Download Egan Ch 13.2 Acid-Base Balance

.
2
A. Electrolytes that ionize in water and
release hydrogen ions are acids; those
that combine with hydrogen ions are
bases.
B. Maintenance of homeostasis depends
on the control of acids and bases in body
fluids.
3
C. Sources of Hydrogen Ions
1.Most hydrogen ions originate as byproducts of metabolic processes
4
Fig18.06
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Aerobic
respiration
of glucose
Anaerobic
respiration
of glucose
Incomplete
oxidation of
fatty acids
Oxidation of
sulfur-containing
amino acids
Hydrolysis of
phosphoproteins
and nucleic acids
Carbonic
acid
Lactic
acid
Acidic ketone
bodies
Sulfuric
acid
Phosphoric
acid
H+
Internal environment
5




Even small hydrogen ion [H+] concentration
changes can cause vital metabolic processes
to fail;
Normal metabolism continuously generates
[H+];
[H+] regulation is of utmost biologic
importance.
Various physiologic mechanisms work
together to keep the [H+] of body fluids in a
range compatible with life.
6



Acid-base balance is what keeps [H+] in normal range
◦ For best results, keeps pH 7.35–7.45
Tissue metabolism produces massive amounts of CO2,
which is hydrolyzed into volatile acid H2CO3
Reaction is catalyzed in RBCs by carbonic anhydrase
Aerobic Metabolism

CO2 + H2O  H2CO3  H+ + HCO3–

(within RBC: H+ + Hb  HHb)
7
◦ The hemoglobin in the erythrocyte (RBC)
immediately buffers the H+, causing no
change in the pH: Isohydric buffering
◦ Lungs eliminate CO2; falling CO2 reverses
Reaction:
Ventilation
↑
CO2 + H2O  H2CO3  H+ + HCO3–
↑
HHb → H+ + HCO3–
8
Bicarbonate & NonBicarbonate buffer
systems
◦ Bicarbonate: composed of HCO3– and H2CO3
 Open system as H2CO3 is hydrolyzed to CO2
 Ventilation continuously removes CO2
preventing equilibration, driving reaction to
the right:
HCO3– + H+ → H2CO3 → H2O + CO2
 Removes vast amounts of acid from body per
day
9

Bicarbonate & Nonbicarbonate buffer
systems (cont.)
◦ Nonbicarbonate: composed of phosphate &
proteins
 Closed system: All the components remain in the
system; no gas to remove acid by ventilation
 Hbuffer/buffer– represents acid & conjugate base
 H+ + buffer– ↔ Hbuf reach equilibrium, buffering
stops
10
.
11

Describes [H+] as ratio of
[H2CO3]/ [HCO3–]
◦ pH is logarithmic
expression of [H+].
◦ 6.1 is the log of the H2CO3
equilibrium constant
◦ (PaCO2 × 0.03) is in
equilibrium with, & directly
proportional to blood
[H2CO3]

Blood gas analyzers
measure pH & PaCO2;
then use H-H equation to
calculate HCO3–
12


The ratio between the plasma [HCO3-] and
dissolved CO2 determines the blood pH,
according to the H-H equation.
A 20:1 [HCO3-]/dissolved CO2 ratio always
yields a normal arterial pH of 7.40
13
Bicarbonate buffer system
◦ HCO3– can continue to buffer H+ as long as
ventilation is adequate to exhale CO2:
H+ + HCO3–
Ventilation

→ H2CO3 → H2O + CO2
 In hypoventilation, H2CO3 accumulates;
only the Nonbicarbonate system can serve
as buffer
14
NonBicarbonate buffer system:
◦ Can buffer any fixed or volatile acid;
◦ As closed system, products of buffering
accumulate & buffering may slow or or reach
equilibrium:
(H+ + Buf- ↔ HBuf).
◦ HCO3– and buf– exist in same blood system
Ventilation

Open: H+ + HCO3– → H2CO3 → H2O + CO2
Closed: Fixed acid → H+ + Buf- ↔ HBuf
15
Open System
 Bicarbonate:
oPlasma
oErythrocyte
Closed System
 NonBicarbonate:
o Hemoglobin
o Organic Phosphates
o Nonorganic Phosphates
o Plasma Proteins
.
Classification of Whole Blood Buffers
16

