Transcript Acid Base Balance

ACID BASE BALANCE
Paula Ruedebusch, ARNP, DNP
ACID-BASE BALANCE

Acid-base balance is carefully regulated to
maintain a normal PH via multiple mechanisms
ACID BASE IMBALANCES

Rare – WHY?

Secondary

ABG needed

Co-exist

Life-threatening
IS PH IMPORTANT?
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Yes!!
pH <6.9 or >7.7: generally incompatible with life
pH determines shape and thus function of many biological
molecules, particularly proteins
Enzymes & ion channels are examples of protein molecules
sensitive to pH (modifies structural bonds, changing shape
and function)
WHERE DOES H+ COME FROM?
 Intake (PO, IV, IM, NG, NJ)
 Food: fatty acids, amino acids
 Drugs : e.g., aspirin, toxins, paraldehyde,
ethylene
glycol, methanol, formaldehyde, others )
 CO2 production:
 CO2 is not an acid
but it combines with water to form
carbonic acid which then dissociates into H+ and
HCO3-
 Metabolic acids:
 Citric acid cycle intermediates (aerobic metabolism)
 Lactic acid (anaerobic metabolism)
 Ketoacids--produced when some fats are
incompletely metabolized.
 Other
organic acid production.
PH
Inverse logarithm of the H+ concentration
 If the H+ are high in number, the pH is low (acidic);
If the H+ are low in number, the pH is high
(alkaline)

PH (CONT’D)
The pH scale ranges from 0 to 14: 0 is very acidic,
14 is very alkaline
 Each number represents a factor of 10


If a solution moves from a pH of 6 to a pH of 5, the H+
have increased 10 times
PH (CONT’D)
Acids are formed as end products of protein,
carbohydrate, and fat metabolism
 To maintain the body’s normal pH (7.35-7.45), the
H+ must be neutralized or excreted
 The bones, lungs, and kidneys are the major
organs involved in the regulation of acid and base
balance

ORGANIC ACID PRODUCTION
 Many
metabolic intermediates are organic acids
(fatty acids, amino acids, citric acid cycle
components, lactic acid produced by anaerobic
metabolism)
Pyruvic acid  pyruvate + H+
 Lactic acid  lactate + H+

 Metabolic
organic acid production can get out
of control, producing an immense acid load
Anerobic metabolism produces lactic acid leading to
lactic acidosis (seen in perfusion & oxygenation
problems)
 Ketoacids from incomplete fat metabolism (diabetes
mellitus, starvation, alcoholism)

ANAEROBIC METABOLISM
Sugar can be burned without oxygen –
anaerobically
 Far more energy is released from burning energy
aerobically
 Glycolysis is anaerobic, and is carried out in the
cytosol

ANAEROBIC METABOLISM
ACID ELIMINATION
Renal elimination in urine
 Respiratory elimination of CO2 (ventilation)
 Emesis/gastric suction
(Buffers keep pH from changing much despite an acid
load)

WHERE DOES BASE COME FROM?
Some foods contain base—not many. Some fruits,
vegetables (broccoli, artichoke, leek, eggplant, others);
they contain an anion that binds H+
 Some drugs contain base (bicarbonate; antacids)

HOW IS BASE ELIMINATED?
There is not normally much base consumption so
most of acid-base balance involves eliminating acid
 Loss of intestinal or colonic fluid results in loss of
base
 Urine can be slightly basic (up to pH 8.0)

PH

1.
2.
3.
MAINTENANCE
How is pH maintained in a narrow range in the face
of great acid intake and production?
Buffers: immediately blunts pH change
Ventilation: rapid response; eliminates 75% of
acid
Renal regulation: slow—takes days
BUFFERING SYSTEMS
A buffer is a chemical that can bind excessive H+
or OH– without a significant change in pH
 Buffers moderate pH change:

If you add H+ to a buffer solution, pH will change less
than one would predict based on the amount of added
H+.
 This is because the buffer has bound up the H+
 Similarly, buffers blunt the effect of added base.

