2. īĒ Arterial blood gas analysis is an essential part of
diagnosing and managing a patientâs oxygenation
status and acid-base balance.
Introduction
3. īĒ Oxygenation (PaO2). The PaO2 is the amount of oxygen
dissolved in the blood and therefore provides initial information
on the efficiency of oxygenation.
īĒ Ventilation (PaCO2). The adequacy of ventilation is inversely
proportional to the PaCO2 .so that, when ventilation increases,
PaCO2 decreases, and when ventilation decreases, PaCO2
increases.
īĒ Acid-base status (pH, HCO3, and base deficit [BD]). A plasma pH
of >7.4 indicates alkalemia, and a pH of <7.35 indicates acidemia.
Despite a normal pH, an underlying acidosis or alkalosis may still
be present.
Arterial blood gas (ABG) provides an
assessment of the following:
4. īĒ The pH is a measurement of the acidity or
alkalinity of the blood.
īĒ It is inversely proportional to the number of
hydrogen ions (H+) in the blood. The more H+
present, the lower the pH will be.
īĒ Likewise, the fewer H+ present, the higher the pH
will be. The pH of a solution is measured on
a scale from 1 (very acidic) to 14 (very alkalotic).
5. īĒ A liquid with a pH of 7, such as water, is neutral
(neither acidic nor alkalotic).
6. īĒ Acids & Bases
īĒ An acid is usually defined as a chemical species that
can act as a proton (H + ) donor, whereas a base is a
species that can act as a proton acceptor (BrÃļnstedâ
Lowry definitions).
Acids
7. īĒ A strong acid is a substance that readily and almost
irreversibly gives up an H + and increases [H + ],
whereas a strong base avidly binds H + and decreases
[H + ].
Strong acids& base
8. īĒ In contrast, weak acids reversibly donate H + ,
whereas weak bases reversibly bind H + ; both weak
acids and bases tend to have less of an effect on [H +
] (for a given concentration of the parent compound)
than do strong acids and bases.
9. īĒ these are compounds that are only partially ionized in solution
īĒ Physiologically important acids include:
īĒ Carbonic acid (H2CO3)
īĒ Phosphoric acid (H3PO4)
īĒ Pyruvic acid (C3H4O3)
īĒ Lactic acid (C3H6O3)
īĒ These acids are dissolved in body fluids.
īĒ Physiologically important bases include:
īĒ Bicarbonate (HCO3
- )
īĒ Biphosphate (HPO4
-2 )
Weak Acids and Bases:
10. īĒ Normal pH 7.35-7.45
īĒ Narrow normal range
īĒ Compatible with life 6.8 - 8.0
___/______/___/______/___
6.8 7.35 7.45 8.0
Acid Alkaline
Normal Acid-Base Balance
11. īĒ pH is the negative logarithm of the hydrogen
ion concentration ([H]). pH is a convenient
descriptor for power of hydrogen. Normally
the [H] in extacellular fluid is 40 nmol/L, a very
small number. By taking the negative log of
this value we obtain a pH of 7.4.
pH SCALE
pH = -log10(H+)
12. īĒLow pH values = high H+ concentrations
īĒUnit changes in pH represent a tenfold
change in H+ concentrations
īĒ Nature of logarithms
pH SCALE
13. īĒ pH = 4 is more acidic than pH = 6
īĒ pH = 4 has 10 times more free H+ concentration
than pH = 5 and 100 times more free H+
concentration than pH = 6
pH SCALE
ACIDOSIS ALKALOSISNORMAL
DEATH DEATH
Venous
Blood
Arterial
Blood
7.3 7.57.46.8 8.0
15. īĒ Severe acidemia is defined as blood pH <7.20 and is associated
with the following major effects:
1) Impairment of cardiac contractility, cardiac output, and the
response to catecholamines.
2) Susceptibility to recurrent arrhythmias and lowering the
threshold for ventricular fibrillation.
3) Arteriolar vasodilation resulting in hypotension
Major consequences of acidemia.
16. 4) Vasoconstriction of the pulmonary vasculature,
leading to increased pulmonary vascular resistance
5) Hyperventilation (a compensatory response)
6) Confusion, and coma
7) Insulin resistance
8) Inhibition of glycolysis and adenosine triphosphate
synthesis
9) Hyperkalemia as potassium ions are shifted
extracellularly
17. Severe alkalemia is defined as blood pH >7.60 and is
associated with the following major effects:
1. Increased cardiac contractility until pH >7.7, when a
decrease is seen.