Lungs:
◦ Excrete CO2, which is in equilibrium with
H2CO3
◦ Crucial: body produces huge amounts of
CO2 during aerobic metabolism
(CO2 + H2O → H2CO3)
◦ In addition, through HCO3– , fixed acids are
eliminated indirectly as byproducts CO2 &
H2O
17

Kidneys
◦ Physically remove H+ from body
◦ Excrete <100 mEq fixed acid per day
◦ Also control excretion or retention of HCO3–
◦ If blood is acidic, then more H+ are
excreted & all HCO3– is retained.
◦ If blood is alkaline, then more HCO3– are
excreted & H+ is retained.
◦ While lungs can alter [CO2] in seconds,
kidneys require hours/days to change
HCO3– & affect pH
18



The lungs regulate the volatile acid content
(CO2) of the blood, while the kidneys regulate
the fixed acid concentration of the blood
In the OPEN bicarbonate buffer system, H+ is
buffered to form the volatile acid H2CO3,
which is exhaled as CO2 into the atmosphere.
In the CLOSED nonbicarbonate buffer system,
H+ is buffered to formed fixed acids which
accumulate in the body.
19

Primary respiratory disturbances:
◦ PaCO2 is controlled by the lung, changes
in pH caused by PaCO2 are considered
respiratory disturbances
 Hyperventilation lowers PaCO2, which
raises pH; referred to as respiratory
alkalosis
 Hypoventilation (PaCO2) decreases
the pH; called respiratory acidosis
20
 Primary metabolic disturbances
◦ Involve gain or loss of fixed acids or HCO3–
◦ Both appear as changes in HCO3– as changes in
fixed acids will alter amount of HCO3– used in
buffering
21
Fig18.12
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Kidney failure
to excrete acids
Excessive production of acidic
ketones as in diabetes mellitus
Accumulation of nonrespiratory acids
Metabolic acidosis
Excessive loss of bases
Prolonged diarrhea
with loss of alkaline
intestinal secretions
Prolonged vomiting
with loss of intestinal
secretions
22

Primary metabolic disturbances (cont.)
◦ Decrease in HCO3– results in metabolic acidosis
◦ Increase in HCO3– results in metabolic alkalosis

Compensation: Restoring pH to
normal
◦ Any primary disturbance immediately
triggers compensatory response
 Any respiratory disorder will be compensated
for by kidneys (process takes hours to days)
 Any metabolic disorder will be compensated for
by lungs (rapid process, occurs within minutes)
23

Compensation: Restoring pH to normal
(cont.)
◦ Respiratory acidosis (hypoventilation)
 Renal retention of HCO3– raises pH toward
normal
◦ Respiratory alkalosis
 Renal elimination of HCO3– lowers pH toward
normal
◦ Metabolic acidosis
 Hyperventilation ↓CO2, raising pH toward
normal
◦ Metabolic alkalosis
 Hypoventilation ↑CO2, lowering pH toward
normal
24
Respiratory acidosis (alveolar
hypoventilation):
◦ Any process that raises PaCO2 > 45 mm Hg
& lowers pH below 7.35
 Increased PaCO2 produces more carbonic
.
acid
.
◦ Causes:
 Anything that results in VA that fails to
eliminate CO2 equal to VCO2
25
Respiratory alkalosis (alveolar
hyperventilation):
◦ Lowers arterial PaCO2 decreases carbonic acid, thus
increasing pH
◦ Causes (see Box 13-4 in Egan)
.
 Any process that increases
. VA so that CO2 is eliminated at
rate higher than VCO2.
 Most common cause is hypoxemia
 Other causes: Anxiety, fever, pain
◦ Clinical signs: early Paresthesia; if severe, may have
hyperactive reflexes, tetanic convulsions, dizziness
26
Fig18.13
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• Anxiety
• Fever
• Poisoning
• High altitude
Hyperventilation
Excessive loss of CO2
Decrease in concentration of H2CO3
Decrease in concentration of H+
Respiratory alkalosis
27