PHYSIOLOGIC BUFFERS
 In
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 In
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 In
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plasma:
HCO3- (goes to H2CO3 then CO2 and H20)
Protein (goes to H+protein compound)
interstitial fluid:
HCO3-
intracellular fluid:
Hemoglobin
Protein
Phosphate
CARBONIC ACID-BICARBONATE PAIR
Operates in the lung and the kidney
 The greater the partial pressure of carbon dioxide,
the more carbonic acid is formed

At a pH of 7.4, the ratio of bicarbonate to carbonic acid
is 20:1
 Bicarbonate and carbonic acid can increase or
decrease, but the ratio must be maintained

CARBONIC ACID–BICARBONATE PAIR
(CONT’D)
If the amount of bicarbonate decreases, the pH
decreases, causing a state of acidosis
 The pH can be returned to normal if the amount of
carbonic acid also decreases


This type of pH adjustment is referred to as
compensation
CARBONIC ACID–BICARBONATE PAIR
(CONT’D)
The respiratory system compensates by increasing
ventilation to expire carbon dioxide or by decreasing
ventilation to retain carbon dioxide
 The renal system compensates by producing acidic or
alkaline urine

COMPENSATION
ACID-BASE IMBALANCES

Normal arterial blood pH
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

Acidosis


7.35 to 7.45
Obtained by arterial blood gas (ABG) sampling
Systemic increase in H+ concentration or decrease in
bicarbonate
Alkalosis

Systemic decrease in H+ concentration or increase in
bicarbonate
ABG NORMS
Lab
Normal Range
pH
7.35 – 7.45
PaO2
80-100
PaCO2
35-45
HCO3
22-26
ACIDOSIS AND ALKALOSIS

Four categories of acid-base imbalances:
Respiratory acidosis—elevation of pCO2 as a result of
ventilation depression
 Respiratory alkalosis—depression of pCO2 as a result
of alveolar hyperventilation
 Metabolic acidosis—depression of HCO3– or an
increase in noncarbonic acids
 Metabolic alkalosis—elevation of HCO3– usually
caused by an excessive loss of metabolic acids

RESPIRATORY ACIDOSIS
RESPIRATORY ACIDOSIS: THE PROBLEM
 Definition:
Alveolar hypoventilation causes
CO2 retention; PaCO2 increases
 Causes:
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suppression of medullary respiratory centers by
drugs (narcotics, sedation, alcohol)
trauma (increased intracranial pressure);
problems with the breathing muscles (paralysis,
anesthesia, weakness) or fatigue;
Thoracic deformities, obesity
Lung problems (COPD, pneumonia, trauma)
RESPIRATORY ACIDOSIS: SIGNS, SYMPTOMS
ABG: acid pH, elevated PaCO2 and HCO3 Observe respiratory symptoms (slow or shallow or
absent breathing)
 Chronic problem: metabolic compensation moves
toward higher HCO3- & higher pH

RESPIRATORY ACIDOSIS: THE COMPENSATION

Increase renal H+ loss and HCO3- retention
RESPIRATORY ACIDOSIS: CLINICAL
MANAGEMENT
Acute problems: increase ventilation (reverse
respiratory suppression, provide mechanical
ventilation, relieve chest wall restriction, restore
muscle function)
 Chronic problems: Support compensation; do not
try to remedy the high HCO3- level; use caution in
administering oxygen; support ventilation

RESPIRATORY ALKALOSIS: DEFINITION &
ETIOLOGY
 Definition:
Alveolar hyperventilation causes
excess CO2 elimination; PaCO2 falls
 Causes:
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Iatrogenic (i.e., caused by care provider: overventilation with mechanical ventilator—can be
accidental or deliberate)
Hypoxemia (induces increased ventilation)
Trauma to medullary respiratory centers
Anxiety, pain
Spontaneous
RESPIRATORY ALKALOSIS - CAUSES
RESPIRATORY ALKALOSIS: SIGNS, SYMPTOMS
alkalotic pH, low PaCO2, low HCO3 Chronic problem: renal compensation
lowers HCO3-; partially corrects pH
 Observe respiratory symptoms
(hyperventilation)
 Irritability
 Paresthesia, cramps, tetany, carpopedal
spasm, Chvostek’s sign, Trousseau’s sign,
cardiac arrhythmias
 ABG:
CHOVSTEK’S SIGN
TROUSSEAU’S SIGN
CHOVSTEK AND TROUSSEAU VIDEO

https://www.youtube.com/watch?v=kvmwsTU0InQ
RESPIRATORY ALKALOSIS: COMPENSATION
Increase renal H+ retention
 This takes several days