2. Refractory ventricular arrhythmias.
3. Coronary artery spasm/vasoconstriction.
4. Vasodilation of the pulmonary vasculature, leading
to decreased pulmonary vascular resistance
Major consequences of alkalemia
18. 5. Hypoventilation (which can frustrate efforts to wean
patients from mechanical ventilation).
6. Cerebral vasoconstriction
7. Neurologic manifestations such as headache,
lethargy, delirium, stupor, tetany, and seizures
8. Hypokalemia, hypocalcemia, hypomagnesemia, and
hypophosphatemia
9. Stimulation of anaerobic glycolysis and lactate
production
19. īĒ pH changes have dramatic effects on normal cell
function
īĒ 1) Changes in excitability of nerve and muscle cells
īĒ 2) Influences enzyme activity
īĒ 3) Influences K+ levels
ACIDOSIS / ALKALOSIS
20. īĒ pH decrease (more acidic) depresses the
central nervous system
īĒ Can lead to loss of consciousness
īĒ pH increase (more basic) can cause over-
excitability
īĒ Tingling sensations, nervousness, muscle twitches
CHANGES IN CELL EXCITABILITY
21. īĒ pH increases or decreases can alter the shape of the
enzyme rendering it non-functional
īĒ Changes in enzyme structure can result in accelerated
or depressed metabolic actions within the cell
INFLUENCES ON ENZYME ACTIVITY
22. īĒ When reabsorbing Na+ from the filtrate of the renal
tubules K+ or H+ is secreted (exchanged)
īĒ Normally K+ is
secreted in much
greater amounts
than H+
INFLUENCES ON K+ LEVELS
K+
K+K+K+K+K+K+
Na+Na+Na+Na+Na+Na+
H+
23. īĒ If H+ concentrations are high (acidosis) than H+ is
secreted in greater amounts
īĒ This leaves less K+ than usual excreted
īĒ The resultant K+ retention can affect cardiac function
and other systems
INFLUENCES ON K+ LEVELS
K+K+K+
Na+Na+Na+Na+Na+Na+
H+H+H+H+H+H+H+
K+K+K+K+K+
25. īĒChemical Buffers
īĒ The body uses pH buffers in the blood to guard against sudden
changes in acidity
īĒ A pH buffer works chemically to minimize changes in the pH of a
solution
ACID-BASE REGULATION
H+
OH-
H+
H+
OH-
OH-
Buffer
26. īĒ Prevent major changes in pH
īĒ Act as spongesâĻ
īĒ 3 main systems
1) Bicarbonate-carbonic acid buffer
2) Phosphate buffer
3) Protein buffer
Buffer Systems
H+
H+
H+
27. īĒ Bicarbonate buffer- most important
Active in ECF and ICF
īĒ Phosphate buffer
Active in intracelluar fluid
īĒ Protein buffer- Largest buffer store
Albumins and globulins
Hemoglobin
Buffer Systems
33. īĒ Respiratory Regulation
īĒ When breathing is increased, the blood carbon
dioxide level decreases and the blood becomes more
basic
īĒ When breathing is decreased, the blood carbon
dioxide level increases and the blood becomes more
acidic
īĒ By adjusting the speed and depth of breathing, the
respiratory control centers and lungs are able to
regulate the blood pH minute by minute
Respiratory Regulation
34. Mechanism of control
īĒ Excretion or retention of
H+ or HCO3
RegulationâĻ.. Slow
īĒ Hours to days to change pH
Renal Regulation
35. īĒ Ratio of 20 to 1 out of balance
īĒ Acidosis (acidemia)
īĒ pH falls below 7.35
īĒ Increase in blood carbonic acid
or
īĒ Decrease in bicarbonate
Acid-Base Imbalances
36. īĒ Alkalosis (alkalemia)
īĒ pH greater than 7.45
īĒ Increase in bicarbonate
or
īĒ Decrease in carbonic acid
Acid-Base Imbalances
37. īĒ Acidosis and Alkalosis can arise in two fundamentally
different ways:
īĒ 1) Excess or deficit of CO2
(Volatile Acid)
īĒ Volatile Acid can be eliminated by the respiratory system