Respiratory alkalosis (cont.)
◦ Compensation is by renal excretion of
HCO3–
 Partial compensation returns pH toward
normal
 Full compensation returns pH to high
normal range
◦ Correction
 Involves removing stimulus for
hyperventilation
 i.e., hypoxemia: give oxygen therapy
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Acid-Base Balance Part 2
29
 Metabolic
acidosis
◦ Low HCO3–, with a low pH
◦ Causes:
 Increased fixed acid accumulation
 Lactic acidosis in anaerobic
metabolism
 Excessive loss of HCO3–
 Diarrhea
 Anion gap can help identify cause
30

Increased anion gap metabolic
acidosis
◦ Normal anion gap = 9 to 14 mEq/L
◦ As fixed acids increase, they dissociate & H+ binds
with HCO3–, leaving unmeasured anion behind,
Increasing anion gap

Normal anion gap metabolic acidosis
◦ HCO3– loss does not cause increased gap
 As HCO3– is lost, it is offset by gain in Cl–
 Also called hyperchloremic acidosis
31
32
Compensation for metabolic acidosis
◦ Hyperventilation is main compensatory
.
mechanism
 Acidosis activates CNS receptors, signaling need to
increase VE
◦ Compensation happens very quickly
 Lack of compensation implies ventilatory defect
◦ Symptoms
 Patients often complain of dyspnea due to
hyperpnea
 Kussmaul’s respiration seen with Ketoacidosis
 Neurologic response may range from lethargy to
coma
33
What would the anion gap be for a metabolic
acidosis caused by the loss of bicarbonate
(HCO3– )?
a.
b.
c.
d.
12-16 mEq/L
3-6 mEq/L
9-14 mEq/L
6-10 mEq/L
34
c.. 9-14 mEq/L
35

Medical intervention to correct
metabolic acidosis:
◦ If pH is >7.2, no correction is required
 Hyperventilation usually brings it above this level
◦ pH below 7.2 can cause serious cardiac
arrhythmias
 In severe acidosis, treat with IV NaHCO3
36
Calculate the anion gap for a patient with the
following electrolytes results: 160 mEq/L for Na+,
108 mEq/L or Cl–, and 27 mEq/L for HCO3– .
a.
b.
c.
d.
11 mEq/L
25 mEq/L
8 mEq/L
30 mEq/L
37
Anion Gap =
=
=
=
[Na+] – ([Cl-] + [HCO3-])
160 – (108 + 27)
160- 135
25
38
Metabolic alkalosis:
◦ Increased [HCO3–], with elevated pH
◦ Causes:
 Due to increased buffer base or
loss of fixed acids
 Loss of fixed acids occurs during
vomiting (HCl)
 Often, it is iatrogenic due to
diuretic use or gastric drainage
39
Metabolic alkalosis
◦ Compensation
 Hypoventilation, despite ensuing hypoxemia
 Metabolic alkalosis blunts hypoxemic stimulation
of ventilation
 PaO2 as low as 50 mm Hg with continued
compensation
◦ Correction
 Restore normal fluid volume, K+, and Cl– levels
 In severe alkalosis, may give dilute HCl in central
line
40
If an anion gap yields a result of 25 mEq/L, what
can be done for the patient to bring the anion gap
back to normal?
a.
b.
c.
d.
treat with intravenous NaHCO2
hypoventilation is required
hyperventilation is required
restrict fluid intake
41
a. treat with intravenous NaHCO2
42

Metabolic acid-base indicators:
◦ Standard bicarbonate
 Attempts to eliminates influence of
CO2 on HCO3–
 In blood gas machine, plasma [HCO3–]
is measured after equilibration to
PaCO2 40 mm Hg
 Flawed process as cannot mimic invivo conditions
43
44
45
46
47
 Mixed
acid-base states
◦ Primary respiratory & primary metabolic
disorders occurring simultaneously
 i.e., pH 7.62, PaCO2 32, HCO3– 29
 High pH caused by low PaCO2 & high
HCO3– : combined alkalosis
 Compensation is not possible
48
a.
b.
c.
d.
PaCO2>45 mmHg and pH<7.35
PaCO2<45 mmHg and pH>7.45
HCO2>26 mEq/L and pH>7.45
HCO3–<22 mEq/L and pH<7.35
49
a. PaCO2>45 mmHg and pH<7.35
50
a.
b.
c.
d.
Kidneys and Lungs
Lungs and Spleen
Heart and Liver
Gallbladder and Appendix
51
a. Kidneys and Lungs