RESPIRATORY ALKALOSIS: CLINICAL
MANAGEMENT
 Fix
acute problems: correct hypoxemia, reduce
rate &/or volume of ventilation, relieve anxiety,
relieve pain, etc
 If anxiety related, consider having the patient
breathe with a paper bag over his face—this
causes him to re-breathe some of his exhaled
CO2 and can raise the PaCO2
 Support compensation if needed
RESPIRATORY ALKALOSIS CASE
 Patient
is a 40 y/o female with chronic asthma;
she now has acute pneumonia (lung infection)
 ABG: pH: 7.6; PaCO2: 24; HCO3- 22mEq/l;
hypoxemia
 S/Sx: hands & feet are twitching; reflexes are
abnormally brisk; positive Chvostek sign;
positive Trousseau’s sign
 Dx: acute respiratory alkalosis; no
compensation
 Rx: administer additional inspired O2 to improve
PaO2, eliminating hypoxic drive to overventilate
ETIOLOGY OF METABOLIC ACIDOSIS
Excess GI HCO3- loss (diarrhea, loss of pancreatic
fluid)
 Excess renal HCO3- loss (some types of renal failure)
 Drugs/toxins: amphotericin B, acetozolamide, others

MORE CAUSES OF METABOLIC ACIDOSIS
Lactic acidosis
 Ketoacidosis
 Drugs/toxins: salicylate, ethylene glycol,
paraldehyde
 Rhabdomyolysis

METABOLIC ACIDOSIS: SIGNS, SYMPTOMS
ABG: acid pH, low HCO3-, low or normal PaCO2
 Observe respiratory symptoms (deep/rapid
respirations)
 Headache, lethargy, progresses to coma
 Anorexia, nausea, vomiting, diarrhea
 Cardiac arrhythmias

METABOLIC ACIDOSIS: THE COMPENSATION

Respiratory: reduce PaCO2 by breathing quickly
and deeply
METABOLIC ACIDOSIS:
CLINICAL
MANAGEMENT
 Fix
acute problems: improve perfusion,
reverse hyperglycemia, etc.
 Support compensation: do not try to remedy
the low PaCO2; observe patient closely for
signs of fatigue—this could slow ventilation
and result in a combination of metabolic
acidosis & respiratory acidosis
 If severe, (pH<7.1), administer sodium
bicarbonate intravenously (IV)
METABOLIC ACIDOSIS CASE
 Patient
is 30 y/o previously healthy man, now
hemorrhaging
 Hypotensive; tachycardic
 Inadequate tissue perfusion, thus anaerobic
metabolism
 ABGs: pH: 7.3; PaCO2: 30; HCO3-: 14mEq/l
 Dx: metabolic acidosis; respiratory compensation
 Rx: Correct problem (stop bleeding, correct
hypotension by administering saline/blood
products); support compensation (i.e., allow him
to continue rapid breathing)
METABOLIC ALKALOSIS: DEFINITION &
ETIOLOGY
Definition: Primary increase in plasma [HCO3-]
 Causes:

Loss of H+ (gastric loss, renal loss)
 Gain of HCO3 Contraction alkalosis

METABOLIC ALKALOSIS: SIGNS, SYMPTOMS
alkalotic pH, high HCO3-; high PaCO2
 Observe respiratory symptoms
(hyperventilation)
 Irritability
 Paresthesia, cramps, tetany, carpopedal
spasm
 Hypokalemia & acidic urine if hypovolemic
 ABG:
METABOLIC ALKALOSIS:
CLINICAL
MANAGEMENT
Correct problem
 Support compensation if needed