īĒ 2) Excess or deficit of Fixed Acid
īĒ Fixed Acids cannot be
eliminated by the
respiratory system
ACIDOSIS / ALKALOSIS
38. Primary cause or origin:
īĒ Metabolic
Changes brought about by systemic
alterations (cellular level)
īĒ Respiratory
Changes brought about by
respiratory alterations
Acid-Base Imbalances
39. Compensation
īĒ Corrective response of kidneys and/or lungs
Compensated
īĒ Restoration of pH and 20 : 1 ratio
Uncompensated
īĒ Inability to adjust pH or 20 : 1 ratio
Acid-Base Imbalances
40. īĒ Respiratory Acidosis
īĒ Respiratory Alkalosis
īĒ Metabolic Acidosis
īĒ Metabolic Alkalosis
Four Basic Types of Imbalance
41. īĒ Carbonic acid excess
īĒ Exhaling of CO2 inhibited
īĒ Carbonic acid builds up
īĒ pH falls below 7.35
īĒ Cause = Hypoventilation
Respiratory Acidosis
H2CO3
42. īĒ Caused by hypercapnia due to hypoventilation
īĒ Characterized by a pH decrease and an increase in
CO2
RESPIRATORY ACIDOSIS
CO2
CO2
CO2
CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
pH
pH
43. īĒ The speed and depth of breathing control the amount of CO2 in
the blood
īĒ Normally when CO2 builds up, the pH of the blood falls and the
blood becomes acidic
īĒ High levels of CO2 in the blood stimulate the parts of the brain
that regulate breathing, which in turn stimulate faster and
deeper breathing
RESPIRATORY ACIDOSIS
48. RESPIRATORY ACIDOSIS
- therapy required to restore metabolic balance
- lactate solution used in therapy is converted to
bicarbonate ions in the liver
H2CO3 HCO3
-
2 40:
Lactate
Lactate
LIVER
HCO3
-
49. īĒ The treatment of respiratory acidosis aims to improve
the function of the lungs
īĒ Drugs to improve breathing may help people who
have lung diseases such as asthma and emphysema
RESPIRATORY ACIDOSIS
50. īĒ Carbonic acid deficit
īĒ Increased exhaling of CO2
īĒ Carbonic acid decreases
īĒ pH rises above 7.45
īĒ Cause = hyperventilation.
Respiratory Alkalosis
H2CO3
51. īĒ Cause is Hyperventilation
īĒ Leads to eliminating excessive amounts of CO2
īĒ Increased loss of CO2 from the lungs at a rate faster
than it is produced
īĒ Decrease in H+
RESPIRATORY ALKALOSIS
CO2 CO2 CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
CO2
54. īĒ Compensation:
īĒ Problem = excess âblowing offâ of CO2
īĒ Result = decrease in carbonic acid and increase in
HCO3
īĒ Response: Kidney excretes excess bicarbonate
Respiratory Alkalosis
55. īĒ Usually the only treatment needed is to slow down
the rate of breathing
īĒ Breathing into a paper bag or holding the breath as
long as possible may help raise the blood CO2 content
as the person breathes carbon dioxide
back in after breathing it out
RESPIRATORY ALKALOSIS
58. īĒ Decreased CO2 in the
lungs will eventually
slow the rate of
breathing
īĒ Will permit a normal
amount of CO2 to be
retained in the lung
RESPIRATORY ALKALOSIS
59. īĒ Base-bicarbonate deficit
īĒ Low pH (< 7.35)
īĒ Low plasma bicarbonate (base)
īĒ Cause = relative gain in H+
(lactic acidosis, ketoacidosis)
or actual loss of HCO3
(renal failure, diarrhea)
Metabolic Acidosis
60. īĒ Any acid-base imbalance not attributable to CO2
is classified as metabolic
īĒ Metabolic production of Acids
īĒ Or loss of Bases
METABOLIC ACIDOSIS
61. īĒ If an increase in acid overwhelms the
body's pH buffering system, the
blood can become acidic
īĒ As the blood pH drops, breathing
becomes deeper and faster as the