The carbonic acid concentration is controlled by the
amount of carbon dioxide excreted by the lungs. The
bicarbonate concentration is controlled by the
kidneys, which selectively retain or excrete
bicarbonate in response to the body's needs.
52
a.
b.
c.
d.
Carbonic acid deficit
Bicarbonate deficit
Bicarbonate excess
Carbonic acid excess
53
d. Carbonic acid excess
An excess of carbon dioxide (hypercapnia) can cause
carbon dioxide narcosis. In this condition, carbon
dioxide levels are so high that they no longer stimulate
respirations but depress them.
54
a.
b.
c.
d.
Carbonic acid deficit
Bicarbonate deficit
Bicarbonate excess
Carbonic acid excess
55
a. Carbonic acid deficit
Excessive pulmonary ventilation decreases hydrogen ion
concentration and thus causes respiratory alkalosis. It can
become dangerous when it leads to cardiac dysrhythmias
caused partly by a decrease in serum potassium levels.
56
a.
b.
c.
d.
Carbonic acid deficit
Bicarbonate deficit
Bicarbonate excess
Carbonic acid excess
57
b. Bicarbonate deficit
The body compensates by using body fat for energy,
producing abnormal amounts of ketone bodies. In an
effort to neutralize the ketones and maintain the acidbase balance of the body, plasma bicarbonate is
exhausted. This condition can develop in anyone who
does not eat an adequate diet and whose body fat must
be burned for energy. Symptoms include headache and
mental dullness.
58
a.
b.
c.
d.
Carbonic acid deficit
Bicarbonate deficit
Bicarbonate excess
Carbonic acid excess
59
c. Bicarbonate excess
In metabolic alkalosis, breathing becomes depressed in
an effort to conserve carbon dioxide for combination
with water in the blood to raise the blood level of
carbonic acid. Symptoms include confusion,
dizziness, numbness or tingling of fingers or toes.
60
a. True
b. False
61
a. True
ABG's are useful in identifying the cause and extent
of the acid-base disturbance and in guiding and
monitoring treatment.
62
a. True
b. False
63
b. False
The major effect is a depression of the central nervous
system, as evidenced by disorientation followed by
coma.
64
a. True
b. False
65
a. True
b.
The muscles may go into a state of tetany and
convulsions.
66
a. True
b. False
67
b. False
Acids are substances having one or more hydrogen
ions that can be liberated into a solution.
Bases are substances that can bind hydrogen ions in
a solution.
68
Case Study 1. A 60 year old man with a history
of COPD presents to the emergency
department with increasing shortness of
breath, pyrexia, and a cough productive of
yellow-green sputum. He is unable to speak in
full sentences. His wife says he has been
unwell for two days. On examination, a
wheeze can be heard with crackles in the
lower lobes; he has a tachycardia and a
bounding pulse. Measurement of arterial
blood gas shows pH 7.20, PaCO2 70 mm Hg,
HCO3- 27 mmol/L, and PaO2 59 mm Hg. How
would you interpret this?
.
.
69
Answer
 This patient has respiratory acidosis (raised
carbon dioxide) resulting from an acute
exacerbation of COPD, with no apparent
compensation. He is in type II respiratory
failure as he is both hypoxemic and
hypercapnic. He should be treated with
bronchodilators, oral steroids, antibiotics, and
controlled oxygen. Most patients can be
treated safely with oxygen, but a few with
COPD rely on their hypoxic drive to breathe.
Take care when giving them oxygen, and
remember to recheck their ABG’s. If the
.
patient does not improve, he or she may
.
require assisted ventilation either noninvasively with a mask or invasively after
sedation and endotracheal intubation.
70
Case study 2. A six year old boy is taken to the
emergency department with vomiting and a
decreased level of consciousness. His
breathing is slow and deep (Kussmaul's
breathing), and he is lethargic and irritable in
response to stimulation. He appears to be
dehydrated—his eyes are sunken and mucous
membranes are dry—and he has a two week
history of polydipsia, polyuria, and weight
loss. Measurement of arterial blood gas shows
pH 7.20, PaO2100 mm Hg, PaCO2 25 mm Hg,
and HCO3- 10 mmol/L; other results are
Na+ 126 mmol/L, K+ 5 mmol/L, and Cl- 95
.
mmol/L. What is your assessment?
.
71
Answer