Compensation = Slowed ventilation: increased
PaCO2
METABOLIC ALKALOSIS CASE
 25
y/o male; 4 day hx of vomiting;
 C/O exhaustion;
 tachycardic, orthostatic hypotension; hypopneic;
brisk reflexes;
 Labs: hypokalemia, hypochloremia; acidic urine
 ABG: pH: 7.5; PaCO2: 48; HCO3-: 36mEq/l
 Dx: metabolic alkalosis, respiratory compensation;
this is “contraction alkalosis” or hypokalemic,
hypochloremic metabolic alkalosis, caused by loss
of GI fluids & sustained by hypovolemia
 Rx: control vomiting; correct saline (extracellular
fluid) deficit; then administer K+; do not try to
increase ventilation
VENTILATION CAN IMPROVE ACID BASE
BALANCE
Ventilation can eliminate metabolically produced
acid (eliminate CO2 thus eliminate acid). This is the
normal way to eliminate 75% of the acid load.
 Ventilation can eliminate excess acid when it is
produced by metabolism or gained. e.g., from
aspirin poisoning. This is called respiratory
compensation for a metabolic acidosis.
 Ventilation can retain acid when the body is too
alkalotic. This is called respiratory compensation for
a metabolic alkalosis.

VENTILATION CAN WORSEN ACID BASE
BALANCE
Decreased ventilation: raises PaCO2; results in
higher H+ levels; called respiratory acidosis
 Increased ventilation: lowers PaCO2; results in
lower H+ levels; called respiratory alkalosis

VENTILATION
High PaCO2 and low PaO2 both stimulate
ventilation
 When PaCO2 rises, this stimulates ventilation; the
patient breathes faster/deeper; this lowers PaCO2
(“blows it off”)
 When PaCO2 is lower than normal, this can inhibit
drive to breathe
 The greater the respiratory rate/depth, the lower will
be the patient’s PaCO2
 The lower the respiratory rate/depth, the higher will
be the patient’s PaCO2

RENAL
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
Kidney normally eliminates about 25% of
the acid load
Filtration: H+ & HCO3- are filtered
Reabsortion & secretion mechanisms:
REMEMBER…
CLEAR YOUR HEAD AND GET READY!
ABGS! ABGS! ABGS!
STEPS FOR ABG ANALYSIS
1.
2.
3.
4.
5.
What is the pH? Acidoticor Alkalotic?
What is the primary disorder present?
Is there appropriate compensation?
Is the compensation acute or chronic?
What is the differential for the clinical processes?
NORMAL ABG VALUES
Lab
Normal Range
pH
7.35 – 7.45
PaO2
80-100
PaCO2
35-45
HCO3
22-26
STEP 1:

Look at the pH: is the blood acidic or alkalemic?

EXAMPLES :

pH: 7.31
 pH: 7.48
 pH: 7.43
STEP 2: WHAT IS THE PRIMARY DISORDER?
What disorder is
present?
pH
PaCO2 or HCO3
Respiratory
Acidosis
Metabolic
Acidosis
pH low
PaCO2 high
pH low
HCO3 low
Respiratory
Alkalosis
pH high
PaCO2 low
Metabolic
Alkalosis
pH high
HCO3 high
ROME
ROME
ROME
STEP 3-4: COMPENSATED VS.
UNCOMPENSATED
 Compensated:
pH is anywhere inside the
normal ranges (Anything between 7.35 to 7.45)
 Uncompensated: pH is anywhere outside the
normal ranges - greater than 7.45 or less than
7.35, and the value (CO2 or HCO3) that does
not match the pH will still be in the normal
range.
 Partially compensated: pH is anywhere outside
the normal ranges, and the value that does not
match the pH will be outside its normal range,
indicating the body is attempting to get the pH
back to normal. For example, if the pH (7.20)
and CO2 (50) are acidotic, the HCO3 should be
on the alkalotic side (27).
TEST YOURSELF!
2. An arterial blood gas value of PaCO2 = 47, pH =
7.30, Bicarbonate = 24 indicates:
A.
B.
C.
D.
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
ABG PRACTICE!

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
pH: 7.40
N
PaCO2: 37 N
HCO3: 23 N
ABG PRACTICE



pH: 7.23
PaCO2: 50
HCO3: 22
N
= Uncompensated
respiratory acidosis
ABG PRACTICE



pH: 7.36
PaCO2: 50
HCO3: 29
N
= Compensated respiratory
acidosis
ABG PRACTICE



pH: 7.50
PaCO2: 18
HCO3: 24 N
= Uncompensated respiratory
alkalosis
ABG PRACTICE



pH: 7.50
PaCO2: 42 N
HCO3: 33
= Uncompensated metabolic
alkalosis
REAL-LIFE IMPORTANCE
QUESTIONS?