body attempts to rid the blood of
excess acid by decreasing the
amount of carbon dioxide
METABOLIC ACIDOSIS
62. īĒ Eventually, the kidneys also
try to compensate by
excreting more acid in the
urine
īĒ However, both mechanisms
can be overwhelmed if the
body continues to produce
too much acid, leading to
severe acidosis and eventually
a coma
METABOLIC ACIDOSIS
63. īĒ The causes of metabolic acidosis can be
grouped into four major categories
īĒ 1) Ingesting an acid or a substance that is
metabolized to acid
īĒ 2) Abnormal Metabolism
īĒ 3) Kidney Insufficiencies
īĒ 4) Severe Diarrhea
METABOLIC ACIDOSIS
66. īĒ Lactic acidosis, keto acidosis (increase acidâĻ no change
in bicarbonate)
1 10
7.10
Metabolic Acidosis
67. īĒ Compensation:
īĒ Problem = low HCO3 (base) or high H+ ion
(acid)
īĒ Response: Lungs hyperventilate
īĒ Get rid of CO2
(decrease PaCO2 and therefore raise level of
HCO3)
Metabolic Acidosis
68. METABOLIC ACIDOSIS
- bodyâs compensation
- hyperactive breathing to â blow off â CO2
- kidneys conserve HCO3
- and eliminate H+ ions in acidic urine
0.75 10:
CO2
CO2 + H2O
HCO3
- + H+
HCO3
-
+
H+
Acidic urine
69. īĒ Metabolic acidosis may be
treated directly
īĒ If the acidosis is mild,
intravenous fluids and
treatment for the underlying
disorder may be all that's
needed
METABOLIC ACIDOSIS
70. īĒ When acidosis is severe,
bicarbonate may be given
intravenously
īĒ Bicarbonate provides only
temporary relief and may
cause harm
METABOLIC ACIDOSIS
71. METABOLIC ACIDOSIS
- therapy required to restore metabolic balance
- lactate solution used in therapy is converted to
bicarbonate ions in the liver
H2CO3 HCO3
-
0.5 10:
Lactate
Lactate
containing
solution
72. īĒ Bicarbonate excess
īĒ High pH (> 7.45)
īĒ Loss of H+ ion or gain of HCO3
īĒ Most common causes vomiting, gastric
suctioning (NG tube)
īĒ Other: Abuse of antacids, K+ wasting diuretics
Metabolic Alkalosis
73. īĒ Reaction of the body to alkalosis is to lower pH
by:
īĒ Retain CO2 by decreasing breathing rate
īĒ Kidneys increase the retention of H+
METABOLIC ALKALOSIS
CO2
CO2
H+
H+
H+
H+
74. METABOLIC ALKALOSIS
- pH = 7.7
- HCO3
- increases because of loss of chloride
ions or excess ingestion of NaHCO3
1 40:
75. METABOLIC ALKALOSIS
- bodyâs compensation
- breathing suppressed to hold CO2
- kidneys conserve H+ ions and eliminate HCO3
- in
alkaline urine
1.25 30
CO2 + H2O
HCO3
- + H+
HCO3
-
H+
+
Alkaline urine
:
78. īĒ Compensation:
īĒ Problem = too much base
īĒ Response: Lungs compensate by
hypoventilating
īĒ Retain CO2, increase PaCO2
īĒ Increase acid level in blood
Metabolic Alkalosis
80. īĒ pH
īĒ Measurement of acidity or alkalinity, based on the hydrogen (H+)
ions present.
īĒ The normal range is 7.35 to 7.45
īĒ
īĒ PaO2
īĒ The partial pressure of oxygen that is dissolved in arterial blood.
īĒ The normal range is 75 to 100 mm Hg.
īĒ
īĒ SaO2
īĒ The arterial oxygen saturation.
īĒ The normal range is 93% to 100%.
īĒ
īĒ PaCO2
īĒ The amount of carbon dioxide dissolved in arterial blood.
īĒ The normal range is 35 to 45 mm Hg.
īĒ
Components of the Arterial Blood Gas
81. īĒ HCO3
īĒ The calculated value of the amount of bicarbonate in
the bloodstream.
īĒ The normal range is 22 to 26 mEq/liter
īĒ
īĒ B.E.
īĒ The base excess indicates the amount of excess or
insufficient level of bicarbonate in the system.
īĒ The normal range is â2 to +2 mEq/liter.