The boy has diabetes mellitus. These results show
that he has metabolic acidosis (low HCO3 -) with
respiratory compensation (low CO2). He has an
increased anion gap (26 mm Hg). Sometimes the
anion gap in patients with diabetic ketoacidosis is
less than expected as a result of urinary excretion
of ketone bodies and metabolic alkalosis
associated with the vomiting.
This patient should be treated in the pediatric
intensive care unit. He should be given
intravenous fluids, insulin by infusion, and
potassium replacement, and he may need cardiac
monitoring.
Metabolic acidosis has many causes, and the anion.
gap can be used to help differentiate between the .
causes. An increase in anion gap occurs when
there is increased production of organic acids,
such as ketones and lactic acid, or reduced
excretion of them.
72
Case study 3. A 12 year old girl attends the
emergency department after falling and
hurting her arm. In triage she is noted to be
tachycardic and tachypneic. She is given some
pain killers. While waiting to be seen by the
doctor, she becomes increasingly hysterical,
complaining that she is still in pain and now
experiencing muscle cramps, tingling, and
paraesthesia. Measurement of arterial blood
gas shows pH 7.5, PaO2 115 mm Hg,
PaCO2 29 mm Hg, and HCO3- 24 mmol/L.
What does this mean?
.
.
73
Answer








The primary disorder is acute respiratory alkalosis (low CO2) due
to the pain and anxiety causing her to hyperventilate. There has
not been time for metabolic compensation. She should be treated
with a stronger analgesic and given reassurance to slow down her
breathing. Some people breathe in and out of a paper bag so that
CO2 is reinhaled and PaCO2 is brought back to normal.
Note that muscle cramps, tingling, and Paresthesia are caused by
low serum calcium, which results from the low H+ ion
concentration (increased pH) promoting an increased binding of
calcium to proteins and a reduction in ionized serum calcium.
Respiratory alkalosis results from hyperventilation. There are
many causes, such as:
Lung disorders—pneumonia, pulmonary embolism, pulmonary
edema
Hypoxia—anemia, high altitude, right to left cardiac shunt
Central nervous system disorders—meningitis
Psychogenesis—pain and anxiety
Drugs—catecholamines, theophylline, and early stage of
.
salicylates overdose.
.
74
Case study 4. An 80 year old woman
presents with a two day history of
persistent vomiting. She is lethargic and
weak and has myalgia. Her mucous
membranes are dry and her capillary
refill takes >4 seconds. She is diagnosed
as having gastroenteritis and
dehydration. Measurement of arterial
blood gas shows pH 7.5, PaO2 85 mm
Hg, PaCO2 45 mm Hg, and HCO3- 37
mmol/L. What acid-base disorder is
shown?
.
.
75
Answer
The primary disorder is metabolic alkalosis (high
HCO3-). As CO2 is the strongest driver of respiration, it
generally will not allow hypoventilation as
compensation for metabolic alkalosis. The patient
should be treated with normal saline and an
appropriate amount of KCl, which should be delivered
slowly, to expand the extracellular fluid volume.[1] As
the body rehydrates, the kidneys will excrete the
excess HCO3- and correct the alkalosis.
Metabolic alkalosis is most commonly associated with:
 Loss of gastric acid from vomiting
 Diuretic—hypokalemia
 Burns—due to volume depletion
 Antacid overdose
.
 Primary hyperaldosteronism.
.
76
