood gases.
Results
43% (n= 40) of patients showed predialysis normal acid-base status. The most
common acid-base disorder in predialysis period was metabolic alkalosis with
chronic hydrogen ion deficiency in 19.3% (n=18). Only 9.7% (n=9) had predialysis
metabolic acidosis. When comparing pre- and post dialysis blood gas analysis, higher
postdialysis levels of pH (7,41 versus 7,50, p<0,01), bicarbonate (21,7mmol/L
versus 25,4mmol/L, p<0,01), and base excess (-2,8 versus 2,4, p<0,01) were
reported, with lower levels of partial pressure of carbon dioxide (34,9 mmHg versus
32,5 mmHg, p<0,01).

Conclusion
At an elevation of 2,640 m.o.s.l., a large percentage of patients are in normal acid-
base status prior to the dialysis session (“predialysis period”). Metabolic alkalosis is
more common than metabolic acidosis in the predialysis period when compared to
previous studies. Paradoxically, despite post dialysis metabolic alkalosis, PaCO2 levels
are lower than those found in the predialysis period.
Background
➢The thesis investigated whether dietary acid load has either short-term (4 to 7 days) or
prolonged (12 weeks) effects on acid-base status at rest and during submaximal and
maximal aerobic exercise;
➢ whether the changes in acid-base balance have a further effect on aerobic exercise
performance.
➢ whether the effects of dietary acid load on acid-base status differ between:
○ adolescents,
○ young adults and the elderly,
○ and between men and women;
Methodology

➢ three different study settings in healthy and recreationally active men and women.
➢ In studies 1 and 2, which followed a crossover study design, participants were
assigned in randomized order to follow a diet with a low or high acid load for 4 or 7
days.
➢ Study 3 was a 12-week longitudinal study in which participants were divided into two
groups of lower and higher acid intake.
➢ Nine 18- to 30-year-old men participated in study 1.
➢ In study 2, 93 men and women were recruited from three age groups: 12 to 15 years,
25 to 35 years and 60 to 75 years.
➢ Forty-nine men and women aged 20 to 50 years participated in study 3.
R
E
S
U
L
T
S
 ➢ The main finding was that dietary acid load has acute and prolonged effects on
C blood and urine acid-base status and may also have effects on exercise
performance.
O ➢ In young and elderly women, in particular, blood was more acidic at rest and during
N submaximal cycling after a 7-day high compared to low acid intake.
➢ In young women, maximal cardiorespiratory measures were lower and time to
C exhaustion shorter after high compared to low acid intake.
L ➢ During exercise, better renal function may be associated with higher bicarbonate ion
availability in blood, which can diminish exercise-induced acidosis and delay fatigue.
U ➢ Moreover, even slightly acidogenic diets combined with regular training may be
accompanied with increased acid load to the body and start to impair kidney
S function.
I ➢ These results emphasize the importance of an adequate intake of fruits and
vegetables as a part of a healthy diet and a physically active lifestyle across the
O lifespan.