īĒ (A negative base excess indicates a base deficit in the
blood.)
82. īĒ The anion gap (AG) estimates the presence of unmeasured
anions. Excess inorganic and organic anions that are not readily
measured by standard assays are termed unmeasured anions.
The AG is a tool used to further classify a metabolic acidosis as
an AG metabolic acidosis (elevated AG) or a non-AG metabolic
acidosis (normal AG). This distinction narrows the differential
diagnosis.
īĒ The AG is the difference between the major serum cations and
anions
īĒ that are routinely measured:
īĒ AG = Na-(HCO3+CL)
īĒ A normal value is 12 mEq/L 4 mEq/L.
The anion gap
83. īĒ Nonanion gap metabolic acidosis results from loss of Na and K or
accumulation of Cl. The result of these processes is a decrease in
HCO3:
īĒ Iatrogenic administration of hyperchloremic solutions
(hyperchloremic metabolic acidosis)
īĒ Alkaline gastrointestinal losses
īĒ Renal tubular acidosis
īĒ Ureteric diversion through ileal conduit
īĒ Endocrine abnormalities
MAJOR CAUSES OF A NONANION
GAP METABOLIC ACIDOSIS
88. 4. Determine level of compensation
Has the body tried to readjust the
pH?
īĒ Uncompensated
īĒ Partly compensated
īĒ Compensated
Interpreting ABGs
89. Uncompensated
īĒ pH abnormal (high or low)
īĒ One component abnormal (high or low
CO2 or HCO3)
īĒ The other component is normal
(The component not causing the acid-base
imbalance is still normal)
Interpreting ABGs
90. Partly compensated
īĒ pH not normal (but moving toward normal)
īĒ Both CO2 and HCO3 are outside normal range
īĒ The component that was normal is changing
in order to compensate
91. Compensated
īĒ pH normal
īĒ Other values abnormal in
opposite directions
īĒ One is acidotic the other alkaline
Interpreting ABGs
92. īĒ Determine amount of hypoxemia present
īĒ Normal PaO2 (adults - room air)
īĒ < 70 years = 75-100 mm Hg
70-79 = 70-100 mm Hg
īĒ Drops 10 mm Hg for each decade
Interpreting ABGs
93. īĒ Hypoxemia = < 70 mm Hg
(for adult < 70 years old)
īĒ Mild = 60-75 mm Hg
īĒ Moderate = 40-60 mm Hg
īĒ Severe = < 40 mm Hg
Interpreting ABGs
95. īĒ 80 year old female with severe pneumonia,
fever
īĒ pH = 7.25
īĒ PaCO2 = 55 mm Hg
īĒ HCO3 = 24 mEq/L
īĒ PaO2 = 65 mm Hg
īĒ O2 sat = 80%
Case 1
96. What is the problem?
Acidosis or alkalosis?
Respiratory or metabolic?
Compensated or not?
Level of hypoxemia?
Diagnoses?
Interventions?
Practice Problems
104. īĒ Teach how to relieve/ prevent anxiety
īĒ Calm environment
īĒ Positioning for comfort
īĒ Assist with relaxation techniques
īĒ Protection from injury
īĒ Education re: drug overdose, esp aspirin
Nursing Management
Respiratory Alkalosis
105. īĒ Frequent assessment of vital signs esp respiratory
rate and rhythm (compensatory mechanisms)
īĒ Safety precautions for confusion
īĒ For ketoacidosis, sodium bicarbonate IV
īĒ Education about diabetes
Nursing Management
Metabolic Acidosis
106. īĒ Monitoring LOC and confusion
īĒ Monitor serum electrolytes, ABGâs
īĒ Administer K and Cl replacement as ordered
īĒ Antiemetics to relieve vomiting
īĒ Seizure precautions
īĒ Teaching/monitoring of diuretic therapy
īĒ Referrals re: eating disorders
Nursing Management
Metabolic Alkalosis
107. īĒ Burn patient 70% (2nd & 3rd degree),with respiratory
distress on 2nd day arterial blood sampling shows:
Case 2
108.
109.
110. īĒ According to ABG results so decision for mechanical
support was made.
īĒ CPAP mode was chosen from start then changed to
fully assisted mode (APRV).
īĒ Another sample was drawn from patient`s radial
artery & showed: